McKown v. Secretary of Health and Human Services ( 2019 )

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 15-1451V
(to be published)
*************************
* Special Master Corcoran
*
CAILEN MCKOWN, *
* Filed: July 15, 2019
Petitioners, *
* Entitlement Decision; Human
v. * Papillomavirus (“HPV”) Vaccine;
* Postural Orthostatic Tachycardia
SECRETARY OF HEALTH AND * Syndrome (“POTS”); Eczema;
HUMAN SERVICES, * Autoimmune Diseases
*
Respondent. *
*
*************************
Clifford J. Shoemaker, Shoemaker, Gentry & Knickelbein, Vienna, VA, for Petitioner.
Debra A. Filteau Begley, U.S. Dep’t of Justice, Washington, DC, for Respondent.
DECISION DENYING ENTITLEMENT1
On December 1, 2015, Cailen McKown filed a Petition under the National Vaccine Injury
Compensation Program (the “Vaccine Program”2), alleging that two doses of the Human
Papillomavirus (“HPV”) vaccine she received on March 20, 2013, and September 3, 2013,
respectively, along with a Hepatitis A vaccine received on March 20, 2013, caused her to suffer
postural orthostatic tachycardia syndrome (“POTS”) and skin rashes (including eczema). Petition
(ECF No. 1) (“Pet.”) at 1-2.
1
This Decision will be posted on the United States Court of Federal Claims’ website in accordance with the E-
Government Act of 2002, 44 U.S.C. § 3501 (2012). This means the Decision will be available to anyone with access
to the internet. As provided by 42 U.S.C. § 300aa-12(d)(4)(B), however, the parties may object to the published
Decision’s inclusion of certain kinds of confidential information. Specifically, under Vaccine Rule 18(b), each party
has fourteen (14) days within which to request redaction “of any information furnished by that party: (1) that is a trade
secret or commercial or financial in substance and is privileged or confidential; or (2) that includes medical files or
similar files, the disclosure of which would constitute a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b).
Otherwise, the entire Decision will be available to the public in its current form. Id.
2
The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,
100 Stat. 3755 (codified as amended at 42 U.S.C. §§ 300aa-10–34 (2012)) (hereinafter “Vaccine Act” or “the Act”).
All subsequent references to sections of the Vaccine Act shall be to the pertinent subparagraph of 42 U.S.C. § 300aa.
A hearing in this matter was held on September 26-27, 2018. After consideration of the
record and testimony provided at hearing, I find that Petitioner is not entitled to a compensation
award. As discussed in more detail below, Petitioner has not demonstrated with reliable scientific
and medical evidence that the HPV or Hep A vaccines could be, or were, causative of her POTS
(or worsening of POTS or her preexisting eczema/skin symptoms). Petitioner’s experts failed to
offer a persuasive, reliable medical theory in support of her claim, and were unpersuasive in their
attempt to establish that Petitioner’s POTS was the rare neuropathic variant that could be
autoimmune in nature.
I. Factual Background
Pre-Vaccine Health History
Ms. McKown was born on January 14, 2000, and received routine vaccinations throughout
her childhood without any reported adverse events. Ex. 1 at 13-14. Her medical history was
significant for eczema (treated with Elidil), diffuse dry skin, and recurrent fever blisters, which
she experienced one to three times per month since the age of six months. Id. at 32-34 (12/1/2010
ten-year-old well-adolescent visit), 36 (2/25/2011 eleven-year-old well-adolescent visit), 38.
Around the time Petitioner received the first dose of the HPV vaccine, she had already
displayed symptoms pertaining to the injuries at issue in this case, in addition to eczema. Thus, on
March 20, 2013, at Petitioner’s thirteen-year-old well-child visit, her mother, Mrs. Tabatha
McKown, reported to treaters that Petitioner had recently experienced lightheadedness with
position changes and two episodes of syncope in the prior three months, both associated with
position changes and without heart palpitations. Ex. 1 at 44. Ms. McKown’s history of dry skin
was also noted, but she was otherwise deemed to be well. Id. The pediatrician’s impression was
neurocardiogenic syncope, and Petitioner was told to increase fluids and salt in her diet, with a
referral to a cardiologist to follow up on the possible cause of these symptoms. Id.
Receipt of HPV Vaccine Doses
Petitioner received the first HPV vaccine dose (along with the Hep A vaccine) on March
20, 2013, at the aforementioned well-child visit. Ex. 1 at 14, 44. No adverse reaction was noted at
the time, and there is no recorded instance of any reaction to the first HPV dose within a month of
its administration. Then, on April 26, 2013 (about five weeks following vaccination), emergency
medical service providers transported Ms. McKown to the emergency room at Eastside Medical
Center in Snellville, Georgia, from a local yogurt shop, where, following an upset stomach, she
had stood up and then immediately began feeling lightheaded, along with a severe headache. Ex.
2
8 at 6-16. Petitioner passed in and out of consciousness for brief intervals several times, and she
was hyperventilating when EMS responders arrived. Id. at 6, 12.
At Eastside Medical Center, the treating ER physician noted that Ms. McKown had
reportedly experienced similar symptoms in the past, observing that she had been recently advised
by her primary care physician (“PCP”) to follow up with a cardiologist. Ex. 8 at 6, 12. Laboratory
results, an EKG,3 and a head CT scan4 were normal, with the exception of revealing left sphenoid
sinus disease. Id. at 8-10, 24-25. The ER physician diagnosed Petitioner with sinusitis (which he
noted could explain her headaches and dizziness), and vasovagal syncope, discharging her that
same day. Id. at 10.
Three days later Ms. McKown followed up with her PCP, Dr. Melissa Magill. Ex. 1 at 47.
Petitioner’s mother recounted Petitioner’s recent syncope symptoms at the yogurt shop, noting that
she had been “lightheaded” and “woozy,” and “trembly,” but not jerking, drifting in and out of
consciousness for five to ten minutes. Id. Following an exam, Dr. Magill assessed Petitioner with
a “known history of neurocardiogenic syncope[,]” and recommended that she increase fluid and
salt intake. Id.
Cardiology Assessment
On May 1, 2013, Ms. McKown saw Dr. Kenneth Dooley, a cardiologist at Sibley Heart
Center in Atlanta. Ex. 7 at 5-7. Dr. Dooley noted that Petitioner reported having passed out a total
of two to five times previously, most recently the week before. Id. Petitioner provided some
additional details about the circumstances of three of the times she had experienced syncope: first,
three years prior after her father had reprimanded her for poor behavior; second, approximately
six months prior while watching a veterinary procedure; and third, five days prior, in the yogurt
shop incident. Id. at 5. She also stated that she felt that her symptoms were worsening. Id. Upon
exam, Dr. Dooley noted that Petitioner almost passed out when asked to sit up. Id. at 6. Her supine
blood pressure was noted to be 104/64 (heart rate: 68), and her standing blood pressure was 90/52
3
An EKG (or “electrocardiogram”) is a noninvasive graphic tracing that records the electrical activity of the heart
muscle. Dorland’s Illustrated Medical Dictionary 597, 599 (32nd ed. 2012) (hereinafter Dorland’s). Each beat of the
heart is triggered by an electrical impulse (generated from cells in the heart), and the EKG records the timing and
strength of these signals. See Electrocardiogram, Mayo Clinic, https://www.mayoclinic.org/tests-
procedures/ekg/about/pac-20384983 (last accessed on June 19, 2019). EKGs are used to detect or diagnose common
heart problems (including irregular heart rhythm, blocked arteries, structural problems, heart attacks, or heart disease).
Id.
4
A CT (or “computerized tomography”) scan combines a series of X-rays taken from different angles around the body
and uses computer processing to create cross-sectional images of the bones, blood vessels, and soft tissues inside the
body. See CT Scan, Mayo Clinic, https://www.mayoclinic.org/tests-procedures/ct-scan/about/pac-20393675 (last
accessed on July 19, 2019). CT images are more detailed than a plain X-ray. Id. This type of scan is used to quickly
examine patients who may have wide-spread internal injuries, and can be used to diagnose or monitor diseases such
as cancer, heart disease, lung nodules, and liver masses. Id.
3
with a pulse of 100. Id. Dr. Dooley diagnosed her with “syncope, possibly vasovagal in origin[,]”
noting that her history and symptoms were most suggestive of simple fainting. Id. He scheduled
Petitioner for a tilt table test5 and recommended she be screened for epilepsy as well. Id.
Petitioner had a follow up appointment with Dr. Dooley two months later, on July 1, 2013.
Dr. Dooley noted that the tilt table test conducted in late May 2013 had been positive for POTS.
Ex. 7 at 8-9; see also Ex. 55. Orthostatic readings taken in conjunction with the test revealed a
significant increase in heartrate (when tilted from the supine position to the standing position),
followed by complaints of dizziness and blurry vision (after approximately eight minutes at
standing). Ex. 55 at 5. Ms. McKown’s blood pressure then dropped significantly (minimum cuff
pressure of 57/32) and her heartrate slowed significantly (into the low fifties) as the tilt returned
to flat. Id. Within five minutes after returning to the supine position, her rates returned to normal.
Id. Dr. Dooley discussed the results of the test, and noted that Petitioner continued to have short
syncopal episodes. Ex. 7 at 8-9. He prescribed Fludrocortisone (0.1 mg, once daily) in addition to
the Valtrex she was currently taking. Id. Dr. Dooley also advised Petitioner to return in six months
(or sooner if the medication did not work), and to have her mother notify him if she experienced
additional episodes. Id.
Repeated Skin-Related Symptoms
A week later, on July 8, 2013, Petitioner’s mother called Dr. Dooley’s office to report that
Petitioner had stopped taking Fludrocortisone, thinking it had caused her to develop a rash and
hives, although these symptoms resolved on their own after treatment with Benadryl. Ex. 7 at 33.
A week later, Petitioner’s mother called again to report that her hives had returned after she drank
a large glass of milk, causing Petitioner’s PCP to diagnose her with a dairy allergy. Id. at 31. Notes
from the telephone call also indicated that Ms. McKown’s PCP suspected her pre-existing eczema
may have been a manifestation of her dairy allergy. Id. Petitioner thereafter restarted
Fludrocortisone, with no initial notable problems at that time. Id. On July 23, 2013, however, her
mother called a third time to report that Petitioner was now suffering from worsening headaches,
and was not “feel[ing] like herself” (i.e., “feeling very tense”), although without any repeat
syncopal episodes. Id. at 30. Dr. Dooley recommended that Ms. McKown start Midodrine as an
alternative to Fludrocortisone. Id.
Petitioner went back to her PCP at Lawrenceville Pediatrics on July 25, 2013, now
complaining of worsening eczema, a rash on her neck, back, and arms, and insect bites. Ex. 1 at
5
A tilt table test is used to evaluate syncope by measuring heart rate and blood pressure in response to the body’s
change in position. Tilt Table Test, Mayo Clinic, https://www mayoclinic.org/tests-procedures/tilt-tabletest/about/pac-
20395124 (last accessed July 5, 2019). The patient begins by lying flat on a table for around 15 minutes. Id. The table
is then quickly tilted upright to change the body’s position from lying down to standing up. Id. The table generally
remains upright for 45 minutes to allow the doctor to monitor the patient's cardiovascular response. Id.
4
50. The pediatric nurse practitioner noted that Ms. McKown’s eczema flared when the weather
was hot, causing her to feel itchy and scratch her skin. Id. It was also noted that Petitioner had been
diagnosed with POTS recently and was waiting to see an electrophysiologist. Id. The nurse
practitioner advised Petitioner to see an allergist, and recommended treatment with various over-
the-counter antihistamines and ointments. Id. A few weeks later, on September 3, 2013, Petitioner
presented again to Lawrenceville Pediatrics with complaints relating to a sore throat and
congestion. Id. at 15-17. She was diagnosed with sinusitis, and now received her second HPV
vaccine dose, with no noted adverse reaction. Id. at 17.
Progression of Skin Symptoms and Efforts to Treat Them
In the ensuing months in the fall of 2013, Ms. McKown’s skin condition continued to
worsen. In November 2013, she had four dermatology appointments at Georgia Skin Cancer and
Aesthetic Dermatology in Athens, Georgia, for treatment of an itchy rash all over her body that
was reported to have been present for months. Ex. 2 at 11-12, 13-16, 20, 25-26. Following
examination, the treating dermatologist (Dr. Jeffrey Moulton) diagnosed her with atopic and
contact dermatitis and eczema. Id. at 25-26. Dr. Moulton recommended that Petitioner take
Clobetasol and/or Vaseline to mitigate her symptoms (in addition to avoiding strong cleansers,
scented detergents, and excessive hand washing). Id. at 25. Patch testing was also performed,
which was positive for numerous chemicals. Id. at 11-12, 13-16, 20. No instances of syncope or
POTS-related symptoms are reported in the medical records from this time period, however, and
Ms. McKown was noted to be alert, oriented, and in “no acute distress.” Id. at 11, 13, 25-26.
One month later, on December 4, 2013, Ms. McKown sought yet another opinion regarding
her skin condition. She presented to Dr. Deidre Crocker, at the Allergy & Asthma Center of
Conyers in Monroe, Georgia, complaining of worsening eczema and a rash. Ex. 3 at 2-4. At this
visit, Petitioner informed Dr. Crocker that she had always had mild eczema, but that her symptoms
had worsened in May 2013 – around the same time she was diagnosed with POTS. Id. at 2. The
rash was aggravated by hot water and sweat, and a variety of treatments (steroid injections,
Benadryl, and changes in shampoos/lotions) had proven ineffective. Id. Increased itching was also
noted with ingestion of wheat products. Id.
On exam, Petitioner displayed multiple scaly, red eczema patches on the neck, arms, and
trunk. Ex. 3 at 2-3. Her diagnosis remained “contact dermatitis and other eczema, due to
unspecified cause.” Id. at 3. Dr. Crocker expressed the view, however, that Ms. McKown’s skin
condition was likely not related to POTS. Id. at 4 (“POTS is not an immune disease so do not feel
that is triggering eczema but possible she has had some st[r]essors contributing to increased
eczema . . . [a]lso possible she may have developed some allergic sensitivities triggering her
eczema”). Id. She advised Petitioner to avoid a number of dermatitis allergens, and prescribed
Mometasone cream. Id.
5
Ms. McKown had a follow-up appointment with Dr. Crocker two weeks later, on
December 19, 2013. It was reported at this time that her eczema had improved, but she still was
experiencing significant itching and a rash. Ex. 3 at 5-6. Her food diary also revealed that every
time she ingested corn products she broke out in hives, with a milder reaction to wheat and other
products. Id. at 5. Blood work conducted on the following day was negative for celiac disease, but
allergy testing was positive for several foods and environmental substances, including fruits, oat,
carrot, barley, sweet potato, corn, and wheat. Id. at 11-13. During this blood testing, Ms. McKown
also had an episode of hypotension, hypoxia, and tachycardia during the blood draw. Ex. 1 at 18;
Ex. 20 at 1. She was reported to have passed in and out for ten minutes until her vitals came back
to normal. Ex. 20 at 1. But this reaction to the testing did not result in any further medical treatment,
emergency or otherwise.
2014 Treatment of Skin and POTS-related Symptoms
On January 2, 2014, Petitioner saw Dr. Crocker again, now reporting that the steroidal
treatment she had been prescribed the prior month had cleared her skin over the holiday, but that
she had experienced flares after playing with dogs and ingesting a wheat cracker. Ex. 3 at 8-9. Her
physical exam was normal but for multiple scaly, erythematous patches of eczema on the face,
neck, elbows, knees and legs. Id. at 9. Additional testing showed strong positives to cat, dust mites,
tree pollen, and grass pollen (as well as certain foods including wheat, corn, and soy). Id. Ms.
McKown was again prescribed oral Prednisone. Id. at 9.
One week later Ms. McKown presented to Dr. Seth Marcus, at GI Care for Kids in Atlanta
for treatment of abdominal pain (with specific concern for possible “allergic gut”), syncope, and
food allergies. Ex. 12 at 5-9; Ex. 1 at 18-21, 75. Similar to the health course described above, Dr.
Marcus noted that Petitioner had experienced minor syncopal episodes in the past, culminating in
her May 2013 complete loss of consciousness for twenty to thirty minutes along with other
associated symptoms. Ex. 12 at 5-6. He noted that these episodes usually arose with stressful or
exciting events, appeared to be more frequent during her menstrual cycle, and generally occurred
two to three times per month. Id. at 5-6. A history of eczema was also noted, along with intermittent
hives and worsening of her eczema in May 2013 (although the contemporaneous record does not
really record increased complaints of eczema before July 2013). Id. at 6. Consistent with Dr.
Crocker, Dr. Marcus expressed uncertainty as to whether Petitioner’s syncopal episodes could be
related to her atopic disease or were an independent phenomenon. Id. at 8-9 (“I am unaware of a
known relationship between POTS and atopy, histamine release, hypereosinophilic syndrome or
eosinophilic gastrointestinal disease”). Id. at 9. He did however opine that her syncope was likely
unrelated to dietary exposures, with the exception of her most recent event that had occurred one
day after exposure to wheat. Id. Labs again ruled out celiac disease. Ex. 5 at 85.
6
On January 27, 2014, Ms. McKown had a follow-up visit with her cardiologist, Dr. Dooley,
seeking clearance for her upcoming colonoscopy and endoscopy to help assess the cause of her
ongoing GI symptoms. Ex. 7 at 10-11, 34. Petitioner now stated she was having one to two
episodes of syncope per month, the last of which was on December 29, 2013, lasting around
twenty-five minutes and resulting in stiffness and eye-rolling (although this incident is not
reflected in any immediately contemporaneous record). Id. Dr. Dooley noted, however, that
Petitioner had not been taking her POTS medication for months, out of the concern that it
exacerbated her rash. Id. The colonoscopy and upper GI endoscopy were performed by Dr. Marcus
on January 31, 2014. Ex. 12 at 19-20. Biopsies showed no significant abnormalities except for
mild esophagitis with rare eosinophils in the distal and mid esophagus. Ex. 5 at 79-84.
On February 21, 2014, Petitioner saw another immunologist, Dr. Karen Freedle, at Emory
Children’s Center in Atlanta for a secondary evaluation of her skin condition. Ex. 1 at 76-79, 85-
87; Ex. 5 at 42-72. Consistent with past treaters, Dr. Freedle’s impression was atopic dermatitis,
chronic urticaria of unclear etiology, chronic nasal and ocular symptoms, intermittent GI
complaints, and multiple food allergies. Ex. 1 at 76. Laboratory results conducted during the visit
were also normal, with the exception of a mildly elevated sedimentation rate and positive ANA at
1:40 with a homogeneous pattern. Ex. 5 at 76-78.
On March 5, 2014, telephonic records establish that Petitioner’s mother called Dr. Dooley
about a recent study in a journal indicating that POTS could be caused by an autoimmune disorder,
and asked whether Petitioner’s treatment would change in light of such findings. Ex. 6 at 25. She
reported that Ms. McKown had been tested for lupus and many allergies, her last syncopal episode
was in December, and that most of her other medications had been eliminated. Id. Dr. Dooley
noted that he had not heard POTS was autoimmune, but that he could refer Petitioner to a
neurologist to explore this concern. Id.
Over the course of the next few months, Ms. McKown’s adverse skin symptoms continued
to worsen. On April 7, 2014, Petitioner again saw her PCP, Dr. Magill, complaining of the same
rash, but with concerns for possible staph infection. Ex. 1 at 22-24. On examination, Petitioner had
diffuse dry skin with “punched out” lesions to the forehead, elbow, wrists, ankles, and knees. Id.
at 23. Her diagnosis remained eczema, and Dr. Magill recommended that she continue taking
clindamycin and acyclovir. Id. That same month Petitioner had a follow-up with Dr. Freedle on
April 21, 2014. Ex. 5 at 35-37. Her examination was normal except for open, excoriated areas of
skin. Id. at 36. A skin biopsy taken at this visit from her right arm revealed subacute spongiotic
dermatitis. Ex. 1 at 93-96.
On May 12, 2014, Ms. McKown saw a different dermatologist, Dr. Zakiya Rice of
Children’s Healthcare of Atlanta, regarding her rash and sores. Ex. 4 at 65-70. The history from
this visit again identified onset as May 2013, with heat causing aggravation of symptoms. Id. at
7
65-66. The examination revealed eczematous papules with excoriations, but well-hydrated skin.
Id. at 68. Dr. Rice assessed Petitioner with “spongiotic dermatitis, steroid responsive,” and
recommended that she restart topical steroids and taper oral Prednisone. Id. At a follow-up
appointment on June 2, 2014, Dr. Rice noted that Petitioner continued to use Prednisone due to
her persist rash. Id. at 50-57. A biopsy taken during the visit was consistent with eczema. Id. at 55.
The following month, Petitioner saw her PCP, Dr. Magill, for her fourteen-year-old well
visit on June 4, 2014. Ex. 1 at 25-30. She now reported that she had been experiencing joint pain
in the shoulders, upper back, wrists, and fingers since October 2013 (in addition to the skin
rashes/eczema and syncopal episodes described above) – although, as the somewhat exhaustive
record review above reveals, no prior treaters had been informed of these newly-reported
symptoms. Id. at 25. Her examination was positive for persistent diffuse dry skin with
lichenification on the elbows and an erythematous rash on the face (consistent with her ongoing
skin symptoms). Id. at 27. Hives were also reported as a current problem (attributable to
overheating, embarrassment, and emotion), but were not noted on exam. Id. at 25, 27. By June 12,
2014, Ms. McKown had completed steroid treatment, but her skin was reportedly still red and
burning, the hives and sores were becoming more severe, and her joints were reported to be
throbbing. Ex. 4 at 32-33; Ex. 5 at 137-38.
Treatment of Joint Pain
On June 30, 2014, Ms. McKown saw a rheumatologist, Dr. Kelly Rouster-Stevens, at
Children’s Healthcare of Atlanta, for evaluation of her joint complaints. Ex. 21 at 1-3; Ex. 23 at
21-24. Dr. Rouster-Stevens noted that Petitioner had been diagnosed with POTS in May 2013, and
then a few months later developed a rash associated with pruritus and burning. Ex. 21 at 1. The
medical history from this visit also states that since her last syncopal episode in December 2013,
Petitioner had experienced some improvement in her POTS symptoms, but had developed joint
pain, and the persistence of her skin rash (initially thought to be related to allergies) was proposed
to possibly have some alternative explanation. Id. On examination, Ms. McKown displayed
eczema patches and multiple tender trigger points in her back and extremities, but no joint swelling
or warmth. Id. at 3. Dr. Rouster-Stevens opined that Petitioner likely did not have lupus, arthritis,
myositis, or any other chronic rheumatologic process, suggesting instead that her exam was most
consistent with amplified musculoskeletal pain syndrome. Id. Lab tests performed at this time did
not support a diagnosis of lupus or other autoimmune connective tissue disease. Id. at 4, 7-8. Dr.
Rouster-Stevens ultimately recommended that Petitioner be evaluated in the pain clinic. Id. at 10.
Roughly one month later, Ms. McKown had follow-up appointments with Drs. Freedle and
Rice on July 21, 2014. Ex. 5 at 20-22; Ex. 4 at 16-21. Dr. Freedle noted that Petitioner’s rash
responded well to steroids, but that she stopped taking them due to how they made her feel
mentally, and that overall she felt she was not experiencing true improvement on this treatment
8
course. Ex. 5 at 20. Her visit with Dr. Rice revealed the same persistent symptoms noted above.
Ex. 4 at 16-21. At this visit, Petitioner and her mother also reported they “worried about this
startign [sic] with Gardasil vaccination 3/2013 and 9/2013[,]” but Dr. Rice offered no opinion
regarding vaccine causation. See id. Otherwise, Dr. Rice noted that a naturopathic consult had been
scheduled for July of that year – at which time Petitioner planned to seek further treatment. Id.6
Cleveland Clinic Evaluation
In mid-August 2014, Petitioner obtained multiple evaluations at the Cleveland Clinic in
Ohio in an attempt to ascertain the etiology for her constellation of symptoms. None of these
Cleveland Clinic treaters concluded that her symptoms were vaccine-related, and few saw any
relationship between the different symptoms she was experiencing.
First, on August 13, 2014, Ms. McKown saw dermatologist Dr. Joan Tamburro, D.O. Ex.
11 at 5-11. The health history taken during the visit indicated that Petitioner reported she had been
itchy with sores all over her body since October 2013, shortly after receiving a second HPV
vaccine dose. Id. at 5. Her POTS diagnosis and joint pain were also noted. Id. at 6. After
examination and consideration of Petitioner’s history, Dr. Tamburro diagnosed her with atopic
dermatitis (consistent with the diagnosis of past treaters) which had not been adequately treated.
Id. at 7. Dr. Tamburro found no evidence to support a diagnosis of connective tissue disease,
determining only that Petitioner likely had an “angry back” (based on previous patch testing)
which explained the numerous allergy positives. Id. Exam notes also indicated that Dr. Tamburro
discussed with Petitioner and her mother that a “persistent rash from Gardasil [wa]s unlikely.” Id.
Lidex and topical ointments were prescribed for her symptoms. Id.
Second, on the following day Petitioner saw two Cleveland Clinic allergists, Drs. Maria
Blanch and Velma Paschall, for an alternative evaluation of what appeared to possibly be chronic
urticaria. Ex. 11 at 12-23. Both physicians noted that Petitioner had a history of eczema since
childhood that had become more severe beginning the summer of 2013. Id. at 12. Episodes of hives
(or urticaria) were also noted to be triggered by heat, stress, showers, and animals. Id. Upon exam,
it was determined that Petitioner’s symptoms were most consistent with severe, chronic urticaria
that was resistant to standard antihistamine treatment, recommending instead an alternative,
newly-approved treatment (Xolair). Id. at 14. Following lab testing, Dr. Paschall sent a letter to
6
In late July 2014, Ms. McKown sought naturopathic care for her persistent symptoms described herein (including
skin rashes, hives, dizziness, and joint pain). See Ex. 19 at 6-8 (visit to Oconee Natural Healthcare Center in
Watkinsville, GA). Ms. McKown’s treater, Dr. Wyler Hecht, reviewed her health history and recommended treatment
with various supplements including Sea Cure (a white-fish dietary supplement), Immuno PRP spray (an immune-
balancing spray), Immuno PRP powder (immune-balancing vitamin supplement), and Curacel (a plant-based vitamin
for cell growth) to aid her symptoms. Id. at 8. Dr. Hecht’s notes also indicated that Petitioner’s mother felt “as though
the Gardasil vaccine triggered the reaction in her daughter[,]” but he offered no opinion regarding causation. See id.
at 6.
9
Petitioner’s mother (dated September 19, 2014) in which she expressed the view that it was
“unlikely that [Petitioner] has autoimmune chronic urticaria” because both her anti-IgE and anti-
IgE receptor antibody tests were negative. Ex. 22 at 1.
Third, on August 15, 2014, Petitioner saw Cleveland Clinic rheumatologist Dr. Andrew
Zeft for a second evaluation for onset of joint symptoms and persistent rash. Ex. 11 at 24-28. The
examination revealed no objective evidence of arthritis. Id. at 28. Dr. Zeft opined that her arthralgia
was mechanical in etiology, and that she had amplified pain from muscle spasm and trigger of
muscle spasm secondarily due to pain and itching from her skin lesions. Id. He thus recommended
treatment of her primary skin lesions, and knee stretching and strengthening exercises. Id.
Subsequent Treatment
The following September through November 2014, Ms. McKown began treatment with
Dr. Phillip DeMio7 in Worthington, Ohio. Ex. 14 at 12. At this time, Petitioner’s mother reported
to Dr. DeMio that she had received a diagnosis of “Gardasil Syndrome (recently spoke with Lloyd
to confirm and Dr. Hitch in Athens),” along with POTS, chronic hives, and dermatitis. Id. She also
specifically told Dr. DeMio that Dr. Rice (the dermatologist Petitioner saw in the spring of 2014)
had determined that “Gardasil triggered all this but . . . won’t go on record to say so.” Id. at 22.
(As noted above, however, the official records from Petitioner’s visits to Dr. Rice do not
corroborate this assertion – and, if anything, undermine it).
Petitioner’s first visit with Dr. DeMio included a discussion of her health history and a
physical exam. Ms. McKown was noted to be “calm and “coop[erative]” on exam. Ex. 14 at 12.
Eczema and hives were present at the time of the visit, and her POTS diagnosis was noted. Id. at
12, 25. Dr. DeMio assessed Petitioner with “adverse rxn to [G]ardasil,” noting that she had
“reported this to many prior practitioners” in the past (albeit ones who wouldn’t “stand for any
suggestion of va[ccine] injury”). Id. at 25, 27. Dr. DeMio recommended that Ms. McKown begin
self-administered vitamin B-12 injections to treat her symptoms. Id. at 59-60. Lab testing revealed
a positive IgM titer for Lyme western blot (but negative IgG), and normal results for toxic/essential
elements and metals. Id. at 36-37, 38-52.
On November 4 through 6, 2014, Mrs. McKown called to report a decline in Petitioner’s
condition, but noted that the B-12 injections had helped “tremendously” to give her more energy.
Ex. 14 at 30. In a handwritten note, Dr. DeMio indicated a “Dx: “Lyme [disease], [and] what
components of current [symptoms] are directly from Lyme: based at least in part on index’s
response.” Id. at 31. Notes taken during the phone consultation reveal that Dr. DeMio
7
Dr. DeMio’s website indicates that his practice focuses on medical testing and treatment for autism, AD/HD
disorders, and Lyme disease. See About Dr. DeMio, http://drdemio.com/dr-phillip-demio/ (last accessed on June 19,
2019).
10
recommended that Petitioner continue with the B-12 injections. Id. He also prescribed ultra-low
dose Naltrexone capsules, Hydroxychloroquine, Doxycycline, Cefdenir, and Valtrex. Id. at 53-58.
At a follow up visit in May 2015, Dr. DeMio ordered blood work relating to static encephalopathy,
metabolic disorder, mineral deficiency, and autoimmune disorder. Ex. 9 at 5-6. The results,
however (including sedimentation rate, iron, c-reactive protein, ammonia, ANA, and lupus), were
normal and negative for autoimmune disorders. Id. at 7-12.
From August 2014 to April 2015, Ms. McKown began attending counseling and started
physical therapy for her joint pain. A counseling note from September 2014 indicated that she had
“learned she no longer has a POTS diagnosis” but rather her symptoms were “actually a part of
the illness related to Gardasil.” Ex. 18 at 7. Notes from October of that year also report that the B-
12 injections were having a positive effect, causing Petitioner to feel much better. Id. at 16-17, 19-
20. In November 2014, her counselor noted that she had been diagnosed with Lyme disease
(presumably on Dr. DeMio’s suspicion), and had started antibiotic treatment in response. Id. at 20-
23. Petitioner’s physical therapy notes from the following April indicated that she reported her
joint and muscles aches were caused by “Gardasil vaccine/Lyme disease.” Ex. 15 at 6. Her health
history included concerns for “Gardasil syndrome[,]” Lyme disease, and POTS. Id. at 7.
Over the next few months, Ms. McKown’s health course began to improve. The following
year, on March 4, 2016, she returned to her PCP for a sixteen-year-old well-adolescent visit at
Lawrenceville Pediatrics. Ex. 24 at 2-8. The evaluating nurse practitioner noted that Ms.
McKown’s mother reported that Petitioner was “still recovering” (presumably from the symptoms
discussed herein), but no current illnesses or chronic problems were noted, with a normal exam.
Id. at 2, 4. The only current medication reported was Mometasone ointment, and Petitioner was
not on any supplements at the time of the appointment. Id. at 2. An additional PCP visit on March
17, 2016, indicated that Ms. McKown presented with complaints of flu-like symptoms, fever, and
moderate nasal congestion (though no medications were prescribed). Id. at 9-11. No further
medical records have been filed.
II. Fact and Expert Witnesses
A. Petitioner’s Witnesses and Hearing Evidence
1. Mrs. Tabitha McKown
Mrs. McKown, Petitioner’s mother, testified about her health history and symptomatology
course following receipt of doses of the vaccines at issue herein. Tr. at 11-97; see also Ex. 63
(narrative statement). Prior to receiving doses of the HPV vaccine, Petitioner was healthy, active,
and energetic. Tr. at 12. She was training for a triathlon, and enjoyed biking, swimming, and
running. Id. In support, Mrs. McKown offered multiple photographs of Petitioner (between in
11
September 2012 and January 2013) showing her interacting with friends and enjoying the above-
noted activities. Id. at 13-15.8
As noted above, Petitioner had multiple pre-existing medical conditions which bear on the
injuries alleged in the present matter (specifically, dry skin and eczema). Mrs. McKown
acknowledged this fact but maintained that her daughter’s symptoms were exacerbated after her
receipt of doses of the HPV vaccine. Tr. at 15, 61; see also Ex. 7 at 31 (dated July 15, 2013). She
described Petitioner’s childhood eczema as mild to moderate (consisting of dry patches on the
folds of the arms and backs of the legs). Tr. at 15, 60-61. Following the administration of Vaseline
or steroid cream, the patches would resolve rather quickly, and before vaccination Petitioner never
experienced eczema on the face, chest, or back. Id. at 15-16.
Mrs. McKown also acknowledged that Petitioner had experienced syncopal episodes (and
lightheadedness with position change) in the past. Tr. at 15-16. She attributed such instances of
lightheadedness to Ms. McKown’s triathlon training, dehydration, and low blood pressure. Id. at
16. Mrs. McKown disputed the accuracy of a record from March 2013 indicating that Dr. Magill
had noted that Petitioner experienced two syncopal episodes in the last three months, maintaining
that she had reported to Dr. Magill the episodes of syncope had occurred over a three-year period
(consistent with reports made to Dr. Dooley), and were triggered in ways distinguishable from
other instances (e.g., following a reprimand for poor behavior or the sight of blood). Id. at 16-17.
According to Mrs. McKown, Petitioner’s overall health began to decline rapidly following
her first dose of the HPV vaccine on March 20, 2013. Tr. at 17.9 She experienced a “pretty quick[]”
onset of migraines thereafter, though Mrs. McKown could not recall the exact date they started.
Id. Five weeks later, Petitioner experienced a syncopal episode while at a yogurt shop with friends.
Id. at 17-18. The event resulted in EMS transporting Petitioner to the local emergency room. Id. at
17. Mrs. McKown recalled that her daughter was diagnosed with POTS within weeks of the yogurt
shop episode. Id. Thereafter, her syncopal episodes became more severe (i.e., lasting anywhere
from a few seconds to thirty minutes) and occurred more frequently. Id. at 17-18.
8
The photographs offered in support of Ms. McKown’s pre-vaccine health (as well as a number also purporting to
demonstrate the progression of her skin-related symptoms) were not filed prior to hearing. Tr. at 12-13. On direct
examination of Mrs. McKown, Respondent objected to the photographs being entered into evidence. Id. at 29-31. I
permitted their admission over this objection, although I cautioned counsel that the evidence had to be properly
authenticated once filed. Petitioner’s counsel filed the photographs on October 31, 2018 (roughly one month following
the hearing), but has not authenticated them. See Exs. 73-74. The photos are also undated.
9
At hearing, Mrs. McKown testified that she initially declined to have her daughter vaccinated against HPV, due to
her age. Tr. at 35. At eleven years old, she felt Petitioner was not highly at risk for HPV, especially given her personal
circumstances (i.e., she was homeschooled and not sexually active). Id.
12
Petitioner subsequently developed new allergies, dramatic exacerbation of her skin
condition (including hives and oozing sores that would cover her body), and joint pain after the
second HPV dose. Tr. at 18-19, 27. Her migraines became more intense, and there were days when
her leg pain was so severe she could not get out of bed. Id. at 19.10 Treaters tested her for multiple
conditions including lupus. Id. at 27. Her syncopal episodes continued through the remainder of
2013. Mrs. McKown recalled an episode of syncope that required a trip to the emergency room at
Clearview Medical Center in December 2013. Id. at 92-93. During this episode, Petitioner’s pulse
and oxygen levels dropped low enough to (in her words) trigger a “code blue” alert, although the
source of this characterization of the incident was the phlebotomist responsible for drawing
Petitioner’s blood. Id. at 92-93.11
Mrs. McKown further posited that Petitioner’s symptoms worsened in January 2014. Tr.
at 28, 54. Her joint pain and fatigue escalated, she could not concentrate on her school work, and
she had no energy and had trouble sleeping at night. Id. The pain triggered by her skin symptoms
and joint pain required morphine treatment (which was ineffective). Id. She also needed assistance
with various personal care tasks (including ambulating and bathing). Id. Petitioner would also wear
long-sleeved clothing to hide the affected areas of skin and hide her face in photographs. Id. at 38-
39, 54.
Next, Mrs. McKown recalled the cardiology appointment with Dr. Dooley that she attended
with Petitioner in May 2013 (around the time she was tested for POTS). Tr. at 64-65. At that time,
Petitioner had reported an episode of syncope lasting twenty-five minutes. Id. at 64-65. Mrs.
McKown testified that these syncopal episodes occurred “dozens” of times. Id. at 65. During the
episodes, Petitioner would experience feelings of cold, her eyes would roll back in her head, and
at times she would convulse. Id. at 66. Mrs. McKown acknowledged that Dr. Dooley (along with
Dr. Magill) recommend that Petitioner schedule an appointment with a neurologist. Id. at 67-68.
But Mrs. McKown decided against a neurology consult because she believed POTS to be strictly
a cardiac condition, fearful that it could be misdiagnosed as “epilepsy” and other conditions. Id. at
67.12 She also did not want to subject her daughter to endless testing. Id. at 69-71.13
10
Notably, however, Respondent submitted evidence revealing that Ms. McKown participated in a 5K race on
November 16, 2013. Tr. at 58.
11
On cross, Respondent pointed out that Ms. McKown had submitted no records memorializing this allegedly drastic
drop in her vitals apart from a hand-written note (filed as Ex. 20 and dated October 9, 2014) prepared by the
phlebotomist responsible for the blood test that immediately triggered the purported reaction. Tr. at 92-93. The only
other documentation in the medical record noting a significant change in vitals is Ex. 55 (her tilt table test results from
May 2013). Id. at 93.
12
Mrs. McKown also testified that she did not recall Dr. Dooley suggesting that Petitioner’s POTS was not
autoimmune in nature (despite the suggestion in the medical record to the contrary). Tr. at 68-69; but see Ex. 7 at 25.
13
According to Mrs. McKown, Petitioner’s treaters at the Cleveland Clinic also did not consider neurology testing to
be necessary for further evaluation of her condition. Tr. at 68. She did, however, admit later in her testimony that she
13
As Mrs. McKown recalled, Petitioner’s skin condition continued to worsen during June
2014. Tr. at 59-60. At this point, Mrs. McKown posited that her daughter was taking six to eight
Zyrtec daily in attempts to combat the rashes and sores. Id. at 59-60. According to Mrs. McKown,
Petitioner’s treaters even suggested that she begin six weeks of chemotherapy (given the persistent
nature of the symptoms) – which prompted her to seek out second opinions regarding the cause of
her condition (and appropriate treatment). Id. at 24-25, 60. (There is no record support for this
recollection, however).
In July 2014, Petitioner was examined by a rheumatologist, Dr. Rouster-Stevens, at Atlanta
Children’s for evaluation of her joint pain, and assessed with “amplified musculoskeletal pain
syndrome.” Tr. at 71-72. Lupus and other autoimmune tissue disease were both ruled out based on
lab results. Id. at 74.14 Mrs. McKown testified, however, that she could not recall the particular
diagnostic opinion offered at this visit, remembering only that Dr. Rouster-Stevens advised
Petitioner to “go back to immunology” (presumably given her skin condition and congruent allergy
testing) or seek treatment at a pain clinic. Id. at 72. As she recalled, Petitioner’s diagnosis often
varied depending on what type of specialist evaluated her symptoms, leading her to feel as if the
family was being shuffled from specialist to specialist with no resulting concrete explanation for
her condition. Id. at 74-75.
Mrs. McKown also testified about the Cleveland Clinic evaluations, starting with
rheumatologist Dr. Zeft in August 2014. Tr. at 76-77. Dr. Zeft diagnosed Petitioner with amplified
musculoskeletal pain (consistent with Dr. Rouster-Stevens) for which he recommended
specialized exercises and pain management. Id. at 76-78. Ultimately, Mrs. McKown
acknowledged these recommendations, but decided against scheduling a pain clinic evaluation. Id.
at 75. Petitioner did, however, participate in some exercises (such as yoga, for example) to help
with her joint pain. Id. at 77.
Mrs. McKown next discussed Petitioner’s appointment with allergist Dr. Paschall. Tr. at
78, 80. Records from this visit indicate that Dr. Paschall assessed Ms. McKown with “chronic
idiopathic urticaria” and discussed the appropriate treatment protocol for the illness, ruling out
autoimmune chronic urticaria. Id. at 84. Despite the record evidence, Mrs. McKown could not
recall any treater opining that Petitioner had chronic urticaria. Id. at 78. She also could not
remember if her daughter took any of the medications prescribed for such a condition, though she
requested a neurologic evaluation at the Cleveland Clinic (along with testing relating to aluminum levels in the blood),
but was rebuffed. Id. at 69-71.
14
Despite the lack of testing evidencing typical autoimmunity markers, Mrs. McKown maintained that Petitioner’s
treaters informed her that her elevated ANA levels indicated she had some form of autoimmune disease. Tr. at 74 (“I
was told that a positive ANA means there is some type of autoimmune somewhere”).
14
allowed for the possibility (given the multitude of treatments that were recommended to treat her
symptoms). Id. at 79-80. She also admitted that Petitioner had tried multiple topical steroid creams
(along with oral steroids) intermittently in the past to assist with her symptoms. Id. at 59-60, 83-
84. She could not recall if Petitioner was currently using any ointments at the time of her Cleveland
Clinic evaluation. Id.
According to Mrs. McKown, it was at the Cleveland Clinic that Petitioner’s treaters first
proposed a connection between the HPV doses she received and her onset of POTS (despite record
evidence to the contrary). Tr. at 22, 24-25.15 Later on in her testimony, Mrs. McKown
acknowledged that she and she daughter learned of the term “Gardasil syndrome” through online
research, and that they began to discuss the concept with treaters – although, as the medical record
reveals, the idea was generally not embraced. Id. at 31-32, 89. Two treaters in particular – Dr. Rice
(Ms. McKown’s dermatologist at Emory) and Dr. Freedle – refused to treat Petitioner further after
the suggestion was made that her HPV doses had resulted in her condition. Id. at 31-32, 85, 87-88.
When confronted with medical records evidencing treater opinions that the HPV vaccine was
likely not the cause for her condition, Mrs. McKown posited that these treaters were simply
unwilling to admit the possibility that the vaccine could have caused Petitioner’s symptoms. Id. at
85, 86-88.
Mrs. McKown also testified about Petitioner’s treatment with Dr. DeMio. Tr. at 32, 85.
She indicated that Dr. DeMio was one of the only physicians who shared her suspicion that her
daughter’s symptoms were caused by the HPV vaccine. Id. at 85-86, 90.16 He started Petitioner on
a “recovery protocol” which included the paleo diet, antibiotics, and various supplements, and
which Mrs. McKown alleged had resulted in a “slow improvement” of Petitioner’s symptoms. Id.
at 32, 85. Over a period of months thereafter, Petitioner’s skin cleared (though Mrs. McKown
testified that she continues to experience flares presently). Id. at 33. Her syncopal episodes were
controlled (i.e., she experienced only one every few months or so). Id. She was also able to compete
in 5K races by April of that year. Id. at 58. As of 2018, Petitioner was successfully attending
college, although she purportedly continues to experience syncopal episodes three to four times
per week that can last up to thirty minutes. Id. at 33. Stress continues to trigger flare-ups of her
skin condition and her headaches continue to be severe. Id. at 33-34.
15
Notes from the Cleveland Clinic evaluations actually suggest that Ms. McKown was able to control her POTS
symptoms through behavior modifications (including physical movements like squeezing her hands or completing
exercises to help with blood flow). Tr. at 90-91.
16
At hearing, Mrs. McKown also testified that one of Petitioner’s pediatricians at Lawrenceville Pediatrics, “Tammie,”
allowed for the possibility that the HPV vaccine caused her condition, but could not recall this treater’s full name. Tr.
at 87-88. Respondent pointed out that at the time of the hearing, Petitioner had submitted no records evidencing an
evaluation from a physician with that first name. Id. Given the discrepancy, counsel indicated that Petitioner would
filed update records following the conclusion of the hearing. Id. at 88-89. However, no additional information has
been filed.
15
2. Photographic and Social Media Evidence
To illustrate her contentions about the course of Petitioner’s skin-related symptoms, Mrs.
McKown offered photographs purportedly taken on various dates ranging from 2013 through
2015, many of which had been posted to social media. Tr. at 21-26; see Ex. 74. As she described,
one photo was taken close-in-time to Ms. McKown’s receipt of the second dose of HPV (in
September 2013), and showed redness and hives scattered over the arms and trunk following
exposure to water. Tr. at 26; see Ex. 74 at 9. Multiple filed photos were taken around December
2013 during the Cleveland Clinic consultations (and showed inflamed patches of skin on the face
and neck). Tr. at 22-23; see Ex. 74 at 3-8. Yet another photo from (mid-April or May 2015)
evidenced a skin eruption after spending time in the sun. Tr. at 21; see Ex. 74 at 1.17
In reaction, Respondent produced additional photographic evidence (spanning the length
of the relevant time period), all of which tended to show that Petitioner’s skin appeared to be
relatively clear at various points throughout 2013 through 2018. Tr. at 41-52; see Exs. P and Q.18
These photographs were taken from Ms. McKown’s Facebook account, with timestamps revealing
that they were posted on various dates between April 2013 and 2018 (although this obviously does
not establish when a particular photo was actually taken). For example, in a photo posted in mid-
November 2013 (or two months following Petitioner’s receipt of the second dose of HPV), Ms.
McKown’s skin appears to be clear and she was not wearing any long-sleeved or high-necked
clothing to cover her skin. Tr. at 41-42. Mrs. McKown explained, however, that her daughter
would routinely repost photos to Facebook that were taken pre-vaccination (and likely did so in
November of that year). Id. at 41-42. Three photos taken in August 2014 and January 2015 also
appear to show Petitioner wearing short-sleeved clothing (with no noticeable skin rashes on her
face or arms). Id. at 42-43. In response, Mrs. McKown testified that Petitioner often edited photos
she posted to social media during her illness in order to remove any evidence of a rash (a practice
Mrs. McKown witnessed her doing throughout 2014). Id. at 43-44, 93-94.
Respondent also offered photos posted on various dates in late 2015 through early 2018, at
which time Petitioner’s skin symptoms began to subside. Tr. at 45-48. A photo dated from April
2018 depicted Ms. McKown on the beach with family members. Id. at 49. Her skin appears to be
17
As previously stated, the photographs (filed as Ex. 74) were not filed prior to hearing, although Petitioner’s counsel
indicated that they would be filed following the hearing (with evidence confirming the dates they were taken). Counsel
did so, but did not offer evidence to confirm the dates upon which they were taken. See generally Ex. 74. I can thus
only rely on the testimony offered by Mrs. McKown (which tends to suggest they were taken following Petitioner’s
receipt of the second dose of HPV in September 2013 through mid-2015). I largely do not, however, find that the
photos do more than illustrate vaguely the existence of eczema flares in this period – a contention not fully disputed,
and one that even if deemed correct does not aid Petitioner in establishing that the HPV vaccine caused the flares.
18
Respondent also filed evidence that Petitioner participated in 5K races in November 2013 and April 2015. See Ex.
R.
16
clear in the photo, and Mrs. McKown admitted at hearing that the sores her daughter had
experienced previously were no longer a problem at this time. Id. She did, however, maintain that
the photograph showed evidence of a rash or “redness” on her hands and back. Id. Overall, after
late 2015, Mrs. McKown posited that Petitioner would have “good days” where her skin remained
clear, but she continued to experience breakouts on and off for the last three years. Id. at 50-54.
3. Dr. Carlo Tornatore
Dr. Tornatore authored one expert report and also testified at the entitlement hearing on
Petitioner’s behalf. See Ex. 56, filed on July 31, 2018 (ECF No. 42-2) (“Tornatore Rep.”). He
opined that Petitioner developed POTS (along with a significant aggravation of preexisting
eczema) following her receipt of HPV vaccine doses on March 20, 2013, and September 3, 2013.
Tr. at 120-21, 135; Tornatore Rep. at 14. In the alternative, if Petitioner’s POTS preexisted her
vaccinations, then the vaccines likely significantly aggravated that condition. Tr. at 135; Tornatore
Rep. at 14.19
Dr. Tornatore is a board-certified neurologist. See Exhibit 57, dated July 31, 2018 (ECF
No. 42-3) (“Tornatore CV”). He graduated from Cornell University with a Bachelor of Arts in
Neurobiology, and attended Georgetown University, where he received a Master of Science in
Physiology. Tr. at 98; Tornatore CV at 2. He subsequently graduated from medical school at
Georgetown University School of Medicine, completing a residency in the Department of
Neurology at Georgetown University Hospital. Tr. at 98; Tornatore CV at 2. He also completed a
fellowship in molecular virology and genetics at the National Institute of Health in Bethesda,
Maryland. Tr. at 98; Tornatore CV at 2. Dr. Tornatore has published multiple articles addressing
cell biology and pathology of demyelinating disorders. Tornatore CV at 8-20. Currently, he serves
as the Chair of the Department of Neurology at Georgetown University Medical Center, and
Interim Chair of the Department of Neurology at Medstar Georgetown University Hospital. Tr. at
98-99; Tornatore CV at 3. He also serves as a director of the neurology clerkship program at
Georgetown University Hospital (which is responsible for training roughly 200 medical students
per year). Tr. at 99; Tornatore CV at 3. During his tenure at Georgetown, Dr. Tornatore also
developed the Neuroimmunology and Multiple Sclerosis Center. Tr. at 99; Tornatore CV at 3. He
also serves as an ad hoc reviewer for several neurology journals. Tr. at 102; Tornatore CV at 7.
Dr. Tornatore is not board certified in immunology or dermatology. Tr. at 133, 139. His
CV also does not evidence any subspecialty in autonomics (or reference any publications or
memberships associated with such a specialty). Id. at 133-34, 135. In his current practice, he
primarily treats multiple sclerosis (“MS”) patients (some of whom have congruent autonomic
19
Upon questioning by the Court, Dr. Tornatore stated that his opinions herein (along with those contained in his
expert reports) were wholly independent from those offered by Drs. Mikovits and Ruscetti. Tr. at 188.
17
issues). Id. at 100, 103. Dr. Tornatore estimated that roughly 600 of his MS patients have POTS
(attributable to various primary illnesses, including deconditioning, cardiovascular issues, or
autonomic problems). Id. at 137-38. He acknowledged, however, that he is not an expert in POTS
or the autonomic nervous system. Id. at 137-38. He also has not performed any testing related to
POTS (i.e., a title table test), but does have some familiarity with orthostatic reading measures. Id.
at 138. In addition, Dr. Tornatore has not treated any MS/POTS patients with dermatologic
problems similar to those describe herein. Id. at 103, 136-37, 140.
Dr. Tornatore characterized POTS as dysfunction of the autonomic nervous system20
resulting from dysregulation of the blood vessels responsible for adjusting the heart rate when the
body changes position. Tr. at 103. Patients suffering from POTS typically experience increased
heart rate, accompanied by a drop in blood pressure, due to the heart’s attempt to compensate for
lack of blood supply to the brain (which can result in dizziness when moving from a lying down
position to a standing one, for example – as evidenced by tilt table testing). Id. POTS can also
present secondarily to central nervous system disorders (like MS, for example). Id. Other
symptoms can include lightheadedness, syncope, and dizziness (something Dr. Tornatore deemed
characteristic of the disease, but not evidence of it). Id. at 156-58. The filed literature suggests
several different triggers can cause an individual to develop POTS, including viruses, bacteria,
deconditioning, and genetics. See C. Gibbons, et al., Structural and Functional Small Fiber
Abnormalities in the Neuropathic Postural Tachycardia Syndrome, PlosOne (2013),
https://doi.org/10.1371/journal.pone/0084716, filed as Ex. 61 (ECF No. 47-5) (“Gibbons”).
In addition, Dr. Tornatore proposed that POTS can be autoimmune in origin. Tr. at 103-
04. An autoimmune disease or disorder features an individual’s immune system reacting
hyperactively, attacking self antigens (at the same time it is reacting to foreign infectious agents).
Dr. Tornatore relied on the presence of certain autoantibodies in patients diagnosed with POTS as
evidence of its autoimmune nature, offering literature (including that authored by Respondent’s
expert, Dr. Gibbons) that he said established this finding. See generally Gibbons at 1-10. The
Gibbons paper analyzed twenty-four POTS patients (along with ten healthy controls) to define the
neuropathology and clinical parameters of neuropathic POTS (as compared to the non-neuropathic
variants). Gibbons at 1. While Gibbons concluded that various subtypes of POTS display
overlapping symptoms, neuropathic POTS patients (experiencing “sudomotor dysfunction”) could
also exhibit symptoms similar to those seen in post-ganglionic dysautonomia. Id. at 6-7. Based on
the above, Dr. Tornatore concluded that there is a specific target antigen associated with
neuropathic POTS) – the “postganglionic proteins” or “ganglia” (which have shown to be virally-
associated with “postganglionic cholinergic dysautonomia”). Tr. at 122-23.
20
Dr. Tornatore defined the autonomic nervous system as the primary regulator of involuntary physiologic processes
(i.e., sweating, bowels, bladder, and respiratory functions). Tr. at 103.
18
In Dr. Tornatore’s opinion, POTS can also be associated with the onset of various skin
eruptions (including eczema and atopic dermatitis). Tr. at 119-20, 181. Dysfunction in the
autonomic nervous system can, he proposed, also cause dysregulation (or inflammation) in the
somatosensory nerves in the skin. Id. at 117-18, 119. Specifically, neural signaling by the sensory
nerves (or “neuroimmune signaling”) can produce neurogenic inflammation, thereby resulting in
the nervous system playing an “active role in inflammation” – attacking the skin directly, and
leading to eczema and atopic dermatitis. Id. at 118-19. He claimed that Ms. McKown’s skin biopsy
from April 2014 (which evidenced markers for inflammation) supported his conclusion. Id. at 152-
53.
On cross, Dr. Tornatore admitted that he had offered no literature directly supporting his
proposition that eczema could be autoimmune in derivation instigated by vaccination. Tr. at 120-
21, 153-54. He nonetheless emphasized that it was reasonable to associate a skin eruption (or
outbreak) with other evidence of autoimmune disease, given that both occur congruently with an
underlying inflammatory process. Id. at 124, 154-55. In support, Dr. Tornatore referenced a single
piece of literature, which he posited shows that eczema can be induced by certain antibodies. Id.
at 153; see T. Voisin, et al., Neuro-Immune Interactions in Allergic Diseases: Novel Targets for
Therapeutics, 29 Int’l Immnol. 247 (2017), filed as Ex. 72 (ECF No. 55-4) (“Voisin”).21 Voisin,
however, discussed allergic inflammation and the interplay between immune cells/inflammatory
mediators as “neurotransmitters” or signalers (which, by way of “cross-talk,” mediate the immune
response to allergens). Voisin at 1. It also made no mention of POTS (nor does it attempt to relate
autoimmune disease to allergies, or connect POTS to eczema). Dr. Tornatore otherwise offered no
evidence that the autoantibodies he discussed as associated with a neuropathic form of POTS could
also be implicated in causing eczema. Tr. at 153-54.
Dr. Tornatore went on to discuss what Petitioner’s actual medical records revealed, in an
effort to bulwark the reasonableness of his theory. First, he noted that Petitioner’s tilt table testing
(completed in May 2013) confirmed she suffers from POTS. Tr. at 169-70, 180. Her subsequent
episodes of prolonged unconsciousness22 (i.e., anywhere from ten to thirty minutes) thereafter were
also in his view likely related. Id. at 165-67, 168-70. Dr. Tornatore could not confirm, however,
which POTS variant best described Petitioner’s specific symptoms. Id. He theorized that Ms.
McKown likely had a form of autoimmune “neurogenic” or “neuropathic” POTS (despite any
treater evidence so opining). Id. at 180-81. In support of this determination, Dr. Tornatore pointed
to Petitioner’s worsening eczema flares (in conjunction with accompanying “skin color changes”)
as evidence of this finding. Id. at 181. He maintained as well that the Voisin article supported his
21
Voisin was filed the day before the hearing. ECF No. 55 (confirming Voisin was filed on September 25, 2018).
22
The fact that one of these prolonged episodes was observed only by a phlebotomist did not alter Dr. Tornatore’s
opinion. Tr. at 165-68. Respondent also noted that these observed episodes were not contemporaneously recorded in
the record (but rather were dictated in letters thereafter or described by Petitioner’s mother only). Id. at 165-68.
19
opinion (given the association of neuroimmune signaling with the pathophysiology of allergic
diseases, such as forms of eczema). Id.
On cross, Dr. Tornatore also posited that “acrocyanosis” – which he described as bluish-
colored limbs – is a “hallmark” of neurogenic POTS. Tr. at 549-50. As he explained, bluish
coloring in the limbs is evidence of some “neurogenic issue” by which the nerves compress the
capillaries. Id. at 549-50. Dr. Tornatore pointed to an instance in the record where one of
Petitioner’s treaters noted such an occurrence. Id. at 550 (citing Ex. 21 at 1), 556. In so maintaining,
he again invoked Voisin, which discussed a 1901 study revealing that nerve stimulation could
result in “vasodilation” (or a change in limb color). Id. at 554; Voisin at 3. As discussed earlier,
however, Voisin makes no mention of POTS at all (and it thus does not consider whether limb
discoloration is a hallmark of neuropathic POTS). Nonetheless, Dr. Tornatore maintained that
evidence of nerve stimulation (and the resulting bluish coloring or “flushing” of the limbs noted
in the medical records) was enough to conclude the best diagnosis was likely
neurogenic/neuropathic POTS. Tr. at 556.23
In reaction to Respondent’s argument that Petitioner’s POTS was more likely attributable
to “hypovolemia” or dehydration, Dr. Tornatore referenced various lab reports in Petitioner’s
records tending to suggest that the relevant markers for hypovolemia were documented as normal
over the course of her illness. Tr. at 556-59. Hypovolemia (or dehydration caused by low blood
volume), he posited, is best evidenced by an elevated BUN24 to creatinine measurement25 (i.e.,
evidence of blood volume depletion). Id. at 559. But, based on his own understanding of the
science, Dr. Tornatore suggested that low levels of creatinine could “falsely elevate” the BUN-
creatinine ration (due to diet or GI issues) – thereby rendering the marker somewhat unreliable at
times as a diagnostic tool. Id. at 558-59. Even so, absent any irregular BUN-creatinine ratio, a
diagnosis of chronic dehydration (associated with POTS) could not be reliably supported in his
reading of the record. Id. at 559-60.
Dr. Tornatore next maintained there was a plausible biologic mechanism by which the HPV
vaccine could cause POTS: molecular mimicry. Tornatore Rep. at 13-14. Molecular mimicry
23
Apart from the above, Dr. Tornatore posited that Respondent’s expert, Dr. Gibbons, offered some evidence that a
“lack of sympathetic tone” in the limbs could result in blood vessel constriction and pooling – thereby causing some
discoloration similar to that noted above. Tr. at 556-57. He could not, however, point to any literature cited by
Respondent relating this specific symptom to POTS. Id. at 557-58.
24
A BUN (or “blood urea nitrogen”) test is a blood test used to measure the amount of urea nitrogen in the blood. See
Blood Urea Nitrogen (BUN) Test, Mayo Clinic, https://www.mayoclinic.org/tests-procedures/blood-urea-
nitrogen/about/pac-20384821 (last accessed on June 19, 2019). Urea nitrogen is a chemical waste product that is
typically removed from the body through the kidneys. Id. A higher than normal BUN test can suggest that the kidneys
or liver may not be working properly. Id.
25
Creatinine is a chemical waste product produced by muscle metabolism. See Creatine Test, Mayo Clinic,
https://www.mayoclinic.org/tests-procedures/creatinine-test/about/pac-20384646 (last accessed on June 19, 2019).
Properly functioning kidneys filter creatine from the blood. Id. A creatine test – which measures the level of creatinine
in the blood – can thus indicate kidney irregularities. Id.
20
occurs when the body is exposed to an environmental factor (such as a vaccine or infection) which
results in a cross-reaction between autoantibodies (produced by the body in response to that
external factor) and a self structure in the body that the foreign antigen has mimicked. In so
proposing, Dr. Tornatore relied on scientific literature establishing homology between protein
components of the HPV vaccine and certain human protein structures. Tr. at 170-71, 547-49; D.
Kanduc & Y. Shoenfeld, Inter-Pathogen Peptide Sharing and the Original Antigenic Sin: Solving
Paradox, 8 Open Immunol. J. 16 (2018), filed as Ex. 69 (ECF No. 53-3) (“Kanduc”).26 Kanduc
examined a nine-protein sequence from HPV16, and recorded amino acid sequence similarities to
the human proteome at the pentapeptide level, concluding that the proteome contains twenty-nine
pentapeptides also found in the HPV16 vaccine – and thus ample mimics for molecular mimicry
to have occurred. Kanduc at 16.
Dr. Tornatore struggled, however, to specify where in the body this autoimmune cross-
reaction was purportedly occurring. At most, he proposed that the immune response triggered by
receipt of the HPV vaccine caused a cross reaction directed at the body’s peripheral nerves (or
some “neuronal element” or epitope). Tr. at 120-21, 171. He also made some suggestion that
Kanduc supported a conclusion that the triggered autoimmune response could be directed against
the human septin-9 protein. Id. at 171; Kanduc at 21. He did not, however, offer literature
evidencing homology between the HPV vaccine components and any specific tissues in the
autonomic nervous system. Tr. at 172. And Kanduc referenced no studies or models indicating
such a cross reaction could occur (in the context of either target). Dr. Tornatore nonetheless
admitted at hearing that he relied solely on Kanduc to establish that components of the HPV
vaccine could interact with septin-9 (or some other “crossreactive target”) and result in POTS
(though, he posited that he could offer more support if given additional time).27 Id. at 171-72, 173,
548; see Kanduc at 21. He maintained, however, the Kanduc paper provided enough support to
conclude such a similarities existed (given the Program’s “more probable than not” preponderance
standard). Tr. at 172.28
26
On cross, Respondent raised concerns regarding the reliability of Kanduc (given that it was published in the Open
Immunology Journal, which Respondent proposed was a disreputable, “predatory” journal). Tr. at 174. Dr. Tornatore,
however, posited that the circumstances of Kanduc’s publication (or the reputation of the authors) did not weigh
heavily on his assessment of the findings discussed in the article. Id. at 175. In his view, the authors simply performed
proteomic searchers (which he deemed “totally objective”), confirming the possibility of homology between the HPV
vaccine components and self structures. Id. at 175-76.
27
Kanduc, like Voisin, was filed the night before the hearing. See ECF No. 53 (confirming Kanduc was filed on
September 25, 2018).
28
In so stating, Dr. Tornatore stepped outside of his demonstrated medical expertise and into the shoes of the person
designated to determine the law in this proceeding – here, the special master. But it is inadvisable for medical or
scientific experts to so comment on the relevant legal standard, as I have noted in other cases. See, e.g., Chinea v.
Sec’y of Health & Human Servs., No. 15-95V, 2019 WL 1873322, at *19, 31 n.42 (Fed. Cl. Spec. Mstr. Mar. 15,
2019), appeal docketed, No. 15-95V (Fed. Cl. Apr. 15, 2019).
21
This inability to establish more than vague contours of how homology between the HPV
vaccine and self proteins might explain a putative autoimmune attack went beyond this narrow
issue, however. Dr. Tornatore offered little in the way of evidence suggesting that the HPV vaccine
has ever been shown from a reliable experiment or study to be pathogenic in the manner proposed
(i.e., to trigger an autoimmune process sufficient to produce the symptoms relevant to this case).
Rather, he relied solely on the fact that Kanduc supported a finding of “human homology” between
HPV vaccine protein components and host proteins – without evidence suggesting the alleged
cross-reactivity could result in an adverse disease process. At most, Dr. Tornatore referenced
Sydenham’s chorea (a known autoimmune disease characterized by rapid, jerking movements) to
explain how an immune response directed against a bacterial infection can “overshoot” and also
lead to different illnesses (rheumatic heart disease, for example). Tr. at 110. As he described, in
the case of Sydenham’s chorea, the body develops an immune response to strep bacteria – and the
autoantibodies produced in response cross-react with host proteins – thus, causing direct damage
to the heart and brain. Id.
Along those same lines, and as another mechanistic explanation in the alternative to
molecular mimicry, Dr. Tornatore briefly discussed the concept of “T cell receptor degeneracy.”
Tr. at 105-07, 189-90; Tornatore Rep. at 14. According to Dr. Tornatore, the body lacks an “army
of T cells” capable of defending against the “millions, if not billions” of antigens it is exposed to
on a regular basis. Id. Thus, it would be impossible for one specific T cell to be directed at one
single antigen. Id. at 105, 566. Rather, T cells are “degenerate” – meaning they can recognize
several different antigens (and mount an immune response against those antigens) without having
to have identifiable homology to every possible foreign antigen, including amino acid chains
whether associated with a particular virus or vaccine. Id. at 105, 546.
Dr. Tornatore characterized the degeneracy concept as either a primary or secondary
adaptive response, but distinguished it from the more typical underlying mechanisms offered in
the Program (i.e., bystander activation and epitope spreading). Tr. at 189. In his view, T cell
degeneracy involves antigen stimulation the of the “same identical T cell clone[,]” rather than by
acceleration of an ongoing immune process by local activation of antigens presenting as a result
of the cross-reactivity. Id. But he stressed that because Kanduc established that the HPV vaccine
has specific homology with self-protein sequences, T cell degeneracy was not a necessary
mechanistic explanation for his theory in this case. Id. at 189 (“we have that specificity for HPV
protein sequence and human sequences to say . . . you don’t need the T cell degeneracy”), 546.
Though, upon further questioning, Dr. Tornatore posited it was possible that both had occurred in
this case – protein cross-reactivity led to the onset of POTS, while T cell degeneracy contributed
to the exacerbation of Ms. McKown’s skin symptoms (in which case it is possible the eczema
worsening was either directly aggravated by the nervous system or stimulated by the underlying
adaptive process attributable to POTS). Id. at 547.
Dr. Tornatore further suggested that Petitioner’s subsequent re-exposure to antigens in the
second dose of the HPV vaccine could have played some role in the molecular mimicry process.
22
Tr. at 107-09. Because of the homology identified between components in the HPV vaccine and
self sequences, nonspecific T cells could attack self structures/amino acid sequences (following
immune system stimulation by the vaccine) in addition to those cells responding specifically to the
vaccine – thereby resulting in a more amplified and inherently more rapid cellular response. Id. at
107-08. Just as a vaccine booster response is intended to assist the body in developing
immunologic memory to certain antigens, Dr. Tornatore posited that memory developed from
exposure to a second dose of HPV could cause the cross-reactivity to occur at a much faster pace.
Id. at 108-09; see Kanduc at 21.
Admittedly, Dr. Tornatore conceded, Kanduc offered multiple possible sequence mimics
that could share homology with numerous self proteins in the entire human genome. Tr. at 112,
552. To account for such a large amount of protein sequence similarities, Dr. Tornatore posited
that genetic risk factors also play a part in how the immune system “overshoot[s]” or reacts in
response to vaccine-induced autoantibodies. Id. at 112-13. Dr. Tornatore offered rheumatologic
disorders as a pertinent illustration. Id. Patients with spondyloarthropathies, for example, have
elevated levels of HLAB-27 (an abnormal haplotype protein located on the immune cells). Id.
These proteins (produced as a result of a genetic rheumatologic disorder) inhibit the body’s ability
to regulate the immune system – thereby resulting in an increased risk for autoimmunity. Id. at
113. Thus, regardless of the number of possible shared sequences, Dr. Tornatore seemed to suggest
that a patient’s genetics will always play some role in susceptibility to develop an autoimmune
disorder. Id. at 190-91, 552-53. He did not indicate, however, what (if any) genetic abnormality
contributed to Petitioner’s onset of symptoms. Id. at 552.
Dr. Tornatore next discussed the evidence (or “combination of things”) in the medical
records that he maintained supported the conclusion that Petitioner likely experienced chronic
inflammation (and resulting immune dysfunction) post-vaccination. Tr. at 127, 179-80. First, Dr.
Tornatore pointed to Petitioner’s POTS – a disease which (as discussed above) “can be
autoimmune” in some circumstances. Id. at 177, 180. He also asserted that eczema “is
inflammatory in nature” which further evidenced some systemic involvement. Id. at 177. Indeed,
Petitioner’s biopsy from April 2014 revealed inflammation in the skin. Id. at 153, 178, 180.
Otherwise, Dr. Tornatore referenced allergy testing – which revealed elevated levels of IgE to
various food and outdoor allergens. Id. at 179 (citing Ex. 1 at 65-66), 180. Even so, Dr. Tornatore
admitted on cross that elevated IgE is not specific to autoimmunity directly, but could suggest a
patient has a “propensity for a hyperimmune state.” Id. at 179. He also agreed that Petitioner’s
records contained no test results establishing the existence of any specific antibodies to neuronal
antigens – though he deemed such testing insignificant. Id.
Apart from the above, Dr. Tornatore concluded that the HPV vaccine doses Petitioner
received were likely responsible for instigating her condition given their close temporal
relationship to her reported onset (and/or worsening) of syncope and rash symptoms. Tr. at 125,
127, 177, 553. In his view, Petitioner’s health course and the “tempo” of her symptoms “changed
dramatically after vaccination, particularly the second vaccination in September.” Id. at 125. She
23
at most experienced situational syncope before her receipt of the HPV vaccine doses, with worse
and longer instances thereafter. Id. at 125-26. Her preexisting eczema also worsened following her
second dose of HPV (as evidenced by the multiple doctor visits she attended over the course of
her illness). Id. at 125-27. Dr. Tornatore also cited to various treater statements indicating their
recognition that Petitioner’s symptoms had worsened in the months following her vaccine doses.
Id. at 125 (citing Ex. 1 at 49), 129 (citing Ex. 3 at 2-4).
While stressing the significance of the above, Dr. Tornatore was dismissive of the fact that
testing performed on Petitioner did not reveal other common, objective indicators of systemic
inflammation (including the CRP29 and ESR30 rates). Tr. at 110-11. In his view, such
measurements are not always elevated in autoimmune disease patients because not all immune
responses result in protein production detectable in the blood. Id. at 110-11. In multiple sclerosis
and myasthenia gravis, for example, inflammation is directed at the nervous system tissue – and
the CRP and ESR testing typically reveal normal results for its patient population (given that
antibodies produced in response to such immune-mediated conditions are deposited in the tissue,
not the blood). Id. at 111-12.31 In addition, Petitioner experienced worsening eczema at the same
time that her CRP and ESR rates were normal (a point conceded by Respondent’s expert). Id. at
111. Thus, as Dr. Tornatore posited, the underlying pathogenesis of an autoimmune disease
process could not be discredited in this case even if some classic tests for inflammation had not
been satisfied. Id. at 177-78.
Dr. Tornatore also acknowledged that Ms. McKown’s medical records evidenced a pre-
vaccination history of two syncopal episodes – but he deemed them “situational” or “vasovagal”
in nature, and thus distinguishable. Tr. at 128, 161-63; see also Tornatore Rep. at 14. In his view,
both instances of past syncope were accompanied by a “significant emotional” component (i.e., a
reprimand for bad behavior and exposure to blood). Tr. at 162. They were therefore not likely
associated with her subsequent autoimmune-instigated POTS, given the above-noted situational
components, the rarity of such occurrences, and lack of other evidence suggest a preexisting
underlying autonomic problem. Id. at 128, 162, 163 (noting “these episodes were 2 ½ years apart”).
By contrast, Ms. McKown clearly experienced more syncopal episodes following her receipt of
two HPV vaccine doses. Id. at 129, 162-63. However, if her pre-vaccine syncopal episodes could
29
CRP is a test used to measure inflammation in the body. C-Reactive Protein Test, Mayo Clinic,
https://www.mayoclinic.org/tests-procedures/c-reactive-protein-test/about/pac-20385228 (last accessed June 20,
2019). It measures the amount of C-reactive protein in the blood via a simple blood test. Id. The results can indicate a
patient's risk for infection or heart disease, for example. Id.
30
ESR is a blood test used to show inflammatory activity in the body. Sed Rate (Erythrocyte Sedimentation Rate),
Mayo Clinic, https://www mayoclinic.org/tests-procedures/sed-rate/about/pac-20384797 (last accessed June 20,
2019). It measures the distance red blood cells fall in a test tube in one hour. Id. The further the cells descend in the
tube, the greater evidence of an existing inflammatory response of the immune system. Id.
31
For further support, Dr. Tornatore posited that the best indicator of a multiple sclerosis diagnosis is an MRI. Tr. at
179. Bloodwork for multiple sclerosis patients is typically normal and does not reveal the presence of systemic
inflammation. Id.
24
be related to POTS, then Dr. Tornatore proposed that the HPV vaccine doses likely aggravated it
given the increased incidence of post-vaccination symptoms. Id. at 128-29, 161-62; Tornatore Rep.
at 14.
As to the timing of the onset of Petitioner’s POTS symptoms, Dr. Tornatore maintained
that she had experienced her first “true” symptoms of syncope on April 26, 2013 (or four to five
weeks post vaccination) at the yogurt shop, and that such timing was medically reasonable. Tr. at
155, 164; Tornatore Rep. at 14. For support, he relied solely on a single epidemiologic study –
involving a totally different disease. See L. Schonberger, et al., Guillain-Barré Syndrome
Following Vaccination in the National Influenza Immunization Program, United States, 1976-
1977, 110 Am. J. Epidem. 105 (1979), filed as Ex. 60 (ECF No. 47-4) (“Schonberger”).
Schonberger’s authors studied the incidence of onset of GBS following receipt of the swine flu
vaccine, concluding that such an increase had occurred mostly within a five-week period thereafter
(although it was possible the risk interval could extend nine to ten weeks). Schonberger at 110.
By contrast, Dr. Tornatore acknowledged outright that Petitioner’s eczema most likely
began pre-vaccination. Tr. at 142. But he felt the symptoms she experienced in this time period
were less recurrent or “episodic” – with the “tempo” of incidents increasing after the second HPV
vaccine dose in September 2013. Id. at 149-50, 151. Despite record evidence suggesting that
Petitioner’s eczema had actually been deemed “recurrent” or “severe” in the past, Dr. Tornatore
maintained that records from close-in-time to her receipt of the vaccine clearly described an
exacerbation of symptoms. Id. at 144-45, 146, 148-49. Dr. Tornatore also pointed to instances in
the record where other treaters categorized Petitioner’s skin condition as “coming and going” (or
at times normal). Id. at 146-48. Ultimately, Dr. Tornatore could not pinpoint the exact day and
time Ms. McKown’s skin symptoms worsened, but maintained that the skin rashes progressively
worsened over a six-month period (beginning in June or July 2013 and later resulting in an
exacerbation or flare-up in September). Id. at 151.
For support on the reasonableness of the eczema exacerbation timeframe, Dr. Tornatore
again referenced Schonberger. Tr. at 116-17. He posited that literature on the topic of ADEM also
supported a conclusion that autoimmune diseases can occur between forty-eight hours and thirty
days following vaccine administration (though, he offered no literature directly addressing eczema
in this context, or why literature pertaining to GBS or some other clearly neuropathic condition
could also be applied to eczema). Id. at 117. Based on Schonberger, Dr. Tornatore also explained
that an initial immune response mediated by T cells could be quick (especially in the context of an
anamnestic response), but could also linger for a period of two months or even longer. Id. at 116.
Given the amount of time it takes to develop immune memory, Dr. Tornatore posited that an
autoimmune response would occur in a similar timeframe (i.e., within a sixty-day period or earlier
if the patient has previous exposure to the same vaccine antigens). Id. at 116-17.
25
2. Drs. Judy Mikovits and Francis Ruscetti
Drs. Mikovits and Ruscetti32 prepared two reports in support of Petitioner’s claim. See
Expert Report, dated Dec. 2, 2016, filed as Ex. 25 (ECF No. 18-2) (“First Mikovits Rep.”); Expert
Report, dated July 19, 2017, filed as Ex. 51 (ECF No. 30-2) (“Second Mikovits Rep.”). Only Dr.
Mikovits testified at hearing, however.33 Dr. Mikovits offered the opinion that the two doses of
HPV, in conjunction with the Hep A vaccine, caused Petitioner to develop POTS and atopic
dermatitis. Contrary to Dr. Tornatore, however, Dr. Mikovits posited that Ms. McKown’s medical
records did not offer persuasive evidence that she indeed suffered from recurrent skin rashes
(characterized as atopic dermatitis) prior to her receipt of the above-noted vaccines – thus, her
opinion does not appear to implicate a significant aggravation theory (at least as it applies to
Petitioner’s skin condition).
Dr. Mikovits is a consultant with MAR Consulting Inc., a group she co-founded, and serves
as an advisor for a private equity investment company. Curriculum Vitae, filed as Ex. 26 (ECF
No. 18-3) (“Mikovits CV”) at 1. She received her undergraduate degree in biology from the
University of Virginia, and a Ph.D. in molecular biology and biochemistry from George
Washington University. Id. at 4. Dr. Mikovits did not attend medical school, however, and is not
a licensed medical doctor. Tr. at 247. She thus has no direct experience treating skin diseases or
autonomic disorders.
From 1992 to 1994, Dr. Mikovits was a post-doctoral fellow in molecular virology at the
National Cancer Institute, Lab of Genomic Diversity, subsequently serving as a staff scientist at
the National Cancer Institute, Lab of Leukocyte Biology, from 1994 to 1998. Mikovits CV at 1-2.
Thereafter, from 1999 to 2001, she served as a Lab Director at the Laboratory of Antiviral Drug
Mechanisms, a division of the National Cancer Institute. Id. at 3. Dr. Mikovits worked in various
capacities at several biotechnology start-up companies from 2002 to 2006, and conducted research
at the Whittemore Peterson Institute for Neuroimmune Disease (“Whittemore”) from 2006 to
2011, studying diseases with inflammatory components and environmentally acquired immune
32
At hearing, Dr. Mikovits testified that both she and Dr. Ruscetti separately reviewed the medical records and case
filings prior to preparing their joint expert report. Tr. at 224. They assumed the factual assertions contained in
Respondent’s Rule 4(c) Report were correct. Id. at 225. She further stated that she and Dr. Ruscetti worked together
to prepare the report, relying on their respective areas of expertise in substance (for Dr. Ruscetti: dendritic cells and
the adaptive immune system; for Dr. Mikovits: mast cells and microglia involvement in disease pathology). Id.
33
According to his CV, Dr. Ruscetti received his B.S. in biology from Boston University, followed by a Ph.D. in
microbiology from the University of Pittsburgh. See Curriculum Vitae, filed as Ex. 27 (ECF No. 18-4) at 1. From
1972 to 1975, Dr. Ruscetti served as a research instructor at the University of Pittsburgh School of Medicine. Id. He
worked for Litton Bionetics as a cell biologist from 1975 to 1978. Id. In 1978, he joined the National Cancer Institute,
and presently serves as Principal Investigator for the Leukocyte Biology Section. Id. at 1-2. He is also an Adjunct
Professor of Biochemistry and Molecular Biology at George Washington University. Id. at 2. Dr. Ruscetti serves on
the editorial board of Stem Cells, and his CV lists multiple authored publications. Id. at 2-33.
26
deficiency. Mikovits CV at 2; Tr. at 221. She has not conducted research since 2012, but now
works as a consultant. Mikovits CV at 1.
Significant and alarming elements of Dr. Mikovits’s professional history were pointed out
at hearing that greatly diminished her credibility as an expert. In particular, while at Whittemore
Dr. Mikovits was accused of stealing laboratory materials, arrested, and fired from her position.
Tr. at 218, 265-66. In addition, a paper Dr. Mikovits published in Science was later retracted
because the results could not be replicated, causing the journal to lose confidence in the report and
the validity of its conclusions. Id. at 216, 258-59. Dr. Mikovits nevertheless has continued to
reference the article on her consulting website without disclosing its retraction. Id. at 265. Dr.
Mikovits has also published works and given presentations which dispute the safety and value of
vaccines, imply a link between vaccines and autism, and/or recommend a moratorium on vaccine
administration generally. Id. at 250-51, 255, 256-58. She has collaborated with an anti-vaccination
publisher and co-author, and regularly speaks at the “AutismOne” conference. Id. She has also
supported a ban on all HPV vaccines and attacked the Vaccine Program as biased. Id. at 255.
Like Dr. Tornatore, Dr. Mikovits testified about Petitioner’s claimed vaccine-caused
diagnoses of POTS and atopic dermatitis, as well the possible causal connection between the HPV
vaccine (and Hep A) and her disease onset. Although the opinions she offered regarding the
vaccines at issue in the case and the appropriate causal mechanism differed from those offered by
Dr. Tornatore, she similarly opined that Ms. McKown’s onset of POTS and atopic dermatitis flares
were caused by an autoimmune process (or reaction) that was likely vaccine-induced.
Dr. Mikovits began by discussing Petitioner’s May 2013 POTS diagnosis. Although Dr.
Mikovits has never treated POTS patients, she filed literature defining POTS as a heterogeneous
disorder characterized by abnormal increments in heart rate upon assumption of the upright
posture, accompanied by orthostatic intolerance and other secondary symptoms. See, e.g., L.
Brinth, et al., Orthostatic Intolerance and Postural Tachycardia Syndrome as Suspected Adverse
Effects of Vaccination Against Human Papilloma Virus, 33 Vaccine 2602 (2015), filed as Ex. 42
(ECF No. 20-7) (“Brinth”).34 Though the cause of POTS is unknown, the onset of its symptoms
can occur following febrile illness, pregnancy, immunization, sepsis, surgery, or trauma. Brinth at
2603; see also E. Benarroch, Postural Tachycardia Syndrome: A Heterogenous and Multifactorial
Disorder, 87 Mayo Clin. Proc. 1214 (2012), filed as Ex. 28 (ECF No. 19-2) (“Benarroch”) (50
percent of POTS cases have an antecedent viral infection, and 25 percent have prior familial
34
Dr. Mikovits expert report stated – incorrectly – that lightheadedness and syncope were not associated with POTS.
Second Mikovits Rep. at 2. She also cited literature positing the same. See S. Blitshteyn, Postural Tachycardia
Syndrome Is Not Caused by Deconditioning, 6 Pulm. Circ. 401 (2016), filed as Ex. 66 (ECF No.49-4) (letter to the
editor). At hearing, she corrected herself and stated she should have said those symptoms were simply not “diagnostic”
of the condition. Tr. at 271.
27
history); First Mikovits Rep. at 5-6.35 Dr. Mikovits also suggested that POTS could be related to a
genetic susceptibility. Tr. at 280-81.36
Dr. Mikovits also characterized POTS as an autoimmune disease. Tr. at 243-44. As she
broadly posited, the “heterogeneity” of the disease suggests it is neuroinflammatory in nature. Id.
at 229; see also S. Blitshteyn, Autoimmune Markers and Autoimmune Disorders In Patients With
Postural Tachycardia Syndrome (POTS), 24 Lupus 1364 (2015), filed as Ex. 64 (ECF No. 49-2)
(“Blitshteyn”). In support, Dr. Mikovits cited to instances in the medical records where various
treaters noted that Petitioner had, post-vaccination, experienced symptoms often associated with
an underlying inflammatory process (including pain, brain fog, weakness, and skin eruptions). Tr.
at 287, 292.37 And she pointed to lab results from December 201338 (revealing increased levels of
IgE and Lyme disease) as evidence of ongoing inflammation. Id. at 287-88. She did, however,
acknowledge that the more traditional biomarkers for inflammation – which she defined as “mast
cell mediators” – were either documented as normal (i.e., CRP and ESR) or never tested (i.e.,
cytokine levels). Id. at 287-88.
Dr. Mikovits went on to argue that relevant literature establishes that at least “half” of all
POTS cases have some neuropathic basis. Tr. at 276-77; M. Thieben, et al., Postural Orthostatic
Tachycardia Syndrome: The Mayo Clinic Experience, 82 Mayo Clin. Proc. 308 (2007), filed as
Ex. 54 (ECF No. 30-5) (“Thieben”); Benarroch at 1215-16. Thieben was a retrospective study of
152 POTS patients seen at the Mayo Clinic over eleven years, and considered the data and test
results obtained during treatment. Thieben at 308. It hypothesized that a particular autoantibody
(the ganglionic acetylcholine receptor) was associated with neuropathic cases of POTS, although
by its own terms the article does not propose or embrace the contention that POTS is in all (or
even most) cases an autoimmune disease. Id. Indeed, as observed in Benarroch (a review article
aimed at cataloging the pathophysiology and subtypes of POTS, including the neuropathic and
hyperadrenergic variants), Thieben only found that fourteen percent of all POTS patients
considered in the study presented with evidence of a ganglionic acetylcholine receptor antibody
35
During her testimony, Dr. Mikovits asserted that POTS is not caused by deconditioning (a contention directly
contrary to what the medical community better versed in POTS understands to be the case in many instances). Tr. at
245; compare Benarroch at 1216-17.
36
Dr. Mikovits spent some time at hearing discussing the MTHFR methylation defect (which she suggested was
present in Petitioner’s family history). Tr. at 280-81. But she could not point to a medical record confirming that Ms.
McKown possessed this particular defect, nor did she offer evidence associating it with POTS. Id. at 281.
37
Upon further questioning, Dr. Mikovits admitted that she relied heavily on the fact of the POTS diagnosis as proof
that Petitioner had experienced post-vaccination neuroinflammation. Tr. at 292.
38
Presumably, Dr. Mikovits is referring to Ex. 1 at 65-66 (dated from December 2013) – which is consistent with Dr.
Tornatore’s testimony. Dr. Mikovits did not reference a particular date during her testimony, however. See Tr. at 287-
88.
28
(which could indicate an immune cause of neuropathic POTS in some cases, but hardly even close
to half. Benarroch at 1215-16.
Dr. Mikovits further relied on various studies associating POTS with other autoimmune
conditions, such as autoimmune inflammatory syndrome induced by adjuvants (“ASIA”)), and
chronic fatigue syndrome (“CFS”). Tr. at 243-45; see, e.g., S. Dahan, et al., Postural Orthostatic
Tachycardia Syndrome (POTS) – A Novel Member of the Autoimmune Family, 25 Lupus 339
(2016), filed as Ex. 65 (ECF No. 49-3) (“Dahan”); S. Cerpa-Cruz, et al., Adverse Events Following
Immunization With Vaccines Containing Adjuvants, 56 Immuno. Res. 299 (2013), filed as Ex. 30
(ECF No. 19-4) (“Cerpa-Cruz”); G. Giannotta, et al., Vaccines and Neuroinflammation, 3 Int’l J.
Public Health Safety 1 (2018), filed as Ex. 68 (ECF No. 53-2) (“Giannotta”). Dr. Mikovits posited
that forty percent of POTS patients congruently suffer from other autoimmune conditions (like
those noted above) – though no specific piece of literature directly supports such an assertion. Tr.
at 272.
In addition, Dr. Mikovits referenced various review articles that “reported” occurrence of
“severe somatoform dysautonomic and neuropathic syndromes” following receipt of the HPV
vaccine, all of which she posited result in symptoms consistent with or overlapping POTS. Tr. at
228-29; First Mikovits Rep. at 7; see B. Palmieri, et al., Severe Somatoform and Dysautonomia
Syndromes After HPV Vaccination: Case Series and Review of Literature, SpringerOnline (2016),
doi 10.1007/s12026-016-8820-z, filed as Ex. 32 (ECF No. 19-6)39; S. Aratani, et al., Murine
Hypothalamic Destruction With Vascular Cell Apoptosis Subsequent to Combined Administration
of Human Papilloma Virus Vaccine and Pertussis Toxin, Scientific Reports (2016),
doi:10.1038/srep36943, filed as Ex. 43 (ECF No. 20-8); M. Martinez-Lavin, Hypothesis: Human
Papillomavirus Vaccination Syndrome—Small Fiber Neuropathy and Dysautonomia Could be Its
Underlying Pathogenesis, Clin. Rheum. (2015), doi:10.1007/s10067-015-2969-z, filed as Ex. 34
(ECF No. 19-8); Brinth at 2602.
Dr. Mikovits next discussed the purported association between Petitioner’s skin symptoms,
which she characterized as atopic dermatitis, and an autoimmune process. Tr. at 277-79. Atopic
dermatitis, in her view, is also immune-mediated – and thus distinct from eczema, for example. Id.
at 230, 277-78. While both conditions are of the same disease family, atopic dermatitis is a
subgroup that is inflammatory in nature, while eczema is not. Id. at 278. To support the purported
neuropathic connection between Petitioner’s skin symptoms and POTS, Dr. Mikovits referenced
Voisin (discussed earlier by Dr. Tornatore), which concluded that immune cells/inflammatory
mediators can act as “neurotransmitters” or signalers (by way of “cross-talk,”), and thereby
mediate allergic inflammation. Id. at 230; Voisin at 1. Dr. Mikovits concluded that “cross-talk”
between neuronal receptors and immune cells can cause skin inflammation – as evidenced by an
onset of itching. Tr. at 230.
39
Exhibit 33 is a corrected version of this article.
29
Based on her review of the record and scientific literature filed in support, Dr. Mikovits
posited that the biologic process responsible for Ms. McKown’s onset of symptoms post-
vaccination likely originated with dysregulation or “overstimulation” of the innate immune system
(which she defined as comprising the body’s “first responders” during an immune response). Tr.
at 196, 227, 289; First Mikovits Rep. at 8. Autoimmunity, in her view, is initiated by an “overactive
immune system” in which various innate immune mediators (including dendritic cells, mast cells,
and microglia) respond to some “perceived threat” (or foreign agent), thereby causing excessive
inflammation in the body. Tr. at 237-38; see also First Mikovits Rep. at 8. The innate system is
capable of recognizing foreign antigens quickly and building a memory response. First Mikovits
Rep. at 8.
Dr. Mikovits next turned to the role a vaccine could play in causing such innate system
overactivity. As. Dr. Mikovits explained, the components of the HPV and Hep A vaccines (both
of which contain aluminum as an adjuvant) dysregulate brain microglia (and mast/dendritic cells
at the mucosal cell surface) – thereby causing chronic neuroinflammation in a genetically
susceptible patient. Tr. at 226-27, 233, 281-82; First Mikovits Rep. at 8-9. After stimulation by a
vaccine, the innate system triggers the overproduction of inflammatory cytokines. Tr. at 227, 233.
Such an overproduction of cytokines could thereafter become chronic, when microglia – non-
neuronal glial cells located in the brain that also play an immune defense role – are primed to
become a source of excess cytokine production, often in reaction some prior insult (such as
vaccination). First Mikovits Rep. at 8-9. In most cases, patients confronted with a cascade of
proinflammatory cytokines can self-regulate the overproduction via a normal immune system
response (with the help of T cells). Tr. at 230-40. Those who experience dysregulation, however,
typically have some form of a genetic susceptibility to autoimmunity (though puberty and/or a
traumatic injury could also spur on such a response). Id. at 240-41.
Dr. Mikovits specifically implicated the IL-1 beta cytokine (which she stated “controls the
local pro-inflammatory cascade”) as responsible for preventing protective immunity from
becoming destructive. Tr. at 230-31. Dr. Mikovits posited that scientific literature on the topic
shows that inhibiting IL-1 beta production can prevent adverse cardiac events from occurring
(though, she did not file any to corroborate her statements). Id. at 231. Based on the above, Dr.
Mikovits concluded that POTS (which is cardiac driven) is likely caused by an inflammatory
response brought about by the overproduction of IL-1 beta. Id.
The receipt of multiple vaccines, Dr. Mikovits maintained, could amount to “damage at a
distance” whereby the immune system cannot adequately respond to the above and properly self-
regulate. Tr. at 232, 295. Inflammatory cytokines can thus more quickly cross from the periphery
(where they originate) and into the central nervous system (thereby interacting with brain
microglia), breaching the blood-brain barrier with the help of macrophages. Id. at 295. Dr.
30
Mikovits posited that histidine and polysorbate 80 (both HPV vaccine ingredients) were also likely
responsible for this breach. Id. at 233. And she allowed for the possibility that “virus-like particles”
contained in the vaccines can “package pieces and parts of other DNA and other retroviruses”
could contribute to the breach, but she could not be more specific as to how (or even what literature
existed that reliably could support such a contention). Id. at 234; see also First Mikovits Rep. at
10.
Along those same lines, Dr. Mikovits discussed the various “excipient[]” components (i.e.,
preservatives or adjuvants) contained in the HPV and Hep A vaccines – which she deemed
responsible for such as response. Tr. at 231-32; First Mikovits at 10-11. In particular, Dr. Mikovits
implicated the aluminum adjuvant40 (which is present in both the HPV and Hep A vaccines) as
causative of the dysregulation of the cytokine balance discussed above. Tr. at 232; R. Gherardi, et
al., Aluminum Adjuvants of Vaccines Injected Into the Muscle: Normal Fate, Pathology, and
Associated Disease, 100 Morphologie 85 (2016), filed as Ex. 49 (ECF No. 21-5); F. Liang & K.
Lore, Local Innate Immune Response in the Vaccine Adjuvant-Injected Muscle, 5 Clin. & Trans.
Immunol. 74 (2016), filed as Ex. 41 (ECF No. 20-6); C. Exley, et al., When an Aluminum Adjuvant
Is Not an Aluminum Adjuvant Used in Human Vaccination Programmes, 30 Vaccine 2042 (2012),
filed as Ex. 39 (ECF No. 20-4) (Letter to the Editor); C. Exley, et al., Aluminum-Based Adjuvants
Should Not Be Used as Placebos In Clinical Trials, 29 Vaccine 9289 (2011), filed as Ex. 38 (ECF
No. 20-3) (Letter to the Editor).
She also referenced literature discussing the concept of ASIA41 (even though Petitioner has
explicitly indicated it is not part of her causation theory)42, and mast cell activation disorder –
which, in her view, establishes that merely 400 micrograms of alum is enough to “cripple[e]” the
microglia – thereby resulting in a disease state characterized by ongoing inflammation. Tr. at 232,
281, 289-90; First Mikovits Rep. at 11; see L. Tomlijenovic, et al., Postural Orthostatic
Tachycardia With Chronic Fatigue After HPV Vaccination as Part of the “Autoimmune/Auto-
Inflammatory Syndrome Induce By Adjuvants”: Case Report and Literature Review, J. Invest.
Med. (2014), doi:10.1177/2324709614527812, filed as Ex. 29 (ECF No. 19-3); M. Frieri, et al.,
Mast Cell Activation Syndrome: A Review, 13 Curr. Allergy Asthma Rep. 27 (2013), filed as Ex.
40 (ECF No. 20-5). The chronic aspect of such a response is attributable to the alum “stay[ing] in
40
At hearing, Dr. Mikovits asserted that the specific aluminum adjuvant present in the HPV and Hep A vaccines has
never been tested for safety despite being used in vaccines for over 80 years. Tr. at 281.
41
On cross, Respondent pointed out that ASIA is not recognized by the World Health Organization as playing a role
in the causation of adverse events related to vaccination. Tr. at 272-73. Dr. Mikovits acknowledged the finding, but
maintained that the ASIA is consistent with the theory that an autoimmune disease can be triggered by various external
agents. Id. at 273.
42
See Pre-Hearing Reply, dated Sept. 21, 2018 (ECF No. 52) (“Respondent spends a good portion of their Pre-Hearing
memorandum addressing the ASIA theory. However, while Drs. Mikovits and Ruscetti reference ASIA, neither they
nor Dr. Tornatore assert ASIA as their theory of causation.”).
31
the macrophage” for “more than one year.” Tr. at 289.43 This interaction (coupled with the
components of her theory discussed below) helps to create the overall autonomic dysfunction
Petitioner alleges to have experienced post-vaccination. Id. at 289-91.44
While maintaining that the autoimmune process resulting in Ms. McKown’s injuries
originated from an innate immune response, Dr. Mikovits posited that the adaptive system (via
molecular mimicry) also likely plays a role in the overall cascade of autoimmune dysfunction. In
addition to sequential homology (between vaccine-induced autoantibodies and self proteins), Dr.
Mikovits explained that “conformational epitope[s]” expressed on the cell surface (in response to
the insulting foreign antigen) are actually responsible for the cross-reactivity. Tr. at 234-35. For
example, the Hep A vaccine contains a “cell line” called MRC-5 (a human cell line from aborted
fetal tissue) that shares homology with endogenous human retroviruses. Id. at 231. The
overlapping mimicry thus stimulates neuroinflammatory pathways and results in some adverse
disease process. Id. In the context of the HPV vaccine doses, Dr. Mikovits posited that the Kanduc
paper (also referenced by Dr. Tornatore) establishes 200 potential immunogenic and cross-reactive
epitopes to HPV vaccine antigens. Id. at 235. This process can also be hastened by subsequent
exposure to the same vaccine antigens, which would be consistent with a “challenge-rechallenge”
response. Id. at 235-36.
B. Respondent’s Witnesses
1. Dr. Christopher Gibbons
Dr. Gibbons filed one written report in this matter and testified at hearing. Tr. at 303-443;
Expert Report, dated May 4, 2018, filed as Ex. D (ECF No. 35-1) (“Gibbons Rep.”). Based upon
the record as a whole and his review of the scientific literature, Dr. Gibbons posited that vaccines
do not cause POTS (nor did they do so in this case).
Dr. Gibbons currently serves as a staff neurologist at Beth Israel Deaconess Medical Center
in Boston, Massachusetts. Curriculum Vitae, filed as Ex. O (ECF No. 54-1) (“Gibbons CV”); Tr.
at 303. In addition to the above, he holds a number of clinical and teaching positions: Associate
43
Dr. Mikovits also made some suggestion that the chronic inflammation (or driver of the “disease engine”) associated
with immune system disorders can also be caused by “oxidative stress” or “reactive nitrogen species”. Tr. at 244. Such
concepts were not discussed in depth – but have been offered in prior Program cases without success. See, e.g., Bast
v. Sec’y of Health & Human Servs., No. 01-565V, 2012 WL 6858040, at *6 (Fed. Cl. Spec. Mstr. Dec. 20, 2012)
(rejecting theory that seizures resulted from vaccine-induced mitochondrial dysfunction associated with oxidative
stress), mot. for review den’d, 117 Fed. Cl. 104 (2014).
44
On cross, when confronted with evidence that humans ingest far more aluminum per day than the considerably
smaller amounts contained in a vaccine, Dr. Mikovits posited that ingesting is not comparable in effect to injecting
cells directly with the adjuvant. Tr. at 282. She did not offer any scientific or medical evidence to corroborate the
assertion, however.
32
Professor of Neurology, Director of the Neurocutaneous Laboratory, Associate Director of the
Autonomic Laboratory, and Director of the Neuropathy Clinic at Beth Israel’s Joslin Diabetes
Center. Tr. at 303. He received his undergraduate degree from Dartmouth College, followed by a
and medical degree from Albert Einstein College of Medicine. Gibbons CV at 1; Tr. at 309. He
completed a neurology residency at Johns Hopkins Hospital in Baltimore, Maryland, and a
fellowship thereafter in clinical neurophysiology (with a subspecialty in autonomic disorders) from
Beth Israel. Tr. at 309.
Over the course of his career, in his clinical practice Dr. Gibbons has repeatedly evaluated
and treated patients with immune-mediated conditions, including autonomic disorders, peripheral
nerve disease, neuropathies, and small fiber neuropathies. Tr. at 303-04. Due to the overlap
between the autonomic and peripheral nervous systems, his treatment focus has been in patients
with Parkinson’s disease (who also display dysautonomia), multiple system atrophy, and diabetic
neuropathy. Id. at 304-05. He also oversees a neurocutaneous skin biopsy lab in which he (and his
students) evaluate biopsy results to determine nerve involvement. Id. at 305. He treats patients
with POTS (and routinely conducts tilt tabling testing). Id. at 306-07, 340. In addition, Dr. Gibbons
serves on the board of various journals focused on autonomic issues, including Autonomic
Neuroscience: Basics and Clinical. Id. at 308. Dr. Gibbons estimated that he spends roughly half
of his time treating patients (while the remaining half is used for teaching and research). Id. at 305-
06, 311. He does not have specialty training in the fields of immunology, dermatology, or
epidemiology, however. Id. at 399.
Dr. Gibbons began his testimony by describing the primary functions of the autonomic
nervous system (along with defining descriptive terms used to describe autonomic nervous system
irregularities, such as “dysautonomia” and “autonomic damage”). Tr. at 315. Dr. Gibbons defined
the autonomic system as the “subconscious” part of the nervous system responsible for controlling
or regulating the body’s involuntary functions (including breathing, heart rate, blood pressure,
sweating, urination, and defecation). Id. “Dysautonomia” or “autonomic dysfunction,” he posited,
is a vague term used in the literature to refer to a “perceived problem” with the autonomic system,
which may or may not be associated with some function in the autonomic system itself. Id. at 315-
16.
In contrast, “autonomic damage” refers to a specific, identifiable injury to the autonomic
system. Tr. at 316-17. For example, Parkinson’s disease is a condition linked to autonomic
damage. Id. at 317. As Dr. Gibbons explained, Parkinson’s can be attributed to a particular protein
in the body (“alpha-synuclein”), the presence of which is identifiable by both microscopic imaging
and testing, and which causes direct damage to the autonomic system. Id. Vasovagal syncope (or
presyncope symptoms: dizziness, lightheadedness, palpitations, or blacking/greying out), on the
other hand, does not necessarily reflect the existence of damage to the autonomic system, but can
33
instead constitute a “normal, completely physiologic, typical response” by an otherwise-healthy
autonomic nervous system. Id. at 316, 336-37.
Dr. Gibbons next defined POTS and its usual symptoms and course. POTS is characterized
by a “heart rate increase that goes up over time beyond what we would consider normal,” resulting
in a number of symptoms (lightheadedness, dizziness, palpitations, tremulousness, feelings of
presyncope, and vasovagal syncope). Tr. at 317-18, 322; see also R. Freeman, et al., Consensus
Statement on the Definition of Orthostatic Hypotension, Neurally Mediated Syncope and the
Postural Tachycardia Syndrome, 161 Autonomic Neurosci. 46 (2011), filed as Ex. D, Tab 1 (ECF
No. 35-2); Gibbons Rep. at 3-4. Skin rashes, in his view, are typically not a presenting symptom
of POTS. Tr. at 436-37.45 In addition, vasovagal syncope is not by itself diagnostic of POTS (or
its inevitable result). Id. at 322, 414, 416 (“people with POTS don’t have to faint”).
POTS is classified as a “syndrome” due to the various etiologies (some of which can be
autoimmune) associated with its onset, including deconditioning, chronic illness, and/or
autonomic neuropathy. Tr. at 317; Gibbons Rep. at 3-4.46 As Dr. Gibbons explained, POTS can be
an “end result of many potential avenues,” including a secondary reaction to a variety of diseases,
like diabetes, thyroid dysfunction, renal dysfunction, or multiple sclerosis. Tr. at 318. The
diagnostic criteria for POTS require (a) an increase in the heart rate of more than 30 bmp or more
from the supine to standing position (or 40 bmp or more if under twenty years of age), (b)
symptoms that are consistent with such a diagnosis (as describe above), and (c) a continuation of
symptoms for greater than six months. Id. at 318-19. POTS is most common in young women
(generally teenagers up to their twenties). Id. at 319.
POTS can be divided into various subgroups with overlapping symptoms (Tr. at 402),
including hypovolemic, hyperadrenergic, and neuropathic. As Dr. Gibbons explained, all the
variants are distinguishable based on laboratory or clinical testing. Tr. at 322, 402. Hypovolemic
POTS is characterized as POTS “related to low blood pressure” (occurring, for example, when an
individual exercises excessively without proper fluid intake). Id. at 320-21. The hypovolemic
variant can also present secondarily to various illnesses associated with deconditioning (including
myalgic encephalomyelitis and CFS). Id. at 419-20. Hyperadrenergic POTS is related to an
adrenaline response (i.e., an increase in norepinephrine). Id. at 321. According to Dr. Gibbons, this
45
As already noted, Petitioner’s experts relied on Voisin as establishing “cross talk” between nerves resulting in onset
of skin rashes that could in turn demonstrate how skin conditions like eczema were the product of the same
autoimmune process that allegedly was causing a person to experience POTS. Tr. at 423-25. In response, Dr. Gibbons
deemed the theory “interesting” but claimed that it did not stand as reliable evidence establishing a reliable medical
association between such conditions (nor evidence that the nerves were indeed damaged in the process). Id. at 423,
433.
46
At hearing, Dr. Gibbons disputed any suggestion that POTS is more often than not caused by neuroinflammation.
Tr. at 325-26.
34
subgroup is more easily differentiated in autonomic testing. Id. Hyperadrenergic POTS can occur
congruently with autoimmune disease (for example, type I diabetes or limb encephalitis), though
in such cases a patient will experience other severe symptomology consistent with the primary
disease process in question. Id. at 314, 357. This subgroup can also be antibody-mediated or
instigated by the presence of toxic substances. Id. at 325.
Finally, Dr. Gibbons discussed neuropathic/neurogenic POTS – a variant he deemed (based
upon his direct experience) “quite rare.” Tr. at 321-22, 377. Dr. Gibbons described this subgroup
as an immune-mediated form of POTS resulting in “some sort of damage to the autonomic nervous
system” which impairs the typical autonomic functions, resulting in the tachycardia associated
with the illness. Id. at 321, 324-35.47 Neuropathic POTS is typically associated with a particular
antibody (the “ganglionic receptor antibody”) that targets the acetylcholine receptor in the
autonomic ganglia, resulting in autoimmune ganglionopathy. Id. at 358. High amounts of the
ganglionic receptor antibody can cause profound autonomic failure (resulting in a total loss of
control of blood pressure, heartrate bowels, bladder, etc.). Id. Based on his knowledge of the
literature, Dr. Gibbons posited that the ganglionic antibody is the only clinically relevant antibody
associated with neuropathic POTS. Id. at 358. He could not identify any other antibody targeted at
the heart,48 but added that he was aware of ongoing research on the topic, although he deemed it
preliminary. Id. at 358, 375-76, 396.49
In addition to the above, Dr. Gibbons questioned the significance of various pieces of
literature offered by Petitioner’s experts to support the conclusion that all (or most) forms of POTS
are neuropathic in nature. In so doing, Dr. Gibbons emphasized the absence of evidence
establishing that the POTS she experienced was consistent with the immune-mediated form of the
condition. Benarroch, for example, discusses the more common POTS subtypes (hypovolemic and
hyperadrenergic), but allows that POTS can be immune-mediated (as Petitioner proposes). Tr. at
361. Dr. Gibbons, however, posited that Benarroch actually supported his earlier conclusion that
the only known antibody associated with neuropathic version of the condition is the ganglionic
acetylcholine receptor antibody – with no other subtype of the disease demonstrated
“convincingly” to be immune mediated. Id.
Thieben, in his view, followed the same pattern: establishing that neuropathic POTS is a
rare subtype specifically involving antibody-mediated, neuronal damage. Tr. at 364. As Dr.
47
A further subset of neuropathic variant is “cholinergic” POTS. Tr. at 324. The cholinergic variant results from
damage to the “sympathetic cholinergic system” associated with gastrointestinal symptoms (and can be associated
with abnormal sweating and nerve damage). Id. at 324, 370-71.
48
Dr. Gibbons posited, however, that structural damage to the heart directly could cause POTS. Tr. at 396-97.
49
As Dr. Gibbons explained, it is difficult to determine if elevated titers of certain circulating antibodies are clinically
relevant absent (a) evidence that high titers are associated with a disease, and (b) evidence that removing those
antibodies prompts a recovery. Tr. at 376.
35
Gibbons explained, Thieben provided evidence that a small number of POTS patients (6 out of 42
or 14 percent) presented with the above-described ganglionic antibody in low positive values. Id.
at 363. But this percentage appeared high to Dr. Gibbons, as he has seen only one POTS patient
with the same ganglionic antibody in the last ten years of his clinical practice. Id. In addition, those
percentages have never been reproduced in further research. Id. at 364, 442-43. Thieben’s authors
similarly made clear that actual damage to the autonomic nervous system did not explain every
POTS subtype. Id.
Dr. Gibbons next discussed the Blitshteyn paper. Tr. at 364-65. Blitshteyn’s authors tested
POTS patients for certain autoimmune biomarkers (e.g., ANA, TTG, SS-A antibodies, etc.),
concluding (based on their positive readings) that autoimmunity must be common in POTS
generally. Id. at 365. Dr. Gibbons, however, criticized Blitshteyn for the inclusion criteria used in
conducting its analyses. Id. at 366. He noted that the study appeared to have self-selected for
patients who suffer from both POTS and an additional autoimmune disease. Id. at 366-67. It was
thus no surprise that many of the studied patients also tested positive for autoimmune biomarkers.
Id. at 367. More importantly, many biomarkers tested for in Blitshteyn had no known association
(in the causation context) to the patient’s underlying disease process – and therefore their presence
did not establish a causal link. Id. at 367. Thus, Blitshteyn could not, in Dr. Gibbons’s opinion, be
invoked to support a conclusion that POTS is generally autoimmune in nature (as Petitioner’s
causation theories implied). Id. at 368.
Dr. Gibbons also addressed the relationship between neuropathic POTS and vasovagal
syncope of the kind relevant to this case. In his experience, neuropathic POTS actually does not
result in, or even feature, syncope. Tr. at 322. Rather, syncope is typically a product of a properly
functioning autonomic nervous system – thus, patients with autonomic damage would likely not
manifest syncope symptoms. Id. at 323, 394, 421 (describing syncope is a “normal physiologic
response”). Rather, the progressive, neuropathic variant of POTS results in orthostatic hypotension
without the tachycardia typically associated with the non-neuropathic subgroups. Id. at 323-24. In
fact, neuropathic POTS should feature a reduction in syncope (given the resulting damage to the
autonomic system). Id. at 349. All in all, Dr. Gibbons concluded that healthy patients can have
vasovagal syncope with no corresponding autonomic damage. Id. at 434, 436.
Relying on his review of the medical records, Dr. Gibbons characterized Petitioner’s
variant of POTS as most likely hypovolemic rather than neuropathic. Tr. at 326, 394. Dr. Gibbons
could not identify any evidence in the record to suggest or corroborate the propriety of a
neuropathic or hyperadrenergic POTS diagnosis. Id. at 394. He further opined that Ms. McKown’s
onset of POTS was not caused or significantly aggravated by either (or both) of her HPV vaccine
doses. Id. at 326, 394. In his practice, Dr. Gibbons regularly treats POTS patients (some of whom
have received the HPV vaccine and some who have not), and has seen no variances in disease
course. Id. at 429-30. Overall, he felt that some of Petitioner’s overall course could be attributable
36
to deconditioning (in light of her physical fitness routines50) and/or genetics (related to her
height51). Id. at 355-56.
In support, Dr. Gibbons referenced record evidence tending to suggest that Petitioner’s
POTS onset was unrelated to any autoimmune process and did not display what he would expect
to see if her POTS was neuropathic. No clinical test results indicated that she was experiencing
any underlying autoimmune disease process. Tr. at 396. A ganglionic receptor antibody test (which
could support a neuropathic variant of the condition) was never conducted. Id. In addition, as noted
above, Dr. Gibbons posited that symptoms indicative of neuropathic harm would be “striking” in
nature (including symptoms such as: fixed/dilated pupils, invariant heart rate, gastroparesis, and
urinary retention). Id. at 439 (describing an event where “essentially every component of the
autonomic nervous system shuts down”). But there was no record evidence that Petitioner
experienced any such drastic symptoms. And other than Dr. DeMio, none of Petitioner’s treaters
proposed autoimmune disease to explain her POTS. Id. at 356.
Rather, Ms. McKown’s course was more consistent with the hypovolemic variant of the
condition. Tr. at 332-33. In support, Dr. Gibbons referenced records detailing her hospital visit in
April 2013 (following the syncopal incident at the yogurt shop). Id. at 332-33. The orthostatic
vitals taken at the time indicated that Petitioner’s blood pressure was stable during the visit. Id. at
332. Her heart rate did increase significantly upon standing, but her syncopal symptoms resolved
following intake of a liter of fluids. Id. The fact that Petitioner’s symptoms ceased following fluid
intake suggested to Dr. Gibbons that she was suffering from the hypovolemic variant. Id. at 332-
33. In addition, laboratory testing completed during her hospital visit in late April 2013 revealed
an elevated BUN to creatine ratio of 20:1. Id. at 333. He considered such a high ratio as indicative
of dehydration (which would explain the resolution of symptoms following fluid intake). Id.52
In addition, Dr. Gibbons referenced Petitioner’s cardiology appointment with Dr. Dooley
(at which time she was officially diagnosed with POTS). In his view, the description of her
symptoms taken during this visit represented a “classic array” of those seen with POTS/vasovagal
50
Deconditioning did not necessarily mean that a person had been physically inactive. Dr. Gibbons referenced the fact
that astronauts (who are physically fit and trained) can develop POTS after returning to earth. Tr. at 355-56 (“[c]ouch
potato[es]” are not the only ones at risk”).
51
Dr. Gibbons suggested that the literature strongly supports an associations between POTS and having a small stature.
Tr. at 355. This point was not, however, developed at hearing or in the parties’ filings, and I therefore do not give it
substantial weight in Respondent’s favor (or against Petitioner).
52
Apart from the above, Dr. Gibbons acknowledged that the ER record also evidence a complaint of GI discomfort.
Tr. at 331. He thus allowed for the possibility that Petitioner’s GI symptoms could have caused her syncopal episode.
Id.
37
syncope patients that he had treated in the past. Tr. at 335.53 Ms. McKown’s orthostatic vitals again
revealed a table blood pressure reading with an increase in heartrate (from 68 to 100) upon position
change – which he deemed as “not quite meeting [POTS] criteria,” though not ruling it out either
(as it was close enough to the diagnostic measures). Id. at 335. Tilt table testing, however,
confirmed the diagnosis thereafter. Id. at 338-39, 342 (“[s]he fainted with her heart rate dropping,
her blood pressure dropping, and then she recovered”). Based on the above, Dr. Gibbons
eliminated the hyperadrenergic variant as a possible explanation, given that her blood pressure
readings were “pretty much the same or lower” (i.e., they didn’t go up). Id. But this record did not
support the neuropathic variant, because Petitioner had experienced syncope upon position change
– which indicated the absence of autonomic system damage. Id. There was also no evidence of
direct cardiac damage indicated on Petitioner’s EKG. Id. at 432. Thus, Dr. Gibbons concluded that
the hypovolemic variant was the form best supported by record evidence. Id.
Other records generated subsequent to Petitioner’s POTS diagnosis were also in Dr.
Gibbons’s view consistent with what would be experienced by a typical patient with non-
neuropathic POTS. Tr. at 345. For example, Dr. Gibbons referenced a record from January 2014,
in which Ms. McKown complained of “minor near-syncopal episodes” with worsening episodes
now resulting in loss of conscious (for twenty to thirty minutes) and abnormal eye movement. Id.
As Dr. Gibbons explained, recurrent episodes of syncope reflected a typical POTS course. Id. at
346.
Petitioner’s purported prolonged episodes of unconsciousness, however, were in Dr.
Gibbons’s view inconsistent with a POTS diagnosis (regardless of the subtype involved). Tr. at
346, 349. Prolonged unconsciousness, Dr. Gibbons reasoned, is instead associated with inadequate
blood flow to the brain or a brain irregularity (i.e, “both [brain] hemispheres . . . are not working”).
Id. at 346. Dr. Gibbons suggested that these prolonged episodes could possibly be attributable to
an underlying seizure disorder, but Petitioner’s presentation was more consistent with vasovagal
syncope. Id. at 347. Moreover, episodes of unconsciousness extending twenty to thirty minutes
would typically be associated with “significant cerebral deficits” which Petitioner did not
experience. Id. As a result, Dr. Gibbons proposed it most likely that these purported episodes of
prolonged unconsciousness were caused by other mechanisms (such as: hyperventilation, fear,
anxiety, fright, worrying, etc.) in which patients are “just unwilling to return to the situation” that
caused the episodes, and therefore did not conform to any form of POTS, neuropathic or otherwise.
Id. at 348-49.
53
This record also indicated that Ms. McKown (or her caretakers) expressed a concern for “recurrent” syncopal
episodes in years past, but Dr. Gibbons could conclude only that those episodes were at least consistent with her more
recent syncopal symptoms in April 2013. Tr. at 334, 405, 433. Later in his testimony, however, he opined that POTS
patients with a predisposition of fainting (in response to blood being drawn, for example) are more commonly placed
in the hypovolemic or hyperadrenergic categories. Id. at 344.
38
Along those same lines, Dr. Gibbons noted that more recent records from 2014 indicated
that Petitioner had been experiencing one to two episodes of POTS-related syncope per month. Tr.
at 350; see Ex. 7 at 10. The frequency of the syncopal episodes, Dr. Gibbons posited, was also
consistent with non-neuropathic POTS (which, as noted earlier, he would expect to diminish, not
increase, syncopal episodes). Tr. at 350-51. By July 2014, records indicated Petitioner’s POTS
symptoms were improving, but she had now experienced a new onset of joint pain. Id. at 351
(citing Ex. 21 at 1). Dr. Gibbons reported that symptoms of pain are not typically indicative of
POTS, unless the pain was attributable to some other underlying disorder. Id. at 352. POTS, in his
view, is not associated with any form of pain syndrome. Id. He therefore also discounted this
symptom as POTS related in any form.
With respect to timing, Dr. Gibbons opined that Petitioner’s POTS symptoms preceded
receipt of the HPV vaccine. He pointed to the records referencing pre-vaccination syncopal
episodes (for which Petitioner was referred to the cardiologist in the first place – on the very day
she received the first HPV dose). Tr. at 326 (citing Ex. 1 at 44). Records from March 2013
indicated that Ms. McKown reported three syncopal episodes with position change (along with
lightheadedness) before the visit – which Dr. Gibbons classified as “classic” POTS
symptomatology. Id. at 327-28.54 Dr. Gibbons ultimately placed onset around six months prior to
her receipt of the first dose of HPV. Id. at 328, 342-43. He also referenced earlier-in-time
orthostatic measurements taken during her wellness checks at ages eleven through fourteen. Id. at
329. Heart rate measurements taken at this time evidenced resting heart rates ranging from 104
beats per minute to 84 – measures he deemed high for a pediatric patient who was also actively
training for triathlons. Id. In his view, heart rate ranges in the 80-100 range suggests something
was occurring even though it might not be overtly clinical. Id. at 330.
Dr. Gibbons also addressed Dr. Tornatore’s arguments that Petitioner’s pre-vaccination
syncopal episodes were distinguishable because they were merely “situational” – a concept he
deemed to be not a “good medical term.” Tr. at 403. Rather, situational syncope and vasovagal
syncope are in his experience essentially synonymous concepts. Id. (describing “situational”
syncope as “vasovagal syncope related to a situation”). Later on in his testimony, however, he
admitted that certain “situations” could trigger vasovagal syncope (for example, having blood
drawn or receiving a reprimand for bad behavior, as is alleged to have occurred with Petitioner).
Id. Ultimately, he proposed that the earlier instances were most likely associated with, rather than
distinguishable from, Petitioner’s later course. Id. at 326-38, 342-43.
Apart from the above, Dr. Gibbons also questioned the strength of independent evidence
purportedly establishing a connection between the HPV vaccine and POTS. Brinth, for example,
identified young women in Denmark who had recently received the HPV vaccine and were then
54
If the prior episodes of syncope were ignored, Dr. Gibbons maintained that he would place onset of Petitioner’s
POTS in May 2013, given the symptoms reported during the visit described above. Tr. at 410-11, 412-13.
39
referred to a syncope clinic due to reported orthostatic intolerance symptoms. Brinth at 2602-05.
Its authors observed 21 cases of POTS out of 35 studied individuals. Id. at 2605. Significantly,
however, as Dr. Gibbons pointed out, all of the patients tested had suspected their POTS was
caused by the HPV vaccine – and were in fact referred to the trial for that reason. Tr. at 381. In his
view, given the self-selection bias in the inclusion criteria for studied individuals, no firm
relationship could be drawn from Brinth’s results. Id. at 382.
In addition, Dr. Gibbons noted that Brinth’s conclusions (which he admitted caused some
“concern” in the medical community regarding vaccine causation) prompted the European Medical
Agency (“EMA”) to conduct a follow-up study, in which it analyzed over 60,000 reports of onset
of POTS following the receipt of the HPV vaccine. Tr. at 383-85; Assessment Report: Human
Papillomavirus (HPV) Vaccines, EMA (2015), filed as Ex. D, Tab 13 (EC 36-4) (“EMA Report”).
The EMA report found that the incidence rate for the number of patients with post-vaccination
POTS (1 reported per 10,000) proved to be smaller than predicted, resulting in an assessment that
disputed associating the HPV vaccine to POTS. Tr. at 385; EMA Report at 38-39. Dr. Gibbons
admitted on cross examination, however, that the EMA report was based on some post-marketing
surveillance (a passive reporting system informing manufacturers of the incidence rate) which,
Petitioner posited, could have resulted in deflated numbers of reported incidence (as low as one
percent). Tr. at 427-28.
Dr. Gibbons also offered other literature supporting his contention that the HPV vaccine
likely plays no role in the development of POTS. Tr. at 387; J. Skufca, et al., Incidence Rates of
Guillain Barre (GBS), Chronic Fatigue/Systemic Exertion Intolerance Disease (CFS/SEID), and
Postural Orthostatic Tachycardia Syndrome (POTS) Prior to Introduction of Human
Papillomavirus (HPV) Vaccination Among Adolescent Girls in Finland, 3 Papillomavirus
Research 91 (2017), filed as Ex. D, Tab 14 (ECF No. 36-5) (“Skufca”). Skufca is a Finish study
which cataloged onset of various autoimmune disease following receipt of the HPV vaccine
beginning in 2013 (although it admittedly included reports from years prior, from 2002 to 2012,
when the HPV vaccine was not administered). Skufca at 91. Skufca’s authors noted a significant
increase in reported POTS cases the year prior to the vaccine being administered. Tr. at 387.
Around this same time, medical awareness of POTS increased (i.e., outreach campaigns were
conducted to inform physicians of the condition and diagnoses increased). Id. Thus, in Dr.
Gibbons’s view, the increase in reported cases could be attributable merely to greater awareness
of POTS, as opposed to an incidence rate increase attributable to vaccination. Id. at 387-88, 392.55
In addition, Dr. Gibbons offered a wide-in-scope review article on POTS’s purported
association with HPV vaccine. Tr. at 392-93; see B. Butts, et al., Human Papillomavirus Vaccine
55
On cross examination, Dr. Gibbons acknowledged that Finland stopped administering the HPV vaccine around
2012. Tr. at 429.
40
and Postural Orthostatic Tachycardia Syndrome: A Review of the Current Literature, J. Child
Neuro (2017), doi:10.1177/0883073817718731, filed as Ex. J (ECF No. 43-5) (“Butts”). Butts
cataloged various items of literature (including peer-reviewed articles, government statements, and
medical advisory committee notes – some of which were filed in the present matter) in an attempt
to gauge the strength of studies purporting to associate the HPV vaccine with POTS. Butts at 1, 3.
Its authors acknowledged the existence of case reports detailing the onset of POTS post-
vaccination, but ultimately determined that the existing epidemiologic evidence did not support a
causal connection. Id. at 7-10; Tr. at 392-93.
2. Dr. Andrew MacGinnitie
Dr. MacGinnitie served as Respondent’s second expert, offering two written reports in the
matter and testifying at hearing. Expert Report, dated Mar. 28, 2017, filed as Ex. A (ECF No. 23-
1) (“First MacGinnitie Rep.”); Expert Report, dated May 5, 2018, filed as Ex. C (ECF No. 34-1)
(“Second MacGinnitie Rep.”). Based on his review of the record, Dr. MacGinnitie opined that the
HPV and Hep A vaccines Petitioner received did not exacerbate her subsequent eczema flares
thereafter, and from an immunologic standpoint could not cause eczema or POTS. Tr. at 454, 455.
Dr. MacGinnitie is an attending physician and the Clinical Director for the Division of
Immunology at Boston Children's Hospital in Boston, Massachusetts. Curriculum Vitae, filed as
Ex. B (ECF No. 26-1) (“MacGinnitie CV”); Tr. at 444-45. He is also an Associate Professor of
Pediatrics at Harvard Medical School. Tr. at 445. Dr. MacGinnitie received his undergraduate
degree from Yale University, followed by both a medical degree and Ph.D. from the University of
Chicago. Id. at 445. He thereafter completed his residency, followed by a fellowship in allergy and
immunology at Boston Children’s. Id. at 445. He is board certified in pediatrics and allergy and
immunology, and has been in practice as an allergist/immunologist since 2004. Id. Further, he has
seen patients with various immunologic diseases, including reactions to vaccines. Id. Ninety
percent of his patients are children. Id. at 446-47. He estimated that he spends two-thirds of his
time treating patients in a clinical setting. Id. at 450.
In his practice, Dr. MacGinnitie treats many allergic conditions (including eczema/ atopic
dermatitis, food and environmental allergies, and urticaria). Tr. at 447. He diagnoses roughly 150-
160 eczema patients per year. Id. at 447-48. Dr. MacGinnitie also performs research and has
produced roughly thirty-five publications on the topic of food allergies (or associated conditions).
Id. at 452. And he has authored a paper on the effects of vaccination on patients with egg allergies.
Id. at 451. Dr. MacGinnitie serves as a medical reviewer for various journals, including Allergy
41
and Immunology. Id. at 452. As he acknowledged at hearing, however, Dr. MacGinnitie is not a
neurologist (or dermatologist), and he has not treated patients with POTS. Id. at 503-04, 505-07.56
Dr. MacGinnitie began his testimony by defining the various medical terms relevant to Ms.
McKown’s skin condition as described herein, including eczema/atopic dermatitis – which he
deemed interchangeable (Tr. at 508) – as compared to urticaria. Eczema is an erythematous, dry,
flaky rash that can persist from hours to days or months, and can chronically relapse. Tr. at 460-
61. Roughly ten to twenty percent of the population experiences eczema at some point in life,
making it a fairly common occurrence. Id. at 461. Ninety percent of patients are diagnosed as
infants, and some eventually outgrown the condition. Id. Eczema can worsen seasonally or flare
unexpectedly, when skin is dry (or in the midst humid conditions). Id. Hormones can also increase
the likelihood of a flare-up. Id. Due to the above, eczema can be difficult to treat. Id. Eczema is
not a true allergic response, but patients diagnosed with eczema are more susceptible to developing
food allergies and asthma later in life. Id. at 460. As Dr. MacGinnitie explained, symptoms of
inflamed, abraded skin (followed by exposure to various foreign antigens) increase the likelihood
later-onset allergies. Id. Vaccines, in his view, are not considered in the medical community to be
causal of eczema. Id. at 462-63.
Dr. MacGinnitie opined that eczema is not an autoimmune condition. Tr. at 462, 501, 544.
It is also not understood to be a presenting symptom of POTS (as he understands the disease). Id.
at 463. Later on in his testimony, however, Dr. MacGinnitie did acknowledge that the condition is
inflammatory (i.e., mediated by T cells) at least as it relates to the skin – and thus, certain immune-
modifying drugs, like Prednisone, can be used to effectively treat it, as was the case herein. Id. at
509-10. He maintained, however, that eczema can only be associated with distinct “subtypes” of
inflammation. Id. at 523. He also posited that the underlying inflammation associated with the
condition is not systemic in nature. Id. at 462.
On cross examination, Dr. MacGinnitie acknowledged that the innate immune system
likely plays some role in the development of eczema (given the increase in eosinophils associated
with the condition). Tr. at 514. He also agreed that cytokines can “drive[]” an “inflammation axis”
for eczema. Id. at 527. Certain drug therapies for eczema exist that are aimed at specific cytokine
receptors, further underscoring the innate system’s connection. Id. at 514, 524. Dr. MacGinnitie
agreed that cytokines can be involved in the pruritus (i.e. itching) associated with eczema. Tr. at
521. Itching, Dr. MacGinnitie posited, could be caused by cytokines stimulating the relevant nerve
fibers in the skin. Id. at 515-17. Thus, nerves are involved in eczema’s symptoms, given that by
56
On cross-examination, Petitioner’s counsel questioned Dr. MacGinnitie about the various grants he received (from
the government and pharmaceutical companies), which enabled him to complete research. Tr. at 504-05. I do not,
however, find that Dr. MacGinnitie’s receipt of such funding reduced his credibility or suggested bias – any more that
I would find that Dr. Tornatore’s frequent appearances on behalf of petitioners in the Vaccine Program is a per se
basis for finding him not credible as a general matter.
42
definition, pruritus is a “phenomenon mediated in the CNS.” Id. at 522. In so stating, he refuted
the suggestion that histamines cause itching (given that antihistamines do alleviate eczema
symptoms). Id. at 514.57
Urticaria, by contrast, is a term used interchangeably with “hives” or “welts.” Tr. at 449.
As Dr. MacGinnitie described, urticaria refers to raised skin lesions that usually “come and go” in
response to a specific allergen (for example, peanuts). Id. at 449-50. Urticaria can also be chronic
in nature – whereby the accompanying lesions persist for six weeks (or longer), often without any
explanation. Id. at 450. In a typical urticarial response, the body’s mast cells release histamine
(often instigated by exposure to an irritant/allergen), causing hives in response. Id. at 466-67. The
initiating allergen, however, is not itself the direct cause of hives. Id. at 466-67. Based on his
review of the medical literature, Dr. MacGinnitie knew of no studied association between
vaccination and onset of hives. Id. at 467. He allowed for the possibility, however, that hives could
be autoimmune in rare circumstances (i.e., where particular antibodies – antithyroid
autoantibodies, for example – are directed at the mast cells). Id. at 475, 544.58
Dr. MacGinnitie described an allergy as an “inappropriate immune response to a harmless
environmental stimuli” (for example, tree pollen, cat dander, or peanut protein). Tr. at 463. Typical
immune responses include sneezing, watery eyes, or anaphylaxis (a more extreme reaction). Id.
Allergies are typically diagnosed via serum-specific IgE testing or “RAST” – though such testing
can also produce false-positives. Id. at 465. A patient’s prior health history (following exposure to
suspected antigens) can also be helpful in evaluating for allergies. Id. An “intolerance,” however,
is not the same as an allergy. Id. at 464. Allergies, he posited, require systemic involvement (as
evidenced by an overall worsening of the response). Id. For example, a patient who is “lactose-
intolerant” will exhibit milder symptoms than a patient with a true milk allergy. As noted earlier,
allergic responses can result in more extreme symptoms (i.e., anaphylaxis). Id. at 465.
Dr. MacGinnitie proposed that allergies are not associated with a predisposition for
infection, autoimmune disease, or severe autonomic dysfunction. Tr, at 468. Similarly, Dr.
57
On cross examination, Petitioner’s counsel presented Dr. MacGinnitie with two articles, neither of which were filed
prior to hearing nor discussed during examination of Petitioner’s own experts. See G. Yosipovitch & A. Papoiu, What
Causes Itch in Atopic Dermatitis, 8 Curr. Allergy & Asthma Reps. 306 (2008), filed as Ex. 75 (ECF No. 61-4); J.
Hamilton, et al., Dupilumab Improves the Molecular Signature In Skin of Patients With Moderate-to-Severe Atopic
Dermatitis, 134 J. Allergy Clin. Immunol. 1293 (2014), filed as Ex. 76 (ECF No. 61-5). Counsel argued that the papers
established that an “overexpression” of interleukins or neutrophils could cause eczema itch. Tr. at 514, 515-17. Based
on his on-the-spot review of the article, however, Dr. MacGinnitie posited that interleukins or neutrophils might only
be “mediators” of pruritis, rather than causal of it. Id. at 517-20. The Hamilton article, counsel posited, reveals that
eczema can be effectively treated by certain anti-inflammatory drugs (including Dupilumab which targets the Th2-
centered inflammatory axis). Id. at 523-27. Indeed, Dr. MacGinnitie agreed that anti-inflammatories can successfully
treat the condition. Id. at 527. In so agreeing, however, Dr. MacGinnitie maintained that anti-inflammatories like
Dupilumab are commonly associated with eczema and food or environmental allergies. Id.
58
Along those same lines, Dr. MaGinnitie posited that it is uncommon for patients to present with both eczema and
urticaria (given the distinctions described above). Tr. at 509. It is even less common for eczema/urticarial patients to
also have POTS. Id. Dr. MacGinnitie testified that he has never treated a patient with all three conditions. Id.
43
MacGinnitie testified that he knew of no causal link between vaccines and onset of allergies (a
theory, he noted had been considered in the past, but not persuasively established). Id. at 466. As
he explained, he has treated patients who experience an allergic reaction to a vaccine, but none
who experience a worsening of allergy symptoms post-vaccination. Id. Indeed, he recommends
that his allergy patients receive vaccinations (particularly those with asthma), as vaccines can
prevent infections (and subsequent asthma exacerbations). Id.
In light of Petitioner’s claim that her skin symptoms worsened following receipt of the
HPV vaccine (along with some form of immune system dysregulation), Dr. MacGinnitie reviewed
the relevant medical records for any evidence consistent with such a response. Leading up to Ms.
McKown’s syncopal episode at the frozen yogurt shop, Dr. MacGinnitie found no record evidence
she possessed an abnormal immune system (beyond the possibility she had pre-existing
environmental allergies). Tr. at 468. At most, the records established that Petitioner clearly had
eczema (most likely in a mild form) as an infant, along with various preexisting environmental
allergies. Id. at 467, 469. He also observed that a CT scan taken during the April 2013
hospitalization revealed evidence of a sinus infection (which could be a result of her allergy
symptoms). Id. at 488.
Thereafter, Dr. MacGinnitie agreed, the post-vaccination records evidenced a worsening
of eczema (and onset of hives) around May 2013 and into the summer. Tr. at 468. But he described
Ms. McKown’s eczema course as a “classic” case (i.e., it was “within the range of what’s typically
seen” with eczema patients). Id. at 512. Any worsening Petitioner experienced could be attributed
to the “waxing and waning” nature of eczema – which, he posited, is normal for patients with the
condition. Id. at 468-69. Petitioner’s April 2014 skin biopsy was also consistent with eczema,
along with the photographic evidence offered on the day of hearing. Id. at 473 (citing Ex. 1 at 93),
477.
The relevant medical records also establish that Petitioner tested positive for various
environmental allergies around this time (including grass, cat dander, tree pollen, dust mite, and
ragweed). Tr. at 470-71 (citing Ex. 3 at 11; Ex. 1 at 42). Dr. MacGinnitie opined that these allergies
likely pre-dated her receipt of the vaccine doses at issue herein. Id. at 469, 471. By contrast, Dr.
MacGinnitie could not say for certain if Petitioner’s food allergy testing clearly evidenced positive
values. Id. at 470-71. He deemed the majority of her allergy testing (related to strawberry, peach,
oat, and so on) to be false-positives. Id. at 471.
During the Cleveland Clinic visit in August 2014, Petitioner was diagnosed with chronic
urticaria (which was thought to have begun in the summer of 2013). Tr. at 473-74 (citing Ex. 11
at 12-14; Ex. 1 at 33), 532-33. The photographic evidence offered at hearing also revealed evidence
of the condition. Id. at 478. Dr. MacGinnitie acknowledged this diagnosis, and noted that the
treating physician categorized the condition as idiopathic (thus could not identify a cause). Id. at
44
474.59 As noted earlier, Dr. MacGinnitie posited that physicians are rarely able to determine the
cause of chronic urticaria (as it can be a diagnosis of exclusion, unrelated to environmental
triggers). Id. But the testing completed during this visit (including CBC, anti-IgE, anti-IgE receptor
antibodies, tryptase,60 thyroid function, and inflammatory markers) clearly ruled out any
autoimmune basis for the urticaria. Id. at 475-76, 545; see Ex. 22.
Along those same lines, Dr. MacGinnitie could find no clear etiology for the episodes of
joint pain noted in Petitioner’s medical record. Tr. at 478. Indeed, her rheumatologic work-up at
the Cleveland Clinic also did not identify a clear trigger. Id. at 479 (citing Ex. 11 at 24-28). As Dr.
MacGinnitie explained, the Cleveland Clinic treaters seemed to first attribute Ms. McKown’s joint
pain to her skin condition, but then later distinguished the two (or at least determined that the pain
was secondary). Id. at 480. There was also no evidence of actual arthritis (or inflammation in the
joints) versus “arthralgias” (or complaints of joint pain). Id. at 479. Even so, Dr. MacGinnitie
posited that eczema and urticaria usually did not result in secondary joint pain or present with
arthralgias. Id. at 479. Indeed, Dr. MacGinnitie testified that he has never treated a patient with
eczema or urticaria also suffering from related joint pain (along with arthralgias, and myalgias).
Id. at 511.
Before the Cleveland Clinic work-up, Petitioner’s appointment with Dr. Rouster-Stevens
in early July 2014 resulted in a diagnosis of “amplified musculoskeletal pain syndrome.” Tr. at
481 (citing Ex. 21). Notably, however, Dr. Rouster-Stevens determined the condition was not
autoimmune in nature. Id. at 481. According to Dr. MacGinnitie, the only proof of autoimmunity
he could identify at this visit was a low ANA titer – which, he considered an unremarkable finding,
and likely a low positive in any event. Id. Lupus and connective tissue disorder were also ruled
out. Id.
All in all, based on his review of the record in its entirety, Dr. MacGinnitie could not
conclude that Petitioner was experiencing an underlying inflammatory process. Tr. at 482. As he
explained, the best markers for ongoing inflammation are the ESR and CRP (both of which
remained relatively stable throughout Petitioner’s symptoms course). Id. Her February 2014 lab
test results showed only a slighted elevated ESR (which Dr. MacGinnitie deemed “unlikely of
clinical importance” at the time) given that almost forty percent of the population have slightly
elevated ANA (many of which do not have an underlying systemic disease). Id. at 483 (citing Ex.
59
On cross examination, Petitioner offered some suggestion that the urticarial lesions were related to a medication she
had taken in the past (Fludrocortisone). Tr. at 534. Dr. MacGinnitie acknowledged that the records indicated a concern
for a reaction to the medication, but he posited that the chronic nature of symptoms described therein made it unlikely
that Fludrocortisone triggered its onset. Id. at 535-36, 537.
60
Along those same lines, Dr. MacGinnitie noted that Petitioner tested negative for mast cell activation disorder or
mastocytosis (which he defined as an increased in the mast cells resulting in various symptoms including: flushing,
urticaria, POTS, cognitive fog, and anaphylaxis). Tr. at 485, 486 (citing Ex. 11 at 21). Mast cell activation is measured
by analyzing a patients tryptase levels. Id. at 485, 486; see C. Akin, Mast Cell Activation Disorders, 2 J. Allergy Clin.
Immunol. Pract. 252 (2014), filed as Ex. A, Tab 21 (ECF No. 25-1).
45
1 at 77); see M. Satoh, Clinical Interpretation of Antinuclear Antibody Tests in Systemic Rheumatic
Diseases, 19 Mod. Rheumatol. 219 (2009), filed as Ex. A, Tab 9 (ECF No. 23-10). Moreover, lab
results from tests conducted in late summer 2014 were also negative for the traditional
inflammatory markers. Tr. at 484. Dr. MacGinnitie agreed with Dr. Tornatore’s earlier point that
a patient could still have an autoimmune disease even absent positive inflammatory markers, but
he would not opine that this was true for non-CNS illnesses of the kind relevant to this action. Id.
at 482.
Dr. MacGinnitie next turned to the medical theories of causation proffered by Petitioner in
support of her claim. As to Dr. Mikovits’s theory, Dr. MacGinnitie noted that he found her opinion
confusing. Tr. at 455. From what he could understand of it, Dr. Mikovits seemed to allege that
various vaccine components (in combination) can lead to immune dysfunction in both the adaptive
and innate systems. Id. Thus, Dr. Mikovits posited that the aluminum adjuvant component, for
example, is “taken up” by macrophages, which then migrate to the CNS and “differentiate” into
the microglia. Id. Retroviral DNA (another vaccine contaminant) was also mentioned in her theory,
though Dr. MacGinnitie knew of no causative mechanism to support such a theory. Id. Dr.
Mikovits similarly relied on the concept (explained primarily by Dr. Tornatore in reliance on the
Kanduc paper) that molecular mimicry between HPV components and self sequence proteins could
have contributed to the purported autoimmune process resulting in Petitioner’s injuries. Id.
But Dr. MacGinnitie found Dr. Mikovits’s theoretical components wholly unpersuasive
and scientifically unreliable. For example, he maintained that he knew of no evidence supporting
a causal connection between retroviral DNA and the onset of any disease process. Tr. at 455-56.
As he explained, ten to fifteen percent of a person’s own DNA is retroviral, rendering it unclear
how the tiny amounts contained in vaccines would have any adverse effect (given that humans are
routinely exposed to it in larger amounts via skin, gut, and everyday infections). Id. at 455-56.
Dr. Mikovits’s aluminum adjuvant61/mimicry component of her theory, was, in his view,
also scientifically unreliable. Dr. MacGinnitie found no evidence in the literature filed in this case
that immune system macrophages can actually absorb the aluminum component in vaccines
sufficient to cause injury, let alone migrate through the CNS and into the brain microglia, given
the fact that the adjuvant originates in the muscle or subcutaneous tissue after injection. Tr. at 456-
57, 498-99. Moreover, such a theory did not explain how such mechanisms could later result in
POTS or eczema (or any medically acceptable disease process for that matter). Id. at 456-57, 500-
01. And Dr. MacGinnitie greatly doubted the sense behind the theory that aluminum in vaccine
could be pathogenic at all. As he explained, adjuvants have been used in vaccines for over one
hundred years, and the applicable scientific studies have found no evidence that aluminum (or any
other adjuvant) is unsafe. Id. at 497. Vaccines also contain miniscule amounts of aluminum
61
Dr. MacGinnitie explained that adjuvants are included in vaccine ingredients to increase the immune response (or
activate a low level of inflammation, so the immune response is higher). Tr. at 497-98.
46
(around 225 micrograms) in comparison to the amounts ingested/inhaled by humans on a daily
basis. Id. at 498.62
Dr. MacGinnitie allowed that proinflammatory cytokines could both trigger and propagate
a disease process in certain circumstances. Tr. at 540. He took issue, however, with Dr. Mikovits’s
suggestion that cytokines likely played a role in the disease/symptoms course relevant herein. Id.
As he explained, the articles offered by Petitioner in support of such a theory show no evidence of
a pathologic process. Id. In Dr. MacGinnitie’s understanding, propagating (or mediating) a disease
is not the same as triggering it. Id. He also pointed out that a cytokine response is an immediate
product of the innate system’s activation (and therefore not an inherently chronic process). Id. at
540. At most, cytokines can trigger some initial inflammation which would only later lead to a
more “long-term” response in the adaptive system, rather than continuing to multiply in unabated
form. Id. Thus, in Ms. McKown’s case, an innate immune response even involving cytokine
upregulation would not inherently cause the onset of an onset of injury months following activation
(given the rapidity nature of its initial response). Id. at 532-33.
Dr. MacGinnitie similarly critiqued the joint mimicry/T-cell degeneracy theories proffered
by Dr. Tornatore as inconsistent and vague. He began by noting that both could not be
simultaneously explanatory. Tr. at 457. As he understood it, the concept of degeneracy involved
T cells not specific to a presenting antigen nevertheless recognizing multiple antigens, leading to
cross-reactivity63 without molecular mimicry – a process that would be contradictory to a
molecular mimicry mechanism (as purportedly supported by Kanduc) involving homology
between specific HPV vaccine components and self proteins. Id. at 457, 489, 542. If degeneracy
best explained the mechanism herein, then any T cell could be responsible for the alleged cross-
reactivity, but it would be impossible to say which64 – rendering degeneracy as an explanatory
mechanism counter to the specificity underlying the mimicry theory. Id. at 489.
Even so, Dr. MacGinnitie disputed the reliability of degeneracy as a possible mechanism
herein. Because in his view any T cell response would be “primary” (i.e., an immediate response
attributable to the innate system), the fact that a T cell is stimulated initially by one antigen does
not mean that the now activated T cell will by default respond to a “clone” thereafter (as Dr.
62
On cross examination, Petitioner argued that injection with aluminum is not the same as ingesting or inhaling the
substance. Tr. at 529. In response, Dr. MacGinnitie suggested a recent (unfiled) paper suggests that patients receiving
immunotherapy are injected with higher doses of aluminum than in vaccination, and yet do not experience increased
autoimmunity. Id. at 529-30. He agreed upon further questioning, however, that such evidence does not rise to the
level of epidemiologic evidence in trustworthiness. Id. at 530.
63
Bystander activation, by contrast, involves “one activated T cell activating other T cells” Tr. at 544.
64
On cross examination, however, Dr. MacGinnitie agreed that humans “can’t generate T cells to every possible
antigen.” Tr. at 542. He also agreed that there is reliable scientific support for the concept that T cells can recognize
different distinct antigens even with a lack of sequence homology. Id.
47
Tornatore suggested). Tr. at 543.65 For support, Dr. MacGinnitie referenced Kanduc, which he
posited actually reveals that subsequent exposure to vaccine antigens results in a less robust
response to variant flu wild virus types thereafter – as if memory of specific, original antigens
“outcompete[s]” future antigens. Id. at 543.
As for the molecular mimicry theory as a mechanistic descriptor applicable herein, Dr.
MacGinnitie did not dispute that Kanduc66 correctly identified homology between the HPV
vaccine and certain self proteins peptide sequences. Tr. at 489-90. The particular peripheral
nervous system protein (septin-9) identified as having been the target in Kanduc, however, has not
been established by independent reliable scientific or medical evidence to have anything to do at
all with the pathogenesis of POTS. Id. at 490. Rather, septin-9 is related to a genetic disorder. Id.
Moreover, Kanduc made no attempt to show that a human (or mouse) injected with HPV proteins
could even generate an immune response to septin-9 in a controlled setting. Id. Thus, the theorized
association between homologous peptides was lacking in sufficient scientific evidentiary support
to deem it reliable. Id. at 489-90.
Along those same lines, Dr. MacGinnitie maintained that the homologies observed in
Kanduc actually undermine the reliability of molecular mimicry as the most likely mechanism for
Petitioner’s injuries, citing literature that demonstrated the prevalence of homology between
foreign antigens and amino acid sequences in the human body. Tr. at 490-92; B. Trost, et al.,
Bacterial Peptides Are Intensively Present Throughout the Human Proteome, 1 SelfNonself 71
(2010), doi:10.4161/self.1.1.9588, filed as Ex. G (ECF No. 43-2) (“Trost”). Trost identified
various bacterial proteomes (both pathogenic and nonpathogenic) in an attempt to catalog
homologous structures shared between the proteomes and self proteins. The study ultimately
identified over 50,000 “ninemers” (or nine amino-acid regions of homology) or mimics shared
between the proteomes and one-third of the human proteome. Tr. at 491. If molecular mimicry
theory was indeed causally mechanistic for autoimmune disease in most cases, the “widespread
overlap” between viral and bacterial proteins “would predict that autoimmune disease should have
a much higher incidence than actually observed” (both in the total number of individuals affected
and the number of autoimmune pathologies per individual). Id. at 492. Dr. MacGinnitie thus found
it difficult to reconcile how molecular mimicry could always be considered potentially explanatory
for onset of autoimmune disease, absent some other, more specific evidence suggesting it
explained a particular disease process. Id. at 492-93.
65
Indeed, Dr. MacGinnitie maintained that the body inherently “deletes” T cells that respond strongly to self antigens.
Tr. at 493.
66
Dr. MacGinnitie expressed some concern regarding Kanduc’s publication credentials. Tr. at 489. In his view, the
article was published in a “predatory” journal. Id. Predatory journals are considered open-access (i.e., they charge
authors a price to publish the article) and are not effectively peer-reviewed prior to publication. Id. at 458-59. As he
stated at hearing, both Kanduc (published in the International Journal of Public Health and Safety) and the Giannotta
paper (published in Bentham Open), are in his view, predatory in nature. Id. at 459.
48
Overall, Dr. MacGinnitie argued that both proffered mechanisms relied on a similar
assumption: that any stimulus from a foreign antigen could potentially cause an autoimmune
disease. Tr. at 458. But if either mechanism was as broadly reliable as asserted, the incidence in
autoimmune disease should be “orders of magnitude higher” (an increase unsupported by the
available scientific literature) – suggesting that other factors (apart from “potentially autoreactive”
T cells in isolation) are more likely involved in the relevant mechanism. Id. at 458, 544. In Dr.
MacGinnitie’s view, “across the range of immune stimuli that humans are exposed to on a daily
basis, immunization is really not particularly notable” as such a potential factor. Id. at 487.
Dr. MacGinnitie went on to evaluate some of the evidence offered by Petitioner
purportedly establishing a direct causal connection between the HPV vaccine and POTS, like case
studies. Tr. at 493-94, 499-500. Although he allowed that such evidence had some limited
reliability, the more sophisticated epidemiologic studies67 considering such a relationship have
consistently shown no discernible increase in POTS following HPV vaccine administration. Id. at
493-94. As a result, Dr. MacGinnitie felt it was more likely that any association between HPV
vaccine and POTS observed in case reports was coincidental – attributable to the fact that the HPV
vaccine is administered around the same time that POTS typically develops (in a young female
population). Id.
One large-scale surveillance study performed in the U.S., for example, followed
approximately 189,00 patients vaccinated with the HPV vaccine (between 2006 and 2008) to
determine the likelihood of developing an autoimmune disease thereafter. Tr. at 494-95; C. Chao,
et al., Surveillance of Autoimmune Conditions Following Routine Use of Quadrivalent Human
Papillomavirus Vaccine, 271 J. Int’1 Med. 193 (2012), filed as Ex. A Tab 6 (ECF No. 23-7)
(“Chao”). Chao (funded but not authored by pharmaceutical manufacturer Merck & Co.) was a
peer-reviewed observational study analyzing a database comprised of the medical histories of
approximately 189,000 women in California to determine whether the studied population had
developed a variety of autoimmune conditions after receiving the HPV vaccine. Chao at 194. The
researchers compared the results of the studied vaccinated population with unvaccinated,
similarly-situated individuals, in order to compare incidence ratios for the identified autoimmune
conditions, but ultimately found no association between onset of autoimmune disease and receipt
of the HPV vaccine. Id. at 194-95. Although Chao’s authors did not specifically include POTS in
the study criteria, Dr. MacGinnitie maintained that the article still cast doubt the concept that a
vaccine can “break[] tolerance” sufficient to cause an autoimmune disease. Tr. at 495.
Dr. MacGinnitie also referenced two additional large-scale epidemiologic studies focusing
on the HPV vaccine. Tr. at 495; L. Grimaldi-Bensouda, et al., Autoimmune Disorders and
Quadrivalent Human Papillomavirus Vaccination of Young Female Subjects, 275 J. Int’l Med.
67
Dr. MacGinnitie acknowledged that epidemiologic studies can never completely disprove causation, but he
nevertheless felt they provide better evidence of causality (or the lack thereof) than the associations observed in case
reports. Tr. at 494.
49
398 (2014), filed as Ex. A, Tab 7 (ECF No. 23-8) (“Grimaldi-Bensouda”); S. Block, et al., Clinical
Trial and Post-Licensure Safety Profile of Prophylactic Human Papillomavirus (Types 6, 11, 16,
and 18) L1 Virus-Like Particles, 29 Pediatric Infect. Dis. J. 95 (2010), filed as Ex. A, Tab 8 (ECF
No. 23-9) (“Block”). Grimaldi-Bensouda was a French case control study of roughly 1,800 patients
(22 percent of whom had received the HPV vaccine), which measured the onset of specific
autoimmune diseases (including: ITP, CN/MS, GBS, lupus, rheumatoid arthritis, type I diabetes,
and autoimmune thyroiditis) following HPV vaccine administration. The Grimaldi-Bensouda
authors found no increased rate of autoimmunity following vaccination. Tr. at 496. The Block
study monitored over 21,000 female patients administered HPV in five clinical trials, and beyond
some evidence of injection site pain following administration, observed no association with any
subsequent autoimmune phenomena. Tr. at 496; Block at 100.68 As with Chao, however, Dr.
MacGinnitie acknowledged on cross examination that neither Grimaldi-Bensouda or Block
included POTS (or dermatologic conditions) when measuring for autoimmunity. Tr. at 528. Even
so, given the lack of evidence associating HPV vaccine administration with other autoimmune
conditions, Dr. MacGinnitie posited that it was unlikely that POTS (which Petitioner has alleged
was autoimmune in nature with respect to herself) could be similarly associated.
III. Procedural History
Ms. McKown filed her Petition on December 1, 2015. Pet. at 1. Following the filing of
pertinent medical records, Respondent filed the Rule 4(c) Report on June 28, 2016 (ECF No. 15),
contesting Petitioner’s right to an entitlement award. I thereafter ordered the parties to file expert
reports in support of their respective positions. Petitioner filed an initial report from Drs. Mikovits
and Ruscetti on December 2, 2016 (ECF No. 18). Respondent’s initial report from Dr. MacGinnitie
was next filed on April 14, 2017 (ECF No. 23). Supplemental expert reports were filed on July 19,
2017 (ECF No. 30) and May 4, 2018 (ECF No. 34), respectively. Congruently, on May 4, 2018,
Respondent filed a report authored by Dr. Gibbons (ECF No. 35), plus Dr. MacGinnitie’s
supplemental report.
Thereafter, Petitioner indicated in her initial pre-hearing brief that she intended to call Dr.
Tornatore as a witness at hearing (and file a report in the matter). See Brief, dated July 13, 2018
(ECF No. 40) at 1-2. This suggestion was made long after the original expert report filing had
concluded (and without my direction or approval). Petitioner did not indicate why she intended to
offer a supplemental report in the matter (though it likely was viewed as necessary to remedy
68
On direct examination, Dr. Mikovits suggested that clinical trials conducted prior to the release of the HPV vaccine
did not include a trial completed with a non-aluminum placebo. Tr. at 496. In response, Dr. MacGinnitie posited that
Block used a non-aluminum placebo to measure for autoimmunity but found no evidence of an increase. Id. at 496-
97.
50
issues relating to the qualifications of Drs. Mikovits and Ruscetti). 69 Nonetheless, Petitioner filed
the report from Dr. Tornatore on July 31, 2018 (ECF No. 42), roughly two months prior to hearing.
I scheduled the matter for hearing on September 26-27, 2018. The hearing took place as
scheduled, and included testimony from the experts identified above (along with testimony from
Petitioner’s mother). Following the hearing’s conclusion, the parties submitted post-hearing briefs.
The matter is ripe for adjudication.
IV. Applicable Legal Standards
A. Claimant’s Burden in Vaccine Program Cases
To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
he suffered a “Table Injury” – i.e., an injury falling within the Vaccine Injury Table, corresponding
to one of the vaccinations in question and also occurring within a statutorily-prescribed period of
time – or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table
Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; see also
Shalala v. Whitecotton, 514 U.S. 268, 270 (1995) (quoting 42 U.S.C. § 11(c)(1)(C)(i)); Moberly
v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010); Capizzano v. Sec’y of
Health & Human Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006).70 Petitioner in this case asserts
only a non-Table claim.
For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. Section 13(1)(a). That is, a petitioner must offer evidence that
leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence
before [he] may find in favor of the party who has the burden to persuade the judge of the fact’s
existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.
476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).
A petitioner may not receive a Vaccine Program award based solely on his assertions; rather, the
petition must be supported by either medical records or by the opinion of a competent physician.
Section 13(a)(1).
69
By this time, other special masters had authored opinions in different cases critiquing the quality of the opinions
offered by Drs. Mikovits and Ruscetti (and/or expressed their view that the testimony offered was unpersuasive in the
causation context). See, e.g., McCabe v, Sec’y of Health & Human Servs., No. 13-570V, 2018 WL 3029175 (Fed. Cl.
Spec. Mstr. May 17, 2018); Barker v. Sec’y of Health & Human Servs., No. 16-1554V, 2018 WL 2772454 (Fed. Cl.
Spec. Mstr. May 11, 2018); Dominguez v. Sec’y of Health & Human Servs., No. 12-378V, 2018 WL 2225540 (Fed.
Cl. Spec. Mstr. Apr. 2, 2018).
70
Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings
concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Human Servs., 59 Fed. Cl. 121,
124 (2003), aff’d, 104 F. App’x 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Human Servs., No. 13-
159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).
51
When a Table Injury claim is successfully established, causation is presumed. 42 C.F.R.
§ 100.3. Table claims must satisfy with evidence the specific elements of the relevant claim,
including the definitions of terms set in the Qualifications and Aids to Interpretation (the “QAI”).
Section 14(b). Case law underscores that, to obtain the benefit of the presumption of causation
associated with a Table claim, the claim’s requirements must be strictly construed. Miller v. Sec’y
of Health & Human Servs., No. 02-235V, 2015 WL 5456093, at *24 (Fed. Cl. Spec. Mstr. Aug.
18, 2015) (requiring petitioner to satisfy the “strict Table definition” of encephalopathy).
For a non-Table claim, proof of medical certainty is not required. Bunting v. Sec’y of Health
& Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). In such circumstances, a petitioner must
demonstrate that the vaccine was “not only [the] but-for cause of the injury but also a substantial
factor in bringing about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health
& Human Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Human
Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). A petitioner asserting a non-Table claim must satisfy
all three of the elements established by the Federal Circuit in Althen v. Secretary of Health &
Human Services, 418 F.3d 1274, 1278 (Fed. Cir. 2005): “(1) a medical theory causally connecting
the vaccination and the injury; (2) a logical sequence of cause and effect showing that the
vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship
between vaccination and injury.”
Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners
must provide a “reputable medical theory,” demonstrating that the vaccine received can cause the
type of injury alleged. Pafford, 451 F.3d at 1355-56 (citations omitted). To satisfy this prong, the
petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”
Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such a theory
must only be “legally probable, not medically or scientifically certain.” Id. at 549.
Petitioners may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009) (citing
Capizzano, 440 F.3d at 1325-26). Special masters, despite their expertise, are not empowered by
statute to conclusively resolve what are essentially thorny scientific and medical questions, and
thus scientific evidence offered to establish Althen prong one is viewed “not through the lens of
the laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant evidence
standard.” Id. at 1380. Accordingly, special masters must take care not to increase the burden
placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras v. Sec’y of
Health & Human Servs., 121 Fed. Cl. 230, 245 (2015), vacated on other grounds, 844 F.3d 1363
(Fed. Cir. 2017).
52
In discussing the evidentiary standard applicable to the first Althen prong, many decisions
of the Court of Federal Claims and Federal Circuit have emphasized that petitioners need only
establish a causation theory’s biologic plausibility (and thus need not do so with preponderant
proof). Tarsell v. United States, 133 Fed. Cl. 782, 792-93 (2017) (special master committed legal
error by requiring petitioner to establish first Althen prong by preponderance; that standard applied
only to second prong and petitioner’s overall burden); Contreras, 121 Fed. Cl. at 245
(“[p]lausibility . . . in many cases may be enough to satisfy Althen prong one” (emphasis in
original)); see also Andreu, 569 F.3d at 1375. At the same time, there is contrary authority from
the Federal Circuit suggesting that the preponderance standard applied when evaluating a
claimant’s overall success in a Vaccine Act claim also bears on the first Althen prong. See, e.g.,
Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1350 (Fed. Cir. 2010) (affirming
special master’s determination that expert “had not provided a ‘reliable medical or scientific
explanation’ sufficient to prove by a preponderance of the evidence a medical theory linking the
[relevant vaccine to relevant injury]”) (emphasis added). Regardless, one thing remains: petitioners
always have the burden of establishing their Vaccine Act claim overall with preponderant
evidence. W.C. v. Sec’y of Health & Human Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations
omitted); Tarsell, 133 Fed. Cl. at 793 (noting that Moberly “addresses the petitioner’s overall
burden of proving causation-in-fact under the Vaccine Act” by a preponderance).
The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Human Servs., 956
F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions
and views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 F.3d
at 1367; Capizzano, 440 F.3d at 1326 (“medical records and medical opinion testimony are favored
in vaccine cases, as treating physicians are likely to be in the best position to determine whether a
‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury’”)
(quoting Althen, 418 F.3d at 1280). Medical records are generally viewed as particularly
trustworthy evidence, since they are created contemporaneously with the treatment of the patient.
Cucuras v. Sec’y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).
However, medical records and/or statements of a treating physician’s views do not per se
bind the special master to adopt the conclusions of such an individual, even if they must be
considered and carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis,
conclusion, judgment, test result, report, or summary shall not be binding on the special master or
court”); Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is
nothing . . . that mandates that the testimony of a treating physician is sacrosanct – that it must be
accepted in its entirety and cannot be rebutted”). As with expert testimony offered to establish a
theory of causation, the opinions or diagnoses of treating physicians are only as trustworthy as the
reasonableness of their suppositions or bases. The views of treating physicians should also be
53
weighed against other, contrary evidence also present in the record—including conflicting
opinions among such individuals. Hibbard v. Sec’y of Health & Human Servs., 100 Fed. Cl. 742,
749 (2011) (not arbitrary or capricious for special master to weigh competing treating physicians’
conclusions against each other), aff’d, 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec’y of Health &
Human Servs., 100 Fed. Cl. 119, 136 (2011), aff’d, 463 F. App’x 932 (Fed. Cir. 2012); Veryzer v.
Sec’y of Health & Human Servs., No. 06-522V, 2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr.
Apr. 29, 2011), mot. for review den’d, 100 Fed. Cl. 344, 356 (2011), aff’d without opinion, 475 F.
App’x 765 (Fed. Cir. 2012).
The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the
phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant
proof that the onset of symptoms occurred within a timeframe which, given the medical
understanding of the disorder’s etiology, it is medically acceptable to infer causation.” Bazan v.
Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what
is a medically acceptable timeframe must also coincide with the theory of how the relevant vaccine
can cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of Health &
Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after remand, 105 Fed. Cl. 353 (2012),
aff’d mem., 2013 WL 1896173 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Human Servs., No.
11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for review den’d (Fed. Cl.
Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).
B. Law Governing Claims of Significant Aggravation
Besides arguing that the HPV and/or Hep A vaccines directly caused her injuries,
Petitioner’s experts have also allowed for the possibility that the vaccines significantly aggravated
her preexisting eczema or previously-undiagnosed POTS. Where a petitioner so alleges, the Althen
test is expanded, and the petitioner has additional evidentiary burdens to satisfy. See generally
Loving v. Sec’y of Health & Human Servs., 86 Fed. Cl. 135, 144 (2009). In Loving, the Court of
Federal Claims combined the Althen test with the test from Whitecotton v. Secretary of Health &
Human Services, 81 F.3d 1099, 1107 (Fed. Cir. 1996), which related to on-Table significant
aggravation cases. The resultant “significant aggravation” test has six components, which require
establishing:
(1) the person’s condition prior to administration of the vaccine, (2) the person’s current
condition (or the condition following the vaccination if that is also pertinent), (3) whether
the person’s current condition constitutes a “significant aggravation” of the person’s
condition prior to vaccination, (4) a medical theory causally connecting such a
significantly worsened condition to the vaccination, (5) a logical sequence of cause and
effect showing that the vaccination was the reason for the significant aggravation, and (6)
54
a showing of a proximate temporal relationship between the vaccination and the
significant aggravation.
Loving, 86 Fed. Cl. at 144; see also W.C., 704 F.3d at 1357 (holding that “the Loving case provides
the correct framework for evaluating off-table significant aggravation claims”). In effect, the last
three prongs of the Loving test correspond to the three Althen prongs.
Subsumed within the Loving analysis is the requirement to evaluate the likely natural
course of an injured party’s preexisting disease, in order to determine whether the vaccine made
the petitioner worse than he would have been but for the vaccination. Locane v. Sec’y of Health &
Human Servs., 685 F.3d 1375, 1381–82 (Fed. Cir. 2012) (upholding special master’s determination
that petitioner had failed to carry her burden of proof in establishing that her preexisting injury
was worsened by the relevant vaccine); Hennessey v. Sec’y of Health & Human Servs., No. 01-
190V, 2009 WL 1709053, at *41-42 (Fed. Cl. Spec. Mstr. May 29, 2009), mot. for review den’d,
91 Fed. Cl 126 (2010). The critical point of examination is thus “whether the change for the worse
in [petitioner’s] clinical presentation was aggravation or a natural progression” of the underlying
condition. Hennessey, 2009 WL 1709053, at *42.71 The Federal Circuit has upheld the
determinations of special masters that worsening was not demonstrated in connection with
establishing a petitioner’s overall preponderant burden of proof for a non-Table causation-in-fact
claim. See, e.g., Snyder/Harris v. Sec’y of Health & Human Servs., 553 F. App’x 994, 999-1000
(Fed. Cir. 2014); Locane, 685 F.3d at 1381-82.72
The mere fact a vaccine might “trigger” a transient negative response in an individual with
an underlying condition or disease is not proof of worsening if that individual would be expected
to experience a similar overall course regardless. Faoro v. Sec’y of Health &Human Servs., No.
10-704V, 2016 WL 675491, at *27 (Fed. Cl. Spec. Mstr. Jan. 29, 2016), mot. for review den’d,
128 Fed. Cl. 61 (Fed. Cl. Apr. 11, 2016) (finding that “the vaccinations would not have changed
her clinical course and thus, the vaccinations did not significantly aggravate her preexisting
71
The legislative history of the Vaccine Act strongly supports interpreting “significant aggravation” as requiring a
claimant to establish that a vaccine rendered a preexisting condition qualitatively worse than it would have been
otherwise – not simply that the affected individual experienced a post-vaccination symptom that contrasts with the
individual’s comparatively better pre-vaccination health. See H.R. Rep. No. 99-908, at 15 (1986) (“This [significant
aggravation] provision does not include compensation for conditions which might legitimately be described as pre-
existing (e.g., a child with monthly seizures who, after vaccination, has seizures every three and a half weeks), but is
meant to encompass serious deterioration (e.g., a child with monthly seizures who, after vaccination, has seizures on
a daily basis” (emphasis added)).
72
This is consistent with the fact (well recognized by controlling precedent) that evidence of “worsening” relevant to
Respondent’s alternative cause burden may reasonably by evaluated by a special master in determining the success of
a petitioner’s prima facie showing. Snyder/Harris, 553 F. App’x at 1000, quoting Stone, 676 F.3d at 1380 (“no
evidence should be embargoed from the special master’s consideration simply because it is also relevant to another
inquiry under the statute”); see also de Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1353 (Fed. Cir.
2008) (“[t]he government, like any defendant, is permitted to offer evidence to demonstrate the inadequacy of the
petitioner’s evidence on a requisite element of the petitioner’s case-in-chief”).
55
condition”). This point has been emphasized in a subcategory of Program cases involving the claim
that a child’s Dravet syndrome (a rare seizure disorder now understood to be caused by the SCN1A
gene mutation) was significantly aggravated by vaccination. Faoro, 2016 WL 675491, at *1. In
such cases, special masters have repeatedly determined that petitioners failed to show that a child’s
expected outcome would have been different but for the vaccination – even though it was not
disputed that the child’s first major seizure had been triggered by vaccination. Id. at *2 (“[a]lthough
H.E.F.’s vaccinations may have caused a low-grade fever or otherwise triggered her first seizure,
neither the initial seizure nor her vaccinations caused or significantly aggravated her Dravet
syndrome and resulting neurological complications”); see also Snyder/Harris, 553 F. App’x at
1003 (special master was not arbitrary in finding that petitioners’ expert failed to show that the
child’s outcome would have been different had he not received the vaccinations at issue).
C. Law Governing Factual Determinations
The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 11(c)(2). The special master is required
to consider “all [] relevant medical and scientific evidence contained in the record,” including “any
diagnosis, conclusion, medical judgment, or autopsy or coroner’s report which is contained in the
record regarding the nature, causation, and aggravation of the petitioner’s illness, disability, injury,
condition, or death,” as well as “the results of any diagnostic or evaluative test which are contained
in the record and the summaries and conclusions.” Section 13(b)(1)(A). The special master is then
required to weigh the evidence presented, including contemporaneous medical records and
testimony. See Burns v. Sec’y of Health & Human Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (it is
within the special master’s discretion to determine whether to afford greater weight to
contemporaneous medical records than to other evidence, such as oral testimony surrounding the
events in question that was given at a later date, provided that such a determination is evidenced
by a rational determination).
Medical records that are created contemporaneously with the events they describe are
presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s
health problems). Cucuras, 993 F.2d at 1528; Doe/70 v. Sec’y of Health & Human Servs., 95 Fed.
Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner’s testimony and his
contemporaneous medical records, the special master’s decision to rely on petitioner’s medical
records was rational and consistent with applicable law”); Rickett v. Sec’y of Health & Human
Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption is based
on the linked propositions that (i) sick people visit medical professionals; (ii) sick people honestly
report their health problems to those professionals; and (iii) medical professionals record what they
are told or observe when examining their patients in as accurate a manner as possible, so that they
are aware of enough relevant facts to make appropriate treatment decisions. Sanchez v. Sec’y of
Health & Human Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr. Apr. 10,
56
2013); Cucuras v. Sec’y of Health & Human Servs., 26 Cl. Ct. 537, 543 (1992), aff’d, 993 F.2d
1525 (Fed. Cir. 1993) (“[i]t strains reason to conclude that petitioners would fail to accurately
report the onset of their daughter’s symptoms. It is equally unlikely that pediatric neurologists,
who are trained in taking medical histories concerning the onset of neurologically significant
symptoms, would consistently but erroneously report the onset of seizures a week after they in fact
occurred”).
Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec’y of Health & Human Servs., No. 03-1585V, 2005
WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical
records are generally found to be deserving of greater evidentiary weight than oral testimony—
especially where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528;
see also Murphy v. Sec’y of Health & Human Servs., 23 Cl. Ct. 726, 733 (1991), aff’d, 968 F.2d
1226 (Fed. Cir.), cert. den’d sub nom. Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United
States v. United States Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that
oral testimony which is in conflict with contemporaneous documents is entitled to little evidentiary
weight”)).
However, there are situations in which compelling oral testimony may be more persuasive
than written records, such as where records are deemed to be incomplete or inaccurate. Campbell
v. Sec’y of Health & Human Servs., 69 Fed. Cl. 775, 779 (2006) (“like any norm based upon
common sense and experience, this rule should not be treated as an absolute and must yield where
the factual predicates for its application are weak or lacking”); Lowrie, 2005 WL 6117475, at *19
(“[w]ritten records which are, themselves, inconsistent, should be accorded less deference than
those which are internally consistent”) (quoting Murphy, 23 Cl. Ct. at 733). Ultimately, a
determination regarding a witness’s credibility is needed when determining the weight that such
testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Human
Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).
When witness testimony is offered to overcome the presumption of accuracy afforded to
contemporaneous medical records, such testimony must be “consistent, clear, cogent, and
compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec’y of Health & Human
Servs., No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In
determining the accuracy and completeness of medical records, the Court of Federal Claims has
listed four possible explanations for inconsistencies between contemporaneously created medical
records and later testimony: (1) a person’s failure to recount to the medical professional everything
that happened during the relevant time period; (2) the medical professional’s failure to document
everything reported to her or him; (3) a person’s faulty recollection of the events when presenting
testimony; or (4) a person’s purposeful recounting of symptoms that did not exist. La Londe v.
Sec’y Health & Human Servs., 110 Fed. Cl. 184, 203-04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir.
57
2014). In deciding whether to afford greater weight to contemporaneous medical records over
contrary testimony, there must be evidence that this decision was the result of a rational
determination. Burns, 3 F.3d at 417.
D. Analysis of Expert Testimony
Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec’y of Health & Human Servs., 219 F.3d
1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to
the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharmaceuticals,
Inc., 509 U.S. 579, 59-96 (1993). See Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328,
1339 (Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316
(Fed. Cir. 1999)). “The Daubert factors for analyzing the reliability of testimony are: (1) whether
a theory or technique can be (and has been) tested; (2) whether the theory or technique has been
subjected to peer review and publication; (3) whether there is a known or potential rate of error
and whether there are standards for controlling the error; and (4) whether the theory or technique
enjoys general acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2
(citing Daubert, 509 U.S. at 592-95).
The Daubert factors play a slightly different role in Vaccine Program cases than they do
when applied in other federal judicial fora (such as the district courts). Daubert factors are usually
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors
are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health
& Human Servs., 94 Fed. Cl. 53, 66-67 (2010) (“uniquely in this Circuit, the Daubert factors have
been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of
expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the
persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88
Fed. Cl. at 742-45. In this matter (as in numerous other Vaccine Program cases), Daubert has not
been employed at the threshold, to determine what evidence should be admitted, but instead to
determine whether expert testimony offered is reliable and/or persuasive.
Respondent frequently offers one or more experts of his own in order to rebut a petitioner’s
case. Where both sides offer expert testimony, a special master’s decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen, 618 F.3d at 1347 (citing Lampe, 219 F.3d at 1362). However, nothing requires the
acceptance of an expert’s conclusion “connected to existing data only by the ipse dixit of the
expert,” especially if “there is simply too great an analytical gap between the data and the opinion
proffered.” Snyder, 88 Fed. Cl. at 743 (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)); see
also Isaac v. Sec’y of Health & Human Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl.
58
Spec. Mstr. July 30, 2012), mot. for review den’d, 108 Fed. Cl. 743 (2013), aff’d, 540 F. App’x
999 (Fed. Cir. 2013) (citing Cedillo, 617 F.3d at 1339).
E. Consideration of Medical Literature
Both parties relied on significant amounts of medical and scientific literature to support
their respective positions. I have reviewed all of the medical literature submitted in this case,
although my decision does not discuss each filed article in detail (nor would it be reasonable to
require a special master to do so – especially in a case like this, where far more literature than was
necessary has been filed). Moriarty v. Sec’y of Health & Human Servs., 844 F.3d 1322, 1328 (Fed.
Cir. 2016) (“[w]e generally presume that a special master considered the relevant record evidence
even though he does not explicitly reference such evidence in his decision”) (citation omitted).
ANALYSIS
I. Overview of POTS, Eczema, and Relevant Prior Decisions
The parties do not dispute the validity of Petitioner’s POTS diagnosis, or that she suffered
from eczema before vaccination. Some discussion of what is known about these
illnesses/conditions, and/or how they have been addressed in prior cases, will help elucidate some
of the grounds for my decision in this case.
POTS
POTS is a subset of orthostatic intolerance, not a wholly separate clinical entity. Benarroch
at 1214-15. It is marked by an increase in heart rate, or tachycardia, caused by a change in body
position from the supine position to the upright position, without an accompanying increase in
blood pressure, and results in feelings of dizziness and lightheadedness, as well as fatigue,
headache, and exercise intolerance. Gibbons at 1-2; Benarroch at 1214. Thus, a claimant alleging
a vaccine injury of POTS is arguing that the relevant vaccine has done something to the autonomic
system sufficient to cause a chronic aberrant response to orthostatic change. The relevant literature
does not indicate that POTS has ever been associated with onset of skin rashes or the exacerbation
of an existing skin condition. See generally Thieben; Butts.
There are several POTS variants with different possible etiologies, although research has
not conclusively established any one as explanatory for the majority of POTS cases. Benarroch at
1214. POTS is often the secondary result of other conditions – lower limb blood pooling,
hypovolemia (meaning decreased blood plasma), or deconditioning due to inactivity (as Dr.
Gibbons best explained). Thieben at 308. Two other proposed etiologies for POTS are a
hyperadrenergic state (meaning elevated norepinephrine concentrations) leading to tachycardia, or
59
a neuropathic variant resulting from autonomic nerve fiber damage. Id. at 308, 313; Benarroch at
1214-15. POTS is more commonly experienced by women. Benarroch at 1214.
A small subset of POTS cases may be autoimmune-mediated. See, e.g., Thieben at 311,
313 (noting that six of forty-two patients tested positive for a particular ganglionic antibody);
Gibbons at 1-2; Benarroch at 1215-16. It appears from more recent studies, however, that
researchers have not embraced autoimmunity as the most likely explanation for POTS in the
majority of individuals, and even Thieben allows that autoimmune-implicated POTS would not be
the most common way in which it occurs – and if it did, would be accompanied by evidence of
“sympathetic denervation.” Thieben at 312-13; see also Butts at 957. Importantly, an individual
suffering from an autonomic neuropathy mediated by autoimmunity would have a number of
presenting symptoms, in addition to orthostatic tachycardia, revealing harm to the autonomic
nervous system. Gibbons at 5-7.
I have had the opportunity several times to consider Vaccine Program claims alleging that
POTS, or other forms of orthostatic intolerance, was attributable to vaccination. See generally
Yalacki v. Sec’y of Health & Human Servs., No. 14-278V, 2019 WL 1061429 (Fed. Cl. Spec. Mstr.
Jan. 31, 2019), appeal docketed, No. 14-278V (Fed. Cl. Mar. 4, 2019); Johnson v. Sec’y of Health
& Human Servs., No. 14-254V, 2018 WL 2051760 (Fed. Cl. Spec. Mstr. Mar. 23, 2018); Combs
v. Sec’y of Health & Human Servs., No. 14-878V, 2018 WL 1581672 (Fed. Cl. Spec. Mstr. Feb.
15, 2018). In all, I have found that the petitioner had not met the burden of proof – primarily
because the claimant failed to successfully establish, with preponderant evidence, a reliable
scientific association between any vaccine and POTS, let alone the HPV vaccine.
In Johnson, a young woman alleged that the HPV vaccine caused her POTS that had been
diagnosed several years after receipt of the vaccine. Johnson, 2018 WL 2051760, at *7 n.11, *26
n.35. In determining that the petitioner had not established a reliable medical causation theory, I
found that she failed to demonstrate that POTS is more often than not autoimmune in origin. Id. at
*24-25. I also determined that the petitioner’s overall disease course, measured from the date of
the alleged causal vaccination to the time her symptoms were thought to possibly reflect POTS,
was simply too meandering and lengthy to deem it a medically reasonable timeframe for vaccine
causation. Id. at *22-25.
Combs, by contrast, involved only the claim that a young woman developed syncope well
after receipt of the HPV vaccine. Combs, 2018 WL 1581672, at *1. Respondent offered persuasive
evidence about the autonomic nervous system and discussed the same kind of orthostatic
intolerance issues raised in this case. After a hearing and full consideration of the evidence and
expert testimony, I found that the petitioner had not established that her condition arose from
damage to the autonomic nervous system (or brain microglia as alleged), since there was no such
evidence in the record to support that contention, nor that her syncope was likely vaccine-caused.
Id.
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In Yalacki, a petitioner alleged that the Hep B vaccine caused her to suffer from POTS
and/or chronic fatigue. Yalacki, 2019 WL 2019 WL 1061429, at *1. In contrast to the above-noted
cases, Respondent in Yalacki raised valid concerns regarding the diagnosis best supported by the
medical record (thereby suggesting petitioner had neither disease) – although there was credible
evidence supporting both injuries as having occurred. Id. at *35. Even so, in determining that the
young woman in Yalacki had not established a reliable medical theory of causation, I found that
she had not established that her POTS course (assuming she in fact had it) was consistent with
what would be expected to occur for the neuropathic variant of POTS – something she had to
establish in order for the vaccine to have been causal. Id. at *34. Petitioner’s significant orthostatic
symptoms prior to vaccination also suggested that her POTS, if it existed, predated vaccination,
but was not exacerbated by it. Id. at *37.
Such decisions certainly do not dictate the outcome of this case. However (and given the
congruity of evidence offered in such cases with that filed herein), they do demonstrate the existing
lack of up-to-date, persuasive scientific evidence associating the HPV vaccine with significant
orthostatic intolerance (beyond recognized, close-in-time reactions like syncope, which is itself a
Table claim for certain vaccines (42 C.F.R. § 100.3 VIII(C) (2018)), as well as the kind of hurdles
a petitioner faces in attempting to obtain an entitlement award based on such a theory. Too often,
such claimants propose a theory dependent on establishing (a) that their POTS was the neuropathic,
autoimmune-mediated variant, and (b) that the relevant vaccine could initiate the process resulting
in POTS, when both the medical record, and existing medical and scientific literature, do not
support either contention.
Eczema
Program cases alleging eczema/atopic dermatitis as the injury have typically involved
allegations of other disease processes as well. The majority of petitioners have combined an
eczema injury claim with the argument that food allergies, or developmental/social delays (and
autism), were also vaccine-caused, but none have succeeded. See, e.g., Gilmore v. Sec’y of Health
& Human Servs., No. 17-2026V, 2019 WL 1468203 (Fed. Cl Spec. Mstr. Feb. 26, 2019)
(dismissed for failure of proof); A.W. v. Sec’y of Health & Human Servs., No. 15-1568V, 2018
WL 1150730 (Fed. Cl. Spec. Mstr. Feb. 1, 2018) (food allergies and eczema not caused by trace
amount of food proteins in vaccines). A few eczema cases (some of which are combined with other
injuries) have, however, resulted in settlement. See, e.g., Williams v. Sec’y of Health & Human
Servs., No. 15-1224V, 2019 WL 994570 (Fed. Cl. Spec. Mstr. Jan. 29, 2019); Parker-Winter v.
Sec’y of Health & Human Servs., No. 13-150V, 2014 WL 657714 (Fed. Cl. Spec. Mstr. Jan. 23,
2014).
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II. Petitioner Has Not Established Her Claim with Sufficient Preponderant Evidence
A. Petitioner’s POTS and Eczema Most Likely Preceded Her March 2013
Vaccinations
Although Ms. McKown argues in the main that the HPV vaccine caused her injuries, she
also (primarily through the testimony of Dr. Tornatore) proposed that the vaccine could have
exacerbated pre-existing POTS or her long-standing but mild eczema. The existing medical record
best supports a significant aggravation claim for most of her claimed injuries, because that record
suggests both conditions existed at the time Petitioner received the first HPV vaccine dose in
March 2013.
There is no dispute that Petitioner had already been diagnosed with mild eczema before
receiving the HPV vaccine, and had been treated for it since a young age. Accordingly, Petitioner
can only succeed in a claim arguing that her eczema was significantly aggravated by vaccination
through satisfaction of the Loving prongs. (I do, however, treat urticaria separately below as a
potentially direct vaccine-caused injury, based on testimony at hearing from Dr. MacGinnitie
distinguishing it from eczema, and the fact that Petitioner does not appear to have suffered from
hives before receipt of the HPV vaccine).
Petitioner’s POTS-based claim also must be considered as a significant aggravation claim
in light of the medical record. The literature filed in this case (along with existing Program
caselaw) supports the conclusion that POTS progresses over a several-month period, and often
precedes formal diagnosis for some time given the difficulties in discerning its symptoms. See Tr.
at 319; Benarroch at 1214 (describing POTS as “chronic”); Thieben at 309 (POTS inclusion
criteria required the presence of symptoms for “more than” three months); see also Johnson, 2018
WL 2051760, at *22. Thus, the very fact that Ms. McKown received her POTS diagnosis in May
2013 from Dr. Dooley – within two months of receiving the first HPV vaccine dose – is almost
too close in time to her receipt of the first HPV vaccine dose to be deemed causal.
More significantly, the record establishes by May 2013 Petitioner had already experienced
three syncopal occurrences, two of which preceded the first HPV dose. And Dr. Tornatore (whose
knowledge of POTS from treating MS patients unquestionably does not render him an expert in
POTS or the autonomic nervous system) was unpersuasive in his effort to distinguish these earlier
episodes as phenotypically different from what otherwise would be deemed incidents of vasovagal
syncope. Indeed, these two prior incidents were raised as a concern at the time Petitioner received
her first HPV vaccine dose, and were also the basis for her referral to the cardiologist, Dr. Dooley,
who provided a POTS diagnosis that was substantiated in the proper manner (with a tilt table test).
See Ex. 1 at 47; Ex. 7 at 5. Accordingly, I find on this record that it is more likely than not that
62
Petitioner’s POTS began before March 2013 – meaning any claim that the HPV vaccine played a
role in her subsequent course is properly analyzed under Loving.73
B. Petitioner Has Not Established a Plausible Causation Theory (Loving Prong 4)
1. Petitioner’s Experts Were Unpersuasive or not Credible
Before discussing the specific merits of Petitioner’s theory, it is appropriate to note the
significant competence and/or qualifications gap separating both sides’ experts. Respondent
offered two experts, one of whom (Dr. Gibbons) possessed direct practice experience treating
patients with POTS (and more generally evaluating autonomic disorders associated with the
condition). Both were credentialed, well-qualified to speak on the issues in dispute, and offered
compelling and persuasive testimony, especially in their willingness to concede points that were
helpful to Petitioner.
Petitioner, by contrast, initially relied on the report jointly authored by Drs. Mikovits and
Ruscetti – but then seems to have decided to hedge her position by adding Dr. Tornatore close in
time to the hearing. Having now heard Dr. Mikovits testify, the prudence of that decision is fairly
evident.
Other special masters have harshly criticized the reliability and validity of the opinions
Drs. Mikovits and Ruscetti have offered – some going so far as to refuse to compensate them for
their time, based on the determination that their opinions were unhelpful in resolving a particular
case. See, e.g., Dominguez v. Sec’y of Health & Human Servs., No. 12-378V, 2018 WL 3028975
(Fed. Cl. Spec. Mstr. May 25, 2018) (awarding Dr. Mikovits a rate of only $75 per hour for work
completed on an expert report after determining she did not assist resolution of the matter);
McCabe v. Sec’y of Health & Human Servs., No. 13-570V, 2018 WL 3029175, at *20-21 (Fed.
Cl. Spec. Mstr. May 17, 2018) (criticizing Dr. Mikovits for diagnosing medical conditions, absent
any medical license or training, and incorrectly stating medical definitions); Barker v. Sec’y of
Health & Human Servs., No. 16-1554V, 2018 WL 2772454, at *1-2 (Fed. Cl. Spec. Mstr. May 11,
2018) (critiquing Drs. Mikovits and Ruscetti for proffering theories based on “misleading
references to medical literature”); Rogero v. Sec’y of Health & Human Servs., No. 11-770V, 2017
WL 4277580, at *23-24 (Fed. Cl. Spec. Mstr. Sept. 1, 2017) (stating Dr. Mikovits’s opinion
regarding vaccine causation was “never clearly or coherently explained” at hearing), mot. for
review den’d, slip op. (Fed. Cl. Jan. 11, 2018), aff’d, 748 F. App’x 996 (Fed. Cir. 2018).
At hearing, Dr. Mikovits lived up to her reputation. She was dismissive and conclusory in
attempting to explain away the many embarrassing episodes from her professional life. Indeed, the
mere fact that she had to recount them at all harmed her credibility from the outset. See, e.g., Tr.
at 217 (“[Whittemore] fired me . . . [and] I get a letter from a lawyer saying you’ve stolen our
73
Below I address only those Loving prongs most relevant to my Decision.
63
intellectual property and data and, basically, defend yourself”), 219 (“I was held [in jail] on
something called a fugitive from justice”), and 259 (“[t]he Whittemores said I manipulated a figure
in order to cover up their misappropriation of federal funds”). The picture painted by these
occurrences in Dr. Mikovits’s professional history was too damaging to ignore. An expert’s
professional past is a relevant consideration when evaluating how much weight to give her
testimony, since it reflects on her overall candor. See, e.g., Cox v. Sec’y of Health & Human Servs.,
30 Fed. Cl. 136, 144 (1993) (“expert’s criminal background[] raised issues of weight and not
admissibility”); Yalacki, 2019 WL 1061429, at *12 n.18 (fact that expert-authored publication was
later retracted impacted expert’s credibility); Weppler v. Sec’y of Health & Human Servs., No. 12-
316V, 2014 WL 4057149, at *2 (Fed. Cl. Spec. Mstr. July 25, 2014) (physician’s prior
“convictions for false statements . . . [and] fraud cast serious doubt on his credibility”).
Other special masters have disregarded expert opinions entirely for comparable improper
conduct. See, e.g., Raymo v. Sec’y of Health & Human Servs., No. 11-0654V, 2014 WL 1092274,
at *13-16 (Fed. Cl. Spec. Mstr. Feb. 25, 2014) (rejecting entire medical opinion as unreliable where
expert credibility issues included a plagiarized report and a failure to reveal a medical license
suspension). Based on what was disclosed about her past at hearing that undermined her
professional competency on immunologic matters, coupled with her lack of specific expertise in
studying or treating either of the conditions at question, I arguably could have simply determined
that Dr. Mikovits’s credibility was so damaged that her opinion was entitled to virtually no weight
at all.74 See, e.g., Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1995)
(concluding that it was reasonable for the special master to use Daubert to evaluate reliability of
an expert’s testimony); Ryman v. Sec’y of Health & Human Servs., 65 Fed. Cl. 35, 40-41 (2005)
(special masters perform gatekeeping function when determining “whether a particular petitioner’s
expert medical testimony supporting biological probability may be admitted or credited or
otherwise relied upon”).
However, despite such sound reasons to ignore her opinion, fairness to the Petitioner
compelled me to evaluate Dr. Mikovits’s opinion for its substance. Even then, her opinion was
wanting. She offered a medical/scientific causation theory that was poorly-supported and utterly
confusing (as Respondent’s experts recognized) – a disorganized hodge-podge of scientific
principles strung together without the persuasive connective “glue” that a competent and
knowledgeable expert would provide. And her opinion relied heavily on ASIA as a mechanistic
explanation for how the vaccines Petitioner received could have injured her - despite the fact that
Petitioner clearly stated she would not be offering ASIA as a component of her case. See Pre-
Hearing Reply (ECF No. 52) at 1 (“while Drs. Mikovits and Ruscetti reference ASIA, neither they
nor Dr. Tornatore assert ASIA as their theory of causation”); Tr. at 6 (“the ASIA literature informs
74
In addition, and as discussed earlier, Dr. Mikovits’s expert reports were co-authored (and signed) by Dr. Ruscetti,
although only Dr. Mikovits testified at hearing. Dr. Mikovits has been criticized in past Program cases for the practice
of testifying alone regarding co-authored reports. See, e.g., Rogero v. Sec’y of Health & Human Servs., No. 11-770V,
2017 WL 4277580, at *23 (Fed. Cl. Spec. Mstr. Sept. 1, 2017), mot. for review den’d, slip op. (Fed. Cl. Jan. 11, 2018),
aff’d, 748 F. App’x 996 (Fed. Cir. 2018).
64
the medical theory, but it’s not the – it’s not the basis for the medical theory”), 8, 294. Overall,
such substantive deficiencies equaled, if not exceeded, the many professional lapses that would
otherwise justify giving Dr. Mikovits’s opinion little to no weight.
My comments on Dr. Mikovits largely do not apply to Dr. Tornatore – a well-credentialed
expert with none of Dr. Mikovits’s substantial professional lapses. He frequently offers fair,
articulate opinions in Program cases, and has served as an expert in many cases I have adjudicated.
But in this case, Dr. Tornatore was the wrong man for the job. His unquestionable expertise in
treating CNS autoimmune illnesses like MS was not accompanied by comparable expertise in
specifically treating or studying POTS or eczema, especially when compared to Drs. Gibbons and
MacGinnitie. He thus could not leverage his personal expertise into a persuasive opinion on POTS
or skin conditions, the interaction between the two, and/or the relationship of either to the HPV
vaccine. He largely seems to have offered an opinion heavily reliant on just two independent items
of literature (Kanduc and Voisin), neither of which were deemed important enough by Petitioner
or her counsel to file in this case before the very eve of trial.
Overall, Petitioner’s expert showing was almost facially inadequate in helping her meet
her preponderant burden of proof – especially when judged against the far more reliable and
scientifically persuasive showing made by Respondent’s experts. Although (again – in the interests
of fairness to the Petitioner), I review below the actual merits of the theories these experts
presented, it is important to emphasize that Petitioner’s experts did not themselves imbue her
causation theory with evidentiary heft based on their own expertise – and in Dr. Mikovits’s case
greatly undermined whatever probative value the expert opinion she offered had on its own.
2. Petitioner’s Causation Theory was Unreliable and Unpersuasive
Having reviewed each side’s expert reports and medical literature, and considered the
testimony at hearing, I find that Petitioner has not presented a plausible theory, supported by
sufficient reliable evidence, that the HPV vaccine can cause, or significantly aggravate, either
POTS or eczema.
An overarching deficiency in Petitioner’s theory is the supposition that her primary,
complained-of injuries – POTS and skin conditions variously characterized as eczema or urticarial
lesions/hives – were more likely than not autoimmune in origin. Petitioner specifically proposed
that a neuropathic form of POTS could be mediated by autoantibodies produced in response to the
implicated vaccine, and thus via an adverse autoimmune process. Admittedly, there is literature
support (such as Thieben, Gibbons, and Benarroch) for the idea that one particular variant of
autonomic neuropathy producing POTS symptoms might be associated with a particular
autoantibody, thereby suggesting autoimmunity as a plausible pathologic mechanism.
Dr. Gibbons (whose direct experience studying the etiology of POTS far outweighed that
of Drs. Tornatore and Mikovits), however, persuasively established that the autoimmune-
65
mediated, neuropathic form of POTS is very rare, occurring only where an individual possesses a
specific ganglionic autoantibody (which Ms. McKown was never demonstrated to possess). The
literature filed with regard to the neuropathic variant, as Dr. Gibbons posited, best supports the
conclusion that this POTS variant is far less common from those deemed non-neuropathic in
etiology. And Drs. Tornatore and Mikovits in no way undercut Dr. Gibbons’s testimony
(corroborated by several items of literature) that the other POTS variants clearly are not
autoimmune in etiology, such as hyperadrenergic POTS or POTS due to deconditioning, or that
these are more common explanations for POTS (which, unlike the neuropathic form, are more
likely to feature syncope of the sort Petitioner actually experienced). Gibbons at 1-10; Tr. at 353-
54, 419-20.
The remaining scientific evidence offered by Petitioner suggesting POTS is typically
autoimmune was thin, relying on case reports – a kind of evidence not given significant weight in
Program cases. See, e.g., Campbell v. Sec’y of Health & Human Servs., 97 Fed. Cl. 650, 668 (2011)
(“[c]ase reports do not purport to establish causation definitively, and this deficiency does indeed
reduce their evidentiary value”). And the evidence linking POTS to other forms of autoimmune
disease (see, e.g., Dahan, Cerpa-Cruz, Giannotta) was too inconclusive, or was rooted in accepting
the abandoned ASIA component of Petitioner’s causation theory. I thus do not find that POTS is
more often than not autoimmune in origin – greatly reducing the likelihood that a vaccine could
initiate an autoimmune process sufficient to cause it.
A secondary weakness of Petitioner’s theory was Dr. Tornatore’s unsuccessful linkage of
POTS with eczema. He proposed that the two could interact via some kind of nervous system
feedback loop, in which the same neuropathic injury could produce both the orthostatic symptoms
of POTS as well as skin-related symptoms. But the primary literature discussing POTS says
nothing about any association between POTS and any symptoms comparable to eczema or
urticaria. See, e.g., Thieben; Butts. To advance this argument in the face of what the medical
community understands about POTS at present, Dr. Tornatore had to stretch certain items of
literature well beyond their actual scope. Voisin, for example, was offered to support the
contention that nerve damage (purportedly the result of an autoimmune cross-reaction) could not
only be associated with POTS but with skin injuries as well. But, as noted earlier, Voisin discusses
only allergic inflammation – it makes no mention of POTS (or the production of autoantibodies
associated with neuropathic variant) or its pathogenesis, nor does it attempt to relate autoimmune
disease to allergies more generally. At bottom, this element of Petitioner’s theory over-relied on
the fact that the nervous system does play some role in adverse skin processes like eczema or
urticaria – even though, as Dr. MacGinnitie established, they cannot be assumed to be allergic in
nature, and are not primarily autoimmune in character either.
Next, even if it is granted that the rare, neuropathic, autoimmune form of POTS could
include symptoms consistent with skin rashes (while also featuring syncope -despite the fact, as
established by Dr. Gibbons, that neuropathic POTS generally does not as it progresses), there
66
remain substantial deficiencies in Petitioner’s theory that the HPV vaccine could trigger or
exacerbate such symptoms via an autoimmune process. For a mechanism75 by which this could
occur, Dr. Tornatore mostly embraced molecular mimicry, relying heavily on Kanduc (an article
that was only deemed important in the days before trial – and which Respondent reasonably
questioned as unreliable simply on the basis of its source of publication). As discussed above,
Kanduc examined the HPV16 polyprotein and recorded amino acid sequence similarities to the
human proteome at the heptamer level, concluding that the proteome contains both heptapeptides
and octapeptides (or enough sequence homology) with the vaccine sufficient to establish potential
cross-reactive sequences. But Kanduc did not test the theoretical cross-reactivity between the
sequences established, nor did it provide any meaningful evidence that the proposed homologous
sequences were in any way pathogenic. And no other evidence was offered suggesting that any of
the self homologous sequences are key to the process by which autoimmune neuropathic POTS
occurs.
Thus, in advancing the contention that molecular mimicry constitutes a reliable scientific
mechanism by which the HPV vaccine could cause or exacerbate POTS, all Petitioner’s experts
have done is observe that protein sequences contained in the HPV vaccine can be shown to possess
some sequential and/or structural similarity with targets of where an autoimmune reaction resulting
in neuropathic POTS is speculated to occur. They have not established that reliable science has
demonstrated that any kind of external insult, whether viral or vaccine, has ever been associated
with an autoimmune reaction resulting in POTS at the proposed homologous situs.
It is common for Program petitioners to propose molecular mimicry as part of a causation
theory – and indeed in many cases it is a persuasive component (especially when accompanied
with other corroborative evidence) that can help establish how a vaccine’s antigenic presentation
might induce an autoimmune pathologic process. But merely chanting the magic words “molecular
mimicry” in a Vaccine Act case does not render a causation theory scientifically reliable, absent
additional evidence specifically tying the mechanism to the injury and/or vaccine in question. See
Devonshire v. Sec’y of Health & Human Servs., No. 99-031V, 2006 WL 2970418, at *15 (Fed. Cl.
Spec. Mstr. Sept. 2006), aff’d, 76 Fed. Cl. 452 (2007). For such reasons I have rejected the blanket
reliance on molecular mimicry under comparable circumstances. See, e.g., Johnson, 2018 WL
2051760, at *26 (theory that HPV vaccine could cause POTS via molecular mimicry not found
scientifically reliable).
Dr. Tornatore’s alternative T cell degeneracy mechanism (which he largely seemed to
abandon at hearing in favor of molecular mimicry) fares no better. Dr. Tornatore posited that T
cells can recognize several different antigens (and mount an immune response against them)
without having any homology to a specific vaccine components, but nevertheless result in the same
75
As I have observed in other cases, petitioners need not offer a mechanism in attempting to establish a causation
theory under the first Althen prong – but if they do, it is fair to evaluate their success in the effort from the standpoint
of whether it is preponderantly established. See, e.g., K.L. v. Sec’y of Health & Human Servs., No. 12-312V, 2017 WL
1713110, at *14 (Fed. Cl. Spec. Mstr. Mar. 17, 2017), mot. for review den’d, 134 Fed. Cl. 579 (2017).
67
autoimmune process presumably ending in POTS. But, and as before, he could not establish that
the HPV vaccine had been shown to have this capacity in any regard, whether in
causing/exacerbating POTS or any other autoimmune condition. And as Dr. MacGinnite
persuasively established, T cell degeneracy as a theory implies that any T cell in the body could
be responsible for an autoimmune cross-reaction (and it would be impossible to determine the
instigator) – an overbroad contention given how infrequently autoimmune diseases actually occur.
Tr. at 491; see also Trost at 71.
The additional mechanistic theories offered by Drs. Mikovits and Ruscetti were similarly
unpersuasive. The proposition that vaccination can induce the production of proinflammatory
cytokines (IL-1 beta specifically), thereby causing inflammation sufficient to create a favorable
environment for autoimmunity, was not preponderately established. Indeed, I have noted in other
cases that this theory – which relies heavily on what vaccines are understood to do
immunologically, but then attempts to convert that into describing a pathologic process – is
scientifically and medically unreliable, absent proof relevant to the disease process or vaccine at
issue. See, e.g., Godfrey v. Sec’y of Health & Human Servs., No. 10-565V, 2015 WL 10710961,
at *10-14 (Fed. Cl. Spec. Mstr. Oct. 27, 2015) (insufficient reliable scientific evidence supported
proposition that cytokine upregulation induced by HPV vaccine was pathogenic enough to cause
juvenile ankylosing spondylitis), mot. for review den’d, slip op. (Fed. Cl. Apr. 29, 2016).
The fact that cytokine upregulation is promoted by vaccination – a medically reliable
assertion standing alone – does not mean that this cytokine increase is definitionally harmful,
especially given (as observed by Dr. MacGinnitie) that it is difficult to establish whether certain
proinflammatory cytokines are instigators or merely mediators of a disease process begun in some
other way. It certainly does not establish that the cytokine upregulation would be sufficiently
chronic to cause harm over an extended period of time. And the ASIA theory (something Dr.
Mikovits could not resist discussing, despite Petitioner’s averment that it was not part of her case),
which posits the aluminum vaccine adjuvant as contributing to the purported pathologic immune
response, is especially suspect from a scientific standpoint, as has been observed repeatedly in the
Vaccine Program. See, e.g., Morris v. Sec’y of Health & Human Servs., No. 12-415V, 2016 WL
3022141, at *12 (Fed. Cl. Spec. Mstr. Apr. 1, 2016) (discussing lack of reliability of ASIA theory);
Rowan v. Sec’y of Health & Human Servs., No. 10-272V, 2014 WL 7465661, at *16 (Fed. Cl.
Spec. Mstr. Dec. 8, 2014), mot. for review den’d, 2015 WL 3562409 (Fed. Cl. May 18, 2015);
D’Angiolini v. Sec’y of Health & Human Servs., No. 99-578V, 2014 WL 1678145, at *60 (Fed.
Cl. Spect. Mstr. Mar. 27, 2014), mot. for review den’d, 122 Fed. Cl. 86 (2015), aff’d, 645 F. App’x
1002 (Fed. Cir. 2016).76
Petitioner also was unable to provide a reliable causation theory that her eczema flares
76
For this very reason, I have not permitted petitioners to assert claims at hearing relying on ASIA for their causation
theory, given the well-established doubts about its scientific reliability. See, e.g., Johnson, 2018 WL 2051760, at *7
n.11.
68
could be vaccine-caused and/or the product of an autoimmune process. A threshold category error
Petitioner made was in attempting to place her skin-related symptoms into a framework of nerve
stimulation also in the context of allergic inflammation. But, as Dr. MacGinnitie (the sole expert
with sufficient credentials and expertise in the fields of allergy and immunology to opine
intelligently on the subject) discussed, allergies are not thought to be associated with or caused by
autoimmune disease or severe autonomic dysfunction (as Petitioner claims). Accordingly,
Petitioner could not persuasively invoke the limited science she offered bearing on how nerves
might interact with allergic responses (primarily Voisin) to also connect those responses to an
autoimmune process.
Finally, Petitioner did not present sufficient reliable scientific or medical evidence
associating the HPV vaccine with POTS or eczema/urticaria. Besides case reports, she offered a
few articles like Brinth or Blitshteyn which, while facially seeming to suggest such an association,
have built-in reliability problems – due to the selection bias at issue in the studied subjects, as
pointed out by Dr. Gibbons, as well as their own lack of a reliable scientific basis. Tr. at 366-67,
381; Brinth at 2603, Blitshteyn at 135; see also Johnson, 2018 WL 2051760, at *24 (critiquing
Brinth as essentially a case study evidencing only a “temporal correlation” between the HPV
vaccine and POTS). Respondent’s experts, by contrast, referenced several reliable and credible
articles (some of which were trustworthy, large-scale epidemiologic studies77) like Chao78, Butts,
Grimaldi-Bensouda, Block, Scufka, and the EMA Report, all noting that the HPV vaccine is not
properly associated either with POTS specifically or other known autoimmune conditions
generally. The evidence against Petitioner’s contentions regarding the HPV vaccine and POTS or
eczema greatly outweighed her own evidence.
No doubt none of the above evidence, pro or con Petitioner’s litigative position, establishes
from a final scientific standpoint whether the HPV vaccine could cause POTS (and it is not my
purview as special master in this case to make such determinations in the first place). It remains
conceivable that scientific evidence may yet reliably establish an association. But the evidence
77
Petitioners in Program cases, when confronted with strong epidemiologic evidence, are often quick to point out that
they cannot be “required” to offer it as part of their evidentiary showing – and therefore (because even a good and
trustworthy epidemiologic study cannot completely refute the possibility that an inherently rare event like a vaccine
injury could occur) merely to consider it constitutes an unfair heightening of their evidentiary burden. See, e.g.,
D’Toile v. Sec’y of Health & Human Servs., 132 Fed. Cl. 421, 430 (2017), aff’d, 726 F. App’x 809 (Fed. Cir. 2018).
But although it is true that petitioners are not obligated to offer epidemiologic evidence to support their claim, it can
be considered (especially when it exists and is especially relevant to the causal theory at issue) in evaluating the
success of a Vaccine Act petitioner in meeting her evidentiary burden. Sound and reliable epidemiologic evidence
relevant to a specific vaccine injury claim cannot be swept under the carpet with the argument that it is categorically
unmentionable.
78
I have in prior decisions discussed Chao in depth, noting its scientific reliability and persuasiveness. See, e.g., Maciel
v. Sec’y of Health & Human Servs., No. 15-362V, 2018 WL 6259230, at *27 (Fed. Cl. Spec. Mstr. Oct. 12, 2018),
mot. for review den’d, slip op. No. 15-362V (Fed. Cl. Apr. 1, 2019); Johnson, 2018 WL 2051760, at *25; Sullivan v.
Sec’y of Health & Human Servs., No. 10-398V, 2015 WL 1404957, at *11-12 (Fed. Cl. Spec. Mstr. Feb. 13, 2015).
69
offered in this case simply does not meet Petitioner’s preponderant burden that it is “more likely
than not” the HPV vaccine could cause or exacerbate POTS or eczema.
C. The Record Does Not Establish That Petitioner’s POTS or Skin Symptoms
Were Exacerbated by the HPV Vaccine (Althen Prong Two/Loving Prong 5)
Petitioner’s obligation under the second Althen prong/Loving prong five is to demonstrate
a logical sequence of cause and effect connecting the particular facts of his case to her medical
theory. Sturdivant v. Sec’y of Health & Human Servs., No. 07-788V, 2016 WL 552529, at *18
(Fed. Cl. Spec. Mstr. Jan. 21, 2016) (discussing Althen prong two). But the record in this case
does not contain preponderant evidence that the HPV vaccine likely exacerbated Petitioner’s
POTS and preexisting eczema via the proposed autoimmune process set forth in her theory. The
medical record does not allow for the conclusion that Ms. McKown’s injuries were the result of
the autoimmune-mediated neuropathic POTS variant.
As Respondent’s experts observed, there is a lack of testing results in the medical record
suggesting that Petitioner was experiencing any of the hallmarks of an autoimmune disease, like
inflammation. Rather ,the more common indicators of underlying systemic inflammation
(including the CRP and ESR rates) remained relatively stable throughout the course of her
illness. Dr. Tornatore posited that those readings could not wholly rule out the possibility that
Petitioner was experiencing a neuropathic condition, but his argument seemed more relevant to
the kinds of CNS-oriented autoimmune diseases he treats, featuring inflammation localized to
the spine or brain, rather than what Petitioner alleges occurred here. Only one record (from July
2014 – hence long after the vaccinations in question) established that Petitioner ever experienced
a slightly elevated ERS and ANA – but, as Dr. MacGinnite persuasively proposed, such slight
elevations likely had no clinical significance (and were themselves barely positive). Tr. at 481.
And even so, Ms. McKown’s treaters consistently ruled out autoimmunity as a cause of her
symptoms. Id.
There is also a paucity of testing results establishing the presence of the putative
autoantibodies that would, under Petitioner’s theory, corroborate that she was experiencing an
autoimmune-oriented disease process, let alone neuropathic POTS. Indeed, none of her treaters
(including the numerous specialists she saw at the Cleveland Clinic) even proposed to test for
them (which they might have done had they harbored any suspicion that autoimmunity explained
her symptoms). The fact that she did test positive for certain allegedly-relevant biomarkers (for
example, her slightly elevated IgE levels to various environmental allergens) cannot be
leveraged into a finding that she was experiencing neuropathic POTS, since (as Dr. Tornatore
admitted during his direct testimony) elevated IgE is not specific to autoimmunity directly.
Moreover, the character of Ms. McKown’s actual symptoms was inconsistent with her
70
allegation that she had suffered a neuropathic form of POTS mediated by an autoimmune process.
Dr. Gibbons (the expert with the most direct experience treating POTS) emphasized that the rare
neuropathic POTS variant discussed in the literature is typically accompanied by profound
autonomic damage – something lacking in this record. Tr. at 358. Neuropathic POTS would also
feature many more debilitating symptoms – none of which Petitioner experienced. At the same
time, the syncopal episodes Petitioner experienced were (as Dr. Gibbons maintained persuasively)
evidence of a properly functioning autonomic nervous system – not one damaged by an
autoimmune neuropathy. Tr. at 323, 394, 421. And Petitioner’s numerous other symptoms
(including joint problems, pain, prolonged episodes of unconsciousness, and eczema) are not
associated with any particular POTS subtype. Tr. at 346, 349, 352.79 Dr. Tornatore’s argument
about the significance of Ms. McKown’s episodes of flushing (or bluish coloring in the limbs) was
especially strained, as none of the literature he relied upon persuasively established that limb
discoloration is associated with the favored POTS variant (beyond a single reference in Voisin –
an article not addressing POTS – to a 1901 study).
Treater support for a finding that Petitioner either experienced a neuropathic form of POTS,
or that at least it had been made worse by vaccination, is similarly absent from the medical record.
Multiple contemporaneous treaters, including her cardiologist Dr. Dooley, informed Petitioner of
their view that the HPV vaccine was not associated with POTS. Ex. 6 at 25. Her dermatologist,
Dr. Rice, also proved unwilling to confirm Petitioner’s fears about vaccine association to her
symptoms. See Ex. 4 at 16-21; Ex. 14 at 22. And treaters at the Cleveland Clinic, who performed
a multi-specialty, comprehensive work-up based on Petitioner’s various complaints, specifically
refuted a connection between the HPV vaccine and skin rashes. Ex. 11 at 7. That work-up
otherwise does not support the conclusion that Ms. McKown’s symptoms had an autoimmune
character or origin.
Admittedly, one treater – Dr. DeMio – reached a contrary conclusion. Ex. 14 at 25, 27. But
(putting aside his questionable medical credentials to offer a reliable opinion on this subject)80, Dr.
79
The evidence is more inconclusive as to what POTS variant best explains Petitioner’s symptoms. Dr. Gibbons
opined that Petitioner’s POTS was likely hypovolemic (or due to dehydration), or attributable to deconditioning related
to her athletic activities but was ultimately uncertain. Tr. at 332-33, 355-56. To support this contention, he referenced
the BUN to creatine ratio measurement (20:1) taken during Petitioner’s initial hospitalization in April 2013, suggesting
the existence of dehydration (with resolution of her symptoms following fluid intake corroborating this possibility).
Id. at 333. In response, Dr. Tornatore reasonably posited that Petitioner otherwise exhibited no clinical signs or
biomarkers for chronic dehydration over the course of her illness, and the BUN-creatine ratio levels were arguably
less meaningful in this case than Respondent’s experts argued. Id. at 559-60. I cannot on this record (especially in the
absence of contemporaneous treater opinions as to the relevant POTS variant in question) determine if the evidence
preponderates for or against Petitioner on this point – other than to conclude that, taken as a whole, the record does
not preponderate in favor of a determination that she had the neuropathic, autoimmune form.
80
Other special masters have observed that Dr. DeMio lacks the expertise to opine regarding the medical theories he
has advanced. See, e.g., Wyatt v. Sec’y of Health & Human Servs., No. 14-706V, 2018 WL 7017751, at *18-19, 21-
22 (Fed. Cl. Spec. Mstr. Dec. 17, 2018) (“[o]nce again, Dr. DeMio has rendered an opinion in a case in which he lacks
the underlying requisite medical expertise. Dr. DeMio has neither specialized training in either autoimmune or
neurological disorders nor has he ever conducted research or written papers in either of these fields”), mot. for review
71
DeMio only saw Petitioner in September 2014 (roughly one year following her second dose of
HPV), and his assessment seemed to turn more on the health course reported by Petitioner than his
own contemporaneous examination. In addition, the testing for autoimmunity performed around
this time was also negative. Ex. 9 at 7-12. I therefore give his opinion far less weight than the more
numerous and more medically-trustworthy prior treaters who reached more evidentiarily-
supported conclusions.
Ms. McKown’s medical record does establish that she experienced a recurring skin
condition, in the form of eczema flares post-vaccination. However, I do not find that she has
established that these flares were attributable to the HPV or Hep A vaccines. As already noted, the
medical record does not support the conclusion that she was experiencing inflammation or an
autoimmune process in the relevant post-vaccination timeframe – and because, as discussed above,
she did not establish a reliable theory that an allergic response like eczema is associated with
autoimmunity in the first place, the presence of such evidence would not make it more likely
vaccination caused her flares. Moreover, none of the dermatologists she saw (including a
Cleveland Clinic specialist) associated her symptoms with either the vaccines she received
specifically or an autoimmune process generally. Otherwise, I do not see on the basis of this
medical record any connection between her skin symptom flares and POTS (beyond the fact that
both were coincidentally occurring in the same general time period).
D. Petitioner’s Urticaria Was Not Vaccine-Caused
Because Petitioner appears not to have experienced hives before vaccination, unlike her
POTS claim she could conceivably establish that this set of symptoms (separate from her
preexisting eczema) was directly vaccine-caused. However, she failed to do so, based on any of
the three Althen prongs.
First, although Respondent’s primary allergy expert, Dr. MacGinnitie, agreed that chronic
urticarial lesions could be autoimmune in nature, Petitioner did not persuasively establish that
either of the vaccines she received beginning in March 2013 could produce this particular outcome
(for which she was first clearly diagnosed in 2014 many months later) – and if so, how. See Ex.
11 at 14; Ex. 1 at 76. Petitioner’s experts lacked the experience and background necessary to offer
a persuasive opinion on the subject of urticaria generally, and (for the same reasons discussed
above) their immunologic theories were scientifically unreliable.
den’d, slip op. No. 14-706V (Fed. Cl. June 5, 2019); Holt v. Sec’y of Health & Human Servs., No. 05-136V, 2015 WL
4381588, at *16 (Fed. Cl. Spec. Mstr. June 24, 2015) (“[Dr. DeMio] is board certified in emergency medicine. He has
no formal specialized training in . . . any of the several areas [pediatrics, immunology, neurology, or gastroenterology],
in which he proffered opinions. His only publications involved chapters on arthritis, gout, inflammation, and nutrition
in an integrative medicine textbook.”).
72
Second, even if Petitioner had satisfied the “can cause” prong, the record does not suggest
that she tested positive for any autoantibodies known to associated with the autoimmune form of
urticaria discussed by Dr. MacGinnitie – and none of the allergists or dermatologic experts she did
see ever proposed or concluded that her hives were vaccine-related, let alone autoimmune in
nature. Indeed, the better evidence in the record (such as that from the summer of 2013, just after
Petitioner was diagnosed with POTS and given medication for it) supports the conclusion that in
certain cases any hives she experienced may have been associated with her medication. See, e.g.,
Ex. 7 at 33. Finally, the timeframe in which Petitioner displayed such hives (beginning no earlier
than three to four months after receipt of the first HPV dose) was not shown by Petitioner’s experts
to be medically reasonable, with her overall stuttering course not reasonably or credibly connected
to some chronic autoimmune process that began with the first dose in March 2013.
E. Other Althen/Loving Prongs
Because my holding turns primarily on the preceding analysis of certain individual Althen
or Loving prongs, I need not consider every single individual other prong. I do, however, make the
following additional findings:
1. Loving Prong 3: Evidence of Worsening
In this case, it is easy to conclude based on the medical record and witness testimony that
in the months and years after receiving the vaccines in question, Ms. McKown experienced more
POTS-associated symptoms, as well as eczema flares, than she had pre-vaccination, and thus in a
literal sense her condition was unquestionably “worse.” Although it was difficult to assess the
accuracy of Petitioner’s claims regarding extended periods of time in which she was unconscious,
I credit her averments that she experienced POTS-related symptoms, as well as bouts of eczema
and hives, more frequently after receiving the two doses of HPV vaccine than before.
But determining that Petitioner’s condition was comparatively worse post-vaccination only
satisfies the second Loving prong, leaving the third unanswered: did her condition reflect an
aggravation of what she otherwise would have expected to consider – as a person previously
diagnosed with eczema, and as likely to have been suffering from POTS even before vaccination?
Locane, 685 F.3d at 1381-82.
Considering only her POTS symptoms, and taking into account the literature filed in this
case along with expert testimony from Dr. Gibbons (the sole expert with a specific focused
background in POTS), I do not find that Petitioner’s course was outside of what most individuals
suffering from POTS will experience. The literature filed in this case establishes that non-
neuropathic POTS can have a number of associated symptoms, including syncopal episodes
(although, as Dr. Gibbons established, such episodes are counterfactually evidence of a properly
73
performing autonomic system). See Benarroch at 1215-16; Gibbons at 1, 5-7. It is also common
for POTS to wax and wane over time, as a patient’s course persists (as Dr. Gibbons posited). See
Tr. at 352 (noting that it is not “unusual” for a POTS course to “fluctuat[e] in the frequency of
symptoms”), 352-53 (“one of the characteristics of POTS is that after you’ve sort of developed the
syndrome, things do get typically worse”), 395. Nothing in Petitioner’s overall treatment history
suggests the POTS symptoms she experienced were outside the norm, and none of her treaters
proposed otherwise.
Petitioner’s experts simply lacked the in-depth knowledge of POTS to opine persuasively
to the contrary. Dr. Tornatore might have accurately described the “tempo” of Petitioner’s
symptoms as picking up post-vaccination, but that does not satisfy the third Loving prong. His
testimony did not establish reliably that Petitioner’s symptoms course went beyond what an
autonomic or cardiologic expert would expect to see. Certainly nothing in the medical record
suggests any treater with expertise in POTS thought Ms. McKown’s symptoms were particularly
alarming or unusual.
Regarding Petitioner’s eczema flares, Dr. Tornatore described a worsening over a six-
month period following Petitioner’s initial doses of HPV and Hep A (beginning in June or July
2013), and later resulting in more significant flares in September of that year (after the second dose
of HPV vaccine). Tr. at 151. But he acknowledged as well that the record evidenced skin-related
symptoms that were “coming and going,” and sometimes even normal. Id. at 146-48. Dr.
MacGinnitie, who treats multiple patients with dermatologic conditions like eczema, agreed but
concluded that Petitioner’s case was nevertheless within the range of what is expected for an
eczema patient. Id. at 486-69, 512. It is not enough for Petitioner to argue that she literally became
“worse” in the days immediately after receipt of the last HPV dose – for that is another way of
simply invoking the temporal relationship between vaccine and injury, a relationship well
understood in the Program to have little evidentiary bearing when determining entitlement. See,
e.g., LaLonde v. Sec’y of Health & Human Servs., 746 F.3d 1334, 1341 (Fed. Cir. 2014) (“[a]
temporal correlation alone is not enough to demonstrate causation”). Accordingly, the record
(supplemented and interpreted with persuasive expert testimony from Dr. MacGinnitie) does not
permit the conclusion that Petitioner’s eczema flares were worse than what would otherwise have
been expected.
2. Althen Prong Three: Timeframe
Petitioner proposes that aggravation of her POTS symptoms in late April 2013 (or four to
five weeks following vaccination), after the yogurt shop incident, was a medically appropriate
timeframe for a vaccine-induced injury to occur. In support, however, she relied almost exclusively
on Schonberger – which studied the incident rate of onset of GBS following receipt of the flu
vaccine -- an injury and vaccine combination that is distinguishable from that alleged herein, other
74
than the fact that it too involves nerve system-related harm. This, plus the broader deficiencies
with Petitioner’s theory (which did not otherwise establish that the HPV (or Hep A) vaccine doses
could directly cause POTS and/or that Petitioner’s POTS was the result of an autoimmune
neuropathy), as well as the lack of evidence that in this timeframe Petitioner was experiencing any
autoimmune or inflammatory process, prevents a finding that the timeframe was medically
acceptable.
The same is true for flares of Petitioner’s preexisting eczema. The records establish that
her flares (a) occurred no earlier than July 2013, or over three months after the first HPV dose, (b)
were associated by treaters with cessation of medicine intended to treat her POTS, (c) were never
deemed autoimmune in nature by any competent treaters, and (d) were not persuasively established
by Petitioner’s experts to have any association with her coterminous POTS diagnosis. Petitioner’s
experts also did not credibly explain how an autoimmune process that could result in a POTS-
related syncopal episode five weeks post-vaccination could then take another two-plus months to
manifest in exacerbation of skin-related symptoms.
CONCLUSION
Petitioner has not carried her burden of proof, and therefore I must DENY entitlement in
this case. In the absence of a timely-filed motion for review (see Appendix B to the Rules of the
Court), the Clerk shall enter judgment in accord with this decision.81
IT IS SO ORDERED.
/s/ Brian H. Corcoran
Brian H. Corcoran
Special Master
81
Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment by filing a joint notice renouncing their
right to seek review.
75