Cerrone v. Secretary of Health and Human Services ( 2023 )

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 17-1158V
(to be published)
*************************
NIKKO CERRONE, *
* Chief Special Master Corcoran
*
Petitioner, * Filed: May 8, 2022
*
v. *
*
SECRETARY OF HEALTH *
AND HUMAN SERVICES, *
*
Respondent. *
*
*************************
Gary Alan Krochmal, Law Offices of Gary A. Krochmal, PLLC, Farmington Hills, MI, for
Petitioner.
Mallori Browne Openchowski, U.S. Department of Justice, Washington, DC, for Respondent.
ENTITLEMENT DECISION 1
On August 28, 2017, Nikko Cerrone filed this action seeking compensation under the
National Vaccine Injury Compensation Program (the “Program”). 2 ECF No. 1. Petitioner alleges
that the human papillomavirus (“HPV”), influenza, and Hepatitis A (“Hep. A”) vaccines he
received on October 7, 2015, caused him to incur ulcerative colitis (“UC”). A two-day entitlement
hearing in the matter was held in Washington, D.C., on May 24-25, 2022.
Having reviewed the record, all expert reports and associated literature, and listened to
those witnesses and experts who testified at the hearing, I hereby deny an entitlement award. As
discussed in greater detail below, Petitioner has not preponderantly established that any of the
1
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. 3758, codified as amended at 42 U.S.C. §§ 300aa-10 through 34 (2012) [hereinafter “Vaccine Act” or “the
Act”]. Individual section references hereafter will be to § 300aa of the Act (but will omit that statutory prefix).
vaccines can cause UC, that they did so herein, or that the timeframe in which his UC manifested
(when measured against the date of vaccination) was medically acceptable.
I. Fact History
Prior Medical History and Receipt of Vaccinations
Mr. Cerrone was sixteen years old when he was evaluated by his primary care physician
(“PCP”) for right jaw and ear pain on October 7, 2015. Ex. 1 at 3, 14. He weighed 165.5 pounds
at the time. Id. at 14. At this visit Petitioner received the three vaccines at issue: HPV (under the
“Gardasil” tradename), influenza (the “Flumist” formulation),3 and Hep A. 4 Id. Before
vaccination, Petitioner’s medical history was significant for attention deficit hyperactivity
disorder, and Petitioner had been taking medication for the condition. Id. There is no
contemporaneous medical record evidence of any immediate vaccine reactions.
The following month, Petitioner had two visits to the ER for physical injuries. Ex. 2 at 31
(November 10, 2015 ER visit for lacerated lip), 34 (November 3, 2015 left wrist injury while
playing football and reports of “left wrist pain due to injury”). He also had a primary care visit on
November 12, 2015, that reported his previous injuries and two ER visits. Ex. 1 at 13. During this
visit he weighed 164 pounds. Id.
The aforementioned records say nothing about a vaccine reaction, and there is no other
medical record evidence for the remainder of 2015 establishing any alleged post-vaccination
symptoms relevant to this claim. Petitioner has, however, personally averred in his affidavit that
he experienced three events relevant to his claim. Affidavit, dated October 12, 2017 (ECF No. 19-
1) (“Cerrone Aff. I”); Affidavit, dated March 20, 2018, (ECF No. 28) (“Cerrone Aff. II”). First, he
maintains that during November 2015, his stamina decreased, and he could not lift weights with
the same repetition or run distances as far or fast. Cerrone Aff. II at 2. Second, he states his stability
became an issue, and he fell for no reason during a football game during that same month. Id.
Third, Petitioner reports that in late December he first observed bloody stools, but was too
embarrassed to tell his mother. 5 Id. at 1.
3
Flumist is a “live attenuated influenza vaccine” (“LAIV”) that is administered as a nasal spray. D'Tiole v. Sec'y of
Health & Hum. Servs., No. 15-085V, 2016 WL 7664475, at *1 n.4 (Fed. Cl. Spec. Mstr. Nov. 28, 2016), mot. for
review den’d, 132 Fed. Cl. 421 (2017), aff'd, 726 F. App'x 809 (Fed. Cir. 2018) (noting that Flumist “contains live,
but attenuated (meaning reduced in virulence), strains of the wild flu virus.”).
4
The records indicate that Petitioner had been receiving yearly flu vaccinations since 2007. Ex. 1. at 1–3.
5
Petitioner also noted (though with no clear date or time at which this occurred) that he was having a hard time playing
sports because of his low energy level and strength. Cerrone Aff. I at 5. Such symptoms (plus continued rectal bleeding
and diarrhea) made it difficult for him to attend college classes. Id.2
Diagnosis of UC After Appearance of Gastrointestinal Symptoms
On February 10, 2016, Petitioner returned to his PCP’s office with complaints of a sore
throat and congestion. Ex. 1 at 4, 12. He was diagnosed with pharyngitis, had a normal physical
exam (with no evidence of unexpected weight loss), and at this time administered a second dose
of Gardasil vaccine. Id. (normal abdominal examination noted). This record (like those before it)
references no gastrointestinal issues either. And no medical records for the prior five to six weeks
have been offered, and thus there is no contemporary evidence prior to this date from the beginning
of 2016 that Petitioner was experiencing any symptoms consistent with his UC.
A few days later, however, on February 13, 2016 (now more than four months after
vaccination), Petitioner presented to the Monroe Regional Hospital (“Monroe”) emergency room
in Monroe, Michigan complaining of three weeks of bright red blood in his stools, with particularly
exacerbated symptoms over the past several days. 6 Ex. 2 at 25–26. He was diagnosed with
hematochezia7 and discharged. Id. at 27, 29–30 (normal hemoglobin and hematocrit values
recorded). On February 17, 2016, Petitioner underwent a stool panel. Ex. 1 at 57–58. The next day
(February 18th), he followed up with his PCP, recounting a history of blood in his stool for three
to four weeks. Id. at 11. He was referred for a gastrointestinal (“GI”) evaluation. Id.Petitioner underwent a flexible sigmoidoscopy 8 performed by gastroenterologist Lesa
Chopra, D.O., on March 14, 2016, which showed proctosigmoiditis with a few ulcerations and
contiguous inflammation to 25 cm. Ex. 3 at 11. His weight had now dropped significantly from
what he had been the month before (down to 158 pounds), and at a follow-up with Dr. Chopra on
March 24, 2016, Petitioner was formally diagnosed with UC. Id. at 6–7, 11. Dr. Chopra also
concluded that the biopsies taken during the sigmoidoscopy were consistent with irritable bowel
disease (“IBD”). Id. at 6. By this time, Petitioner was experiencing persistent daily rectal bleeding
despite use of a suppository. Id.; see also Ex. 1 at 10 (March 30, 2016 PCP visit reiterating the UC
diagnosis and persistent bloody stools).
6
This history (which is consistent with the PCP record from February 18, 2016) would place onset of Petitioner’s
symptoms approximately fifteen weeks after his October 7, 2015, receipt of the HPV vaccine, or by the last week of
January 2016. Ex 1 at 11. During this February 18, 2016 visit, Petitioner’s weight was 170.8 pounds. Id.7
Hematochezia is the medical term for the passage of bloody stools. Hematochezia, Dorland’s Medical Dictionary
Online, https://www.dorlandsonline.com/dorland/definition?id=21736&searchterm=hematochezia (last visited May
8, 2023).
8
A sigmoidoscopy is an inspection of the sigmoid colon through a sigmoidoscope. Sigmoidoscopy, Dorland’s Medical
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=45800&searchterm=sigmoidoscopy (last
visited May 8, 2023).
3
UC Treatment
On May 19, 2016, Petitioner returned to the Monroe ER for a lower GI bleed and acute
abdominal pain. Ex. 2 at 19–24. He gave a history of bloody stools for five months with associated
diarrhea, constipation, abdominal pain, and hemorrhoids (putting onset anywhere between mid-
December 2015 to mid-January 2016. Id. Petitioner’s mother reported that he had been “doubled
over” with pain, but it had since resolved. Id. Petitioner also had a facial rash for one day after
recent completion of a course of oral steroids that reportedly did not help with his symptoms. Id.;
Ex. 3 at 1. He was started on another suppository and fiber, and discharged to follow up with Dr.
Chopra the following week. Ex. 2 at 23–24.
Petitioner thereafter continued treatment through the early fall of 2016, but his rectal
bleeding did not diminish. Ex. 3 at 1-4 (May and August 2016 treatment visit). In the interim, on
June 24, 2016, Petitioner saw his PCP for testing after he swam in a lake with high levels of E.
coli. Ex. 1 at 8. He reported abdominal pain and diarrhea the day before. Id. At that visit, Petitioner
received a third Gardasil vaccination. Id. at 4, 8. There is no medical record evidence suggesting
any reaction to this dose of vaccine, and Petitioner has not alleged it exacerbated his symptoms.
That September, Petitioner was seen in the Monroe ER for chest pain and shortness of
breath, which was diagnosed as costochondritis with no need for further cardiology workup. Ex. 2
at 13, 18–19; 100. He also reported a recent upper respiratory infection two weeks earlier. Id. at
13. A history of IBD with iron deficiency anemia, abdominal pain, melena, 9 and hematochezia
was noted. Id. at 13–14. Petitioner was on steroids for UC and being followed by a GI specialist,
but they could not control or stop his bleeding and diarrhea. Id. at 88. He was reportedly still eating
okay and functioning well. Id.On October 3, 2016, Petitioner was evaluated by Nirmal Kaur, M.D., at the Henry Ford
IBD Center. Ex. 4 at 9. At that visit, Petitioner indicated specifically (for the first time in the
medical record) 10 “that he began having some intermittent rectal bleeding during December of
2015,” but did not seek further evaluation or workup at that time. Id (emphasis added). He
subsequently began having “nausea with epigastric pain as well as worsening frequency of blood
in his stools.” Id. By March 2016, Petitioner had daily pain with associated nausea. Id.9
Melena is the passage of dark-colored, tarry stools, due to the presence of blood altered by the intestinal juices.
Melena, Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=30249&searchterm=melena (last visited May 8, 2023).
10
Petitioner reported a history of bloody stools beginning in December 2015 on multiple subsequent occasions. Ex. 4
at 17; Ex. 5 at 15, 24, 1247; but see Ex. 1 at 11; Ex. 2 at 25. The history also indicates that Petitioner was first seen by
Dr. Chopra on February 26, 2016, although Dr. Chopra’s records (filed collectively as Petitioner’s Exhibit 3) do not
appear to contain a record of this visit.
4
In October 2016, Petitioner was continuing on his medication, but still had five to six stools
per day with visible blood in every bowel movement. Ex. 4 at 9. He now weighed 140 pounds—a
20-pound unintended weight loss since March 2016. Id. at 14. Dr. Kaur discussed with Petitioner
and his mother the concerns for “active disease that is not controlled on his current therapy.” Id.
at 11. Another endoscopic evaluation with flexible sigmoidoscopy was planned. Id. A repeat
endoscopy performed on October 6, 2016 showed “Mayo 2 colitis from rectum, 35 cm.” and Mr.
Cerrone was switched again to another new medication. Ex. 5 at 15.
From October 2016 to the present, Petitioner has continued to obtain treatment for his UC,
which on some occasions presented acutely and required in-patient treatment. See, e.g., Ex. 2 at
9–12; Ex. 5 at 12–13, 15 (October 2016 hospitalization). By November 2016, pancolitis 11 was
observed, and Petitioner underwent a colectomy with a diverting ileostomy 12 on December 12,
2016. Ex. 5 at 1247, 1265–70, 2788, 2918–19. He required additional emergency or in-patient care
in early 2017. Ex. 2 at 1; Ex. 5 at 3064–66, 3377–89. He has otherwise continued to follow up
with his specialists and PCP for his UC. See generally Exhibit 69.
II. Witness Testimony and Expert Reports
A. Petitioner’s Experts
1. David Rosenstreich, M.D. – Dr. Rosenstreich, a licensed clinician and
immunologist (though not a gastroenterologist), prepared two written reports and an affidavit, and
testified for Petitioner in support of the contention that the three vaccines he received (HPV,
Flumist, and Hep. A) can cause UC, and did so to him. See generally Tr. at 6–143, 324–34. Report,
dated September 12, 2018, filed as Ex. 8 (ECF No. 39-2) (“Rosenstreich First Rep.”); Report,
dated October 22, 2019, filed as Ex. 48 (ECF No. 63-2) (“Rosenstreich Second Rep.”); Affidavit,
dated July 15, 2020, filed as Ex. K (ECF No. 97-2) (“Rosenstreich Aff.”).
Dr. Rosenstreich obtained his undergraduate degree from the City College of New York
and his medical degree from New York University School of Medicine. Curriculum Vitae, filed
as Exhibit 35 on September 13, 2018 (ECF No. 42-2) (“Rosenstreich CV”) at 1. He is currently a
Professor in the Departments of Medicine, Otolaryngology, and Microbiology/Immunology at the
Albert Einstein College of Medicine. Tr. at 6; Rosenstreich CV at 1; Rosenstreich First Rep. at 1.
He is also the Director of the Division of Allergy & Immunology in the Department of Medicine
11
Pancolitis is defined as inflammation of the entire colon. Pancolitis, Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=36502&searchterm=pancolitis (last visited May 8, 2023).
12
A colectomy is excision of a segment of the colon and ileostomy is establishment of a fistula through which the
ileum discharges directly to the outside of the body. Stedman’s, supra note 2 at 407, 946.
5
at the Albert Einstein College of Medicine and Montefiore Medical Center. Tr. at 6; Rosenstreich
CV at 1; Rosenstreich First Rep. at 1.
Dr. Rosenstreich actively sees patients with vaccine-induced problems and performs
differential diagnostic techniques. Tr. at 7. His clinical work does not focus on the care and
treatment of GI patients, however, and he does not diagnose patients with UC or IBD. Id. at 103–
04. He has also never provided a diagnosis where a vaccine or combination of vaccines was
suspected to have caused UC. Id. at 133. Dr. Rosenstreich is board certified as an Internal Medicine
specialist by the American Board of Internal Medicine and as an Allergy/Immunology specialist
by the American Board of Allergy and Immunology. Id. at 6–7; Rosenstreich CV at 2; Rosenstreich
Aff. at 1; Rosenstreich First Rep. at 1. He also has an additional qualification in Diagnostic
Laboratory Immunology. Rosenstreich CV at 2; Rosenstreich Aff. at 1; Rosenstreich First Rep. at
1. Dr. Rosenstreich has published over 200 scientific papers in the field of allergy and immunology
and has edited 4 books in the fields of clinical allergy and basic immunology. Tr. at 7; Rosenstreich
First Rep. at 2. The focus of his publication and research work is not on reporting vaccine-related
autoimmune problems, though he mentioned one recent paper specific to the COVID-19 mRNA
vaccines. Tr. at 104–05.
Dr. Rosenstreich accepted Petitioner’s UC diagnosis, 13 given Petitioner’s colonoscopy
findings and disease pathology. Tr. at 11–12. He defined UC to be an immunologically-mediated
inflammatory disease14 of the large intestine. Id. at 12–13, 16, 333; Rosenstreich First Rep. at 5;
S. Friedman & R. Blumberg, Harrison's Principles of Internal Medicine 8 (McGraw-Hill Global
Education Holdings 19 th ed. 2015) (“Friedman”); R. Ungaro et al., Ulcerative Colitis, 389 Lancet
1756, 1756 (2017), filed as Ex. 10 (ECF No. 39-4) (“Ungaro”). In UC, immune tolerance 15 is
broken and regulatory processes in the gut fail. Tr. at 62; Rosenstreich First Rep. at 5. In particular,
gastrointestinal T cell lymphocytes 16 become immunologically activated, increase in number, and
13
Although the experts agree on the diagnosis, they use UC and IBD interchangeably throughout their discussions.
14
Dr. Rosenstreich differentiated autoimmune diseases from immune-mediated diseases. An autoimmune disease is
where the antigen sparking an aberrant immune reaction is part of the patient’s makeup (even if something else might
trigger the antigen beforehand—like a vaccine), whereas an immune-mediated disease occurs due to the impact of an
external agent. Tr. at 13–14; Ex. 38. UC, Dr. Rosenstreich explained, is both an autoimmune disease and immune-
mediated disease; there are autoantibodies against epithelial cells, which are self antigens, and there is an immune
reaction against external or commensal gut bacteria (external antigens). Tr. at 15–17; see, e.g., Friedman at 4; Ungaro
at 1757–59; I. Ordas et al., Ulcerative Colitis, 380 Nature 1606, 1607 (2012), filed as Ex. 12 (ECF No. 39-6).
Respondent’s experts agreed with Dr. Rosenstreich that UC is an inflammatory immune-mediated disease, even
though they did not concede a vaccine can be causal of it ab initio. Tr. at 17–19.
15
Immune tolerance is where the body does not recognize the antigen and thus does not have an immune response.
Tr. at 61. Breaking immune tolerance means the gut bacteria is now exposed to the systemic immune system
improperly. Id. at 66.
16
The T cell lymphocytes are located in the lamina propria of the intestine underneath the epithelial cells. Tr. at 64.
These cells monitor antigens that are in the gut and protect against infection. Id.
6
initiate an intense reaction against gut microbial constituents, with production of large amounts of
inflammatory cytokines such as tumor necrosis factor. Tr. at 62; Rosenstreich First Rep. at 5. This
produces UC’s characteristic symptoms—blood in the stool and diarrhea, and in severe cases
symptoms can also include incontinence, fatigue, increased frequency of bowel movements, and
abdominal discomfort. Ungaro at 1759.
There is not one single understood trigger of UC. Rather, UC has various infectious and/or
genetic etiologies, although for the majority of patients its etiology cannot be determined. Tr. at
20–24, 26, 58–59; Rosenstreich First Rep. at 5, 7–8; K. Gradel et al., Increased Short and Long-
Term Risk of Inflammatory Bowel Disease After Salmonella or Campylobacter Gastroenteritis,
137 Gastroenterology 495, 495, 499–500 (2009), filed as Ex. 11 (ECF No. 39-5) (“Gradel”)
(finding particular genetic mutations increase the risk of developing IBD); 17 B. Khor et al.,
Genetics and Pathogenesis of Inflammatory Bowel Disease, 474 Nature 307 (2011), filed as Ex.
18 (ECF No. 40-3) (“Khor”) (reviewing the genetics of IBD in this genome-wide association study
and finding 200 different genes that could be associated in IBD patients, compared to patients
without the disease). In addition, Dr. Rosenstreich maintained, specific environmental factors (e.g.,
smoking, antibiotics, vaccines, or infections) can in a susceptible host (meaning someone with
likely, if unidentified, genetic propensities) come together to cumulatively/interactively disrupt
immunologic homeostasis,18 producing a chronic state of dysregulated inflammation common to
IBD/UC. Tr. at 57–58, 118; Rosenstreich First Rep. at 5; Khor at 314–15.
Next, Dr. Rosenstreich sought to explain how the three vaccines Mr. Cerrone received
could theoretically cause UC. Tr. at 28. By his own admission, he reached his opinion by reasoning
“backwards” from UC’s symptomatic presentation, characterized by colonic inflammation, to the
vaccines. Id. at 76, 117–18. And he ultimately invoked the effects, or proposed impact, of the
differing vaccines involved (one of which—Flumist—is administered nasally) at different stages
of his theory, attempting to associate these sub-conceptions with what Petitioner’s experience
revealed.
First, Dr. Rosenstreich broadly referenced the mechanistic theory of molecular mimicry
often invoked to explain the pathophysiologic process of an autoimmune disease, identifying it as
the most likely explanation for chronic disease inflammation in this case. Rosenstreich First Rep.
at 7; Rosenstreich Second Rep. at 5. In particular, he proposed that (in the context of the immune
17
Also cited as Respondent’s Exhibit AA.
18
Dr. Rosenstreich defined immunological homeostasis to be the balance between immune stimulation and immune
suppression. Tr. at 61. This is disrupted with an infection or vaccine when excessive stimulation sets up a negative
feedback with immune regulation and suppresses the reaction that would otherwise shut down an autoimmune/aberrant
process. Id.
7
stimulation 19 generally attributable to vaccination) some cross-reactivity of antibodies or T cells,
due to vaccine antigens and “intestinal epithelial cell antigens” being similar—sequentially or
structurally—to each other, 20 allowed gut bacteria to penetrate the intestinal mucosa, setting up a
chronic immune-mediated reaction to the bacteria characteristic of UC. Tr. at 67, 75–76, 139–42,
325; Rosenstreich First Rep. at 5–7; Ungaro at 1758; I. Ordas et al., Ulcerative Colitis, 380 Nature
1606, 1608 (2012), filed as Ex. 12 (ECF No. 39-6).
The antigen-specific signal sufficient to spark cross-reactivity due to mimicry could have
come from any of the three vaccines Petitioner received, Dr. Rosenstreich maintained. Tr. at 76,
139. However, he particularly focused on the possibility that the Gardasil vaccine contained
proteins that could mimic intestinal brush-border proteins, noting that there are often “unexpected
similarities” between viral proteins and relevant UC proteins. Id. at 77–78; Rosenstreich First Rep.
at 7; Rosenstreich Second Rep. at 6; C. Natale et al., Computer-Assisted Analysis of Molecular
Mimicry Between Human Papillomavirus 16 E7 Oncoprotein and Human Protein Sequences, 78
Immunology & Cell Biology 580, 580 (2000), filed as Ex. 21 (ECF No. 40-6) (“Natale”).
Respondent’s experts later disputed this possibility, observing the plain fact that intestinal proteins
are not found in the HPV vaccine—including the specific HPV viral strain discussed in Natale—
but Dr. Rosenstreich emphasized that he only raised the possibility of this occurring, and could not
provide specifics to corroborate his speculation. Tr. at 77–79 (“[i]n this case, I have no idea what
they are, but they can exist”).
Alternatively, Dr. Rosenstreich offered an analogy to what is scientifically known about
how a Campylobacter jejuni bacterial infection can result (via molecular mimicry) in the
production of autoantibodies driving Guillain-Barré syndrome (“GBS”). Tr. at 72; Rosenstreich
First Rep. at 7; N. Shahrizaila & N. Yuki, Guillain-Barre Syndrome Animal Model: The First
Proof of Molecular Mimicry in Human Autoimmune Disorder, J. Biomedicine & Biotechnology
1–4 (2010), filed as Ex. 20 (ECF No. 40-5) (“Shahrizaila”). Though the host structure for target
antigens would be different for GBS (the GM1 antigen, as opposed to the epithelial cells for UC),
there is scientific support for the proposition that a C. jejuni infection results in the production of
19
At each of the sites of vaccination (three in total here), the vaccine antigens would be taken up by antigen-presenting
cells locally, where they probably migrated into the regional lymph nodes and stimulated activation of B cells, which
produced antibodies and T cells. Tr. at 67–68. The antibodies and T cells then enter circulation in the body and return
to the site of injection to cause a local reaction. Id. This ongoing stimulation creates memory T cells and memory B
cells—which can also be cross-reactive if the antigen that underlies the B or T cells is a mimic of a self structure or
amino acid sequence. Id.
20
Molecular mimicry would occur during the immune system’s adaptive response—a phase Dr. Rosenstreich
differentiated from the initial, innate response. Tr. at 83–84. The innate immune reaction is the first line of
immunologic defense—a nonspecific reaction to invading pathogens, in which immune cells rapidly, but generally,
react to danger signals to start releasing cytokines and initiate an immune reaction. Id. The adaptive arm occurs
thereafter, and features more specificity to the precise antigenic attackers. Id.
8
cross-reactive antibodies capable of causing myelin damage in GBS—and the same mechanism
was plausible herein. Tr. at 73; Rosenstreich First Rep. at 7; Shahrizaila at 2–4.
In addition to molecular mimicry, Dr. Rosenstreich opined that the three vaccines
Petitioner had received also probably induced the activation of other immune cells through less
immunologically-specific mechanisms. Some, he proposed, might be attributable to the alum
adjuvant included in some of the vaccines at issue. 21 Tr. at 82–83; Rosenstreich First Rep. at 7.
Such adjuvants increase vaccine immunogenicity because they stimulate cells like macrophages,
which then releases cytokines like interleukin 1 that augment immune reactions. Tr. at 83. Without
them, the vaccine antigens alone often will not stimulate a very powerful response sufficient to
encourage the intended response. Id.22 In addition, an aberrant immune reaction could occur as a
result of polyclonal activation and or bystander activation. 23 Id. at 81; Rosenstreich First Rep. at
7. Less specific immune cells, located in the lamina propria of the gut, could be stimulated by an
ongoing intense immunologic inflammatory context, becoming activated and producing cytokines
that would only further the inflammatory reaction. Tr. at 81–82.
To support the theory, Dr. Rosenstreich discussed or referenced several different items of
medical literature. Tr. at 29. First, he considered the vaccine package inserts, starting with Gardasil.
This package insert revealed that the vaccine’s manufacturers had looked at the incidence of IBD
in patients in a vaccinated group versus control group. Id. at 30–31, 126–28; Gardasil Package
Insert, filed as Ex. 13 on Sept. 12, 2018 (ECF No. 39-7) (“Gardasil Package Insert”), at 8–9.24
Although Dr. Rosenstreich admitted that the HPV vaccine trials found no difference overall in the
IBD incidence for vaccine recipients compared to patients who had received an alum control, the
fact that Petitioner had at the same time also received Flumist—a live attenuated influenza vaccine,
or “LAIV”—was a significant confounding factor, since suggested it would cause “different
degrees of immune stimulation and immune dysregulation.” Tr. at 30–31.
On cross examination, Dr. Rosenstreich was confronted with the fact that some clinical
trial findings disclosed in the Gardasil Package Insert were inconsistent with vaccine causation.
21
The Flumist vaccine does not contain an adjuvant. D'Tiole, 2016 WL 7664475, at *9.
22
Johnson v. Sec'y of Health & Hum. Servs., No. 14-254V, 2018 WL 2051760, at *10 (Fed. Cl. Spec. Mstr. Mar. 23,
2018). (explaining the immunologic function of the alum adjuvant).
23
“Bystander activation occurs when immune system cells that were previously suppressed, or anergic, are broken
down by an existing/ongoing immune response to infection (or an autoimmune response to vaccination), causing
immune tolerance created by those cells to similarly be destroyed and thereby allowing the dysregulation of the
immune response to continue or expand.” Lozano v. Sec'y of Health & Hum. Servs., No. 15-369V, 2017 WL 3811124,
at *4 (Fed. Cl. Spec. Mstr. Aug. 4, 2017), mot. for review den’d, 958 F.3d 1363 (Fed. Cir. 2020), aff'd, 958 F.3d 1363(Fed. Cir. 2020).
The Gardasil Package Insert was filed by Petitioner twice (as Exhibit 13 and 45), and also filed by Respondent as
24
Exhibit JJ, Tab 2.
9
Tr. at 126-29. In particular, for a subgroup of the trial sample (specifically, 9 to 26 year old boys,
which would have included Petitioner, comparing more than three thousand vaccinated individuals
versus approximately 2,300 who received an alum or saline placebo), not only was there no
increased incidence for IBD seen in the vaccinated population, but the incidence for the vaccinated
group was lower. Id. at 128; Gardasil Package Insert at 9 (Table 10). Dr. Rosenstreich questioned
the reliability of these results, however, because some of the control group received an alum
adjuvant alone, which was concerning to him as alum could (in theory) cause an aberrant immune
response. Tr. at 128; Rosenstreich First Rep. at 2, 9; G.P. de Chambrun et al., Aluminum Enhances
Inflammation and Decreases Mucosal Healing in Experimental Colitis in Mice, 7 Mucosal
Immunology 589, 589 (2014), filed as Ex. 49 (ECF No. 63-3) (“Chambrun I”).
Dr. Rosenstreich went on to address the package inserts for the two other vaccines. The
Flumist Package Insert noted that because that vaccine is a LAIV formulation, it functions through
introduction of weakened live viral particles, causing different degrees of immune stimulation and
dysregulation. Tr. at 32; Rosenstreich First Rep. at 6; Flumist Quadrivalent Package Insert, filed
as Ex. 14 on Sept. 12, 2018 (ECF No. 39-8) (“Flumist Package Insert”), at 12–13. Thus, the
response to it would be more akin to the impact of a wild virus infection, with the attendant
dangers. Flumist Package Insert at 12. And the Hep. A Package Insert revealed that it included
(like the HPV vaccine) an alum adjuvant—meaning that Petitioner had received a “double dose”
of alum at the time he was vaccinated (and thus a greater risk of an adverse response due to
excessive inflammation). Tr. at 33; Rosenstreich First Rep. at 6, 9; Rosenstreich Second Rep. at 2.
HAVRIX Package Insert, filed as Ex. 15 on Sept. 12, 2018 (ECF No. 39-9) (“Hep. A Package
Insert”), at 9. While the Flumist and Hep. A package inserts did not reveal any concern that IBD
was a quantifiable side effect of those vaccines, they also did not disclosure pre-release testing
relevant to that question. Tr. at 129. And there was no evidence that any studies about the effects
of receiving all three vaccines at one time had ever been conducted. Id. at 330; Rosenstreich First
Rep. at 6, 9; Rosenstreich Second Rep. at 8.
Second, Dr. Rosenstreich discussed a number of case reports that he deemed supportive of
a causal relationship between the vaccines Petitioner received and his UC. Tr. at 33–34. He
acknowledged that case reports lack the same scientific evidentiary value as full-scale
epidemiologic studies, but deemed them nevertheless to be reliable “signals” to the scientific
community of a potential vaccine-UC relationship worthy of further consideration. Id. at 46–47,
55, 326. Dr. Rosenstreich later admitted, however, that if case reports deserved weight even though
they amount to an “n-of-one” study (a one-person sample), then larger studies involving bigger
sample populations could not simply be rejected as incapable of detecting the rare event of a
vaccine injury. Id. at 138.
In one case report, pancolitis (an infection of the entire colon) was observed after
administration of a flu vaccine to a 70-year-old woman with a history of diabetes. Tr. at 36–37,
10
130; L. Luca et al., Pancolitis After Influenza Vaccination, 59 Allergy 362, 367 (2004), filed as
Ex. 27 (ECF No. 41-3) (“Luca”); Rosenstreich First Rep. at 7. The Luca patient had received at
least six prior flu vaccines, developing onset of GI symptoms within hours of receipt of an
additional dose. Tr. at 130; Rosenstreich Second Rep. at 3; Luca at 367. Dr. Rosenstreich admitted,
however, that Mr. Cerrone’s flu vaccine had been administered in a different manner—and that
his onset was not nearly as sudden. Tr. at 131. In another case report, a patient developed
panniculitis 25 after a flu vaccine that he had previously tolerated, indicating a delayed
hypersensitivity reaction. 26 Id. at 37–38; C. Pauwels et al., Cytophagic Histiocytic Panniculitis
After HlNl Vaccination: A Case Report and Review of the Cutaneous Side Effects of Influenza
Vaccines, Dermatology 217, 217–19 (2011), filed as Ex. 28 (ECF No. 41-4) (“Pauwels”).27
Pauwels also referenced 17 cases of systemic vasculitis, an immune-mediated inflammatory
reaction, in association with the flu vaccine. Tr. at 38–39; Pauwels at 218. Dr. Rosenstreich deemed
such evidence to establish an association between the flu vaccine and different, but comparable,
forms of immune-mediated inflammatory reactions. Tr. at 39.
Third, Dr. Rosenstreich referenced VAERS reports 28 establishing an association between
vaccines and UC. He was able to identify 75 specific reports of colitis 29 associated with the
administration of either the Gardasil, flu, or Hep. A vaccines. Tr. at 40, 42, 135; Rosenstreich First
Rep. at 8; Rosenstreich Second Rep. at 5. He also found five VAERS reports associating colitis
with the Gardasil vaccine alone. Tr. at 42–43.30 In testimony he represented that there were other
VAERS reports of patients who had received multiple vaccines at the same time and then
experienced UC, but none were filed. 31 Id. at 43–45. As with case reports, Dr. Rosenstreich
admitted that VAERS reports were not capable of establishing causality (especially in the absence
25
Panniculitis is an inflammatory reaction of subcutaneous fat. Panniculitis, Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=36598&searchterm=panniculitis (last visited May 8, 2023).
26
Dr. Rosenstreich explained that immediate reactions are those mediated by antibodies and immunoglobulins, similar
to an allergic reaction whereas delayed reactions are skin or pathological reactions that take several days to develop,
which are usually mediated by activated T cells. Tr. at 38.
27
Pauwels was filed by Petitioner twice, as Exhibit 28 and Exhibit 42.
28
The Vaccine Adverse Event Reporting System (“VAERS”) is a database maintained by the Center for Disease
Control (“CDC”) to compile information from the public about reactions to immunizations listed on the Vaccine Injury
Table, Section 14(a).
29
Colitis is different from UC, Dr. Rosenstreich acknowledged, since it was more likely to be time-limited in overall
course. Tr. at 125.
30
These are set forth in Ex. 29, which appears to be a self-made document referencing the five VAERS reports with
a short write-up. The exhibit has no other citations, however, so the accuracy of its contents cannot be verified simply
from its face.
31
During the hearing, Respondent noted that proof of these instances had not been filed. Tr. at 44. I informed
Petitioner’s counsel they could file such evidence after the hearing. Tr. at 45. This did not occur.
11
of information about background rates of disease instances or total vaccines administered in a
specific population group), but he deemed them nevertheless of value in suggesting causation. Id.
at 41, 56, 124–26, 326–27; Rosenstreich Second Rep. at 8–9. At the same time, he acknowledged
reliability problems with such data; in particular, an adverse event report is not verified before its
creation, meaning the underlying truth of a VAERS report cannot be ascertained merely from its
existence. Tr. at 45–46, 124–25, 136–38.
Besides these categories of evidence, Dr. Rosenstreich highlighted a meta-analysis study 32
filed by Respondent, focusing on the occurrence of IBD after receipt of a specific live vaccine
(poliomyelitis). Tr. at 53; G.P. de Chambrun et al., Vaccination and Risk for Developing
Inflammatory Bowel Disease: A Meta-Analysis of Case–Control and Cohort Studies, 13 Clinical
Gastroenterology & Hepatology 1405, 1405 (2015), filed as Ex. Y (ECF No. 53-11) (“Chambrun
II”); Rosenstreich Second Rep. at 9. Chambrun II sought to combine the findings from eight case
control studies plus three cohort studies (although none involved the HPV or Hep. A vaccines).
Tr. at 53; Chambrun II at 1405, 1410. It proposed that there was potential higher risk of IBD after
receiving multiple vaccines at the same time. Chambrun II at 1413. Dr. Rosenstreich also
maintained that live vaccines might add to this risk, although only the Flumist vaccine contained
live viral components. Tr. at 54–55. Importantly, however, Chambrun II’s overall conclusion was
that the childhood vaccines it considered were not likely to increase the risk of IBD—and to the
extent receiving multiple vaccines at one time was itself a risk factor, Chambrun II’s authors
deemed that partially attributable to the fact that many of the studies incorporated into the meta-
analysis had not focused on single vaccine causality. Chambrun II at 1412–13, 1414.
Dr. Rosenstreich disputed the value of other literature offered by Respondent’s experts—
in particular articles that purportedly found no increased risk of UC after receipt of the HPV
vaccine. Tr. at 47–48; J. Skufca et al., The Association of Adverse Events With Bivalent Human
Papilloma Virus Vaccination: A Nationwide Register-Based Cohort Study in Finland, 36 Vaccine
5926, 5926 (2018), filed as Ex. CC (ECF No. 53-15) (showing no significant increased risk of UC
in 11 to 13-year-old girls with the Gardasil vaccine) (“Skufca”). In his view, studies like Skufca
were ultimately not sensitive enough to detect a rare occasion like a vaccine injury, especially
since genetics and previous medical history can make an individual unusually susceptible to an
adverse event. Tr. at 48. He also criticized studies that in essence confirmed the safety of certain
of the vaccines at issue. See, e.g., M-G. Angelo et al., Post-Licensure Safety Surveillance for
Human Papillomavirus-16/18-AS04-Adjuvanted Vaccine: More Than 4 Years of Experience, 23
Pharmacoepidemiology & Drug Safety 456, 463 (2014), filed as Ex. R (ECF No. 53-4); (“[c]linical
studies conducted during vaccine clinical development are essential, but usually too limited in size
32
A meta-analysis is defined as “a method for systematically combining pertinent qualitative and quantitative study
data from several selected studies to develop a single conclusion that has greater statistical power.” Himmelfarb Health
Sciences Library, Meta-Analysis, https://himmelfarb.gwu.edu/tutorials/studydesign101/metaanalyses.cfm (last visited
May 8, 2023).
12
to detect rare [adverse events]. . . .”) (“Angelo”). Had such studies established a risk, the vaccine
would not have been approved in the first place—but that did not mean that a vaccine could never
be causal of injury in rare circumstances. Tr. at 48.
Dr. Rosenstreich next focused on Mr. Cerrone’s medical history, arguing that his
experiences were consistent with the causation theory. Tr. at 9, 57; Rosenstreich First Rep. at 8–
9. As a general matter, Dr. Rosenstreich felt it likely that Petitioner was a genetically-susceptible
host. Khor, he noted, had identified 200 potential genes that may drive IBD—with only three or
four needed for disease to occur. Tr. at 58, 60; Rosenstreich First Rep. at 5, 7, 9; Rosenstreich
Second Rep. at 2–3; Khor at 315; Ungaro at 1756. He acknowledged, however, that there was no
testing evidence from this case that would establish whether Petitioner actually possessed any risk
factors for IBD. Tr. at 118–19, 121; Rosenstreich First Rep. at 2; Ex. 72 at 13. There was also no
notation in the records that he had a family history of IBD (although Petitioner’s mother’s status
as an adopted child greatly diminished the possibility of obtaining such evidence on a family basis).
Tr. at 118–19. In effect (and as admitted elsewhere), Dr. Rosenstreich was reasoning backward
from the fact of injury to his conclusion of genetic susceptibility (an especially problematic
approach given that unvaccinated patients develop IBD, while the majority of patients that receive
vaccines do not). Id. at 120.
It was also possible, Dr. Rosenstreich opined, that other environmental factors had
contributed to Petitioner’s development of UC. For example, Mr. Cerrone may have developed a
clinically-inapparent viral infection such as cytomegalovirus or enterovirus, which could have
altered his intestinal microbial constituents and magnified the aberrant response to vaccination. Tr.
at 121; Rosenstreich First Rep. at 9. However, Dr. Rosenstreich could not identify any record
evidence in support of this contention. Tr. at 122. Indeed, part of Petitioner’s workup for his UC
involved an analysis of his stool; infectious agents were checked, but none of the usual stool
pathogens were found. 33 Id.Dr. Rosenstreich derived additional evidence in support of his opinion from witness
statements. In particular, Petitioner had alleged in his affidavit an increased loss of stamina a few
weeks after his vaccination but before the onset of his clinical GI symptoms (bloody stools on
December 27 th). Cerrone Aff. II at 2. Stability was also an issue, according to Petitioner’s affidavit,
and Petitioner reported falling during a pickup football game on November 3, 2015, fracturing his
wrist. Tr. at 107; Cerrone Aff. II at 2. Dr. Rosenstreich deemed these incidents significant,
considering them manifestations of ongoing systemic inflammation even before Petitioner’s more
obvious GI-associated symptoms. Tr. at 94–96, 105, 107, 114–15; Rosenstreich Second Rep. at 1,
9.
33
Dr. Rosenstreich also could not opine on other, more direct potential factors that might have impacted the
development of UC, such as Mr. Cerrone’s diet or the quality of his drinking water. Tr. at 121.
13
At the same time, however (and as Dr. Rosenstreich admitted), these symptoms34 of loss
of stamina and lack of stability were not mentioned in any of the contemporaneous medical
records. Tr. at 106–07. Indeed, from October 7, 2015 (date of Petitioner’s vaccinations) until
January 2016, there are in the record no primary care appointment or medical encounters reporting
malaise, stability, or stamina issues. Id. at 107–08. Petitioner had previously reported instances of
fatigue prior to vaccination (for example, on December 17, 2014), suggesting he would have done
so later if such concerns existed. Id. at 112–13; Ex. 1 at 15. Nevertheless, Dr. Rosenstreich still
opined the references to post-vaccination symptoms (again reiterating fatigue) were significant.
Tr. at 113; Rosenstreich Second Rep. at 1, 8. K. Ozawa et al., Suspected Adverse Effects After
Human Papillomavirus Vaccination: A Temporal Relationship Between Vaccine Administration
and the Appearance of Symptoms in Japan, 40 Drug Safety 1219, 1227 (2017), filed as Ex. 31
(ECF No. 41-7) (“Ozawa”) (discussing general fatigue, along with headache, limb pain, and
weakness as possible Gardasil vaccine-related adverse effects).
Petitioner’s purported worsening of symptoms after the receipt of his second HPV vaccine
dose on February 10, 2016, was also evidence supporting causation, Dr. Rosenstreich maintained.
Tr. at 96–97, 328; Rosenstreich Second Rep. at 8. He maintained that the immune response after
a second exposure to vaccination is inherently faster/more robust. Tr. at 97–98, 116; Rosenstreich
First Rep. at 6, 10; Rosenstreich Second Rep. at 8; C-A. Siergrist, Vaccine Immunology, Vaccines
17, 23 (2008), filed as Ex. 77 (ECF No. 90-3) (“Siergrist”). However, Dr. Rosenstreich struggled
to comport this alleged worsening with the lack of evidence of a reaction after Petitioner received
a third Gardasil dose in June 2016 (by which time Petitioner was receiving treatment for his UC).35
Tr. at 116, 328. Dr. Rosenstreich also acknowledged that Petitioner’s treating physicians had not
expressed concern about the role of any vaccines in causing his UC, and in fact recommended he
received vaccinations even after his UC diagnosis. Id. at 117.
Finally, Dr. Rosenstreich proposed that the timeframe for Petitioner’s symptoms onset was
medically acceptable. Tr. at 334; Rosenstreich First Rep. at 8. To do so, he began by setting forth
his understanding of the progression of UC. The intestinal epithelial damage associated with UC’s
symptoms would begin, he maintained, after sufficient activated T cells are present in the gut. Tr.
at 92–93; Rosenstreich First Rep. at 8. And it would take approximately 30 days post-insult to
develop inflammation, and for the body to reach peak antibody response. Tr. at 93, 140–42;
34
Dr. Rosenstreich continuously emphasized Petitioner’s alleged fatigue as well, although fatigue was not actually
mentioned in Petitioner’s affidavit as a symptom in November of 2015 (in comparison to complaints of stability or
stamina problems). Cerrone Aff. II at 2. Low energy level and decreased strength, by contrast, were, though the
timeline of those symptoms is unclear. Cerrone Aff. I at 5.
35
At most, Dr. Rosenstreich maintained that it was hard to discern the impact of this third HPV vaccine dose, since
by this time Petitioner was both quite ill and receiving treatment—factors that might have obscured what the reaction
was. Tr. at 329; Rosenstreich Second Rep. at 8.
14
Siergrist at 23. After that immune response is at its maximum, there would be an aberrant process
of cell death and regrowth in the gut, progressing to the point where the immune system destroys
enough cells to cause holes in the gut because the cells cannot regrow fast enough to counter
existing bacteria. Tr. at 93; Rosenstreich First Rep. at 8.
An influx of such commensal bacteria would take a while to peak as well before their
damage potentiality would be realized. Tr. at 93–94; Siergrist at 23. Dr. Rosenstreich then
proposed another 20 days would likely pass before there is full-blown destruction of the gut
epithelium and visible bleeding. Tr. at 94. Throughout this 80-day process, a patient might be
experiencing inflammation of a sub-acute nature. Id. at 90, 94. (Of course, Dr. Rosenstreich had
also opined that the fatigue had clinically manifested in November 2015 was part of the vaccine
reaction process leading to the more obvious and specific UC manifestations, although the record
reveals no other instances of obvious inflammation from the date of vaccination until late
December 2015 at the earliest).
Here, Petitioner had been vaccinated in October 2015, and approximately 81 days later
experienced bloody stools on or around December 27 th. 36 This, Dr. Rosenstreich proposed, was an
indication that Petitioner was experiencing colitis-associated inflammation. Tr. at 27, 86, 333;
Rosenstreich First Rep. at 8. There was subsequently an unbroken sequence between the bleeding
Petitioner reports first experiencing on December 27 th and his ultimate diagnosis a few months
later. Tr. at 86–88; Rosenstreich First Rep. at 8.
Such a timeframe was consistent with Petitioner’s literature, Dr. Rosenstreich contended.
Gradel, for example, had observed a delay between the time of recovery from patients’ IBD-
initiating infection (during which time they were presumably asymptomatic—although some of
the studied sample had been hospitalized) and when they began to experience IBD symptoms, with
the temporal gap peaking at around four to five months.37 Tr. at 25–27, 89; Rosenstreich Second
Rep. at 4; Gradel at 498; Angelo at 463–64. Further support for the timeframe question was found
in a study specific to the flu-GBS association. See L. Schonberger et al., Guillain-Barré Syndrome
Following Vaccination in the National Influenza Immunization Program, United States, 1976–
1977, 110 Am. J. Epidemiol. 105, 112 (1979), filed as Ex. 16 (ECF No. 39-10) (“Schonberger”).
Although Schonberger documented an increased risk for GBS concentrated primarily within the
five-week period after vaccination, some cases occurred as much as nine or ten weeks after. Tr. at
90–91; Schonberger at 105, 112 Figure 4 (determining that from week ten the relative risks no
36
Though this first instance of bloody stools did not lead to Petitioner visiting a physician, he reported this event in
his affidavit. Tr. at 87; Cerrone Aff. II at 1.
37
Gradel also found that a prior gastroenteritis infection can cause IBD with up to a one-year latency period. Tr. at
122; Gradel at 499. Dr. Rosenstreich did not give an outer limit on what he would consider a medically acceptable
timeframe for vaccine-caused UC, however, maintaining that it would have to be evaluated on a case-by-case basis in
the end. Tr. at 122–23.
15
longer remained significantly different, but observing some cases after). In fact, Schonberger
observed cases as late as 12 weeks (84 days) after vaccination. Tr. at 332, 334; Rosenstreich
Second Rep. at 4; Schonberger at 112–13. This was also consistent with findings in Respondent’s
literature. Tr. at 49–51; Angelo at 460 (noting that for GI disorders, the authors found four cases
beginning at five weeks after vaccination, as well as two cases around 17 weeks and one case
around 36 weeks).
2. John J. Santoro, D.O. – Dr. Santoro, a gastrointestinal physician, prepared
one written report and an affidavit (but did not testify at trial) 38 for Petitioner in support of the
contention that the three vaccines Petitioner received can cause UC, and did so in this case. 39 See
generally Report, dated August 16, 2019, filed as Ex. 36 (ECF No. 59-2) (“Santoro Rep.”);
Affidavit, dated July 15, 2020, filed as Ex. 81 (ECF No. 90-7) (“Santoro Aff.”). Dr. Santoro’s
report was not discussed at length in Petitioner’s pre- or post-hearing briefs, and for the most part
the opinion he offered was duplicative of Dr. Rosenstreich’s reports and testimony. But because it
remains in evidence, I will address his points briefly.
Dr. Santoro reiterated the dates and evidence provided in the medical records, and provided
background comments on IBD consistent with Dr. Rosenstreich’s reports and testimony. Santoro
Rep. at 3–8. Dr. Santoro also suggested a theory of molecular mimicry due to the presence of
serum and mucosal autoantibodies against intestinal epithelial cells (described in further detail by
Petitioner’s other expert. Id. at 9–10. Dr. Santoro opined that one of Petitioner’s vaccines caused
his UC because there were no other antecedent or concurrent events that could explain his
symptoms, and there was no evidence in his medical records that he suffered from IBD prior to his
vaccinations. Id. at 10–11. And though there is no definite answer in the medical literature for an
appropriate temporal relationship between IBD and the vaccines, Dr. Santoro found from his
experience that patients might have several months of indolent symptoms before a firm diagnosis
can be made, given the waxing and waning nature of the disease—thus suggesting the timeframe
for Petitioner’s onset was acceptable. Id.; D-W. Lee, et al., Diagnostic Delay in Inflammatory
38
Dr. Santoro is deceased. He obtained his undergraduate degree from the LaSalle College in Philadelphia, PA and
graduated with his doctorate of osteopathic medicine from the Philadelphia College of Osteopathic Medicine.
Curriculum Vitae, filed as Exhibit 47 on August 16, 2019 (ECF No. 60-4) (“Santoro CV”) at 1. He then completed a
rotating internship in internal medicine at the John F. Kennedy Memorial Hospital, and a residency in internal
medicine and fellowship in gastroenterology at the University of Medicine & Dentistry in Stratford, NJ. Santoro CV
at 1. He was a Medical Director of clinical research at Atlantic Gastroenterology Associates and the Co-Director of
the groups Inflammatory Bowel Disease Center. Santoro CV at 3; Santoro Rep. at 2. He also held a clinical Associate
Professorship at Rowan University School of Osteopathic Medicine. Santoro CV at 3; Santoro Rep. at 2. He cared for
more than 300,000 patients and specialized in diagnosing, treating, and researching various gastrointestinal diseases
like IBD. Santoro Rep. at 2. He was board certified in internal medicine and gastroenterology by the American
Osteopathic Board of Internal Medicine. Santoro CV at 2; Santoro Aff. at 1.
39
Dr. Romberg argued that Dr. Santoro was not qualified to opine on the molecular underpinnings of inflammatory
diseases. Tr. at 262–63; Romberg Second Rep. at 2.
16
Bowel Disease Increases the Risk of Intestinal Surgery, 23 World J. Gastroenterology 6474, 6478–
80 (2017), filed as Ex. 46 (ECF No. 60-3).
B. Respondent’s Experts
1. Chris Liacouras, M.D. – Dr. Liacouras, a practicing pediatric
gastroenterologist, prepared two written reports and an affidavit for Respondent, and also testified
for Respondent in support of the contention that Petitioner’s UC was not vaccine-associated. See
generally Tr. at 146–211. Report, dated May, 31, 2019, filed as Ex. O (ECF No. 53-1) (“Liacouras
First Rep.”); Report, dated January 21, 2020, filed as Ex. HH (ECF No. 71-1) (“Liacouras Second
Rep.”); Affidavit, dated December 11, 2020, filed as Ex. LL (ECF No. 97-2) (“Liacouras Aff.”).
Dr. Liacouras received his undergraduate degree from Johns Hopkins University and his
medical degree from Harvard University. Tr. at 146; Curriculum Vitae, filed as Exhibit NN on
May 19, 2022 (ECF No. 120-1) (“Liacouras CV”) at 1. He is currently a Professor of Pediatrics at
the Children’s Hospital of Philadelphia (“CHOP”), University of Pennsylvania School of
Medicine. Tr. at 146; Liacouras CV at 2. He also currently holds hospital positions as a co-director
at the Center for Pediatric Eosinophilic Disorders, a director and medical director at CHOP Exton
Specialty Center, and a pediatric gastroenterologist at the Children’s Hospital of Philadelphia at
three satellite locations. Liacouras CV at 3. He has over 30 years of clinical and endoscopic
experience treating children and adolescents with gastrointestinal, liver and dietary disorders,
including more than 2,500 patients with inflammatory bowel. Liacouras Aff. at 1. Dr. Liacouras
sees approximately two to 3,000 patients a year in both an inpatient and outpatient setting, with
approximately 85 percent of his work devoted to such patient care. Tr. at 147. He is licensed to
practice medicine in Pennsylvania and is board certified in pediatric gastroenterology, hepatology,
and nutrition by the American Board of Pediatrics. Liacouras Aff. at 1. He has approximately 80-
90 peer-reviewed articles and has helped write or organize several textbooks in pediatric
gastroenterology. Tr. at 148–49.
Dr. Liacouras accepted that Petitioner most likely suffered from UC. He defined UC as a
chronic, ulcerative condition of the colon (often grouped in the same category as IBD because they
are treated similarly). 40 Tr. at 149–51, 154; Liacouras First Rep. at 4. UC is considered an
autoimmune or immune-mediated disease but its etiology is largely unknown, with genetic,
environmental, autoimmune and bacterial factors all possible explanations. Tr. at 150, 188–90,
204, 208; Liacouras First Rep. at 3, 6, 8; Liacouras Second Rep. at 4. It causes severe irritation of
the mucosa and submucosa of the colon. Tr. at 149–50. UC occurs somewhere around one to five
patients for every 10,000 patients—common enough that the diagnosis occurs frequently in Dr.
40
Colitis alone, by contrast, just means inflammation of the colon, and is most commonly an acute, short lived, self-
resolving condition, whereas UC is severe and chronic. Tr. at 150–51; Liacouras First Rep. at 7.
17
Liacouras’s practice. Id. at 152. In pediatric patients, it presents with some degree of rectal
bleeding accompanied by diarrhea and abdominal pain. Id. at 151; Liacouras First Rep. at 4;
Liacouras Second Rep. at 2.
The bleeding associated with UC can be severe enough that patients develop anemia or
weight loss, which can lead to other systemic features like fatigue or lethargy. Tr. at 152; Liacouras
First Rep. at 4–5. The average age of onset is around 10-12 years old, but patients can present with
UC at any age. Tr. at 152–53; L. Higuchi & A. Bousvaros, Clinical Presentation and Diagnosis of
Inflammatory Bowel Disease in Children, UpToDate 1, 2–3 (2020), filed as Ex. LL, Tab 1 (ECF
No. 97-3). Treatment ranges from oral medicines to surgery, relying on biologic therapies in severe
cases. Tr. at 153–54; Liacouras First Rep. at 3–4.
Mr. Cerrone’s disease progression, Dr. Liacouras contended, helped establish why his
vaccinations were likely unrelated to his UC. In the month following vaccination, Petitioner was
seen by medical providers in the ER twice. 41 Tr. at 155–56; Liacouras First Rep. at 2; Ex. 2 at 30
(November 10, 2015 ER visit for laceration of his lip), at 34 (November 3, 2015 ER visit for left
wrist injury). Yet at these times he did not mention or demonstrate any GI symptoms (in fact, his
GI evaluations were normal). Tr. at 156–58; Liacouras First Rep. at 1, 2, 6; Ex. 1 at 13; Ex. 2 at
30, 34. Indeed, even later records (after Petitioner’s purported onset, moreover) revealed few issues
relevant to UC. Thus, on February 10, 2016, Petitioner had a primary care visit for a sore throat,
cough, and congestion, but his examinations revealed no abnormal abdominal findings nor
evidence of UC symptoms. Tr. at 158–59; Ex. 1 at 12. He also now received his second dose of
HPV vaccine, with no evidence of any reaction. Tr. at 159; Liacouras First Rep. at 2; Ex. 1 at 12.
The first record that formally memorialized an instance of lower gastrointestinal bleeding
was from February 13, 2016. Tr. at 159; Liacouras First Rep. at 2–3; Ex. 2 at 20, 25–26. But other
than general GI complaints (discussed as blood in his stool for the last three weeks), Petitioner
displayed no evidence of dizziness, weakness, or fatigue, and his abdominal exam was otherwise
normal. Tr. at 159; Liacouras First Rep. at 2; Ex. 2 at 20, 25–26. Only by mid-March 2016 was
there evidence from testing of significant issues fully reflective of UC (thus suggesting the severity
of his problem had progressed considerably over this timeframe). Tr. at 161–62; Ex. 3 at 11. By
March 2016, Petitioner was 158 pounds, and he dropped more weight in the ensuing months. Tr.
at 162–63; Ex. 3 at 6; Ex. 5 at 14. But even after significant treatment for UC, Petitioner was still
allowed to receive a third HPV vaccine dose. Liacouras First Rep. at 2; Ex. 1 at 4, 8.
41
In fact, Petitioner was evaluated no less than four times between the date of his first Gardasil vaccine dose on
October 7, 2015, and the first reported visit for abdominal complaints on February 13, 2016. Liacouras First Rep. at
5.
18
Given Petitioner’s medical history and disease progression (as best evidenced by the
record), 42 Dr. Liacouras deemed it unlikely that the vaccines Petitioner received (alone or in
concert) had caused his UC, since there was no real evidence of any disease process until much
longer after vaccination. Tr. at 179, 208; Liacouras First Rep. at 3, 7–8; Liacouras Second Rep. at
3. There was virtually no medical record of anything GI-associated from October 2015 to the end
of January/early February 2016. At best, Petitioner alleged that he had experienced decreased
stamina and loss of stability in November 2015, but Dr. Liacouras characterized such symptoms
as associated with UC only when presenting with (or in the wake of) significant anemia—which
the record did not reveal to exist in the fall of 2015. Tr. at 167–68; Liacouras First Rep. at 8. And
in Dr. Liacouras’s view, there were plenty of other causes of fatigue or loss of stamina for
teenagers, and Petitioner had previously reported fatigue prior to vaccination (allowing the
question of why he had not done so formally in November 2015). Tr. at 168; Ex. 1 at 15. In
addition, none of Petitioner’s treaters had counseled against his receipt of additional HPV vaccine
doses despite his UC diagnosis. Tr. at 177–79; Ex. 3 at 7 (documenting as a preventative measure
that Petitioner should receive the pneumococcal vaccine every five years and the annual flu
vaccine); Ex. 5 at 1135 (talking about ordering Hep. B and varicella vaccines as per the GI
recommendations). In fact, patients with active IBD are routinely vaccinated. Liacouras First Rep.
at 5. And Dr. Liacouras could not find record evidence that Petitioner’s second or third HPV doses
had caused a worsening of UC symptoms (although the record does clearly establish general
worsening between February and March 2016). Tr. at 169–70.
Dr. Liacouras only briefly discussed the alleged causal association (or lack thereof)
between the vaccines and UC, leaving the immunologic issues such matters raised to Respondent’s
other expert, Dr. Romberg. Tr. at 171, 191–93, 196, 200–01, 209. He indicated, however, that he
had been unable to locate in his own literature searches evidence associating vaccines with UC,
adding that in fact the contrary seemed to be better supported. Id. at 173–76, 203–04; Liacouras
First Rep. at 5, 7; Liacouras Second Rep. at 2, 4; Skufca at 5926 (evaluating several hundred
thousand individuals and finding no significant evidence indicating there were any adverse effects
related to the development of UC or fatigue after receipt of the HPV vaccine); S. Dezfoli & G.
Melmed, Vaccination Issues in Patients with Inflammatory Bowel Disease Receiving
Immunosuppression, 8 Gastroenterology & Hepatology 504, 507–08 (2012), filed as Ex. Z (ECF
No. 53-12) (“Dezfoli”) (concluding that there was no increased risk associated abnormalities for
IBD after the Hep. A or HPV vaccines); R. Davis et al., Measles-Mumps-Rubella and Other
Measles-Containing Vaccines do not Increase the Risk of Inflammatory Bowel Disease, 155
Archives Pediatrics & Adolescent Med. 354, 354 (2001), filed as Ex. T (ECF No. 53-6)
(“[c]hildren vaccinated with MMR who were older than 18 months were at significantly decreased
42
In Dr. Liacouras’s view, Dr. Rosenstreich relied too much on Petitioner’s affidavits and amended petition rather
than the contemporaneous medical records. Liacouras First Rep. at 6.
19
risk for IBD”)(emphasis added); Chambrun II at 1414 (“results of this meta-analysis do not support
a role of childhood immunization or H1N1 vaccination in the development of IBD”).
Dr. Liacouras’ opinion also included consideration of Petitioner’s onset and its relationship
to causation. He noted that symptoms of UC typically progress between a few weeks to up to two
months after what might be considered an instigating trigger (like an infection). Liacouras First
Rep. at 4. 43 In his view, the records best supported the conclusion that Petitioner’s UC symptoms
began around mid to late January 2016—or about three to four months after his October 7, 2015
vaccinations. Tr. at 169; Liacouras First Rep. at 6. Dr. Liacouras acknowledged that Petitioner
alleged his symptoms began earlier, in late December 2015 (even if they were not formally
reported or treated at that time), but in his opinion even such an onset would not make vaccine
causation more likely. Tr. at 169, 209; Cerrone Aff. II at 1.
Dr. Liacouras also disputed the evidence offered by Dr. Rosenstreich for the contention
that UC can occur anywhere between five weeks to almost a year after instigation in patients.
Angelo, for example (which Respondent filed but Dr. Rosenstreich attacked) did not look at this
issue. Tr. at 175; Angelo at 460–64. At most, Angelo showed the possibility of UC in the sample
group of patients, but it did not correlate the risk to the HPV vaccine using a case control group or
patient. Tr. at 176; Angelo at 463. In fact, Dr. Liacouras would expect even more cases of UC in
the normal population if an association with the vaccine was likely, given the commonality of this
disease. Tr. at 176. Angelo ultimately had failed to identify any significant relationship between
the development of UC and the HPV vaccine, undermining the significance of any proposed risk
interval. Id.; Angelo at 464.
2. Neil Romberg, M.D., – Dr. Romberg, an immunologist and medical doctor
focused on the care for children with immunological disorders, testified on behalf of Respondent,
and submitted two expert reports and an affidavit. See generally Tr. at 211–323; Report, dated
May, 6, 2019, filed as Ex. A (ECF No. 50-1) (“Romberg First Rep.”); Report, dated January 14,
2020, filed as Ex. GG (ECF No. 70-1) (“Romberg Second Rep.”); Affidavit, dated December 11,
2020, filed as Ex. JJ (ECF No. 98-2) (“Romberg Aff.”). Dr. Romberg did not find a casual
association between the vaccines Petitioner received and UC.
Dr. Romberg received his undergraduate degree from the University of Michigan, and his
medical degree from Pennsylvania State University, College of Medicine. Tr. at 211; Curriculum
Vitae, filed as Ex. MM (ECF No. 119-1) (“Romberg CV”) at 1. 44 He completed a pediatric
residency and a chief residency in pediatrics at New York University, School of Medicine and
43
Respondent cited to Ex. FF by an author named Croft, but this pages for this exhibit are cut off and it is unclear on
the authors name or title of the article.
44
This is the most updated version filed by Respondent.
20
completed his training at Yale University, School of Medicine, with a three-year allergy clinical
immunology fellowship. Tr. at 211; Romberg CV at 1. Dr. Romberg is currently an Assistant
Professor of Pediatrics at the University of Pennsylvania and an attending physician at the
Children’s Hospital of Philadelphia where he holds the Jeffrey Modell Endowed Chair of Pediatric
Immunology Research. Romberg CV at 1; Romberg First Rep. at 1. He is licensed to practice
medicine in New York, Connecticut, and Pennsylvania, and is board certified by the American
Board of Pediatrics and the American Board of Allergy and Clinical Immunology. Tr. at 214;
Romberg First Rep. at 1; Romberg CV at 2. Dr. Romberg has published approximately 40-50 peer-
reviewed publications. Tr. at 217.
Dr. Romberg deferred to Dr. Liacouras regarding Petitioner’s UC diagnosis, and instead
focused on Petitioner’s three mechanistic theories. He understood them to be as follows: that (a)
the innate immune system would mount an overly exuberant response to vaccine components (due
in part to the alum adjuvant); (b) molecular mimicry between antigenic vaccine components and
epithelial cell structures would results in a cross-reaction against the gut, damaging it and also
encouraging an inflammatory setting; and (c) the vaccines could also induce an immune response
that upsets the equilibrium between the mucosal immune system in the gut and the mensural
bacteria. Tr. at 220–21, 281; Romberg First Rep. at 4. Although Dr. Romberg admitted he could
not say with certainty that there was absolutely a zero percent chance the vaccines at issue could
induce such processes resulting in disease, in his estimation the chance approached zero, given
the submitted literature and evidence. Tr. at 320–21.
First, Dr. Romberg addressed Petitioner’s contentions about the role of the innate immune
system in the context of this case. Tr. at 221, 309. The innate immune system, he explained,
responds quickly after it detects evidence of pathogens or other damaging external factors. Id. at
222, 310–11. By contrast, the adaptive response moves slowly and secondarily, and is more
selective about what it recognizes as a foreign invader. Id. at 223. Thus, where the innate immune
system typically responds the same every time (and quickly as well), the adaptive immune system
has features of immunological memory, and thus will only react more rapidly to antigenic stimuli
it has encountered before. Id. at 223, 275.
Dr. Romberg opined that an aberrant innate response would not be hidden or remain
subacute for a lengthy period of time. Rather, hyperactivation of the innate response (for example,
due to the alum adjuvant) would result in clinical manifestations or other evidence that could be
obtained from testing. Tr. at 225. The immune response to alum (which occurs within minutes of
vaccination) has been well described and characterized. Id. When alum is detected by a protein
called NLRC3, it stimulates a macromolecular structure called the inflammasome, leading to the
upregulation of certain proinflammatory cytokines. Id.; Romberg First Rep. at 7; S. Eisenbarth et
al., Crucial Role for the Nalp3 Inflammasome in the Immunostimulatory Properties of Aluminum
Adjuvants, 453 Nature 1122, 1122 (2008), filed as Ex. K (ECF No. 50-11). If those cytokines stay
21
in the tissue, they cause fever or “induration” (swelling and redness at the injection site). 45 Tr. at
225; Romberg First Rep. at 7. Subsequently, the antigens sparking the innate response will be
taken to lymph nodes, where they interact with the B and T cells and start the adaptive immune
response. Tr. at 225–26, 285; Romberg First Rep. at 7. To get a more systemic reaction that can
result in disease or worse symptoms, there must be an uncontrolled series of events. Tr. at 226.
Dr. Romberg similarly did not accept the argument that the alum adjuvant might have
heightened the initial vaccine response, deeming the fact that Petitioner received two vaccines with
the adjuvant simultaneously as not atypical. Tr. at 228. Dr. Rosenstreich had cited a study
regarding oral ingestion of large amounts of aluminum in mice and its relation to IBD (Chambrun
I), but this was not a comparable situation to vaccination in Dr. Romberg’s estimation. Id.;
Chambrun I at 589. The studied mice in Chambrun I had been force-fed large amounts of
aluminum for 31 days, in comparison to the amounts Petitioner had received in a single day. Tr. at
229; Romberg Second Rep. at 5–6. And the dosage mattered, since the amount of alum contained
in vaccines is far dwarfed by what the experimental mice had received. Tr. at 230, 303; Romberg
Second Rep. at 5–6. Most importantly, Chambrun I’s authors determined that exposure to alum
alone did not cause colonic inflammation, so its own results did not support Dr. Rosenstreich’s
contentions. Tr. at 229–30, 306–07; Romberg Second Rep. at 5–6; Chambrun I at 590 (citing
supplementary Figure 1, and noting “[t]hese four weeks’ oral administration of aluminum did not
induce any macroscopic, histological, or molecular colonic inflammation”). As Dr. Romberg later
admitted, however, Chambrun I does also state that the dose and route of aluminum administration
used in the study had relevance to human exposure, even if the study methodology used artificial
conditions so that effects could be reasonably evaluated for experimental purposes. Tr. at 304;
Chambrun I at 597.
In addition, the receipt of multiple vaccines on a single day, Dr, Romberg opined, was not
itself likely to encourage an aberrant reaction. In fact, the immune system can easily handle
multiple vaccines at once without the occurrence of any immune-mediated harm. Tr. at 252. The
CDC has no difficulty recommending multiple vaccines be administered at a single pediatric visit,
and many vaccines are intentionally formulated to be multi-antigen (like the DTaP or
pneumococcal vaccine, which contains several pneumococcal serotypes). Id. Thus, Petitioner’s
receipt of three vaccines at one time was not contrary to accepted pediatric standards of care. Id.at 252–53.
45
Fever is the number one sign that a specific proinflammatory cytokine, IL-1β, is circulating in the blood and has
reached (or at least communicated with) the brain. Tr. at 226; Pek v. Sec'y of Health & Hum. Servs., No. 16-0736V,
2020 WL 1062959, at *5, n.8 (Fed. Cl. Spec. Mstr. Jan. 31, 2020) (defining IL-1β as a “type of cytokine that mediates
antigen-specific responses through direct activation of lymphocytes”). The clinical/symptomatic response is malaise
and fatigue. Tr. at 226.
22
Second, Dr. Romberg deemed unpersuasive the component of Petitioner’s causation theory
positing an autoimmune cross-reaction due to molecular mimicry. As he explained, molecular
mimicry is a theory of mistaken identity in which the immune system reacts to the protein of an
exogenous antigen (like a vaccine or infection), creating an immune response to that protein—but
where the original antigenic agent has some resemblance (whether due to amino acid sequence or
structure) to a self-protein component or structure. 46 Tr. at 230; Romberg First Rep. at 4. This can
lead to the immune system mistakenly attacking the self tissue, due to its component resemblance
to a pathogenic microbe or other foreign invader. Tr. at 230–31.
In Dr. Romberg’s view, however, while molecular mimicry has a reasonable scientific
basis as a theory, it does not follow that it is the likely mechanism in any given autoimmune disease
process. Tr. at 231; Romberg First Rep. at 5; C. Benoist & D. Mathis, Autoimmunity Provoked by
Infection: How Good is the Case for T Cell Epitope Mimicry?, 2 Nature Immunology 797, 797–
98 (2001), filed as Ex. F (ECF No. 50-6) (“Benoist”); L. Albert & R. Inman, Molecular Mimicry
and Autoimmunity, 341 N Eng. J. Med. 2068, 2073 (1999), filed as Ex. G (ECF No. 50-7). Rather,
evidence supporting its role must be identified. Some in the immunologic field rely on a four-
pronged framework 47 to determine if molecular mimicry is the likely disease mechanism. Tr. at
231, 287; Romberg First Rep. at 5; Benoist at 797–98; C. Ang et al., The Guillain-Barré Syndrome:
A True Case of Molecular Mimicry, 25 Trends Immunology 61, 62–65 (2004), filed as Ex. H (ECF
No. 50-8) (“Ang”). 48
The first criterion of this framework, Dr. Romberg explained, looks for epidemiologic
support for a vaccine-injury association generally. Tr. at 231, 287. The second asks whether
autoreactive T cells or B cells that might recognize some sort of a human target have been
identified. Id. at 240–41, 300; Romberg First Rep. at 6. The third criterion looks for a proposed
antigen on the vaccine/infection side that might sufficiently resemble a self structure to spark a
cross-reaction (in the wake of the immune system’s reaction to the initial foreign antigen). Tr. at
241, 300. And the fourth criterion evaluates whether an animal model exists that could reproduce
46
Dr. Romberg provided more detail for his explanation of molecular mimicry in his first report. As he noted, the
concept is that an immune cell mistakes a self-antigen loaded in an HLA molecule for a foreign antigen and mounts
an inflammatory response. Romberg First Rep. at 4; Tr. at 286–87. As different HLA alleles present antigens
differently, autoimmune diseases occur more often in people with certain HLA alleles, and so molecular mimicry may
provide an explanation why some people develop inflammatory diseases when others do not. Romberg First Rep. at
4.
47
This framework was originally created by Dr. Diane Mathis, and has since been relied upon by immunologists
interested in autoimmune diseases as a way to gauge whether molecular mimicry actually might “explain” a disease’s
pathogenesis. Tr. at 242; Benoist at 797–98; Ang at 62–65.
48
Dr. Rosenstreich, by contrast, maintained that this four-prong framework demanded a degree of proof far in excess
of what would be deemed sufficient in the context of a Vaccine Program injury claim. Rosenstreich Second Rep. at
5–6. This point has merit, as I discuss below (although I take some notice of the framework as generally illuminating
the kinds of evidence needed to support molecular mimicry as explanatory of an autoimmune process).
23
experimentally the proposed autoimmune process relying on molecular mimicry. Id. at 241–42.
The ability to meet all four provides strong support for molecular mimicry as relevant to a disease
process, in Dr. Romberg’s view—whereas if none are fulfilled, the argument that molecular
mimicry is part of the disease process is unpersuasive. Id. at 243.
In this case, Dr. Romberg maintained, none of these criteria could be met. Tr. at 243;
Romberg First Rep. at 5. First, he could identify no persuasive or reliable epidemiologic evidence
establishing a vaccine association generally, noting that the placebo-controlled clinical trial data
discussed in the Gardasil Package Insert undercut contentions of a relationship. Tr. at 233; Gardasil
Package Insert at 8–9. In these seven clinical trials, development of new autoimmune diseases
were assessed two and six months after either administration of a vaccine or placebo. Romberg
First Rep. at 5; Gardasil Package Insert at 8–9. The study compared 10,944 females who had
received the Gardasil vaccine compared to 9,412 females receiving a placebo, but found only seven
cases in the Gardasil group, versus ten cases in the placebo group, of IBD. Tr. at 234; Romberg
First Rep. at 5; Gardasil Package Insert at 8. The same analysis was done for males (though in
fewer numbers, with 3,093 males in the vaccine group and 2,303 in the placebo group). Tr. at 234;
Romberg First Rep. at 5; Gardasil Package Insert at 9.
In discussing this evidence from the Gardasil Package Insert, Dr. Romberg rejected Dr.
Rosenstreich’s concerns that alum in the placebo group doses might have impacted a reaction
alone. Tr. at 234, 296. If, he reasoned, alum was the “bad actor” prompting IBD, there would be
cases just in the alum group and not in the saline group (whereas if it was the protein that caused
disease there would be evidence in the group receiving the vaccine, as opposed to the controls).49
Id. at 235. In fact, the study saw fewer cases of IBD in the placebo group than in the treatment
group, suggesting there is probably no effect of the alum adjuvant. Id. at 235, 296–97. This clinical
trial study evidence thus negated any HPV vaccine association—and Petitioner had offered no
other evidence pro or con relating to Flumist or Hep A. 50 Id. at 293; Romberg First Rep. at 5.
Second, Dr. Romberg maintained that no evidence established what autoreactive T cells or
autoantibodies would be driving a cross-reactive process. Tr. at 241; Romberg First Rep. at 6.
Indeed, there was no evidence of the presence of any such potential offending T or B cells in
49
The Gardasil Package Insert also disclosed that in seven clinical trials (five amorphous aluminum hydroxy sulfate
(“AAHS”) controlled, one saline placebo controlled, and one uncontrolled), there were 15,706 patients in the Gardasil
group, 13,023 patients in the AAHS control group, and only 594 patients in the saline placebo group, which Dr.
Romberg admitted was generally large enough to detect rare events for the saline placebo group. Tr. at 297–98;
Gardasil Package Insert at 4.
50
By comparison, Dr. Romberg noted that there were many good examples where molecular mimicry likely does
contributes to autoimmune human diseases, such as in the context of Streptococcal infection-associated rheumatic
fever, or the infections/flu vaccine association with GBS. Romberg First Rep. at 5. In such cases, reliable and
persuasive epidemiological data exists that links the exposure with onset of disease. Id.24
Petitioner’s blood. Romberg First Rep. at 6. Dr. Rosenstreich had cited to a case report, Luca, to
suggest that colitis could be T cell-induced after receipt of the flu vaccine, but Luca not only
involved a totally different version of the vaccine (which was injected rather than administered
intranasally like Flumist) but also featured onset within two hours (not 11 weeks). Id. at 6–7; Luca
at 367. Nor was Dr. Rosenstreich able, in Dr. Romberg’s view, to identify what the mimic for the
vaccine antigen even was. At most, Petitioner proposed that the HPV16 E7 protein was
molecularly similar to an intestinal brush-border transport protein, but the former protein is not
contained in the HPV vaccine—let alone the other two. Tr. at 214, 241; Romberg First Rep. at 7;
Rosenstreich First Rep. at 7; Gardasil Package Insert at 12 (listing a complete list of ingredients in
the vaccine).
The final criterion was also unmet, in Dr. Romberg’s estimation. He noted the existence of
many animal models for IBD (identifying his familiarity with 66 models as of the date of his first
report), but he was aware of none that had attempted to induce IBD or UC via Gardasil, Hep. A,
any form of seasonal flu vaccine, or the components thereof (including the alum adjuvant). Tr. at
242, 302–03; Romberg First Rep. at 6. Though Dr. Romberg acknowledged that more research on
rare conditions was always called for, he emphasized that IBD is a major topic for biomedical
research and is frequently evaluated, so in his view the absence of research evidence on this subject
was telling. Tr. at 243. On the other hand, clinical guidelines routinely recommended that IBD/UC
patients be vaccinated. Tr. at 235–36; K. Chaudrey et al., Updates in Vaccination:
Recommendations for Adult Inflammatory Bowel Disease Patients, 21 World J. Gastroenterology
3184, 3184 (2015), filed as Ex. I (ECF No. 50-9). If vaccines were factors in contributing to IBD,
adverse events would be far more commonly reported. Tr. at 236–37.
Dr. Romberg went on to discuss the case report evidence relied upon under Petitioner’s
theory, deeming them to generally be worthy of relatively little evidentiary weight. Tr. at 237. In
the hierarchy of scientific/medical evidence, he contended, the most persuasive and reliable proof
was to be found in meta-analyses of placebo-controlled blinded studies of a large number of
patients. Id. at 231–32, 290. Below this level would be placebo-controlled blinded studies,
followed by epidemiologic evidence like case control series. Id. at 232. At the bottom would be
case series reports, with single-patient case reports the least persuasive category of causation
evidence. Indeed, in Dr. Romberg’s estimation many in the scientific community might not deem
the latter to be of any evidentiary value at all, given the lack of controls and individual patient
samples. Id. at 233.
Besides lacking general value as causation evidence, Dr. Romberg deemed the specific
case reports cited by Dr. Rosenstreich to be unpersuasive or unhelpful to Petitioner’s case. Luca,
for example, involved a single patient who could be distinguished from Mr. Cerrone in terms of
25
age, gender, preexisting conditions, and timeframe for onset. 51 Tr. at 238; Luca at 367. The same
was true for Pauwels. Tr. at 238–39; Romberg Second Rep. at 8; Pauwels at 217–19. That case
report involved a wholly-different disease (panniculitis), not to mention a form of the flu vaccine
with a different composition and method of administration. Tr. at 239; Romberg Second Rep. at
8. Flumist accesses the mucosal immune system in the nose, with the intention of creating a
controlled infectious process therein, distinguishing it from a peripherally-administered
intramuscular vaccine which aims to send the vaccine antigens more directly into the lymphatic
system. 52 Tr. at 239–40; Romberg Second Rep. at 8. Dr. Romberg also deemed the VAERS data
establishing 75 cases of post-vaccine colitis to be unsurprising, given the passive nature of this
kind of evidence. Tr. at 240; Romberg First Rep. at 5. He deemed unverified reporting of adverse
events to be no better than a last resort, useful only when there is no other data relevant to causal
issue. Tr. at 240. Yet in this case, such data exists (although it is unhelpful to Petitioner’s case) Id.;
Romberg First Rep. at 5.
Dr. Romberg found equally unpersuasive Dr. Rosenstreich’s contention that the vaccines
(alone or in concert) could somehow interfere with gastrointestinal equilibrium. In making this
argument, Dr. Rosenstreich had analogized the impact of the relevant vaccines to infectious agents
understood to induce autoimmune disease, such as C. jejuni. But because the HPV vaccine is not
(nor does it contain) an intraluminal microbe, the nature and source of this balance disruption could
not be illuminated either way. Tr. at 245–46. Otherwise, Dr. Romberg denied that vaccines had
been credibly linked to the abnormal imbalance between commensal bacteria and the immune
system characteristic of IBD. Id.Another argument raised by Petitioner but questioned by Dr. Romberg was the possibility
that Petitioner’s second HPV vaccine dose, 53 received on February 10, 2016, evidenced
rechallenge, 54 or a quicker adaptive immune response upon second exposure, since the medical
record showed that Petitioner’s UC progressed drastically from mid-February to March 2016. Tr.
at 243–44, 314–16; Romberg Second Rep. at 8–9. In Dr. Romberg’s view, the very concept of
rechallenge in this case (in which the first dose did not result in evident clinical manifestations for
51
Dr. Romberg also noted that the Luca case report did not appear to have been peer-reviewed, and its assertionsabout
the patient considered and her condition could not be verified. Romberg First Rep. at 6.
52
In addition, Dr. Romberg explained, with a live vaccine there is a delayed innate immune response (around five to
eight days) because the live viruses in the vaccine need to replicate several times before an immune reaction will
occur. Tr. at 239.
53
Dr. Romberg was unaware whether Mr. Cerrone had also previously received the Hep. A or Flumist vaccines, so
he focused on the HPV vaccine in addressing this issue. Tr. at 244.
54
See generally Nussman v. Sec'y of Health & Hum. Servs., No. 99-500V, 2008 WL 449656, at *9 (Fed. Cl. Spec.
Mstr. Jan. 31, 2008), aff'd, 83 Fed. Cl. 111 (2008) (defining challenge-rechallenge as “when a person (1) is exposed
to one antigen, (2) reacts to that antigen in a particular way, (3) is given the same antigen again, and (4) reacts to that
antigen similarly”).
26
over two months) was belied by the fact that Mr. Cerrone received a third HPV vaccine dose on
June 24, 2016, after his diagnosis and while he was being actively treated, but showed no renewed
or worsened symptoms thereafter. Id. at 244–45, 315; Romberg Second Rep. at 9.
Dr. Romberg was questioned on cross examination about Dezfoli, a ten-year old abstract
review article. Tr. at 315–16. Although Dezfoli concluded that IBD patients receiving
immunosuppressive treatments were not put at risk by receipt of the HPV or Hep. A vaccines, it
did classify LAIVs like Flumist to be contraindicated. Dezfoli at 505, 509-10. Dr. Romberg
maintained, however that in Dezfoli the flu vaccine had been administered to 575 IBD patients
who were receiving immunosuppressive therapy, with no control group. Tr. at 316; Dezfoli at 506.
IBD patients are known to have flares, and therefore it was not surprising to Dr. Romberg that
Dezfoli observed flares in five percent of the sample post-vaccination. Tr. at 316; Dezfoli at 506.
Thus, whether there was a likely causal connection with that specific vaccine was not reliably
established. Tr. at 316. And Dezfoli’s authors stressed generally that their recommendations
flowed from the broader view that generally “live vaccines should be avoided among patients who
are immunosuppressed,” as opposed to a determination that this category of vaccine posed causal
risks for disease initiation. Dezfoli at 509, 510.
Dr. Romberg concluded with a discussion of whether Petitioner’s UC onset was medically
acceptable under the circumstances. He acknowledged that the medical record in this case could
support an onset as having occurred between 81 to 100 days after vaccination. Tr. at 224, 319–20;
Romberg First Rep. at 7–8. But Dr. Romberg found it difficult to identify what period might be
most medically reasonable, based on the evidence submitted. Tr. at 246–47. Schonberger, for
example, best supported a post-vaccination onset for the autoimmune disease it focused on (GBS)
of around 21 days, 55 but it involved a distinguishable vaccine and injury. Id. at 247; 289–292;
Romberg First Rep. at 7–8; Schonberger at 112.
Dr. Romberg also pointed out that Schonberger’s results had been corroborated by animal
models 56—but there was little comparable evidence that could shed light on what the proper
timeframe for vaccine-caused UC/IBD would be. Tr. at 248. At best, one could look to an IBD-
specific mouse model, and to that end he referenced the Dextran Sulfate Sodium model. Id. at 248–
49; Romberg Second Rep. at 7; B. Chassaing et al., Dextran Sulfate Sodium(DSS)-Induced Colitis
in Mice, 104 Current Protocols Immunology 1, 1 (2015), filed as Ex. GG, Tab 3 (ECF No. 70-4)
(“Chassaing”). But the response observed in Chassaing was significantly faster—occurring within
three to four days. Tr. at 249–51; Romberg Second Rep. at 7; Chassaing at 8. Another study had
55
Specifically, Schonberger indicates that most GBS cases after the flu vaccine occurred around 13-17 days, with
their latest happening 41 days. Schonberger at 112.
56
Dr. Romberg acknowledged that animal testing was not fully comparable to what would be expected to occur with
humans, but noted that were reasonable models that could provide fair comparison to comparable diseases in humans
(specifically pointing to one that was used in mice as a proxy for peripheral neuropathies in humans, like GBS). Tr. at
249–50; Romberg First Rep. at 7–8.
27
reached a similar conclusion. See, e.g., E. Antoniou et al., The TNBS-Induced Colitis Animal
Model: An Overview, 11 Annals Med. & Surgery 9, 13 (2016), filed as Ex. GG, Tab 4 (ECF No.
70-5) (describing a separate mouse colitis model for Crohn’s disease, and finding that test subjects
demonstrated colon-impacting symptoms within three days, dying by day seven). Thus, what
evidence existed relevant to UC did not support even the shortest vaccine-symptoms interval
possible in this case (81 days). Tr. at 251; Romberg Second Rep. at 7.
Dr. Romberg commented about what the medical record said (or did not) about onset and
vaccine association with Petitioner’s UC. He did not see any evidence of local inflammatory
symptoms such as induration, redness, or fever after the October 2015 vaccination date. Tr. at 226,
280, 319; Romberg First Rep. at 3, 7. And Petitioner’s contentions that he had experienced loss of
stamina that November had not been contemporaneously reported to any of his providers. Tr. at
227–28. Dr. Romberg also noted (like Dr. Liacouras) that teenagers might experience fatigue or
low energy for a number of reasons unrelated to vaccination (e.g., growth, hormonal activity, or
sleep disturbances). Id. at 227. And these kind of symptoms were not commonly associated with
gut inflammation in any event. Id. at 226–27; Romberg First Rep. at 5.
IV. Procedural History
After the case’s initiation in August 2017, Petitioner filed medical records, affidavits, an
amended petition, and statement of completion by October 2017. Respondent’s Rule 4(c) Report
was filed on February 28, 2018, contesting Petitioner’s right to compensation. ECF No. 25. Expert
reports were subsequently filed through early 2020, and thereafter the special master to whom the
case had been assigned requested a briefing from the parties in advance of potential adjudication
to determine a ruling finding for entitlement, a decision denying entitlement, or an order
scheduling the case for a hearing. ECF No. 78. Petitioner submitted his brief on July 15, 2020,
Respondent filed her response on December 11, 2020, and Petitioner replied on February 26, 2021.
ECF Nos. 90, 97, 102.
The case had been set for an October 2021 trial, but was transferred to me due to a conflict
of interest involving the prior special master. I subsequently set the matter for a two-day hearing
for May 2022. ECF No. 115. The trial occurred as scheduled, and the parties submitted post hearing
briefs on August 5, 2021. ECF Nos. 133–34. The matter is now ripe for resolution.
V. Applicable Legal Standards
A. Petitioner’s Overall 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 within a statutorily prescribed period of time
or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table
28
Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §
11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed.
Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006).57
In this case, Petitioner does not assert a 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).
Proof of medical certainty is not required. Bunting v. Sec’y of Health & Hum. Servs., 931 F.2d
867, 873 (Fed. Cir. 1991). In particular, 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 & Hum. Servs., 165 F.3d 1344,
1352–53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed.
Cir. 2006). 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).
In attempting to establish entitlement to a Vaccine Program award of compensation for a
Non-Table claim, a petitioner must satisfy all three of the elements established by the Federal
Circuit in Althen v. Sec'y of Health & Hum. Servs., 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
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, a
petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”
Knudsen v. Sec’y of Health & Hum. 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
57
Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Hum. 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 & Hum. Servs., 59 Fed. Cl. 121,
124 (2003), aff’d 104 F. Appx. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Hum. Servs., No. 13-159V,
2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).
29
theory. Andreu v. Sec’y of Health & Hum. 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, 121 Fed.
Cl. at 245.
In discussing the evidentiary standard applicable to the first Althen prong, the Federal
Circuit has consistently rejected the contention that it can be satisfied merely by establishing the
proposed causal theory’s scientific or medical plausibility. See Boatmon v. Sec’y of Health & Hum.
Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019); see also LaLonde v. Sec’y of Health & Hum. Servs.,
746 F.3d 1334, 1339 (Fed. Cir. 2014) (“[h]owever, in the past we have made clear that simply
identifying a ‘plausible’ theory of causation is insufficient for a petitioner to meet her burden of
proof” (citing Moberly, 592 F.3d at 1322)); Howard v. Sec'y of Health & Hum. Servs., No. 16-
1592V, slip op. at *6 (Fed. Cl. Feb. 27, 2023) (confirming that “[t]he standard has been
preponderance for nearly four decades”). Otherwise, petitioners always have the ultimate burden of
establishing their Vaccine Act claim with preponderant evidence. W.C. v. Sec’y of Health & Hum.
Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted); Tarsell v. United States, 133 Fed.
Cl. 782, 793 (2017) (noting that Moberly “addresses the petitioner’s overall burden of proving
causation-in-fact under the Vaccine Act” by a preponderance standard).
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 & Hum. 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 & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).
Medical records and statements of a treating physician, however, 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 & Hum. Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is nothing . . . that mandates
30
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 be weighed against other, contrary
evidence also present in the record—including conflicting opinions among such individuals.
Hibbard v. Sec’y of Health & Hum. 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); Veryzer v. Sec’y of Dept. of Health & Hum. Servs., No. 06-522V,
2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review denied, 100 Fed.
Cl. 344, 356 (2011), aff’d without opinion, 475 F. Appx. 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.” de Bazan
v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what
is a medically acceptable timeframe must align 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 & Hum.
Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after remand, 105 Fed. Cl. 353 (2012), aff’d
mem., 503 F. Appx. 952 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V,
2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for rev. denied (Fed. Cl. Dec. 3,
2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).
B. Legal Standards 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 & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir.
1993) (determining that 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 determination
is evidenced by a rational determination).
31
As noted by the Federal Circuit, “[m]edical records, in general, warrant consideration as
trustworthy evidence.” Cucuras, 993 F.2d at 1528; Doe/70 v. Sec'y of Health & Hum. 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”), aff'd, Rickett v. Sec'y of Health & Hum.
Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). A series of linked
propositions explains why such records deserve some weight: (i) sick people visit medical
professionals; (ii) sick people attempt to 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 & Hum. Servs., No. 11–685V,
2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr. Apr. 10, 2013); Cucuras v. Sec'y of Health & Hum.
Servs., 26 Cl. Ct. 537, 543 (1992), aff'd, 993 F.2d at 1525 (Fed. Cir. 1993) (“[i]t strains reason to
conclude that petitioners would fail to accurately report the onset of their daughter's symptoms”).
Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec'y of Health & Hum. Servs., No. 03–1585V, 2005 WL
6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical records
are often 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 & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff'd per curiam, 968 F.2d
1226 (Fed. Cir. 1992), cert. den'd, 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, the Federal Circuit has also noted that there is no formal “presumption” that
records are accurate or superior on their face to other forms of evidence. Kirby v. Sec’y of Health
& Hum. Servs., 997 F.3d 1378, 1383 (Fed. Cir. 2021). There are certainly situations in which
compelling oral or written testimony (provided in the form of an affidavit or declaration) may be
more persuasive than written records, such as where records are deemed to be incomplete or
inaccurate. Campbell v. Sec'y of Health & Hum. 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 & Hum. Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).
32
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 & Hum. 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 of Health
& Hum. Servs., 110 Fed. Cl. 184, 203–04 (2013), aff'd, 746 F.3d 1334 (Fed. Cir. 2014). In making
a determination regarding whether to afford greater weight to contemporaneous medical records
or other evidence, such as testimony at hearing, there must be evidence that this decision was the
result of a rational determination. Burns, 3 F.3d at 417.
C. 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 & Hum. 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 Pharm., Inc., 509
U.S. 579, 594–96 (1993). See Cedillo v. Sec’y of Health & Hum. Servs., 617 F.3d 1328, 1339 (Fed.
Cir. 2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999).
Under Daubert, the 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).
In the Vaccine Program the Daubert factors play a slightly different role than they do when
applied in other federal judicial settings, like the district courts. Typically, Daubert factors are
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable or could confuse a jury. By contrast, in Vaccine Program cases these factors are
used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec'y of Health &
Hum. 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
33
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 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 v. Sec'y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (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 & Hum.
Servs., No. 08–601V, 2012 WL 3609993, at *17 (Fed. Cl. 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). Weighing the relative persuasiveness of competing expert testimony, based on
a particular expert's credibility, is part of the overall reliability analysis to which special masters
must subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d at 1325–26
(“[a]ssessments as to the reliability of expert testimony often turn on credibility determinations”);
see also Porter v. Sec'y of Health & Hum. Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this court
has unambiguously explained that special masters are expected to consider the credibility of expert
witnesses in evaluating petitions for compensation under the Vaccine Act”).
D. Consideration of Medical Literature
Both parties filed numerous items of medical and scientific literature, but not all such items
factor into the outcome of this decision. While I have reviewed all the medical literature submitted,
I discuss only those articles that are most relevant to my determination and/or are central to
Petitioner’s case—just as I have not exhaustively discussed every individual medical record filed.
Moriarty v. Sec’y of Health & Hum. Servs., No. 2015–5072, 2016 WL 1358616, at *5 (Fed. Cir.
Apr. 6, 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); see also Paterek v. Sec’y of Health & Hum. Servs., 527 F. App’x 875, 884 (Fed. Cir.
2013) (“[f]inding certain information not relevant does not lead to—and likely undermines—the
conclusion that it was not considered”).
34
ANALYSIS
Petitioner was unable to meet any of his causation prongs under Althen.
I. Althen Prong One
At the outset, I reiterate that the evidentiary standard for the first Althen prong is
preponderance. Boatmon, 941 F.3d at 1359 (Fed. Cir. 2019); LaLonde, 746 F.3d at 1339. Although
Petitioner has not directly challenged this legal conclusion, his briefing emphasized other
commentary and characterizations that the Federal Circuit has provided about the “can cause”
prong—and that in turn might stand for a slightly different, and effectively lower, standard. See
generally Petitioner’s Post-Hearing Brief, dated August 5, 2022 (ECF No. 133) (“Br.”), at 1–19.
Thus, his post-trial brief repeatedly notes that the theory offered by an expert must merely be
“reputable” (suggesting in turn that only evidence that the theory was not reputable—i.e., that it
would not warrant publishing in peer-reviewed articles, or would otherwise be soundly rejected by
the medical community—would be sufficient to rebut Petitioner’s showing), or that a “plausible”
theory suffices. Br. at 1–3, 11–12.
It is firmly established in the Vaccine Program that no particular class or type of evidence
must be included in the mix of proof (circumstantial and direct) a petitioner offers. See Perekotiy
v. Sec'y of Health & Hum. Servs., No. 16-997V, 2020 WL 12904810, at *13 (Fed. Cl. Spec. Mstr.
Apr. 20, 2020), mot. for review denied, No. 16-997V, 2020 WL 5887548 (Fed. Cl. Sept. 17, 2020)
(citing Andreu, 569 F.3d at 1378–79) (“[p]etitioners may satisfy the first Althen prong without
resort to medical literature, epidemiological studies, demonstration of a specific mechanism, or a
generally accepted medical theory”). Thus, for example, I cannot (and would not) dismiss a case
for failing to offer any epidemiologic evidence supporting a vaccine-injury association.
But the evidence a claimant offers must, in totality, always accomplish one thing in the
end: preponderantly establish that the vaccine(s) at issue more likely than not can cause the
relevant disease. Thus, the reputable quality of individual items of literature offered in the case, or
plausibility of a theory, does not mean this burden has been carried, unless the overall weight of
evidence (which includes evidence Respondent in rebuttal) balances out in a claimant’s favor. It
is not demanding certainty to find that certain items of literature or studies, no matter where
published, do not sufficiently aid Petitioner in crossing the preponderant “line,” especially after all
the evidence is weighed together. Application of any other standard amounts to asking that the
burden of proof be lowered. See L.C. v. Sec'y of Health & Hum. Servs., No. 17-722V, 2021 WL
3630315, at *19 (Fed. Cl. Spec. Mstr. July 2, 2021) (citing Hodges v. Secretary of Health & Hum.
Servs., 9 F.3d 958, 961 (Fed.Cir.1993) (“while ‘the [Vaccine Act] does the heavy lifting’ when a
claimant seeks to establish a Table injury, in the causation-in-fact context ‘the heavy lifting must
be done by the petitioner, and it is heavy indeed’)).
Here, it was not preponderantly demonstrated that UC can be vaccine-caused—and if so,
that the immunologic processes would work as proposed to cause it (even if UC is immune-
35
mediated, as the experts generally agreed). The associations between the specific vaccines in
question and UC, for example, were not well-established with sufficient evidence. Respondent, by
contrast, offered several individual reliable items of evidence (including studies performed in
association with initial vaccine safety trials) that found no causal relationship. See, e.g., Skufca at
5926; Dezfoli at 507–08; Chambrun II at 1414; Gardasil Package Insert at 8–9.58 While Petitioner
was never obligated to identify his own favorable epidemiologic evidence or direct proof of a
vaccine association, the existence of some evidence going the other way was reasonably included
in my evidentiary weighing process. Chambrun II was especially inconsistent with Petitioner’s
theory, since it specifically found no association between two of the three vaccines at issue and
IBD (and only deemed the LAIV a risk factor because of its inclusion of live viral components—
a danger at best in the context of existing IBD, and/or where a patient is receiving
immunosuppressive therapies).
The individual mechanistic theories offered by Dr. Rosenstreich were also inadequately
supported by reliable evidence, and ultimately were unpersuasive. His contention that molecular
mimicry, in particular, as an explanation for some of the processes leading to UC relied too much
on borrowing its substantiation with respect to other autoimmune diseases, even though the theory
is not a “one size fits all” credible explanation for all alleged vaccine-caused injuries. See McKown
v. Sec'y of Health & Hum. Servs., No. 15-1451V, 2019 WL 4072113, at *50 (Fed. Cl. Spec. Mstr.
July 15, 2019) (“[b]ut 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”) (emphasis in original).
In addition, a variety of additional evidence needed to bulwark Petitioner’s claim was not
provided. On the issue of molecular mimicry, for example, Dr. Rosenstreich’s theory did not rise
above plausibility, and was not bulwarked by studies or other evidence showing that mimicry in
this context was likely disease-causing or at least contributory. Dr. Rosenstreich could not identify
what specific components of any of the relevant vaccines might be at the center of such a process.
He at most posited the possibility of some cross-reaction between antibodies or T cells reacting to
HPV vaccine components and epithelial cells in the gut, even though the study relied upon for this
contention involved a protein not included in Gardasil. Compare Gardasil Package Insert at 12
58
There was some discussion at trial about the Gardasil Package Insert in particular, and the clinical trials it disclosed
did bear on whether IBD was a likely adverse event. But package inserts are generally afforded very little weight in
Vaccine Program cases as proof of causation. Christiansen v. Sec'y of Health & Human Servs., No. 08-244V, 2012
WL 6766650, at *12 (Fed. Cl. Spec. Mstr. Nov. 13, 2012). All vaccines covered by the Program are considered “safe”
for administration in an overall sense, but that fact never rebuts an individual claim that a vaccine might have caused
a specific injury (or even that in rare circumstances some vaccines might cause certain injuries more often). I thus
have not given this item of evidence significant weight in my overall balancing.
36
with Natale at 580. 59 The fact that many other autoimmune diseases can proceed this way does not
make up for this omission.
In so finding, I am not requiring Petitioner’s evidentiary showing to meet the “four factors”
Dr. Romberg relied upon in explaining why he did not deem molecular mimicry established as the
likely immune process underlying vaccine-caused UC. These factors do not constitute a court-
established test that must be met in Vaccine Act cases, independent from or in addition to a
claimant’s general obligation to establish the “can cause” prong preponderantly. The factor that
looks for epidemiologic support for molecular mimicry, in particular, is not something Petitioners
must ever demonstrate to prevail on the first Althen prong, as I have noted above (even though
epidemiologic evidence, to the extent it exists and is otherwise relevant to a claim, does bear on a
Petitioner’s success, and may be considered by a special master). My finding that Petitioner has
not persuasively established vaccine-caused molecular mimicry can result in UC is not a function
of my determination that all of these factors could not be satisfied.
However, Dr. Romberg persuasively explained why he took into account such factors in
assessing whether molecular mimicry reasonably applied in this case. His consideration of them
does not amount to his requiring certainty, or otherwise invalidates his opinion. In fact, he
expressly noted that he could not say for certain that Petitioner’s theory was wrong, even if he
rejected it overall. Tr. at 320–21. Rather, the factors reflect what knowledgeable members of the
relevant scientific community would deem important when determining if molecular mimicry
explains a likely disease process. I differentiate that from my own legal analysis of the evidence
(which would permit me to find causation even in the absence of reliable epidemiologic proof).
The role the innate response might play in the disease process—and specifically how it
would lead into, or encourage, a molecular mimicry-driven cross reaction—was also not
persuasively or reliably established by Dr. Rosenstreich. Little probative evidence was offered to
show an aberrant innate response would likely spark UC. Alum per se as an adjuvant ingredient
was not shown to constitute a risk factor—even when included in more than one vaccine, as here.
Reliance on alum as doing so bordered on the discredited Program theory of “ASIA” (autoimmune
syndrome induced by adjuvants). See, e.g., McGuinness v. Sec'y of Health & Hum. Servs., No. 17-
0954V, 2021 WL 5292343, at *17 n.17 (Fed. Cl. Spec. Mstr. Oct. 20, 2021); Morris v. Sec'y of
Health & Human Servs., No. 12-415V, 2016 WL 3022141, at *12 (Fed. Cl Spec. Mstr. Apr. 1,
2016); 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.
Spec. Mstr. Mar. 27, 2014), mot. for review den'd, 122 Fed. Cl. 86 (2015), aff'd, 645 F. App'x 1002(Fed. Cir. 2016). And such an immune-driven process would most likely be associated with a
59
In fact, Natale’s purpose to no small extent was to use its findings to argue for the importance of developing therapies
(including vaccines) that would allow the immune system to generate antibodies against the studied HPV16 E7
oncoprotein—thus underscoring the fact that the existing version of the vaccine (and certainly the one at issue in this
case) does not perform this function because it does not contain such an antigen. Natale at 580, 584.
37
closer-in-time reaction (i.e., some evidence of inflammation) or evidence of greater disease
manifestation, both of which are absent from the record (and indeed Dr. Rosenstreich was arguing
for a sub-acute process that would take more than two months to manifest with any recognizable
UC symptoms).
The argument about gut bacteria/immune equilibrium balance being impacted by
vaccination was similarly not bulwarked with evidence that this balance could be disrupted by
vaccination(s) received several weeks before onset. And Petitioner over-relied on classes of
evidence—case reports or VAERS data—to support a vaccine-injury relationship that are not
generally given much weight in Program cases, for the reasons provided by Respondent’s experts.
See, e.g., Tompkins v. Sec'y of Health and Human Servs., No. 10–261V, 2013 WL 3498652, at *16
(Fed. Cl, Spec. Mstr, June 21, 2013) (“VAERS is a stocked pond,” and its individual reports lack
scientific reliability), mot. for review den'd, 117 Fed. Cl. 713 (2014); Campbell v. Sec'y of Health
& Hum. 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,” even if they should
receive some weight). Such proof simply records instances in which UC, or a comparable
condition, temporally followed vaccination—not that evidence was derived (in a study or test or
some kind) that lent support to a causal association. The fact that any one case report was published
in a peer-reviewed journal, or serves as a signal worthy of further study, does not suddenly elevate
this class of evidence into something meriting greater weight. 60 And case reports for
distinguishable illnesses or involving different kinds of patients (Luca or Pauwels) were even less
probative.
60
In this vein, I do not find persuasive Petitioner’s citation to a 2012 publication by the Institute of Medicine (the
“IOM”) suggesting that case reports can stand as “strong mechanistic evidence” that can outweigh epidemiologic
studies involving larger numbers of subjects or vaccinations. Br. at 9 (citing Committee to Review Adverse Effects of
Vaccines, Adverse Effects of Vaccines: Evidence and Causality, 1, 46–47 (K. Stratton et al. eds., 2012), filed as Ex.
85 (ECF No. 116-3) (“Stratton”)). The citation has been taken out of context. Putting aside the fact that Petitioner
purported to file the entire text of a work more than 800 pages at length, the quote selected comes from a discussion
of the authors’ different “causality conclusions” for specific vaccines and injuries, and their explanations for certain
terms they employ therein. The cited section notes that they would employ the term “convincingly supports” where
vaccine causality evidence included “one case report in which convincing evidence exists that the vaccine indeed did
cause the adverse event,” adding that they would also consider “the detection of laboratory-confirmed, vaccine-strain
virus compelling evidence to attribute the disease to the vaccine-strain virus and not other etiologies.” Id. (emphasis
added). Stratton’s authors here also discussed the fact that they would associate a vaccine with a specific adverse event
despite epidemiologic evidence going the other way, but only where that evidence proved of “limited confidence or
insufficient.” Stratton at 47.
Thus, the cited portion from Stratton does not stand for the proposition that case reports alone—lacking other
corroborative proof, and without “laboratory-confirmed, vaccine-strain virus compelling evidence”—would carry the
day, that case reports always do so, or that they inherently outweigh epidemiologic studies that are not of “limited
confidence or insufficient.” Rather, it deems them significant when presented with other highly-reliable scientific
evidence linking the vaccine to an injury. It does not establish a basis for elevating case reports to a level of reliable
or probative evidence they are not presently provided in Program cases.
38
Overall, Dr. Rosenstreich’s opinion was not bulwarked with enough reliable independent
scientific/medical evidence to be persuasive—and the opinion he offered did not gain credibility
from demonstrated study of the immunologic issues it involved. Certainly (and ignoring his lack
of specific GI experience) Dr. Rosenstreich had sufficient qualifications to offer an opinion on the
purported immunologic processes due to vaccination that theoretically could cause UC. But he
relied on no specific research or experience of his own that could be brought to bear in support of
his theory (which applies to the specific context of a gastrointestinal disease). Although Dr.
Rosenstreich acted in good faith in offering the theory he did, his opinion ultimately seemed more
designed to serve the needs of Petitioner in this case than to reflect an independently trustworthy
view. Thus, (as he admitted a trial), he had attempted to support the theory based on reasoning
backward from the injury (Tr. at 76), and relied on literature searches conducted for this case rather
than his own expertise in immunologic/autoimmune illness (Tr. at 10).
Respondent’s testifying experts, by contrast, were collectively more credentialed, better
able to connect their testimony to their personal expertise, and proved significantly more
persuasive in explaining why the three vaccines Petitioner received could not likely cause UC,
based on their experiential understanding of the medical scientific issues as well as fair readings
of the filed literature. They persuasively rebutted Petitioner’s contention that his causation theory
was “legally probable,” and did not (as Petitioner has contended) apply a standard of certainty in
so determining. Br. at 9. And I found their rejection of Petitioner’s theory to be derived less from
a claim-oriented desire to assist their side to prevail, but more to reflect their own independent and
honest assessment of the theories and facts at issue.
Petitioner’s theory ultimately rested on a combination of the temporal association with
injury (as association that relies on a somewhat attenuated temporal period), the case and VAERS
reports of post-vaccination UC, and the theory’s “biological plausibility.” Tr. at 101. This does not
amount to a preponderant showing, even if individual items of evidence offered in this case had
their own specific reliability or reputability—or even if the core idea that vaccines could cause UC
has some degree of plausibility.
II. Althen Prong Two
The record does not permit the conclusion that any of the vaccines in question likely “did
cause” Mr. Cerrone to experience UC. First, no treaters ever proposed any association between the
vaccinations and Petitioner’s subsequent diagnosis. In fact, doctors expressed no hesitancy (and in
some cases even recommended) administering the remaining two doses of HPV vaccine in
commonly-prescribed regimen, as evidenced by the record. Ex. 1 at 4, 8, 12; Ex. 3 at 7; Ex. 5 at
1135. Second (and as noted above), the medical record is not consistent with Petitioner’s theory.
There is no evidence of any initial vaccine reaction that would reflect the start of an inflammatory
process, for example; no testing evidence that Petitioner possessed any putatively-causal
39
autoantibodies (ignoring that Petitioner never identified what they might be); 61 and no record
corroboration of the symptoms Petitioner reports experiencing in November 2015 (symptoms
which, it should be emphasized, are nonspecific for UC, not uncommon for teens to experience,
and which if present in UC would likely follow other manifestations—not precede them). 62 It
cannot even be concluded that Petitioner’s alleged fatigue and stamina issues were related to his
onset of UC several weeks later.
Petitioner’s rechallenge argument was similarly unsupported by the record. It is admittedly
the case that Petitioner more obviously worsened symptomatically after his receipt of a second
HPV vaccine dose in February 2016, and close in time to it as well. But the temporal gap between
any likely UC-related symptoms (which occurred no earlier than the end of December) and the
first HPV dose exceeded two months, evidencing no initial “challenge” that could reasonably be
measured against his medical history after the second dose. In addition, some of the initial records
(in February 2016) where Petitioner first complained of rectal bleeding suggest it had been ongoing
since mid to later January—even prior to the second HPV vaccine dose, and thus somewhat
undermining the contention that he had in fact worsened after it. Ex 2 at 25–26. It is as likely that
Petitioner was already progressing symptomatically, independent of the second dose. And then,
importantly, the third dose Petitioner received that summer reveals no further rechallenge at all.
This case thus does not provide the sort of facts where an initial vaccination prompts an identifiable
reaction, with a second, more pronounced reaction after the second vaccine exposure, thereby
supporting vaccine causality.
III. Althen Prong Three
The timeframe (measured from vaccination) in which Petitioner’s UC symptoms
manifested has not been shown to be medically acceptable. Although my first prong determination
impacts how the third Althen prong is resolved (because Petitioner cannot show the vaccines can
61
It also has not been established that Petitioner was genetically susceptible to injury of this kind. Although Petitioner
argues in his brief, with the support of his expert, that it “is probable that [he] has genes that uniquely make him
susceptible. . .”, there is nothing in the record to support this assertion. Br. at 19. He uses evidence from the Luca case
report, noting that the patient there had skin test results supportive of such findings. Luca at 362. But such testing did
not occur in this case.
62
Although I can accept for purposes of argument that Petitioner’s reported November 2015 symptoms did occur as
alleged, their lack of record corroboration limits their evidentiary utility—and Dr. Rosenstreich’s straightforward
reliance on their accuracy, over the actual records from the timeframe, is harmful somewhat to his opinions. For
example, it was not until November 3, 2015, when Petitioner fractured his wrist that there was a contemporaneous
medical record from the emergency room. Tr. at 108–09; Ex. 2 at 34. However, on this encounter Petitioner reports
only symptoms from pain and dull aching from the injury. Tr. at 111; Ex. 2 at 34. The next medical visit once again
lacked the reporting of symptoms discussed in Petitioner’s affidavit. Tr. at 111–12. Less than ten days later, Petitioner
was back in the ER on November 10th for a lacerated lip while at the movie theater. Tr. at 111; Ex. 2 at 30–31. During
this visit there was no record of fatigue, loss of stability, strength, or stamina. Tr. at 112.
40
cause UC, the onset of his UC is immaterial), this prong itself was not preponderantly established,
given Dr. Rosenstreich’s theory.
Although some of Petitioner’s symptoms allegations lack record corroboration, I accept his
contention that he first began to experience bloody stools in late December 2015 (December 27th
specifically, even though he delayed in reporting them to treaters for more than a month). Dr.
Liacouras (the most credentialed and qualified GI disease expert who offered an opinion in this
case) seemed comfortable with a December onset, even if he noted the medical records better
supported onset beginning in January 2016. Petitioner therefore needed to establish that an 81-day
(or more than 11 weeks) post-vaccination onset was medically acceptable. Petitioner offered some
reliable evidence to support a several-week onset (albeit for a variety of autoimmune diseases,
most of which are facially distinguishable from UC, like Schonberger). Indeed, Gradel (which was
specific to IBD and UC) posited a risk period of months to a year or longer (although it based its
findings not on vaccinations but gastroenteritis caused by bacterial infections, attenuating its
relevance to this context). Gradel at 498–99. The timeframe in this case from vaccination to
obvious UC manifestations falls within the four to five-month period Dr. Rosenstreich seemed to
allow as medically acceptable overall. Tr. at 89–90.
But Petitioner’s actual causation theory—which relied on a somewhat-confusing and
overlapping combination of innate and adaptive aberrant immune responses, occurring at different
stages—is ultimately not consistent with such a lengthy timeframe, nor does sufficient reliable
science support it. The theory as presented, and as connected to Petitioner’s actual history, relies
on his experiencing a mix of clinical and subacute reactions—with initial inflammation largely
due to the HPV vaccine alone or alum found in it plus the Hep. A vaccine, followed later by cross-
reactive autoantibody production, and then immune system balance dysfunction in the gut. But the
actual record does not reflect Petitioner’s theory for how, and when, UC would unfold or manifest
due to receipt of the Hep. A, HPV, and Flumist vaccines.
For example, the aspect of Petitioner’s theory that focuses on an innate response (likely
stimulated by the alum adjuvant) would reasonably involve some kind of reaction close-in-time to
the October vaccinations. But the medical record itself shows no immediate reaction to vaccination
at all, nor does it support the conclusion that a lengthy sub-acute process was underway,
manifesting only in late December. There is simply no medical record support that would establish
an aberrant, subacute immune response was occurring in November or most of December 2015,
that would (a) later manifest 81 days after vaccination, but (b) remain tolerable another four to six
weeks, before becoming severe enough to encourage Petitioner to seek emergency treatment. Dr.
Romberg, by contrast, persuasively established that a theory relying on an innate immune response
as aberrant and/or contributing to a later-manifesting disease should have record corroboration of
some initial reaction. Tr. at 225–26.
To get around this record omission, Petitioner alleges he did experience symptoms
associated with his later-diagnosed UC: fatigue or stamina loss/strength issues in November 2015.
41
Dr. Rosenstreich agreed (as indicated in his testimony from Petitioner’s rebuttal case) that the
initial symptoms alleged by Petitioner were important to his theory’s validity. Tr. at 333 (admitting
that disregarding the witness testimony of November fatigue or stamina issues would “weaken”
his feelings about the theory, and that Petitioner’s “descriptions of his symptoms I think are an
important part of my understanding of the development of his disease”).
But not only are these witness contentions lacking in corroboration (there is no medical
records reflecting stamina or fatigue issues), but these kinds of symptoms have not been shown to
be precursors of the more typically-expected UC symptoms. On the contrary, and as Dr. Liacouras
established, if stamina loss and fatigue occur in the context of UC, they would likely manifest only
later, as a result of anemia associated with bleeding caused by gut inflammation. Tr. at 152, 167–
68. At most, Petitioner offered some evidence specific to the HPV vaccine that unconvincingly
links it to fatigue. 63 And even if Petitioner had persuasively demonstrated that a common HPV
vaccine reaction is fatigue or stamina loss, he did not also show that this symptom (which
otherwise has not been associated with UC generally) could be both the transient product of one
of the three vaccines received, and also a precursor of the kinds of symptoms classically associated
with UC’s onset.
The other components of Petitioner’s causation theory relevant to onset timeframe were
also unsupported by sufficient reliable independent proof. He relied heavily on case reports, for
example, that were facially inconsistent with the timeframe at issue, with one in particular
involving an extremely short onset period not at all compatible to what occurred herein. Luca at
367. Other case reports involved distinguishable injuries. See generally Pauwels. Indeed, on the
question of onset generally, Petitioner referenced several items of literature having nothing to do
with UC. See, e.g., Schonberger at 112. I do not accept the suggestion that “any” autoimmune and
vaccine-caused illness is likely to occur in the same timeframe—such that findings in Schonberger,
for example, can be readily transposed to the present case.64
At the same time, animal models specific to IBD and UC suggested a very rapid response
time after insult—less than one week. See, e.g., Chassaing at 7–8. While I do not in this case make
a finding, generally, as to what period of time post-vaccination would be most “medically
acceptable” for vaccine-caused UC—and as noted, the 81-day post-vaccination timeframe is
63
In particular, Dr. Rosenstreich offered Ozawa, which discusses purported dysautonomic effects of the HPV vaccine
in Japanese girls. Ozawa at 1220. I have had the occasion in several prior cases to address Ozawa (specific to claims
that the HPV vaccine causes a variety of orthostatic issues), but have noted that it is not a reliable or persuasive item
of literature. See, e.g., McDonald v. Sec'y of Health & Hum. Servs., No. 15-612V, 2023 WL 2387844, at *5, 11, and
22 (Fed. Cl. Spec. Mstr. Mar. 7, 2023).
64
Schonberger is not fully supportive of Petitioner’s timeframe contentions in any event. It showed the autoimmune
process causing GBS peaking within two to three weeks, dwindling down significantly to no real risk by 10 weeks
(less than the 11-week period herein). First Romberg Rep. at 7; Schonberger at 112 Figure 4.
42
consistent with Dr. Rosenstreich’s opinion—this kind of evidence at least shows that a lengthy
timeframe has reliability issues that Petitioner’s evidence did not fully address or refute.
In the end, Petitioner’s onset contentions ultimately amount to an attenuated version of
what many claimants argue—that the fact of post-vaccination illness (even at some distant time
after vaccination) inherently implicates the vaccine. This kind of post hoc reasoning, however, has
never been deemed evidentiarily persuasive in the Program. Pafford, 451 F.3d at 1358. It is even
less so when the timeframe exceeds two months, 65 but where the medical record does not
corroborate the purported immune process at work.
CONCLUSION
A Program entitlement award is only appropriate for claims supported by preponderant
evidence. Here, Petitioner has not made such a showing. Petitioner is therefore not entitled to
compensation.
In the absence of a motion for review filed pursuant to RCFC Appendix B, the Clerk of the
Court SHALL ENTER JUDGMENT in accordance with the terms of this Decision.66
IT IS SO ORDERED.
/s/ Brian H. Corcoran
Brian H. Corcoran
Chief Special Master
65
Notably—and somewhat contradictory to Schonberger—most special masters have been unwilling to deem the
onset of GBS after the flu vaccine medically acceptable if onset exceeds six to eight weeks, or up to 56 days. See
Chinea v. Sec'y of Health & Hum. Servs., No. 15-095V, 2019 WL 1873322, at *29 (Fed. Cl. Spec. Mstr. Mar. 15,
2019) (citing Barone v. Sec'y of Health & Human Servs., No. 11-707V, 2014 WL 6834557 (Fed. Cl. Spec. Mstr. Nov.
12, 2014) (eight weeks is the longest reasonable timeframe for a flu/GBS injury)). An onset of nearly four weeks
longer, as here, would readily be rejected, underscoring why (even if I accepted Petitioner’s invocation of Schonberger
in a distinguishable context) the timeframe at issue is too great.
66
Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment if (jointly or separately) they file notices
renouncing their right to seek review.
43