Exum v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 21-1513V

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PORTIA EXUM, * Chief Special Master Corcoran

*

Petitioner, * Dated: May 27, 2025

*

v. *

*

SECRETARY OF HEALTH AND *

HUMAN SERVICES, *

*

Respondent. *

*

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Amber Diane Wilson, Wilson Science Law, Washington, DC, for Petitioner.

Mary Novakovic, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION ON REMAND 1

On June 25, 2021, Portia Exum filed a petition seeking compensation under the National

Vaccine Injury Compensation Program (the “Vaccine Program”). 2 Petitioner alleges that the

tetanus-diphtheria-acellular pertussis (“Tdap”) and measles-mumps-rubella (“MMR”) vaccines

she received on August 20, 2018, caused her to develop autoimmune hepatitis (“AIH”). Pet. at 1.

A one-day Entitlement Hearing was held on March 7, 2024, and after listening to the

witnesses’ testimony and evaluating the record, I determined that Petitioner was not entitled to

compensation. However, Petitioner prevailed on a motion for review, and the Court has ordered

me on remand to more fully describe the rationale for my conclusions (including my decisions to

accept, reject, and/or credit certain medical literature and expert testimony), and to revise my

analysis pertaining to alternative causes. Remand Order, dated Feb. 26, 2025 (ECF No. 82)

1

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 whole Ruling will be available to the public in

its present 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) (“Vaccine Act” or “the Act”).

Individual section references hereafter will be to § 300aa of the Act (but will omit that statutory prefix).

(“Remand Order”) at 44, 50–51. I have now done so—but I reach the same conclusion that I did

after hearing. For, as discussed below, Petitioner was unable to preponderantly establish that the

Tdap and MMR vaccines can cause AIH, or did so in her case.

I. Factual Background

Pre-Vaccination History

Ms. Exum was born on January 29, 1988. Prior to the vaccinations at issue, she had a

history of gastrointestinal reflux issues, small intestinal bacterial overgrowth, and kidney stones.

Ex. 2 at 9–12; Ex. 3 at 273–75, 265–71. Notably, during a May 2018 ER visit for treatment of

kidney stones, Petitioner’s AST and ALT levels (liver enzymes) were tested but found to be

normal. Ex. 3 at 268. She also reported to an endocrinologist (who she saw in July 2018 for follow-

up regarding her kidney stone issues) that she had been taking certain mushrooms as an immune

booster, in anticipation of a trip she planned for later that year. Ex. 1 at 14.

Petitioner began preparing for overseas travel to Kenya and Tanzania in mid-August 2018.

See Declaration, dated June 8, 2021, filed as Ex. 11 (ECF No. 7-2) (“Exum Decl.”) at 1 ¶7. As part

of that preparation, she received anti-malarial medication on August 17, 2018. Ex. 3 at 74. She

was instructed to begin taking the medication two days before visiting areas with high risk for

malaria, and to continue taking it for seven more days after leaving. Id. Three days later, on August

20, 2018, as additional preparation for her trip, she received the MMR and Tdap vaccines from her

employer’s health clinic, but declined the typhoid vaccine. Id. at 72–73; Exum Decl. at 1 ¶7.

Petitioner also at this time was provided traveler’s advisory information about risks of mosquito-

borne illnesses, diarrhea, and “malaria prophylaxis.” Ex. 3 at 72.

There is no medical record evidence that Petitioner experienced any immediate reaction to

either of the vaccines she received on August 20th, or any notable symptoms in the more than one-

week period before travelling abroad.

Post-Vaccination Period and Symptoms Onset

Petitioner traveled to Kenya and Tanzania as planned, from August 29 to September 8,

2018. Ex. 4 at 35; Exum Decl. at 1 ¶8. While abroad, she reports having received four or five bug

bites. Ex. 4 at 35. Upon return, she felt fatigued, and had symptoms of gastroesophageal reflux

disease (“GERD”) and indigestion in late September. Id.; Ex. 4 at 8. There is no other record

evidence from the month of September suggesting Petitioner was experiencing unusual

inflammation or signs of an infectious process.

2

Petitioner has alleged that she began to experience daily nausea in October 2018. Ex. 4 at

35; Exum Decl. at 1 ¶¶10–11. But there is no record evidence she sought treatment for it at this

time. At most, in a medical encounter in January 2019, Petitioner stated that her nausea felt

especially strong after a workout in mid-October. Ex. 4 at 8.

Later that same month, on October 26, 2018 (now over two months since the vaccinations

at issue—and six weeks after return from travel), Petitioner had a routine physical for life insurance

purposes. The record from this visit memorializes no complaints or reports of gastrointestinal

concerns, fatigue, or any other clinical symptoms. However, testing performed at this time revealed

the presence of elevated liver enzymes. Ex. 4 at 42 (ALT of 818 U/L with a 0-45 U/L normal

range, AST of 546 U/L with a 0-33 U/L normal range). She did not at this time, however, test

positive for biomarkers supporting the presence of inflammation, like “BUN” or creatinine, 3 and

she tested negative for Hepatitis C antibody (which would have suggested the presence of an acute

or chronic infection that could result in liver disease). Id. at 40–41.

Petitioner followed up with a gastroenterologist a month later, on November 28, 2018, to

address both the elevated liver enzymes and her ongoing nausea, as well as related GI symptoms.

Ex. 3 at 280. An abdominal exam was unremarkable, with no signs of liver enlargement or

tenderness. Id. A physician’s assistant (“PA”) noted her recent abnormal liver function tests,

however, and that Petitioner reported right-sided distress. Id. at 282. The PA recommended testing

for an H. pylori bacterial infection, and that Petitioner try an over-the-counter anti-acid medication,

plus diet modifications to ease her GERD and related symptoms. Id. Petitioner was also referred

to a hepatologist to have an MRI of her liver. Id. at 283. Test results two days after this visit showed

even higher AST and ALT levels, but yielded negative results for H. pylori. Id. at 67–69.

Petitioner’s next treatment event occurred over five weeks later, at a visit to her primary

care physician (“PCP”) on December 7, 2018. Ex. 3 at 61. She now reported upper right quadrant

abdominal pain, nausea, fatigue, and yellow eyes. Id. An abdominal exam was unremarkable, and

her PCP referred her to a hepatologist. Id. at 63. She also had her inter-uterine device (“IUD”)

removed on December 6, 2018, to eliminate it as a potential source for her liver-related issues. Id.

at 242–43. She then visited the same PCP on December 14, 2018. Id. at 57. She now reported that

she had not completed the antimalarial drug course prescribed for her, and that some “doctor

3

The BUN (or “blood urea nitrogen”) test is used to measure the amount of urea nitrogen in the blood. See Blood

Urea Nitrogen (BUN) Test, Mayo Clinic, https://www.mayoclinic.org/tests-procedures/blood-ureanitrogen/about/pac-

20384821 (last visited on May 27, 2025). Urea nitrogen is a chemical waste product usually removed from the body

through the kidney, so a higher-than-normal BUN test result can stand as evidence that the kidneys or liver may not

be working properly. Id. Creatinine is a chemical waste product produced by muscle metabolism, and also filtered out

by the kidneys (and thus a high reading is further proof of kidney issues). See Creatine Test, Mayo Clinic,

https://www.mayoclinic.org/tests-procedures/creatinine-test/about/pac-20384646 (last visited on May 27, 2025). An

elevated BUN to creatinine measurement is evidence of blood volume depletion. McKown v. Sec. of Health & Human

Services, No. 15-1451V, 2019 WL 4072113, at *15 (Fed. Cl. Spec. Mstr. July 15, 2019).

3

friends” of hers had expressed informal views that her condition could be the product of malaria

or other insect diseases resulting from big bites she had received while in Tanzania. Id.

The PCP ordered additional lab work, and referred her to an infectious disease specialist.

Ex. 3 at 59. The lab work again showed elevated AST and ALT, but autoantibody testing for

biomarkers associated with AIH (anti-nuclear antibodies and anti-smooth muscle antibodies) were

negative. Id. at 58.

On December 19, 2018, Petitioner saw hepatologist Dr. Omobonike Oloruntoba for

evaluation of her elevated liver enzymes. Ex. 3 at 232–38. Petitioner denied the presence of known

risk factors for liver disease, such as alcohol consumption or IV drug use, as well as any medicines

or supplements (with the exception of “starting Reishi mushrooms” at some unspecified time). Id.

at 232. She did, however, acknowledge taking antimalarial medication for ten days in connection

with her oversees travel in August-September. Id.

Dr. Oloruntoba noted that Petitioner displayed no signs of decompensated liver disease,

including icterus, jaundice, confusion, melena, hematochezia, hematemesis, bruising, weight loss,

or abdominal swelling, and an abdominal exam was again unremarkable. Ex. 3 at 232–33, 235.

But a liver MRI revealed the presence of two hyper-intense lesions consistent with adenomas

versus focal nodular hyperplasia (“FNH”), and asymmetric dilation of the left renal vein. Id. at

235–36. The diagnostic differential offered by Dr. Oloruntoba included “persistently elevated”

liver function tests (“LFTs”), but with a “negative serologic work up,” deeming lab results to be

“fortunately . . . not consistent with acute liver failure,” and hepatic adenoma versus FNH. Id. at

237. Additional lab results again showed elevated LFTs, but no signs of an active hepatitis

infection. Ex. 8 at 73. Dr. Oloruntoba ordered a liver biopsy and a repeat liver MRI with contrast

to be performed in six months. Ex. 3 at 237.

Subsequent Treatment for Hepatitis

Petitioner underwent the liver biopsy on January 3, 2019. Ex. 3 at 227–31. Results

established the presence of “marked chronic inflammation,” as well as “patchy moderate interface

necrosis.” Id. at 229. The findings were deemed by treaters to support a “broad differential

diagnosis” that included “infection, the effects of medications/drugs/herbal remedies, Wilson

disease, 4 and autoimmune hepatitis.” Ex. 3 at 229.

4

Wilson disease is a rare, inherited disorder in which the body fails to eliminate excess copper, leading to its

accumulation in organs such as the liver or eyes. Wilson Disease, Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=70938&searchterm=Wilson+disease (last visited on May 27,

2025). The build-up of copper can cause significant organ damage and various symptoms, including liver problems.

Id.

4

The next day, Petitioner saw hematology and oncology specialist Dr. Charles Eisenbeis,

who prepared a write-up/summary of his views on January 12, 2019. Ex. 3 at 221–26. The medical

history obtained at this time was consistent with what is described above—that testing had begun

to reveal abnormal LFTs in October 2018 and remained elevated thereafter, along with the liver

MRI findings. Id. at 223. Dr. Eisenbeis also noted, however, that Ms. Exum had experienced no

more than mild fatigue as a clinical symptom, and that she had not tested positive for the presence

of hepatitis B or C. Id. And his own physical exam revealed nothing but the prior-reported nausea

plus dyspepsia. Id. at 225.

Dr. Eisenbeis observed elevated serum ferritin (iron) levels, which he attributed to

“obvious liver disease” (adding that testing for a hereditary condition that could cause excess iron

deposits was negative). Ex. 3 at 222. He also suggested Petitioner was experiencing hepatitis, but

noted that “[w]orkup so far has been unrevealing for a cause of her liver disease.” Id.

In mid-January, Petitioner received additional treatment for kidney stones and the lower

quadrant pain/nausea she had previously reported. Ex. 2 at 28–30. Labs from this visit also revealed

“very elevated” ALT and AST levels. Id. at 28. Petitioner also purports to have received an AIH

diagnosis around this time frame—although no direct record proof has been offered in which Dr.

Oloruntoba, or any other qualified hepatologist, is memorialized to have offered this diagnosis.

On January 29, 2019, petitioner saw an infectious disease specialist, Henry Wu, M.D., for

a second opinion regarding the purported AIH diagnosis she had just received. Ex. 4 at 6. At this

time, her international travel from the early fall of 2018 was discussed, and she reported that she

had entered bodies of water (“she did swim in the Indian Ocean and was in a bay to wade in the

water to access the boats”), received several insect bites, and had felt extreme fatigue upon return.

Id. at 8. Dr. Wu noted that Petitioner was taking a four-to-six-week course of prednisone. Id. at 6.

He affirmed Petitioner’s hepatitis diagnosis (deeming it more likely chronic than attributable to an

acute infection) and ordered lab work. Id. at 8. The results revealed Petitioner had experienced an

Epstein-Barr viral infection at some prior point. Id. at 12; Ex. 3 at 207. Her LFTs had also improved

but were still elevated. Ex. 3 at 204. Otherwise, no infectious explanation for Petitioner’s AIH

could be identified. Id. at 7.

Petitioner’s LFT levels thereafter trended downwards during February and March 2019.

Ex. 3 at 43–51. During a GI visit for reflux management in February, Petitioner’s treater noted that

she was taking kidney-oriented medication in addition to the prednisone to treat her liver issues.

Id. at 197. Her PCP later noted in April 2019 that her AIH was “improving.” Id. at 36–37. A visit

to a hepatologist that same month revealed continued LFT improvement, although levels remained

above normal. Id. at 192–96. She also continued to report some ongoing fatigue. Id. at 34.

5

Petitioner visited her hepatologist again in August 2019. Ex. 3 at 162–65. Her LFTs

remained elevated, and the hepatologist ordered a metabolic screen to rule out hepatoxicity, and

instructed her to continue with her previously-prescribed medications. Id. at 165. Labs taken

shortly thereafter in September 2019 showed slightly elevated LFTs, but otherwise normal results.

Id. at 20–31.

By the first half of 2020, Petitioner’s liver concerns had mostly resolved, and testing from

this time to 2022 revealed normal LFTs. Ex. 10 at 56–61; Ex. 3 at 154. A repeat liver biopsy

performed in February 2021, however, showed “chronic hepatitis with minimal interface activity

and mild portal fibrosis (stage 1 of 4).” Ex. 14 at 41; Ex. 15 at 83. But a hepatology follow-up in

March 2022 revealed no signs of liver disease, and the latest records filed in this case show no

signs of liver disease through November 2023. Ex. 14 at 36–41; Ex. 46 at 6–7.

II. Hearing Witnesses

A. Petitioner’s Expert – Dr. Robert Gish, M.D.

Dr. Gish prepared two reports in this case. Gish First Report, dated July 11, 2022, filed as

Ex. 16 (ECF No. 18-1) (“First Gish Rep.”); Gish Supplemental Report, dated Mar. 21, 2023, filed

as Ex. 38 (ECF No. 28-1) (“Second Gish Rep.”). He also testified at the hearing. Tr. at 5–116. Dr.

Gish was the sole expert presented at trial in support of Petitioner’s claim.

Dr. Gish received his M.D. from the University of Kansas, and completed his internship

and residency at the University of California, San Diego. Curriculum Vitae, filed on July 11, 2022,

as Ex. 37 (ECF No. 20-1) (“Gish CV”) at 3. He then completed a fellowship in gastroenterology

and hepatology, with a special rotation in liver transplantation, at UCLA. Id. He is board-certified

in internal medicine and gastroenterology, and has a separate board certification for hepatology

that is part of the Certificate of Advanced Qualification in liver transplantation. Id. at 2. He is a

member of multiple professional societies including the National Viral Hepatitis Round Table, the

American Association for the Study of Liver Disease, and the American Liver Foundation. Id. at

4. He is a licensed physician in California, Arizona (inactive), and Nevada. Id. at 2. He has been

active as a clinician and researcher for thirty-six years and has served on the editorial boards of

many prestigious journals in his field, including Hepatology and the Journal of Viral Hepatitis.

Gish First Rep. at 1.

Presently, Dr. Gish is a Clinical Adjunct Professor of Medicine at the University of Nevada

School of Medicine in both Reno and Las Vegas, and UCSD Skaggs School of Pharmacy and

Pharmaceutical Sciences. Gish CV at 1. He is also the Medical Director of the Hepatitis B

Foundation, which is the nation’s leading nonprofit research and advocacy organization for

hepatitis B (HBV). Id. Dr. Gish acknowledged, however, that he is not an expert in immunology

6

(and significantly for purposes of this decision, no such expert was presented by Petitioner). Tr. at

90.

Dr. Gish began his testimony by discussing Petitioner’s medical history prior to

vaccination—which he deemed not to suggest the existence of developing liver disease or

alternative causes. Tr. at 15. For example, she had no physical exam results indicating liver issues,

and four normal liver panel tests before receiving the vaccine. Id. When a patient has normal liver

enzyme tests, “the chance of that person having active liver disease that is hidden in some way is

extremely small.” Id. at 18. He also noted that liver disease patients typically present with

symptoms like fatigue, liver pain, jaundice, rashes, and mental confusion. Id. at 19. When

reviewing Petitioner’s medical history, Dr. Gish looked for common causes of liver disease, such

as alcoholism, needle sharing, high-risk sexual behavior, and having medical procedures in

developing countries—but no such factors were evident. Id. at 19–20. Dr. Gish further pointed out

that Petitioner had tested negative for Epstein-Barr virus and Hepatitis B and C, which are also

significant risk factors. Id. at 22.

Dr. Gish admitted that Petitioner’s receipt of anti-malarial medication before traveling to

Africa was a risk factor for AIH, “but that’s typically brief, transient, and doesn’t result in

autoimmune disease long-term.” Tr. at 22. He compared Petitioner’s course to that of the patient

in a case report whose hepatitis presented acutely after taking an anti-malarial medication. Id.; B.

Beretta-Piccoli et al., Atovaquone/Proguanil-Induced Autoimmune-Like Hepatitis, 1 Hepatology

Comm. 293 (2017), filed as Ex. A Tab 10 (ECF No. 25-10) (“Beretta-Piccoli”). The patient

evaluated in Beretta-Piccoli displayed symptoms like jaundice and dark urine—obvious clinical

signs of liver disease, but unlike Petitioner (at least when her elevated LFT levels were first

observed). Tr. at 82; Beretta-Piccoli at 293. Further, Petitioner had already stopped taking all of

her medications and supplements after receiving her October 2018 lab results. Tr. at 80. Thus, had

the two herbal supplements Petitioner had been taking caused her elevated liver enzymes, the

levels should have normalized once she stopped taking them—but she continued to have elevated

liver enzymes. Id. The above, plus Dr. Gish’s view that her disease onset had begun within a few

weeks of vaccination, permitted him to conclude that she fit the “ideal profile” for an adverse

reaction to the vaccine. Id. at 22.

In proposing how the vaccines Petitioner received could have caused AIH, Dr. Gish

focused on the measles component of the MMR vaccine as capable of triggering an immune-

mediated disease process. Tr. at 38. AIH, he maintained, would usually be initiated by some kind

of environmental trigger. Id. at 23. The MMR vaccine Petitioner received is an attenuated but live

vaccine, which contains components that can “live in the body as a virus” and thereby “manipulate

the immune system.” Id. at 35; First Gish Rep. at 11. As a result, the measles component could

temporarily suppress the immune system so that the virus can replicate and persist. Tr. at 36. In an

individual with a functioning immune system, regulatory safeguards can turn back on, regulating

7

the virus and shutting down the immune response. Id. But Petitioner’s immune response remained

chronically activated. Id. at 49.

In support, Dr. Gish pointed to filed literature that he maintained established the capacity

of the MMR vaccine to suppress the immune response, in ways comparable to the wild measles

virus. Tr. at 38–42; R. Nanan et al., Measles Virus Infection Causes Transient Depletion of

Activated T. Cells from Peripheral Circulation, 12 J. of Clin. Virology 201 (1999), filed as Ex. 31

(ECF No. 19-7) (“Nanan”); T. Munyer et al., Depressed Lymphocyte Function after Measles-

Mumps-Rubella Vaccination, 132 J. of Infectious Diseases 75 (1975), filed as Ex. 32 (ECF No.

19-8) (“Munyer”); First Gish Rep. at 22 (“[s]ufficient clinical studies confirm that MMR vaccine,

even though attenuated, can induce a temporary immune suppression that can last for months”).

Here, the suppression of bystander immune cells by the measles virus component of the

vaccine allowed an autoimmune cross-reaction to occur. Tr. at 58. Dr. Gish proposed that the

pathogenic mechanism responsible for the onset of Petitioner’s AIH involved the breaking of self-

tolerance to hepatic autoantigens (located on the surface or in the mitochondria of liver cells). Id.

at 54–55. Normally, a healthy person’s immune cells will not cross-react with these hepatic

autoantigens, in part from T cell regulation. Id. But when T cells are dysregulated, they can

incorrectly recognize the hepatic autoantigens on a person’s liver cells as being foreign—and

attack them. Id. at 58. Dr. Gish thus theorized that, in clearing the vaccine-induced measles

infection from Petitioner’s body, non-measles specific immune cells remained chronically

activated thereafter, resulting in a persistent autoimmune condition affecting her liver. Id. at 46–

49.

In addition, Dr. Gish maintained that the measles component of the MMR vaccine could

directly infect immune cells. Tr. at 38; L. Rennick, Live-Attenuated Measles Virus Vaccine Targets

Dendritic Cells and Macrophages in Muscle of Nonhuman Primates, 89 J. of Virology 2192-2000

(2015), filed as Ex. 33 (ECF No. 19-9) (“Rennick”). This was additional confirmation of the

possibility that the measles virus could not only persist in the body post-vaccination but could

negatively impact immune function (or at least engage in ongoing immune suppression). First Gish

Rep. at 20, 23.

An autoimmune reaction to the measles vaccine was likely compounded by Petitioner’s

simultaneous receipt of the Tdap vaccine. Tr. at 62. 5 Petitioner’s age and records confirmed for

5

Dr. Gish’s initial report also suggested that an adjuvant (a compound included in a vaccine to boost immunogenicity)

in the Tdap or MMR vaccine may have also played a role in causing injury. First Gish Rep. at 10, 21, 23. However,

at trial he explicitly stepped away from reliance on this possible mechanism. Tr. at 60, 166–68. This was wise—the

Program has consistently rejected causation theories relying on the pathogenic impact of vaccine adjuvants. McKown

v. Sec'y of Health & Hum. Servs., No. 15-1451V, 2019 WL 4072113, at *50 (Fed. Cl. Spec. Mstr. July 15, 2019)

(noting that the ASIA theory, “which posits the aluminum vaccine adjuvant as contributing to the purported pathologic

immune response, is especially suspect from a scientific standpoint”) (citations omitted).

8

Dr. Gish the fact that Petitioner had previously received a whole cell pertussis-containing vaccine

(since replaced by the acellular form due to concerns about adverse events). First Gish Rep. at 12,

21–22. Studies have established the need for pertussis boosters to maintain immunity—and also

that production of a specific kind of T helper cell 6 “believed to play an important role in the

development of a variety of autoimmune diseases, including autoimmune liver disease” is

encouraged in individuals who had previously received the whole cell pertussis form of the

vaccine, but then receive as a booster the acellular form. Id. at 22; F. Lafdil et al., Th17 Cells and

Their Associated Cytokines in Liver Diseases, 7 Cellular & Molecular Immuno. 250–54 (2010)

(ECF No. 20-2) (“Lafdil”). 7 The antigen-specific response generated by this booster vaccine may

have amplified the existing response to the measles vaccine, and also itself peaked more quickly

(since Petitioner was receiving a booster). Tr. at 62; First Gish Rep. at 23.

As additional support for causation, Dr. Gish relied on a number of case reports (discussed

below). He deemed them reasonable evidence of causation under the circumstances, since vaccine

injury was rare as a general matter, and given the absence of relevant larger-scale epidemiologic

studies. Second Gish Rep. at 1–2. Case reports, he proposed, were at least “signals of issues to be

aware of” for clinicians, and they stood as real-world evidence of how a proposed theory might

actually unfold. Id. at 2, 3 (“if something did happen in another person, then logically the event

can happen in this patient”). At the same time, Dr. Gish accepted the possibility of mere

coincidence between receipt of a vaccine and development of AIH. Id. at 1.

Dr. Gish then briefly discussed an item of literature that he proposed established a

secondary explanation for how an individual like Petitioner might experience AIH. See S.

Subramanian et al., Postinfectious Autoimmune Hepatitis-Induced Liver Failure: A Consequence

of Hepatitis A Virus Infection, 7 ACG Case Reports J. 1 (2020), filed as Ex. 25 (ECF No. 19-1)

(“Subramanian”). But he did not reference Subramanian for its primary findings (which focused

on how a hepatitis A wild virus infection could secondarily result in autoimmune hepatitis), but

instead for a separate item of literature it discussed, “Vento” (which Petitioner never filed in this

case). 8 In Vento, researchers followed family groups that developed autoimmune hepatitis after

hepatitis A infections. Tr. at 66–68. The results of the Vento study supported the concept that a

genetic disposition could render patients susceptible to AIH, and Dr. Gish felt that this in turn

6

T helper cells are a kind of immune cell that assist B cells in the production of antibodies. Zacharski v. Sec'y of

Health & Hum. Servs., No. 21-317V, 2025 WL 1235431, at *18 (Fed. Cl. Spec. Mstr. Mar. 26, 2025). They serve a

different purpose from the type of T cells responsible for directly attacking foreign pathogens.

7

Although Lafdil is identified on Petitioner’s Exhibit List (ECF No. 45-4) as Exhibit 35, it is erroneously marked as

Ex. 36 in the filed copy.

8

See Exhibit List, filed December 26, 2023 (ECF No. 45-4). Despite the fact that Vento was never filed as evidence

in this case, Dr. Gish characterized it as a “very, very interesting and compelling report,” as well as “a[n] excellent

paper that would describe what happened to Ms. Exum.” Tr. at 67, 69. It is exceedingly difficult to understand why

Petitioner (despite demonstrated opportunity) never chose to file this article, if it is in fact so compelling and

persuasive.

9

suggested that Petitioner was likely genetically susceptible as well. Id. at 69. But he admitted that

no genetic testing had been performed that would corroborate the contention about Petitioner’s

susceptibility. Id. at 96. (And of course, as already noted, the vaccines Petitioner received did not

include hepatitis A).

Dr. Gish also reviewed Petitioner’s clinical course, deeming it consistent with his causal

theory. Tr. at 70. In particular, he opined that Petitioner’s AIH symptoms onset began within an

acceptable timeframe for an environmental trigger (in this case the vaccine). Id. He pointed to

Petitioner’s fluctuating but elevated liver enzymes (as evidenced by test results obtained between

October 2018 and January 2019) as establishing the existence of ongoing AIH, confirmed by the

biopsy taken in January 2019. Id. at 70–74, 75. Thus, he concluded that “the timing of symptoms,

the timing of laboratory tests, the liver biopsy, all fits a classic triggering event and onset of

autoimmune disease.” Id. at 82.

Dr. Gish did not provide a precise proposal for Petitioner’s most likely true onset, however.

On the one hand, in his first expert report he seemed to embrace the discovery of elevated LFT

results, in connection with Petitioner’s October 26, 2018 physical exam (occurring 68 days post-

vaccination) as a significant evidentiary point establishing the presence of AIH at that time. First

Gish Rep. at 24; Second Gish Rep. at 10. But during the hearing, he refined his view, maintaining

that onset likely occurred sometime before these testing results were obtained. Tr. at 114.

Ultimately, Dr. Gish seemed to embrace any onset as occurring within ten weeks of vaccination

as medically acceptable. Id. at 70. But he also seemed to view a timeframe of up to five or six

months as acceptable, based on science suggesting that the immune response could remain robust

for such a period of time. Second Gish Rep. at 10; Claire-Anne Siegrist, Vaccine Immunology, in

Plotkin’s Vaccines 16-34 (S. Plotkin et al. eds., 7th ed. 2018) (“Siegrist”), filed as Ex. 20 (ECF No.

18-5).

On cross-examination, Dr. Gish acknowledged that he has seen patients who developed

AIH after traveling, and after taking herbal supplements as well. Tr. at 91–92. He denied that

Petitioner’s previous small bowel overgrowth (“SIBO”) could have caused her AIH, explaining

that SIBO is linked to a specific type of AIH which Petitioner did not have. Id. at 94. He

acknowledged that Petitioner’s AIH could have been idiopathic, however, and admitted that an

environmental trigger can typically only be identified in half of cases. Id. at 95.

When asked about the molecular mimicry aspect of his causal theory, Dr. Gish agreed that

he had not identified a specific homology between any amino acid sequences found in proteins of

the relevant vaccine components and liver proteins. Tr. at 108. He also attempted to further explain

the immune suppression mentioned in his earlier testimony and report, and how the MMR vaccine

“both suppresses and activates the immune system” at the same time. Id. at 112–16. He specified

that the innate immune response is suppressed, leading the adaptive immune response to

10

compensate. Id. at 113. Concurrently, a variety of antigen-presenting cells are activated, producing

“off-target effects.” Id. Then, in a genetically susceptible individual, “[y]ou end up stimulating an

arm of the immune system that isn’t getting turned off. These are the T-regs that are suppressed in

some ways or can[no]t be activated and the immune system goes down this long pathway.” Id.

B. Respondent’s Experts

1. Jeffrey Crippin, M.D. — Dr. Crippin authored one report in this case, and

testified at the hearing. Crippin Report, dated Oct. 31, 2022, filed as Ex. A (ECF No. 23-1)

(“Crippin Rep.”); Tr. 117–41.

Dr. Crippin received his medical degree from the University of Kansas, and completed an

internal medicine residency at Kansas University Medical Center, where he served as chief

resident. Curriculum Vitae, dated Mar. 4, 2024, filed as Ex. E (ECF No. 56-1) (“Crippin CV”) at

1–2. He then completed a three-year fellowship in Gastroenterology and Hepatology at the Mayo

Clinic in Rochester, Minnesota. Crippin CV at 2. He currently works at the Barnes-Jewish Hospital

in St. Louis, and is a Professor of Medicine at the Washington University School of Medicine. Id.

at 1. He is board certified in internal medicine and gastroenterology, and has received the

Certificate of Added Qualification in transplant hepatology. Id. at 6–7. He has extensive

experience in treating patients with autoimmune hepatitis—he has treated 300–400 patients with

the disease over the course of his career. Crippin Rep. at 1.

Dr. Crippin agreed with Petitioner’s AIH diagnosis, but denied that the vaccines she

received were more likely than not the cause of her illness. Tr. at 123. Rather, he pointed out

numerous other potential causal factors in her record, although he was unable to specify one as

most likely. Id. at 125–27. These factors included Petitioner’s international travel in the months

prior to her illness; her use of anti-malarial medication and herbal supplements; and a prior history

of kidney stones, an IUD, and her SIBO. Id. at 125–27, 128–29. Further, she had tested positive

for Epstein-Barr virus antibodies in December 2018. Id. at 127; Ex. 3 at 207. Dr. Crippin admitted,

however, that it was impossible to determine when she had Epstein-Barr from that test (“[i]t could

have been earlier that year, it could have been five years ago”). Tr. at 127. Although Petitioner

experienced fatigue (a symptom of the virus) upon returning from travel, she was not tested for

the virus at the time. Id. at 128. He also noted that a large number of AIH cases are idiopathic,

meaning that no specific trigger can be identified. Id. at 130.

Dr. Crippin then discussed one of the case reports Petitioner filed most relevant to this case,

pointing out differences from Petitioner’s clinical course. Tr. at 131; W. Saliba & M. Elias, Acute

Hepatitis Following MMR Vaccination, 16 Euro. J. of Internal Med. 379 (2005), filed as Ex. 21

(ECF No. 18-6) (“Saliba”). Although Saliba involved the MMR vaccine, it featured a patient who

experienced acute hepatitis rather than AIH, with a post-vaccination onset of two weeks (not the

11

six to eight weeks likely in this case). Tr. at 131–32; Saliba at 379. The Saliba patient had also

recently given birth, putting her at greater risk of viruses due to pregnancy-related immune

suppression, and no liver biopsy was performed to help determine the cause of her hepatitis. Tr. at

131–32; Saliba at 379.

Dr. Crippin also noted that he had been unable to locate any controlled studies showing a

link between AIH and either the MMR or Tdap vaccines. Tr. at 130. And he similarly was unaware

of studies establishing that the combined administration of both vaccines at once constituted a risk

factor for AIH. Id. at 133. On cross, he reiterated his prior testimony that he could not determine

when Petitioner was infected with Epstein-Barr virus, and that there were no other infections noted

in her records. Id. at 135. Ultimately, Dr. Crippin declined to identify which of the various factors

he deemed the most likely cause, and stated again that this could be an idiopathic case. Id. at 137–

38, 140–41.

2. Andrew MacGinnitie, M.D., Ph.D. — Dr. MacGinnitie wrote one report in

this case, and testified at the hearing. MacGinnitie Report, dated Oct. 27, 2022, filed as Ex. C (ECF

No. 23-3) (“MacGinnitie Rep.”); Tr. at 141–92.

Dr. MacGinnitie is the Chief of the Division of Allergy, Asthma, and Immunology at

Children’s Hospital of Wisconsin, and a Professor of Pediatrics at Medical College of Wisconsin.

Tr. at 142–43. He graduated from the University of Chicago Pritzker School of Medicine with both

an M.D. and a Ph.D. from the Department of Pathology. Curriculum Vitae, dated Oct. 31, 2022,

filed as Ex. D (ECF No. 23-4) (“MacGinnitie CV”). He then completed a residency in pediatrics

in the Boston Combined Residency Program, training at Boston Children’s Hospital and Boston

Medical Center, followed by an allergy/immunology fellowship at Boston Children’s Hospital. Id.

at 1. He is board certified in both allergy/immunology and pediatrics. Id. at 11. He maintains an

active clinical practice seeing more than 1600 patients annually and has extensive experience in

caring for children and adults with a variety of immunologic diseases, including reactions to

vaccines. MacGinnitie Rep. at 2. Dr. MacGinnitie also performs research and has published articles

in a number of areas related to allergy/immunology including food allergy, vaccine reactions, and

primary immunodeficiency. Id. Dr. MacGinnitie was the sole immunology expert to offer

testimony in this case.

Dr. MacGinnitie opined that the vaccines Petitioner received had no likely relationship to

her AIH. Tr. at 148. First, he criticized Dr. Gish’s reliance on case reports (in the absence of

epidemiological studies connecting AIH and the Tdap and MMR vaccines). Id. at 150. In his view,

case reports cannot reliably connect a vaccine to an illness because they do not provide an accurate

comparison with the baseline rate of an illness in the general population. Id. Further, none of the

case studies filed involved instances of simultaneous administration of the Tdap and MMR

vaccines. Id. at 151; see, e.g., M. van Gemeren et al., Vaccine-Related Autoimmune Hepatitis: The

12

Same Disease as Idiopathic Autoimmune Hepatitis? Two Clinical Reports and Review, 52

Scandinavian J. of Gastroenterology 18 (2017) (involving a combination of Tdap and hepatitis A

vaccines), filed as Ex. 26 (ECF No. 19-2) (“van Gemeren”); see also P. Perumalswami et al.,

Vaccination as a Triggering Event for Autoimmune Hepatitis, 29 Seminars in Liver Disease 331

(2009) (discussing hepatitis A and yellow fever vaccines), filed as Ex. 27 (ECF No. 61)

(“Perumalswami”). And although Saliba did involve the MMR vaccine, the relevant patient only

experienced an acute form of hepatitis. Tr. at 152; Saliba at 379. In another case report offered by

Dr. Gish, the patient received six vaccines at the same time, and although the MMR vaccine was

one of them, it was impossible to isolate the effects of only one or two of the listed vaccines. Tr.

at 152–53; G. Veerappan et al., Vaccination-Induced Autoimmune Hepatitis, 50 Digestive Diseases

and Sci. 212 (2005), filed as Ex. 24 (ECF No. 58-1) (“Veerappan”).

Second, Dr. MacGinnitie took issue with Petitioner’s invocation of molecular mimicry as

a possible mechanism for vaccine-induced AIH. Tr. at 156. After explaining the concept briefly,

he noted that Dr. Gish had not identified any specific homology (meaning molecular similarity)

between amino acid sequences in the vaccines’ protein components and the liver cell antigens

where an autoimmune cross-reaction would begin or occur—a crucial starting point if molecular

mimicry was to stand as a reasonable explanation for Petitioner’s injury. Id. at 158. Moreover,

even a demonstration of homology would not be sufficient to prove the theory in Dr. MacGinnitie’s

view, as there is a “massive overlap between microbial and human proteins” in nature that does

not commonly result in autoimmunity. Id. He also criticized Petitioner’s reliance on bystander

activation of secondary/nonspecific immune cells as a possible disease mechanism, noting that

articles filed in the case specific to AIH did not consider this to be a pathologic explanation. Id. at

160; C. Mack et al., Diagnosis and Management of Autoimmune Hepatitis in Adults and Children:

2019 Practice Guidance and Guidelines from the American Association for the Study of Liver

Diseases, 72 Hepatology 671 (2020), filed as Ex. A, Tab 1 (ECF No. 25-1) (“Mack”). Beyond this,

Petitioner had not displayed clinical signs of significant inflammation, which would have occurred

shortly after vaccination had such an autoimmune response been underway. Tr. at 159.

Dr. MacGinnitie also addressed Petitioner’s argument that her immune system was likely

suppressed by the measles vaccine, allowing an autoimmune response to occur. He noted the

absence of strong evidence showing that the measles vaccine (as opposed to the wild virus)

suppresses the immune system pathologically. Tr. at 162; MacGinnitie Rep. at 8–9. He deemed

articles filed to support this contention as lacking in clinical value and/or outdated. Tr. at 162–64;

Nanan (published in 1999); Munyer (published in 1975). Up-to-date clinical manuals relied upon

by treaters, however, acknowledge the immune-suppressive nature of the wild measles virus, but

not the vaccine (the receipt of which functions to prevent this immune suppression in the first

place). Tr. at 165–66; American Academy of Pediatrics, Red Book (2021): Report of the

Committee on Infectious Diseases 503 (32d ed. 2021), filed as Ex. C, Tab 4 (ECF No. 26-4) (“AC

of Pediatrics”); see also M. Mina, Measles, Immune Suppression, and Vaccination: Direct and

13

Indirect Nonspecific Vaccine Benefits, 74 J. Infection S10, S15 (2017), filed as Ex. C, Tab 3 (ECF

No. 26-3) (“Mina”) (noting the benefit of measles vaccine in blunting the immunosuppressive

character of a wild measles virus infection). Dr. MacGinnitie also noted that a theory dependent

on immunosuppression did not fit with AIH’s likely pathogenesis. Since AIH is considered

autoimmune in character, it reflects an aberrantly overstimulated/overactive immune process—not

one that has been suppressed (allowing another opportunistic infectious process might occur). Tr.

at 162.

Dr. MacGinnitie challenged Dr. Gish’s argument that whole cell pertussis 9 could itself

stimulate a class of T-helper cells (which encourage the production of certain proinflammatory

cytokines)—and thus, because Petitioner had likely received the whole cell pertussis vaccine as a

child, the Tdap booster she had received in 2018 might have increased the possibility of a

comparable immune memory response. Tr. at 169. He acknowledged the importance of the

relevant T-helper cells in fighting bacterial and fungal infections, but deemed the re-stimulation of

them unlikely to cause autoimmune disease. Id. at 170. Thus, although Petitioner had offered a

study showing that patients vaccinated with whole cell pertussis produced more inflammatory

cytokines than those initially vaccinated with acellular pertussis, the study did not also establish

that the produced cytokines rose to levels anywhere near sufficient to propagate an autoimmune

inflammatory environment. Id. at 171–72; R. da Silva Antunes et al., Th1/Th17 Polarization

Persists Following Whole-Cell Pertussis Vaccination Despite Repeated Acellular Boosters, 128 J.

Clin. Investigation 3853 (2018), filed as Ex. 34 (20-1) (“da Silva Antunes”). And since Petitioner

had not been tested for these cytokines, it was pure speculation to propose she likely possessed

them in pathologic levels after vaccination. Tr. at 173.

Dr. MacGinnitie concluded with a brief consideration of the onset interval of one to five

months Dr. Gish proposed for vaccine-induced AIH. Tr. at 174. Although he opined that case

reports should carry little evidentiary weight, he noted that the case reports Dr. Gish cited showed

documented hepatitis (not simply the first symptoms) beginning within a far shorter timeframe:

ten to thirty days of vaccination. Id.; see, e.g., T. Sasaki et al., Autoimmune Hepatitis Following

Influenza Virus Vaccination: Two Case Reports, 97 Med. 1 (2018), filed as Ex. 28 (ECF No. 19-

4) (“Sasaki”) (documenting one week onset and one month onset). Other items of literature

Petitioner referenced for a shorter onset timeframe involved distinguishable diseases or vaccines.

Tr. at 175–76; L. Schonberger et al., Guillain-Barré Syndrome Following Vaccination in the

National Influenza Immunization Program, United States, 1976-1977, 110 Am. J. of Epidemiology

105, filed as Ex. 39 (ECF No. 28-2) (“Schonberger”) (discussing the flu vaccine and Guillain-

Barré syndrome (“GBS”)).

9

The now largely-discontinued DPT vaccine included whole cell pertussis, but the version administered today (Tdap)

employs an acellular form of pertussis thought to be less likely to cause certain side effects. See Andreu v. Sec'y of

Health & Hum. Servs., 569 F.3d 1367, 1375 n.1 (Fed. Cir. 2009) for discussion of case law on the safety concerns

prompting the switch to an acellular formulation.

14

III. Review of Filed Literature

Ample Program authority establishes that special masters are not required to describe

and/or analyze in a written decision every item of literature filed in support of or against a claim.

See, e.g., Snyder v. Sec'y of Health and Hum. Servs., 36 Fed. Cl. 461, 466 (1996), aff'd, 117 F.3d

545 (Fed. Cir. 1997). Indeed, the failure to specifically mention a filed item in a decision does not

allow for the inference that it was not included in the special master’s overall weighing of evidence.

Hazlehurst v. Sec'y of Health and Hum. Servs., 604 F.3d 1343, 1352 (Fed. Cir. 2010) (noting that

a reviewing court presumes that the fact finder has considered all of the material in the record,

regardless of whether it is individually mentioned in his or her decision); see also 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); 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”).

There is also the fact that this matter went to a live hearing. A hearing provides the parties

the opportunity to succinctly but fully explain their take on a case in the best possible manner. In

holding hearings, special masters reasonably focus their attention on the items of literature the

parties deem most worthy of verbal mention during an expert’s testimony. Presenting an

entitlement claim is not a game of “hiding the ball,” where a claimant seeds the record with

numerous items of literature, references only some at hearing, and then later objects on appeal

when certain filed items do not receive a full airing in a written decision. Echols v. Sec’y of Health

& Hum. Servs., 165 Fed. Cl. 9, 12 (2023) (“the evidence heard by the special master should be the

“main event” rather than a mere “tryout”).

The Remand Order nevertheless has identified some items of literature as requiring more

discussion, in order to disclose the full extent of my reasoning. Remand Order at 40–44.

Accordingly—and because I ultimately reach the same conclusion that I initially did—I will

provide a detailed summary of every single item of literature filed by Petitioner in this case. 10

10

Petitioner filed a relatively modest 22 articles or studies. See Petitioner’s Exhibit List as of December 26, 2023,

filed Feb. 9, 2024 (ECF No. 53-2).

15

A. Petitioner’s Literature 11

1. Mack

Both sides offered this article. Mack provides an overview of AIH, and guidelines for its

diagnosis and treatment. See generally Mack. Petitioner offered Mack to explain AIH’s

immunopathogenesis, and to establish that Petitioner was properly diagnosed with AIH. First Gish

Rep. at 7. But Petitioner’s diagnosis is not questioned in this case. To the extent Mack bears on

causation, it is discussed in greater detail in the analysis section of this Decision.

2. U. Christen & E. Hintermann, Pathogens and Autoimmune Hepatitis, 195 Clin. and

Experimental Immuno. 35-51 (2019), filed as Ex. 18 (ECF No. 18-3) (“Christen”).

Petitioner has offered Christen in support of her argument that multiple viruses, including

the measles virus, are implicated in the pathogenesis of AIH. First Gish Rep. at 10. Christen is a

review article discussing some of the possible environmental triggers for AIH. Christen at 35.

Unquestionably, the article mentions “pathogen infections and vaccinations” as possible

environmental factors that can interact with a preexisting genetic risk factor. But Christen solely

discusses wild viral or bacterial pathogens, focusing on the most obvious (hepatitis viruses) or the

Epstein-Barr virus. Id. at 40–43.

In a brief section addressing “other pathogens” possibly capable of triggering AIH,

Christen notes the existence of “two studies from the 1980s” in which AIH patients were found to

possess evidence of a measles virus infection, but adds that the studies relied on diagnostic

definitions for AIH that would no longer be valid—and that another epidemiologic study had

subsequently revealed “no significant difference” between a studied population and AIH patients

who generated measles virus antibodies. Christen at 43. 12 At most, Christen posits that some case

reports involving AIH after a measles infection allow for the hypothetical possibility of measles

virus as an infectious trigger—although the sole reference for this case report is the same article

mentioned by Dr. Gish but never filed, Vento. Id. at 43 n.111. Christen also acknowledges that

little evidence supports the hypothesis that AIH is driven by molecular mimicry, although (unlike

Mack) Christen does mention bystander activation, at least as a theoretical mechanism. Id. at 37,

38.

11

I refer to an article’s abbreviated title in all cases where the item was previously defined in this manner in this

Decision.

12

Petitioner filed one of the two 1980s articles referenced herein—Robertson (see Christen at 43 n.109), plus the

epidemiologic article that Christen notes undermined a measles virus—AIH connection (Mieli-Vergani I—Christen

at 43 n.110). Both are discussed below.

16

3. C. Benn et al., A Small Jab – A Big Effect: Nonspecific Immunomodulation by Vaccines,

34 Trends in Immuno. 431-39 (2013), filed as Ex. 19 (ECF No. 18-4) (“Benn”).

Petitioner cites Benn to support her contention that vaccines can activate nonspecific

bystander immune cells. First Gish Rep at 10. Benn notes that “[r]ecent epidemiological studies

have shown that, in addition to disease-specific effects, vaccines against infectious diseases have

nonspecific effects on the ability of the immune system to handle other pathogens.” Benn at 431.

The authors of Benn explain that each exposure to infection or vaccination leaves an imprint on a

person’s immune system, which can affect future innate and adaptive responses to new pathogens.

Id. at 433. This concept of “heterologous immunity” could explain why vaccines may have

nonspecific effects—because the vaccines encode antigens that cross-react with other pathogens.

Id. The authors conclude, therefore, that cross-reactive T-cell-mediated heterologous immunity is

likely a common determinant in the pathogenesis of infections. Id. at 433–34.

Benn, however, primarily focuses on the positive rather than pathologic indirect effects of

vaccination. In Benn’s discussion of the measles vaccine, for example, the authors emphasize the

vaccine’s observed survival benefits. Benn at 432, 436 (“[e]xisting studies suggest a general

pattern, namely that the live vaccines: [including measles vaccine] are associated with beneficial

nonspecific effects, leading to reduced all-cause mortality . . . .” (emphasis added)). Measles-

vaccinated children have substantially lower mortality than can be explained by measles-related

deaths, suggesting that the vaccine comes with a host of nonspecific beneficial effects. Id. at 432.

Benn does not purport to state how vaccines most likely induce these nonspecific effects, but it

does not support the conclusion that the live vaccines it discusses have pathologic potential due to

their nonspecific effects (at best allowing for the need to identify when those effects could be

detrimental, so that concurrent therapeutic interventions could be developed to inhibit negative

outcomes). Id. at 437. 13 And Benn says nothing specific about AIH and its purported vaccine

association.

4. Siegrist

Siegrist is an excerpt from a larger publication, and it provides a general explanation for

how a vaccine activates the immune system. Among other things, it highlights the role of T cells

in the induction of high-affinity antibodies and immune memory. Siegrist at 16. It also notes that

live vaccines (like MMR) “rapidly disseminate throughout the vascular network to reach their

target tissues” in a pattern that is “very similar to that occurring after a natural infection.” Id. at 20.

13

At most, Benn contains a discussion of some instances where “detrimental heterologous immunity can lead to severe

immunopathology.” Benn at 434. But the instances discussed involve studies featuring immunization of animal

subjects with different vaccines, resulting in other forms of disease not bearing on this case, or where receipt of one

form of a vaccine can “lock” an immune response to subsequent forms, causing a vaccine to have “detrimental effects

on the outcome of secondary infections.” Id. at 435.

17

But Siegrist also, in Petitioner’s estimation, has something to say about the impact of

receipt of the non-live, Tdap vaccine. She received Adacel, a Tdap booster, and that vaccine was

expected to activate Petitioner’s immune memory cells and result in a rapid increase of antibody

titer. First Gish Rep. at 23. According to Figure 2.3 in Siegrist, booster exposure to antigen

reactivates immune memory and results in an increase of IgG antibody titer within seven days of

receipt. Siegrist at 24. Short-lived plasma cells responsible for production of antibodies thereafter

maintain peak antibody levels for a few weeks. Id. And six months after booster vaccination, long-

lived plasma cells reach survival niches in the bone marrow and continue to produce antigen

specific antibodies. Id.

Petitioner cited to Siegrist to support her arguments about the medically-acceptable

timeframe in which her AIH manifested post-vaccination. First Gish Rep. at 24. Petitioner started

to experience fatigue in the weeks after vaccination, but then continued to suffer increased

symptoms in the five months up to her formal diagnosis in January 2019. Petitioner argues that

this symptom progression fits within the one to five-month timeframe suggested in Siegrist. First

Gish Rep. at 24.

5. Saliba

As discussed above, Petitioner has offered Saliba to support her argument that the MMR

vaccine can cause a person to develop hepatitis. Saliba is a one-page “letter to the editor” which

reports an instance in which a 24-year-old woman developed acute hepatitis two weeks after

receiving the MMR vaccine, with her hepatitis thereafter resolving within a month (as reflected by

LFT results). Saliba at 379. The sequence of events, together with the lack of potential causes for

elevated liver enzymes, “strongly suggest[ed]” to its authors that the patient’s development of

hepatitis was related to vaccination. Id. The proposed mechanism was a cytotoxic, cell-mediated,

immunological response with injury of the hepatocytes. Id. But Saliba notes (at least as of the time

of its publication) that “there is still no evidence that [the vaccine’s viral components] are directly

cytopathic to the hepatocytes,” although it referenced an older article (not filed in this case)

purportedly establishing that biopsies of patients with rubella infection have revealed “necrosis of

liver cells” and suggesting that “cytotoxin T cell lymphocytes play an important role in liver

injury.” Id. Saliba’s short onset timeframe is self-evidently distinguishable from this case.

6. J. McMahon et al., Measles Vaccine Virus RNA in Children More Than 100 Days after

Vaccination, 11 Viruses 636-48 (2019), filed as Ex. 22 (ECF No. 18-7) (“McMahon”).

McMahon is another instance of an article cited by Petitioner as supporting a point that the

article itself only stands for secondarily. Noting the general dangers of a wild measles infection

(especially because of its immunosuppressive character), and the corresponding benefit of the

measles vaccine, McMahon’s authors evaluated some instances of “extremely delayed” detection

18

of the measles vaccine in a sample of more than 9,000 children. McMahon at 638-39. Ordinarily,

RNA from a measles virus strain found in the vaccine is commonly detected for up to at least 14

days post-vaccination. Id. at 638, 643. But McMahon confirmed that the strain can be detected

between 100- and 800-days post-vaccination, albeit based on a subset of only eleven samples. Id.

at 638.

McMahon’s findings were deemed consistent with the understood persistence of a wild

virus measles infection, and its authors also noted the significance of the fact that the vaccine

component RNA was specifically identified in the respiratory tract of the studied patients

(underscoring the degree to which lymphoid tissue—to which a natural infection would spread as

immune cells encountered the virus—was a likely situs for the virus to remain in the body).

McMahon at 643. But its authors in no way implicated the vaccine as dangerous or pathologic in

connection with its immune persistence (except in the limited circumstance of a person known to

be immunodeficient or receiving immunosuppressive treatments). Id. Indeed, McMahon’s authors

expressly observed that the vaccine remained safe and highly important in the prevention of

measles, and that the exceedingly small sample size relied upon for its findings prevented drawing

larger conclusions from the study. Id. at 644.

Dr. Gish relied in part on McMahon for the contention that persistence of the measles virus

in Petitioner could have later contributed to her development of chronic liver inflammation. Tr. at

50; First Gish Rep. at 24. But McMahon certainly does not equate persistence with pathogenicity—

active or potential. Indeed, as Dr. MacGinnitie observed, McMahon did not show that the studied

children actually had an infection in their liver—the measles vaccine virus RNA was only present

in their respiratory secretions. Tr. at 176. And although the eleven samples had more often than

not presented pre-detection with some infectious-like symptoms, McMahon’s authors noted that

they could not confirm whether other, concurrent viral infections were not explanatory—and even

more importantly, that “detection of [vaccine component measles RNA] alone does not allow for

any assessment of whether infectious virus is present.” McMahon at 644.

7. P. Berry & G. Smith-Laing, Hepatitis A Vaccine Associated with Autoimmune Hepatitis,

13 World J. of Gastroenterology 2238-39 (2007), filed as Ex. 23 (ECF No. 18-8)

(“Berry”).

Berry is a case report in which a 56-year-old man developed acute liver injury consistent

with autoimmune hepatitis ten days after he received the hepatitis A vaccine. Berry at 2238.

Notably, the patient in Berry had also been diagnosed with acute hepatitis five months before the

administration of the vaccine. Id. This case is thus distinguishable from Petitioner’s case, involving

not only an entirely different vaccine—the hepatitis A vaccine—but a patient who had experienced

a relapse of hepatitis post-vaccination.

19

8. Veerappan

Veerappan is another case study offered for the general proposition that autoimmune

hepatitis is associated with vaccination. First Gish Rep. at 16. In Veerappan, a 35-year-old male

developed severe flu-like symptoms one week after receiving multiple vaccinations—typhoid,

hepatitis A, oral polio, diphtheria/tetanus, and MMR. Veerappan at 212. A liver biopsy performed

one month after initial presentation showed severe chronic hepatitis, which was deemed to be

consistent with AIH. Id. The authors concluded that AIH may be a complication in patients who

receive multiple vaccinations simultaneously. Id. at 213. But Veerappan’s authors provide no

explanation for the significance of the receipt of so many vaccines at once, deeming them “a novel

inciting event” worthy of consideration (but not shown to be likely pathogenic). Id. And

Petitioner’s onset was not nearly so quick in this case.

9. Subramanian

Subramanian is yet another, facially-inapposite case report. Here, a 45 year-old woman

who had been diagnosed with a hepatitis A infection was hospitalized a month later, and her

presenting symptoms and lab work were later deemed consistent with AIH. Subramanian at 1–2.

Thus, the studied individual had not received any vaccine at all (let alone the MMR or Tdap

vaccines), and was suspected to have developed AIH from her prior hepatitis infection (evidence

of which was detected after her disease onset and which “remained positive” during her treatment.

Id. at 2.

Petitioner nevertheless (as noted above) relied on Subramanian, with Dr. Gish maintaining

that it stood as evidence of the genetic susceptibility for AIH. Tr. at 69. But as noted above, Dr.

Gish’s primary interest in Subramanian arises from its reference to an unfiled article (Vento) in

which two relatives developed autoimmune hepatitis within five months of an acute hepatitis

infection. Subramanian at 2 n.4. The authors concluded that a genetic disposition (specifically, a

type of T cell defect) made the patients susceptible to AIH following the impact of infection. Id.

In Dr. Gish’s view, Petitioner similarly likely suffered some kind of “T cell defect” due to genetic

susceptibility, like the patients in Vento, but triggered here by a different acute immunologic

stimulus. Id. at 69. But Dr. Gish later admitted that no genetic testing had been performed that

would corroborate Petitioner’s susceptibility. Id. at 96. And Subramanian itself does not suggest

that exposure to a measles wild virus or vaccine component could have the same impact on a

genetically susceptible individual as a hepatitis A infection.

10. van Gemeren

van Gemeren discusses two women in their 20s who developed AIH after receiving various

vaccines. van Gemeren at 18–19. One developed AIH a month after receiving vaccines against

hepatitis A and hepatitis B. Id. at 18. The other developed AIH ten days after she was vaccinated

20

against hepatitis A, diphtheria, whooping cough, and tetanus. Id. at 19. The article suggested that

vaccination, especially vaccination against hepatitis A, may trigger AIH in genetically susceptible

individuals. Id. at 21–22. However, van Gemeren acknowledges that no conclusive evidence has

been found for a causal association between vaccines and the occurrence of autoimmune diseases.

Id. at 21. Otherwise, this case report does not involve the MMR vaccine (the focus of Petitioner’s

causation theory), does not discuss the impact of the tetanus-containing vaccine to any significant

degree, and does a better job underscoring the possible impact of hepatitis-oriented vaccines.

11. Perumalswami

The Perumalswami case report discussed a 31-year-old woman who developed

autoimmune hepatitis 11 days after receiving hepatitis A and yellow fever vaccines. Perumalswami

at 331. After vaccination and prior to developing symptoms, she had traveled to Nigeria for five

days. Id. Perumalswami’s authors raised the possibility that these two vaccines may have been a

triggering agent for AIH (but admitted that this was a novel finding). Id. at 333. Like the other case

reports discussed above, however, this article says less about the potential pathogenicity of the

vaccines at issue than it does about the risks of a hepatitis vaccine.

12. Sasaki

Sasaki is the final case report offered by Petitioner to substantiate a vaccine-AIH

relationship. In Sasaki, two female patients presented with AIH within one week and one month,

respectively, after receiving the flu vaccine. Sasaki at 1–2. The authors admitted that a causal link

could not be established, but hypothesized that the flu vaccine could trigger the development of

AIH, given the possible link between immunization and other autoimmune diseases. Id. at 3. But

as Dr. MacGinnitie pointed out, flu vaccine administration is so widespread that it is very likely

that the development of AIH after vaccination in these cases was mere coincidence. Tr. at 155. And

yet again—Sasaki, like prior case reports, does not involve the relevant vaccines in this case.

13. D. Robertson et al., Persistent Measles Virus Genome in Autoimmune Chronic Active

Hepatitis, 330 The Lancet 9-11 (1987), filed as Ex. 29 (ECF No. 19-5) (“Robertson”).

Robertson, a study from 1987, involves the measles virus and its putative association with

“chronic active hepatitis.” Robertson at 9. 12 out of 18 studied patients with confirmed

autoimmune chronic active hepatitis were found also to possess the measles virus genes. Id. at 10.

Robertson’s authors concluded that the presence of high-titer antibodies to the measles virus in

patients with AIH “suggests that these particular viruses may have a causal role in the condition.”

Id. They also surmised that the patients’ exposure to measles resulted in a persistent incomplete

infection occurring as a result of continued production of measles antigen and ineffective

elimination of the virus. Id. at 11.

21

The Robertson study briefly mentions the measles vaccine but does not offer a potential

causal mechanism, and suggests even that the measles vaccine might have prevented some

instances of measles-caused AIH (resulting in onset only in older cohorts). Robertson at 10. In

addition (and as noted in my discussion of Christen above), there is reason to doubt whether the

defined group of individuals with “autoimmune chronic active hepatitis” would be suffering from

what is currently understood to be AIH. Otherwise, Robertson’s authors admitted that the finding

of persistent measles virus in the small set of subjects could simply be attributable to an

“epiphenomenon” 14—meaning a secondary effect arising from, but not causal of, a primary

process (and thus not causal of the studied, hepatitis-like illness).

14. G. Mieli-Vergani et al., Measles and Autoimmune Chronic Active Hepatitis, 334 The

Lancet 688 (1989), filed as Ex. 30 (ECF No. 19-6) (“Mieli-Vergani I”).

Petitioner deemed Mieli-Vergani I to substantiate an association between the measles

vaccine and AIH. Mieli-Vergani I’s authors (in a single-paragraph summary 15 published in the

Lancet) mentioned a study observing that 8 out of 12 children with autoimmune hepatitis had

received the measles vaccination and had tested positive for low titers of measles antibody. Mieli-

Vergani I at 688. The authors surmised that there could be a causal link between measles and

autoimmune hepatitis, at least in childhood. Id; First Gish Rep. at 19. But the cursory discussion

of these findings prevents any greater scrutiny of their reasonableness. And as noted expressly in

Christen—published 30 years later, and thus with the benefit of further study (as well as perhaps

a full copy of the article)—Mieli-Vergani I did not find the existence of the measles antibody titers

significant, when comparing sick individuals with a control, healthy population—thereby reducing

the evidentiary value of this somewhat-stale article. Christen at 43.

15. Nanan

Nanan’s authors sought to investigate the impact of measles infection-induced immune

suppression (which has also been observed to a lesser extent in vaccination) by seeking to analyze

T cells extracted from serum of four pediatric subjects with measles infections, plus four older

individuals who had received the measles vaccine. Nanan at 202. In particular, it sought to observe

the expression of leukocyte function-associated antigen 1 (LFA-1)—a cell surface protein found

on human T cells, and deemed important to a functioning immune process. Id. at 201–02.

14

“Epiphenomenon” is defined as “an accessory, exceptional, or accidental occurrence in the course of an attack of

any disease.” Epiphenomenon, Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=16902&searchterm=epiphenomenon (last visited on May 27,

2025).

15

Petitioner has not filed a full version of Mieli-Vergani I.

22

Nanan found that there was a “remarkable loss” of LFA-1-bright cells during natural

measles infection, and after measles vaccination. Nanan at 204–05. The findings suggested to the

authors that sequestration of T cells is a feature of the measles virus infection and vaccination. Id.

at 209. This is problematic, since the integration and control of immune responses depend on

regulated trafficking of lymphocytes. Id. The disruption of lymphocyte trafficking by random

distribution of T cells in all areas of lymphoid organs could impair host defenses and result in

immune suppression. Id.

Petitioner cited Nanan to support her contention that the measles component of the MMR

vaccine could initiate immune dysfunction, leading in some form to an autoimmune response

(although Nanan itself does not discuss such secondary disease in the context of measles-induced

immunosuppression). Tr. at 40–41; First Gish Rep. at 19. While Dr. Gish admitted that there is no

evidence in this case that Petitioner likely ever suffered from a prolonged measles vaccine-induced

suppression, he contended that this was not necessary to meet Petitioner’s burden of proof on

causation. Tr. at 45–46. And it was likely in any event that immune activation persisted even if

Petitioner’s system had cleared measles post-vaccination. Id. at 49. In response, Dr. MacGinnitie

emphasized that the authors of Nanan did not provide evidence that the observed decrease of LFA-

1 was clinically meaningful, nor did they offer evidence that the small group of patients they

considered had experienced any actual immune suppression sufficient to cause disease. Tr. at 163.

There is no reason to doubt the validity of Nanan’s specific findings, and I deem its

methodology reliable. Indeed, its findings are consistent with the already-understood

immunosuppressive impact of the wild measles virus. But Nanan cannot be read to support the

conclusion that receipt of a measles-containing vaccine is likely pathologic for this same reason –

or that AIH is more likely in the context of a prior measles vaccination. It thus stands as somewhat

weak evidence overall for the contention that the MMR vaccine has the capability to produce

disease-encouraging immune suppression.

16. Munyer

Munyer is a 1975 study that sought to consider the impact of receipt of the version of MMR

vaccine used at the time on T cell responses in the blood of children. Sera was drawn from an

unspecified number of vaccinated children (pre and post-vaccination), then stimulated ex vivo.

Munyer at 75–76. An impairment in lymphocyte response to stimulation with antigen was

observed in the vaccinated samples (via an in vitro test), with the impairment lasting for one to

five weeks post-vaccination. Id. at 77. From this, Munyer’s authors concluded that the MMR

vaccine could cause a depression of lymphocyte function - although the degree of impairment was

deemed likely more pronounced for an active infection than vaccination. Id. at 77–78.

Munyer also, however, noted the following:

23

no significant alteration was observed in the absolute number of lymphocytes in the

peripheral blood of vaccinated subjects, either in comparison with base line (before

vaccination) counts or with counts from a group of unvaccinated controls.

Similarly, no decrease in either the percentage or the absolute number of peripheral

blood T-lymphocytes was observed after vaccination.

Munyer at 76. Thus, although experimental stimulation of blood samples revealed an impairment

in immune cells, actual, in vivo vaccination did not. It is the results of the latter that are ultimately

in contention in this case.

Petitioner cites Munyer for the same reason as Nanan—to support her argument that the

measles vaccine could have induced immunosuppression in Petitioner, leading to the development

of AIH. First Gish Rep. at 19. Dr. MacGinnitie criticized this article during his testimony, however,

noting that it was 50 years old (and hence outdated), and claiming that its authors used “rather

primitive techniques.” Tr. at 163. More importantly, however, Dr. MacGinnitie observed that

Munyer did not provide evidence that the immunosuppression observed was meaningful from a

clinical standpoint (as opposed simply to an observed, absolute phenomena). Id. The above-

referenced block quote citation from the article directly corroborates this opinion.

My reaction to Munyer is consistent with my reading of Nanan. While Munyer’s findings

may narrowly be based on a methodologically-reliable experiment, the article stands only as a

single (and facially-outdated) “brick” in the causation theory “wall” Petitioner seeks to build—

and it does not itself establish vaccine-related pathology. Rather, it constitutes additional evidence

that the measles component of the MMR vaccine may cause an experimentally-observable amount

of immune suppression—but whether that is of a magnitude sufficient to result in an autoimmune

disease is not addressed. And it cannot be concluded from Munyer that the vaccine when actually

administered in vivo does cause observable immune suppression, and/or has pathologic outcomes.

Munyer’s own findings suggest the opposite.

17. Rennick

Rennick noted that despite the widespread use of measles vaccines, “little is known about

the attenuation profile of the vaccine virus or what cells it targets upon vaccination.” Rennick at

2197. Accordingly, Rennick’s authors sought to compare the immunogenicity of the vaccine

compared to its biologic viral parent, specifically by looking to identify the vaccine’s antigenic

targets after administration by injection. Id. The study (using animal subjects) determined that

infected cells after vaccination are predominantly macrophages and dendritic cells in subcutaneous

tissues, found abundantly at the site of injection (rather than muscle cells). Id. at 2199.

24

Petitioner has cited Rennick as establishing that the measles vaccine virus strain likely

infected Petitioner’s immune cells. Tr. at 38. But the means by which the immune system takes up

the vaccine does not also lead to the conclusion that pathology was an expected, or even possible,

outcome due to vaccination. And Rennick says other things about the impact of a measles infection

that are inconsistent with Petitioner’s theory. For example, Rennick notes that the measles wild

virus has a much shorter, preclinical latency period after infection (10 to 14 days) than what is

proposed in this case, undermining Petitioner’s general argument that once vaccinated, pathology

remains possible months later. Rennick at 2192. Rennick also underscores the principal danger of

a wild measles infection—the increase in “susceptibility to opportunistic infections”—in addition

to direct risk from the infection itself (and here, the evidence that Petitioner’s AIH is attributable

to an opportunistic hepatitis infection is wholly lacking).

18. da Silva Antunes

da Silva Antunes constitutes one of the few articles offered in this case to link the Tdap

vaccine to Petitioner’s injury. Its authors sought mainly to better understand the effects of the

transition from the use of whole cell pertussis-containing vaccines to the acellular form (which in

the U.S. replaced whole cell pertussis, due to concerns that the former version was associated with

adverse events). da Silva Antunes at 3856. Accordingly (and in the wake of evidence that pertussis

disease was increasing even in places where the acellular form was used), da Silva Antunes’s

authors attempted to compare the immune responses of children who received whole cell pertussis

originally versus those who first received the acellular form, comparing both groups after they

received an acellular pertussis booster. Id. at 3855. The study revealed that subjects who had been

previously vaccinated with whole cell pertussis produced more of a specific form of T helper cell

(Th17 cells). Id. at 3856–58. In effect, despite the adverse events associated with the largely-

discontinued whole cell pertussis, receipt of that form of the vaccine was deemed to impart greater

immunity overall. Id. at 3869–70.

Petitioner cited da Silva Antunes to show how an increase in Th17 cells could lead to

autoimmune hepatitis. Tr. at 169–70. Dr. Gish reasoned that Th17 cells are critical to regulate both

protective and pathogenic immune responses. First Gish Rep. at 22. Because Petitioner was likely

administered the whole cell pertussis vaccine as a child, she would produce more Th17 cells after

she received the Tdap booster vaccine. Id. Dr. MacGinnitie argued in response, however, that Dr.

Gish had never explained how the production of Th17 cells would actually result in AIH

(specifically by causing damage to cells in the liver). Tr. at 173. And Petitioner’s Th17 levels were

never tested, so there was no way to know if they were elevated at all. Id.

As with other items of literature filed by Petitioner in this case, there is no reason to doubt

the validity of da Silva Antunes’s findings. But the article does not seek to evaluate vaccine

pathology, but instead to measure vaccine effectiveness. And the fact that it suggests that the Tdap

vaccine can cause an increase of a certain kind of immune cell does not mean that the ordinary

25

receipt of the vaccine is likely to cause that immune cell to proliferate so much that it becomes the

driver of a pathologic autoimmune process.

19. Lafdil

Lafdil appears to have been offered to link the findings from da Silva Antunes discussed

above to Petitioner’s theory in this case. Lafdil is a review article discussing other studies that have

observed the role that Th17 T-helper cells play in the development of autoimmune liver disease.

Lafdil at 250. It defines Th17 cells to be “a subset of T helper cells that play important roles in

host defense against extracellular bacteria as well as in the pathogenesis of autoimmune disease.”

Id. Studies show that IL-17 is significantly elevated in a variety of chronic liver diseases, and

Lafdil specifically discusses (a) a laboratory animal model form of hepatitis driven by T cells, (b)

alcoholic liver disease, (c) chronic hepatitis B and C viral-induced liver infections, and (d)

autoimmune liver disease. Id. at 251–52. The latter category arguably relates to AIH (although that

term is not used in the section discussing autoimmune liver disease), but Lafdil refers mainly to

studies showing increased levels of a T helper cell-associated cytokine in studies involving

cirrhosis 16—which Ms. Exum does not have—and otherwise the authors only say that the

mechanisms for why these T helper cells increase in this context are unknown, along with their

role in aiding pathogenesis of disease. Id. at 252.

20. I. Amanna et al., Duration of Humoral Immunity to Common Viral and Vaccine Antigens,

357 N. Eng. J. Med. 1903-15 (2007), filed as Ex. 36 (ECF No. 20-3) (“Amanna”)

Amanna sought to evaluate “the issue of antibody maintenance after infection or

vaccination,” by reviewing 630 serum samples drawn from 45 subjects, and where the blood serum

samples had been drawn regularly and “banked” over an average period of 15 years. Amanna at

1905. The study’s authors looked to evaluate the temporal length of antibody maintenance (and

whether the antibodies were at protective levels to fight off future disease) for a number of

infections, including most of the viruses that the vaccines Petitioner received were aimed against

(such as the MMR components). Id. at 1906). Amanna’s authors determined that the antibody

responses to a live viral infection were generally longer than to responses to the kind of

nonreplicating protein antigens often contained in vaccines. Id. at 1911. But even exposure to the

latter conferred some long-term benefit; the authors specifically found a comparatively-rapid

decrease in tetanus-specific antibodies over a more than ten-year period. Id. at 1908.

Dr. Gish generally relied upon Amanna to support his contentions about the medically-

acceptable timeframe in which Petitioner’s post-vaccination AIH began, although he did not

16

Cirrhosis is a condition in which an individual’s liver is found to be scarred and permanently damaged, due to

alcoholism or some other disease process. Cirrhosis, National Institute of Diabetes and Digestive and Kidney

Diseases, https://www.niddk.nih.gov/health-information/liver-disease/cirrhosis#:~:text=Print%20All%20Sections-

,Definition%20%26%20Facts,your%20liver%20begins%20to%20fail. (last visited on May 27, 2025).

26

explain in detail how it supported his contentions (which seemed more to embrace the idea that

the Tdap booster caused a faster immune response due to Petitioner’s prior receipt of the whole

cell pertussis form of vaccine). First Gish Rep. at 23.

21. Schonberger

Schonberger is an epidemiologic study performed after the 1970s swine flu epidemic, and

considers the impact of the immunization program initiated by the federal government in response.

The study evaluated over 1,000 individuals who had experienced Guillain-Barré syndrome

(“GBS”) in the 1976–77 timeframe, comparing those who received the version of the vaccine used

at that time (now nearly fifty years ago) versus those who did not, and finding that the incidence

rate for GBS was higher among those who had received the vaccine. Schonberger at 109.

Schonberger also made findings about the post-vaccination timeframe in which individuals

developed GBS, peaking within two to three weeks but significantly declining after ten. Id. at 112.

Schonberger is consistently cited in the Program by virtually any claimant seeking to

establish how the flu vaccine could cause a demyelinating autoimmune disease of the peripheral

or central nervous system. Hence, it has no direct relevance to this case, which involves different

vaccines and a different injury. Schonberger is also commonly invoked to support arguments about

what constitutes a reasonable post-vaccination timeframe for development of an antibody-driven

autoimmune disease - and here, Dr. Gish contended that it supported the conclusion that there was

risk of a possible autoimmune, post-vaccination injury up to ten weeks after. Second Gish Rep. at

10.

22. Excerpts, Institute of Medicine, Adverse Effects of Vaccines: Evidence and Causality, 556-

62 (Kathleen Stratton, Andrew Ford, Erin Rusch & Ellen W. Clayton, eds., 2012), filed as

Ex. 45 (ECF No. 45-3) (“2012 IOM Rep.”)

The 2012 IOM Report is a book-length evaluation of different risks associated with a

variety of commonly-administered vaccines. Petitioner has offered a collection of excerpts from

it, highlighting a few points: (a) that evaluating a potential adverse effect of vaccination involves

consideration both of what the underlying natural infection does as well as the adverse event’s

known pathophysiology (2012 IOM Rep. at 40); (b) what the committee did in evaluating the

adequacy of evidence of a particular outcome (Id. at 12–13); (c) that no studies (as of 2012) were

considered in assessing the risk of hepatitis due to the MMR vaccine (Id. at 211); and (d) that case

studies have associated the MMR vaccines with hepatitis, but that the mechanistic evidence of an

association (whether with respect to the MMR or hepatitis A vaccine) is weak, given what is known

about the natural infection (Id. at 212, 429–30).

27

B. Respondent’s Literature 17

1. G. Mieli-Vergani et al., Autoimmune Hepatitis, 4:18017 Nat. Rev. Dis. Primers 1-21

(2018), filed as Ex. A Tab 2 (ECF No. 25-2) (“Mieli-Vergani II”)

The primary author of this review article is the same as Mieli-Vergani I, cited by Petitioner.

Mieli-Vergani II notes some basic facts about AIH, largely consistent with Mack. However, it also

makes observations about AIH that are somewhat contrary to what Petitioner gleaned from Mieli-

Vergani I. In particular, Mieli-Vergani II deems the cause of AIH to be unknown (Mieli-Vergani II

at 10), and in discussing potential mechanisms for its pathogenesis, like molecular mimicry, it

makes no mention of measles virus (as Christen noted Mieli-Vergani I had done), focusing instead

on case reports involving hepatitis infections (Id. at 4). But Mieli-Vergani II does propose a role

for T helper cells in propagating disease, as well as the loss of immune tolerance—both of which

Petitioner relies upon in her causation theory.

2. Beretta-Piccoli

Beretta-Piccoli is a case report showing the counter-risk posed by anti-malarial medicine

in causing AIH. It discusses a 65-year-old woman who made yearly visits to Tanzania, and took

an anti-malarial drug, Malarone (atovaquone/proguanil), on each trip. Beretta-Piccoli at 293–94.

The year before the illness at issue, she had become jaundiced with an acute hepatitis following

her trip, and her illness was thought to be drug-induced liver injury due to an antibiotic (although

she had also been taking Malarone), although it resolved in two weeks. Id. at 294, 296. The

following year, she returned to Tanzania and again took Malarone. Id. at 294. Shortly after she

returned, she went to the hospital with fatigue, jaundice, and dark urine. Id. at 293. She reported

that she had stopped taking Malarone four days earlier due to the appearance of jaundice. Id. at

294. After performing a liver biopsy and several lab tests, doctors tentatively diagnosed the patient

with AIH. Id. at 295. The patient’s liver inflammation took a long time to resolve, allowing a firm

diagnosis only three years after presentation. Id. at 297. Beretta-Piccoli’s authors concluded that

the anti-malarial medication was the likely cause of the patient’s liver pathology, but they

acknowledged that a second case would be needed to confirm “the rare but potentially severe

hepatotoxicity of this commonly used antimalarial prophylaxis/treatment.” Id. at 296–97.

Respondent cited Beretta-Piccoli as evidence that anti-malarial medication can cause AIH.

Crippin Rep. at 4–5. And there are similarities between this patient and Ms. Exum. Both traveled

to Tanzania, and both needed prolonged therapy with corticosteroids/prednisone after falling ill.

However, there are also significant factual differences. The patient in Beretta-Piccoli developed

17

Respondent offered 38 items of literature. Exhibit List, filed January 24, 2024 (ECF No. 49). But Respondent does

not bear the burden of proof in this matter, and therefore it is far less critical from a fairness standpoint that I unpack

each item of literature he filed. I instead review herein only those items filed by Respondent that are most important

to my analysis.

28

very clear signs of liver injury (jaundice, dark urine) while she was actively taking the anti-malarial

medication, but Petitioner did not develop symptoms (other than fatigue) in such a short timeframe.

3. 2012 IOM Report 18

Respondent also referenced portions of the 2012 IOM Report, in support of his contention

that Petitioner had not presented sufficient evidence to support a molecular mimicry mechanism.

Tr. at 184. The relevant excerpts of the 2012 IOM Report confirm that proof of homology (between

different amino acid sequences in a foreign antigen and self protein structure) is insufficient to

prove a molecular mimicry reaction. See 2012 IOM Report at 60 (deeming it “problematic” to

prove autoimmunity due to molecular mimicry, and noting that homology is common in nature

and usually not pathogenic). Yet Dr. Gish did not even attempt to demonstrate homology in the

first place.

Additionally, the 2012 IOM Report notes that pathogenic molecular mimicry may serve as

a causal explanation for an autoimmune disease if the theory is corroborated with evidence of an

autoimmune attack in vivo, evidenced by proof of “local binding of antibody with activation of

the complement cascade, activation of the appropriate co-stimulatory T cells signals and cytokines,

and/or involvement of other pathogenic effector mechanisms in a biologically relevant tissue site.”

2012 IOM Report at 71. Thus, Dr. MacGinnitie contended, Petitioner would need to show that

there were antibodies or T cells that cross-reacted in her case with vaccine components, and that

they were actually present in vivo. Tr. at 185. Furthermore, Petitioner would have to show that

these immune cells were actually capable of mediating organ damage. Id. But no such evidence

existed in this matter.

4. Mina

Mina is a review article discussing the significantly positive impact of receipt of the

measles vaccine worldwide. See Mina at S11. It notes that “[m]easles immune suppression is an

invisible hallmark of measles infection, predisposing to secondary infections, the major cause of

measles associated mortality.” Mina at S13. But “[m]easles vaccination programs have been

among the greatest public health achievements” in eliminating the measles infection across the

globe. Id. at S10. This is attributed to “direct heterologous benefits of the measles vaccines that

enhance innate and adaptive immune responses.” Id. Receipt of the measles vaccine thus not only

prevents directly a subsequent measles infection, but reduces the likelihood of experiencing some

secondary, opportunistic infection or illness (since the immunosuppression caused by an initial

measles infection is eliminated). Id. at S13–15. The measles infection can have a longer-term

impact on the immune system—what Mina terms “measles virus associated immune-amnesia.” Id.

at S14.

18

See Ex. C Tab 2 (ECF No. 26-2)—the portions filed by Respondent are different than what Petitioner highlighted.

29

Respondent cited Mina to refute Petitioner’s argument that the measles vaccine is capable

of suppressing the immune system to any comparable pathologic degree. Tr. at 164; MacGinnitie

Rep. at 8–9. As Dr. MacGinnitie explained, the measles vaccine in fact prevents the profound

immune suppression caused by the measles virus (precisely what Petitioner argues in part caused

her to experience AIH). Tr. at 165.

5. AC of Pediatrics

AC of Pediatrics is an annually-updated clinical manual relied upon by treaters. It

acknowledges the immune-suppressive nature of the wild measles, but not the vaccine. It

specifically notes that “children who have had measles have long-term blunted immune responses

to other pathogens and increased mortality attributable to the known effects of the measles virus

on lymphocytes.” AC of Pediatrics at 503. It then discusses the importance of measles prevention

(i.e. by receiving the measles vaccine). Id. at 503–04. Like Mina, AC of Pediatrics was cited to

refute Petitioner’s argument that the measles vaccine can cause clinically meaningful immune

suppression, in comparison to the known impact of the underlying wild virus. Tr. at 165–66.

6. T. Safranek et al., Reassessment of the Association between Guillain-Barre Syndrome

and Receipt of Swine Influenza Vaccine in 1976-1977: Results of a Two-State Study, 133

Am. J. of Epidemiology 940-51 (1991), filed as Ex. C-19 (ECF No. 26-19) (“Safranek”).

Safranek, which involved the swine flu vaccine and GBS, found that there was an increased

risk of developing GBS within six weeks of vaccination, with no increased risk after. Safranek at

940. Respondent cited Safranek to support his argument that the onset of autoimmune diseases (if

vaccine-related) typically occurs no more than six weeks of vaccination (rather than up to five

months, as Petitioner contended); Tr. at 176 (Dr. MacGinnitie deeming six weeks “the outer limit”

for a vaccine-triggered autoimmune injury).

IV. Procedural History

As noted above, the case was initiated in 2021. Respondent filed his Rule 4(c) Report

disputing Petitioner’s right to compensation on August 19, 2022. Expert reports were filed through

the end of 2022, and the trial was held in March 2024. I initially denied entitlement on August 29,

2024. On September 30, 2024, Petitioner filed a motion for review.

The Court granted the motion in part, and remanded the case on February 26, 2025, with

instructions to elaborate on my rational for my conclusions. In particular, the Court has directed

the following:

- “provide a rationale for crediting or discrediting the medical literature filed in

this case; such a rationale supporting any conclusions here is necessary to

30

confirm that the prong one 19 legal standard was correctly applied,” in order to

“sufficiently articulate the legal, factual, and evidentiary bases” for my

conclusion that the first prong for causation was not met (Remand Order at 43–

44);

- “provide a more fulsome explanation . . . regarding (1) the probative weight of

the medical literature Petitioner cited, including Petitioner’s case reports

involving relevant vaccines and vaccine antigens, (2) his rationale for accepting

or rejecting that evidence; and, as necessary, (3) the extent to which he is

crediting each expert’s testimony; and (4) his rationale for doing so” (Remand

Order at 44);

- “to the extent that, on remand, . . . analysis of prong one affects [my] findings

pertaining to Petitioner’s prong two logical sequence of cause and effect, [I]

should revise and explain those findings accordingly” (Remand Order at 47);

and

- “(1) revise [my] findings on prong two, only to the extent that [my] prong one

analysis on remand affects those findings, (2) revise [my] analysis pertaining to

alternative causes, insofar as [I] improperly required Petitioner to “persuasively

limit or exclude all of them,” and, importantly, (3) fully describe [my] rationale

for all of his prong two conclusions in the remand decision” (Remand Order at

50–51).

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

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). 20

There is no Table injury for AIH, so Petitioner can only assert a causation-in-fact claim.

19

Prong references are to the Federal Circuit’s decision that established the causation standard applied in Vaccine

Program cases—Althen v. Sec'y of Health and Hum. Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005).

20

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,

31

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 and 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 Althen prong 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

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. Distinguishing between “preponderant evidence” and “medical certainty”

is important because special masters must take care not to impose an evidentiary burden that is too

124 (2003), aff’d 104 F. App’x. 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).

32

high. Bunting v. Sec'y of Health & Human Servs., 931 F.2d 867, 873 (Fed.Cir.1991) (“The standard

of proof required by the [Vaccine] Act is simple preponderance of evidence; not scientific

certainty.... [I]t is not plaintiff's burden to disprove every possible ground of causation suggested

by defendant nor must the findings of the court meet the standards of the laboratorian.”) (citations

and internal quotation marks omitted).

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 Kalajdzic v. Sec’y of Health &

Hum. Servs., No. 2023-1321, 2024 WL 3064398, at *2 (Fed. Cir. June 20, 2024) (arguments “for

a less than preponderance standard” deemed “plainly inconsistent with our precedent” (citing

Moberly, 592 F.3d at 1322)); Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359

(Fed. Cir. 2019); see also Demore v. Sec'y of Health & Hum. Servs., No. 20-1265V, 2024 WL

4542934 (Fed. Cl. Spec. Mstr. Sept. 26, 2024), aff'd, No. 20-1265V, 2025 WL 868902, at *4 (Fed.

Cl. Mar. 20, 2025) (rejecting the argument that a petitioner’s burden is to prove that a causation

theory is plausible and instead requiring petitioner to prove the theory by a preponderance of the

evidence) (emphasis added). And petitioners always have the ultimate burden of establishing their

overall 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) (“Snyder II”) (“there is nothing . . .

that mandates that the testimony of a treating physician is sacrosanct—that it must be accepted in

33

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 den’d, 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. den’d 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. den’d (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).

34

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).

35

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

36

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 II,

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”).

ANALYSIS

I. Treatment of AIH in Prior Cases

The parties agree that Ms. Exum was properly diagnosed with AIH. But even though this

is undisputed, some brief discussion of AIH’s characteristics will help in the analysis of causation

in this matter.

According to Mack, AIH occurs when “a break in self-tolerance to hepatocyte autoantigens

initiates immunological responses causing progressive hepatic necroinflammation and

fibrogenesis.” Mack at 675, Figure 1. Mack deems AIH to be a “complex genetic disease that

requires interplay among genetic, epigenetic, immunologic, and environmental factors.” Id. at 674.

It allows that environmental factors like “viral infections or xenophobic disorders” can defeat

immune tolerance against autoantigens in genetically-susceptible persons, although it does not

mention vaccines. Id. Nonspecific symptoms like fatigue and arthralgias are common to its

37

presentation. Id. at 680; Crippin Rep. at 3, 6. An AIH diagnosis can be confirmed by liver tissue

biopsy. Crippin Rep. at 6.

The primary articles regarding AIH offered by either side do not appear to embrace the

concept that vaccines might in rare cases cause it. At best, they propose an immune-mediated

process for how it unfolds. Mack, for example, describes the pathogenesis of AIH as involving a

breaking of immune tolerance mediated by a variety of T cells, while cross-reactive autoantibodies

(here, presumably incurred due to vaccination) are generated. Mack at 674–76. This is largely

consistent with Petitioner’s proposed mechanistic theory. Mack also sets forth a number of specific

autoantibodies associated with AIH (although Petitioner has never been shown to have possessed

any). Id. at 676–78. But Mack makes no mention of the measles virus as a potential cause of AIH—

and its discussion of vaccination-related risks is limited to the context of existing AIH patients

receiving immunosuppressive treatments, as opposed to individuals not already experiencing AIH.

Id. at 686. 21 Indeed—immunosuppression is a favored treatment of AIH. Mieli-Vergani II at 1, 2,

11 (“AIH should always be treated with immunosuppressive drugs with very few exceptions”).

The Vaccine Program has previously considered whether certain covered vaccines can

cause AIH—but the trend seems to be against a finding of causation. See, e.g., Porter v. Sec’y of

Health & Hum. Servs., 663 F.3d 1242 (Fed. Cir. 2011) (reversing Court’s rejection of special

master determination that hepatitis B vaccine was not shown to cause AIH; special master’s

decision was reasonably based on credibility determinations about the competing expert opinions,

as well as other record evidence). In addition, most such prior claims logically focused on the

hepatitis A or B vaccines, since their viral cognates are understood to lead to hepatitis (and indeed,

the bulk of the case reports filed in this case better support that kind of causation case than what

is advanced here).

There are comparatively fewer cases involving the MMR or Tdap vaccines—but those that

exist are not favorable to Petitioner. See, e.g., Rivas v. Sec'y of Health & Hum. Servs., No. 21-

1683V, 2025 WL 551570, at *2 (Fed. Cl. Spec. Mstr. Jan. 24, 2025) (“[P]etitioner has not carried

her burden of presenting a minimally persuasive case that the Tdap vaccine and hepatitis A and B

vaccines can cause and/or worsen autoimmune hepatitis”).

II. Petitioner Has Not Met her Burden of Proof under Althen

The failure to establish even one of the three Althen prongs in the context of a causation-

in-fact claim is sufficient basis for a claim’s dismissal. Dobrydnev v. Sec’y of Health & Hum.

Servs., 566 Fed. Appx. 976, 980 (Fed. Cir. 2014). Upon remand, I once again determine that

Petitioner did not preponderantly establish causation—at least with respect to the first two Althen

21

Mack actually notes the importance of vaccinating “[p]atients unprotected against infection with hepatitis A virus

(HAV) and hepatitis B virus )(HBC)” before they undergo immunosuppressive treatment for AIH. Mack at 686.

38

prongs. (But although the Remand Order affirms the fact that a special master is not compelled to

perform analysis of each prong individually, if at least one is found not to have been satisfied

(Remand Order at 51), I am including herein my analysis of all three prongs).

A. Prong One

Petitioner contends that the MMR and Tdap vaccines—alone or in combination—more

likely than not can cause AIH. Some elements of the theory are wholly noncontroversial, since

they begin with propositions rooted in what is known about the pathogenesis of AIH. Thus, AIH

likely occurs due to some combination of individual susceptibility and an environmental trigger.

But the theory in its totality lacks sufficient preponderant support, even if some individually-

reliable items of literature have been offered in this case. In order to fully meet the Court’s remand

mandate, I have explicitly broken down each element of my reasoning for why I find causation

has not been demonstrated.

1. Petitioner has Not Preponderantly Demonstrated a Link Between

the Measles Component of the MMR Vaccine and AIH

The primary thrust of Petitioner’s causation argument was that the measles component of

the MMR vaccine has the capacity to suppress the immune response, opening the door thereafter

to AIH (with the Tdap vaccine possibly playing a secondary role). There are several flaws with

the theory.

To an overarching degree, Petitioner’s theory is rooted in a false equivalence between the

immunologic impact of the measles wild virus versus the vaccine. 22 Certainly Program claimants

often base their theories on the impact a vaccine’s wild viral or bacterial counterpart can have from

a pathologic standpoint (since that opens the door to the possibility that a vaccine based on that

same wild virus could achieve a comparable effect). And there is reliable evidence that the wild

measles infection can cause pathologic harm due to immune suppression—even after the virus has

been successfully treated and/or cleared.

But the measles wild virus has not been shown to be directly associated with AIH (and

instances of liver disease or even AIH associated with hepatitis infections of any kind cannot

inform the analysis herein). And it cannot be disputed that the danger posed by the wild measles

virus is far greater than the vaccine, all things being equal. See, e.g., McMahon at 635 (measles

infections “complications, often due to [virus] induced immunosuppression, occur in up to 30% of

cases, and can result in pneumonia, encephalitis, and, in rare cases, death”). Accordingly, it is not

facially compelling for Petitioner to assume that vaccination per se involves a risk comparable to

the impact of the wild measles infection.

22

See, e.g., Tr. at 37 (Dr. Gish responding affirmatively to the question, “[w]ould it be expected that Mrs. Exum

suffered a mild vaccine strain measles infection from the administration of her vaccine?”).

39

More specifically, however, the contention that the measles vaccine is capable of

pathologic immune suppression has not been preponderantly established—even if some of the

items offered to support this concept have scientific reliability. Both Munyer and Nanan support

the narrow proposition that the measles vaccine has been experimentally observed to produce some

depression of T cell lymphocyte function—but that is where their findings end. Neither article

stands for the conclusion that the studied patients experienced meaningful immune suppression,

such that any disease became more likely after receipt of the vaccine (let alone AIH). See, e.g.,

Munyer at 76. The dated quality of these two items of literature further reduces the weight to be

given to them, since they were never followed by confirmatory studies that substantiate the

importance of their findings. If it has been known for over twenty years that a measles virus-

containing vaccine could produce a dangerous degree of immune suppression, where are the

subsequent studies evaluating or testing this purported risk?

Thus, the concept that some fairly-old studies produced some evidence of possible vaccine-

related suppression needed to be linked to other evidence fleshing out the proposition—not

necessarily specific to AIH, but at least to some comparable autoimmune injury. But the evidence

Petitioner has offered does not fill these holes in the theory very well. Christen, for example, only

briefly mentions the measles vaccine, but notes that evidence connecting it to AIH was not

corroborated over time. Christen at 43. Christen similarly mentions a case series article never filed

in this case (Vento), and which observed only a temporal association between measles and AIH.

And it references Mieli-Vergani I as the ultimately-uncorroborated measles virus-AIH

connection—while the same primary author (in the more recently-published Mieli-Vergani II)

made no mention at all of measles virus as a putative AIH trigger (suggesting that in the 30 years

that passed between the two articles, the measles trigger hypothesis was no longer considered

important).

Robertson is fairly weak support for the proposed measles-AIH link. It may well show (in

a small sample) that a preexisting measles infection might be associated with an AIH-like

condition. Yet (and in addition to the fact, noted in Christen, that Mieli-Vergani I did not

corroborate its potential findings—and that the illness considered may not be on all fours with

AIH) it says little about the impact of receipt of a measles-containing vaccine. I therefore do not

find that even the nascent possibility outlined in Nanan and Munyer has been subsequently

confirmed or carried forward—meaning in turn that this aspect of Dr. Gish’s theory lacks sufficient

reliable support to corroborate it.

I also emphasize that the argument that the measles vaccine component can cause

pathologic immune suppression is hardly new to the Program. In fact, it was a central pillar of the

causation theory advanced in the Omnibus Autism Proceeding (the “OAP”) over 15 years ago,

about the alleged capacity of the MMR vaccine to cause autism. But (after a matter characterized

40

by a lengthy and laborious degree of fact-finding unheard of in the Program, before or since) 23 the

idea that pathologic immune suppression could be caused by this vaccine was firmly rejected. See,

e.g., Snyder v. Sec'y of Health & Hum. Servs., No. 01-162V, 2009 WL 332044, at *104 (Fed. Cl.

Spec. Mstr. Feb. 12, 2009) (“petitioners have failed to demonstrate that the MMR vaccine causes

immunosuppression. There is no evidence that children receiving the vaccine have higher rates of

infection in the months after vaccination than children who do not receive the vaccine”), mot. for

review den’d, 88 Fed. Cl. 706 (2009).

Notably, Nanan and Munyer were published before Snyder’s issuance—again raising the

question as to why, if they stand as reliable and persuasive evidence of MMR vaccine-caused

immune suppression, there are not any more recent follow-up studies corroborative of their

findings. And subsequent decisions considering the same proposition (admittedly, also in the

context of an autism injury claim) have rejected the theory again, even where such articles were

expressly invoked in support. See, e.g., Reed v. Sec'y of Health & Hum. Servs., No. 08-650V, 2018

WL 6844458, at *47 (Fed. Cl. Spec. Mstr. Dec. 4, 2018) (rejecting contention that MMR vaccine

can cause clinically meaningful immunosuppression resulting in autism, and discussing Munyer’s

limits as persuasive evidence to that point).

Petitioner’s immunosuppression argument is further weakened by Respondent’s

counterevidence, which supports the conclusion that the measles vaccine actually makes immune

suppression far less likely—simply by reducing the possibility of a measles infection in the first

place. See e.g., Mina at S10 (noting that measles vaccine is correlated with large reductions in

childhood mortality because direct heterologous benefits of the vaccine enhance innate and

adaptive immune responses). And there is a contradictory quality to arguing that immune

suppression would cause a disease reaction that is the product of an uncontrolled immune

response—since autoimmunity involves an unregulated attack by the immune system against self.

In fact, as Dr. Crippin noted, immunosuppressive treatments are used for AIH, and Petitioner

herself received them (Crippin Rep. at 3). How does measles-induced immunosuppression lead to

a disease that itself is treated by immune suppressive drugs? Mieli-Vergani II at 1, 2, 11. This

contradiction is unanswered by Dr. Gish.

Otherwise, the evidence of a direct MMR vaccine-AIH connection is largely absent. 24 It is

limited to a single case report, Saliba (with Veerappan providing one additional case involving the

23

See Hooker v. Sec'y of Health & Hum. Servs., No. 02-472V, 2017 WL 3033940, at *4–6 (Fed. Cl. Spec. Mstr. Apr.

11, 2017), for a summary of the OAP process. The work performed by the three special masters who jointly heard

evidence in the OAP, and then wrote the formidably-long entitlement decisions thereafter, was exemplary—and thus

findings made therein that have relevance to other kinds of Vaccine Act claims deserve considerable weight, even if

they do not control the outcome herein.

24

My observation that this evidence is lacking is not the same as requiring it. I am simply noting that the evidence of

a more direct vaccine-AIH association is not evident (underscoring the degree to which Petitioner must rely on more

indirect and circumstantial proof—and here, that proof too proves inadequate).

41

MMR, but too many other additional vaccines to separate out possible triggers). This is not enough

of a link to remedy the other deficiencies in this aspect of Petitioner’s causation theory.

I thus do not find on this record that it is preponderantly likely that the MMR vaccine can

cause sufficient levels of immune suppression to have a clinically-meaningful impact—such that

it could establish conditions for an autoimmune disease like AIH.

2. Evidence About the Putative Role of the Tdap Vaccine in

Causing AIH is Weak or Lacking

Dr. Gish devoted less time at trial to explaining his theory for how the Tdap vaccine could

play into the proposed pathogenesis for AIH. But this aspect of the overall theory made

assumptions about the impact of the Tdap vaccine (and its promotion of inflammation through

stimulation of T-helper cells) that arise more from supposition than independent evidence.

Petitioner contends that an upregulation of T helper cells due to receipt of a Tdap booster

could in turn cause pro-inflammatory cytokines secreted by those T helper cells to encourage an

autoimmune disease process. First Gish Rep. at 21–22. The limited evidence that he offered for

this was unconvincing. In van Gemeren, for example, a woman developed AIH after receiving

multiple vaccines, including the Tdap vaccine. van Gemeren at 19. But the authors of this case

report did not include any discussion of the Tdap vaccine. Id. Instead, they narrowed in on the

hepatitis A vaccine as a potential trigger. Id. at 21–22.

da Silva Antunes admittedly provided some evidence relevant to this argument, finding

that people previously vaccinated with the whole cell pertussis vaccine produce more IL17

cytokines after booster vaccination (for the subset of the sample that previously received a whole

cell pertussis version of the vaccine—presumably true of Petitioner as well). da Silva Antunes at

3–4. But does this mean that the levels of cytokines generated in reaction would be enough to be

pathogenic—if not in the specific context of AIH, then with respect to any autoimmune disease?

da Silva Antunes does not say. And its more limited observation was rooted in an evaluation of

the comparative immunologic value of acellular versus whole-cell pertussis - not the pathogenic

potential of the Tdap vaccine. da Silva Antunes at 3855–56. The article includes no discussion of

AIH. And Dr. MacGinnitie persuasively also pointed out that the sample size of the da Silva

Antunes study was limited, that it did not observe large increases in the production of these

cytokine-generating helper cells, and otherwise that these T cells themselves are not considered

per se pathogenic in any event. First MacGinnitie Rep. at 9–10.

Lafdil does not bridge this evidentiary gap sufficiently. It does observe that T-helper cells

play some role in the development of autoimmune liver disease—in particular through

encouragement of a kind of pro-inflammatory cytokine associated with different kinds of liver

illnesses—some of which are analogous to AIH. Lafdil at 250, 251–52. Again, however—does

42

this lead to the conclusion that receipt of a Tdap booster is likely to raise these cytokines to

pathogenic levels, and thereupon spur on AIH? Lafdil does not so conclude, and it is speculative

to do so here. Petitioner has only shown that there is scientific support for the conclusion that this

kind of T helper cell is involved in an AIH-like disease process. But that is not the same as the

determination that vaccination likely leads to the disease process. There are too many missing

links in the causation chain to so conclude.

Overall, this element of the causation theory reflects Petitioner’s continued effort to

transmute narrow, scientifically-reliable facts (derived from limited but methodologically

reasonable studies) into a basis for pathology which itself is ultimately speculative. Even if a Tdap

booster results in the production of certain T cells that could be associated with autoimmune

disease, this does not mean they drive or initiate that disease—or that they are upregulated by

vaccination in amounts sufficient to cause disease. And Petitioner’s showing, in the absence of

other evidence implicating the Tdap vaccine (or its viral/bacterial components) to AIH, is even

more faint in supporting causation.

3. Insufficient Evidence Was Offered to Establish

The Risk of Receiving Two Vaccines at Once

Dr. Gish argues that the administration of both vaccines at the same time raised the risk of

an aberrant response. Tr. at 51, 63. But this is a barely plausible contention that lacked

corroboration from materials filed in this case. No studies were offered that evaluated via a

trustworthy methodologic experiment the impact of receiving two vaccines at the same time – in

the context of any autoimmune disease. At most, some case reports were filed in which at least

one of the relevant vaccines was administered. See, e.g., Veerappan, van Gemeren. While the

authors of Veerappan suggest that AIH may be a complication in patients who receive multiple

vaccinations simultaneously, they do not explain why. Veerappan at 212. And in Veerappan, the

patient received four vaccines simultaneously, as opposed to Petitioner’s two. (Otherwise, and as

discussed in greater detail below, there is no evidence in the contemporaneous medical record at

all of any suspect, close-in-time reaction to the vaccines Petitioner received on August 20, 2018—

further distinguishing the present case from Veerappan).

4. Dr. Gish’s Molecular Mimicry Mechanism for Driving

AIH Due to Vaccination Was Inadequately Corroborated

Admittedly, Petitioner in this case did not primarily rely on a theory that antigenic

similarity between components of either vaccine she received and protein components in the liver

caused an autoimmune cross-reaction, resulting in AIH. Dr. Gish, however, did invoke the concept

as a reliable mechanistic explanation for autoimmune disease. See, e.g., First Gish Rep. at 10, 17,

43

20–21. But he did not substantiate it adequately either, such that I could find it might stand as a

reliable mechanism explaining how the two relevant vaccines, alone or in combination, could lead

to AIH.

Some autoimmune diseases can be mediated by mistaken self-attacks propagated by

antibodies generated in response to a foreign antigen that (due to molecular and/or structural

similarities with a self-antigen protein) then cross-react with the self tissue, often in a

chronic/persistent manner. See, e.g., Bielak v. Sec'y of Health & Hum. Servs., No. 18-761V, 2023

WL 35509, at *33 (Fed. Cl. Spec. Mstr. Jan. 3, 2023) (“[m]olecular mimicry is predominantly

driven by B cell activity, occurring when antibodies are produced in response to antigenic

components of the vaccine—but which (due to mimicry between the presenting vaccine antigens

and self-tissues) cause harmful cross-reactions, by mistakenly attacking the self antigens”).

Because vaccines are usually designed to encourage an adaptive response to a foreign

antigen specifically by “teaching” the immune response to create antibodies to attack the antigen

in future exposures, the mechanism of molecular mimicry fits well with theories that the immune

response to vaccination could become pathologic. But litigants who invoke molecular mimicry to

explain how a vaccine could have triggered an autoimmune disease commonly attempt to show at

a minimum (a) what homology might exist between a vaccine’s antigens and a self-structure

relevant to the situs of harm (here the liver), and (b) what evidence exists that the vaccine would

cause the production of the likely pathogenic antibodies. See K.A. v. Sec'y of Health & Hum. Servs.,

No. 16-989V, 2022 WL 20213037, at *9 (Fed. Cl. Spec. Mstr. Apr. 18, 2022), mot. for review

den’d, 164 Fed. Cl. 98 (2022), aff'd, 2024 WL 2012526 (Fed. Cir. May 7, 2024) (“[b]ecause

homology is common in nature (given the total limited number of amino acids that constitute

proteins), it is important to focus on homology specific to the “disease-related” situs for the cross-

reactive attack”).

Here, however, Dr. Gish has not made a homology showing—which, as Dr. MacGinnitie

noted, is by itself not enough evidence to conclude an autoimmune process linked to vaccination

has been established. He also did not otherwise offer evidence suggesting that the vaccines or their

wild viral counterparts are associated with any antibodies thought to drive AIH or be involved in

its pathogenesis. There is thus very little evidence in this record that would support molecular

mimicry due to vaccination as a mechanistic explanation for AIH.

In reaching my conclusion about the strength and applicability of molecular mimicry as a

mechanism in this case, I acknowledge that petitioners need not offer any mechanism at all in

proving causation. Andreu, 569 F.3d at 1378–79. But what does this mean, in a case where the

Petitioner’s expert did offer several possible mechanisms? Is the special master obligated to avert

his eyes from the strength of the evidence at issue? Must he simply assume a briefly-invoked

mechanism reasonable, without consideration of the weaknesses noted in it by Respondent?

Relevant and controlling case law says otherwise. Howard v. Sec'y of Health & Hum.

Servs., No. 16-1592V, 2022 WL 4869354, at *24 (“[o]f course, petitioners are never required to

44

establish mechanism—but they often attempt to do so, and therefore it is reasonable to evaluate

their success in the effort”) (Fed. Cl. Spec. Mstr. Aug. 31, 2022), mot. for review den’d, 2023 WL

4117370 (Fed. Cl. May 18, 2023), aff'd, 2024 WL 2873301 (Fed. Cir. June 7, 2024). I may evaluate

whether a proposed pathologic mechanism has been evidentiarily supported—and this one has not.

Claimants cannot both invoke a possible mechanism to flesh out their causation theory, but then

evade its deficiencies by objecting they were never obligated to prove it in the first place.

5. Case Reports are Weak Causation Evidence, and

Those Offered Were Largely Unhelpful to Petitioner

Petitioner offers a number of case reports in support of her causation argument. See Saliba,

Sasaki, Perumalswami, Subramanian, van Gemeren, Berry, Veerappan. At the outset, however, it

is plain that several of them (Berry, Perumalswami, Sasaki) do not involve the Tdap or MMR

vaccines (or even comparable wild virus infections). Berry, Perumalswami, and van Gemeren

involve the hepatitis A and/or B vaccine; Subramanian a hepatitis A wild infection; and Sasaki the

flu vaccine. This fundamental fact distinction greatly saps such case reports of evidentiary value

in the context of this case. See Herms v. Sec'y of Health & Hum. Servs., No. 19-70V, 2024 WL

1340669, at *21 (Fed. Cl. Spec. Mstr. Mar. 4, 2024) (“Petitioner does not explain how data from

other unrelated vaccines could be extrapolated to the vaccines at issue here and accordingly, the

data is not persuasive”), mot. for review den’d, 173 Fed. Cl. 1 (2024); see also Deshler v. Sec'y of

Health & Hum. Servs., No. 16-1070V, 2020 WL 4593162, at *19–21 (Fed. Cl. Spec. Mstr. July 1,

2020) (declining to attribute case reports on the flu vaccine to the causation potential of

pneumococcal vaccines).

Saliba is the most factually-relevant case report, since it involves a patient who developed

hepatitis after receipt of the MMR vaccine. Saliba at 379. But the patient in Saliba experienced

acute hepatitis, which is distinguishable from AIH, a chronic condition. Additionally, the patient

in Saliba developed obvious symptoms of liver disease within two weeks of vaccination, while

Petitioner’s first confirmed symptom (elevated liver enzymes) appeared two months post-

vaccination. It is thus factually distinguishable in important respects.

In a larger sense, case reports are of limited value in determining causation—even when

they are factually relevant. Special masters have repeatedly observed that case reports present only

a temporal sequence of events, and thus stand as very thin evidence of causation. Demore v. Sec'y

of Health & Hum. Servs., No. 20-1265V, 2024 WL 4542934, at *7 (Fed. Cl. Sept. 26, 2024), aff'd,

No. 20-1265V, 2025 WL 868902 (Fed. Cl. Mar. 20, 2025); see also 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”).

45

Dr. Gish devoted much of his supplemental expert report to attempting to defend case

reports, especially given the rarity of vaccine injuries. See generally Second Gish Rep. at 1–4. But

his reasoning rings hollow. A case report may be the place to start a causation inquiry, but that

effort must then build upon other evidence that suggests the temporal/coincidental observation of

post-vaccination injury is scientifically meaningful. And here, the paucity of case reports specific

to the vaccines at issue and AIH do not appreciably add to the total picture. Dr. Gish reasons that

case reports suggest a one-time occurrence might repeat elsewhere (Second Gish Rep. at 3 (“if

something did happen in another person, then logically the event can happen in this patient”)—but

this kind of logic does not pass muster in the Vaccine Program when uncorroborated with other

evidence.

6. Other Proposed Mechanisms Were Inadequately Developed

Petitioner’s causation showing included a number of additional independent theories or

mechanisms that were only briefly touched upon, but never substantiated into something sufficient

to be deemed preponderantly established. These contentions accordingly merit even less weight

than the better fleshed-out aspects of the causation theory discussed above, like the proposed

impact of measles vaccine-associated immune suppression.

For example, as evidence for the contention that the measles vaccine component could

literally “infect” certain immune cells, Petitioner referenced Rennick. But as I have noted above,

an article like Rennick has more to say about the function of the measles vaccine from an

immunologic standpoint than it does about the vaccine’s allegedly-pathogenic capacity (which is

what is at issue in this case). Its observation about the way the vaccine’s antigens are taken up by

immune cells cannot be alone stretched into a finding that this in turn increases the likelihood the

vaccine will, at some later time, unexpectedly cause measles-associated immune suppression of

some kind. Thus, Rennick stands as another instance in which Petitioner seeks to take anodyne

scientific findings about vaccine performance and speculatively recast them into proof of

pathology.

Petitioner proposed bystander activation of nonspecific immune cells (and/or suppression

leading to expansion of these immune cells) as another way AIH might occur. First Gish Rep. at

9, 10; Tr. at 42, 58. But there was inadequate evidence supporting this mechanism as likely causal

of AIH due to vaccination. 25 Dr. MacGinnitie persuasively explained that usually bystander

activation would only be thought to occur in the presence of active inflammation due to an

infectious process (which was never shown to have happened in this case). Tr. at 158–60. And

25

In fact, articles like Mack did not even mention bystander activation as an understood mechanism for AIH (Tr. at

160)—although Dr. MacGinnitie admitted on cross-examination that Mina mentioned bystander activation as

something a vaccine could encourage—blunting this contention somewhat.

46

articles like Benn are focused on the positive, secondary effects of this kind of nonspecific immune

stimulation, rather than supporting the contention that vaccine-associated bystander activation is

harmful. Benn at 432, 436–37.

Dr. Gish also spoke generally of immune tolerance being broken by a T cell-driven process,

resulting in harm to liver cells. Tr. at 53–54; Petitioner’s Post-Hearing Brief, filed May 31, 2024

(ECF No. 73) (“Br.”) at 9. This is consistent with how AIH likely unfolds—but a description of

the pathogenesis of the disease in question does not also establish causation, if not yoked to

sufficient reliable proof to conclude the vaccine can be an aspect of the disease process. I have

already observed above that explanations like measles-associated immunosuppression, or Tdap

booster-driven T helper cell increases, do not “work.” And certainly no other, more direct evidence

was offered to show how these vaccines would break immune tolerance. Petitioner could not

simply take a truism about the illness in question and then turn that into evidence of vaccine-

instigated pathology, without better and more persuasive proof.

7. Respondent’s Experts Were More Persuasive

Than Dr. Gish on the Question of Vaccine Causation

Another factor bearing on my prong one determination is my assessment of the experts,

who I saw and heard live at hearing. Dr. Gish was certainly qualified to offer an opinion in this

case as a general matter, given his expertise in hepatology. But he has no specific expertise

studying AIH’s pathogenesis (even if he has a background in the treatment of liver-associated

diseases, and has some reasonable insights gleaned from that experience). In addition, he was

matched against another, equally-qualified hepatologist (Dr. Crippin) who also reasonably relied

on his own experience in questioning causation. Worse, Dr. Gish lacks demonstrated expertise in

the field of immunology—and the opinions he offered on this subject were persuasively rebutted

by Dr. MacGinnitie—the sole immunologist who testified herein. I therefore have given Dr. Gish’s

generalized and somewhat broad contentions about the alleged immune process that could lead to

AIH post-vaccination less weight than the Respondent’s experts’ testimony.

This is not a case where I deemed an expert to have lacked core “credibility.” 26 But

weighing of expert testimony is not limited to determining bare-bones questions of personal

honesty or truthfulness. Nor does Program law ever compel me to accept an expert’s ipse dixit.

Snyder II, 88 Fed. Cl. at 743. While Dr. Gish presented an opinion favorable to Petitioner, that

was not the end of my evaluation of it—and as discussed herein, I deem it ultimately wanting, since

26

I do, however, share the opinion offered by Dr. MacGinnitie that it was “difficult to follow a logical, step by step

theory of causation in Dr. Gish’s Report,” which was excessively wordy, meandering, and unclear in the theory it

embraced. MacGinnitie Rep. at 6. His enunciation of that theory at hearing was not much more illuminating—and

although I have attempted to summarize his views in a more ordered fashion, it has not been easy (and this also detracts

from the theory’s persuasiveness).

47

it was unsupported by sufficient corroborating evidence. Dr. Gish too often tried to leverage things

known about AIH into proof of vaccine pathology, without sufficient connective evidence;

exaggerated the impacts of the measles vaccine into a disease process; and relied on older studies

that have not been subsequently shown to have the same significance they might once have been

thought to possess. Dr. Gish’s theory did not add up, independent of his expertise as a hepatologist,

and even if some of its components were individually reliable.

In summary: Petitioner was unable to establish that the Tdap vaccine and/or MMR vaccine

can likely cause autoimmune hepatitis. I make this finding based on an in-depth review of all the

evidence presented by both parties. Petitioner has not provided enough reliable evidence that the

MMR vaccine causes clinically significant immunosuppression leading to an autoimmune disease

like AIH. For these reasons, I find that the first Althen prong is unsatisfied.

B. Althen Prong Two

Under the second Althen prong, a petitioner must prove actual causation—that the

vaccine(s) at issue “did cause” the alleged injury/illness—by a preponderance of the evidence.

Boatmon, 941 F.3d at 1355.

The evidence in the record for this matter does not so preponderate. I mostly base this

determination on the absence of objective record proof from which it could be inferred that

Petitioner’s August 20, 2018 vaccinations caused any aberrant reaction. Thus, Petitioner’s medical

records contemporaneous to her vaccination date are devoid of evidence that she experienced any

close-in-time vaccine reaction. In addition, she never tested positive for inflammation biomarkers

that might corroborate that she was experiencing some kind of inflammatory event before her liver

test values became elevated. Petitioner was not shown to have possessed an active measles

infection (key to Dr. Gish’s opinion about suppression), and was not demonstrated to be

experiencing any form of hepatitis infection, or even any other opportunistic infectious process

that could be thought to have occurred in the wake of the alleged measles vaccine-caused immune

suppression (and thus might demonstrate indirectly that she was then suffering from immune

suppression). I also have not ascertained any instance where any of Petitioner’s treaters proposed

the vaccinations explained her AIH (including Drs. Oloruntoba or Wu).

What remains is the fact that Petitioner experienced some post-travel nonspecific

symptoms which did not immediately merit treatment (and which arguably were consistent with

her pre-vaccination health). While these concerns (in particular, fatigue) seem likely related to

Petitioner’s subsequently-diagnosed AIH, they are not enough of a basis to conclude that the two

vaccines Petitioner received “did cause” her AIH. Petitioner received the two vaccines, traveled

abroad, then a few weeks later felt fatigue, and then inadvertently was found to possess elevated

LFTs. To deem this sufficient to establish “a logical sequence of cause and effect” as required for

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the “did cause” prong would be to elevate the temporal relationship between vaccination and injury

(here, already somewhat attenuated) into compelling proof of causation. Grant v. Sec'y of Health

& Hum. Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992) (“[a] proximate temporal association alone

does not suffice to show a causal link between the vaccination and the injury”). 27

It is also very important to give weight to the circumstances in which Petitioner received

these vaccines—for her vaccinations did not occur in a vacuum. While Dr. Gish did observe the

absence of some risk factors for AIH relevant to Petitioner (for example, she had not tested positive

for a hepatitis viral infection), he did not persuasively account for the risk factors that were present

—even though he acknowledged the relevance of this kind of evidence to causation. Tr. at 20 (Dr.

Gish testifying that reviewing an individual’s medication history is “really key” to determining

what may have caused AIH). Petitioner’s recent post-vaccination foreign travel (which clearly

could have exposed her to any number of possible pathogens), plus her acknowledged receipt of

anti-malarial medications and supplements, were all potential causal factors.

The anti-malarial medication Petitioner received is an example of the kind of confounding

factor undermining vaccines as causal in this case. It is well-established that medication toxicity

is a risk factor for liver dysfunction. See e.g., Tr. at 86 (Dr. Gish acknowledging the existence of

drug-induced liver disease). And in Beretta-Piccoli, a patient developed long-term autoimmune

hepatitis (comparable to AIH) while taking the same anti-malarial medication as Petitioner.

Beretta-Piccoli at 293–95. The fact that this case report patient developed hepatitis on two separate

occasions while taking this medication led the authors to conclude that the medication was “likely”

the cause of the patient’s liver pathology. Id. at 296. And the patient in Beretta-Piccoli stopped

taking the anti-malaria meds four days before she presented at the hospital, but still developed

AIH. Beretta-Piccoli at 294.

Admittedly, it cannot be concluded from this record that the anti-malarial medication likely

caused Petitioner’s AIH. Dr. Gish reasonably noted that this medication typically does not result

in long-term autoimmune disease, and/or should cause harm closer-in-time to when the medication

is being taken. He similarly pointed out some factual differences in the form of hepatitis at issue,

as well as the relevance of when the medication is taken in comparison to onset. And I am reluctant

to give great weight to a case report of any kind – whether offered by Respondent or Petitioner. 28

27

For this same reason, I do not give weight to the pre-vaccination absence of evidence of liver disease or hepatitis

as proof of the vaccine’s role in causing what manifested after. The fact a claimant was not sick before the vaccination,

but sick after, is simply another form of post hoc ergo propter hoc reasoning that the Program rejects.

28

Of course, if the “signal” of otherwise-factually distinguishable case reports like Saliba should be viewed as credible

evidence of causation—as Petitioner urges—then there is no reason to downplay the findings of Beretta-Piccoli simply

because Dr. Gish observes some factual distinctions between that case and the present facts. The same distinctions are

true for Saliba, which involved acute hepatitis and a short onset—and as the adage goes, “sauce for the goose is sauce

for the gander.” I also note that Beretta-Piccoli is considerably more substantive in its analysis than Saliba – the most

on-point case report offered by Petitioner, but which takes the form of a one-page “letter to the editor,” and includes

far less consideration of causality.

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But this medication is clearly something that had a demonstrated capacity to increase Petitioner’s

possible hepatitis risk, and she received it after vaccination (and hence closer in time to her

possible onset).

I am not, on the basis of this record, able to determine what did likely cause Petitioner’s

AIH—and I do not find Respondent preponderantly established a different trigger. But entitlement

is not properly granted simpl

This text is long and has been trimmed here. Open the source document for the complete record.