VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_18-vv-00925
Package ID: USCOURTS-cofc-1_18-vv-00925
Petitioner: Jose Gamboa-Avila
Filed: 2018-06-27
Decided: 2023-09-11
Vaccine: pneumococcal
Vaccination date: 2017-11-13
Condition: Guillain-Barré syndrome
Outcome: denied
Award amount USD: 

AI-assisted case summary:
Jose Gamboa-Avila, a 48-year-old male with HIV-AIDS, filed a petition alleging that a pneumococcal vaccine received on November 13, 2017, caused him to develop Guillain-Barré syndrome (GBS). He reported symptoms including body aches, headache, night sweats, and numbness starting around the vaccination date, progressing to facial droop, difficulty eating, and weakness. He was hospitalized and diagnosed with GBS in December 2017. The case proceeded as an off-Table claim, requiring proof of causation. Petitioner's expert, Dr. Lawrence Steinman, proposed a molecular mimicry theory, suggesting that components of the pneumococcal vaccine, specifically phosphoglycerol and phosphocholine, could cross-react with nerve myelin, leading to GBS. He also proposed a secondary theory involving the vaccine's conjugate component. Respondent's expert, Dr. J. Lindsay Whitton, countered that the pneumococcal vaccine's components are not known to cause GBS, that the underlying bacterium is not associated with GBS, and that the vaccine's structure differs significantly from known GBS triggers like Campylobacter jejuni. Dr. Whitton also argued that studies cited by Dr. Steinman, particularly those related to Multiple Sclerosis (MS), were not applicable to GBS. The Chief Special Master denied entitlement, finding that Petitioner failed to preponderantly establish that the pneumococcal vaccine can cause GBS, which was a sufficient basis for dismissal. The court later affirmed this decision on review, agreeing that the Chief Special Master applied the correct preponderance standard and that the evidence presented did not establish the necessary causal link.

Theory of causation field:
Off-Table

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_18-vv-00925-0
Date issued/filed: 2023-10-06
Pages: 42
Docket text: PUBLIC DECISION (Originally filed: 9/11/2023) regarding 84 DECISION of Special Master. Signed by Chief Special Master Brian H. Corcoran. (ag) Service on parties made.
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Case 1:18-vv-00925-DAT Document 85 Filed 10/06/23 Page 1 of 42
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 18-925V
(to be published)
* * * * * * * * * * * * * * * * * * * * * * * * * * * * *
* Chief Special Master Corcoran
JOSE GAMBOA-AVILA, *
*
*
Petitioner, * Dated: September 11, 2023
*
v. *
*
SECRETARY OF HEALTH *
AND HUMAN SERVICES, *
*
Respondent. *
*
* * * * * * * * * * * * * * * * * * * * * * * * * * * * *
Curtis R. Webb, Attorney at Law, Monmouth, OR, for Petitioner.
Colleen Clemons Hartley, U.S. Dep’t of Justice, Washington, DC, for Respondent.
ENTITLEMENT DECISION1
On June 27, 2018, Jose Gamboa-Avila filed a petition for compensation under the National
Vaccine and Injury Compensation Program (the “Vaccine Program”).2 (ECF No. 1) (“Petition”).
Petitioner alleges that a pneumococcal vaccine he received on November 13, 2017, caused him to
incur Guillain-Barré syndrome (“GBS”). Id.
The parties have agreed that the matter could reasonably be resolved via ruling on the
record and filed briefs in support of their respective positions. See Petitioner’s Motion, dated
January 14, 2022 (ECF No. 72) (“Mot.”); Respondent’s Opposition, dated April 29, 2022 (ECF
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 Decision 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) [hereinafter “Vaccine Act” or “the
Act”]. Individual section references hereafter will be to Section 300aa of the Act (but will omit the statutory prefix).

Case 1:18-vv-00925-DAT Document 85 Filed 10/06/23 Page 2 of 42
No. 76) (“Opp.”); Petitioner’s Reply, dated June 2, 2022 (ECF No. 80) (“Reply”). In addition,
counsel presented oral argument on February 13, 2023. ECF No. 83 (transcript of proceedings).
Having reviewed the above plus the filed medical records, expert reports, and associated
literature, I hereby deny an entitlement award. As discussed in greater detail below, Petitioner has
not preponderantly established that the pneumococcal vaccine can cause GBS—and this alone is
a sufficient basis for dismissal. I have reached the same determination in several prior Program
cases, based on a comparable theory, and nothing advanced by Petitioner in this case supports an
alternative finding, or reflects new scientific/medical developments that would provide the
occasion to reconsider my prior reaction to the theory.
I. Factual Background
The core facts of this case need not be given considerable time herein, since it is my
determination that the claim’s resolution turns on the “can cause” causation prong.3 Petitioner,
then 48 years old, received the pneumococcal vaccine during a routine visit for care of his existing
HIV-AIDS diagnosis on November 13, 2017. Ex. 2 at 6–12. He then sought treatment on
November 27, 2017, complaining of generalized body aches, a headache, night sweats, and
numbness since November 13, 2017, the date of his last visit (although the accuracy of this record
is disputed). Id. at 17–21.
The next day, Petitioner again obtained treatment, reporting ongoing complaints that
petitioner reported had been present for seven days, including that his eyes felt swollen; his face
and body felt numb; he was having difficulty eating and could not taste food; his legs hurt when
he walked; he had difficulty sitting or standing for “too long;” and his hands were weak. Ex. 2 at
28–30. On examination, infectious disease specialist Leila Hojat, M.D., observed that Petitioner
had a mild right-sided facial droop, with reduced sensation on the left side of his face and in both
legs. Id. But he had full strength in all of his extremities. Id.
Petitioner went to the emergency room that very night, now complaining of whole-body
muscle pain and numbness that he described as “tingly,” as well as facial weakness, and that these
symptoms made it difficult for him to talk and walk. Ex. 2 at 31–38. Over the next several days,
Petitioner was hospitalized for suspected GBS, and eventually diagnosed with it after discharge in
December 2017. Id. at 63–64, 96, 192–93. There is, however, later evidence in the record in which
physicians contested that diagnosis.
Treaters did discuss the vaccine and its potential relationship with Petitioner’s GBS
beginning as early as November 28, 2017 and lasting until the end of the year. Such statements
3 The parties do disagree as to the accuracy of the GBS diagnosis (see, e.g., Opp. at 13–18), and that this remains an
open issue that would also require resolution if this Decision is reversed. But in the interests of brevity, I focus only
on whether the pneumococcal vaccine can even cause GBS.
2

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were discussed by ten treaters. See, e.g., Ex. 2 at 30, 71–72, 76, 84, 90, 94, 96, 102, 105, 107, 112,
115, 120, 126, 130, 136, 141–42, 145, 151, 155, 207. His treaters discuss the temporal relationship
of his vaccination to his GBS, with some discussing causality. See, e.g., Ex. 2 at 30 (“[h]e was
subsequently hospitalized and is suspected to have [GBS] from his recent Prevnar vaccine”), 72
(“[r]ecent vaccine may potentially predispose to GBS”), 76 (“[p]ossibly triggered by recent
pneumonia vaccine”). However, other treaters simply repeat past impressions. See, e.g., Ex. 2 at
87, 102, 105, 112, 155 (“[v]accine may have been trigger.”).
II. Expert Reports
A. Petitioner’s Expert – Lawrence Steinman, M.D.
Dr. Steinman, a neurologist, prepared four written reports for the Petitioner. Report, dated
June 21, 2020, filed as Ex. 15 (ECF No. 38-1) (“Steinman First Rep.”); Report, dated April 25,
2021, filed as Ex. 39 (ECF No. 55-1) (“Steinman Second Rep.”); Report, dated September 5, 2021,
filed as Ex. 46 (ECF No. 62-1) (“Steinman Third Rep.”); Report, dated January 22, 2022, filed as
Ex. 71 (ECF No. 68-1) (“Steinman Fourth Rep.”). All told, Dr. Steinman prepared more than 100
pages in support of Petitioner’s claim (although many are either devoted to the disputed GBS
diagnosis, or reflect reproduction of charts and wholesale sections of a variety of secondary sources
he has relied upon).
As shown in his CV, Dr. Steinman received his undergraduate degree from Dartmouth
College, and his medical degree from Harvard Medical School. Curriculum Vitae, filed as Ex. 16
on July 16, 2020 (ECF No. 38-2) (“Steinman CV”) at 1. He then completed residencies in
neurology and pediatrics at Stanford University. Id. He has worked as a professor of neurology
and pediatrics at Stanford for the past 40 years. Id.; Steinman First Rep. at 1. He is board certified
in neurology from the American Board of Psychiatry and Neurology. Steinman CV at 2. Dr.
Steinman has also published hundreds of peer-reviewed publications on neurology and
autoimmune diseases. Id. at 6–49. He holds several patents related to the diagnosis and treatment
of autoimmune and demyelinating diseases. Id. at 2–3. He presently serves as the George A.
Zimmerman Professor of Neurological Sciences, Neurology, Genetics and Pediatrics at Stanford
University. Id. at 1.
First Report
After several pages discussing his credentials, Dr. Steinman’s first report summarized the
medical records, accepting Petitioner’s GBS diagnosis. Steinman First Rep. at 4–7. He also
provided an overview of GBS, denying that Petitioner’s preexisting HIV was a likely explanation
for his injury. Id. at 8–9.
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With respect to causation, Dr. Steinman proposed that the pneumococcal vaccine contains
a “molecular mimic” relevant to the pathogenesis of GBS, the “polar head group of the
phosphoglycerol and phosphocholine molecules.” First Steinman Rep. at 11. Thus, his theory
parallels what is often provided in many Program cases: that the mechanism of molecular
mimicry—in which antibodies produced in reaction to a vaccine’s antigenic components cross-
react with/mistakenly attack self structures in the body that resemble the antigens—was the
foundational explanation for how the pneumococcal vaccine would also lead to GBS.
Of course, Dr. Steinman needed to show how molecular mimicry would specifically apply
in this context, and he endeavored to do so. As the “Prevnar-13” package insert indicates,4 the
vaccine comprises a sterile suspension of saccharides of the capsular antigens of Streptococcus
pneumoniae from 13 strains, or serotypes (1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F and 23F),
individually linked to non-toxic diphtheria CRM protein.5 Id. at 10–13 (citing Pneumococcal
197
Package Insert, filed as Ex. 25 on July 16, 2020 (ECF No. 40-9) (“Pneumococcal Package Insert”),
at 24);6 see generally D. Wang et al., Uncovering Cryptic Glycan Markers in Multiple Sclerosis
(MS) and Experimental Autoimmune Encephalomyelitis (EAE), Drug Dev. Res. 172, 185–86
(2014), filed as Ex. 31 (ECF No. 41-5). Certain phospholipids (phosphatidyl serine and
phosphatidyl choline) are also present in the vaccine, expressed in association with its
polysaccharide antigens. Steinman First Rep. at 12. In addition, the CRM protein conjugate
197
requires functional glycerol phosphate “side chains” be retained in the vaccine’s formulation (for
the conjugate to perform its immune-boosting task). Id. at 13.
At the same time, Dr. Steinman stressed (invoking his own personal research in support)
that “phospholipids are components” of the nerve myelin, and are moreover “targeted by
antibodies in neuroinflammation.” First Steinman Rep. at 13–14; P. Ho et al., Identification of
Naturally Occurring Fatty Acids of the Myelin Sheath That Resolve Neuroinflammation, 4 Sci.
Translational Med. 1, 1 (2012), filed as Ex. 22 (ECF No. 27-1) (“Ho”). Ho, however, did not
involve GBS specifically, but multiple sclerosis (“MS”)—a demyelinating autoimmune disease of
the central nervous system—and although it suggests the studied antibodies might contribute to
MS’s pathogenesis, it did not determine that they were the likely instigating spark for an
autoimmune disease. Compare Ho at 1 with First Steinman Rep. at 17–18.
4 Prevnar-13 is a trade name for a form of the pneumococcal vaccine that is covered under the Vaccine Act.
5 “CRM is a nontoxic variant of diphtheria toxin isolated from cultures of Corynebacterium diphtheriae strain Cy
197
(β197) grown in a casamino acids and yeast extract-based medium. CRM is purified through ultrafiltration,
197
ammonium sulfate precipitation, and ion-exchange chromatography.” Pneumococcal Package Insert at 24. It is
included to induce “immunity through a T cell-dependent response.” Deshler v. Sec'y of Health & Hum. Servs., No.
16-1070V, 2020 WL 4593162, at *19 (Fed. Cl. Spec. Mstr. July 1, 2020).
6 Also cited as Respondent’s Ex. M, Tab 5.
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Dr. Steinman offered several other items of literature to support the conclusion that
“phosphosaccharides with the same polar head groups are critical for the immunogenicity” of the
vaccine. First Steinman Rep. at 15; J. Chang et al., Relevance Of O-Acetyl and Phosphoglycerol
Groups for the Antigenicity of Streptococcus Pneumoniae Serotype 18C Capsular Polysaccharide,
30 Vaccine 7090, 7091 (2012), filed as Ex. 32 (ECF No. 41-6) (“Chang”) (demonstrating that a
phospholipid linkage is necessary for immunogenicity of these capsular polysaccharides); C.
Lugowski & H. Jennings, Structural Determination of the Capsular Polysaccharide of
Streptococcus Pneumoniae Type 18C, 131 Carbohydrate Res. (1984), filed as Ex. 44 (ECF No.
68-4) (same); J. Ohori et al., Phosphorylcholine Intranasal Immunization with a 13-Valent
Pneumococcal Conjugate Vaccine can Boost Immune Response Against Streptococcus
Pneumoniae, 38 Vaccine 699, 699 (2020), filed as Ex. 24 (ECF No. 41-8) (“Ohori”); Yi-Ping
Chuang et al., Impact of the glpQ2 Gene on Virulence in a Streptococcus pneumoniae Serotype
19A Sequence Type 320 Strain, 83 Infection & Immunity 682, 682 (2015), filed as Ex. 28 (ECF
No. 27-7) (“Chuang”).
Chang, for example, was offered to establish the immunologic significance of the serotype
18C polysaccharide found in the vaccine’s antigenic components, in order to demonstrate that
“[t]he phosphoglycerol linkage is critically preserved to ensure the vaccine’s function.” First
Steinman Rep. at 15–16; Chang at 7095. This is, however, not a precise construction of Chang’s
findings. It is true that the pneumococcal vaccine must, to be effective, induce the production of
anti-capsular polysaccharide antibodies. Chang at 7090. However, the S. pneumoniae bacteria’s
polysaccharide antigens can have their immunogenicity affected by the manner in which the
conjugated version of the vaccine (deemed the “vaccine of choice to target child protection”) is
manufactured/formulated. Id. Chang’s authors therefore conducted an animal study in which the
relevant capsular polysaccharide used in most versions of the vaccine was treated and prepared in
different ways, then injected into the animal subjects, in order to evaluate “a suitable modification-
conjugation procedure” that would ensure preservation of the most important antigenic features of
the vaccine. Id. at 7095; see also 7091–92. Chang concluded that preservation of the glycerol
phosphate group was more important than the O-acetyl group. Id. at 7095–96. Thus, Chang says
nothing about those antigens being pathogenic, but only that they must exist in the vaccine if it is
to perform as intended.
Dr. Steinman also maintained that Ohori showed “[a]dditional [intranasal] immunization
with [phosporylcholine (“PC”)] after PCV13 immunization, which is currently conducted under a
periodic vaccination program, can produce a booster effect comparable to that achieved by
additional systemic immunization as well as PC-specific mucosal immune response, thereby
providing protection against S. pneumoniae serotypes not contained in PCV13.” First Steinman
Rep. at 16–17; Ohori at 699. Ohori’s focus, however, was on establishing ways to improve the
body’s immune response to the intramuscularly-administered pneumococcal vaccine—here, by
supplementing it with phosphorylcholine administered intranasally, after initial vaccination. Ohori
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at 700 (“the transmucosal administration of PC can induce systemic as well as mucosal immune
responses and thus provide a higher preventative efficacy compared with conventional vaccines”).
Thus, while Ohori may confirm that the vaccine contains PC, it says nothing at all about how the
presence of it could prove pathogenic.
Dr. Steinman did not, however, merely speculate that the putatively-pathogenic antibodies
should be found in the vaccine—he concluded that in fact they “ARE.” First Steinman Rep. at 19
(capitalization in original), citing Chuang. In particular, Dr. Steinman maintained, Chaung
demonstrated that the phospholipid phosphorylcholine is expressed in the 19A serotype
component, which is key in the pathophysiology of the pneumonia infection. Steinman First Rep.
at 19. The enzyme for metabolizing lipids and producing phosphorylcholine was also present in
strains 3, 6B, 19A, and 19F—with three of those strains (strains 3, 19A, and 19f) all included in
the Prevnar formulation. Chuang at 682.
Another article was referenced by Dr. Steinman to show more specifically that the
antibodies of the kind that would (theoretically) be produced by the pneumococcal vaccine are
known to be associated with GBS. B. Gilburd et al., Autoantibodies to Phospholipids and Brain
Extract in Patients with Guillain-Barre Syndrome: Cross-Reactive or Pathogenic?16
Autoimmunity 1, 23–27 (1993), filed as Ex. 27 (ECF No. 41-1) (“Gilburd”); First Steinman Rep.
at 18. However (and ignoring that Gilburd was published nearly 30 years ago, yet does not appear
to have encouraged much, if anything, in the way of follow-up research), the article is more notable
for its caveats and limitations. Thus, Gilburd admits at its outset that “the autoantigen of GBS has
not yet been identified”—still a truism so many years later. Gilburd at 23. Further, its authors note
something even more fundamental—that “it is not settled whether the autoantibodies in GBS
induce the nerve damage or are induced by the demyelination and liberation of autoantigens.” Id.
(emphasis added). Otherwise, Gilburd’s findings were based on testing involving an exceedingly
small sample (16 GBS patients), and its authors reiterated the uncertainty as to what the temporal
role was for these autoantibodies. Id. at 24, 26–27.
The same qualifications apply to a case report filed by Dr. Steinman. First Steinman Rep.
at 18–19; G. Nakos et al., Anti-Phospholipid Antibodies in Serum from Patients with Guillain-
Barré Syndrome, Intensive Care Med. 1401, 1404 (2005), filed as Ex. 28 (ECF No. 41-2)
(“Nakos”). Nakos, Dr. Steinman maintained, observed that “phospholipid antibodies were found
in patients with GBS.” First Steinman Rep. at 18. In Nakos, a small sample of nine patients with
the AIDP (meaning “acute inflammatory demyelinating polyneuropathy”) GBS variant had their
blood tested for the presence of anti-phospholipid antibodies over a period of several days, with
results revealing “a wide range” of these antibodies in comparison to controls. Nakos at 1405.
Nakos did observe phosphatidylcholine (which has a phosphoglycerol component) as one of the
main antigens in the tested sample. Id. at 1405–07. But Nakos’s authors did not purport to
determine the precise role of the autoantibodies in GBS’s pathogenesis, allowing that they could
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simply “represent a part of a more extensive immunoreaction that takes place in the GBS,” rather
than a primary/initial causal factor. Id. at 1406. Thus, evidence of the presence of the putatively-
pathogenic antibody was not the same as evidence it is pathogenic.
Dr. Steinman's own research, he added, had shown that phospholipids are components of
the nerve’s myelin sheath in humans, and that they are targeted by antibodies in the context of
existing neuroinflammation. Steinman First Rep. at 7; J. Kanter et al., Lipid Microarrays Identify
Key Mediators of Autoimmune Brain Inflammation, 12 Nat. Med. 138 (2005), filed as Ex. 21 (ECF
No. 26-8) (“Kanter”). Employing an experimental animal model, Kanter7 determined that (given
the extent to which nerve myelin is comprised of lipids) lipid-specific autoantigens likely played
some role in the pathogenesis of MS—although Kanter is not specific to peripheral neuropathies
like GBS. Kanter at 138, 142. It also did not suggest this role was initial or primary. To the
contrary, Kanter’s authors also noted that prior studies had suggested that the lipid-oriented attacks
might be secondary to ongoing autoimmune-mediated damage, occurring as a result of “epitope
spreading” encouraged by other antibodies. Id. at 141.
Finally, Dr. Steinman endorsed the onset of Mr. Gamboa’s GBS as having occurred in a
medically-acceptable timeframe when measured from date of vaccination. First Steinman Rep. at
20. For support, he invoked an item of literature specific to the 1976 swine flu vaccine (and
something he has cited in virtually every single one of his expert reports involving neuropathies
that I have reviewed since becoming a special master). L. Schonberger et al., Guillain-Barré
Syndrome Following Vaccination in the National Influenza Immunization Program, United States,
1976–1977, 110 Am. J. Epidemiol. 105 (1979), filed as Ex. 30 (ECF No. 27-9) (“Schonberger”).
Because Petitioner’s onset occurred approximately nine days after vaccination, it fell within
Schonberger’s observed risk interval. Schonberger at 109. In so maintaining, Dr. Steinman
proposed that what is known about timing in Schonberger could be applied herein, although he
also admitted that more detailed studies specific to GBS and the pneumococcal vaccine do not
exist. Steinman First Rep. at 9.
Second Report
Dr. Steinman’s next report reacted to the reports filed by each of Respondent’s experts—
although for present purposes only his efforts to rebut Dr. Whitton’s opinion merit discussion. See
generally Second Steinman Rep. at 1–14. First, he contended that in fact S. pneumoniae is
associated with GBS. Id. at 1–3. But he offered only two case reports to substantiate this
contention. H. El Khatib et al., Case Report: Guillain-Barré Syndrome With Pneumococcus – A
New Association in Pediatrics, 11 IDCases 36 (2018), filed as Ex. 40 (ECF No. 56-1) (“El Khatib”)
(13 year old GBS patient was discovered to be suffering from existing case of acute pneumonia);
7 Kanter is another MS-specific study involving several of Ho’s co-authors (in fact, Kanter pre-dates Ho and was cited
therein). See Ho at 2 n.3.
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N. Yuki & K. Hirata, Fisher’s Syndrome and Group A Streptococcal Infection, 160 J. Neurol. Sci.
64 (1998), filed as Ex. 41 (ECF Mo. 56-2) (17 year-old presenting with what was later determined
to be streptococcal tonsilitis later developed Miller-Fisher GBS variant).
Neither case report corroborates a purported association, however. It is, for example, not
self-evident that the El Khatib subject even had GBS, since the patient had an intercurrent wild
infection. Thus, El Khatib demonstrates that the individual in question had Streptococcus
bacteremia from an ongoing bacterial infection, rather than a post-infectious condition that could
be reasonably analogized to a vaccination. El Khatib at 37. And both case report’s authors admitted
that no such association had even been scientifically established. See, e.g., El Khatib at 36
(“Streptococcus pneumoniae . . . has never been associated with GBS in the pediatric age group”).
Even Dr. Steinman acknowledged that the association was less common than C. jejuni. Second
Steinman Rep. at 3.
Second, Dr. Steinman endeavored to rehabilitate his prior argument that the pathologic
process leading to GBS involves the targeting of phospholipid structures in the myelin. See
generally Second Steinman Rep. at 3–9. In reaction to Dr. Whitton’s point that literature (like
Nakos) suggested that the anti-phospholipid antibodies might not be directly causal of GBS, but
instead be generated by the disease process itself, Dr. Steinman protested that this was “not
inconsistent” with his theory. Id. at 3. His point, rather, was that (a) these antibodies “are found”
in GBS, and (b) that they could theoretically be generated by the vaccine. Id. However, Dr.
Steinman nevertheless insisted they did likely play a role in direct disease pathogenesis. Id. (citing
Ho (“antibodies from patients with multiple sclerosis target the phosphate polar hear group (the
phosphoglycerol and phosphocholine moiety) in the phospholipids of the central nervous system”).
And he maintained that it was reasonable to rely on items of literature, like Ho or Kanter, that
focused on MS rather than peripheral neuropathies like GBS, given the “similarity of the antibody
targets” in both diseases. Second Steinman Rep. at 5.
Relatedly, Dr. Steinman attempted to establish that the polar head groups could also, like
gangliosides (about which far more is known, it must be underscored), be the specific target for
the autoimmune cross-reactive processes leading to GBS. Second Steinman Rep. at 5–8. He
contested Dr. Whitton’s argument about the specificity of different kinds of bacterial structures
(and that some were less likely to express ganglioside mimics), maintaining that pneumococcus
was not ruled out despite its structure (although he offered only his case reports, like El Khatib, as
evidence of this). Id. at 5. He also again stated that studies had shown the presence of the antibodies
to phospholipids in the blood sera of GBS patients. Id. at 6–7 (citing Nakos).
More specific to the point at issue, Dr. Steinman maintained that Dr. Whitton’s analysis of
the nature of an antibody attack on the polar head groups misconstrued his actual argument—
which was that the polar heads themselves were a target, as opposed to the “side chains that adorn
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the phosphoglycerol or the phospholipid molecule as a whole.” Second Steinman Rep. at 6. In
support, he referenced Ho. See Ho at 3–4 (“[t]his suggests that autoantibodies present in RRMS
CSF target the phospholipids’ phosphate head group and that the affinity of antibody-lipid binding
is not specific to a particular phospholipid.”). Thus, even though Dr. Steinman conceded that
“gangliosides generally do not contain polar head groups,” and gangliosides might be “important”
in GBS, they were not necessarily the sole disease attack point/trigger (although his substantiation
for this point was quite thin). Second Steinman Rep. at 7–9.8
Third Report
For his next supplemental report, Dr. Steinman opted to write more than 40 pages—almost
the total length of the first two reports put together (and raising the obvious question of why a
responsive report would ever need to be so long).9 Although Dr. Steinman again used the
opportunity to react to both of Respondent’s experts and their criticisms, three-fourths of the report
was aimed at addressing Dr. Whitton.
Dr. Steinman first sought to explain why studies involving MS, which he had relied on in
his earlier reports (see, e.g., Kanter, Ho) could have applicability in the context of GBS. Third
Steinman Rep. at 2–3. He emphasized his expertise researching “[h]ow the immune system attacks
the nervous system,” but otherwise repeated his conclusion that what was seen in the MS context
likely applied to GBS as well. Id. at 2. At most, he admitted that MS’s chronic nature made it
somewhat easier to study.
8 Dr. Steinman also engaged in a lengthy effort to bulwark his prior argument that one of the vaccine’s strains contains
glycerol phosphate, against Dr. Whitton’s contention that it does not. Second Steinman Rep. at 10–11. In so doing, he
noted that articles like Chang established that other strains in the vaccine could also be shown to contain a
phosphoglycerol group, and that its inclusion was important, because it ensured the vaccine’s function. Id. at 11–12;
Chang at 7095 . Dr. Whitton also engaged in this debate in his subsequent reports, protesting that Dr. Steinman was
flat-out wrong. See, e.g., Second Whitton Rep. at 4–5.
I do not highlight this dispute (or attempt to parse which expert ended up “on top” with respect to the particulars of
this sub-debate), because my Althen prong one determination turns more on questions about the general associations
between the vaccine and GBS, as well as the known pathogenic course of GBS—factors that are preponderantly
unsupportive of Dr. Steinman’s theory, even if he is correct that the pneumococcal vaccine’s effectiveness depends in
part of phospholipid molecular structures, or that enough serotypes of the S. pneumoniae bacteria included in the
vaccine contain phosphoglycerol molecules.
9 Of course, much of this wholly-excessive length was not due to the inclusion of actual expert thought or comment.
Rather, and as is common with Dr. Steinman’s expert reports in Program cases, this third report was chock-full of
reproductions of charts or intricate molecular structure images taken from his source materials. Indeed, by my
admittedly-cursory count, the third report alone contains more than 15 chart or figure reproductions (not to mention
numerous lengthy block-quotes from his own prior reports or Dr. Whitton’s). See generally Third Steinman Rep. at
1–30.
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Second, Dr. Steinman again ventured to show how the pneumococcal bacterium could be
associated with GBS, despite Dr. Whitton’s contention that the most reliable authority never
included it in lists of likely antecedent triggers. Third Steinman Rep. at 3–6. He specifically
referenced one such article. See generally A. Jasti et al., Guillain-Barre Syndrome: Causes,
Immunopathogenic Mechanisms and Treatment, 12 Expert Rev. Clinical Immunology 1175
(2016), filed as Ex. A, Tab 17 (ECF No. 45-7) (“Jasti”). Although, Dr. Steinman admitted, Jasti
provided “a long list” of potential triggers for GBS that did not also include S. pneumoniae, it also
supported the conclusions that (a) molecular mimicry was the most likely mechanistic explanation
for how any trigger would lead to GBS, and (b) that a wide array of external insults (viral as well
as bacterial) could cause GBS. (He also made some less-well-supported contentions about Jasti,
such as representing that it demonstrated gangliosides were not the only possible target for cross-
reaction. Jasti at 1184).10
From this, Dr. Steinman moved to a slightly different contention: that the pneumococcal
vaccine could theoretically cause GBS even if a natural pneumococcal infection could not,
reasoning that “the vaccine is very different from the microbe itself.” Third Steinman Rep. at 3. In
so arguing, he noted that the vaccine did not merely contain bacterial serotypes, but was conjugated
to the non-toxic diphtheria CRM protein, to improve its immunogenicity for its targeted
197
“audience” (young children and the elderly). Id. at 4–5. But that protein was only slightly different
from the diphtheria toxin. Id. at 4.
Later in his third report, Dr. Steinman explained this contention in more detail. Third
Steinman Rep. at 17–18, 23–29. All 13 of the vaccine’s polysaccharide serotypes are “covalently
linked” to the CRM conjugate (which Dr. Steinman described as “reductive amination”). Id. at
197
18. This was necessary to preserve “the chemical structure of the phosphoglycerol moiety.” Id.
But in addition to providing this function, the conjugate also contained an additional mimic that
could cause GBS (although he deemed it not mutually exclusive to the primary antigenic,
phosphoglycerol-containing components that his prior reports had focused on). Id. at 24.
Specifically, the conjugate includes Contactin-1, a molecule “that is targeted in some cases
of GBS.”11 Third Steinman Rep. at 24; Y. Miura et al., Contactin I IgG4 Associates to Chronic
Inflammatory Demyelinating Polyneuropathy with Sensory Ataxia, 138 Brain 1484, 1486 (2015),
filed as Ex. 56 (ECF No. 63-10) (“Miura”) (aiming to describe the clinical and serological features
10 For good measure, Dr. Steinman threw in the proposition that the Petitioner had tested negative for anti-ganglioside
antibodies. Third Steinman Rep. at 3. To some extent, however, this raises a question relevant to the second Althen
prong, and hence I do not discuss it. If the pneumococcal vaccine cannot likely cause GBS, it does not matter what
kinds of antibodies Petitioner was shown by testing to possess (or not).
11 Contactin-1 is a molecule that some studies have identified as a target in the myelin damage central to GBS.
Trollinger v. Sec'y of Health & Hum. Servs., No. 16-473V, 2023 WL 2521912, at *8 (Fed. Cl. Spec. Mstr. Feb. 17,
2023), mot. for review den’d, No. 16-VV-473, 2023 WL 5249583 (Fed. Cl. July 31, 2023).
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of Japanese patients with CIDP displaying the anti Contactin-1 antibodies). A different article, Dr.
Steinman proposed, established the possibility that the conjugate could express a mimic for
Contactin-1. Third Steinman Rep. at 29; R. Raju et al., Epitopes for Human CD4+ Cells on
Diphtheria Toxin: Structural Features of Sequence Segments Forming Epitopes Recognized by
Most Subjects, 25 Eur. J. Immunology 3207, 3207 (1995), filed as Ex. 55 (ECF No. 63-9) (“Raju”)
(focusing on the generation of T helper cells in reaction to diphtheria toxin—not showing that
antibodies would cross react with Contactin-1).
To identify the possible molecular congruence, Dr. Steinman conducted a “BLAST”
search12 focusing on Contactin-1 in comparison with the conjugate’s components. Third Steinman
Rep. at 24. He thus performed the same desktop computer analysis he has offered in countless
Program cases,13 where he seeks to establish the potentiality of molecular mimicry. Specifically,
he (a) attempted to propose the degree of amino acid homology that would be necessary, arguing
that five out of a twelve amino acid string is sufficient (Id. at 25) (b) performed searches with the
BLAST online government database for the components of the pneumococcal vaccine, to identify
the amino acids comprising them, and determine whether other researchers identified the same
epitope(s)14, and (c) compared them to the molecular composition in identified portions of myelin.
Id. at 25–29. He concluded from the foregoing that “a compelling theory” existed in support of his
contention that even based on the conjugate itself, “molecular mimics in the [pneumococcal
vaccine] can cause GBS.” Id. at 29.
Dr. Steinman also sought to add heft to his prior contention that the vaccine could likely
induce cross-reactive antibodies specific to neuronal polar head groups found in or on the nerve
myelin. Third Steinman Rep. at 8–13. He stressed that the vaccine contained phosphoglycerols in
at least some of its included polysaccharide strains, and that they played an important role in
ensuring immunogenicity. Id. at 8–9, 14–15, citing Chang at 7095. Because (as established in
Chang) the phosphoglycerol structure was important to the bacteria’s ability to cause infection in
12 Basic Local Alignment Search Tool (“BLAST”) is a medical/scientific internet resource that assists researchers in
finding regions of similarity between biological sequences of amino acids. The program compares nucleotide or
protein sequences to sequence databases and calculates the statistical significance. BLAST, U.S. National Library of
Medicine, https://blast.ncbi nlm nih.gov/Blast.cgi (last visited Feb. 17, 2023). A BLAST search involves review of an
online database to “compare[] nucleotide and protein sequences, to search for a homology between the . . . vaccine
and [the body's myelin basic protein].” Montgomery v. Sec'y of Health & Hum. Servs., No. 15-1037V, 2019 WL
2511352, at *5 (Fed. Cl. Spec. Mstr. May 21, 2019).
13 Schilling v. Sec'y of Health & Hum. Servs., No. 16-527V, 2022 WL 1101597, at *5 (Fed. Cl. Spec. Mstr. Mar. 17,
2022) (“[Dr. Steinman] also (as he has done many times before) performed online BLAST searches to identify amino
acid sequence homology. . . .”).
14 Dr. Steinman first tested the sequence WEQAKALSVE and identified it as an area of alignment between contactin-
1 and CRM , determining it is “an epitope in diphtheria toxin, which provide the basis for CRM .” Steinman Third
197 197
Rep. at 28. Dr. Steinman tested a second sequence, EYMAQACAGNRVRR, which also has “known cross-reactivity
with epitopes described in humans and on the c. diphtheria microbe that is the basis for CRM .” Id. at 29.
197
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the lung, it was also a “critical target” for an immune response intended (due to the vaccine) to
arrest the bacterial progress. Third Steinman Rep. at 16; Chang at 7090, 7095.
Other literature more specifically demonstrated, in Dr. Steinman’s estimation, the degree
to which the pneumococcal vaccine’s phosphoglycerol components likely sparked a directed
immune response. Third Steinman Rep. at 17; Bryson et al., Structures of Preferred Human IgV
Genes-Based Protective Antibodies Identify How Conserved Residues Contact Diverse Antigens
and Assign Source of Specificity to CDR3 Loop Variation, 196 J. Immunology 4723, 4725, 4727–
28 (2016), filed as Ex. 65 (ECF No. 79-4) (“Bryson”). Bryson, he explained, showed that the
immune response to the vaccine “targets” phosphoglycerol in serotype 23F. Third Steinman Rep.
at 9–10, 12 (deeming the evidence from Bryson on this point to “UNEQUIVOCALLY” support
his contention (emphasis in original)); Bryson at 4723–24. Further, the fact that phosphoglycerol
was not present for all 13 of the vaccine’s serotypes did not make a difference to Dr. Steinman.
The vaccine, he maintained, was intended to generate an individual response to each separate
serotype, and thus only one serotype including phosphoglycerol was needed to generate the
antibodies against the polar heads. Third Steinman Rep. at 13.
Otherwise, Dr. Steinman reiterated points he had already covered in his two prior efforts.
For example, he maintained that epidemiologic studies might establish the vaccine’s general
safety, but could not disprove the possibility of vaccine-caused injury. Third Steinman Rep. at 6–
7; P. Haber et al., Post-Licensure Surveillance of 13-Valent Pneumococcal Conjugate Vaccine
(PCV13) in Adults Aged 19 Years Old in the United States, Vaccine Adverse Event Reporting
System (VAERS), June 1, 2012–December 31, 2015, 34 Vaccine 6330, 6330, 6333–34 (2016), filed
as Ex. M, Tab 7 (ECF No. 78-7) (“Haber”); H. Tseng et al., Pneumococcal Conjugate Vaccine
Safety in Elderly Adults, Open Forum Infectious Diseases 1, 1 (2018), filed as Ex. M, Tab 8 (ECF
No. 78-8) (“Tseng”). Tseng, in fact (in Dr. Steinman’s reading) revealed what he deemed an
unexplained “high incidence” of GBS for those receiving the pneumococcal vaccine versus an
expected background rate (four cases in a 1–42 period for a sample of 313, 136 vaccinated
individuals, versus one case for 78,284 individuals). Tseng at 7.
Fourth Report
Dr. Steinman’s final written report focused more on Dr. Whitton’s rejoinders than
commenting on Dr. Chaudhry’s final opinions. See generally Fourth Steinman Rep. at 1–14.
Dr. Steinman relied on some recent studies, one of which he co-authored, to bulwark the
mechanistic aspect of his theory. See Fourth Steinman Rep. at 1, 5–6; W. Robinson & L. Steinman,
Epstein-Barr Virus and Multiple Sclerosis, 21 Science 375:264 (2022), filed as Ex. 72 (ECF No.
68-2) (“Robinson & Steinman”); T. Lanz et al., Clonally Expanded B Cells in Multiple Sclerosis
Bind EBV EBNA1 and GlialCAM, 603 Nature 1 (2022), filed as Ex. 73 (ECF No. 68-3) (“Lanz”).
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Of course—and as Dr. Steinman conceded—these articles relate solely to MS and a possible
disease-driving mimic between self amino-acid sequences and the Epstein-Barr virus (“EBV”),
and thus specifically say nothing about a different vaccine and different disease. Fourth Steinman
Rep. at 1; Lanz at 1; Robinson & Steinman at 1. However, Dr. Steinman deemed them relevant
because they undermined the degree of homology Dr. Whitton had argued was necessary for a
likely cross-reaction. Fourth Steinman Rep. at 5–6.
Otherwise, Dr. Steinman’s fourth report simply repeated his prior contentions in the tit-for-
tat debate between him and Dr. Whitton evident from their prior written exchanges. He again
argued that MS-specific studies had evidentiary value, summarizing the findings from articles
previously discussed, like Ho (which showed polar head targeting in MS), and connecting them to
Nakos (which he now maintained revealed “more antibody to phospholipid than to ganglioside in
patients with GBS”). Fourth Steinman Rep. at 1–2. He repeated the same comparison, while adding
in references to Chang, Chuang, and Bryson, to defend the contention that the phosphoglycerol-
specific antibodies could cross-react with polar group heads, stressing again the point that reliable
science showed the existence of phosphoglycerol in the 23F serotype strain. Id. at 2–4.15 Lastly,
Dr. Steinman took on directly Dr. Whitton’s criticisms of his data search methodology and analysis
(discussed below), arguing that it had scientific reliability and merit. Id. at 4–14.
B. Respondent’s Expert16 – J. Lindsay Whitton, M.D., Ph.D. – Dr. Whitton, an
immunologist, submitted three expert reports for the Respondent in support of the argument that
the pneumococcal vaccine does not likely cause GBS. Report, dated September 2, 2020, filed as
Ex. A (ECF No. 44-1) (“First Whitton Rep.”); Report, dated August 3, 2021, filed as Ex. G (ECF
No. 61-1) (“Second Whitton Rep.”); Report, dated November 23, 2021, filed on November 23,
2021 (ECF No. 67-1) (“Third Whitton Rep.”). Dr. Whitton disputed the contention that the
phosphoglycerol/glycerophosphate-containing polysaccharides in certain pneumococcal vaccine
antigens could induce an antibody response that causes GBS, or that the conjugate could similarly
spark an autoimmune attack.
Dr. Whitton obtained his undergraduate, medical, and doctorate degrees from the
University of Glasgow in Scotland. Curriculum Vitae, filed as Ex. B on September 2, 2020 (ECF
No. 45-12) (“Whitton CV”) at 1; Whitton Rep. at 1. He then began working as a senior research
associate at the Scripps Research Institute in La Jolla, California, where he studied immunology,
vaccinology, and viral pathogenesis. Whitton CV at 1; Whitton Rep. at 1. Dr. Whitton has
conducted extensive research in these subject areas and has published numerous articles on the
15 He also copied wholesale charts and images in the final report from his earlier offerings. Compare Third Steinman
Rep. at 10–11 with Fourth Steinman Rep. at 3–4.
16 Although diagnostic expert, Dr. Vinauy Chaudhry, also prepared several written reports, I do not summarize them
because of my focus herein on the first causation prong.
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subjects. Whitton CV at 2–15. In addition to his research, Dr. Whitton also serves as a professor
in the department of Immunology and Microbial Science at Scripps Research Institute. Whitton
CV at 1. In both his research and teaching, Dr. Whitton has focused on viral pathogenesis, innate
and adaptive immune responses, and molecular mimicry. Whitton Rep. at 1–2. Dr. Whitton does
not have board certification in the United States to practice medicine. Id. at 2.
Dr. Whitton began with a lengthy discussion of the pneumococcal vaccine itself. First
Whitton Rep. at 3–6. The vaccine aims to immunize against a bacterial infection caused by S.
pneumoniae, or “pneumococcus.” Id. at 3. The S. pneumoniae bacterium is surrounded by a
“capsule” made of polysaccharides. Id. at 3–4. Polysaccharides are made up of sugar molecules
and occur throughout nature, but are distinguishable from a protein (which is comprised of chains
of amino acids). Id. Amino acids contain only two attachment points, so amino acid chains have a
linear character. Id. at 4. Sugars, on the other hand, have several different points at which they can
link, resulting in different molecular “shapes.” Id.; J. Prestegard et al., Oligosaccharides and
Polysaccharides, Essentials of Glycobiology 1, 4 (2017), filed as Ex. A, Tab 1 (ECF No. 44-2).
Thus, because of such variation, the pneumococcal vaccine can only “teach” the immune system
to respond to the specific strains it “sees” (based on the strains in the vaccine), with each being
separate. First Whitton Rep. at 5. There are close to 100 serotypes17 of pneumococcus, and they
are distinguished based on having structurally-different polysaccharide capsules. Id.
In addition, Dr. Whitton explained the “conjugated” character of the version of the
pneumococcal vaccine at issue—Prevnar-13. Although adults can mount a robust immune
response when exposed simply to the bacterial polysaccharides alone, it has been found that
children (especially infants) do not. First Whitton Rep. at 5. As a result, to boost the immune
response (and in particular the intended production of antibodies to the S. pneumoniae bacterium),
the vaccine’s antigenic components are linked, or conjugated, to a protein that “can trigger a
reasonably strong T cell response” (and in this case Dr. Whitton referred to “helper T cells”—
lymphocytes that assist B cells in production of antibodies specific to the vaccine’s polysaccharide
antigens).18 Id. at 6.
Only the conjugated version of the pneumococcal vaccine is “covered” by the Vaccine
Program,19 and many studies have noted not only its general safety, but the fact that it (or at least
17 Dr. Whitton defined serotype to mean “this organism is distinguished from related organisms on the basis of how it
is recognized by the antibody response.” First Whitton Rep. at 5 (emphasis in original).
18 For a more detailed discussion of the CRM conjugate’s function, see Bielak v. Sec'y of Health & Hum. Servs.,
197
No. 18-761V, 2022 WL 18058244, at *31 (Fed. Cl. Spec. Mstr. Dec. 9, 2022).
19 Another version—Pneumovax 23—is not similarly conjugated, and because it is only recommended for adults, it
cannot be the basis of a Program claim. Whitton Rep. at 6; Louvaris v. Sec'y of Health & Hum. Servs., No. 21-416V,
2021 WL 4955690, at *1–2 (Fed. Cl. Spec. Mstr. Sept. 27, 2021)
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the antigenic components common to both versions) is not associated with an increased risk of
disease—including GBS. First Whitton Rep. at 10 (citing Haber). Dr. Whitton admitted that Haber
relied on passive VAERS20 reports (which are not verified for accuracy) rather than
epidemiologically-verified data, but maintained that its findings still had value since the “early
warning system” benefits provided by VAERS undercut the concept that GBS might have some
relationship to the pneumococcal vaccine. He also noted that Dr. Steinman’s report had itself cited
a large, proper epidemiologic study that reached the same conclusions. First Whitton Rep. at 10;
R. Baxter et al., Lack of Association of Guillain-Barre Syndrome with Vaccinations, 57 Clinical
Infection Diseases 197, 201 (2013), filed as Ex. 37 (ECF No. 42-1) (“Baxter”). Although Baxter
had only considered the non-covered version of the pneumococcal vaccine, Dr. Whitton still
deemed its findings significant, since that vaccine (like Prevnar-13) did not contain the antigenic
molecules (discussed below) that he deemed more likely to be capable of causing GBS.
Dr. Whitton also included in his first report some discussion of GBS—and in particular the
pathogenic mechanisms most likely to trigger it. See generally First Whitton Rep. at 7–10. GBS
was known to be associated more often than not with a pre-onset infection of some kind, and was
believed to be mediated by some autoimmune process. Id. at 7; J. Winer et al., A Prospective Study
of Acute Idiopathic Neuropathy – Antecedent Events, 51 J. Neurology, Neurosurgery, & Psychiatry
613 (1988), filed as Ex. A, Tab 12 (ECF No. 45-2). Antibodies, he agreed, were a more likely
driver of the autoimmune cross-attack in GBS, with “host gangliosides” present in peripheral
nerves their most well-understood target. P. van Doorn et al., Clinical Features, Pathogenesis, and
Treatment of Guillain-Barré Syndrome, 7 Lancet Neurol. 939 (2008), filed as Ex. A, Tab 6 (ECF
No. 44-7). Thus, anti-ganglioside antibodies observed in the blood sera of GBS patients likely
played a “pathological role” in driving GBS. First Whitton Rep. at 7.21
20 VAERS is a database maintained by the CDC to compile information from reports about reactions to immunizations
listed on the Vaccine Injury Table, 42 U.S.C. § 300aa–14(a). See About VAERS, VAERS, https://vaers
hhs.gov/about.html (last visited Feb. 17, 2023).
21 In fact, Dr Whitton maintained that Dr. Steinman had (in literature he co-authored) acknowledged that gangliosides
were the most likely GBS autoimmune target in any case of GBS, as opposed to phosphoglycerol structures. First
Whitton Rep. at 13, citing Kanter at 138 (“[a]utoimmune responses directed against phospholipids and gangliosides
contribute to the pathogenesis in systemic lupus erythematosus and [GBS], respectively”). Dr. Whitton interpreted
this sentence construction (and the word “respectively” at its end) to mean that the phospholipid target reference is
only specific to lupus, not GBS—a wholly reasonable construction in my view. Dr. Steinman later denied this reading,
however, protesting variously that it did not reflect the views of “all” of Kanter’s authors, or was otherwise a
misreading. See, e.g., Second Steinman Rep. at 8–9.
This is not the first time this expert pair has disputed the interpretation of this sentence from Kanter in the context of
a claim that the pneumococcal vaccine can cause GBS. Trollinger, 2023 WL 2521912, at *4, 16. While (as before) I
deem Dr. Whitton’s reading of the sentence to be more compelling and grammatically accurate, I do not also view
this to be a full-on concession by Dr. Steinman about weaknesses in his theory. Rather, it simply underscores that
science has more consistently understood gangliosides as the GBS target for certain autoimmune processes or
triggers—and thus underscores the degree to which the alternative target proposed in this case is not all that well-
supported by existing literature, even if it has some reasonable theoretic underpinnings. There would simply be other
items of literature discussing GBS mediated by attacks on phosphoglycerol/phospholipid targets if the contention had
reliable support.
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GBS was also, Dr. Whitton acknowledged, understood to be associated with some kinds of
infections. In particular, medical science was aware of the connection between Campylobacter
jejuni bacteria (which typically cause some form of gastrointestinal disease) and GBS. First
Whitton Rep. at 7–8. But Dr. Whitton stressed that the strains/serotypes in question still mattered—
because not all bacteria (not even all strains of C. jejuni) expressed “lipo-oligosaccharides”
(“LOS”), or “lipopolysaccharides” (“LPS”)—antigens capable of triggering the development of
anti-ganglioside antibodies, due to their ganglioside-like structures. Id. at 8; I. Nachamkin et al.,
Campylobacter Species and Guillain-Barré Syndrome, 11 Clinical Microbiology Rev. 555, filed
as Ex. A, Tab 18 (ECF No. 45-8). Thus, Dr. Whitton emphasized that “triggering of GBS by C.
jejuni appears to be quite strain-specific, and appears to be determined by some aspect of the
particular strain’s LPS molecule.” First Whitton Rep. at 8 (emphasis in original).
S. pneumoniae, by contrast, was not similarly associated with GBS. First Whitton Rep. at
8. Indeed, it was not included in larger lists of viral and bacterial infections so associated. Id.; Jasti
at 1177–79 (discussing the causes and immunopathogenic mechanisms of GBS). This raised for
Dr. Whitton a foundational weakness in Dr. Steinman’s theory: if the antigenic components of the
vaccine could be causal of GBS, then why was there no recognized association with the underlying
antigens from the actual infectious bacterial strains included in the vaccine? First Whitton Rep. at
9.
This in turn, Dr. Whitton opined, illuminated a second limitation for a causal theory
proposing that antigens derived from S. pneumoniae bacterial strains could be just as causal of
GBS as distinguishable bacteria like C. jejuni. Some bacteria known to be associated with GBS,
like C. jejuni, are “gram negative,”22 (meaning their poly saccharide capsule is “thin”) but the S.
pneumoniae capsule is “gram positive,” or thick. First Whitton Rep. at 9. Gram-negative bacteria
include an outer membrane in which is “embedded” the LOS or LPS molecules believed to be
capable of triggering autoantibodies against ganglioside structures—the pathogenic process
leading to GBS. Id. Indeed, all but one of the wild bacteria already understood to be associated
with GBS are gram negative. Id. at 9–10; Jasti at 1176. Thus, the S. pneumoniae bacterium (and
the vaccine containing its antigenic strains) “lack the very molecules that are thought to trigger
GBS.” First Whitton Rep. at 9 (emphasis in original).
Dr. Whitton then turned to the primary contentions contained in Dr. Steinman’s first report.
First, he repeated his point that Dr. Steinman had made no effort to explain how causality was
22 Bacteria can be subdivided into two groups based on the nature of their cell walls, using a procedure called gram
staining to distinguish the groups. First Whitton Rep. at 9. Gram-positive bacteria have thick capsules with no outer
membrane. Id.; G. Zhang et al., On the Essentiality of Lipopolysaccharide to Gram-Negative Bacteria, 16 Current Op.
Microbiology 779, 779 (2013), filed as Ex. A, Tab 19 (ECF No. 45-9) (“Zhang”). In contrast, gram-negative bacteria
have a flimsy capsule that is surrounded by an outer membrane. Zhang at 779.
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possible for a vaccine to cause GBS when its wild antigenic contents had never been so associated.
First Whitton Rep. at 11. This was especially troubling, given the distinction between Gram-
positive and negative bacteria that Dr. Whitton had observed (which explained why a different
bacterial infection was associated with GBS). Second, Dr. Whitton maintained that Dr. Steinman
overemphasized studies that had observed the presence of antibodies to phospholipids in the blood
of GBS patients, noting that the existence of such antibodies could simply be “the result of the
disease,” as the authors of the literature at issue openly admitted. Id.; citing Nakos, Gilburd. And
he disputed the relevance of studies specific to MS, a distinguishable neuropathic illness occurring
in the central nervous system, and which had likely different targets for cross-reactive autoimmune
attacks. First Whitton Rep. at 11–12.
Next, Dr. Whitton took issue with Dr. Steinman’s contention that polar head groups (which
Dr. Whitton defined as “small molecular components”) could be an autoimmune target in GBS—
in addition to gangliosides. First Whitton Rep. at 12–13. Overall, he deemed the concept
speculative—especially in comparison to how much more was known by medical science about
gangliosides. Id. at 12. Phospholipids with polar head groups were in fact structurally
distinguishable from gangliosides, using a diagram comparing the polar head group
phosphocholine with a ganglioside to visually illustrate their differences. Id. at 12–13, 16. Thus,
even if the pneumococcal vaccine could induce antibodies specific to polar head groups of the kind
identified by Dr. Steinman, these antibodies could not themselves plausibly cross-react with myelin
gangliosides. Id. at 13.
In addition, Dr. Whitton characterized as speculative and unsupported Dr. Steinman’s
argument that glycerol phosphate was integral to the pneumococcal vaccine’s function (and hence
made it more likely that the vaccine would induce antibodies against it). First Whitton Rep. at 13–
14. Indeed, Dr. Whitton maintained that strain 10A of the pneumococcal bacterium identified in
Dr. Steinman’s report in fact did not contain glycerophosphate. Id. at 14. Nor did Dr. Whitton
accept Dr. Steinman’s contention that phosphorylchlorine had a stimulative/booster effect if part
of a vaccine, noting that his reading of the literature offered to support this aspect of Dr. Steinman’s
theory did not in fact establish this to be the case. Id.
Second Report
Dr. Whitton’s next report provided a point-by-point reaction to Dr. Steinman’s rebuttal
efforts. First, he reiterated his prior argument that because MS and GBS are distinguishable, “one
should not be used as a model for the other,” and therefore studies specific to MS were not relevant
in this case. Second Whitton Rep. at 1. He denied that the two diseases could be lumped together
as having a common pathogenesis, and noted that no literature support for Dr. Steinman’s
argument had been provided.
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Second, Dr. Whitton revisited his general contention that S. pneumoniae is not thought by
prevailing medical science to be associated with GBS (unlike numerous other bacterial or viral
infections). Second Whitton Rep. at 1–2. All Dr. Steinman had offered for an association, he noted,
were two case reports (including El Khatib), even though they only established a temporal link.
Id. at 2–3 (discussing case report evidence in detail). Dr. Whitton also provided some additional
literature further demonstrating that a lengthy list of GBS bacterial or viral triggers did not include
pneumococcus. See, e.g., R. Hughes et al., Guillain-Barré Syndrome in the 100 Years Since its
Description by Guillain, Barré and Strohl, 139 Brain 3041, 3044 (2016), filed as Ex. G, Tab 1
(ECF No. 61-2) (“Hughes”) (“[b]esides Campylobacter and Zika virus, the other principal
infections established as occurring before GBS more often than chance are cytomegalovirus,
Mycoplasma pneumoniae,23 Epstein-Barr virus, Haemophilus influenzae and hepatitis E”).
Finally, Dr. Whitton elaborated on his prior argument that phosphoglycerol and polar head
groups in nerve myelin were not likely GBS targets, addressing Dr. Steinman’s effort to bulwark
that concept but still deeming the overall contention to be speculative. Second Whitton Rep. at 3–
4. Dr. Whitton noted that (a) not all of the vaccine’s serotypes featured phosphoglycerol-containing
polysaccharides in the first place, (b) the same polysaccharides were contained in the wild bacteria
(thus again raising the question why the wild S. pneumoniae was not associated with GBS if its
counterpart vaccine could), and (c) reliable literature discussing GBS, such as Hughes, said
nothing about polar heads groups as a putative target for an autoimmune attack, but repeatedly
mentioned gangliosides. Id. at 4; see also J. Kwan & S. Biliciler, Guillain-Barré Syndrome and
Other Acute Polyneuropathies, 37 Clinics Geriatric Med. 313 (2021), filed as Ex. G, Tab 3 (ECF
No. 61-4) (“Kwan”), at 318 (“[i]t is postulated that the epitopes on the surface of pathogens mimic
components of the peripheral nerve ganglioside, triggering an aberrant activation of the immune
system”) (emphasis added). Dr. Whitton also questioned the strength of Dr. Steinman’s argument
that the pneumococcal strain that did contain phosphoglycerol (18C), was significant for
conjugation—for if so, its chemical structure would be altered and the immunogenicity of the strain
effectively destroyed. Second Whitton Rep. at 4.
Third Report
The last written report prepared by Dr. Whitton briefly addressed some of Dr. Steinman’s
reiterated prior arguments and his responses (which require no further repetition herein), but he
also discussed new issues raised in the third Steinman report, as well.
Dr. Whitton spent some time reacting to the contention (first set forth in Dr. Steinman’s
third report) that the pneumococcal vaccine’s conjugate component could also trigger antibodies
cross-reactive against self mimics, and thereby drive GBS. Third Whitton Rep. at 2–3, 6–8. He
23 This is not the same as S. pneumoniae.
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pointed out that in the first two reports filed in this case Dr. Steinman had proposed, without
evidence, that phosphoglycerols were a vital link in the attachment of the conjugate to the vaccine’s
polysaccharide serotypes. Third Whitton Rep. at 6–7, referencing First Steinman Rep. at 12 and
Second Steinman Rep. at 13 (suggesting Dr. Steinman’s view that phosphorylcholine is itself
attached to the conjugate, rather than the polysaccharide serotypes). This assertion, Dr. Whitton
maintained, was erroneous. In fact, (a) this “attachment” concept did not account for the serotypes
not shown to contain phosphoglycerol, but to which the conjugate also managed to attach, and (b)
Dr. Steinman had not explained how (given Chang’s findings) the phosphoglycerol so important
to the vaccine’s immunogenicity would not be altered (thereby eliminating its allegedly-
foundational immunogenicity) if it served as a link to the protein conjugate. Id. at 7.
Dr. Whitton then engaged in an extended criticism of Dr. Steinman’s use of BLAST search
data24 to demonstrate the potentiality of mimicry between components of the CRM conjugate
197
and Contactin-1. Third Whitton Rep. at 8–14. He maintained that the BLAST database was
arguably being misused by Dr. Steinman “to try to identify possibly-immunologically-significant
tracts of protein,” when the database served a more general purpose, and that the short homologic
sequences that Dr. Steinman looked for in his case-specific research were not deserving of
“immunological weight.” Id. at 10–13. He also argued that the common amino acid sequences
shared between Contactin-1 and CRM that Dr. Steinman had identified were “cherry picked,”
197
with Dr. Steinman focusing only on the results that supported his contentions while ignoring the
unhelpful results. Id. at 13.
Ultimately, Dr. Whitton concluded that no evidence beyond the scientifically-unreliable
homologies revealed via Dr. Steinman’s BLAST searches supported the possibility of a cross-
reaction with the conjugate. Dr. Steinman had pointed to Raju as identifying a potentially cross-
reactive amino acid sequence, but that article did not in fact establish that antibodies generated
against the CRM protein would likely cross-react with Contactin-1. Instead, Raju had focused
197
on the generation of T helper cells in reaction to the actual diphtheria toxin (which is
distinguishable from the conjugate, even if the latter synthetically simulates features of the former).
Third Whitton Rep. at 17; Raju at 3210. The very sequence at issue was not even one of the peptide
sequences that Raju’s authors noted had been recognized by the studied subject immune responses,
whereas “other regions of the diphtheria toxin” were more prominent in stimulating a response.
Third Whitton Rep. at 17. Otherwise, the “vast majority” of homologies could not be shown by
medical science to always, or likely, result in autoimmune cross-reactive pathologic processes. Id.
at 14–15 (discussing, for sake of argument, homologies demonstrable between influenza A protein
24 Dr. Whitton similarly criticized Dr. Steinman’s “filter funnel” framework for how he reasoned his way to the
conclusion that the homologies he demonstrated via BLAST searches reliably established a likely cross-reaction. Third
Whitton Rep. at 15–17. He deemed this analytic approach to not only include a number of faulty stages (such as the
very effort of looking for homologous sequences), but ultimately reflected circular logic, allowing Dr. Steinman to
reach in any case the result most favorable to a petitioner. Id. at 17.
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sequences in a common vaccine and body show large numbers of common sequences without
evidence of actual disease occurring).
Besides the foregoing, Dr. Whitton again addressed the portion of Dr. Steinman’s opinion
that proposed vaccine-induced antibodies could cross-react with neuronal polar head groups found
in nerve myelin. He again deemed the theory speculative and lacking in reliable scientific/medical
support, and denied that the vaccine even required an immune response to phosphoglycerol
specifically for it to function. Third Whitton Rep. at 3. On the contrary, Dr. Whitton maintained
that “[t]he role of the phosphoglycerol in bacterial virulence is not relevant” in this context, and
that articles like Chang did not establish the existence of an immune response specific to
phosphoglycerol, even if its inclusion was important to the vaccine’ effectiveness otherwise. Id. at
4; Chang at 7091.
Dr. Whitton also commented on Bryson,25 which Dr. Steinman had contended proved an
immune response to the vaccine’s 23F serotype specific to phosphoglycerol. Third Whitton Rep.
at 4–5. He noted that Bryson’s authors had actually observed that the immune response to this
serotype was specific to “L rhamnose,” a large molecule “of which the phosphoglycerol is just one
part.” Id. at 4; Bryson at 4727–28. The targeting observed in Bryson was thus not specific to the
smaller phosphoglycerol moiety—and if it were, not only would the immune response to this
serotype be sufficient to protect against other serotypes (completely contrary to the understanding
that the vaccine needed multiple serotypes to confer protection, since immune responses were so
specific to individual strains), but also (and again), then the wild pneumococcal 23F strain should
similarly be capable of causing GBS (yet no reliable evidence suggested this to be the case). Id. at
5. In fact, 23F was not even contained in Prevnar-13 (and it was speculative for Dr. Steinman to
assume comparable phosphoglycerol structures were found in other strains that are in the vaccine).
Id.
25 Independent of Dr. Whitton’s criticism, Bryson in fact says even less about causation herein than Dr. Steinman
proposes. Bryson focused not on the immunogenicity of the pneumococcal vaccine, how antibodies with affinity for
phospholipid components might cause/contribute to GBS, or any other issue directly relevant to this case. Rather, its
authors clearly indicated that their study’s focus was the role of preferred genes responsible for coding antibodies to
certain pathogens. Bryson at 4724. Thus, Bryson considered two particular antibodies—one formed in response to
the 23F antigenic serotype, and one formed in reaction to the wild cytomegalovirus—choosing them specifically
because both rely on a “pair of . . . preferred genes” for their generation, even though the two pathogenic incitements
are distinguishable. Id. at 4723–24. Its authors subsequently looked at the specific structures of the antibodies, finding
that they “provide structural evidence that the same . . . genes . . . can assume different roles in protective [antibodies]”
due to distinct configurations—and in turn establishing that “evolutionary pressure by pathogens to retain certain . . .
genes can collaborate with two stochastic processes.” Id. at 4724. Bryson’s authors concluded that their finding
“illustrates how a limited set of human germline genes can contribute to the creation of binding suites for a variety of
highly diverse [antigens].” Id. at 4729. Bryson seems to have only been cited by Dr. Steinman because it featured a
chart showing that the 23F serotype includes phosphoglycerol, and he wished to reproduce it in his written reports.
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III. Procedural History
As noted, the Petition in this matter was filed five years ago. Pet. at 1. After some delay
attributable to records-gathering efforts, Respondent filed a Rule 4(c) Report in March 2020
contesting Petitioner’s right to compensation. ECF No. 34. Expert reports were filed thereafter,
and then the matter was transferred to me in January 2021. Additional reports were filed over the
ensuing year, and I subsequently set a schedule for briefing of a ruling on the record in the winter
of 2022, along with a date for oral argument on the competing motions. Docket entry, dated
February 17, 2022. After some extensions of time, briefing was completed, the oral argument was
held in February 2023, and the matter is now fully ripe for resolution.
IV. Parties’ Briefs and Oral Argument
A. Briefing
Petitioner maintains that he has met his causation-in-fact burden based on the factors
established by the Federal Circuit in Althen v. Sec'y of Health & Hum. Servs., 418 F.3d 1274 (Fed.
Cir. 2005); Mot. at 32–51, 56–60; Reply at 17–32. While much of his briefing focuses on the
disputed diagnosis or the other two Althen prongs, he also discussed in detail what he believes
supports his prong one, “can cause” showing. Since that is the basis for my decision dismissing
the claim, I will only summarize those subsections of his briefing, as well as Respondent’s
countervailing brief—although Petitioner made a number of very specific arguments pertaining to
that aspect of his claim.
Petitioner’s Motion
Petitioner breaks down his causation theory into two parts: one in which the pneumococcal
vaccine sparks a cross-reaction as a result of antibodies produced in reaction to
phosphoglycerol/phosphocholine found in at least one of the vaccine’s polysaccharide serotypes,
and one in which the conjugate itself is the basis for the purported cross-reaction. Mot. at 32, 39.
With respect to the former, Petitioner relies heavily on articles submitted by Dr. Steinman about
MS, and what they show with respect to phosphate groups on the myelin sheath targeted by
autoantibodies, reasoning that they are useful in the GBS context, as well. Id. at 33–34, citing Ho.
He then notes that some of the vaccine’s serotypes have been shown not only to contain these
phospholipid-oriented molecules, but that they are critical to immunogenicity. Mot. at 35–37,
citing Chuang, Chang. Finally, he maintains that articles like Bryson demonstrate that antibodies
are generated in response to the phosphoglycerol molecules in at least one of the vaccine’s 13
serotypes. Thus, he contends that via the widely-accepted biologic mechanism of molecular
mimicry, these subcomponents of the vaccine trigger the production of autoantibodies specific to
polar head structures in the myelin, thereby mistakenly attacking them, relying both on what is
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generally known about molecular mimicry in the context of GBS and other wild infections, like
C. jejuni, and cases (discussed below) where this theory has been accepted. Mot. at 37–39.
Petitioner spends comparatively less time discussing the aspect of his theory relying on the
vaccine conjugate. He explains, however, its essence: that Dr. Steinman’s database research had
established two possible amino acid sequences that were shared by the conjugate and Contactin-
1, a protein found in myelin, and that the lengths of these sequences were sufficient for a cross-
reaction to occur. Mot. at 40–44. But this aspect of Dr. Steinman’s opinion does not possess
anywhere near the same degree of research suggesting any actual evidence of the theorized cross-
reactivity (other than what is found in articles like Lanz—which are specific to MS and the Epstein
Barr virus), and Petitioner’s brief does not cite any items of literature to this specific end.
In addition, Petitioner’s brief asserts that certain items of literature actually reveal medical
community support for a pneumococcal vaccine-GBS association—although the actual articles
make no such affirmative finding, and the readings given them by Petitioner are somewhat
strained. Mot. at 56–60. Haber, for example, was deemed by Dr. Steinman as at least “reassuring”
in its determination that the vaccine is not associated with a disproportionate number of GBS cases,
but he maintained (especially since it relies on VAERS data) that it could not disprove an
association. Id. at 57. Tseng did not compare its findings regarding vaccinated individuals who
experienced GBS against a background incidence rate, while seeing some instances of GBS
regardless. Id.at 58–59. And Baxter did not involve the relevant vaccine, and had other limitations.
Id. at 60.
Respondent’s Brief
Respondent denies that the first Althen prong has been satisfied. Opp. at 18–23.26 The fact
that the underlying S. pneumoniae bacterium is not associated with GBS is a fatal flaw to the
theory, and nothing offered specific to it could overcome this foundational problem. Id. at 18–19.
This might be because the kinds of molecules found in other bacteria that are so associated, like
C. jejuni, express a different kind of molecule known to mimic aspects of myelin. Id. at 19. And
Petitioner did not offer evidence associating the vaccine with GBS, while the existing
epidemiology undercuts an association. Id. at 19–20.
The theory offered herein otherwise relies on unsubstantiated contentions about molecular
mimicry that have been rejected in prior cases also involving the pneumococcal vaccine (as
26 Respondent also makes some arguments about the adequacy of Dr. Steinman’s expert opinion, given his propensity
in prior cases (which I have observed myself) to act more as an advocate than independent expert. Opp. at 7–8. But
my determination herein relies on the “face value” of Dr. Steinman’s opinion (albeit weighed against my prior
exposure to it) and thus I do not comment on his individual proclivities in Program cases generally (beyond how
needlessly long and diagram-laden his reports tend to be).
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discussed below). Opp. at 20. In particular, it assumes without preponderant evidence that (a)
phospholipid polar head groups can be a target of GBS much like ganglioside structures (even
though substantially more science supports the latter, with hardly any going the other way), and
(b) antibodies to these polar head groups can drive disease, simply based on the fact that in a few
studies they have been found in the blood of GBS patients. Id. at 21, citing Nakos, Gilburd. Dr.
Steinman also maintained that phosphoglycerols were vital to the vaccine’s immunogenicity—
when in fact, as Dr. Whitton established, Petitioner’s own literature suggested that they would not
exist after the vaccine’s manufacture (which involves connection of all included serotypes to the
protein conjugate) if they functioned as proposed. Id. at 21–22, citing Chang.
Respondent also criticized Dr. Steinman’s BLAST searches, which were specific to the
conjugate “side” of his theory, as not probative of causation. Opp. at 22. Not only did Dr. Steinman
not show that Contactin-1 is a likely GBS-instigating target, but he also demonstrated insufficient
numbers of amino acid sequences to trigger a cross-reaction, as explained by Dr. Whitton. Id. And
he relied on case reports that were factually distinguishable, like El Khatib. Id. at 23.
Reply
Only a portion of Petitioner’s reply focuses on his prong one showing, and it mostly
reiterates the arguments addressed above. Reply at 17–23. Petitioner does, however, propose that
evidence offered in the case shows that gangliosides are not the only target in GBS, and that
autoantibodies to phospholipids are seen in connection with GBS patients in some studies. Id. at
18–19, citing Nakos. The evidence favoring gangliosides as a target, Petitioner maintained, is only
specific to C. jejuni infections, and thus does not suggest that “different immune challenges” could
not involve different aspects of the myelin. Reply at 19. (And in any event, the record evidence
does not establish that Petitioner tested positive for anti-ganglioside antibodies). Id.
Petitioner also maintained that even if articles like Nakos expressly decline to say whether
anti-phospholipid antibodies are causal of GBS (as opposed to the indirect product of the myelin
damage associated with GBS), other articles do support the conclusion—albeit in the
distinguishable context of MS. Reply at 20, citing Ho. He also notes the numerous other decisions
accepting Dr. Steinman’s reasoning, deeming them the equivalent of case reports. Reply at 20–21
(citations omitted). And he again walks through Dr. Steinman’s BLAST search-supported theory
involving the vaccine’s CRM component. Id. at 22–23.
197
B. Oral Argument
The parties agreed to have their respective counsel present live argument in court, rather
than conduct a hearing featuring expert testimony, and to that end I heard both sides in February
2023. At that time, Petitioner maintained he had successfully established all elements of his claim,
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but in so maintaining offered substantial commentary on the Althen prong one issues I am focusing
upon in this Decision. See generally Tr. at 7–19, 25–47, 66–71. The argument lasted two hours.
In particular, Petitioner’s counsel reiterated the elements and components of Dr.
Steinman’s causation theory, noting its two main alternative mechanistic contentions (cross-
reaction to phosphoglycerol moieties, plus cross-reaction against the conjugate)27 and also
highlighting literature already discussed above. Tr. at 7–12 (mentioning Bryson, Chang, Nakos,
and Ho, among other items). He proposed that the theory offered was comparable to what is known
about the C. jejuni—GBS relationship. Id. at 12.28 And he noted that several prior special masters
had ruled favorably on the theory, whereas the sole decision that I had issued at the time of hearing
stood as an outlier, and also did not involve a theory presented by Dr. Steinman.29 Id. at 15, 17–
18.
I also asked questions of counsel about how the preponderance standard should be applied
generally in causation cases—and in effect, although counsel agreed the standard of proof was
preponderance, he proposed that to deny that Petitioner had met it herein on the first prong would
be to improperly heighten his burden. Thus, counsel maintained that questions about whether anti-
phosphoglycerol antibodies likely cause GBS (as opposed to appearing merely in the context of
the disease)30—questions that literature filed by Petitioner expressly do not propose to answer—
amounted to “the ‘when’ and the ‘what’” questions that “may be necessary for scientific certainty
but not for a preponderance of the evidence or legal probability.” Tr. at 16. Thus, as long as a
claimant has offered individually-reliable items of literature that are not shown to be false or
scientifically-untrustworthy, plus a qualified expert (like Dr. Steinman) embracing the theory, “we
meet Althen 1.” Id. at 35, 38. Any weighing performed by the special master should thus be limited
to either evaluating if in fact the items offered are as individually reliable as they are held out to
be, whether they have been rebutted by counter-evidence offered by Respondent that contradicts
their findings (such as additional studies on the same topic), or whether other kinds of evidence
27 Counsel did acknowledge indirectly that the first theoretical contention was “the stronger theory,” although
Petitioner has not abandoned the aspect of the theory relying on the conjugate. Tr. at 6.
28 Counsel acknowledged, however, that the evidence of an association between the underlying wild S. pneumoniae
bacteria and GBS was wanting (or at least far less robust than associations known with other wild viruses or bacteria,
such as C. jejuni). Tr. at 27–28, 69. But he later stressed that vaccine’s formulation as a conjugated vaccine might
explain why the vaccine would more likely spark an autoimmune disease than the wild bacteria. Id. at 67–68.
29 At the time of oral argument, my third-published pneumococcal vaccine-GBS decision (which specifically discussed
Dr. Steinman’s theory as offered herein) had not yet been issued—but was the following week. See Trollinger, 2023
WL 2521912, at *4–6.
30 By “context,” I mean that the antibodies might be generated mid-disease course—not from driving the disease
initially, and/or arising as the body reacts to the damage from the disease rather than increasing the disease tempo or
worsening it. Certainly, Petitioner’s literature filings say nothing about the likelihood that the antibodies drive
initiating the autoimmune process leading to GBS.
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(such as a particularly persuasive epidemiologic study—evidence I acknowledge does not exist in
this case) merit greater weight.
Respondent offered his own argument in favor of dismissal. Tr. at 48–66. His counsel
contended that my prior decisions provided a reasoned roadmap for resolving this case, especially
since nothing different had actually been proposed as grounds for finding entitlement in this record,
and that Petitioner was in effect relying on the flu vaccine-GBS theory but in a disparate context.
Id. at 50–51. Dr. Steinman’s theory was in fact not reliable, for the reasons discussed above in my
summary of Dr. Whitton’s opinion. Id.at 51–52, 57–59. Respondent thus maintained that the
collective weight of Petitioner’s evidence offered in support of the theory was not preponderantly
sufficient to meet the “can cause” prong standard. In Respondent’s view, “where” or “when”
evidence specific to the putative role of anti-phosphoglycerol antibodies was lacking, and it did
not amount to an unreasonable heightening of the preponderant burden to require such evidence.
Id. at 64–65 (“they need to have evidence to show that the autoantibodies would be pathogenic”).
V. Applicable Law
A. Standards for Vaccine Claims
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).31
In this case, Petitioner cannot assert a Table claim (as there is no such claim with respect to the
pneumococcal vaccine).
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
31 Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Hum. Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings
concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Hum. Servs., 59 Fed. Cl. 121,
124 (2003), aff’d 104 F. Appx. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Hum. Servs., No. 13-159V,
2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).
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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, 418 F.3d at 1278: “(1) a medical theory causally connecting the vaccination and
the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason
for the injury; and (3) a showing of proximate temporal relationship between vaccination and
injury.”
Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners
must provide a “reputable medical theory,” demonstrating that the vaccine received can cause the
type of injury alleged. Pafford, 451 F.3d at 1355–56 (citations omitted). To satisfy this prong, a
petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”
Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such a theory must
only be “legally probable, not medically or scientifically certain.” Knudsen, 35 F.3d 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. Accordingly, special masters must take care not to increase the burden
placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras, 121 Fed.
Cl. at 245.
In discussing the evidentiary standard applicable to the first Althen prong, the Federal
Circuit has consistently rejected the contention that it can be satisfied merely by establishing the
proposed causal theory’s scientific or medical plausibility. See Boatmon v. Sec’y of Health & Hum.
Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019); LaLonde v. Sec’y of Health & Hum. Servs., 746 F.3d
1334, 1339 (Fed. Cir. 2014) (“[h]owever, in the past we have made clear that simply identifying a
‘plausible’ theory of causation is insufficient for a petitioner to meet her burden of proof” (citing
Moberly, 592 F.3d at 1322)); see also Howard v. Sec'y of Health & Hum. Servs., 2023 WL
4117370, at *4 (Fed. Cl. May 18, 2023) (“[t]he standard has been preponderance for nearly four
26

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decades”), appeal docketed, No. 23-1816 (Fed. Cir. Apr. 28, 2023). 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) (“there is nothing . . . that mandates
that the testimony of a treating physician is sacrosanct—that it must be accepted in its entirety and
cannot be rebutted”). As with expert testimony offered to establish a theory of causation, the
opinions or diagnoses of treating physicians are only as trustworthy as the reasonableness of their
suppositions or bases. The views of treating physicians should be weighed against other, contrary
evidence also present in the record—including conflicting opinions among such individuals.
Hibbard v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 742, 749 (2011) (not arbitrary or capricious
for special master to weigh competing treating physicians’ conclusions against each other), aff’d,
698 F.3d 1355 (Fed. Cir. 2012); Veryzer v. Sec’y of Dept. of Health & Hum. Servs., No. 06-522V,
2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review denied, 100 Fed.
Cl. 344, 356 (2011), aff’d without opinion, 475 F. Appx. 765 (Fed. Cir. 2012).
The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the
phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant
proof that the onset of symptoms occurred within a timeframe which, given the medical
understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan
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v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what
is a medically acceptable timeframe must align with the theory of how the relevant vaccine can
cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of Health & Hum.
Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after remand, 105 Fed. Cl. 353 (2012), aff’d
mem., 503 F. Appx. 952 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V,
2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for review denied, (Fed. Cl. Dec. 3,
2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).
B. Law Governing Analysis of Fact Evidence
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).
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 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
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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. denied, 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 testimony may be more persuasive than written records, such as where records are
deemed to be incomplete or inaccurate. Campbell v. Sec'y of Health & 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).
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.
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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 Pharmaceuticals,
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)). “The Daubert factors for analyzing the reliability of testimony are: (1) whether a
theory or technique can be (and has been) tested; (2) whether the theory or technique has been
subjected to peer review and publication; (3) whether there is a known or potential rate of error
and whether there are standards for controlling the error; and (4) whether the theory or technique
enjoys general acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2
(citing Daubert, 509 U.S. at 592–95).
The Daubert factors play a slightly different role in Vaccine Program cases than they do
when applied in other federal judicial fora (such as the district courts). Daubert factors are usually
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors
are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health
& 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
expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the
persuasiveness and reliability of expert testimony has routinely been upheld. See e.g., Snyder, 88
Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases), Daubert has not
been employed at the threshold, to determine what evidence should be admitted, but instead to
determine whether expert testimony offered is reliable and/or persuasive.
Respondent frequently offers one or more experts of his own in order to rebut a petitioner’s
case. Where both sides offer expert testimony, a special master’s decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen 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. 136, 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 rev. denied, 108 Fed. Cl. 743 (2013), aff’d, 540 F. Appx. 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
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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”).
Expert opinions based on unsupported facts may be given relatively little weight. See
Dobrydnev v. Sec’y of Health & Hum. Servs., 556 F. Appx. 976, 992–93 (Fed. Cir. 2014) (“[a]
doctor’s conclusion is only as good as the facts upon which it is based”) (citing Brooke Group Ltd.
v. Brown & Williamson Tobacco Corp., 509 U.S. 209, 242 (1993) (“[w]hen an expert assumes
facts that are not supported by a preponderance of the evidence, a finder of fact may properly reject
the expert’s opinion”)). Expert opinions that fail to address or are at odds with contemporaneous
medical records may therefore be less persuasive than those which correspond to such records. See
Gerami v. Sec’y of Health & Hum. Servs., No. 12-442V, 2013 WL 5998109, at *4 (Fed. Cl. Spec.
Mstr. Oct. 11, 2013), aff’d, 127 Fed. Cl. 299 (2014).
D. Consideration of Medical Literature
Both parties filed numerous items of medical and scientific literature in this case, but not
every filed item factors into the outcome of this Decision. While I have reviewed all the medical
literature submitted in this case, I discuss only those articles that are most relevant to my
determination and/or are central to Petitioner’s case—just as I have not exhaustively discussed
every individual medical record filed. Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322,
1328 (Fed. Cir. 2016) (“[w]e generally presume that a special master considered the relevant record
evidence even though he does not explicitly reference such evidence in his decision”) (citation
omitted); see also Paterek v. Sec’y of Health & Hum. Servs., 527 F. Appx. 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”).
E. Standards for Ruling on the Record
I am resolving Petitioner’s claim on the filed record, in accordance with the parties’ wishes
as well as my own assessment of how best to decide the claim. The Vaccine Act and Rules not
only contemplate but encourage special masters to decide petitions on the papers where (in the
exercise of their discretion) they conclude that doing so will properly and fairly resolve the case.
Section 12(d)(2)(D); Vaccine Rule 8(d). The decision to rule on the record in lieu of hearing has
been affirmed on appeal. Kreizenbeck v. Sec’y of Health & Hum. Servs., 945 F.3d 1362, 1366 (Fed.
Cir. 2020); see also Hooker v. Sec’y of Health & Hum. Servs., No. 02-472V, 2016 WL 3456435,
at *21 n.19 (Fed. Cl. Spec. Mstr. May 19, 2016) (citing numerous cases where special masters
decided case on the papers in lieu of hearing and that decision was upheld). I am simply not
required to hold a hearing in every matter, no matter the preferences of the parties. Hovey v. Sec’y
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of Health & Hum. Servs., 38 Fed. Cl. 397, 402–03 (1997) (determining that special master acted
within his discretion in denying evidentiary hearing); Burns, 3 F.3d at 417; Murphy v. Sec’y of
Health & Hum. Servs., No. 90-882V, 1991 WL 71500, at *2 (Fed. Cl. Spec. Mstr. Apr. 19, 1991).
ANALYSIS
I. Overview of Prior Decisions
Much is known about GBS’s likely pathogenesis, as well as its association with one
particular vaccine covered by the Program: the flu vaccine. There are several reliable evidentiary
components supporting this association, as I have discussed in other cases.32 Trollinger v. Sec'y of
Health & Hum. Servs., No. 16-473V, 2023 WL 2521912, at *25 (Fed. Cl. Spec. Mstr. Feb. 17,
2023), mot. for review den’d, No. 16-VV-473, 2023 WL 5249583 (Fed. Cl. 2023); Bielak v. Sec'y
of Health & Hum. Servs., No. 18-761V, 2022 WL 18058244, at *34 (Fed. Cl. Spec. Mstr. Dec. 9,
2022). These evidentiary components have been deemed sufficient (on numerous prior occasions)
to preponderantly demonstrate the flu vaccine can likely cause GBS. Mason v. Sec'y of Health &
Hum. Servs., No. 17-1383V, 2022 WL 600415, at *26 (Fed. Cl. Spec. Mstr. Feb. 4, 2022) (noting
that the flu vaccine-GBS association is supported by a “mix of (a) knowledge about how molecular
mimicry “works” in GBS's pathogenesis, (b) trustworthy animal experiments that model
demyelinating injuries in the context of the molecular mimicry mechanism, and (c) solid (if
somewhat old) epidemiologic evidence . . . establishing a higher incidence of GBS after
vaccination when compared to an unvaccinated population”). As a result, there are many reasoned
Program determinations recognizing the strength of the association.33 Indeed, GBS after the flu
vaccine is a Table claim, as well. 42 C.F.R. § 100.3(a)(XIV)(D).
The same is not true for the pneumococcal vaccine, however. On the contrary: to date I
have issued three lengthy decisions explaining in detail why it is unlikely that the pneumococcal
vaccine can cause GBS. See generally Trollinger, 2023 WL 2521912, at *27–30; Bielak, 2022 WL
32 Although I decide this case based on the evidence before me, it is not only useful, but prudent, to take into account
prior determinations—both for guidance and to avoid “reinventing the wheel” when deciding like Program cases.
33 See, e.g., Chinea v. Sec’y of Health & Human Servs., No. 15-095V, 2019 WL 1873322 (Fed. Cl. Spec. Mstr. Mar.
15, 2019); Strong v. Sec’y of Health & Human Servs., No. 15-1108V, 2018 WL 1125666 (Fed. Cl. Spec. Mstr. Jan.
12, 2018); Stitt v. Sec’y of Health & Human Servs., No. 09-653V, 2013 WL 3356791 (Fed. Cl. Spec. Mstr. May 31,
2013); Stewart v. Sec'y of Health & Human Servs., No. 06-777V, 2011 WL 3241585, at *16 (Fed. Cl. Spec. Mstr. July
8, 2011). Such cases often also rely on the theory of molecular mimicry, proposing that antibodies produced by B cells
in response to a vaccine’s viral antigen components can cross-attack the myelin sheath (because the target antigen and
gangliosides of the myelin sheath share structural homology), thereby causing demyelination of peripheral nerves.
Chinea, 2019 WL 1873322, at *15.
32

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18058244, at *33–37 (pneumococcal vaccine not shown to cause GBS); Deshler v. Sec'y of Health
& Hum. Servs., No. 16-1070V, 2020 WL 4593162 (Fed. Cl. Spec. Mstr. July 1, 2020).
Bielak and Trollinger involved theories largely comparable to what was offered here, as in
both cases the petitioner argued that phosphoglycerol components of the pneumococcal vaccine
caused antibodies to cross-react against relevant portions of the myelin, and both also involved
nearly all of the same items of literature, like Ho, Gilburd, Nakos, etc. See Trollinger, 2023 WL
2521912, at *19; Bielak, 2023 WL 35509, at *15–17, 33–34. The Trollinger petitioner also
featured the expert input of Dr. Steinman, whose report (after an initial, slightly-different iteration)
ended up consistent with what has been proposed in this case (and with Dr. Whitton serving the
role as Respondent’s expert, as well).
My determination in Deshler, 2020 WL 4593162, also bears on the outcome herein, if less
directly. The Deshler petitioner relied on the second component of Dr. Steinman’s theory: that the
conjugate component of the Prevnar-13 vaccine itself had caused an aberrant, mimicry-driven
autoimmune process relating to the vaccine’s antigens. Deshler, 2020 WL 4593162, at *27. That
petitioner’s expert opined the subsequent B cell reaction (the primary goal of the vaccine) was
driven by the polysaccharide component of the vaccination, although (unlike this case) he
conceded that he could not demonstrate mimicry between the S. pneumoniae polysaccharides and
self-structures. Id. Respondent’s expert in Deshler (Dr. Whitton again) argued in reaction that the
polysaccharides contained in the vaccine did not share structural homology with self-structures of
the peripheral nervous system, and thus could not contribute to the pathogenesis of GBS via a
molecular mimicry-driven cross-reaction to the vaccine’s antigens. Id. at *27. I concurred with
Respondent, while also finding that the petitioner relied too heavily on the temporal association
between vaccination and onset as evidence of causation (and that there was another potential
explanation for the claimant’s GBS that had not been rebutted). Id. at *22, 27.
It is unquestionably the case (as I previously observed in Trollinger and Bielak) that other
special masters have accepted Dr. Steinman’s theory regarding GBS and the pneumococcal
vaccine. See, e.g., Gross v. Sec'y of Health & Hum. Servs., No. 17-1075V, 2022 WL 9669651
(Fed. Cl. Spec. Mstr. Sept. 22, 2022); Maloney, 2022 WL 1074087; Pierson v. Sec'y of Health &
Hum. Servs., No. 17-1136V, 2022 WL 322836 (Fed. Cl. Spec. Mstr. Jan. 19, 2022); Koller v. Sec’y
of Health & Hum. Servs., No. 16-439V, 2021 WL 5027947 (Fed. Cl. Spec. Mstr. Oct. 8, 2021).
However (and although I am not bound by these determinations in any event), I do not find them
persuasive. They largely seem to have embraced the framework for the existing flu vaccine-GBS
association, but without convincingly explaining why Respondent’s counter-arguments deserved
less weight given the disparate context. I have also observed that these favorable cases cite the
same items of literature that I determined (after close analysis) are not especially reliable or
persuasive. See, e.g., Bielak, 2022 WL 18058244, at *15–17, 32 (discussing in detail Chang,
Gilburd, Ho, Kanter, and Nakos).
33

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Ultimately, as I explained in Trollinger, Bielak, and Deshler, the theory that the
pneumococcal vaccine “can cause” GBS seeks to demonstrate a link between indirectly-present
components34 of the vaccine and molecules found in myelin structures (in this case, lipids), but
without additional sufficient evidence persuasively establishing likely pathogenicity. In effect,
claimants seek application of the flu vaccine-GBS association in a context in which it does not
work—and to accept it would be to find causation mostly because a claimant’s GBS post-dated
vaccination, reverse-engineering causation from the temporal association.
II. Petitioner Has not Carried His Althen Prong One Burden of Proof
My analysis herein focuses solely on whether the pneumococcal vaccine “can cause”
GBS.35 As noted above, I have now on three occasions found that this is unlikely—and no new or
alternative evidence was presented in this case that would provide compelling grounds for
revisiting the issue, or finding the burden met here where it was not before.
In short, Dr. Steinman’s theory is unreliable and unpersuasive when evaluated in its totality
(even if it does possess subcomponents that are scientifically reliable or reasonable in isolation).
As in many cases, he embraces molecular mimicry as a mechanism36 for how the vaccine’s
components could cause the immune system to produce autoantibodies that would then attack
myelin-associated structures that mimic vaccine antigens or components like the conjugate (which
is not included in the vaccine for the purpose of encouraging immunity to it in the future
specifically. But although molecular mimicry is well-established in the Vaccine Program as
providing a reliable scientific explanation for how GBS may often occur after receipt of the flu
vaccine specifically, it cannot be invoked summarily in all circumstances and then deemed to
resolve causation. McKown v. Sec'y of Health & Hum. Servs., No. 15-1451V, 2019 WL 4072113,
at *50 (Fed. Cl. Spec. Mstr. July 15, 2019) (“merely chanting the magic words ‘molecular
mimicry’ in a Vaccine Act case does not render a causation theory scientifically reliable, absent
additional evidence specifically tying the mechanism to the injury and/or vaccine in question”)
(emphasis in original), mot. for review denied, 76 Fed. Cl. 452 (2007)).
34 By indirect, I mean only that the vaccine is not manufactured or engineered to specifically include phospholipids or
phosphoglycerol—although the polysaccharide antigens in the vaccine themselves happen to contain these sub-
structures, and their existence within the polysaccharides might have some internal significance.
35 I thus do not also decide if Petitioner likely had GBS, or if he met the other two Althen prongs. The question of
diagnosis is in fact hotly-disputed, and would have to be addressed were my Althen prong one finding deemed in error.
However, because of my prior exposure to the questions surrounding this aspect of causation, I find it in the interest
of judicial efficiency to evaluate only the “can cause” question herein.
36 Although Program claimants are not required to propose a mechanism in support of a causation theory, they often
attempt to do so—and thus invite reasonable scrutiny into whether the proposed mechanism is persuasive and/or has
preponderant support. Andreu, 569 F.3d at 1378–79 (citing Capizzano, 440 F.3d at 1325–26).
34

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Here, there are too many foundational deficiencies and holes in the overall theory to
embrace molecular mimicry as likely driving GBS after receipt of the pneumococcal vaccine. At
the outset, Dr. Steinman cannot explain convincingly why the pneumococcal vaccine would be
more likely to cause GBS than its wild bacterial infectious analog (which unquestionably is not so
associated). He vaguely points to the conjugate as the “X factor,” but his theory does not rely on
it as explanatory (and in fact proposes a separate mechanism involving the conjugate that could
independently also cause GBS, although he admits this is a less-substantiated theory (see Tr. at
6)). In fact, Dr. Whitton persuasively explained (offering a comparison of C. jejuni with S.
pneumoniae) why one bacterium is known to be associated with GBS, while the other is not, noting
that this likely has something to do with the differing polysaccharide capsules that protect the
bacteria. First Whitton Rep. at 5. Although it is not a baseline requirement in Program cases to
prove a vaccine’s wild infectious counterpart is associated with a particular disease, claimants
certainly highlight the connection when it exists—and it is absent herein.
Next, Dr. Steinman proposes an antigenic/autoimmune self-target for GBS’s
pathogenesis—polar head groups containing phospholipid components—that is not accepted
overall by medical science specific to GBS, let alone addressed in reputable publications or studies.
(In effect, if Dr. Steinman is correct, he has made a major discovery about GBS that others in the
field more well-versed in the specific study of peripheral neuropathies have fully missed. Compare
Hughes, Kwan). It is simply speculative to propose that GBS could be mediated by an attack on
this target, based solely on the logic that the myelin contains it—and the degree of speculation is
highlighted by the comparatively larger amount of evidence that associate gangliosides as a likely
target. He further assumes the vaccine can cause antibodies specific to phospholipid structures to
be produced when that is not even the primary intent of the vaccine, and relies for support on case
reports or literature that expressly acknowledges that the presence of these antibodies in the blood
sera of GBS patients does not mean they were causal of GBS. See, e.g., Gilburd, Nakos. And he
also cannot show that the anti-phosphoglycerol autoantibodies would react against the gangliosides
either.
Many items of evidence offered in support of Dr. Steinman’s theory may have individual
reliability, but do not appreciably aid construction of his theory. He repeatedly, for example,
invokes literature specific to MS—not the disease at issue, even if it has some common features
with other demyelinating conditions. (The same goes double for his citation to recent, admittedly
ground-breaking research about an association between MS and the EBV infection). He identifies
studies in which the presence of anti-phosphoglycerol antibodies are seen in the blood sera of GBS
patients, but where the study’s authors do not propose to explain the role of the autoantibodies.
Chang at 7091–92; Gilburd at 27. And he goes to great lengths to attempt to argue that
phosphoglycerols must be in the pneumococcal vaccine, or play some role in its immunogenicity—
when that only “sets the stage” for his mechanistic arguments that fail to persuade for many other
reasons.
35

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Dr. Steinman’s secondary causal theory—that the conjugate in the vaccine is an alternative
source for a protein (rather than sugar) molecular mimic comparable to a myelin component—
fares no better. Indeed, although this aspect of the theory was not at issue in Trollinger or Bielak,
it was in Deshler, and Dr. Whitton (who served as Respondent’s expert in both that case and this
one) has now effectively rebutted the concept twice. As I noted in Deshler, CRM is lab-created,
197
and although it is comparable to diphtheria toxin, it is not the same, reducing the value of
analogizing the results of research articles like Raju to the present context. Deshler, 2020 WL
4593162, at *11. In addition, while the conjugate’s inclusion in the pneumococcal vaccine is
intended to boost immunogenicity, the conjugate is not itself added to provide an additional
beneficial antigenic component (since Prevnar-13 aims to protect against pneumococcus
bacteria—not diphtheria), further reducing the likelihood that it would cause the production of
antibodies specific to it that would in turn cross-react with self mimics. Dr. Steinman’s speculative
theory about the immune response to this ingredient is otherwise unsupported by sufficient science
specific to the conjugate itself and its purported capacity to induce an aberrant response. And
Petitioner offered hardly any evidence (in comparison to the other aspect of his theory) that vaccine
recipients mount a response to the conjugate that would produce Contactin-1 antibodies, let alone
that Contactin-1 is a likely GBS pathogenic target.
Other arguments for causation were no more persuasive, although of lesser significance.
For example, although both experts spent a great deal of energy arguing about the utility of BLAST
searches as well as Dr. Steinman’s preferred analytical structure for evaluating causation, this case
does not turn on whether a five, ten, or twenty amino acid sequence must be shown to establish
reliable homology. Rather, as I have noted many times now in prior decisions (often in response
to Dr. Steinman’s “in silica” desktop database search efforts), more than homology must be shown
to preponderantly demonstrate that a vaccine likely causes cross-reactive damage via the
mechanism of molecular mimicry. See, e.g., Trollinger, 2023 WL 2521912, at *29; Schilling v.
Sec'y of Health & Hum. Servs., No. 16-527V, 2022 WL 1101597, at *5, 19–20 (Fed. Cl. Spec.
Mstr. Mar. 17, 2022); McKown, 2019 WL 4072113, at *50. Dr. Steinman’s success in establishing
sequential homology (ignoring Dr. Whitton’s reasoned objections to the utility of BLAST
searches) does not make it more likely the pneumococcal vaccine causes GBS without other
corroborative evidence that has not been offered in this case. Certainly nothing new and on point
was filed to that end that I have not already considered in my prior cases involving the
pneumococcal vaccine.37
37 Lanz or Robinson & Steinman do qualify as more recent publications, but they involve MS and a different viral
infection, not GBS and pneumococcus bacteria. Accordingly, the fact that they might provide ballast for Dr.
Steinman’s argument about what amino acid chain length is sufficient for a cross-reaction is of little regard. Indeed,
the existence of such studies—which have been hailed as breakthroughs in proposing a possible infectious trigger for
MS—underscore the comparative lack of comparable reliable proof in this case. Where is the study showing a similar
link between GBS and S. pneumoniae? The usual excuses offered for why more specific evidence was not possible (it
cannot be done; the disease is too rare; it is unfair to demand such proof in a field bereft of certainty; etc.) wilt in the
face of strong research supporting other causal connections in disparate contexts.
36

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I similarly do not give great weight to the fact that some treaters speculated that the vaccine
was causal of Petitioner’s GBS. I acknowledge that such evidence has relevance to the Althen
prong one inquiry, even though treater views usually are thought to have more significance in the
context of determining whether the second, “did cause” prong has been satisfied. But it is not
evident from the record that treater speculation on this subject was informed by the scientific
specificity displayed by both sides’ experts on prong one. And the case report evidence (a class of
proof not usually deemed deserving of significant weight as it is) offered herein, like El Khatib,
was especially thin, and hardly supported Dr. Steinman’s more sweeping contention that a GBS-
pneumococcal vaccine association is “recognized.” Second Steinman Rep. at 2.
Petitioner endeavored to fend off the weaknesses in his theory, but was unsuccessful. For
example, he argues that gangliosides are not necessarily the exclusive target in GBS (and that in
any event, it cannot be shown in this case that he possessed antibodies to them). This, however,
misapprehends the importance of the target “question.” Dr. Whitton established that medical
science already knows a great deal about likely GBS targets, comparing that information to the fact
that GBS authorities generally have not embraced phospholipid polar group heads as a target (or
S. pneumoniae as a trigger for that matter). And numerous items filed in this case specific to GBS
note that no conclusions can credibly be drawn about the role anti-phosphoglycerol antibodies play
in GBS, even if they are found in the blood of GBS patients. Nakos at 1406–07; Gilburd at 23. It
is also incorrect for Petitioner to suggest gangliosides are only relevant when GBS is thought to
have been caused by a C. jejuni infection, since in numerous Program cases gangliosides as a target
are discussed in the context of vaccine causation. Pierson, 2022 WL 322836, at *24 (remarks from
another special master that note “[f]lu vaccine-GBS cases often rely upon the theory of molecular
mimicry, specifically proposing that antibodies produced by B cells in response to the vaccine's
viral antigen components cross-attack the myelin sheath (where the target antigen and gangliosides
of the myelin sheath share structural homology), causing demyelination of peripheral nerves.”)
Respondent, by contrast, effectively and persuasively rebutted Petitioner’s theory. Dr.
Whitton could not deny that phosphoglycerol is found in at least some of the vaccine’s 13
polysaccharide antigens. But he established (based on the literature filed herein) that it is unlikely
that (a) antibodies are generated to the phosphoglycerol-specific aspects of some of the vaccine’s
antigenic serotypes, (b) they can in turn react with host tissue phospholipid polar head structures,
or (c) GBS is primarily or initially mediated by such a cross-reaction, with articles like Nakos and
Gilburd admitting that the existence of such antibodies (which could be the product of an ongoing
disease started by something distinguishable) does not in turn imply pathogenic primacy. Indeed,
as other Program cases have acknowledged, antibodies often exist or are found in blood sera but
are not definitionally pathogenic. Scott v. Sec'y of Health & Hum. Servs., No. 03-2211V, 2006 WL
2559776, at *19 (Fed. Cl. Spec. Mstr. Aug. 21, 2006) (“Some agents may trigger the production
of antibodies without also triggering the disease.”). I give more weight overall to Dr. Whitton when
opining on the biochemistry and immunologic topics relevant to the causation theory.
37

Case 1:18-vv-00925-DAT Document 85 Filed 10/06/23 Page 38 of 42
I do not find all of Petitioner’s arguments unpersuasive or (at least in this narrow context)
unreliable. For example, this is not a case in which persuasive epidemiologic evidence weighs
against the offered causation opinion. Articles like Haber, Tseng, and Baxter either involve the
kind of passive data never deemed particularly compelling in Program cases, or did not involve
reliable findings based on a comparison of results specific to a vaccinated sample against an
incidence rate for the unvaccinated. My prior decisions consistent with the present, like Bielak and
Trollinger, also did not turn on the weight given to such items of evidence. (Of course, I do not
find persuasive Petitioner’s suggestion that these studies or articles establish a medical community
consensus in favor of a pneumococcal vaccine-GBS relationship—if anything, the opposite is true,
as Dr. Whitton proposed, when he pointed out how existing GBS literature never proposes that the
wild S. pneumoniae infection is associated with GBS. But either way, the existing epidemiologic
studies discussed in this case by both sides were not probative of a relationship or lack thereof).
In addition, reliable evidence establishes that individuals with central nervous system
neuropathies, like MS, have been shown in small sample studies to possess antibodies specific to
myelin-containing phospholipids. I do not find reason to dispute the homologies observed in Dr.
Steinman’s BLAST searches, or that, despite Dr. Whitton’s contentions, the chain lengths were
inadequate (although as already noted the case turns on more fundamental questions of GBS
pathogenesis than homology).38 And Petitioner did show that phosphoglycerols are found in both
some of the vaccine’s antigens as well as nerve myelin.
But it remains preponderantly unlikely that anti-phospholipid/phosphoglycerol antibodies
drive GBS in its initial stages, or that they do so by targeting polar group heads specifically, or that
the pneumococcal vaccine causes GBS in a way that other medical science has yet to recognize.
What remains is a theory that does no more than attempt to “connect the dots” between vaccine
components and some molecular components of nerve myelin—a theory that largely hopes to
replicate the logic supporting a link between the flu vaccine and GBS. But that vaccine is not
interchangeable with the pneumococcal vaccine. They have wholly different ingredients and
function differently, and are also aimed at different kinds of illnesses.
III. Petitioner Misapprehends the Evidentiary Weighing Process
As noted, the parties opted for oral argument by counsel in lieu of a hearing. This afforded
Petitioner’s counsel not only the chance to highlight the aspects of his case he deemed most
38 I thus do not give great weight to Dr. Whitton’s argument that Dr. Steinman’s practice of employing BLAST
searches constitutes a misuse of the database, and I do not dispute the baseline utility it provides him in establishing
potential homologic sequences when comparing a variety of compounds, protein or otherwise, common to vaccines
and human tissue—although the science-heavy showing he made on this front did more to obscure and confuse than
support the theory that the vaccine can cause GBS.
38

Case 1:18-vv-00925-DAT Document 85 Filed 10/06/23 Page 39 of 42
important, but also to comment on how his prong one showing should be evaluated, in light of
the Vaccine Program’s preponderance evidentiary standard.
At argument, Petitioner proposed that I might be mistakenly “raising” his burden in the
context of the evidentiary weighing that special masters perform. He maintained that the evidence
offered was sufficient to meet his burden, since Respondent could not show that the scientific
literature was unreliable or false, and Dr. Steinman was qualified to opine on the subject. In
addition, the fact that other special masters had found this same showing adequate highlighted
my error. These arguments merit comment.
There is no doubt that the Program is structured in many ways to be favorable to its
claimants to serve the policy goal of encouraging vaccination—in particular, by ensuring a means
of compensating those injured by a vaccine through no fault of their own. No rules of evidence,
for example, limit the proof that can be offered and considered; on the contrary, an expansive
array of evidence, more often than not circumstantial, is reasonably relied upon and evaluated
when deciding if the Althen prongs are met. In addition, cases are supposed to be resolved
expeditiously, 39 with the special masters applying “inquisitorial” methods to direct a case toward
its proper conclusion rather than passively conducting proceedings. And to ensure a competent
bar exists to represent injured parties, the Act incorporates perhaps the most generous fee-shifting
provisions found in the federal system, paying fees in failed cases as often as in successful
matters.
All of the above, however, does not mean that petitioners prevail simply by offering
evidence in an exercise of “checking off” boxes from the Althen framework, then stepping back
and declaring their work is done. Rather, the balance of evidence is necessarily weighed by the
special master—not only in an initial, prima facie sense (for some cases do not even cross that
threshold), to determine that some evidence relevant to each prong has been offered, but also to
determine how Petitioner’s arguments and proof stack up against what Respondent marshals. For
a finding of entitlement, the probative value/quality and persuasiveness of a petitioner’s evidence,
considered in toto, must at least barely outweigh the Respondent’s. Some overall mix of evidence
must exist suggesting that a given vaccine could cause an injury (and, where a mechanism is
proposed, that this mechanism was preponderantly established).
After repeated careful consideration of the science and medical thinking about the
pneumococcal vaccine and GBS, I have concluded that the proof available is simply too
insubstantial to preponderantly show the pneumococcal vaccine can cause GBS. Petitioner is only
able to identify some molecular consistency between sub-components of the vaccine and myelin,
39 This goal has been hard to meet in the past ten-plus years, owing to the ever-growing number of cases filed in the
Vaccine Program—but it remains a very important consideration, and one I am always mindful of when processing
claims and scheduling cases for trial or other resolution.
39

Case 1:18-vv-00925-DAT Document 85 Filed 10/06/23 Page 40 of 42
coupled with other evidence suggesting (from small test samples, moreover) that antibodies
relevant to these consistent components might exist in the context of GBS. This does not mean
that it is likely they drive GBS (especially given how much is known about the exogenous factors
that likely do drive GBS, or the self antigenic targets), or that they do so by attacking myelin
structures wholly distinguishable from those already believed by science to be autoimmune
targets.
Is my determination simply masking a demand for scientific certainty? Only if the
weighing process I am tasked with performing did not involve consideration of Respondent’s
arguments and evidence, or if it were limited solely to evaluation of the reliability of individual
scientific studies or the credentials and expertise of a claimant’s expert—as Petitioner suggested
in oral argument. But this is not how special masters function, as the Court has recognized. On
the contrary—I am properly tasked with weighing both the probative value of individual items of
evidence and the credibility and persuasiveness of an expert’s testimony against the evidence
offered contra. I am never compelled to accept what is offered at face value—by either side—
any more than any fact finder would be. Sword v. United States, 44 Fed. Cl. 183, 188 (1999)
(“[e]ven more than ordinary fact-finders, this Court has recognized the unique ability of Special
Masters to adjudge cases in the light of their own acquired specialized knowledge and expertise
. . . The Special Master's sole professional responsibility for years has been to preside over
vaccine cases . . . No judge or jury can be forced to accept or reject an expert's opinion or a party's
theory at face value”). Denying entitlement after performing such weighing, in a quest for
sufficient evidence, does not mean certainty was demanded. Hodges v. Sec’y of Health & Hum.
Servs., 9 F.3d 958, 962 (Fed. Cir. 1993) (noting rejection of medical opinion on causation did not
amount to requiring certainty, but instead reflected the special master’s inquiry into whether
“some degree of acceptable scientific support” existed to conclude preponderance standard had
been met).
If anything, Petitioner’s arguments reflect a desire to lower his burden—something the
Circuit instructs is as inappropriate as requiring certainty. Boatmon, 941 F.3d at 1359–60. But in
some circumstances, the existing scientific and medical evidence relevant to a particular disease
and vaccine simply does not support causation, and it is no objection to maintain in response that
what a petitioner can offer should be deemed sufficient if it is “science-y” enough. Caves v. Sec'y
of Health & Hum. Servs., 100 Fed. Cl. 119, 143 (2011), aff’d, 463 F. App'x 932 (Fed. Cir. 2012)
(“the standard of proof does not operate as a sliding scale that varies depending on the quantity
and quality of the scientific evidence that is available”). It has not been shown to be likely that
the pneumococcal vaccine can cause GBS, because the evidence that exists on the topic is too
sparse overall to constitute a persuasive preponderant showing, after the weighing of evidence
pro and con has been performed.
40

Case 1:18-vv-00925-DAT Document 85 Filed 10/06/23 Page 41 of 42
Finally, what of the fact that other special masters have reached a different result? In many
cases, because the mix of evidence and nature of the theory presented from case to case can vary,
inconsistent outcomes are easier to accept. Not so here. And while special masters often take
refuge in the legal truism that their colleagues’ determinations do not bind them, Petitioner not-
unreasonably notes the fact that I am (so far) alone in my negative assessment of this causation
theory.
In response, I return to my analysis herein (which recapitulates Bielak and Trollinger)
highlighting the specific weaknesses of the theory that GBS can be caused by the pneumococcal
vaccine. As I have now exhaustively stated several times, the evidence associating the vaccine
(along with its wild bacterial cognate) with GBS is notably weak—substantially weaker than the
evidence linking the flu vaccine, or even wild flu virus. Arguments that antibodies produced in
response to the pneumococcal vaccine can attack nerve structures and instigate GBS rely on
articles I discussed at length in Bielak and Trollinger—but found wanting. See Bielak, 2022 WL
18058244, at *15–17, 32 (discussing Chang, Gilburd, Ho, Kanter, and Nakos); Trollinger, 2023
WL 2521912, at *28–29 (same). Those same articles were offered in the successful cases. See,
e.g., Gross, 2022 WL 9669651, at *15-17, 28; Pierson, 2022 WL 322836, at *12, 16. And Dr.
Whitton convincingly explained why it could not be assumed, and had not been shown, that an
antibody produced in response to one of the vaccine’s phosphoglycerol-containing
polysaccharides would even be recognized by a myelin phospholipid structure, let alone attack
the polar head groups (which have not been shown to be likely GBS targets in any event). A bare
demonstration of a cross-reactive potential is not enough to prevail, especially in the absence of
corroborative evidence that associates GBS with the pneumococcal vaccine or its wild bacterial
counterpart. Bielak, 2022 WL 18058244, at *33, 36. And I have also previously addressed
comparable arguments about the role of the conjugate. Deshler, 2020 WL 4593162, at *20–21.40
Overall, the opinion offered herein is wholly consistent with theories I have reviewed—
and rejected—three times before. My prior, and present, determinations were the product of
careful evaluation of the evidence, expert reports, and scientific literature (with identical items
filed in all of these matters). I did not accept at face value Petitioner’s arguments for what the
literature says, but read the filed items carefully, weighing them against Respondent’s criticisms.
Although I would always prefer to be guided by the collective wisdom of the other special
masters, I do not deem the cited counter-determinations to be sufficiently persuasive in their
analysis to suggest that I am in error. Rather, like Boatmon, those cases may reflect instances in
40 In fact, although my determinations in Trollinger and Bielak squarely contend with the findings in some other
decisions, my determination in Deshler with respect to the conjugate was not addressed in such cases, which
distinguished it on the grounds that Dr. Steinman’s phosphoglycerol theory had not been offered in Deshler. See, e.g.,
Gross, 2022 WL 9669651, at *36; Pierson, 2022 WL 322836, at *26, 31.
41

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which the proper evidentiary standard was inadvertently lowered, based on the unexamined
assumption that what “works” for the flu vaccine-GBS association works for any vaccine.41
CONCLUSION
Claimants must carry their burden of proof—here, by preponderantly establishing, via an
offering of sufficient evidence specific to the pneumococcal vaccine in question, how it could
cause GBS. This has not been accomplished in this case. Accordingly, I deny entitlement.
In the absence of a motion for review filed pursuant to RCFC Appendix B, the Clerk of the
Court SHALL ENTER JUDGMENT in accordance with the terms of this Decision.42
IT IS SO ORDERED.
/s/ Brian H. Corcoran
Brian H. Corcoran
Chief Special Master
41 Of course, if (as was determined in prior cases) it is enough to find that a vaccine has some cross-reactive potentiality
with self tissues on the basis of Dr. Steinman’s argument, it may as well be concluded that all covered Program
vaccines are capable of causing GBS, so long as an expert like Dr. Steinman is willing to provide a series of lengthy
expert reports so opining. At that point, of course, the special masters would be creating a new Table claim.
42 Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment if (jointly or separately) they file notices
renouncing their right to seek review.
42

================================================================================
DOCUMENT 2: USCOURTS-cofc-1_18-vv-00925-1
Date issued/filed: 2024-03-21
Pages: 10
Docket text: JUDGE VACCINE REPORTED OPINION (PUBLIC VERSION) re: 95 Order on Motion for Review, Judge Vaccine Order/Opinion. Signed by Judge David A. Tapp. (smr) Service on parties made.
--------------------------------------------------------------------------------
Case 1:18-vv-00925-DAT Document 97 Filed 03/21/24 Page 1 of 10
In the United States Court of Federal Claims
No. 18-925
Filed: March 21, 2024†
JOSE GAMBOA-AVILA,
Petitioner,
v.
SECRETARY OF HEALTH AND
HUMAN SERVICES,
Respondent.
Curtis R. Webb, Curtis R. Webb, Attorney at Law, Monmouth, OR, for Petitioner.
Colleen C. Hartley, Assistant Director, Traci R. Patton, Assistant Director, Heather L.
Pearlman, Deputy Director, C. Salvatore D’Alessio, Director, and Brian M. Boynton, Principal
Deputy Assistant Attorney General, Torts Branch, Civil Division, United States Department of
Justice, Washington, D.C., for Respondent.
MEMORANDUM OPINION AND ORDER
TAPP, Judge.
Dissimilar circumstances justify disparate outcomes. Jose Gamboa-Avila (“Mr.
Gamboa”), petitioned for compensation pursuant to the Vaccine Act, alleging that he suffered
from Guillain-Barre syndrome (“GBS”)1 after receiving the pneumococcal vaccine. (Pet., ECF
No. 1). Specifically, Mr. Gamboa alleged he experienced fatigue, generalized body aches,
headaches, insomnia, loss of strength, numbness, and facial paralysis. (Id. at 1–2). The Chief
† This Order was originally filed under seal on February 26, 2024. (ECF No. 95). The Court
provided parties the opportunity to review this opinion for any proprietary, confidential, or other
protected information and submit proposed redactions no later than March 11, 2024. The parties
failed to file a Joint Status Report requesting redactions. Thus, the sealed and public versions of
this Order are identical, except for the publication date and this footnote.
1 GBS is “a rare disorder in which your body’s immune system attacks your nerves. Weakness
and tingling in your hands and feet are usually the first symptoms. These sensations can quickly
spread, eventually paralyzing your whole body.” Guillain-Barre syndrome, Mayo Clinic, (last
reviewed Dec. 22, 2023), https://www.mayoclinic.org/diseases-conditions/guillain-barre-
syndrome/symptoms-causes/syc-20362793.

Case 1:18-vv-00925-DAT Document 97 Filed 03/21/24 Page 2 of 10
Special Master reviewed Mr. Gamboa’s claim, ultimately concluding that Mr. Gamboa was not
entitled to compensation because he did “not preponderantly establish[] that the pneumococcal
vaccine can cause GBS—and this alone is a sufficient basis for dismissal.” Gamboa-Avila v.
Sec’y of Health & Hum. Servs., No. 18-925, 2023 WL 6536207, at *1 (Fed. Cl. Spec. Mstr. Sept.
11, 2023), (Decision, ECF No. 84). Consequently, the Chief Special Master denied entitlement.
Id. at *1, 32.
Mr. Gamboa seeks review, (ECF No. 86), arguing that the Chief Special Master
impermissibly raised the burden of proof—requiring a higher burden than preponderance—so his
decision should be reversed. (Mem. Mot. for Rev. (“Pet’r’s Mem.”), ECF No. 88).2 As explained
below, the Court denies Mr. Gamboa’s Motion for Review and affirms the Chief Special
Master’s ruling.
I. Background
Mr. Gamboa received the pneumococcal vaccine on November 13, 2017 during a routine
visit for his existing HIV-AIDS3 diagnosis. Gamboa-Avila, 2023 WL 6536207, at *1 (citing
Pet’r’s Ex. 2 at 6–12, ECF No. 30-2). On November 27, 2017, Mr. Gamboa reported generalized
body aches, a headache, night sweats, and numbness since his November 13 visit. (Pet’r’s Ex. 2
at 17–21). The next day, Mr. Gamboa returned to his provider complaining of body aches
(particularly leg and foot pain), facial numbness on his left side that began the night before, and
insomnia. (Id. at 28). His physician noted that since the pneumococcal vaccine Mr. Gamboa “has
generally felt unwell, described vague [symptoms] including . . . feel[ing] swollen, face/body
feels numb, difficult to eat, [does not] taste food, legs hurt when he walks, hard to sit or stand for
too long, [and] hand weakness. [Symptoms] affecting [right] side more than [left].” (Id.). Mr.
Gamboa’s physician also documented a mild right facial droop and reduced sensation on the left
side of his face. (Id. at 29). However, Mr. Gamboa’s physician noted that his strength remained
intact in all extremities, and he exhibited a normal gait.
That night, November 28, Mr. Gamboa visited the emergency department complaining of
facial numbness and weakness, lip swelling, difficulty talking and walking, and generalized body
aches that he described as “tingly” and intermittent. (Id. at 31). The emergency physician noted
that his “whole body pain and numbness” first began “about [five to six] days ago,” (id.), thereby
dating the onset of symptoms to on or around November 22 or 23. The emergency physician and
Mr. Gamboa’s HIV physician speculated the symptoms were caused by a recent medication
change and/or vaccine. (Id. at 31 (“symptoms started about [five to six] days ago, after one of his
2 The citations correspond with the Adobe-Acrobat Pro pagination, not the assigned page number
on which the document appears.
3 “Acquired immunodeficiency syndrome (AIDS) is a chronic, potentially life-threatening
condition caused by the human immunodeficiency virus (HIV). By damaging your immune
system, HIV interferes with your body's ability to fight infection and disease.” HIV/AIDS, Mayo
Clinic, (last reviewed Dec. 22, 2023), https://www.mayoclinic.org/diseases-conditions/hiv-
aids/symptoms-causes/syc-20373524.
2

Case 1:18-vv-00925-DAT Document 97 Filed 03/21/24 Page 3 of 10
ART meds was switched and he received a pneumovax shot”), 33–34 (“HIV [physician] believes
this is possibly caused by a recent change to his medication regimen”)).
Mr. Gamboa’s physicians hospitalized him from November 30 to December 9, 2017, and
diagnosed Mr. Gamboa with GBS. (Id. at 50, 54, 57, 63–64, 96, 192–93). Throughout his
hospitalization, Mr. Gamboa’s treaters continued to note his symptoms in relation to both a
change in medication and the pneumococcal vaccine. (E.g., id. at 57 (“symptoms coincide with
recent change in ART meds and pneumovax administration”), 59 (“unclear if patient’s
neuropathic symptoms are 2/2 medication changes or pneumovax”), 71 (“received
[pneumococcal vaccine] on November 13, also switched [medications] on that day”), 87
(“admitted with recent onset facial diplegia4 and paresthesias5 . . . [v]accine may have been
trigger”), 94 (“presenting with generalized pain and facial weakness which developed [one
week] after receiving pneumococcal vaccine . . . was originally switched to [different
medication] on same clinic visit that vaccine was received), 102 (“vaccine may have been
trigger”)).
Mr. Gamboa petitioned for vaccine compensation on June 27, 2018, claiming the
pneumococcal vaccine caused his GBS, entitling him to compensation under the Vaccine Act.
(See generally Pet.). Under the Vaccine Act, petitioners may demonstrate eligibility for an award
through two methods: (1) an injury listed on the Vaccine Injury Table occurred within the
requisite period, or (2) an unlisted injury was caused-in-fact by a vaccine listed on the Table. 42
C.F.R. § 100.3; 42 U.S.C. § 300aa-11(c)(1)(C). Here, Mr. Gamboa petitioned for an unlisted
injury, so he was required to establish causation. To establish actual causation, Mr. Gamboa was
required to “show by preponderant evidence” (1) a medical theory connecting the vaccination
and 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.” Althen v. Sec’y of Health & Hum. Servs., 418 F. 3d 1274, 1278 (Fed. Cir. 2005). The
Chief Special Master determined that Mr. Gamboa failed to preponderantly establish that his
specific pneumococcal vaccine can cause GBS. Gamboa-Avila, 2023 WL 6536207, at *1–2, 42.
The Chief Special Master’s finding that Mr. Gamboa failed to satisfy Althen prong one
chiefly relied on a review of scientific literature and expert testimony. Id. at *2–19, 26–29. Mr.
Gamboa’s expert, Dr. Lawrence Steinman (“Dr. Steinman”),6 advanced a theory that “the
pneumococcal vaccine contains a ‘molecular mimic’ relevant to the pathogenesis
[(development)] of GBS[;]” in other words, the vaccine contains molecules that confuse the body
into attacking its own nervous system’s myelin, leading to GBS. Id. at *2 (quoting First
4 Diplegia is when “[p]aralysis occurs on the same area on both sides of the body. For example,
paralysis affects both arms, both legs or both sides of the face.” Paralysis, Cleveland Clinic, (last
reviewed Dec. 22, 2023), https://my.clevelandclinic.org/health/diseases/15345-paralysis.
5 Paresthesia is “the feeling of tingling, numbness or ‘pins and needles.’” Paresthesia, Cleveland
Clinic, (last reviewed Dec. 22, 2023), https://my.clevelandclinic.org/health/symptoms/24932-
paresthesia.
6 Admitted as expert in neurology. Gamboa-Avila, 2023 WL 6536207, at *2.
3

Case 1:18-vv-00925-DAT Document 97 Filed 03/21/24 Page 4 of 10
Steinman Rep. at 11, ECF No. 38); (see also Pet’r’s Mem. at 8–9 (outlining four element theory7
connecting pneumococcal vaccine to GBS)). Dr. Steinman attempted to show that molecular
mimicry led to Mr. Gamboa’s GBS, by testifying (based on his own research) that specific
phospholipids—phosphoglycerol and phosphocholine—are present in both the pneumococcal
vaccine and nerve myelin that are “targeted by antibodies in neuroinflammation.” Id. at *3–5
(quoting First Steinman Rep. at 13–14, 19). He continued that the pathogenic antibodies “are
found” in the pneumococcal vaccine and are known to be associated with GBS. Id. at *4 (citing
First Steinman Rep. at 19).
Dr. Steinman also cited literature to support his molecular mimicry theory, including Ho
who studied fatty acids of the myelin sheath that resolve neuroinflammation and Gilburd to show
that “the antibodies of the kind that would (theoretically) be produced by the pneumococcal
vaccine are known to be associated with GBS.” Id. at *3–4 (citing Pet’r’s Ex. 22, ECF No. 27-1
(“Ho”); Pet’r’s Ex. 27, ECF No. 41-1 (“Gilburd”)). However, the Chief Special Master
determined the literature did not necessarily advance Dr. Steinman’s theory. Id. at *3–10. For
example, Ho studied the autoimmune response in multiple sclerosis (“MS”),8 not GBS, and
Gilburd noted that the antibodies in GBS have not been proven to induce nerve damage. Id. at
*3–4. Further, Dr. Steinman cited two case reports that linked pneumococcus with GBS, but the
Chief Special Master found that “both case report’s authors admitted that no such association had
even been scientifically established.” Id. at 5–6 (citing Pet’r’s Ex. 40, ECF No. 56-1 (“El
Khatib”); Pet’r’s Ex. 27, ECF No. 56-2 (“Yuki”)). Dr. Steinman also cited Nakos, which
sampled the blood of nine patients with an “acute inflammatory demyelinating polyneuropathy”9
GBS variant. Id. at *4, 6 (citing Pet’r’s Ex. 28, ECF No. 41-2 (“Nakos”)). Nakos found that a
7 Dr. Steinman theorizes that: “1. The human immune system targets the phosphoglycerol and
phosphocholine polar head groups in lipids in the central nervous system of some patients with
[MS]. 2. Pneumococcal conjugate vaccine (Prevnar 13) generates an immune response to the
phosphoglycerol and phosphocholine moieties in the polysaccharide capsule of several serotypes
of the streptococcus pneumonia bacteria. 3. Phosphoglycerol and phosphocholine containing
lipids in the peripheral nervous system are targets of the aberrant immune response in some cases
of GBS. 4. The immune response that targets the phosphoglycerol or phosphocholine moiety of
the polysaccharide capsule of streptococcus pneumonia bacteria can also, on rare occasions,
target the phosphoglycerol or phosphocholine moiety in the myelin of lipids in the peripheral
nerves and cause [GBS].” (Pet’r’s Mem. at 8–9).
8 MS “causes damage to nerve fibers in the central nervous system. Over time, it can lead to
vision problems, muscle weakness, loss of balance or numbness.” Multiple Sclerosis (MS),
Cleveland Clinic, (last reviewed Jan. 11, 2024),
https://my.clevelandclinic.org/health/diseases/17248-multiple-sclerosis.
9 Acute inflammatory demyelinating polyneuropathy (AIDP), also known as
polyradiculoneuropathy, is an autoimmune disorder characterized by the rapid onset of weakness
and sensory loss in the limbs due to inflammation and damage to the peripheral nerves’ myelin
sheath. Acute inflammatory Demyelinating Polyneuropathy, Polyradiculoneuropathy (AIDP),
Yale Medicine, (last reviewed Jan. 22, 2024) https://www.yalemedicine.org/clinical-
keywords/acute-inflammatory-demyelinating-polyneuropathy-polyradiculoneuropathy.
4

Case 1:18-vv-00925-DAT Document 97 Filed 03/21/24 Page 5 of 10
“wide range” of antibodies were observed, although the precise role of the antibodies’ in the
development of GBS was not determined. Id. Put simply, Nakos showed that antibodies were
present in patients with GBS, including one with a phosphoglycerol component, but were not
proven to cause GBS. See id.
Following pushback from the Secretary’s expert, Dr. Steinman advanced another distinct
theory that “the pneumococcal vaccine could theoretically cause GBS even if a natural
pneumococcal infection could not, because ‘the vaccine is very different from the microbe
itself.’” Id. at *7 (citing Third Steinman Rep. at 3, 17–18, 23–29) (emphasis in original). Dr.
Steinman testified that the conjugated vaccine—a type of vaccine that only uses a portion of the
germ and coats that germ in a polysaccharide (a sugar)10—contained an additional mimic that
could cause GBS. Id. at *7–8 (citing Third Steinman Rep. at 24). Dr. Steinman opined that
mimic would likely spark an immune response, leading to the body to attack its own myelin. See
id. at *7–9.
The Secretary’s expert, Dr. J. Lindsay Whitton (“Dr. Whitton”),11 testified that it is
unlikely the pneumococcal vaccine would cause GBS. Id. at *10. He explained that because of
sugar and protein molecules in the pneumococcal vaccine, the vaccine “can only ‘teach’ the
immune system to respond to specific strains it ‘sees’ (based on the strains in the vaccine), with
each being separate.” Id. (citing First Whitton Rep. at 5, ECF No. 44-1). Dr. Whitton continued
that triggering GBS was “quite strain-specific” and that S. pneumoniae, at issue here, was not
associated with GBS. Id. at *12 (quoting First Whitton Rep. at 8). Dr. Whitton distinguished the
polysaccharide capsules in S. pneumoniae—which are “gram positive” or “thick”—with those of
C. jejuni—which are “gram negative” or “thin”—because C. jejuni is known to be associated
with GBS. Id. (citing First Whitton Rep. at 7–10). Dr. Whitton contended that because of the
capsule differences, the pneumococcal vaccine lacks the molecular structure understood to cause
GBS, so it is improbable that the vaccine caused Mr. Gamboa’s GBS. Id. at *12–13. Dr. Whitton
also distinguished GBS from MS, arguing that the diseases do not have a common pathogenesis,
so MS-focused literature (like Ho) is not relevant to Mr. Gamboa’s condition. Id. at *13. The
Chief Special Master found Dr. Whitton’s rebuttal convincing. Id. at *10–15, 26–29.
The Chief Special Master also looked to prior decisions to determine that Mr. Gamboa
failed to satisfy Althen prong one. Id. at *24–25. Specifically, the Chief Special Master noted
that Mr. Gamboa relied on unpersuasive theories and literature used in other cases. Id. In Bielak
and Trollinger, petitioners relied on nearly all the same literature as Mr. Gamboa to argue that
10 Conjugate vaccines “use only portions of the germ. Many bacteria molecules are coated by a
sugar called polysaccharide. This coating hides or disguises the germ (antigens) so that the
immature immune systems of infants are not able to recognize it. Therefore, scientists attach the
polysaccharide to a stronger protein. When the immune system responds to the protein, it also
responds to the polysaccharide. Examples include . . . Pneumococcal Conjugate Vaccine
(Prevnar®).” Types of Vaccines), Health.mil, (last reviewed Jan. 22, 2024),
https://www.health.mil/Military-Health-Topics/Health-Readiness/Immunization-
Healthcare/Clinical-Consultation-Services/Types-of-Vaccines.
11 Admitted as expert in immunology. Gamboa-Avila, 2023 WL 6536207, at *10.
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phosphoglycerol in the vaccine caused antibodies to attack myelin. Id. at *25 (citing Ho, Gilburd,
& Nakos (distinguished above)); Trollinger v. Sec’y of Health & Hum. Servs., No. 16-473V,
2023 WL 2521912, at *25 (Fed. Cl. Spec. Mstr. Feb. 17, 2023), mot. for review denied, No. 16-
473, 2023 WL 5249583 (Fed. Cl. Aug. 15, 2023); Bielak v. Sec’y of Health & Hum. Servs., No.
18-761V, 2022 WL 18058244, at *34 (Fed. Cl. Spec. Mstr. Dec. 9, 2022. Further, in Deshler, the
Chief Special Master rejected the petitioner’s theory, also advanced by Mr. Gamboa, that the
conjugate component of the vaccine caused an autoimmune response relating to the vaccine’s
antigens. Gamboa-Avila, 2023 WL 6536207, at *25; Deshler v. Sec’y of Health & Hum. Servs.,
No. 16-1070V, 2020 WL 4593162 (Fed. Cl. Spec. Mstr. July 1, 2020). The Chief Special Master
concluded that Dr. Steinman’s theory is “unreliable and persuasive.” Gamboa-Avila, 2023 WL
6536207, at *26–32. Accordingly, the Chief Special Master determined Mr. Gamboa did not
carry his Althen prong one burden of proof12 and, therefore, was not entitled to compensation
under the Vaccine Act.
II. Analysis
Under the Vaccine Act, the Court of Federal Claims reviews a special master’s decision
upon the timely request of either party. See 42 U.S.C. § 300aa-12(e)(1)–(2) (2018). In motions to
review, the Court must determine if the decision is “arbitrary, capricious, an abuse of discretion,
or otherwise not in accordance with law[.]” 42 U.S.C. § 300aa-12(e)(2)(B). The Court applies
the arbitrary and capricious standard to factual findings and reviews all legal conclusions de
novo. Munn v. Sec’y of Health & Hum. Servs., 970 F.2d 863, 870 n.10 (Fed. Cir. 1992). When
the Court reviews mixed questions of law and fact, it must determine whether answering it
primarily involves legal or factual work. U.S. Bank Nat. Ass’n ex rel. CWCapital Asset Mgmt.
LLC v. Vill. at Lakeridge, LLC, 138 S. Ct. 960, 967 (2018) (involving determination by
bankruptcy court).
Importantly, the Court does not “reweigh the factual evidence,” or “assess whether the
special master correctly evaluated the evidence.” Lampe v. Sec’y of Health & Hum. Servs., 219
F.3d 1357, 1360 (Fed. Cir. 2000) (quoting Munn, 970 F.2d at 871). Neither does the Court
“examine the probative value of the evidence or the credibility of the witnesses.” Id. Rather, the
Court upholds the special master’s decision if they “considered the relevant evidence of record,
dr[ew] plausible inferences and articulated a rational basis for the decision[.]” Hines on behalf of
Sevier v. Sec'y of Health & Hum. Servs., 940 F.2d 1518, 1528 (Fed. Cir. 1991) (holding that
“reversible error [is] extremely difficult to demonstrate”). The standard of review is “highly
deferential.” Cucuras v. Sec’y of Dep’t of Health & Hum. Servs., 26 Cl. Ct. 537, 541 (1992),
aff’d, 993 F.2d 1525 (Fed. Cir. 1993). The Court cannot “substitute its judgment for that of the
special master merely because it might have reached a different conclusion.” Snyder v. Sec’y of
Dep’t of Health & Hum. Servs., 88 Fed. Cl. 706, 718 (2009).
To determine causation, the special master and this Court apply the Althen test, listed
above. 418 F.3d at 1278. A petitioner must satisfy all three prongs to demonstrate causation-in-
fact. Id. at 1274. Under Althen prong one, the petitioner must provide a “reputable medical
12 Because the Chief Special Master determined that Mr. Gamboa did not establish prong one of
Althen, he did not address prongs two or three. See generally Gamboa-Avila, 2023 WL 6536207.
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theory” that the vaccine at issue can cause the type of injury alleged. Id. at 1278; Pafford v. Sec’y
of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). Petitioner’s medical theory must
be supported by “sound and reliable medical or scientific explanation[,]” however, medical or
scientific certainty is not required. Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 548–
49 (Fed. Cir. 1994). Further, mere plausibility of petitioner’s medical theory is insufficient.
Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019); LaLonde v.
Sec’y of Health & Hum. Servs., 746 F.3d 1334, 1339 (Fed. Cir. 2014) (“[h]owever, in the past we
have made clear that simply identifying a ‘plausible’ theory of causation is insufficient for a
petitioner to meet her burden of proof” (quoting Moberly ex rel. Moberly v. Sec’y of Health &
Hum. Servs., 592 F.3d 1315, 1322 (Fed. Cir. 2010))). When evaluating expert testimony, a
special master “may conclude that there is simply too great an analytical gap between the data
and the opinion proffered.” Cedillo v. Sec’y of Health & Hum. Servs., 617 F.3d 1328, 1339 (Fed.
Cir. 2010) (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)). Ultimately, special
masters must determine whether the medical theory advanced by the petitioner and their expert is
“more probable than not[.]” Althen, 418 F.3d at 1279–80 (citing Hellebrand v. Sec’y of Health &
Hum. Servs., 999 F.2d 1565, 1572–73 (Fed. Cir. 1993)).
Mr. Gamboa challenges the Chief Special Master’s decision on one ground, that the
Chief Special Master impermissibly raised the burden of proof to determine Mr. Gamboa did not
satisfy Althen prong one. (Pet’r’s Mem. at 12–27).13 Specifically, Mr. Gamboa asserts the Chief
Special Master required scientific certainty by improperly comparing Mr. Gamboa’s claim to a
vaccine table injury, requiring more fulsome evidence than necessary, and discounting GBS-
specific medical science. (Id. at 14–19). Mr. Gamboa also argues the Chief Special Master
impermissibly required epidemiological evidence connecting the pneumococcal disease or
vaccine conjugate to GBS. (Id. at 20–24). Further, Mr. Gamboa argues the Chief Special Master
did not give proper weight to the opinions of Mr. Gamboa’s treating physicians. (Id. at 24–27).
Mr. Gamboa requests that this Court reverse the Chief Special Master’s decision and remand the
petition to apply the correct burden of proof. (Id. at 27). The Secretary argues the Chief Special
Master applied the correct standard of preponderance to Althen prong one, and his factual
findings were not arbitrary and capricious. (Resp’t’s Resp. at 11–21, ECF No. 90). The Court
agrees with the Secretary.
13 Mr. Gamboa asserts that the Chief Special Master required a higher burden of proof than other
special masters who determined the pneumococcal vaccine was causally connected to GBS. (Id.
at 12–14 (citing Gross v. Sec’y of Health & Hum. Servs., No. 17-1075V, 2022 WL9669651 (Fed.
Cl. Spec. Mstr., Sept. 22, 2022), Maloney v. Sec’y of Health & Hum. Servs., No. 19-1713, 2022
WL 1074087 (Fed. Cl. Spec. Mstr., March 17, 2022), Pierson v. Sec’y of Health & Hum. Servs.,
No. 17-1136V, 2022 WL 322836 (Fed. Cl. Spec. Mstr. Jan. 19, 2022) (Koller v. Sec’y of Health
& Hum. Servs., No. 16-439V, 2021 WL 5027947 (Fed. Cl. Spec. Mstr. Oct. 8, 2021))). The
Chief Special Master explained that the other special masters’ decisions “may reflect instances in
which the proper evidentiary standard was inadvertently lowered” so his review was more
rigorous. Gamboa-Avila, 2023 WL 6536207, at *31 (emphasis added). The Court will address
the burden of proof in more detail below, but notes that special masters are not bound by the
decisions of their colleagues. Boatmon, 941 F.3d at 1358–59.
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As an initial matter, Mr. Gamboa’s argument that the Chief Special Master impermissibly
raised his burden of proof by requiring scientific certainty is a mixed question of law and fact.
(Pet’r’s Mem. at 14–19). When faced with a mixed question, the Court must determine whether
answering it primarily involves legal or factual work. See U.S. Bank Nat. Ass’n, 138 S. Ct. at
967. Here, Mr. Gamboa disguises a factual disagreement as a legal challenge. See e.g., Echols v.
Sec’y of Health & Hum. Servs., 165 Fed. Cl. 9, 17 (2023).
First, Mr. Gamboa argues that the Chief Special Master raised the burden of proof
beyond preponderance by comparing the quality of his evidence to evidence connecting the flu
vaccine to GBS and invoking evidence linking the Epstein-Barr virus to MS. (Pet’r’s Mem. at
14–17). Mr. Gamboa identifies that a flu vaccine is a Vaccine Table Injury and argues that robust
evidence connecting the flu vaccine with GBS comes from studies that are “rare in science.” (Id.
at 15). Mr. Gamboa also asserts that the scale of the study proving with scientific certainty that
the Epstein-Barr virus causes MS far exceeds the preponderance standard. (Id. at 16–17
(referencing study of “more than [ten] million young adults” to test causal connection between
the Epstein-Barr virus and MS)). Therefore that “degree of certainty” should not be applied to
literature studying the connection between the pneumococcal vaccine and GBS. (Id. at 15 (citing
42 CFR § 100.3(a)XIV(D) and (b)(15)). Mr. Gamboa mischaracterizes the Chief Special
Master’s decision.
The Chief Special Master did not “require” Mr. Gamboa to produce comparable
evidence. Gamboa-Avila, 2023 WL 6536207, at *24–31. Rather, the flu and Epstein-Barr
evidence illustrated the relative weakness of the medical literature provided by Mr. Gamboa. Id.
at *27 n.37 (asserting the robustness of those studies “underscore the comparative lack of
comparable reliable proof in this case.”). As explained above, Mr. Gamboa provided medical
literature that discussed MS (Ho), failed to establish an association between pneumococcus and
GBS (El Khatib), and did not identify the precise role of antibodies in GBS’s development
(Nakos). Id. at *4–6, 10, 25, 27–28, 31. Accordingly, evidentiary comparisons did not raise Mr.
Gamboa’s burden of proof but underscored the weakness of Mr. Gamboa’s theory.
Further, Mr. Gamboa argues the Chief Special Master disregarded the value of those
studies and their specificity to GBS. (Pet’r’s Mem. at 17–19). Specifically, Mr. Gamboa argues
Ho was reliable because it showed how the immune systems of people with MS target
phospholipids, and such knowledge can “help us understand other demyelinating diseases” like
GBS. (Id. at 18). Similarly, Mr. Gamboa argues that Nakos was reliable because it identified
anti-phospholipid antibodies in GBS patients, which supported Dr. Steinman’s molecular
mimicry theory. (Id. at 19). However, it is not the role of the Court to “reweigh the factual
evidence” or second-guess the special master’s scientific evaluation. Lampe, 219 F.3d at 1360.
So long as the Chief Special Master “considered the relevant evidence of record, dr[ew]
plausible inferences and articulated a rational basis for the decision,” the Court will not disrupt
his decision. Hines, 940 F.2d at 1528. Here, the Chief Special Master discussed at length how
and why he was unconvinced that those studies established the pneumococcal vaccine could
cause GBS. Gamboa-Avila, 2023 WL 6536207, at *26–29. The Court agrees. Thus, the Chief
Special Master did not raise Mr. Gamboa’s burden of proof or arbitrarily or capriciously reject
his evidence.
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Second, Mr. Gamboa argues that the Chief Special Master required epidemiological
evidence connecting the pneumococcal disease and/or conjugate vaccine to GBS. (Pet’r’s Mem.
at 20–24). Mr. Gamboa asserts that the absence of epidemiological evidence was considered a
“critical flaw” in his medical theory. (Id. at 20). Here again, the Chief Special Master did not
“require” epidemiological evidence nor impermissibly raise Mr. Gamboa’s burden of proof. The
Chief Special Master did not violate Capizzano where the Federal Circuit held that “requiring
either epidemiologic studies . . . or general acceptance in the scientific or medical communities
to establish a logical sequence of cause and effect” is contrary to Althen. Capizzano v. Sec’y of
Health & Hum. Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006) (internal citation omitted). Instead,
the Chief Special Master noted the lack of epidemiological evidence, particularly given the
relative weakness of the literature provided by Mr. Gamboa to show the pneumococcal vaccine
can cause GBS. Gamboa-Avila, 2023 WL 6536207, at *26–29. Again, the Court declines to
reweigh the Chief Special Master’s factual findings.
Lastly, Mr. Gamboa argues the Chief Special Master failed to “seriously consider” the
medical opinions of Mr. Gamboa’s treating physicians. (Pet’r’s Mem. at 24–27). Mr. Gamboa
emphasizes that multiple physicians speculated the pneumococcal vaccine “triggered” his GBS.
(Id. (citing Pet’r’s Ex. 2 at 30, 59, 72, 76, 155)). Mr. Gamboa argues that such language provides
“clear evidence” that Mr. Gamboa’s physicians recognized a potential connection between the
pneumococcal vaccine and GBS diagnosis. (Id. at 25–26). Mr. Gamboa further argues that
although the Chief Special Master acknowledged those medical records were relevant to Althen
prong one, he disregarded them because they did not display “scientific certainty.” (Id. at 26).
This is purely an issue of fact.
To be upheld by this Court, the Chief Special Master need only consider relevant
evidence, make plausible inferences, and articulate a rational basis for the decision. See Hines,
940 F.2d at 1528. Generally, medical records are considered trustworthy evidence and given
substantial weight. Cucuras, 993 F.2d at 1528; e.g., Lowrie v. Sec’y of Health & Hum. Servs.,
No. 03–1585V, 2005 WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). However,
physician notes largely focused on temporality do not relieve the petitioner from providing “a
reputable medical or scientific explanation that pertains specifically to [his] case,” Broekelschen
v. Sec'y of Health & Hum. Servs., 618 F.3d 1339, 1345 (Fed. Cir. 2010) (quoting Knudsen, 35
F.3d at 548–49). Here, the Chief Special Master weighed the opinions of Mr. Gamboa’s treating
physicians against the medical literature and Dr. Whitton’s testimony to determine Mr. Gamboa
failed to establish the pneumococcal vaccine can cause GBS. Gamboa-Avila, 2023 WL 6536207,
at *28. Specifically, he found that the physicians’ notes were speculative and not informed by the
level of scientific specificity found in the medical literature provided by both Mr. Gamboa and
the Secretary. Id.
Mr. Gamboa’s physicians noted there could be a connection between the pneumococcal
vaccine and his GBS but advanced other theories as well. (E.g., Pet’r’s Ex. 2 at 57 (“symptoms
coincide with recent change in ART meds and pneumovax administration”), 59 (“unclear it
patient’s neuropathic symptoms are 2/2 medication changes or pneumovax”), 71 (“received
[pneumococcal vaccine] on November 13, also switched [medications] on that day”)). Therefore,
the Chief Special Master was within his purview to weigh the factual evidence and examine its
probative value. Porter v. Sec’y of Health & Hum. Servs., 663 F.3d 1242, 1249 (Fed. Cir. 2011).
When the finding of fact is “based on evidence in the record that [is] not wholly implausible,
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[this Court is] compelled to uphold the finding as not being arbitrary or capricious.” Porter, 663
F.3d at 1249 (internal citation omitted). The Chief Special Master plausibly found that Mr.
Gamboa’s physician notes were less convincing than the Secretary’s evidence, explained above.
Accordingly, the Court upholds the factual findings as neither arbitrary nor capricious.
Based on the foregoing, the Court finds that the Chief Special Master considered the
relevant evidence of record, drew plausible inferences, and articulated a rational basis for his
decision that Mr. Gamboa failed to satisfy the preponderance standard. Accordingly, the Chief
Special Master’s September 11, 2023 ruling was not arbitrary, capricious, an abuse of discretion,
or contrary to law.
III. Conclusion
For the stated reasons, the Court hereby DENIES Mr. Gamboa’s Motion for Review,
(ECF No. 86), and AFFIRMS the Chief Special Master’s September 11, 2023 decision. The
Clerk is directed to enter judgment accordingly.
The Court has filed this ruling under seal. The parties shall confer to determine proposed
redactions to which all parties agree. Per Vaccine Rule 18(b), no later than March 11, 2024, the
parties shall file a joint status report indicating their agreement with the proposed redactions,
attaching a copy of those pages of the Court’s ruling containing proposed redactions, with all
proposed redactions clearly indicated.
IT IS SO ORDERED.
s/ David A. Tapp
DAVID A. TAPP, Judge
10