Jaye v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 20-672V

************************* Chief Special Master Corcoran

*

RICHARD JAYE, * Filed: July 18, 2024

*

Petitioner, *

*

v. *

*

SECRETARY OF HEALTH AND *

HUMAN SERVICES *

*

Respondent. *

*

*************************

Scott Rooney, Nemes Rooney, P.C., Farmington Hills, MI, for Petitioner.

Lynn Schlie, U.S. Dep’t of Justice, Washington, DC, for Respondent.

ENTITLEMENT DECISION 1

On June 2, 2020, Richard Jaye filed a petition for compensation under the National Vaccine

and Injury Compensation Program (the “Vaccine Program”) 2 (ECF No. 1), alleging that a

pneumococcal vaccine he received on December 8, 2017, caused him to incur Guillain-Barré

syndrome (“GBS”). (Petitioner previously alleged that a flu vaccine administered to him in early

October of that same year may also have been causal, but seems to have abandoned that aspect of

his claim).

Because of my prior experience resolving Vaccine Program claims asserting a similar

causation theory, I determined that the matter could reasonably be resolved via ruling on the

record, and to that end the parties have filed briefs in support of their respective positions. See

Petitioner’s Motion, dated September 29, 2023 (ECF No. 81-1) (“Mot.”); Respondent’s

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).

Opposition, dated January 30, 2024 (ECF No. 86) (“Opp.”); Petitioner’s Reply, dated March 6,

2024 (ECF No. 88) (“Reply”).

Having reviewed the above plus the filed medical records, expert reports, and associated

literature (including items filed only in connection with this claim), 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 grounds for dismissal. I have reached

the same determination in several prior Program cases, based on a comparable theory, and no

scientific or medical evidence offered in this case that I have not previously considered supports

an alternative finding, or reflects new scientific/medical developments suggesting that rejection of

the theory should be revisited.

I. Factual Background

The relevant facts can be briefly summarized. Petitioner (then 72 years old) received the

pneumococcal vaccine on December 5, 2017, in the context of an annual physical exam. Ex. 17 at

33. Less than two weeks later, he sought emergency care due to two days of chest pain (coupled

with bilateral leg pain). Ex. 4 at 27. Then, on December 19, 2017 (now two weeks post-

vaccination), he informed his primary care physician that he was experiencing generalized

arthralgias and myalgias, plus difficulty walking. Ex. 17 at 34. A few days thereafter, he sought

treatment from a physical medicine and rehabilitation specialist for arm and leg pain, weakness,

and difficulty standing and maintaining balance. Ex. 12 at 23–24. He also saw a neurologist on

December 22, 2017, at which time he specifically reported onset of weakness on December 13th.

Ex. 3 at 11–12.

Based on exam and presentation, the neurologist opined Petitioner might be experiencing

GBS. Ex. 3 at 11–12. Petitioner subsequently went to the emergency room, where cerebrospinal

fluid testing produced results consistent with GBS. Ex. 4 at 104–09. He was then hospitalized,

receiving immunodeficiency treatments and later in-patient rehab. Petitioner’s diagnosis was

refined over time to be an axonal form of GBS, and he continued to experience sequelae from the

disease into 2019 and even later. Ex. 14-1 at 83; Ex. 13 at 16–19, 79–80; Ex. 12 at 35–36.

II. Expert Reports

A. Petitioner’s Expert – Lawrence Steinman, M.D.

Dr. Steinman, a neurologist, prepared two written reports for the Petitioner. Report, dated

July 26, 2022, filed as Ex. 28 (ECF No. 68-1) (“First Steinman Rep.”); Report, dated April 2, 2023,

filed as Ex. 29 (ECF No. 78-1) (“Second Steinman Rep.”).

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. 28

2

Ref. 3 (ECF No. 70-3) (“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.

The opinions expressed in Dr. Steinman’s two reports (especially his initial report) are

consistent in all material ways to what was offered—also by Dr. Steinman—in two prior cases I

decided, also involving the contention that the pneumococcal vaccine can cause GBS. See

Gamboa-Avila v. Sec'y of Health & Hum. Servs., No. 18-925V, 2023 WL 6536207, at *2-10 (Fed.

Cl. Spec. Mstr. Sept. 11, 2023), mot. for review den’d, 170 Fed. Cl. 441 (2024), appeal docketed,

No. 24-1765 (Fed. Cir. May 1, 2024); 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).

The similarity of Dr. Steinman’s opinions offered in this case with the opinions he offered

in Gamboa-Avila and Trollinger is unmistakable—in ways large and small. For example, in reports

filed in each of these cases, Dr. Steinman included a graphic from his seminal Scientific American

article about molecular mimicry (a graphic that he likely has included in every one of the hundreds

of reports filed in the Program). 3 More specific to the causation theory at issue, the reports filed

herein also include the previously-offered contentions that (a) phospholipids are found in the

antigenic components of the pneumococcal vaccine, (b) GBS patients can be shown to possess

antibodies to these antigens, (c) “polar head groups” on the myelin sheath covering nerves are

putative targets for the antibodies, and (d) the vaccine’s conjugate component (which is included

in the formulation almost wholly to increase its immunogenicity, rather than to engender immunity

per se to it) contains a mimic to Contactin-1, a protein also found in myelin. 4

In addition, all three report “collections” 5 contain virtually identical explanations for Dr.

Steinman’s “filtration” methodology for finding the degree of observed amino acid homology

evidentiarily significant, in defense of Dr. Whitton’s contentions that his showing of molecular

mimicry is not enough to render his theory preponderantly convincing. First Steinman Rep at 25–

3

Compare First Steinman Report at 9 to Dr. Steinman’s first report in Gamboa-Avila. (ECF No. 38-1). (I recognize

that the Gamboa-Avila filings are not evidence in this case, but cite to them solely to substantiate that the opinion Dr.

Steinman has previously offered is consistent with what he proposes herein).

4

Compare First Steinman Rep. at 9–19 with Gamboa-Avila ECF No. 38-1 at 10–20.

5

In this case, two reports authored by Dr. Steinman were filed – whereas in Gamboa-Avila and Trollinger, four reports

were prepared and filed. Gamboa-Avila, 2023 WL 6536207, at *2; Trollinger, 2023 WL 2521912, at *3.

3

29. And an informal comparison of literature cited in the reports from all three cases reveals that

more than 20 items identical to those he also offered in these two prior cases have been cited in

this case as well. 6

Because of the foregoing, I do not include a detailed summary of the opinions contained in

Dr. Steinman’s reports filed in this matter—as I have already repeatedly considered the same exact

theory. See, for example, Gamboa-Avila, 2023 WL 6536207, at *26–29; Trollinger, 2023 WL

2521912, at *27–30. As before, Dr. Steinman maintains that an autoimmune cross-reaction

stimulated by components of the pneumococcal vaccine was sufficient to cause the demyelination

characteristic of GBS. He specifically argues 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 19. Because of sequential/structural identity

in a chain of molecules making up that group and a chain found in components of the vaccine,

phospholipid structures in the nerve myelin are mistakenly attacked by the vaccine-generated

antibodies, leading to pathology. Id. And these antibodies, he maintains, are often found in the

context of GBS (although Dr. Steinman struggles to show they are primarily, initially, or in any

manner at all pathogenic of GBS, as opposed to being merely a measurable by-product of a disease

process that has a different primary cause). Dr. Steinman also argued that the vaccine’s CRM197

conjugate contains mimicking molecules for a different myelin protein, Contactin, and thus act as

a separate basis for the proposed cross-reaction (even though that conjugate is not included in the

vaccine with the goal of stimulating the production of antibodies, but instead merely improves the

vaccine’s immunogenicity). Id.

Admittedly, (and perhaps partially owing to the fact that his second report was prepared in

the spring of 2023—and hence reflects a slight evolution of his thinking on the theory presented

in this case, in comparison to earlier matters), Dr. Steinman has offered some “newer” (meaning

not previously referenced, as opposed to recently published) items of medical or scientific

literature in support of his arguments, refining a few of his arguments in the process. But none

appreciably aid the core theory offered.

For example, Dr. Steinman has cited some items of literature I have not previously

confronted to show that (contrary to Dr. Whitton’s contention that molecular mimics abound in

nature, but do not commonly result in autoimmune disease) in some cases experiments where

direct mimics were introduced into humans resulted in disease. See Second Steinman Rep. at 3; L.

Kappos et al., Induction of Non-Encephalitogenic Type 2 T Helper-Cell Autoimmune Response in

Multiple Sclerosis After Administration of Altered Peptide Ligand in a Placebo-Controlled,

Randomized Phase II Trial, 6 Nat. Med. 1176 (2000), filed as Ex. 29-1 (ECF No. 90-1)

(“Kappos”); B. Bielekova et al., Encephalitogenic Potential of the Myelin Basic Protein Peptide

6

Compare First Steinman Rep. at 32–34, with Gamboa-Avila, ECF No. 38-1 at 22–23.

4

(Amino Acids 83-99) in Multiple Sclerosis: Results of a Phase II Trial with an Altered Peptide

Ligand, 6 Nat. Med. 1167 (Oct. 2020), filed as Ex. 29-2 (ECF No. 90-2) (“Bielekova”).

But these items of literature are distinguishable, or only indirectly support the causal theory

Dr. Steinman champions. Kappos, for example, was focused on Multiple Sclerosis (“MS”)—a

central nervous system demyelinating disease that is largely distinguishable from GBS, even

though both involve demyelination 7—and specifically experimental efforts to positively regulate

the response to an autoimmune attack at the likely site of demyelination, which in turn involved

how certain immune cells react to myelin basic protein, a nerve myelin “building block.” Kappos

at 1176, 1177. Its authors directly immunized 142 patients who already were diagnosed with MS

with either placebos or varying amounts of an altered peptide ligand (“APL”) that was theorized

to induce an ameliorative cross-reaction that would reduce the likelihood of clinical relapses. Id.

at 1177. Because of concerns about observed adverse reactions to the experimental treatment, the

study was halted, but Kappos’s authors concluded based on data they initially collected that the

induced autoimmune response (which largely involved T cells—not B cell-production of

antibodies) might be a helpful treatment for MS. Id. at 1180. Thus, Kappos actually stands for the

proposition that mimicry might (more often than not) result in beneficial autoimmunity, rather than

the generalized and unsubstantiated dangers Dr. Steinman seeks to establish. And since it involved

individuals who were already suffering from MS, the impact of receipt of the APL directly is not

the same as the contention that a single vaccine might instigate disease through unplanned cross-

reactions attributable to molecular mimicry.

Bielekova was published in the same journal (even issue) as Kappos, and also deals with

experimental ways of introducing altered peptide ligands designed to cross-react, positively, with

MBP demyelination situses in the treatment of MS. Bielekova at 1167. It involved a smaller pool

of subjects than Kappos (24 patients), and it too resulted in discontinuation due to poor tolerance

of the treatment. Id. at 1167. This study’s results also either observed no improvements in disease

course, or (in a small subset of patients) worsening. Id. at 1172. Ultimately, Bielekova’s authors

concluded that while “target antigens” identified in other kinds of studies could have experimental

significance when applied to in vivo study efforts, “a better understanding of the complexities of

the pathogenesis of T-cell mediated autoimmune disease” was needed in attempting to design

ameliorative immunotherapies. Id. at 1173. As with Kappos, Dr. Steinman’s reference to

Bielekova seems aimed at underscoring that experimental and directed “immunization” can

produce cross-reactions specific to nerve myelin. But there is a wide gulf between the kind of

experimentally-targeted immunizations at issue in these studies, and the receipt of a vaccine

7

MS is a chronic condition, not acute and monophasic like GBS; it impacts the spine and brain, not peripheral nerves;

and to date only the Epstein-Barr Virus has been associated with its development, whereas other kinds of viral and

bacterial infections are associated with GBS. More significantly for present purposes, MS is generally thought to be

mediated by T cell attacks—not cross-reacting auto-antibodies produced by B cells, which any vaccine causation

theory would rely upon (since antibody production is an initial, prime goal of vaccination). Kappos at 1176.

5

(which is not designed at all to react in this way)—and it is glib to elide vaccination and

immunization in the way Dr. Steinman does.

Dr. Steinman also offers an older item of literature to rebut Dr. Whitton’s contention that

the size of the phosphoglycerol molecule is likely too small to prompt cross-reaction. Second

Steinman Rep. at 4; E. Barbar et al., Binding of Phenylphosphocholine-Carrier Conjugates to the

Combining Site of Antibodies Maintains a Conformation of the Hapten, 35 Biochem. 2958 (1996),

filed as Ex. 29-3 (ECF No. 90-3) (“Barbar”). Barbar (authored nearly 30 years ago, but without

demonstrated follow-up in the literature confirming its importance or even its findings) sought in

general to evaluate the role of the protein “carrier” that many vaccines feature, and what impact

the carrier will have on antibody production in response to the smaller, “hapten” 8 molecules

attached to the protein. Barbar at 2966. The pneumococcal vaccine at issue in this case includes a

protein carrier/conjugate, which is intended to assist the immune process even though the bacterial

polysaccharides conjugated to it are intended to be the primary antigenic components. Package

Insert: Prevnar-13 at 25, filed on October 6, 2022 as Ex. 28-10 (ECF No. 70-11).

But Barbar was not a study of the pneumococcal vaccine—or even any vaccine designed

to protect against S. Pneumoniae. Indeed, Barbar’s authors noted that “the choice of haptens was

made in order to evaluate the contribution of the carrier to binding, and its effect on hapten

conformation in the active site [of that same binding].” Barbar at 2958. Thus, although Dr.

Steinman is accurate in citing Barbar for the limited fact that it involves a phosphocholine

molecule, the study does not make it more or less likely that comparable components of the

pneumococcal vaccine produce a cross-reaction to demyelinating target sites on the nerve myelin.

In fact, were it the case that an article published nearly 30 years ago stood for the proposition that

antibody attacks on, or cross-reactions in association with, phosphoglycerol were possible despite

the molecule’s size, then it is a mystery why the association Dr. Steinman gleans (which suggests

an alternative cause for GBS) is not recognized more widely. Barbar thus offers limited additional

support for Petitioner’s causation theory.

Another set of previously-unfiled items of literature are invoked by Dr. Steinman as

“showing that phospholipids are targeted in GBS, including very early in the disease.” Second

Steinman Rep. at 6, 7-11; T. Al-Temeemi et al., Antiphospholipid Antibody in Serum of Guillain-

Barré Syndrome Patients, 10 Iraqi J. Med. Sci. 191 (2012), filed on May 9, 2024 as Ex. 29-4 (ECF

No. 90-4) (“Al-Temeemi”); J. Terryberry et al., Myelin- and Microbe-Specific Antibodies in

Guillain-Barré Syndrome, 9 J. Clin. Lab. Anal. 308 (1995), filed on May 9, 2024 as Ex. 29-6 (ECF

8

“Hapten” is defined as “a small molecule, not antigenic by itself, that can react with antibodies of appropriate

specificity and elicit the formation of such antibodies when conjugated to a larger antigenic molecule, usually a

protein, called in this context the carrier or schlepper. Antibody production involves activation of B lymphocytes by

the hapten and helper T lymphocytes by the carrier.” Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=21432&searchterm=hapten (last accessed July 12, 2024).

6

No. 90-6) (“Terryberry”). 9 This is a foundational element of Petitioner’s theory, necessary to

establish if the vaccine is to be found causal of disease (especially so, given the absence of evidence

that the bacterial infection the vaccine seeks to protect against—S. Pneumoniae—is not associated

with GBS). Whitton First Rep. at 18–20. As a result, such articles could well support causation in

ways Dr. Steinman’s theory fell short in Gamboa-Avila and Trollinger.

But they do not. Al-Temeemi, for example, is not particularly recent (raising the question

of why it was not previously offered—in this case or any of the other multiple parallel cases for

that matter). In it, a group of Iraqi researchers performed a case-control study involving a

particularly small sample size—eleven patients—to evaluate the presence of antiphospholipid

antibodies in the blood serum of GBS patients. Al-Temeemi at 191. Their focus on this group of

relevant antibodies stemmed from their determination that GBS was often comorbid in patients

also suffering from other known autoimmune diseases, like lupus, and therefore “[n]early any

neurological manifestation may occur in patients” who possess this particular antibody. Id. at 192.

Al-Temeemi’s authors wished to evaluate the titer levels of the antiphospholipid antibodies in the

subjects when compared to comparable healthy individuals, and at different times. Id.

Determinations about levels in comparison to timing amongst the sick subjects mostly

produced statistically-insignificant results, although Al-Temeemi’s authors did observe a negative

correlation between more recently-produced antibody levels and illness duration (consistent with

articles discussed in prior comparable cases). 10 But even though Al-Temeemi noted (and at a

statistically-significant level) higher antiphospholipid antibody levels in GBS patients in the initial

illness stage than healthy controls, they deemed this likely attributable to “a more extensive

immune reaction beyond the well known antiganglioside production, which has been related to

the demyelination of the peripheral nerves.” Al-Temeemi at 198 (emphasis added). In other words,

Al-Temeemi did not find the phospholipid-targeting antibodies were pathogenic in GBS. Indeed—

Al-Temeemi speculates the antiphospholipid antibodies may be protective (based on different

levels when evaluating severity of the GBS and the degree of treatment required in the studied

patients). Id. Thus, Al-Temeemi (and based on extremely limited data) only supports the existence

of this antibody in GBS patients, reaching no reliable conclusions about how it comes into

existence—or whether it plays any pathogenic role.

9

Petitioner also filed an article referencing the presence of lipid-related antibodies in a small study set of GBS patients.

See S. Mata et al., Anti-GM1, Anti-Central Myelin Proteins, and Anti-Cardiolipin Autoantibodies During Plasma-

Exchange in Guillain-Barré Syndrome (GBS), 13 J. Clin. Apheresis 155 (1998), filed as Ex. 29-5 (ECF No. 90-5)

(“Mata”). But Mata deals with measurement of a different kind of phospholipid antibody – cardiolipin—and deems

the antibody’s pathogenic role “less known” in comparison to anti-ganglioside antibodies. Mata at 155. Petitioner also

has filed only a two-page excerpt from Mata, making it impossible to evaluate its findings completely.

10

See Bielak v. Sec'y of Health & Hum. Servs., No. 18-761V, 2023 WL 35509, at *36 (Fed. Cl. Spec. Mstr. Jan. 3,

2023) (stating that the articles “actually suggest that the phospholipid antigenic targets on the myelin either serve a

protective, immune-modulating role, or at worst are damaged by an ongoing autoimmune process only after it has

begun—thus greatly undermining the contention that antibodies to these lipid myelin components initiate it”).

7

Terryberry (yet another fairly old item of literature) evaluated the blood sera of a larger

cohort (56 GBS patients), compared to controls that were healthy or suffered from other kinds of

conditions also involving demyelination, with a focus on levels of 18 antibodies believed to be

cross-reactive with myelin, including cardiolipin (a phospholipid antibody). Terryberry at 308–09.

Nearly half of the studied subjects possessed anti-cardiolipin antibodies. Id. at 311. Moreover,

many of the blood specimens tested positive for resolved S. pneumoniae infections—although this

cannot be extrapolated to constitute proof of a causal association, since there would be no way to

know when these prior infections occurred in association with GBS’s onset. Indeed, Terryberry’s

authors observed that “some patients had antibodies to as many as 15 infectious agents.” Id. at 310,

312 (Tables 3 and 4). The study concluded, among other things, that its results “illustrate the

difficulties in determining whether infection by a specific organism triggers the disease in

individual patients”—a difficulty that has not diminished in the more than 25 years since

Terryberry was published. Id. at 315.

Another “new” article was offered to bulwark Dr. Steinman’s contentions about the

potentiality of an autoimmune cross-reaction between the vaccine’s conjugate and Contactin,

which Dr. Steinman maintains “is targeted in some cases of GBS.” Second Steinman Rep. at 12;

J. Devaux et al., Nodal Proteins are Target Antigens in Guillain-Barré Syndrome, 17 J. Periph.

Nerv. Syst. 62 (2012), filed on May 9, 2024 as Ex. 29-7 (ECF No. 90-7) (“Devaux”). Devaux

sought to obtain more information about to the degree to which the “nodes of Ranvier”—gaps

along the otherwise-myelinated nerve axon—are targets of autoimmune attack in GBS, given that

more is known about ganglioside structure-directed autoantibody attacks in driving the disease.

Devaux at 62–63. It thus looked for evidence of autoantibodies against different proteins specific

to these nodes, such as neurofascin (which is comparable to Contactin). Id. at 63. Blood sera from

150 Japanese patients (50 of whom were suffering from chronic immune demyelinating

polyneuropathy, or “CIDP”—a distinguishable GBS variant) were tested on animal subjects, with

findings that (a) the nodes were in fact targets, and (b) neurofascin was a specific target, but (c)

anti-neurofascin antibodies were better associated with an axonal form of GBS (in which other

antibodies to gangliosides were detected, and more likely were driving the disease in a primary

manner), and (d) it could not be determined from the study “[t]he causes generating these

autoantibodies in GBS,” with no identified antecedent illnesses. Id. at 67–70.

Thus, Devaux (like many other studies offered in the effort to prove the pneumococcal

vaccine can cause GBS) sheds a dim light on another possible GBS-associated antibody in addition

to anti-ganglioside antibodies. But it gives no additional reason to find the pneumococcal vaccine

is likely causal of that antibody—let alone capable of producing it at the pathogenic levels

necessary to drive disease, and in the absence of an existing/ongoing disease process as well. And

the study’s focus was not on Contactin either, even if in a subset of patients’ antibodies to it were

observed. Second Steinman Rep. at 13. Once again, Dr. Steinman offers an item of literature that

8

only glancingly supports his theory, observing a plausible connection but not appreciably

supporting the conclusion that the identified GBS target is a likely disease driver.

Dr. Steinman’s efforts to elevate the argument that the pneumococcal vaccine conjugate

element might instigate production of autoimmune antibodies extended to other items of literature

not previously filed. For example, he referenced two articles to support the argument that Caspr211

is “an antigen targeted in GBS.” Second Steinman Rep. at 23; R. Rosch et al., Guillain-Barré

Syndrome Associated with CASPR2 Antibodies: Two Paediatric Cases, 19 J. Periph. Nerv. Syst.

246 (2014), filed on May 9, 2024 as Ex. 29-10 (ECF No. 90-10) (“Rosch”); X. Tan et al., Guillain-

Barré Like Syndrome: An Uncommon Feature of CASPR2 and LGI1 Autoimmunity, 269 J. Neurol.

5893 (2022), filed on May 9, 2024 as Ex. 29-11 (ECF No. 90-11) (“Tan”).

Once again, these items are far less helpful than supposed. Rosch is a case report discussing

two children (a two and six-year old) who developed GBS, both after different viral infections.

Rosch at 246–47. The children in each case tested positive for autoantibodies against a Contactin-

associated protein (which Dr. Steinman alleges could be the self mimic for the pneumococcal

vaccine’s conjugate), but not the more-expected ganglioside antibodies. Id. at 247. However (and

besides the fact that the subjects were children), neither had been vaccinated pre-onset. Rosch’s

authors ultimately noted that although the reports supported the theory that these specific

autoantibodies “might potentially contribute to peripheral nerve pathology in GBS,” existing

studies involving these kinds of autoantibodies “reported to date have not characteristically

involved demyelination.” Id. at 248. Thus, Rosch hardly stands for solid evidence of pathology—

and certainly does not support an association between the pneumococcal vaccine and the

production of anti-Contactin/Caspr2 antibodies.

Tan is a case report involving an adult who tested positive for the anti-Contactin antibodies

proposed by Dr. Steinman as potentially causal herein, and who experienced a “GBS-like”

syndrome (although the patient’s presentation was more typical of a different neurologic condition,

Morvan syndrome 12). Tan at 5893. Indeed, Tan noted the relevant autoantibodies were more

associated with Morvan syndrome. Id. at 5894. Tan otherwise listed a few other comparable case

reports (including Rosch). Id. at 5896–97. As with Rosch, Tan stressed the possibility that the

identified autoantibodies might play some causal role in GBS, but observed the need for further

11

CASPR2 is a “neuronal cell surface protein.” CASPR2 antibodies are “usually associated with peripheral nervous

system involvement.” Rosch at 246.

12

Morvan syndrome is a manifestation of syringomelia, “a slowly progressive syndrome of cavitation in the central

segments of the spinal cord, generally in the cervical region, but sometimes extending up into the medulla oblongata”

that “results in neurologic deficits, usually segmental muscular weakness and atrophy with a dissociated sensory loss.”

In Morvan Syndrome, “the subcutaneous tissues of the hands become thickened, edematous, soft, swollen, cyanotic”

along with “analgesic ulceration of the fingertips and paresthesia and atrophy of the hands and forearms.” Dorland’s

Medical Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=48639 and

https://www.dorlandsonline.com/dorland/definition?id=111022 (last accessed July 12, 2024).

9

study. Id. at 5899. Tan otherwise makes no mention of the propensity for any vaccine to trigger

production of anti-Contactin antibodies in levels sufficient to become pathologic. Thus, these two

articles are weak evidence that the identified antibodies more likely than not “can cause” GBS.

Only one of the not-previously-filed articles was actually published too recently to have

been offered in prior cases like Gamboa-Avila. See D. Erkan et al., Clinical Manifestations of

Antiphospholipid Syndrome, www.uptodate.com (Apr. 2024), filed on May 9, 2024 as Ex. 29-14

(ECF No. 90-14) (“Erkan”). Dr. Steinman referenced Erkan to justify his reliance on MS or other

central nervous system-specific diseases and the antibodies thought causal in those contexts.

Second Steinman Rep. at 28. But Erkan is an overview/review article discussing a distinguishable

autoimmune condition, “antiphospholipid syndrome,” which it defines as a “multisystem disorder

characterized by arterial, venous, or small vessel thromboembolic events, pregnancy morbidity,

and/or nonthrombotic events (e.g., thrombocytopenia) in the presence of persistent

antiphospholipid antibodies.” Erkan at 1. Thus, Erkan at the outset involves an illness wholly

unrelated to GBS, and it pertains to this case solely because anti-phospholipid antibodies are

theorized there as pathogenic in a distinguishable context. It bears not at all on the possibility that

this antibody could promote an inflammatory neurologic condition like GBS; indeed, Erkan admits

that those neurologic disorders suspected to be associated with the antibody (stroke, transient

ischemic attack, epilepsy, chorea, migraines, etc.) have never been persuasively so linked. Id. at 5,

11.

B. Respondent’s Experts

Respondent offered two written reports, 13 including a single report authored by Lindsay

Whitton, Ph.D.—an immunologist and Dr. Steinman’s counterpart in the Trollinger and Gamboa-

Avila cases. Report, dated November 30, 2022, filed as Ex. A (ECF No. 73-1) (“Whitton Rep.”).

Like Dr. Steinman’s showing, however, Dr. Whitton’s report filed in this case is almost wholly

consistent with what he offered in these prior matters. Gamboa-Avila, 2023 WL 6536207, at *10-

15; Trollinger, 2023 WL 2521912, at *13-18. I therefore do not include an extensive review or

summary of the opinions he has offered in this case.

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The second of Respondent’s reports was prepared by Dr. Thomas Leist. Report, dated November 8, 2022, filed as

Ex. C (ECF No. 74-1). However, Dr. Leist is primarily a neurologist, and while he possesses sufficient general

expertise to comment on proposed immunologic causes of GBS, I find his opinion to have overlapped Dr. Whitton’s

to a large degree, but without adding any details worthy of evaluation (and without Dr. Whitton’s demonstrated

specific competence in addressing questions of biochemistry and immunology). Accordingly (and also since I have

now repeatedly found the causal theory offered herein deficient solely on the basis of the arguments Dr. Whitton

raises), I do not include a discussion of Dr. Leist’s opinion.

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III. Procedural History

As noted, the Petition was filed approximately four years ago. Pet. at 1. Once most

documents deemed necessary to adjudicate the claim had been filed, the matter was activated out

of “pre-assignment review” in the spring of 2021 and initially assigned to the “special processing

unit,” since it facially involved the kind of claim often easily settled (GBS as an injury after receipt

of the flu vaccine). But after Respondent filed a Rule 4(c) Report in September 2021 contesting

Petitioner’s right to compensation (ECF No. 34), the claim was transferred to my own docket, and

I set a schedule for the filing of expert reports (while noting that the timeframe between the

Petitioner’s receipt of the flu vaccine and GBS onset was too attenuated to support a Table claim,

meaning the claim should be limited to causation associated with the pneumococcal vaccine).

Order, dated December 7, 2021 (ECF No. 64). Expert reports were filed through the summer of

2023, and then I set a deadline for briefing the claim. The matter has been ripe for resolution since

the filing of Petitioner’s reply in March of this year.

IV. Parties’ Briefs

Petitioner

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 48; Reply at 4.

Petitioner breaks down his causation theory into two parts: one involving the proposal

that 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 the second focusing on the conjugate. Mot. at 33, 43. With respect to the former,

Petitioner relies on studies that he contends show increased levels of anti-phospholipid

antibodies in the blood of GBS patients, though he posits that these studies do not determine the

role of the antibodies in the pathogenesis of GBS. B. Gilburd et al., Autoantibodies to

Phospholipids and Brain Extract in Patients with the Guillain-Barré Syndrome: Cross Reactivity

of Pathogenic?, 16 Autoimmunity 23 (1993), filed on October 6, 2022 as Ex. 28-11 (ECF No.

70-12) (“Gilburd”); G. Nakos et al., Anti-phospholipid Antibodies in Serum From Patients with

Guillain-Barré Syndrome, 31 Intensive Care Med. 1401 (2005), filed on October 6, 2022 as Ex.

28-12 (ECF No. 70-13) (“Nakos”). 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. Id. at 35–37, citing J. Chang et al., Relevance of O-acetyl Phospoglycerol

Groups for the Antigenicity of Streptococcus Pneumoniae Serotype 18C Capsular

Polysacchaaride, 30 Vaccine 7090 (2012), filed on October 6, 2022 as Ex. 28-13 (ECF No. 70-

14) (“Chang”) . Finally, he maintains that antibodies are generated in response to the

phosphoglycerol molecules in at least one of the vaccine’s 13 serotypes. Id. at 38–43. Thus, he

contends that via the widely-accepted biologic mechanism of molecular mimicry, these

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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 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. Id.

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 43–44. But this aspect of Dr. Steinman’s opinion does not possess

anywhere near the same degree of independent medical or scientific support suggesting any actual

evidence of the theorized cross-reactivity, 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 referenced

articles make no such affirmative finding, and the readings given them by Petitioner are somewhat

strained. Mot. at 47. One, 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. P. Haber et. al., Post-licensure Surveillance of 13-valent Pneumococcal Conjugate Vaccine

(PCV13) in Adults Aged P19 Years Old in the United States, Vaccine Adverse Event Reporting

System (VAERS), June 1, 2012–December 31, 2015, 34 Vaccine 6330 (2016), filed on October 6,

2022 as Ex. 28-32 (ECF No. 70-33). And another did not involve the relevant vaccine, and had

other limitations. Id. at 25.

Respondent

Respondent denies that the first Althen prong has been satisfied. Opp. at 14. 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 15–16. 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. And Petitioner

did not offer evidence associating the pneumococcal vaccine with GBS, while the existing

epidemiology undercuts an association. Id. at 16–18.

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

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

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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 21–22, citing Nakos, Gilburd.

Respondent further criticizes Dr. Steinman’s reliance on the Bryson study, noting that it does not

provide any connection between the immunogenicity of phosphoglycerol and the pathogenesis of

GBS. Id. at 22–23; S. 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 (2016), filed on October 6, 2022 as

Ex. 28-16 (ECF No. 70-17).

Respondent further criticized Dr. Steinman’s BLAST searches, which were specific to the

conjugate “side” of his theory, as not probative of causation. Opp. at 24. Not only did Dr. Steinman

not show that Contactin-1 is a likely GBS-instigating target, but he failed to acknowledge that

sequence homology occurs “frequently between human tissues and antigens without pathological

significance,” as explained by Dr. Whitton. Id. Further, he relied on case reports that were factually

distinguishable, since they involved GBS variants believed to be driven by different antibodies

and/or involving different antigenic targets. Id. at 23; Y. Miura et al., Contactin-1 IgG4 Associates

to Chronic Inflammatory Demyelinating Polyneuropathy with Sensory Ataxia, 138 Brain 1484

(2015), filed on October 6, 2022 as Ex. 28-20 (ECF No. 70-21).

Reply

In his short reply, Petitioner reiterates the Althen prong one arguments made above. Reply

at 3–4. He also attempts to refute Respondent’s remarks regarding Dr. Steinman’s bias towards

Petitioners devaluing his theories, listing cases in which “theories posited by Petitioner’s expert

withstood the appropriate scrutiny.” Id. at 2. He then responds to criticism of Dr. Steinman’s

BLAST search methods, noting that is only one portion of a multi-step research process. Id.

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). 14

14

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

13

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

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

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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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 Kalajdzic v. Sec’y of Health &

Hum. Servs., No. 2023-1321, 2024 WL 3064398, at *2 (Fed. Cir. June 20, 2024) (arguments “for

a less than preponderance standard” deemed “plainly inconsistent with our precedent” (citing

Moberly, 592 F.3d at 1322)); Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359

(Fed. Cir. 2019); 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 decades”), aff’d, 2024 WL

2873301 (Fed. Cir. June 7, 2024) (unpublished). 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

15

that the testimony of a treating physician is sacrosanct—that it must be accepted in its entirety and

cannot be rebutted”). As with expert testimony offered to establish a theory of causation, the

opinions or diagnoses of treating physicians are only as trustworthy as the reasonableness of their

suppositions or bases. The views of treating physicians should be weighed against other, contrary

evidence also present in the record—including conflicting opinions among such individuals.

Hibbard v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 742, 749 (2011) (not arbitrary or capricious

for special master to weigh competing treating physicians’ conclusions against each other), aff’d,

698 F.3d 1355 (Fed. Cir. 2012); Veryzer v. Sec’y of Dept. of Health & Hum. Servs., No. 06-522V,

2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review denied, 100 Fed.

Cl. 344, 356 (2011), aff’d without opinion, 475 F. Appx. 765 (Fed. Cir. 2012).

The third Althen prong requires establishing a “proximate temporal relationship” between

the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the

phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant

proof that the onset of symptoms occurred within a timeframe which, given the medical

understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan

v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what

is a medically acceptable timeframe must align with the theory of how the relevant vaccine can

cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of Health & Hum.

Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after remand, 105 Fed. Cl. 353 (2012), aff’d

mem., 503 F. Appx. 952 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V,

2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for review denied, (Fed. Cl. Dec. 3,

2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

B. 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).

16

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

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).

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C. 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”).

D. Standards for Ruling on the Record

I am resolving Petitioner’s claim on the filed record. 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 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 have now ruled on four prior occasions that it is preponderantly unlikely that the

pneumococcal vaccine “can cause” GBS. See, e.g., Gamboa-Avila, 2023 WL 6536207, at *24;

Trollinger, 2023 WL 2521912, at *25; Bielak v. Sec'y of Health & Hum. Servs., No. 18-761V,

2022 WL 18058244, at *34 (Fed. Cl. Spec. Mstr. Dec. 9, 2022); Deshler v. Sec'y of Health & Hum.

Servs., No. 16-1070V, 2020 WL 4593162, at *19 (Fed. Cl. Spec. Mstr. July 1, 2020). In each

instance, I conducted a detailed review of the medical/scientific support offered for the proposed

causation theory—and as noted above, in two of these prior cases Dr. Steinman offered an opinion

18

favoring causation (also opposed, as here, by Dr. Whitton). Gamboa-Avila, 2023 WL 6536207, at

*26–29; Trollinger, 2023 WL 2521912, at *27–30. 15

As already observed, the causation theory that was at issue in these earlier-decided matters

is virtually the same as what has been proposed in this case. In Bielak 16 and Trollinger, petitioners

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; P. Ho et al., Identification of Naturally Occurring Fatty Acids of

the Myelin Sheath That Resolve Neuroinflammation, 4 Sci. Translational Med. 1 (2012), filed on

October 6, 2022 as Ex. 28-7 (ECF No. 70-7).

My determination in Deshler, 2020 WL 4593162, also bears on the outcome herein. 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 that 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. 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.

Most recently, I again denied entitlement in Gamboa-Avila. This time (and based on the

wishes of the parties), I held an oral argument, to provide counsel the chance to articulate verbally

how and why that claimant had met the relevant evidentiary standard. Gamboa-Avila, 2023 WL

6536207, at *18. In turn, this permitted me the opportunity to address questions I had about the

preponderant legal standard as applicable in a causation case—questions that went to the heart of

the adequacy of the petitioner’s evidentiary showing. Id. I again found the causation theory

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At the same time, Dr. Steinman has also been the expert in virtually every case decided by a different special master

involving the same theory. See, e.g., Sprenger v. Sec'y of Health & Hum. Servs., No. 18-279V, 2023 WL 8543435

(Fed. Cl. Spec. Mstr. Nov. 14, 2023); 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).

16

Although the Bielak petitioner did not utilize Dr. Steinman, his expert borrowed the literature that Dr. Steinman

offered in Trollinger and Gamboa-Avila. Bielak, 2022 WL 18058244, at *8–9.

19

deficient, however. Id. at *29. I also observed that the petitioner’s legal arguments leaned heavily

on the concept that weighing the petitioner’s showing against Respondent’s, but finding the

evidence did not preponderate in petitioner’s favor, was in effect a heightening of the legal

standard—an argument that would, if accepted, seem to require special masters to find for

petitioners in any case involving molecular mimicry and some showing of homology (in the

absence of evidence that the literature offered to support the theory was suspect, or the homology

showing otherwise in error). I rejected that contention as legally erroneous. Id. at 29–31. 17

Ultimately (and as I have now explained several times in prior decisions), the theory that

the pneumococcal vaccine “can cause” GBS seeks to demonstrate a link between indirectly-present

components 18 of the vaccine and molecules found in myelin structures (in this case, lipids), but

without additional sufficient evidence persuasively establishing likely pathogenicity, and with an

over-reliance on either a showing of possible molecular homology or the presence of antibodies

theorized to be produced by the vaccine (but certainly not intended to) in some limited studies

involving GBS patients. In so arguing, claimants seek application of the flu vaccine-GBS

association “template” in a context in which it does not work. To accept it would be to find

causation mostly because a claimant’s GBS post-dated vaccination, reverse-engineering causation

from the temporal association plus some molecular similarities, but without compelling evidence

that a pathogenic reaction is likely.

Because of the foregoing, my skepticism about the viability of the causation theory

presented in this case does not reflect personal bias, but is the product of my actual experience

considering near-identical theories. 19 Admittedly, I am not bound to reach the same conclusion

here despite my decisions in parallel matters. A new “twist” on the proposed theory, coupled with

more recent studies or scientific findings, a different expert’s thinking on the topic, or even

different facts about the claimant’s medical history, might justify reconsideration of a theory I have

rejected many times before. But it is otherwise appropriate for me to rely on my learned experience

as a special master adjudicating comparable cases, and to apply that experience in resolving

comparable subsequent matters. Doe v. Sec'y of Health & Hum. Servs., 76 Fed. Cl. 328, 338–39

17

I acknowledge that Gamboa-Avila is currently on appeal at the Federal Circuit, and there is thus a chance my

reasoning will be rejected. However, having considered the theory so many times, and having had it challenged twice

at the Court, it is fair to rely on my prior determinations as likely holding, and hence not to await a Circuit ruling

before dismissal of this claim.

18

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.

19

I am not treating my prior determinations akin to a system of precedential “claim preclusion,” whereby earlier

determinations control the outcome in all similar cases to come. My earlier decisions do not have such legal preclusive

force. But to take note of my familiarity with the relevant theory, and to require a claimant to establish how the theory

before me differs in substance from what I have previously—and exhaustively—considered, is not the same a pre-

deciding a subsequent case.

20

(2007) (“[o]ne reason that proceedings are more expeditious in the hands of special masters is that

the special masters have the expertise and experience to know the type of information that is most

probative of a claim”) (emphasis added). It would be a dereliction of my duty to plug my ears,

pretend such prior decisions were never issued, and “reinvent the wheel” in evaluating this claim.

The Program does not demand that special masters start over, so to speak, each time a new case is

filed, and ignore what they have already learned about an oft-repeated theory of vaccine injury

causation.

Was anything offered in this case different than the evidence put forth in the prior matters?

Recent Federal Circuit precedent suggests that even when taking into account experience resolving

prior relevant cases, special masters should still ensure that their determinations are ultimately

based on the evidence before them in the relevant case. See Kalajdzic, 2024 WL 3064398, at *3.

As a result, I have carefully reviewed the new versions of Dr. Steinman’s reports filed

herein, looking for any arguments that addressed the kinds of prior concerns I had voiced in

Gamboa-Avila or Trollinger about the theory’s deficiencies. I also scrutinized items of literature

not previously offered in the comparable earlier cases—and I included my review of many of those

items in my otherwise-abbreviated summary of Dr. Steinman’s reports above.

Having performed this exercise, I do not find that the new versions of Dr. Steinman’s

reports advance Petitioner’s contentions better than what I have considered before. The reports

cite no recently-published scientific studies or reports more directly linking the pneumococcal

vaccine to GBS, let alone the vaccine’s wild infectious counterpart. They also do not persuasively

expand on Dr. Steinman’s contentions about phospholipid targets for GBS-driving antibodies

created in reaction to the pneumococcal vaccine. And any items of literature not previously offered

in cases I have decided do not demonstrably increase the likelihood Petitioner is correct.

For example, Al-Temeemi and Terryberry do not persuasively support the conclusion that

GBS is likely driven by phospholipid-instigated, autoantibody attacks on antigenic nerve structure

targets previously-unknown to the medical scientists who specifically study peripheral

neuropathies, but which Dr. Steinman has somehow (and tellingly, solely in conjunction with his

expert efforts in this case—not as a result of his own personal research in the field) uncovered.

Others, like Rosch and Tan, are mere case reports unworthy of significant weight in determining

causality as a general matter. Pearson v. Sec’y of Health & Human Servs., No. 17-489V, 2019 WL

1150044, at *11 (Fed. Cl. Spec. Mstr. Feb. 7, 2019) (concluding that case reports receive only

limited evidentiary weight and cannot cure Althen prong one deficiencies); see also Harris v. Sec’y

of Health & Human Servs., No. 10-322V, 2014 WL 3159377, at *18 (Fed. Cl. Spec. Mstr. June

10, 2014) (noting that “case reports are generally not a valuable form of evidence”)). And these

reports at best only link anti-Contactin antibodies to GBS, while saying nothing about GBS

occurring in the context of pneumococcal vaccine administration (let alone the wild bacterial

21

infection). I also (again) note that recent studies specific to MS and the Epstein-Barr Virus—which

Dr. Steinman has in many prior cases cited to bulwark his general contentions about the pathologic

character of molecular mimicry—are not otherwise relevant to a case involving a different vaccine

and a different injury. Nothing recently published and offered in this case would render the

proposed association between the pneumococcal vaccine and GBS more likely.

Thus, the expert reports filed in this case, along with their scientific and medical references,

do not establish grounds for taking a fifth look at my prior, comprehensive determinations that the

pneumococcal vaccine cannot likely cause GBS. It still has not been credibly established that anti-

phospholipid or phosphoglycerol antibodies antibodies likely drive GBS—the lynchpin to a

determination that the vaccine could spark it in the first place, by causing the pathogenic antibodies

to come into existence. All Dr. Steinman has done is establish the existence of some biochemical

similarities between molecular components of the vaccine’s antigens and nerve components. This

cannot be enough to preponderantly show causation (and if it is, then all special masters may as

well conclude that all covered vaccines can cause GBS equally, since a showing of molecular

mimicry would never fail to establish homology, given how common it is in nature). And

arguments about cross-reactivity between the conjugate in the vaccine and nerve components has

been reasonably addressed, but rejected, in other prior cases like Deshler; at most, Dr. Steinman

merely identifies a possible homologous mimic, but does not establish causation would likely flow

from this showing. Deshler, 2020 WL 4593162, at *20.

I also repeat what I have noted previously about my rejection of contrary determinations from

other special masters who have found that the pneumococcal vaccine can cause GBS. Gamboa-

Avila, 2023 WL 6536207, at *25; 20 compare Cooper v. Sec'y of Health & Hum. Servs., No. 18-

1885V, 2024 WL 1522331 (Fed. Cl. Spec. Mstr. Mar. 12, 2024); Gross v. Sec'y of Health & Hum.

Servs., No. 17-1075V, 2022 WL 9669651 (Fed. Cl. Spec. Mstr. Sept. 22, 2022); Maloney v. Sec'y

20

One more recent such ruling underscored the overlap between my findings on the science and the contrary cases –

perhaps with the intent of emphasizing how little actually separates my findings on this subject from my colleagues’

determinations. See Cooper v. Sec'y of Health & Hum. Servs., No. 18-1885V, 2024 WL 1522331, at *16 (Fed. Cl.

Spec. Mstr. Mar. 12, 2024) (“even when reaching a different result, there has still been agreement that record evidence

comparable to what has been presented in this case” establishes that “phyosphoglycerol is found in the pneumococcal

vaccine; that the immune system produces antibodies in reaction to the relevant antigens containing the

phosphoglycerol; and that individuals with neuropathies (although some suffer from the distinguishable disease MS)

have been shown in small sample studies to possess antibodies specific to myelin-containing phospholipids” (quoting

Trollinger, 2023 WL 2521912, at *28)).

In fact, the varying outcomes in these cases more likely results from differences of opinion about proper application

of the Althen prong one evidentiary standard. In effect, some special masters deem a merely plausible argument about

mimicry – and one that does apply to the flu vaccine and GBS - enough to put “evidence on the scale” in a petitioner’s

favor, ending the analysis. They seem to consider any counter-weighing of Respondent’s arguments (for why

molecular mimicry cannot always persuasively explain every demyelinating post-vaccination injury, or why the

impact of the pneumococcal vaccine cannot be deemed identical to the flu vaccine) to amount to an unfair heightening

of the preponderant evidentiary standard. I, by contrast, view the evidence they call persuasive as inadequate – and its

acceptance to be an exercise in lowering the preponderant standard.

22

of Health & Hum. Servs., No. 19-1713V, 2022 WL 1074087 (Fed. Cl. Spec. Mstr. Mar. 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).

I am of course not bound by these determinations—any more than the special masters who

decided these claims were beholden to my analysis. But I otherwise do not find the legal reasoning

expressed in those decisions to be persuasive. Rather, those decisions simply adopt the framework

for the existing flu vaccine-GBS association, but without convincingly explaining why

Respondent’s counter-arguments merit less weight. I have also observed that these reasoned

decisions cite the same items of literature that I have determined (after very close analysis) are not

especially reliable or persuasive. See, e.g., Bielak, 2022 WL 18058244, at *15–17, 32. Although

future research or studies may better substantiate the alleged association between the

pneumococcal vaccine and GBS, existing science on the subject is simply not favorable to the

theory. To hold otherwise is to treat GBS as a “universal” vaccine injury, associated with virtually

every covered vaccine, so long as the claimant has offered an expert opinion comparable to what

Dr. Steinman has fashioned for this case.

CONCLUSION

Claimants must carry their burden of proof. Here, Petitioner had the burden of

preponderantly establishing that the pneumococcal vaccine can 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. 21

IT IS SO ORDERED.

/s/ Brian H. Corcoran

Brian H. Corcoran

Chief Special Master

21

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.

23