VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_22-vv-00335
Package ID: USCOURTS-cofc-1_22-vv-00335
Petitioner: Charles Taylor
Filed: 2022-03-28
Decided: 2025-07-08
Vaccine: influenza
Vaccination date: 2020-10-05
Condition: Guillain-Barré syndrome (GBS)
Outcome: compensated
Award amount USD: 130000

AI-assisted case summary:
Charles Taylor, an adult, received an influenza vaccine on October 5, 2020. Within days, he began experiencing symptoms including fatigue, headaches, tingling in his hands and feet, and generalized weakness. He was hospitalized and diagnosed with Guillain-Barré syndrome (GBS), an autoimmune disorder affecting the peripheral nervous system. The court found that his case met the criteria for a Table claim, meaning the vaccine is presumed to have caused the GBS. The respondent argued that a cytomegalovirus (CMV) infection was the sole substantial cause, but the court found insufficient evidence to support this claim, concluding that the vaccine was a substantial factor in causing the GBS. The court awarded Mr. Taylor $130,000 for actual pain and suffering, acknowledging the severity and duration of his GBS symptoms, which included a five-day hospitalization, a course of IVIg treatment, and residual weakness and numbness for approximately six months post-vaccination.

Theory of causation field:
Influenza vaccine on October 5, 2020, adult age stated in DB as 35, followed within days by fatigue, headache, tingling, weakness, hospitalization, and Guillain-Barre syndrome. COMPENSATED as a Table GBS case. Respondent argued cytomegalovirus infection was a factor unrelated/sole substantial cause, but Chief Special Master Corcoran found the record did not prove CMV displaced vaccine causation. Damages decision filed July 8, 2025 awarded $130,000 for pain and suffering. No unreimbursable expenses were included in the staged damages summary.

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_22-vv-00335-0
Date issued/filed: 2025-04-28
Pages: 31
Docket text: PUBLIC ORDER/RULING (Originally filed: 03/25/2025) regarding 56 Ruling on Entitlement. Signed by Chief Special Master Brian H. Corcoran. (mva) Service on parties made.
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Case 1:22-vv-00335-UNJ Document 62 Filed 04/28/25 Page 1 of 31
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 22-335V
* * * * * * * * * * * * * * * * * * * * * * * * * Chief Special Master Corcoran
*
CHARLES TAYLOR, *
* Filed: March 25, 2025
Petitioner, *
*
v. *
*
SECRETARY OF HEALTH AND *
HUMAN SERVICES, *
*
Respondent. *
*
* * * * * * * * * * * * * * * * * * * * * * * * *
Elizabeth K. Abramson, mctlaw, Washington, DC, for Petitioner.
Nina Y. Ren, U.S. Department of Justice, Washington, DC, for Respondent.
RULING ON ENTITLEMENT1
On March 28, 2022, Charles Taylor filed a petition for compensation under the National
Vaccine Injury Compensation Program (the “Vaccine Program”).2 See Petition (ECF No. 1).
Petitioner alleges that an influenza (“flu”) vaccine administered to him on October 5, 2020, caused
him to experience Guillain-Barré syndrome (“GBS”). Id.
The elements of a Table flu vaccine-GBS claim are met by the records filed in this matter.
But because Respondent has argued that evidence supported an alternative cause for Petitioner’s
injury, I proposed that the parties brief whether Respondent could carry his shifted burden of proof.
See Petitioner’s Motion, dated Aug. 9, 2024 (ECF No. 50-1) (“Mot.”); Respondent’s Opposition,
1 "Under Vaccine Rule 18(b), each party has fourteen (14) days within which to request redaction “of any information
furnished by that party: (1) that is a trade secret or commercial or financial in substance and is privileged or
confidential; or (2) that includes medical files or similar files, the disclosure of which would constitute a clearly
unwarranted invasion of privacy.” Vaccine Rule 18(b). Otherwise, the whole Ruling will be available to the public in
its present form. Id."
2 The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,
100 Stat. 3758, codified as amended at 42 U.S.C. §§ 300aa-10 through 34 (2012) [hereinafter “Vaccine Act” or “the
Act”]. Individual section references hereafter will be to § 300aa of the Act (but will omit that statutory prefix).

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dated Sep. 9, 2024 (ECF No. 53) (“Opp.”); Petitioner’s Reply, dated Sep. 16, 2024 (ECF No. 54)
(“Reply”).
Now, having reviewed the above plus the filed medical records, expert reports, and
associated literature, I hereby find that Respondent has not preponderantly demonstrated that a
“factor unrelated” – namely a cytomegalovirus (“CMV”) infection3 – was the more likely, and
sole, explanation for Petitioner’s GBS. Accordingly, entitlement is established.
I. Factual Background
Mr. Taylor has a pre-vaccination history of migraine headaches, and had experienced
several tick bites in 2019 and 2020 requiring prophylactic treatment with Doxycycline. Ex. 2 at
49, 51-54, 57-60.4 He received the flu vaccine in question on October 5, 2020, in New York City.
Ex. 1 at 1. There is no record evidence of any immediate reaction or symptoms close-in-time to
vaccination.
A week later (October 12th), Petitioner sought treatment for reported left shoulder pain,
which he said had started after working on his cabin. Ex. 5 at 5-10. Exam revealed no acute injuries
or abnormalities, and no neurological deficits were observed on physical examination. Id. at 9.
Also, no reference to the vaccination was made (or to any neurologic-like symptoms later
reported). Petitioner was diagnosed with left shoulder tendonitis and discharged after receiving a
Toradol (nonsteroidal) injection. Id. at 10.
Ten days after vaccination (October 15, 2020), Petitioner took himself to the Columbia
University Student Health Center complaining of fatigue, headaches, tingling in his hands and feet,
and generalized weakness, beginning five days before (meaning October 10th). Ex. 2 at 43. He also
confirmed a history of tick bites, along with the fact that he had been experiencing headaches
(distinguishable from migraines) for up to two weeks (which would predate vaccination). Id. at
43-44. Blood testing performed that day yielded unremarkable results, except for slightly elevated
liver function tests (“LFTs”) (AST: 48 IU/L and ALT: 61 IU/L). Id. at 41, 84. And another
neurologic test resulted in normal findings. Id. at 44-45. Petitioner was assessed with “unspecified
disturbances of skin sensation.” Id. at 45.
Then, on the evening of October 16th, Petitioner went to an emergency room, again
reporting left shoulder pain (which he associated with heavy chores and lifting his daughter) and
limited range of motion, with an initial exam confirming his complaints (but identifying no
neurologic concerns). Ex. 3 at 7-8. He was assessed with a probable rotator cuff injury and received
3 CMV is a common, incurable virus that is part of the herpes family, and can linger in the body even after the
infection’s resolution. Clinical Overview of CMV and Congenital CMV, Center for Disease Control,
https://www.cdc.gov/cytomegalovirus/hcp/clinical-overview/index.html (last visited Feb. 6, 2025).
4 Although Petitioner reported on several occasions to treaters that he had experienced the tick bites (perhaps in the
belief they could have played some role in his subsequent injury), the parties seem to concur that such bites do not
likely explain his GBS, and I therefore do not include discussion of them as potentially causal in this Decision.
2

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a steroid injection prior to his discharge. Id. at 8, 18. Petitioner’s shoulder concerns persisted (to
the point where he felt unable to move his arm), however, and the next day (October 17th) he
returned to the Student Health Center for additional treatment. Ex. 2 at 35-36. Petitioner was
advised to seek orthopedic assistance and was urged to otherwise continue with self-help
treatments, supplemented by some pain-oriented prescriptions. Id. at 36.
Petitioner thereafter continued to experience shoulder pain-related issues, but also began
expressing concerns about other symptoms that could be considered more neurologic in character.
For example, on October 19, 2020, Petitioner contacted treaters about his previously-reported hand
and feet paresthesia, plus worsening weakness, and questioned whether a neurologic consult was
needed in addition to further orthopedic evaluations. Ex. 2 at 27, 30. He also reported difficulty
walking up stairs and getting out of bed, and trouble with temperature regulation, leading him to
question whether his condition had a neurologic explanation. Id. at 33 (Petitioner informing treater
by email that “this sounds like peripheral neuropathy”).
Petitioner took himself to New York Presbyterian Hospital’s emergency department on
October 21, 2020, complaining of pain and weakness in his arms and neck, plus tingling in his
hands and feet, and leg weakness that inhibited his movement. Ex. 4 at 35. Petitioner was admitted
to the hospital for further evaluation, including a neurology consult, and additional testing was
ordered. Id. In the process of his intake, Petitioner fell down and remained prone until he was
found by treaters, leading the hospital to take extra precautions with him going forward. Id. at 38.
After admission, Petitioner underwent an initial neurology consultation with Dr.
Christoforos Koumas. Ex. 4 at 69-72. Dr. Koumas’s assessment noted Petitioner’s recent history
of numbness and hand/foot tingling plus weakness, adding that (in addition to the previously-
treated left shoulder pain) Petitioner had also begun to experience comparable right shoulder pain
the day before admission (making him wonder if numbness was ascending). Id. at 69. And Dr.
Koumas recorded Petitioner’s complaints of generalized weakness and ambulation impacts, as
well as the fact that Petitioner denied other symptoms or infections beyond “several tick bites this
year.” Id.
Petitioner’s neurologic exam while hospitalized now confirmed diminished strength and
reflexes, plus gait abnormalities. Ex. 4 at 70-71. The initial diagnostic differential included
peripheral neuropathy, radiculoneuropathy, or cervical cord pathology, although more workup was
deemed necessary before a particular etiology could be embraced. Id. at 72.
Petitioner underwent a more comprehensive neurologic evaluation on October 22, 2020,
when two neurologists (other than Dr. Koumas) saw him. Ex. 4 at 38-45. In setting down the
medical history, some additional details were added, such as (a) progression of Petitioner’s
paresthesia from fingertips and toes upward, (b) temperature regulation difficulties, and (c) fatigue
that not only limited Petitioner’s exercise ability but made it hard to engage in mundane activities
of daily living. Id. at 39. But it was also stated that he had previously experienced episodes of
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“incapacitating back pain” that would cause him to require a day of complete rest before
resumption of activities, and Petitioner’s spouse speculated that his current presentation was
qualitatively similar. Id. The neurologic treaters further noted that Petitioner denied any pre-onset
illness or infections (including ones he might have been exposed to via his infant daughter), and
that he had received the flu vaccine earlier that month (plus the aforementioned tick bites that same
year). Id. at 40.
Thereafter, treaters expressed greater confidence in a GBS diagnosis, which was supported
by additional testing evidence. Additional neurologic exams continued to reveal Petitioner’s
weakness, diminished reflexes, and other comparable symptoms consistent with his presentation
and primary complaints. Ex. 4 at 42. A lumbar puncture and cerebral spinal fluid (“CSF”) analysis
(performed on October 22, 2020), revealed elevated proteins consistent with GBS (and did not
identify possible pathogenic explanations). Id. at 45, 76, 128–29. An electromyogram and nerve
conduction study were also consistent with GBS (although not specific for it, as the results did not
demonstrate the presence of demyelination). Id. at 28, 49. Treaters proposed Petitioner receive a
course of intravenous immunoglobulin (“IVIg”)5 and neuropathic pain medications – treatments
common in the setting of GBS. Id. at 38, 158.
At the same time, however, one set of testing revealed results relevant to the dispute herein
regarding a potential etiology for Petitioner’s GBS. Testing performed on Petitioner around
October 21, 2020, revealed the presence of a recent, active CMV infection. Ex. 4 at 49 (“CMV
quantitative PCR from blood returned at 990, serum IgG and IgM6 were also positive”), 126. A
“curbside”7 infectious disease consult was performed on October 23, 2020, to discuss the test
results. The infectious disease team opined that the positive results were more likely reflective of
a latent CMV reactivation infection, secondary to Petitioner’s GBS, than evidence of an active
infection, and treatment was not deemed necessary in the context of ameliorating Petitioner’s
5 “Intravenous Immunoglobulin (IVIG)” is defined as “[a] therap[y] prepared from a pool of immunoglobulins
(antibodies) from the plasma of thousands of healthy donors. Immunoglobulins are made by the immune system of
healthy people for the purpose of fighting infections…IVIG/SCIG work in different ways to prevent the body from
attacking itself and to decrease several types of inflammation in the body.” IVIG,
https://rheumatology.org/patients/intravenous-immunoglobulin-ivig (last visited Mar. 24, 2025).
6 IgG and IgM are types of immunoglobulins, which are also referred to as antibodies. Antibodies are proteins that the
immune system makes to fight germs. IgG antibodies, which are present in all body fluids, are very important for
fighting bacteria and viruses. The body keeps a "blueprint" of all the IgG antibodies that have been created - so if a
person is exposed to the same germs again, the immune system can quickly make more antibodies. IgM antibodies,
which are found in the blood and lymph fluid, are the first antibodies the body makes after it is exposed to germs.
They provide short-term protection while the body makes other antibodies. “Immunoglobulins Blood Test,” Medline
Plus, https://medlineplus.gov/lab-tests/immunoglobulins-blood-test/ (last visited Mar. 6, 2025).
7 According to Dr. Collins, a curbside consultation involves “a casual request for information in which the consulting
service does not review the chart or examine the patient” but “[i]nstead. . . are given a very brief summary of a
particular question the team has.” First Collins Rep. at 4.
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immediate symptoms. Id. at 49 (CMV infection “[u]nlikely to be contributory to the current
picture”), 93.
After receiving a three-day course of IVIg, Petitioner was discharged on October 25, 2020,
with a diagnosis of GBS “likely in the setting of recent flu vaccine.” Ex. 4 at 47, 49. He continued
to experience common post-treatment GBS sequelae thereafter. Ex. 2 at 19. However, Petitioner
made slow progress in recovering. Id. at 15. By February 2021, he was still experiencing some
range of motion limitations plus weakness and numbness, and was advised to expect symptoms to
linger for six months or so from onset (meaning through spring 2021). Ex. 2 at 11-12. By April
2021, Petitioner felt he was “about 70% back to baseline.” Ex. 4 at 12. He continued to bear the
diagnosis of GBS, AIDP (acute inflammatory demyelinating polyneuropathy) variant. Id.at 25.
II. Expert Reports8
A. Respondent’s Expert – Kathleen L. Collins, M.D., Ph.D.
Dr. Collins, an infectious disease specialist and medical school professor, offered two
written reports in this case for Respondent. Report, dated July 1, 2023, filed as Ex. A (ECF No.
34-1) (“First Collins Rep.”); Report, dated Apr. 23, 2024, filed as Ex. C (ECF No. 43-1) (“Second
Collins Rep.”).
Dr. Collins is a Professor of Internal Medicine and Microbiology and Immunology at the
University of Michigan Medical School. CV, dated July 12, 2023, filed as Ex. B (ECF No. 34-21)
(“Collins CV”). She received her medical degree and her Ph.D. from Johns Hopkins University
School of Medicine. Collins CV at 1. She completed a residency in internal medicine at Brigham
and Women’s Hospital in Boston, MA, and a fellowship in infectious diseases at various hospitals
in the Boston area. Id. She also completed a research fellowship at Harvard University and a
postdoctoral fellowship in immunology at Massachusetts Institute of Technology. Id. Dr. Collins
is board certified in infectious disease. First Collins Rep. at 1. Her clinical practice at University
of Michigan has focused on inpatients with complicated infectious disease problems. Id. Dr.
Collins also runs a research laboratory that studies molecular mechanisms of HIV persistence, and
she has published over 70 papers. Id.
First Report
After summarizing her own credentials and Petitioner’s medical history, Dr. Collins
provided her core opinion: that a CMV infection was more likely the cause of Petitioner’s GBS
than the flu vaccine. First Collins Rep. at 1-5. She began with an overview of GBS’s known causes
– highlighting the extent to which a variety of infections are deemed likely etiologic explanations.
For example, a C. jejuni bacterial infection is a well-accepted GBS cause; the excess risk of GBS
following this infection is 60-fold, and 20% of all GBS cases are attributable to this pathogen. Id.
8 Because this matter turns on Respondent’s success in carrying the “factor unrelated” burden, I begin my analysis
with a summary of the opinion offered by Respondent’s expert.
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at 5; C. Tam et al., Guillain-Barre Syndrome and Preceding Infection with Campylobacter,
Influenza and Epstein-Barr Virus in the General Practice Research Database, 2 PLOS One 1, 1
(2007), filed as Ex. A-3 (ECF No. 34-4). The risk of developing GBS following a C. jejuni
infection is much higher than the background rate for individuals not so infected. First Collins
Rep. at 5; N. Yuki, Infectious Origins of, and Molecular Mimicry in, Guillain-Barre and Fisher
Syndromes, 1 The Lancet 29, 31 (2001), filed as Ex. A-4 (ECF No. 34-5) (“Yuki”).
The same, evidentiarily-supported association exists for a CMV infection, and Dr. Collins
provided a number of evidentiary bases for this aspect of her opinion. See generally First Collins
Rep. at 5-6. A meaningful number of patients with GBS (up to a fifth) have been seen to possess
IgM antibodies to CMV, establishing evidence of a recent infection – and the incidence of GBS
after such a primary infection is comparable to the risk from a C. jejuni infection (compared to the
background rate for the general population). See J.B. Winer et al., A Prospective Study of Acute
Idiopathic Neuropathy, 51 J. of Neurol., Neurosurg. and Psych. 613, 616 (1998), filed as Ex. A-5
(ECF No. 34-6) (“Winer”); B.C. Jacobs et al., The Spectrum of Antecedent Infections in Guillain-
Barre Syndrome, 51 Neurology 1110, 1113-14 (1998), filed as Ex. A-6 (ECF No. 34-7) (“Jacobs”);
D. Orlikowski et al., Guillain-Barre Syndrome following Primary Cytomegalovirus Infection: A
Prospective Cohort Study, 52 Clin. Infect. Diseases 837, 842 (2011), filed as Ex. A-8 (ECF No.
34-9) (“Orlikowski”).
In describing the risk of GBS attributable to a CMV infection, Dr. Collins stressed several
points specific to that virus. In particular, she noted that because the symptoms of a CMV infection
are “usually self-limiting and not unique,” they are not usually diagnosed at the time of infection.
First Collins Rep. at 5. In fact, a CMV infection can manifest asymptomatically – with only some
kinds of tests confirming its existence. Id. And (as discussed below), Dr. Collins felt Petitioner’s
own testing results were consistent in this regard. Dr. Collins also noted that medical science
suggests that a CMV-caused GBS would be “more commonly associated with objective sensory
defects,” suggesting in turn “that the virus itself is directly or indirectly implicated and raises the
question of whether CMV therapy would aid treatment for CMV-associated GBS.” Id. at 6;
Orlikowski at 843.
Dr. Collins also proposed that CMV-caused GBS might be mediated differently than other
versions of GBS attributable to other kinds of triggers, maintaining that molecular mimicry (a
common mechanistic explanation for how an autoimmune disease like GBS might occur)9 might
not be applicable in this context. First Collins Rep. at 6. Orlikowski, for example, proposed that
the kind of anti-ganglioside antibodies often thought to be produced via molecular mimicry, and
that might in turn attack nerve myelin cross-reactively, might be produced by a primary CMV
9 “Molecular mimicry occurs as a result of amino acid sequences shared between a vaccine's viral or bacterial particles
and structures in human tissue. . . The immune system's reaction to the foreign vaccine antigens produces immune
cells that in turn can cross-react against the similar human tissue antigens, mistakenly identifying self-structures as
foreign.” Mason v. Sec'y of Health & Hum. Servs., No. 17-1383V, 2022 WL 600415, at *5 (Fed. Cl. Spec. Mstr. Feb.
4, 2022).
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infection, but were not also seen “to significantly influence the pathogenesis of CMV- GBS.” First
Collins Rep. at 6; Orlikowski at 843 (“Our results confirm that the anti-GM2 IgM response is more
closely associated with primary CMV infection than with GBS . . . .”).
Other studies emphasized different targets for autoimmune attack in GBS attributable to
CMV infection, and were unable to identify evidence of CMV antigens as triggering the production
of attacking autoantibodies. See S. Sawai et al., Moesin is a Possible Target for Cytomegalovirus-
related Guilllain-Barre Syndrome, 83 Neurology 113, 116 (2014), filed as Ex. A-9 (ECF No. 34-
10). Still more items of literature (including case series reports) seemed to associate a T cell-driven
autoimmune attack in CMV-caused GBS, in comparison to patients whose GBS was associated
with C. jejuni, or even no infection at all. R.D. Hadden et al., Preceding Infectious, Immune
Factors, and Outcome Guillain-Barre Syndrome, 56 Neurology 758, 763 (2001), filed as Ex. A-
13 (ECF No. 34-14). Dr. Collins acknowledged, however, that research on this topic had not yet
reliably established any of its hypotheticals. First Collins Rep. at 6.
Dr. Collins provided several substantive bases for her view that a CMV infection best
explained Petitioner’s GBS. The medical record, she argued, established that Petitioner had
experienced an active CMV infection around the time his GBS symptoms manifested. First Collins
Rep. at 6. In support, she noted that Petitioner had tested positive for both IgG and IgM CMV
antibodies when hospitalized in October 2020. Id. at 4. In addition, liver function tests revealed
fluctuating abnormalities between mid- and late-October, when he was discharged. Id. at 3-4. Such
a finding was associated with a CMV infection. See T. Friel, Epidemiology, Clinical
Manifestations, and Treatment of Cytomegalovirus Infection in Immunocompetent Adults, Wolters
Kluwer Health – UptoDate, https://www.uptodate.com/contents/epidemiology-clinical-
manifestations-and-treatment-of-cytomegalovirus-infection-in-immunocompetent-adults (last
updated Mar. 9, 2022), filed as Ex. A-1 (ECF No. 34-2) (“Friel”). Dr. Collins also noted that
several test results from his October hospitalization showed an increase in absolute lymphocytes.10
Id. Treaters had considered this evidence of “possible viral infection,” and it was further indirect
proof of the existence of the CMV infection. Ex. 2 at 30; Friel at 7.
The flu vaccine, by contrast, was less likely causal of GBS (even though the Vaccine
Program clearly recognizes the claim). First Collins Rep. at 6-9. One 2001 UK study found less of
a risk of developing GBS from the flu vaccine than from a wild flu infection. J. Stowe et al.,
Investigation of the Temporal Association of Guillain-Barre Syndrome With Influenza Vaccine
and Influenzalike Illness Using the United Kingdom General Practice Research Database, 169
Am. J. of Epidemiology 382, 385 (2009), filed as Ex. D (ECF No. 52-1) (“Stowe”). Another
epidemiologic prospective study reached a comparable conclusion. L. Grimaldi-Bensouda,
Guillain-Barre Syndrome, Influenzalike Illnesses, and Influenza Infection During Seasons With
10 A lymphocyte is type of white blood cell that determines the specificity of the body’s immune response to infectious
microorganisms and other foreign substances. Lymphocyte, Britannica Online,
https://www.britannica.com/science/lymphocyte (last visited Mar. 17, 2025).
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and Without Circulating A/H1N1 Viruses, Am. J. of Epidemiology 326, 334 (2011), filed as Ex.
A-14 (ECF No. 34-15) (“Grimaldi-Bensuda”) (“Influenza infections and influenza-like illnesses
are likely risk factors for GBS and should therefore be considered serious confounders in future
studies of GBS and vaccination. On the other hand, no new concerns about influenza vaccination,
notably use of the A/H1N1 vaccine, have been identified”). A third article concluded the same,
but also observed that some of the association between vaccination and GBS might be attributable
to the fact that vaccination efforts also occurred in the midst of wild viral outbreaks, confounding
findings that the vaccine’s antigens alone were causal of GBS. S. Greene, Guillain-Barre
Syndrome, Influenza Vaccination, and Antecedent Respiratory and Gastrointestinal Infections: A
Case Centered-Analysis in the Vaccine Safety Datalink 2009-2011, 8 PLOS One 1, 6 (2013), filed
as Ex. A-15 (ECF No. 34-16) (“Greene”). And another item of literature provided evidence that
(given the undeniable connection between the wild flu virus and GBS) vaccination against the
virus could be seen as reducing instances of GBS. C. Vellozzi et al., Cumulative Risk of Guillain-
Barre Syndrome Among Vaccinated and Unvaccinated Populations During the 2009 H1N1
Influenza Pandemic, 104 Am. J. of Pub. Health 696, 700 (2014), filed as Ex. A-16 (ECF No. 34-
17).
Second Report
Dr. Collins’s supplemental report endeavored to respond to the arguments of Dr. Kelesidis
(Petitioner’s expert). Before entering into her point-by-point rebuttal, however, she noted the areas
of agreement between both sides. In particular (and in addition to the fact that the GBS diagnosis
is not disputed), she observed that Dr. Kelesidis had acknowledged (a) that most cases of GBS
have an infectious etiology, (b) that Petitioner was found to have a CMV infection in the course
of his hospitalization, and (c) that a CMV infection is a GBS risk factor. Second Collins Rep. at 1.
Otherwise, Dr. Collins maintained that her opinion had withstood Petitioner’s attacks.
First, she disputed Dr. Kelesidis’s overall point that only a severe CMV infection with clear
symptoms (of the kind that Petitioner did not report or experience) had the capacity to result in the
“post-infectious etiology of his neurological manifestation.” Second Collins Rep. at 1. The
evidence offered by Dr. Kelesidis for this contention either focused on how GBS might present in
severe cases, or discussed liver disturbances in the context of GBS, but without also reviewing the
CMV-GBS association Dr. Collins maintained was established by independent literature. See A.
de Jager, Clinical Signs in Severe Guillain-Barre Syndrome: Analysis of 63 Patients, 104 J. of
Neuro. Sci. 143, 143 (1991), filed as Ex. 19 (ECF No. 42-3) (“de Jager”); P. Oomes et al., Liver
Function Disturbances in Guillain-Barre Syndrome: A Prospective Longitudinal Study in 100
Patients, 46 Neurology J. 96, 98 (1996), filed as Ex. 20 (ECF No. 42-4). Nor was the presence of
organ involvement in the context of a CMV infection a necessary prerequisite. Not only was there
some evidence of possible organ involvement here (the liver function test results), but no
independent evidence otherwise supported this argument. Second Collins Rep. at 3-4.
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In fact, Dr. Collins maintained, evidence she had offered rebutted the contention that a
CMV infection would need to be severe for GBS to be an associated risk. Orlikowski, for example,
based its findings of a CMV-GBS relationship on individuals like Petitioner, where serum testing
simply revealed evidence of IgM antibodies to CMV. Orlikowski at 839. This evidence of the
presence of infection was accepted by the medical community, and thus Dr. Collins did not put
stock in Dr. Kelesidis’s contentions that “CMV IgM may not be specific for primary infection.”
Second Collins Rep. at 5. (She admitted, however, that in this case, unlike in Orlikowski, there
was no evidence of the “avidity”11 of Petitioner’s IgG response, although IgG testing was
consistent with a CMV infection’s presence. Second Collins Rep. at 2.)
There was also “clear evidence” of the CMV virus circulating in Petitioner’s blood. Second
Collins Rep. at 2; Ex. 4 at 49, 23, 123. And Dr. Collins denied that “the amount of CMV DNA”
found in testing was relevant to the severity of the infection. Second Collins Rep. at 5. The fact
that GBS was post-infectious, she noted, was what was relevant (meaning that it could occur in
the wake of a prior infection, regardless of severity). Nor did Dr. Collins consider significant the
amount of CMV detected in cerebrospinal fluid testing, since in the majority of cases (as reflected
in literature referenced by Dr. Kelesidis) “most (69%) of patients with CMV seropositivity and
GBS did not have CMV DNA in their spinal fluid.” Id.; C. Steininger, Presence of
Cytomegalovirus in Cerebrospinal Fluid of Patients with Guillain-Barre Syndrome, 189 J. of
Infectious Diseases 984, 986 (2004), filed as Ex. 33 (ECF No. 42-17) (“Steininger I”).
In addition, Dr. Collins reiterated that CMV infections were more often than not
asymptomatic in presentation. Second Collins Rep. at 3; Orlikowski at 839 (noting that a minority
of studied patients presented with GI symptoms or fever). At the same time, however, Petitioner
did complain of sensory deficits consistent with “CMV-associated GBS.” Orlikowski at 840. And
his liver function testing was also akin to what CMV-caused GBS would look like. Second Collins
Rep. at 3.
Second, Dr. Collins took issue with Dr. Kelesidis’s proposal that Petitioner’s CMV
infection was likely only a reactivation (and hence less likely to be causal of GBS). Second Collins
Rep. at 4-5. She noted in response that the lab findings in this case confirming the presence of a
CMV infection would have been deemed a sufficient basis to have included Petitioner in studies
like Orlikowski, which considered those findings evidence of a “primary cytomegalovirus
infection.” Orlikowski at 837 (“We diagnosed 63 (12.4%) CMV-GBS cases by immunoglobulin
(Ig) M detection and IgG avidity”). The fact that Petitioner was being treated for GBS was also
not the cause of the alleged CMV reactivation. Rather, the infection likely predated findings of its
11 IgG avidity is defined as “the strength with which IgG binds to antigenic epitopes expressed by a given protein. . .
Low CMV IgG avidity is an accurate indicator of primary infection within the preceding 3 to 4 months, whereas high
avidity excludes primary infection within the preceding 3 months.” H. Prince & M. Lape-Nixon, Role of
Cytomegalovirus (CMV) IgG Avidity Testing in Diagnosing Primary CMV Infection During Pregnancy, 21 Clin. and
Vaccine Immunology 1377, 1377 (2014), filed as Ex. 61 (ECF No. 49-24) (“Prince”). IgG avidity testing “is
increasingly considered the ‘gold standard’ for distinguishing primary from nonprimary CMV infection.” Prince at
1377.
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presence, since “[i]t takes time following exposure to a virus for IgM and IgG to become
detectable.” Second Collins Rep. at 6. Existing studies supported the conclusion that Petitioner’s
infection exposure began several days before testing revealed it. Id.; Ex. 4 at 126. But Petitioner’s
GBS symptoms did not manifest until October 15th (although the record of this visit suggests an
onset five days prior). And treatments that might have had an impact on CMV reactivation, like
steroids, began later as well. Dr. Collins did not deem Petitioner’s age to make it more likely any
CMV infection he experienced was a reactivation. Second Collins Rep. at 6.
More significantly, however, Dr. Collins noted a lack of evidence offered by Petitioner in
support of the conclusion that only a primary infection could present a GBS risk. Second Collins
Rep. at 5, 7-8. Dr. Kelesidis seemed to assume only immunocompromised individuals would be
threatened by a reactivated infection, but offered no good evidence to support this supposition. Id.
at 7. No other evidence offered by Petitioner, Dr. Collins argued, established a lack of association
between GBS and reactivation of CMV – while literature suggested that reactivation could still be
GBS-associated. Second Collins Rep. at 6; C. Steininger, Primary Cytomegalovirus Infection in
Patients with Guillain-Barre Syndrome, 183 J. of Neuroimmunology 214, 218 (2007), filed as Ex.
32 (ECF No. 42-16) (“Steininger II”). The degree of risk had not been shown to be dependent on
the proper characterization or nature of the infection.
Third, Dr. Collins reiterated her view that the lab findings she had highlighted (such as
lymphocytosis or liver function/transaminitis) were consistent with a CMV infection. Second
Collins Rep. at 4. Dr. Kelesidis had suggested that the timing of different findings during the course
of Petitioner’s treatment was evidence of an “inconsistent progression,” especially in light of the
lack of confirming symptoms manifestations. Id. But the core fact of Petitioner’s infection (as
evidenced by antibody findings) was not impacted by these other lab findings (even though Dr.
Collins had deemed them significant). And no evidence referenced by Dr. Kelesidis stood for the
proposition that the progression of these other lab findings had anything to do with the degree of
GBS risk in the wake of a CMV infection. Id.
Dr. Collins went on to discuss what the record indicated about Petitioner’s treaters, and
their possible views about the etiology of his GBS and/or relationship to a prior infection. Second
Collins Rep. at 7. Although the record does show that some infectious consult occurred in the
course of Petitioner’s treatment, Dr. Collins noted that it has an informal and cursory nature,
referred to in the actual record as “curbside” (meaning casual and based on a very brief summary).
Id. The intent of this evaluation, moreover, was only to decide if the discovered CMV infection
warranted treatment – a consideration independent of whether the infection was associated with
Petitioner’s GBS (something that this set of records said nothing about). Dr. Collins concurred
with the decision not to treat, observing that “CMV typically resolves without specific treatment
in an immunocompetent person.” Id.
Dr. Collins concluded her second report with more discussion of the relative risks of GBS
post-vaccination versus post-infection and engaged in a pointed effort to rebut some of Dr.
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Kelesidis’s contentions on this topic. Second Collins Rep. at 8-11. However, I do not deem that
question to be particularly in dispute – and since this is otherwise a Table claim, the causal
association of the flu vaccine with GBS is also not in question. Accordingly, the debate between
the experts on this point is academic for present purposes.
B. Petitioner’s Expert – Theodoros Kelesidis, M.D., Msc., Ph.D.
Dr. Kelesidis is (like Dr. Collins) an infectious disease specialist and medical academic,
and he authored two reports in support of Petitioner. Report, dated Jan. 11, 2024, filed as Ex. 17
(ECF No. 42-1) (“First Kelesidis Rep.”); Report, dated Aug. 2, 2024, filed as Ex. 39 (ECF No. 49-
2) (“Second Kelesidis Rep.”).
Dr. Kelesidis is an Associate Professor in the Division of Infectious Diseases at University
of Texas Southwestern Medical Center. CV, dated Jan. 11, 2024, filed as Ex. 18 (ECF No. 42-2)
(“Kelesidis CV”). He received his medical degree from Athens University Medical School in
Athens, Greece, and received his Ph.D. from the Department of Microbiology, Immunology and
Molecular Genetics at UCLA. Kelesidis CV at 1. Dr. Kelesidis completed a residency in internal
medicine at St. Elizabeth’s Medical Center in Boston, MA and completed a fellowship in
infectious diseases at UCLA. Id. He is board-certified in infectious disease. First Kelesidis Rep. at
1. His clinical practice has focused on patients with complicated infectious disease problems and
his research laboratory studies molecular mechanisms of immunopathogenesis of viral infections.
Id. Dr. Kelesidis has published over 150 papers. Id.
First Report
Dr. Kelesidis accepted both Dr. Collins’s summation of the medical history, as well as
Petitioner’s ultimate GBS diagnosis. First Kelesidis Rep. at 1. But he denied a CMV infection
could explain Petitioner’s GBS, and he provided several points to support his opinion.
Dr. Kelesidis disputed that the medical record established that Petitioner had experienced
any infection of sufficient severity to cause GBS. First Kelesidis Rep. at 1-3. Most cases of GBS
deemed viral in origin would be preceded by evidence of infectious-associated symptoms, from
upper respiratory complaints to gastrointestinal issues. Id. at 1; de Jager at 144. But the medical
record in this case revealed no such complaints prior to Petitioner’s onset of neurologic symptoms.
He had not even experienced a sore throat (a common CMV-associated symptom), nor had he been
caring for an infant or young child – the “main vector in primary CMV infections in late
adulthood.” First Kelesidis Rep. at 2; A. Al-Omari et al., Cytomegalovirus Infection in
Immunocompetent Critically Ill Adults: Literature Review, 6 Annals of Intensive Care 1, 2 (2016),
filed as Ex. 22 (ECF No. 42-6) (“Al-Omari”). (The record in this case does establish Petitioner had
an infant daughter, although there is no evidence the child displayed any infection-related
symptoms before Petitioner’s onset. Ex. 13 at 2. And Al-Omari says only that CMV is more
commonly acquired in childhood – not that children transmit it to adults).
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CMV, Dr. Kelesidis agreed, could be largely subclinical in its course, and “[m]ost healthy
individuals who acquire CMV infection are able to clear the infection within a short length of time
with no adverse sequelae.” First Kelesidis Rep. at 2. But severe symptoms were also possible, and
they could run the gamut, from GI-associated concerns to “life-threatening complications” that
could result in organ damage. Id. Liver impact, in Dr. Kelesidis’s view, would be rare, and if
present, would result in obvious secondary symptoms, “including fever and mononucleosis like
syndrome (sore throat, swollen lymph nodes).” Id.
Dr. Kelesidis proposed that the record evidence only established, at most, a reactivation of
a prior CMV infection – insufficient in his view to be causal of GBS. See generally First Kelesidis
Rep. at 3-4. He agreed that Petitioner as of October 15, 2020, displayed elevated liver enzymes, or
“transaminitis,” but maintained that the levels subsequently “self-resolved.” Id. at 2. The same was
true for test results demonstrating lymphocytosis, with Dr. Kelesidis considering the results to
show only mild elevations that could not be considered atypical – and which also did not persist.
Id. It certainly was not the degree of abnormality which had been seen in studies of CMV infections
involving mononucleosis. D. Felsenstein et al., Phenotypic Properties of Atypical Lymphocytes in
Cytomegalovirus-Induced Mononucleosis, 152 J. of Infect. Diseases 198, 201-02 (1985), filed as
Ex. 27 (ECF No. 42-11). And lymphocytosis was not specific to a CMV infection in any event,
further diminishing the significance of those findings here. First Kelesidis Rep. at 2. Otherwise,
Petitioner had displayed no signs of an active CMV infection. For example, he had no fever, and
no signs of the kind of mononucleosis (associated with CMV) that might establish the presence of
an infection. Id.
A CMV reactivation, was, in Dr. Kelesidis’s view, more likely to have occurred in this
case. First Kelesidis Rep. at 3. As a general matter, an adult of Petitioner’s age would be unlikely
to have never had CMV in his life before – and CMV is known to be a virus that could remain
latent in the body, well after exposure to it as a child. Friel at 2; P. Lachance, Association Between
Cytomegalovirus Reactivation and Clinical Outcomes in Immunocompetent Critically Ill Patients:
A Systematic Review and Meta-Analysis, 4 Open Forum Infect. Diseases 1, 1 (2017), filed as Ex.
29 (ECF No. 42-13) (“Lachance”). The testing performed on Petitioner also revealed an overall
low viral load – especially in comparison with the kind of especially-virulent infection that would
be associated with significant pathology. P. Griffiths & M. Reeves, Pathogenesis of Human
Cytomegalovirus in the Immunocompromised Host, 19 Nature Rev. Microbio. 759, 759 (2021),
filed as Ex. 31 (ECF No. 42-15) (“. . . [I]f the immune system is compromised, HCMV can
replicate to high levels and cause serious end organ disease”). The presence of IgM CMV
antibodies, even in patients with GBS, was not evidence of an active infection, as recognized in
relevant literature. Steininger II at 218. Petitioner’s cerebrospinal fluid testing had not revealed
evidence of an active infection (as it should have if his GBS were CMV-caused). Id. at 215. In
addition, CMV reactivation could have occurred due to Petitioner’s GBS (as opposed to the latter
caused by the former). See Lachance at 1 (“This state of latency allows CMV to reactivate when
host defenses become compromised, such as in critical illness. Cytomegalovirus reactivation in
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critically ill patients is well recognized with as high as 71% incidence. . .”). In fact, Petitioner’s
treaters had expressed the view that Petitioner’s CMV infection was merely a reactivation “in the
setting of illness,” and that it did not merit treatment on its own. First Kelesidis Rep. at 3.
A reactivated CMV infection, moreover, was less likely to result in GBS. First Kelesidis
Rep. at 3-4. But to establish this point, Dr. Kelesidis relied primarily on the absence of affirmative
evidence from literature that reactivated CMV infections in “immunocompetent patients” (which
would presumably be a fair characterization of Petitioner) were associated with GBS. At most,
some evidence (such as case reports) suggested that individuals severely ill from a CMV infection
might in rare circumstances secondarily develop GBS. Id. at 4.
Dr. Kelesidis felt, by contrast, that it was far more likely Petitioner’s GBS was vaccine-
caused. First Kelesidis Rep. at 4-7. In so opining, he summarized existing medical science
supporting the mechanism for an association (occurring via molecular mimicry between vaccine
antigens and self-structures on the nerve myelin) and highlighted a number of studies that he felt
continued to show a possible link from an epidemiologic standpoint (in contrast to the items of
literature offered by Dr. Collins to undermine that conclusion). Id. at 5-6.12 And he deemed
contrary evidence to be limited either by methodologic issues (such as insufficiently-large
samples) or by the fact that rare occurrences like GBS cannot be predicted with epidemiology. Id.
at 6. Dr. Kelesidis also proposed that an onset of a week to two weeks post-vaccination was
medically acceptable, based on the likely autoimmune mechanism at issue – molecular mimicry.
Id. at 4.
Second Report
Dr. Kelesidis’s final report attempted to defend his overall opinion that Petitioner’s CMV
infection could not have caused his GBS.13 He sought to bulwark his argument that Petitioner’s
infection was overall insufficiently severe to have resulted in GBS. Second Kelesidis Rep. at 1-4.
He again emphasized the lack of evidence of any significant clinical manifestations of a CMV
infection prior to its discovery. Id. at 1. He also maintained that the absence of such symptoms
plus results from “IgG avidity testing,” did not support the conclusion that Petitioner had
12 I do not include a specific discussion of these items of literature – both because the vaccine’s capacity to cause GBS
is not relevant in the context of a Table claim (where causation is presumed), but also because Dr. Collins’s efforts
were focused more on an equally-indisputable point: that the wild flu virus is far more likely to cause GBS than the
flu vaccine. And a distinction between population-level risk and individual risk matters not. Epidemiologic evidence
on this sub-issue (vaccination risk versus wild virus risk) still preponderates against the relative risk of vaccination
compared to infection. Arguments that “no study can ever disprove the possibility of individual causation”
misapprehend the weight that such evidence deserves – when it exists. Kelly v. Sec'y of Health & Hum. Servs., No. 16-
878V, 2021 WL 5276373, at *26 n.24 (Fed. Cl. Spec Mstr. Oct. 18, 2021).
13 Dr. Kelesidis also repeated many of his arguments about the flu vaccine’s association with GBS (see generally
Second Kelesidis Rep. at 11-12), but I do not recapitulate these secondary points, for the same reasons I have not
addressed their treatment in Dr. Collins’s second report.
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experienced a primary infection. Id. at 1-2, citing Steininger II at 217-18. And Dr. Collins, as noted
above, had admitted that these findings were not available.
This left Dr. Collins to rely on secondary proof, like the liver functionality testing results.
But Dr. Kelesidis deemed these nonspecific in nature, and therefore likely evidence of other kinds
of issues beyond a CMV infection. Second Kelesidis Rep. at 2. In fact, the liver function results
could have been the product of Petitioner’s self-medication with Tylenol to treat his headaches
before he sought medical assistance. Id.; Jorge Herrera & Alisa Likhitsup, Medications and the
Liver, Am. College of Gastroenterology, https://gi.org/topics/medications-and-the-liver (last
updated August 2022), filed as Ex. 60 (ECF No. 49-23) (stating that Tylenol is the best-known
medication that can cause damage to the liver).
The record in fact, Dr. Kelesidis maintained, was consistent with the conclusion that
Petitioner had experienced a reactivated infection rather than primary. Second Kelesidis Rep. at 5-
8. Because of a lack of IgG avidity testing, Orlikowski could not be credibly invoked by Dr. Collins
as supporting the conclusion that Petitioner’s infection was primary. Id. at 6. Other evidence
offered by Dr. Collins stood as support for CMV reactivation being a risk factor for GBS only in
cases where the individual was “critically ill,” and thus likely immunocompromised. Id. at 6-7; A.
Caliendo, Approach to the Diagnosis of Cytomegalovirus Infection, Wolters Kluwer Health –
UptoDate, https://www.uptodate.com/contents/approach-to-the-diagnosis-of-cytomegalovirus-
infection (last updated May 16, 2024), filed as Ex. A-7 (ECF No. 34-8); L. Papazian et al.,
Cytomegalovirus Reactivation in ICU Patients, 42 Intensive Care Med. 28, 28-29 (2016), filed as
Ex. 49 (ECF No. 49-12). The IgM evidence was not necessarily dispositive proof of a recent
infection, since IgM antibodies could persist up to a year after initial encounter with the infectious
agent or could simply reflect reactivation. Second Kelesidis Rep. at 7; H. Prince & M. Lape-Nixon,
Role of Cytomegalovirus (CMV) IgG Avidity Testing in Diagnosing Primary CMV Infection
During Pregnancy, 21 Clin. and Vaccine Immunology 1377, 1378 (2014), filed as Ex. 61 (ECF
No. 49-24) (“Prince”). Petitioner’s adult status made it likely he had been exposed to CMV in his
life before, and because the CMV virus tended to remain latent in the body, it was simply more
credible that this is what had occurred in this case. Second Kelesidis Rep. at 11.
Such a less-virulent reactivated infection was unlikely to result in GBS. Second Kelesidis
Rep. at 7. In so arguing, Dr. Kelesidis maintained that no mechanism had been identified linking
any form of CMV infection with GBS, proposing that the studies Dr. Collins generally relied upon
all displayed “major limitations” that made it impossible to give them probative weight. Id. at 7-
8. Otherwise, Dr. Kelesidis maintained that Petitioner’s own testing levels for CMV viral load
were low, consistent with a reactivation, and that it was more likely his GBS contributed to that
reactivation than vice-versa. Id. at 8.
Dr. Kelesidis further sought to identify record proof that he deemed more consistent with
a vaccine-caused GBS than infectious-caused. Had Petitioner’s GBS been due to a CMV infection,
progression of the illness process should have been evident in testing. Second Kelesidis Rep. at 4.
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But the “inconsistent presence of lymphocytosis and atypical lymphocytes” seen in testing results
in this case did not make an infectious cause more likely, and were in fact nonspecific, or even due
to GBS. Id. And Petitioner’s treaters did not deem the CMV infection to be a possible causal factor,
with Dr. Kelesidis downplaying the “curbside” nature of the infectious consult Petitioner received.
Id. at 8.
III. Procedural History
This claim was initiated in March 2022. In April 2023, Respondent filed his Rule 4(c)
Report contesting entitlement. Respondent filed an expert report from Dr. Collins in July 2023,
and Petitioner filed a responsive report from Dr. Kelesidis in January 2024. Three months later, in
April 2024, Respondent filed a supplemental report from Dr. Collins. In August 2024, Petitioner
filed his final expert report from Dr. Kelesidis, along with a Motion for Ruling on the Record.
Respondent filed his Opposition and Petitioner followed up with his Reply. The matter is now ripe
for resolution.
IV. Parties’ Arguments
Respondent
Respondent contends that Petitioner’s GBS was caused by an active, if asymptomatic,
CMV infection, as supported by definitive laboratory testing results. Opp. at 1, 8-9. According to
Friel, “acute [CMV] infection is strongly suggested by the detection of either CMV-specific IgM
antibody or a four-fold or greater rise in CMV-specific IgG performed in paired specimens
obtained at least two weeks apart.” Friel at 5. And Petitioner possessed CMV-specific IgM
antibodies. Opp. at 9; Ex. 4 at 126. While Petitioner argues that he needed to have an IgG avidity
score performed simultaneously with his IgM result to establish that he had a recent primary CMV
infection, IgM results without avidity scores were used in multiple peer-reviewed articles
evaluating the associations between CMV and GBS. Opp. at 10; Second Collins Rep. at 5. Because
Petitioner had positive IgM, he would have been included in studies showing that a recent CMV
infection is a risk factor for the development of GBS. Opp. at 12; see also Winer at 2 (“The
presence of IgM antibodies was taken to indicate recent CMV infection”); Jacobs at 2 (CMV
infection was “defined as the presence of IgM”). Moreover, Petitioner argues that the lack of
another test is inadequate to overcome Respondent’s preponderant showing. Opp. at 10.
Additionally, Petitioner had elevated atypical lymphocytes at ten percent. Opp. at 9; Ex. 4
at 123. According to the medical literature, “the presence of more than [ten] percent atypical
lymphocytes on peripheral blood smear” is a hematologic abnormality that indicates an active
CMV infection. Friel at 6-7. Further, Petitioner had abnormal AST and ALT levels, and
“[s]ubclinical transaminitis is the most common finding in immunocompetent patients[.]” Opp. at
9; Friel at 9. Petitioner also had elevated liver transaminases. Opp. at 9; Ex. 4 at 123. All of this
led Dr. Collins to conclude that Petitioner likely had an ongoing CMV infection at the time of
vaccination. Opp. at 10.
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Respondent further argues that Petitioner not only failed to establish that his CMV infection
was a reactivation rather than primary infection, but that this distinction matters. Opp. at 10. In
support of his argument, Petitioner notes that he did not have any symptoms. Id. But Respondent
contends that this is not unusual, since “[i]nfection in the immunocompetent host is generally
asymptomatic[.]” Id. at 9 (citing Friel at 1).
Petitioner also argues that his CMV viral load was low, but as Dr. Collins explains, CMV
viral load is related to severity, not whether an infection is present in the first place. Opp. at 11.
Petitioner’s claim that GBS or steroid use can reactivate a CMV infection is simply unsupported.
Id. Respondent notes that Petitioner’s only evidence in support of this claim is LaChance, which
discusses CMV activation in critically ill patients, unlike Petitioner. Id.; LaChance at 1. Opp. at
11. Finally, the infectious disease team’s cursory statement that Petitioner’s CMV was “likely re-
activation [in setting of] recent illness, would not treat” does not overcome Respondent’s showing.
Id. Curb-siding reflects a minimal clinical evaluation, and CMV typically resolves without specific
treatment in an immunocompetent person. Id.
Respondent also argues that Petitioner has not provided any support for his contention that
severe or symptomatic CMV infection is a prerequisite to general causation of GBS. Opp. at 13.
Dr. Kelesidis recognizes that most primary CMV infections are subclinical, and that “active
infection has been linked to GBS.” Id.; Second Collins Rep. at 3-4; First Kelesidis Rep. at 4. And
Dr. Kelesidis’s claim that viral damage and release of antigens increases based on the severity of
the infection stands in stark contrast to his subsequent attempt to ascribe causation to the flu
vaccine, which did not cause Petitioner to experience effects anywhere near the same level as a
viral infection. Opp. at 13.
Respondent maintains that a great deal of data supports the conclusion that infection is an
important cause of GBS. Opp. at 14; see also Yuki at 1; Greene at 1-8. Notably, CMV “is the most
common viral antecedent infection” of GBS. Opp. at 14 (citing Yuki at 1). Respondent argues,
contrary to Petitioner’s demand, that he need not elucidate a mechanism causally connecting CMV
to GBS. Id. at 15. Respondent’s theory is sufficiently supported by expert testimony and
epidemiological evidence. Id. Moreover, some Program decisions support Respondent’s
contentions about the greater chance of a wild flu virus causing GBS over the flu vaccine. Bielak
v. Sec'y of Health & Hum. Servs., No. 18-761V, 2023 WL 35509, at *30-31 (Fed. Cl. Spec. Mstr.
Jan. 3, 2023) (noting “viral infections have also been found associated with GBS—further
supporting the contention that the flu vaccine could be causal”); Mason v. Sec'y of Health & Hum.
Servs., No. 17-1383V, 2022 WL 600415, at *5-6, *26 (Fed. Cl. Spec. Mstr. Feb. 4, 2022)
(summarizing petitioner’s expert’s molecular mimicry theory, which hinged upon research
associating infections, including CMV, with GBS).
Respondent concludes with the proposition that Petitioner’s CMV infection caused his
GBS within a medically acceptable timeframe. Opp. at 16. Dr. Collins opined that Petitioner’s
CMV “infection was recent and ongoing because the IgM was positive and because viral DNA
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was detected.” First Collins Rep. at 6. Even if Petitioner had a CMV reactivation, it is the infection
per se that is significantly associated with GBS. Opp. at 17; Second Collins Rep. at 4-8. In contrast
to the strong evidence linking CMV infections and GBS, the medical literature does not show an
association between the flu vaccine and GBS. Opp. at 18; Stowe at 1-2; Grimaldi-Bensuda at 1-2;
Greene at 1. In sum, the record shows that the flu vaccine had no more than a coincidental
relationship to Petitioner’s GBS. Opp. at 20; First Collins Rep. at 9. Petitioner’s active CMV
infection was the preponderant sole substantial cause of Petitioner’s GBS. Opp. at 20.
Petitioner
Petitioner asserts he can meet the elements for a Table claim of GBS after receipt of the
seasonal flu vaccine. Mot. at 18. Five days after receiving the vaccine on October 5, 2020,
Petitioner developed tingling and generalized weakness in bilateral hands, feet, and mouth. Id.;
Ex. 2 at 43. Two weeks later (on October 25, 2020), Petitioner was diagnosed with “GBS [ ] likely
in the setting of recent flu vaccine” and was treated with a three-day course of IVIg. Mot. at 19;
Ex. 4 at 48-49. Because Petitioner developed GBS within the statutorily-defined timeframe of 3-
42 days, he has satisfied the prima facie criteria for an on-Table claim. Mot. at 19.
Respondent asserts that Petitioner’s GBS was caused by an active CMV infection. Mot. at
19. But Petitioner denies the “factor unrelated” burden has been carried. Respondent has failed to
demonstrate that Petitioner was experiencing an active CMV infection, or that such an infection
was the sole substantial factor leading to his development of GBS. Id.
Petitioner argues that Respondent’s expert, Dr. Collins, offered studies that failed to
elucidate a mechanism linking CMV to the development of GBS. Mot. at 19-20. Orlikowski, for
example, found that the serum GM2 IgM – while closely associated with primary CMV infection
– is unlikely to significantly influence the development of CMV-associated GBS. Id. at 20 (citing
Orlikowski at 843). Unable to prove a causal mechanism, Dr. Collins relies on small
epidemiological studies that may establish an association, but do not establish causation. Mot. at
20. Winer and Jacobs both identified a small subset of patients with CMV-specific IgM antibodies,
which are thought to be indicative of a recent primary CMV infection (although a latent CMV
infection could not be excluded). Id. at 20-22; Winer at 617; Jacobs at 1110. The authors discussed
possible mechanisms to explain the link between CMV and GBS, but Dr. Collins questioned the
applicability of some of these mechanisms and explicitly rejected the molecular mimicry theory.
Mot. at 21-22; First Collins Rep. at 6. Dr. Collins’s reliance on Orlikowski is also inapplicable
because the patients in Orlikowski were experiencing a “recent primary infection,” while the
medical records in this case support a finding that Petitioner was experiencing a reactivation of
CMV secondary to his onset of GBS. Mot. at 23; Ex. 4 at 49, 93.
Respondent also points to Petitioner’s abnormal LFTs, lab test results identifying IgM and
IgG antibodies to CMV, the presence of lymphocytosis, and neurological manifestations as all
“consistent with CMV-associated GBS.” Mot. at 24-30. Dr. Collins argues that a person with an
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asymptomatic CMV infection can exhibit mild increases in liver transaminases, without additional
symptoms of infection. Id. at 25; First Collins Rep at 5-6. But Friel, which Dr. Collins uses to
support her argument, indicates that increases in liver transaminases can be observed in
symptomatic CMV infections. Mot. at 25; Friel at 9. Petitioner points out that his transient
transaminitis was more likely caused by his GBS, NSAID medications, and/or his IVIg treatments.
Mot. at 26.
Dr. Collins also relies on lab tests that show the presence of both IgM and IgG antibodies
to CMV. Mot. at 27. But these findings do not allow for the differentiation between a recent or
active primary infection, in comparison to CMV reactivation in the setting of a critical illness. Id.
Petitioner explains that the presence of IgG antibodies indicates that a person was, at some point
in their life, infected with CMV. Id. at 28. While IgM antibodies can indicate a recent primary
infection, they are also produced during a secondary infection and reactivation. Id.; see also
Steininger II at 215; Steininger I at 984. The only reliable means of distinguishing between an
active CMV infection and a latent CMV infection is IgG avidity testing, which Petitioner did not
undergo. Mot. at 29. Therefore, the available antibody studies in this case do not stand as strongly
persuasive evidence of a primary CMV infection. Id. at 30.
Respondent also argues that Petitioner’s lymphocytosis and elevated levels of atypical
lymphocytes suggest the presence of an ongoing CMV infection, but he fails to acknowledge that
both are observed in a number of conditions besides CMV infection. Mot. at 30; H. Hamad & A.
Mangla, Lymphocytosis, StatPearls (2023), filed as Ex. 48 (ECF No. 49-11); T. Shiftan & J.
Mendelsohn, The Circulating “Atypical” Lymphocyte, 9 Hum. Pathology 51 (1978), filed as Ex.
47 (ECF No. 49-10).
Finally, Respondent claims that Petitioner demonstrated neurological manifestations that
are most consistent with CMV-associated GBS, like objective sensory defects. Mot. at 31.
Petitioner responds by arguing that this opinion far exceeds Dr. Collins’s area of expertise, given
her lack of training in neurology. Id. at 32. Furthermore, Dr. Collins ignores the fact that the GBS
subtype Petitioner was diagnosed with, AIDP, is typically characterized by symmetric motor
flaccid weakness and sensory abnormalities. Id. at 33. And the literature that Dr. Collins uses to
support her argument, Friel, describes inconsistent results in studies seeking to identify common
neurologic manifestations that could help distinguish CMV-associated GBS. Id.; Friel at 10. Facial
nerve palsies appear to be the only neurologic manifestation that has consistently been observed
at higher rates in CMV-associated GBS, and Petitioner never demonstrated facial nerve palsy.
Mot. at 33-34; Friel at 10.
Turning to the third Althen prong, Petitioner argues that Respondent failed to demonstrate
a proximate temporal relationship between Petitioner’s CMV and GBS. Mot. at 37. The studies
offered by Respondent suggest that the onset of GBS typically occurs two weeks after a CMV
infection. Id. at 34; Winer at 4; Orlikowski at 839. Respondent contends that Petitioner was
infected with CMV prior to October 13, 2020, but this assumption is based on medical literature
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describing IgG and IgM responses to coronavirus infections – not CMV. Mot. at 35; (citing H.
Hou et al., Detection of IgM and IgG Antibodies in Patients with Coronavirus Disease 2019, 9
Clin. & Translational Immunology 1, 1-6 (2020), filed as Ex. C-2 (ECF No. 43-3); X. Liu et al.,
Patterns of IgG and IgM Antibody Response in COVID-19 Patients, 9 Emerging Microbes &
Infections 1, 1-6 (2020), filed Ex. C-3 (ECF No. 43-4)). CMV-specific literature does not support
Dr. Collins’s proposed timeline of events, as IgM antibodies to CMV can persist for over a year.
Mot. at 36; Prince at 1379. Therefore, the presence of IgM antibodies in Petitioner’s blood sheds
no light on when Petitioner contracted his CMV infection. Mot. at 37.
V. Applicable Legal Standards
A. Petitioner’s Overall Burden in Vaccine Program Cases
To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
he suffered a “Table Injury”—i.e., an injury falling within the Vaccine Injury Table—
corresponding to one of the vaccinations in question within a statutorily prescribed period of time
or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table
Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §
11(c)(1)(C)(ii)(I); see also Moberly, 592 F.3d at 1321; Capizzano v. Sec’y of Health & Hum.
Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006).14 Mr. Taylor asserts a Table claim of GBS after
receipt of the flu 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, 165 F.3d at 1352–53); 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
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
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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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.” Id. at 549.
Petitioners may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu, 569 F.3d at 1378–79 (citing Capizzano, 440 F.3d at 1325–26). Special masters,
despite their expertise, are not empowered by statute to conclusively resolve what are essentially
thorny scientific and medical questions, and thus scientific evidence offered to establish Althen
prong one is viewed “not through the lens of the laboratorian, but instead from the vantage point
of the Vaccine Act’s preponderant evidence standard.” Id. at 1380. Accordingly, special masters
must take care not to increase the burden placed on petitioners in offering a scientific theory linking
vaccine to injury. Contreras, 121 Fed. Cl. at 245.
In discussing the evidentiary standard applicable to the first Althen prong, the Federal
Circuit has consistently rejected the contention that it can be satisfied merely by establishing the
proposed causal theory’s scientific or medical plausibility. See Boatmon v. Sec’y of Health & Hum.
Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019); see also LaLonde v. Sec’y of Health & Hum. Servs.,
746 F.3d 1334, 1339 (Fed. Cir. 2014) (“[h]owever, in the past we have made clear that simply
identifying a ‘plausible’ theory of causation is insufficient for a petitioner to meet her burden of
proof” (citing Moberly, 592 F.3d at 1322)); Howard v. Sec'y of Health & Hum. Servs., No. 16-
1592V, slip op. at *6 (Fed. Cl. Feb. 27, 2023) (confirming that “[t]he standard has been
preponderance for nearly four decades”), appeal docketed, No. 2023-1816 (Fed. Cir. Apr. 28
2023). Otherwise, petitioners always have the ultimate burden of establishing their Vaccine Act
claim with preponderant evidence. W.C. v. Sec’y of Health & Hum. Servs., 704 F.3d 1352, 1356
(Fed. Cir. 2013) (citations omitted); Tarsell v. United States, 133 Fed. Cl. 782, 793 (2017) (noting
that Moberly “addresses the petitioner’s overall burden of proving causation-in-fact under the
Vaccine Act” by a preponderance standard).
The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375–77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. Servs., 956
F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions
and views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 F.3d
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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 den’d, 100 Fed.
Cl. 344, 356 (2011), aff’d without opinion, 475 F. Appx. 765 (Fed. Cir. 2012).
The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the
phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant
proof that the onset of symptoms occurred within a timeframe which, given the medical
understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan
v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what
is a medically acceptable timeframe must align with the theory of how the relevant vaccine can
cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of Health & Hum.
Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after remand, 105 Fed. Cl. 353 (2012), aff’d
mem., 503 F. Appx. 952 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V,
2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for rev. den’d (Fed. Cl. Dec. 3,
2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).
B. Legal Standards Governing Factual Determinations
The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 11(c)(2). The special master is required
to consider “all [ ] relevant medical and scientific evidence contained in the record,” including
“any diagnosis, conclusion, medical judgment, or autopsy or coroner's report which is contained
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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 at 1525 (Fed. Cir. 1993) (“[i]t strains reason to
conclude that petitioners would fail to accurately report the onset of their daughter's symptoms”).
Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec'y of Health & Hum. Servs., No. 03–1585V, 2005 WL
6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical records
are often found to be deserving of greater evidentiary weight than oral testimony—especially
where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528; see also
Murphy v. Sec'y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff'd per curiam, 968 F.2d
1226 (Fed. Cir. 1992), cert. den'd, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United States
v. United States Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that oral
testimony which is in conflict with contemporaneous documents is entitled to little evidentiary
weight.”)).
However, the Federal Circuit has also noted that there is no formal “presumption” that
records are accurate or superior on their face to other forms of evidence. Kirby v. Sec’y of Health
& Hum. Servs., 997 F.3d 1378, 1383 (Fed. Cir. 2021). There are certainly situations in which
compelling oral or written testimony (provided in the form of an affidavit or declaration) may be
more persuasive than written records, such as where records are deemed to be incomplete or
inaccurate. Campbell v. Sec'y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“like any
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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.
C. Analysis of Expert Testimony
Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec’y of Health & Hum. Servs., 219 F.3d 1357,
1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to the
factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509
U.S. 579, 594–96 (1993). See Cedillo v. Sec’y of Health & Hum. Servs., 617 F.3d 1328, 1339 (Fed.
Cir. 2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999).
Under Daubert, the factors for analyzing the reliability of testimony are:
(1) whether a theory or technique can be (and has been) tested; (2) whether the
theory or technique has been subjected to peer review and publication; (3) whether
there is a known or potential rate of error and whether there are standards for
controlling the error; and (4) whether the theory or technique enjoys general
acceptance within a relevant scientific community.
Terran, 195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592–95).
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In the Vaccine Program the Daubert factors play a slightly different role than they do when
applied in other federal judicial settings, like the district courts. Typically, Daubert factors are
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable or could confuse a jury. By contrast, in Vaccine Program cases these factors are
used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec'y of Health &
Hum. Servs., 94 Fed. Cl. 53, 66–67 (2010) (“uniquely in this Circuit, the Daubert factors have
been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of
expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the
persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88
Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases), Daubert has not
been employed at the threshold, to determine what evidence should be admitted, but instead to
determine whether expert testimony offered is reliable and/or persuasive.
Respondent frequently offers one or more experts in order to rebut a petitioner’s case.
Where both sides offer expert testimony, a special master's decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec'y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe, 219 F.3d at 1362). However, nothing requires the acceptance of an expert's conclusion
“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743
(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)); see also Isaac v. Sec'y of Health & Hum.
Servs., No. 08–601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. for
review den'd, 108 Fed. Cl. 743 (2013), aff'd, 540 F. App’x. 999 (Fed. Cir. 2013) (citing Cedillo,
617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony, based on
a particular expert's credibility, is part of the overall reliability analysis to which special masters
must subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d at 1325–26
(“[a]ssessments as to the reliability of expert testimony often turn on credibility determinations”);
see also Porter v. Sec'y of Health & Hum. Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this court
has unambiguously explained that special masters are expected to consider the credibility of expert
witnesses in evaluating petitions for compensation under the Vaccine Act”).
D. Consideration of Medical Literature
Both parties filed numerous items of medical and scientific literature in this case, but not
all such items factor 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., No. 2015–5072,
2016 WL 1358616, at *5 (Fed. Cir. Apr. 6, 2016) (“[w]e generally presume that a special master
considered the relevant record evidence even though he does not explicitly reference such evidence
in his decision”) (citation omitted); see also Paterek v. Sec’y of Health & Hum. Servs., 527 F.
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App’x 875, 884 (Fed. Cir. 2013) (“[f]inding certain information not relevant does not lead to—
and likely undermines—the conclusion that it was not considered”).
E. 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. Petitioner Has Met His Prima Facie Burden of Proof for
a Table Flu Vaccine-GBS Claim
The parties agree that Petitioner has alleged a Table claim in this case. Mot. at 11; Opp. at
7. GBS is listed as a Table injury for the flu vaccine, and thus a claimant seeking to meet its
requirements must show (a) receipt of a covered form of the flu vaccine, (b) that the claimant did
in fact experience GBS as defined in the Table’s “qualifications and aids to interpretation,” and
(c) that onset (whether or not GBS could then be diagnosed, or was) occurred between three and
42 days after vaccination. 42 C.F.R. § 100.3.
All of these elements exist and/or have been satisfied in this case. There is no dispute that
Petitioner received a covered version of the flu vaccine, and his GBS diagnosis is not contested.
In addition, his onset occurred no sooner than October 10, 2020, since he reported weakness and
tingling in his hands and feet having begun five days prior to his October 15th initial treater visit.
Ex. 2 at 43. An onset occurring within five days of his October 5, 2020 vaccination falls within
the timeframe set for a successful Table flu-GBS claim. Thus, the record preponderantly supports
the prima facie elements of Petitioner’s Table claim—meaning that Respondent can only prevail
if he carries his shifted burden to prove a “factor unrelated.” Section 13(a)(1)(B).
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II. Respondent Has Not Established That Petitioner’s CMV Infection
Was the Likely Sole Substantial Factor in Causing Petitioner’s GBS
A. Legal Standards for “Factor Unrelated” Showing
The nature of Respondent’s “factor unrelated” burden in this case warrants explanation.
While the evidentiary standard of preponderance applicable under Althen also applies in cases
involving the shifted “factor unrelated” burden Respondent bears, governing authority has
characterized this burden to be “higher”—or, more accurately, including an additional obligation
not placed on claimants.
When a petitioner successfully establishes a prima facie case of causation, “the burden then
shifts to the government to prove alternative causation by a preponderance of the evidence.”
Cedillo, 617 F.3d at 1338. The Vaccine Act defines “factors unrelated to the administration of the
vaccine” to be matters “documented by the petitioner's evidence or other material in the record,”
such as “infection, toxins, trauma (including birth trauma and related anoxia), or metabolic
disturbances which have no known relation to the vaccine involved, but which in the particular
case are shown to have been the agent or agents principally responsible for causing the petitioner's
illness, disability, injury, condition, or death.” Section 13(a)(2)(B) (emphasis added).
As noted by the Court of Federal Claims in Stone v. Sec'y of Health & Hum. Servs., 95 Fed.
Cl. 233, 237 (2010),
the standard for proving a “factor unrelated” is higher than the petitioner's burden
of proving a prima facie case. Although a petitioner is required to show that the
vaccine was a “substantial factor” in causing his or her injury, ‘the petitioner need
not show that the vaccine was the sole or predominant cause of her injury.’ (de
Bazan, 539 F.3d at 1351). The respondent’s burden, by contrast, is to ‘identify[ ] a
particular [unrelated] factor (or factors) and present [ ] sufficient evidence to
establish that it was the sole substantial factor in bringing about the injury.’ Id. at
1354 (emphasis added). In order to prevail, therefore, the respondent must
‘exclude[ ] the vaccine as a substantial factor.’
Id. Stone went on to observe that “[t]he difference between “substantial factor” and “sole
substantial factor” is a meaningful one,” noting that compensation could still be awarded even in
cases where a factor unrelated had been shown to be substantial—but not “solely” substantial.
Stone, 95 F.3d at 237 n.5 (citations omitted). This, in effect, describes what is sometimes referred
to as a “Shyface analysis”—where two factors, including vaccination, are deemed potentially
causal, but one cannot be found to predominate over the other. Shyface v. Sec'y of Health & Hum.
Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999).
In applying this standard, then, to the question of whether a factor unrelated explains an
injury, special masters must conclude that the factor unrelated was the “sole substantial factor”—
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although in so doing, the evidence deemed sufficient to reach that conclusion must only be
preponderant, allowing the determination that it is “more likely than not” the factor unrelated was
the sole substantial factor. That, in turn, leaves room for doubt (just as there is doubt in any
preponderant determination that barely crosses the preponderant line). Thus, a finding that the
vaccine has been excluded must only cross the “more likely than not” line, even if Respondent
bears this obligation when petitioners never do. In practice, special masters have found the factor
unrelated burden met by Respondent based on the same mix of evidence and weighing of items of
literature versus expert testimony that they encounter when considering Petitioner’s obligations.15
Importantly for present purposes, the strength of a claimant’s prong one showing does not
per se make it less likely that the proposed factor unrelated was not the sole substantial factor
(although the evidence offered pro and con must still be weighed, and therefore evidence relevant
to a claimant’s initial showing will in many cases get additional airing while performing the
burden-shifted analysis). And I am aware of no case law suggesting that once a claimant offers
preponderant evidence sufficient to meet the Table elements for a claim, that showing somehow
disadvantages Respondent in attempting to prove factor unrelated. The concession of causation
implicit in a Table claim does not mean the relevant vaccine can be assumed to have played some
role in causation, regardless of the role the factor unrelated is demonstrated to have played.
B. Nature of CMV Infection
CMV is a herpes virus with an estimated seroprevalence of 45%-100% in the general,
worldwide population. R. Lachmann et al., Cytomegalovirus (CMV) Seroprevalence in the Adult
Population of Germany, 13 PLOS One 1,1 (2018), filed as Ex. 51 (ECF No. 49-14) (“Lachmann”).
Primary CMV infection usually occurs during childhood and early adolescence, after which the
virus establishes a latent phase mainly within leukocytes. Al-Omari at 1. Transmission of the virus
can occur through contact with CMV-infected body fluids during primary infection or reactivation.
Lachmann at 1. Although CMV infections are typically asymptomatic in immunocompetent hosts,
they can cause life-threatening complications in immune-compromised individuals. Id.
C. Respondent Has Not Carried his Shifted Burden
The parties’ experts agree that Petitioner tested positive for CMV while being treated for
GBS (even if they disagree as to the precise severity of the infection). They further concur that
GBS frequently is attributable to an antecedent infection. And it is also likely the case – as
preponderantly established by Respondent – that a broad array of infections are more likely
15 To give one example, after remand of the Stone case (where Respondent maintained that a child’s Dravet syndrome
was solely due to a genetic mutation rather than vaccination), the special master was readily able to conclude under
the proper standard that Respondent had met his burden, relying on a showing that included (a) the determination to
give more weight to Respondent’s expert testimony than Petitioner’s, (b) the highly persuasive evidence of the
alternative cause, and (c) an absence of record evidence that the vaccine itself had caused any harm to the child’s brain
(as would needed to have been shown to conclude the vaccine caused injury in accordance with the theory alleged).
Stone v. Sec'y of Health & Hum. Servs., No. 04-1041V, 2011 WL 836992. at *3 (Fed. Cl. Spec. Mstr. Jan. 20, 2011),
mot. for review den’d, 99 Fed. Cl. 187 (2011), aff’d, 676 F.3d 1373 (Fed. Cir. 2012).
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explanatory of GBS than any vaccine. First Collins Rep. at 7. But Respondent must still
demonstrate that in this case, the established CMV infection was itself the sole causal factor of
Petitioner’s GBS.
Respondent has unquestionably succeeded in establishing several disputed issues in his
favor. It has been preponderantly established, for example, that a CMV infection “can cause” GBS.
See e.g., Yuki at 1. I also find persuasive Dr. Collins’s contention that medical science does not
require a CMV infection to be clinically obvious, and/or especially virulent, with unmistakable or
severe symptoms for it to cause GBS. Special masters routinely find a vaccine caused a subsequent
injury based on records containing little to no evidence of any post-vaccination reaction – and it is
therefore just as possible that a latent infection with an almost subclinical course could equally
result in disease later. And correspondingly, the fact that a CMV infection reflects a reactivation,
rather than an acute/initial infectious process, does not undermine the capacity of the infection to
cause GBS.
The parties also disagree as to the relevance of Petitioner’s own infectious severity. And
on this point, the evidence is in equipoise. On the one hand, it cannot be disputed that Petitioner
had no CMV infection symptoms at all before either onset of his GBS or discovery of the infection
through testing. Certainly, it was not a severe infection with obvious manifestations. But the
significance of this fact is unclear. Dr. Collins did persuasively establish that severity of infection
is not a prerequisite to GBS’s development – and she also successfully demonstrated that the risk
from a merely reactivated infection was not necessarily less than that from a primary infection. At
the same time, Petitioner’s infectious work-up did not deem the infection particularly significant
– although that work-up was clearly cursory and did not at all delve into the possible relationship
between the infection and Petitioner’s GBS.
Ultimately, I do not accept Petitioner’s effort to give great weight to the severity of the
infection in resolving whether the infection could have caused his GBS. But I nevertheless still do
not find Respondent has carried his “factor unrelated” burden – despite his other successes. For on
this record, I cannot conclude that preponderant evidence establishes that Petitioner’s CMV
infection likely “did cause” his GBS – the second Althen prong (which applies when evaluating
Respondent’s factor unrelated showing). See Knudsen, 35 F.3d at 549.
The record simply does not reveal enough about Petitioner’s personal health circumstances
to conclude that the discovered CMV infection likely was the reason he developed GBS – even if
in most cases such an infection would have more explanatory value than receipt of the flu vaccine.
Even if I ignore the question of infectious severity, there is nothing from the medical record that
suggests in this context that the infection was causal. Rather, the record presents evidence that an
infection (which may or may not have existed at the time of vaccination, or began after, or reflected
an unexplained reactivation) merely existed. I fully accept Respondent’s contention that a CMV
infection could cause GBS generally, and even that it is more likely to result in GBS than a flu
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vaccine. But I would require additional corroborative proof to find that in this case, it did so – and
that evidence is lacking.
Dr. Collins’s careful reading of the testing results does not change my analysis. All she has
done is show results – the liver functioning or lymphocyte – corroborating the CMV infection.
This does not make it more likely the infection did cause GBS (even if some items of literature
show instances in which it was determined that a CMV infection likely caused GBS because of
the results of those tests). Simply because the infection was present around the time of Petitioner’s
onset does not support the conclusion that it also likely caused those initial GBS-oriented
symptoms as well. And her arguments about the significance of certain results, or Petitioner’s
clinical manifestations and what they say about the best explanation for Petitioner’s GBS, were
ultimately unavailing.
In finding as I have, I stress the fact that the medical record does not allow me to conclude
it “more likely than not” that the CMV infection explains Petitioner’s GBS. In effect, Respondent
is arguing that the established fact of the infection, and its high association with GBS when
compared to the flu vaccine, makes it the “only” possible cause. But I routinely reject that kind of
logic when offered by petitioners in causation-in-fact cases, where the burden has not shifted.
Thus, a silent or incomplete record that shows no evidence of a vaccine reaction, or other
testing results consistent with some vaccine-associated process, can result in denial of entitlement
on the second Althen prong. See, e.g., Bender v. Sec'y of Health & Hum. Servs., No. 11-693V,
2018 WL 3679637, at *34-35 (Fed. Cl. Spec. Mstr. July 2, 2018) (record did not support finding
that a Hepatitis A vaccine did cause a claimant’s TM, given absence of proof of record
corroboration of vaccine-instigated process), mot. for review den’d, 141 Fed. Cl. 262 (2019).
Indeed, I frequently call petitioners and their experts to task for assuming that the required “logical
sequence of cause and effect” is demonstrated merely by the temporal association between a
vaccine’s administration and subsequent illness or other injury. See e.g., M.R. v. Sec'y of Health &
Hum. Servs., No. 16-1024V, 2023 WL 4936727, at *34 (Fed. Cl. Spec. Mstr. June 30, 2023) (“At
bottom, the ‘best’ evidence of a vaccine-injury association that can be mustered is the fact that [the
injury] occurred within a week of vaccination. But without other proof, that kind of temporal
showing is not and has never been enough of a basis for a favorable entitlement decision” (citing
Grant, 956 F.2d at 1148)). Claimants do not get to breeze past Althen prong two once they show
a vaccine could be causal of a specific injury.
I have also found for Respondent in cases involving the factor unrelated analysis – but
those results underscore what is absent in this case. See, e.g., White v. Sec'y of Health & Hum.
Servs., No. 20-1319V, 2023 WL 4204568 (Fed. Cl. Spec. Mstr. June 2, 2023), mot. for review
den’d, 168 Fed. Cl. 660 (2023), appeal docketed, No. 24-1372 (Fed Cir. Jan. 23, 2024). In White,
as here, I determined that the Table elements of a claim for GBS after receipt of the flu vaccine
had been met – leading Respondent to attempt to carry his shifted, “factor unrelated” burden.
White, 2023 WL 4204568, at *15. The record in White also revealed that the claimant had an
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obvious H. influenzae infection16 that could have been causal. Id. at *17. But that infection not
only required treatment due to its virulence, but could be shown as having begun after vaccination
while also closer in time to Petitioner’s GBS onset. Id. at *18. Here, by contrast, I cannot ascertain
when Petitioner’s CMV infection began – and even if a reactivated infection can still cause GBS
(something I find Respondent did establish), I am unable to find the infection was primary or
reactivated. In addition, treaters in White agreed the infection was a good etiologic explanation for
his injury. Id. at *17. Such facts relevant to the prong two analysis are absent in this case.
The foregoing is not impacted by Respondent’s strong success in associating the CMV
infection with GBS. This is because a claimant’s obligation to submit sufficient preponderant
evidence on the “did cause” Althen prong cannot be ignored or deemed subsumed within a
claimant’s success on the first prong. The same is true for the parties’ debate over the relative risks
of vaccination versus a CMV infection. Respondent has shown not only that infections in most
cases are better associated with GBS than vaccination, but also that a CMV infection is itself a risk
factor for GBS. See e.g., Yuki at 1 (“Cytomegalovirus is the most common viral antecedent
infection [to GBS]”). But this does not mean that when both factors are present, that the better-
associated cause was the likely, or sole, cause. Shyface itself rejects that reasoning, allowing for
the possibility that a vaccine could always be an important causal factor even if another causal
factor exists, and/or is more likely causal in most circumstances. Shyface, 165 F.3d at 1353. That
determination does not depend on absolute causal risks, outside the context of the facts of a specific
case.17 Rather, the medical record relevant to a claimant’s unique circumstances bears heavily on
resolution of the question – and here, that record is too silent on the actual likely cause of
Petitioner’s GBS to conclude it could only have been the infection.
This case also does not turn on which expert was more persuasive overall, or whose
marshalling of the evidence was the most successful. Dr. Collins made many effective and
persuasive contentions about the CMV infection and its general association with GBS. Dr.
Kelesidis, by contrast, strained to demonstrate the comparative risk of the flu vaccine as equivalent,
and did not otherwise undermine Respondent’s contentions that a CMV infection could cause GBS
even if the infection was only a reactivation. But I simply cannot discern on this record that the
CMV infection “more likely than not” caused Petitioner’s GBS. The propensity of the flu vaccine
to cause GBS really does not weigh one way or another on this determination.
16 In White, the severity of the infection, and obvious evidence of its clinical presence, proved particularly relevant –
and this, coupled with the fact that the infection was (all things being equal) more likely to cause GBS, resulted in a
factor unrelated finding for Respondent. Here, as noted above, I do not give great weight to the absence of clinical
evidence of a CMV infection (and it certainly does not suggest a CMV infection is less likely to cause GBS if the
infection is not active or virulent). But it remains the case that the lack of objective evidence of the infection’s impact
on Petitioner bears somewhat on analysis for the second Althen prong.
17 Indeed, in almost any vaccine injury case, it is far more likely other factors can cause an injury in question than the
vaccination the claimant received. But just as the general safety of vaccines for most of the population is not relevant
to whether a specific claimant was harmed, the low likelihood of a vaccine causing the injury in absolute terms – and
when compared to other known causes – does not mean it could not have caused the injury to the specific claimant.
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In the end, Respondent did not fail in proving factor unrelated because he could not exclude
the vaccine as causal. I do not even reach that question herein – and the existence of the Table
claim of GBS after receipt of the flu vaccine does not mean that in every case where such a vaccine
has been administered, the flu vaccine should be assumed to have played some role in causing
GBS subsequent to it. Rather, Respondent’s inability to prove that CMV in this case “did cause”
Petitioner’s GBS was dispositive.18
CONCLUSION
Petitioner has prevailed in his Table claim. A damages order will follow this Decision.
IT IS SO ORDERED.
/s/ Brian H. Corcoran
Brian H. Corcoran
Chief Special Master
18 Admittedly, this matter presents a very close evidentiary determination, with evidence pro and con on the disputed
“did cause” element. In such circumstances, Program case law counsels deciding the issue in a petitioner’s favor.
Althen, 418 F.3d at 1280. Even though a CMV infection clearly can cause GBS – and likely does so far more often
than the flu vaccine – I cannot find sufficient evidence that it likely did so here, given the ambiguous nature of the
demonstrated infection and its impact on Petitioner’s health.
31

================================================================================
DOCUMENT 2: USCOURTS-cofc-1_22-vv-00335-1
Date issued/filed: 2025-08-08
Pages: 9
Docket text: PUBLIC DECISION (Originally filed: 07/08/2025) regarding 64 DECISION of Special Master Signed by Chief Special Master Brian H. Corcoran. (ppa) Service on parties made.
--------------------------------------------------------------------------------
Case 1:22-vv-00335-UNJ Document 68 Filed 08/08/25 Page 1 of 9
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 22-335V
* * * * * * * * * * * * * * * * * * * * * * * * *
CHARLES TAYLOR, * Chief Special Master Corcoran
*
Petitioner, * Filed: July 8, 2025
*
v. *
*
SECRETARY OF HEALTH AND *
HUMAN SERVICES, *
*
Respondent. *
*
* * * * * * * * * * * * * * * * * * * * * * * * *
Elizabeth K. Abramson, mctlaw, Washington, DC, for Petitioner.
Emily Hanson, U.S. Dep’t of Justice, Washington, DC, for Respondent.
DAMAGES DECISION1
On April 4, 2021, Charles Taylor filed a petition for compensation under the National
Vaccine Injury Compensation Program (the “Vaccine Program”).2 Petitioner alleged his receipt of
an influenza (“flu”) vaccine on October 5, 2020, caused him to suffer Guillain-Barré syndrome
(“GBS”). Petition (ECF No. 1) at 5. I ruled on the record for entitlement in Petitioner’s favor. See
Ruling on Entitlement, filed Mar. 25, 2025 (ECF No. 56) (“Entitlement Ruling”).
The parties were unable to resolve damages on their own and have therefore submitted
their dispute to me for resolution (which solely involves the magnitude of the actual pain and
suffering award). See Petitioner’s Brief, filed Apr. 4, 2025 (ECF No. 59) (“Br.”); 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 § 300aa of the Act (but will omit that statutory prefix).

Case 1:22-vv-00335-UNJ Document 68 Filed 08/08/25 Page 2 of 9
Opposition, filed Apr. 14, 2025 (ECF No. 60) (“Opp.”); Petitioner’s Reply, filed Apr. 15, 2025
(ECF No. 61) (“Reply”).
For the reasons set forth in greater detail below, I find that Petitioner is entitled to an
award of damages in the amount of $130,000.00 for actual pain and suffering.
I. Factual Background
A more complete summary of the relevant medical history and factual background is
contained in my Entitlement Ruling, and is incorporated by reference herein. See generally
Entitlement Ruling at 2–5.
In short, Petitioner received the subject flu vaccine on October 5, 2020. Ex. 1 at 1. A week
later, he sought treatment for left shoulder pain which he attributed to working on his cabin. He
was diagnosed with tendonitis, treated, and discharged. Ex. 5 at 5–10. Then, on October 15, 2020,
Petitioner presented to his primary care provider at the Columbia University Student Health Center
with “fatigue, headaches, tingling in his hands, feet, and mouth, and generalized weakness.” Ex. 2
at 43.
The next day (specifically the evening of October 16, 2020) Petitioner reported to the
emergency room with increased shoulder pain and range of motion issues, which were then
attributed to Petitioner lifting his young daughter and doing heavy chores. Ex. 3 at 7–8. An exam
revealed no neurological concerns, and he was diagnosed with a rotator cuff injury and given a
steroid shot. Id. at 8, 18. His shoulder pain continued, however, and he began to experience other
possibly neurologic symptoms. On October 19, 2020, Petitioner contacted his PCP regarding his
previously reported hand and feet paresthesia, worsening weakness, and difficulty climbing stairs
and getting out of bed. Ex. 2 at 27, 30, 33. Petitioner himself questioned whether these symptoms
were rooted in a neurologic issue. Id. at 33.
On October 21, 2020, Petitioner went to the emergency department of New York
Presbyterian Hospital complaining of pain and weakness in his arms and neck, tingling in his hands
and feet, and leg weakness that inhibited his movement. Ex. 4 at 35. He was admitted for further
evaluation. Id. While in the ER, Petitioner fell to the floor and remained prone until he was found
by treaters, leading them to designate him as a fall risk. Id. at 38. An initial neurology assessment
noted that he had begun to experience right shoulder pain comparable to that in his left shoulder.
Id. at 69. A neurologist confirmed diminished strength, reflexes, and gait abnormalities. Id. at 70–
71.
During a more comprehensive neurologic exam on October 22, 2020, Petitioner’s treating
neurologists noted the progression of his paresthesias from fingertips and toes upwards, his
temperature regulation difficulties, and excessive fatigue. Ex. 4 at 39. While Petitioner had
previously experienced episodes of “excruciating back pain” and had reported several tick bites in
2020, he denied any pre-onset illness or infections. Id. at 39–40. A lumbar puncture and
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cerebrospinal fluid analysis performed on October 22 revealed elevated proteins consistent with
GBS, and an electromyogram (“EMG”) and nerve conduction study were also consistent with
(though not specific for) GBS. Id. at 45, 28. While testing revealed the presence of an active CMV
infection, the infectious disease team opined that the infection was a latent reactivation and
secondary to Petitioner’s GBS. Id. at 49.
Petitioner began a three-day course of intravenous immunoglobulin (“IVIg”) and
neuropathic pain medications. Ex. 4 at 38, 158. He was discharged on October 25, 2020, with a
diagnosis of GBS “likely in the setting of recent flu vaccine.” Id. at 47, 49. He continued to
experience common post-treatment GBS sequelae and made slow progress in recovery. Ex. 2 at
15, 19. By February 2021, Petitioner was still experiencing some range of motion limitations,
weakness, and numbness, and was advised to expect symptoms to linger for six months or so from
onset (meaning through spring 2021). Ex. 2 at 11–12. By April 2021, Petitioner felt he was “about
70% back to baseline.” Ex. 4 at 12. He has since continued to bear the diagnosis of GBS, AIDP
(acute inflammatory demyelinating polyneuropathy) variant. Id. at 25.
II. Parties’ Arguments
As noted, the sole damages component in dispute is actual pain and suffering. Petitioner seeks
$150,000.00, while Respondent argues for the lesser sum of $90,000.00.
Petitioner
Petitioner notes that he began experiencing symptoms such as “headaches, numbness and
tingling, weakness, and fatigue” within two weeks of his vaccination. Br. at 14 (citing Ex. 2 at 27,
43). Over the course of his five-day hospitalization, Petitioner underwent an MRI, lumbar
puncture, electrodiagnostic studies, and three IVIg treatments. Id. Though he did not require
inpatient or outpatient physical therapy, Petitioner did experience residual GBS symptoms for six
months after his vaccination, including “weakness, discomfort, fatigue, and reduced endurance.”
Id.
To support his proposed demand, Petitioner offers two comparable cases where claimants
received pain and suffering awards of $160,000.00. See generally Gross v. Sec'y of Health & Hum.
Servs., No. 19-0835V, 2021 WL 2666685 (Fed. Cl. Spec. Mstr. March 11, 2021); Robinson v.
Sec'y of Health & Hum. Servs., No. 18-0088V, 2020 WL 5820967 (Fed. Cl. Spec. Mstr. Aug. 27,
2020). The petitioner in Gross was diagnosed with GBS and required a five-day hospitalization
with a five-day course of IVIg treatment, an EMG, and a lumbar puncture, though she declined
outpatient physical therapy. Gross, 2021 WL 2666685 at *4. That individual continued to
experience “numbness, tingling, and difficulty with balance” for several months, though treaters
were unable to conclusively rule out her preexisting conditions as the cause of the sequelae. Id.
The Robinson petitioner required a six-day hospitalization involving an MRI, CT scan, two lumbar
punctures, a five-day course of IVIg, and twenty outpatient physical therapy sessions to treat her
GBS. Robinson, 2020 WL 5820967 at *2–3. She was able to return to work three months after the
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onset of her symptoms and experienced few symptoms thereafter, though her hospitalization and
recovery interfered with her ability to care for her young children. Id. at *6.
Petitioner suggests that his case resembles those of the referenced petitioners, noting that
they all underwent MRIs, lumbar punctures, electrodiagnostic testing, and courses of IVIg. Br. at
14–15. He posits that his course of treatment was more similar to that of the Gross petitioner (five-
day hospitalization, no outpatient physical therapy), but that the duration of his symptoms was
more like the petitioner in Robinson (Petitioner feeling “70% back to baseline” six months post-
onset compared to Robinson’s return to work three months post-onset). Id. at 15. Petitioner
acknowledges that his course of IVIg was shorter than those in either proposed comparable case,
but adds that this is reflected in the lower proposed award. Id.3
In his reply brief, Petitioner criticizes the comparable cases offered by Respondent – in
particular Granville v. Sec'y of Health & Hum. Servs., No. 21-2098V, 2023 WL 6441388 (Fed. Cl.
Spec. Mstr. Aug. 30, 2023). He argues that Granville should not be considered because it was
“predicated on a now withdrawn damages decision.” Reply at 4 (referencing Geschwindner v.
Sec'y of Health & Hum. Servs., No. 17-1558V, 2022 WL 177372 (Fed. Cl. Spec. Mstr. Jan 28,
2022)). Petitioner also argues that his case is more severe than that of the petitioner in Koonce v.
Sec'y of Health & Hum. Servs., No. 21-1560V, 2024 WL 3567368 (Fed. Cl. Spec. Mstr. July 8,
2024) due to Petitioner’s ongoing “substantial weakness,” and that Petitioner’s emotional distress
makes his situation factually distinguishable from both Koonce and Granville. Id. at 7–8.
Respondent
Respondent argues for a lesser award of $90,000.00. Opp. at 1. He maintains that Petitioner
had an “uncomplicated and short course and recovery” from GBS. Id. at 6. Petitioner was
discharged to home after a four-day hospital stay and three-day course of IVIg, and was able to
walk up four flights of stairs to his apartment and even travel from New York to Virginia to visit
family. Id. Respondent distinguishes both Robinson and Gross from the instant case, arguing that
Petitioner’s illness was less severe. Id. at 6–8. The petitioner in Robinson experienced a
“traumatic” hospitalization, enduring severe migraines and painful testing, and a “horrible” return
home that involved three months of leave from work and significant ongoing symptoms. Id. at 7–
8 (citing Robinson, 2020 WL 5820967 at *4. The petitioner in Gross had significant “residual GBS
3 Petitioner also proposes that yet another comparable case establishes a “’floor’ for Program cases involving GBS”
at $130,000.00. Br. at 12 (citing Quirino v. Sec'y of Health & Hum. Servs., No. 17-989V, 2025 WL 407117 (Fed. Cl.
Spec. Mstr. Jan. 8, 2025) at *8). But I do not endorse the idea that any damages determination – including my own –
amounts to binding precedent (as opposed to a practice guideline). Thus, while I have often informed SIRVA claimants
that cases involving surgery will more often than not justify a six-figure pain and suffering award, the individual
circumstances of the case ultimately are what matters. See, e.g., Richardson v. Sec'y of Health & Hum. Servs., No. 20-
0674V, 2023 WL 6180813, at *8 (Fed. Cl. Spec. Mstr. Aug. 16, 2023). Here too, although the alarming nature of GBS
as a vaccine injury justifies a higher-than-usual pain and suffering award, the actual calculation of that award comes
down to the specific circumstances of the case.
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symptoms” that required an increase to her dose of gabapentin. Opp. at 8 (citing Gross, 2021 WL
2666685 at *4).
To support his preferred pain and suffering award, Respondent offers two cases involving
comparably-moderate GBS injuries - Koonce (in which $70,000.00 was awarded) and Granville
($92,500.00). Opp. at 9. The Koonce petitioner was also discharged to home after a “relatively
uncomplicated” hospital stay for GBS (four days in the hospital, lumbar puncture, and IVIg), and
did not attend physical therapy. Opp. at 9 (citing Koonce, 2024 WL 3567368, at *4). And Granville
involved a mild GBS injury that required a five-day hospitalization, a lumbar puncture, five IVIg
treatments, six PT sessions, and one OT evaluation. Granville, 2023 WL 6441388, at *4.
III. Relevant Law
A. General Principles in Calculating a Pain and Suffering Award
Compensation awarded pursuant to the Vaccine Act shall include “[f]or actual and
projected pain and suffering and emotional distress from the vaccine-related injury, and award not
to exceed $250,000.00.” Section 15(a)(4). There is no mathematic formula for assigning a
monetary value to a person’s pain and suffering and emotional distress. I.D. v. Sec’y of Health &
Hum. Servs., No. 04-1593V, 2013 WL 2448125, at *9 (Fed. Cl. Spec. Mstr. May 14, 2013)
(“[a]wards for emotional distress are inherently subjective and cannot be determined by using a
mathematical formula”); Stansfield v. Sec’y of Health & Hum. Servs., No. 93-0172V, 1996 WL
300594, at *3 (Fed. Cl. Spec. Mstr. May 22, 1996) (“the assessment of pain and suffering is
inherently a subjective evaluation”).
Factors to be considered when determining an award for pain and suffering include: 1)
awareness of the injury; 2) severity of the injury; and 3) duration of the suffering. I.D., 2013 WL
2448125, at *9 (citing McAllister v. Sec’y of Health & Hum. Servs., No. 91-1037V, 1993 WL
777030, at *3 (Fed. Cir. 1995)). I may also consider prior pain and suffering awards to aid my
resolution of the appropriate amount of compensation for pain and suffering in this case. See, e.g.,
Doe 34 v. Sec’y of Health & Hum. Servs., 87 Fed. Cl. 758, 768 (2009) (finding that “there is
nothing improper in the chief special master’s decision to refer to damages for pain and suffering
awarded in other cases as an aid in determining the proper amount of damages in this case.”). And
of course, I may rely on my own experience adjudicating similar claims. Hodges v. Sec’y of Health
& Hum. Servs., 9 F.3d 958, 961 (Fed. Cir. 1993) (noting that Congress contemplated that the
special masters would use their accumulated expertise in the field of vaccine injuries to judge the
merits of individual claims.
Although pain and suffering in the past was often determined based on a continuum, that
practice was cast into doubt by a decision from several years ago. Graves v. Sec’y of Health &
Hum. Servs., 109 Fed. Cl. 579 (Fed. Cl. 2013). Graves maintained that to do so resulted in “the
forcing of all suffering awards into a global comparative scale in which the individual petitioner’s
suffering is compared to the most extreme cases and reduced accordingly.” Id. at 590. Instead,
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Graves assessed pain and suffering by looking to the record evidence and prior pain and suffering
awards within the Vaccine Program. Id. at 595. Under this alternative approach, the statutory cap
merely cuts off higher pain and suffering awards—it does not shrink the magnitude of all possible
awards as falling within a spectrum that ends at the cap. Although Graves is not controlling of the
outcome in this case, it provides reasoned guidance in calculating pain and suffering awards.
B. Pain and Suffering Awards in GBS Cases
Table claims alleging GBS after receipt of the flu vaccine are common in the “special
processing unit” (“SPU”)—the process used by OSM for resolving matters it reasonably
anticipates are amenable to fast resolution or settlement. I therefore include herein some discussion
of the kinds of pain and suffering awards obtained in such cases.
As of July 1, 2024, on nearly every occasion that SPU has had to resolve the appropriate
award for GBS pain and suffering (49 cases), over $100,000.00 has been awarded in every case
but one (and there only the slightly lesser sum of $92,500.00 was awarded). The first-quartile value
is $155,000.00, the median is $165,000.00, the third-quartile value is $178,000.00, and the largest
award was $192,500.00. Holmberg v. Sec’y of Health & Hum. Servs., No. 21-1132V, 2024 WL
4607929, at *3–5 (Fed. Cl. Spec. Mstr. Oct. 7, 2024).
A consistent starting consideration in reaching these determinations is that “GBS pain and
suffering awards generally should be higher than those awarded to petitioners who have suffered
a less frightening and physically alarming injury, such as SIRVA.”4 Gross v. Sec’y of Health &
Hum. Servs., No. 19-0835V, 2021 WL 2666685, at *5 (Fed. Cl. Spec. Mstr. Mar. 11, 2021); see
also Castellanos, 2022 WL 1482497, at *10 (emphasizing recognition of “the seriousness of GBS
as a general matter,” in awarding a six-figure sum); Voeller v. Sec’y of Health & Hum. Servs., No.
20-1526V, 2023 WL 5019830, at *10 (Fed. Cl. Spec. Mstr. July 6, 2023) (noting GBS’s
“frightening” nature).
But not every GBS case is equally severe. Further details of the initial medical course are
considered—including any mistake or delay in diagnosing GBS; any in-patient hospitalization
and/or in-patient rehabilitation (and the duration of any such stays); diagnostic procedures (e.g.,
bloodwork, lumbar punctures, electrodiagnostic studies, imaging); the severity of symptoms at
their nadir (e.g., involving incontinence or respiratory failure); the extent and effectiveness of
treatment (e.g., IVIg plasmapheresis, pain medications); other interventions (e.g., feeding tubes,
breathing tubes, catheterization); and any complications (e.g., sepsis during hospitalization).
Also relevant is a petitioner’s long-term course—as evidenced by out-patient therapies,
neurology evaluation, and other medical appointments concerning GBS; the results of repeat
electrodiagnostic studies and other relevant tests; medical providers’ assessments of the degree of
4 Shoulder injury related to vaccine administration (“SIRVA”) is another Table injury. 42 C.F.R. §§ 100.3(a), (c)(10).
6

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recovery achieved; ongoing reliance on assistive devices and medications; and relevant treatment
gaps. Previous opinions have recognized that “a substantial recovery does not mean that [an
individual] has fully recovered from his GBS and has no ongoing sequela. It is common for
petitioners to experience ongoing symptoms of GBS, such as numbness and fatigue, even with a
good recovery.” Elenteny v. Sec’y of Health & Hum. Servs., No. 19-1972V, 2023 WL 2447498, at
*5 (Fed. Cl. Spec. Mstr. Mar. 10, 2023). But symptoms of that nature are typically folded into a
“typical” past pain and suffering award, and will not justify a future component. See, e.g., id.;
Miller v. Sec’y of Health & Hum. Servs., No. 21-1559V, 2023 WL 2474322, at *8 (Fed. Cl. Spec.
Mstr. Feb. 10, 2023).
“The mere fact that a claimant had pre-vaccination comorbidities does not per se diminish
the impact of [the vaccine injury] on his life—especially one as alarming and potentially life-
altering as GBS—and therefore is not alone reason for a lower award.” Bircheat v. Sec’y of Health
& Hum. Servs., No. 19-1088V, 2021 WL 3026880, at *4 (Fed. Cl. Spec. Mstr. June 16, 2021).
However, a special master is statutorily required to consider to what extent a petitioner’s pain and
suffering is truly “from the vaccine-related injury,” Section 15(a)(4) (emphasis added), and nor
from any unrelated preexisting or subsequently-developed medical issues. See, e.g., Bircheat, 2021
WL 3026880, at *4; Gross, 2021 WL 2666685, at *5.
Finally, the injury’s impact on a petitioner’s personal circumstances, including his or her
family and other personal obligations, and professional life (whether or not lost wages are directly
claimed), is properly taken into account as well. All of these factors are primarily gleaned from
the medical records—although sworn statements and/or other evidence may also be considered,
especially if they supplement, and do not contradict, the facts reflected in the medical records.
ANALYSIS
In this case, awareness of the injury is not disputed. The record reflects that at all times
Petitioner was a competent adult with no impairments that would impact his awareness of his
injury. I therefore analyze principally the severity and duration of Petitioner’s injury. In performing
this analysis, I have reviewed the record as a whole, including the medical records, affidavits, and
all assertions made by the parties in written documents and at hearing. I have also considered prior
awards for pain and suffering issued in comparable cases, although I ultimately base my
determination on the circumstances of this case.
The record shows that Petitioner, a 35-year-old graduate student with a history of migraine
headaches and tick bites, presented multiple times between October 12 and October 19, 2020, with
left shoulder pain, followed by “fatigue, headaches, tingling in his hands, feet, and mouth, and
generalized weakness.” Ex. 2 at 43. Each time, testing found no abnormal results and Petitioner
was discharged. Thus, this is not a case in which Petitioner’s suffering was clearly exacerbated by
treatment errors or miscalculations about the nature of his injury. Instead, his progression and
presentation was too nonspecific to identify its exact character.
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On October 21, 2020, Petitioner was admitted to the hospital for a neurological workup.
Ex. 4 at 35. Petitioner was thereafter hospitalized for five days and diagnosed with GBS after
undergoing extensive testing, including a lumbar puncture and EMG/NCV study, and a three-day
course of IVIg treatment that was not repeated later. Id. at 45–49. Petitioner was discharged on
October 25, 2020, with a diagnosis of GBS “likely in the setting of recent flu vaccine” and
prescriptions for gabapentin and Percocet. Ex. 4 at 47, 49; Pet. at 4.
The record further indicates that Petitioner continued to experience common post-treatment
GBS sequelae after returning home (rather than any extreme post-illness sequelae). Ex. 2 at 19.
His recovery progress was, however, relatively slow, and he continued to feel weakness and
numbness and experience a limited range of motion though February 2021. Id. at 11. By April
2021, now six months after vaccination, he reported feeling “about 70% back to baseline.” Ex. 4
at 12. Petitioner claimed that he was abstaining from physical therapy until the COVID-19
pandemic was “more controlled.” Ex. 2 at 12. Petitioner, a graduate student, resigned from his
freelance consulting job due to his inability to keep up with the workload on account of his GBS
sequelae. Ex. 13. He found it difficult to run or to carry his daughter, and managed ongoing pain
with over-the-counter medicines. Ex. 6 at 14.
Based on the foregoing, and considering the parties’ written arguments, I find that
Petitioner suffered a moderate GBS injury—although as a class, GBS injuries are distinguishable
in their nature and overall severity from many other kinds of more discrete or mechanical Program
vaccine injuries. Gross, 2021 WL 2666685, at *5. Petitioner’s personal experience with his injury
justifies a six-figure pain and suffering award, but less than the $150,000.00 requested by
Petitioner.
The comparable pain and suffering determinations offered by Petitioner, while helpful,
reflect distinguishable circumstances in their higher amounts. Gross is difficult to reconcile with
the facts at hand because that petitioner’s more severe ongoing symptoms may have had something
to do with to a preexisting condition (and thus the added suffering that claimant experienced due
to the intervening vaccine injury warranted a higher award). Gross, 2021 WL 2666685 at *5. And
while the Robinson petitioner experienced a similar hospital stay duration, course of IVIg
treatments, and inability to care for her children, her hospitalization was significantly more
traumatic. Robinson, 2020 WL 5820967 at *2–6. That petitioner was in constant agonizing pain
due to her treatments, which included a second lumbar puncture, and attended 20 sessions of
physical therapy after discharge. Id. at *3–4. Mr. Taylor, in contrast, did not attend any physical
therapy after discharge and did not report such excruciating pain. Ex. 2 at 12.
At the same time, Respondent’s recommendation of $90,000.00 is too modest and does not
give sufficient credence to the seriousness of GBS as a general matter, or to the facts of this specific
case. Nor are Respondent’s proposed comparables significantly more useful than what Petitioner
has offered. The Koonce petitioner, for example, experienced a milder case of GBS, featuring
decreased sensation in his extremities but not weakness or difficulty walking like Petitioner. 2024
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WL 356768 at *1. The Koonce petitioner’s GBS had also mostly resolved within a month of his
vaccination, with Mr. Koonce having returned to regular exercises with only complaints of some
numbness in his toes. Id. at *2. In contrast, Petitioner was still experiencing issues with his range
of motion and weakness for more than six months after his vaccination.
The facts of Granville are more consistent with Petitioner’s experience. That petitioner
incurred a five-day hospitalization with five IVIg treatments, a lumbar puncture, and an MRI, after
which she was discharged with some continual numbness and tingling in her hands and feet.
Granville, 2023 WL 6441388 at *3. Her symptoms then continued for about seven months, during
which she returned to work part-time and attended six physical therapy appointments, and she later
represented that she felt “fully recovered” from her GBS. Id. at *3–4.
Granville does support the proposition that not every case of GBS warrants an award of
more than $150,000.00 – especially ones involving a single hospitalization and otherwise short
course. But as Petitioner has noted, the Granville award arose in part because the petitioner therein
relied (as a comparable case) on the amount of the award granted in Geschwindner – a case in
which the pain and suffering award was later increased, to $120,000.00, following a granted
motion to vacate the original judgment due to ineffective assistance of counsel. Geschwindner v.
Sec’y of Health & Hum. Servs., No. 17-1558V, 2024 WL 938952 (Fed. Cl. Spec. Mstr. Feb. 5,
2024). As a result, the precise determination from Granville loses some of its heft as guidance.
Overall, then, I find that the most fair sum to award lies somewhere between Petitioner’s
demand and the corrected amount from Geschwindner. I therefore will award $130,000.00 in
actual pain and suffering in this case.
CONCLUSION
Based on the record as a whole and arguments of the parties, I award Petitioner a lump sum
payment of $130,000.00 for past pain and suffering, to be paid through an ACH deposit to
Petitioner’s counsel’s IOLTA account for prompt disbursement. This amount represents
compensation for all damages that would be available under 42 U.S.C. § 300aa-15(a).
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.5
IT IS SO ORDERED.
/s/ Brian H. Corcoran
Brian H. Corcoran
Chief Special Master
5 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.
9