H.C. v. Secretary of Health and Human Services

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Originally Filed: May 9, 2022
Refiled in Redacted Form: July 20, 2022

* * * * * * * * * * * * * * *
H.C., * PUBLISHED
*
Petitioner, * No. 16-4V
*
v. * Special Master Nora Beth Dorsey
*
SECRETARY OF HEALTH * Entitlement; Influenza (“Flu”) Vaccine;
AND HUMAN SERVICES, * Ramsay Hunt Syndrome.
*
Respondent. *
*
* * * * * * * * * * * * * * *

Robert J. Krakow, Law Office of Robert J. Krakow, P.C., New York, NY, for petitioner.
Colleen Hartley, U.S. Department of Justice, Washington, DC, for respondent.

DECISION1

I. INTRODUCTION

On January 4, 2016, H.C. (“petitioner”) filed a petition under the National Vaccine Injury
Compensation Program (“Vaccine Act” or “the Program”), 42 U.S.C. § 300aa-10 et seq. (2012)2
alleging that as a result of an influenza (“flu”) vaccination on January 4, 2013, petitioner suffered

1
Because this Decision contains a reasoned explanation for the action in this case, the
undersigned is required to post it on the United States Court of Federal Claims’ website in
accordance with the E-Government Act of 2002. 44 U.S.C. § 3501 note (2012) (Federal
Management and Promotion of Electronic Government Services). This means the Decision will
be available to anyone with access to the Internet. In accordance with Vaccine Rule 18(b),
petitioner has 14 days to identify and move to redact medical or other information, the disclosure
of which would constitute an unwarranted invasion of privacy. If, upon review, the undersigned
agrees that the identified material fits within this definition, the undersigned will redact such
material from public access.
2
The National Vaccine Injury Compensation Program is set forth in Part 2 of the National
Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended,
42 U.S.C. §§ 300aa-10 to -34 (2012). All citations in this Decision to individual sections of the
Vaccine Act are to 42 U.S.C. § 300aa.

1
from Ramsay Hunt syndrome.3 Petition at 2-3, 7 (ECF No. 1). Respondent argued against
compensation. Respondent’s Report (“Resp. Rept.”) at 1 (ECF No. 46).

After carefully analyzing and weighing the evidence presented in this case, in accordance
with the applicable legal standards, the undersigned finds petitioner has failed to provide
preponderant evidence that the flu vaccine she received caused her Ramsay Hunt syndrome.
Therefore, this case must be dismissed.

II. ISSUES TO BE DECIDED

The parties agree that petitioner received the flu vaccine on January 4, 2013, that
petitioner was diagnosed with Ramsay Hunt syndrome, and that the condition “results from
reactivation of the varicella zoster virus” (“VZV”). Joint Submission, filed Mar. 9, 2021, at 1-2
(ECF No. 221).

The parties identify three factual issues in dispute: (1) “[t]he cause of petitioner’s
reactivation of Ramsay Hunt syndrome in June 2013 and recurrences thereafter;” (2) “[t]he
timeline for petitioner’s development of [eosinophilic granulomatosis with polyangiitis
(“EGPA”)], and specifically whether petitioner had eosinophilia4 years prior to developing
EGPA (also referred to as Churg-Strauss syndrome),5 which was diagnosed in 2017; and (3)
“[t]he role, if any, [ . . . ] petitioner’s clinical picture.” Joint Submission at 1 (emphasis omitted).
The undersigned’s findings relative to the factual issues are integrated into the causation analysis
portion of this Decision.

Regarding causation, the parties dispute whether the flu vaccine caused petitioner’s
Ramsay Hunt syndrome pursuant to the analysis set forth in Althen v. Secretary of Health &
Human Services, 418 F.3d 1274 (Fed. Cir. 2005). Joint Submission at 2.

Petitioner proffers experts Dr. Scott Zamvil and Dr. M. Eric Gershwin. Petitioner’s Post-
Hearing Submission (“Pet. Post-Hearing Br.”), filed Sept. 9, 2021, at 2, 14 (ECF No. 250). Dr.
Zamvil opines that the petitioner’s flu vaccination caused reactivation of VZV, which triggered

3
Initially, petitioner alleged that she suffered from Bell’s palsy and/or Ramsay Hunt syndrome.
See Petition at 7 (ECF No. 1). Once complete records and expert reports were filed, petitioner
dropped her references to Bell’s palsy, and thus, the relevant diagnosis is Ramsay Hunt
syndrome. See Joint Submission, filed Mar. 9, 2021, at 1 (ECF No. 221). Thus, this Decision
refers only to Ramsay Hunt syndrome.
4
Eosinophilia is “the formation and accumulation of an abnormally large number of eosinophils
in the blood” or “the presence of eosinophils in a location where they are not normally found.”
Eosinophilia, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=16719 (last visited Apr. 14, 2022).
5
Some of the experts and treating physicians used the phrase Churg-Strauss syndrome, which is
the older term for EGPA. Petitioner’s Exhibit (“Pet. Ex.”) 33 at 1. For clarity and consistency,
the undersigned uses the newer reference, EGPA, throughout this Decision.

2
her Ramsay Hunt syndrome. Id. at 14. Dr. Gershwin also opines as to the significance of
petitioner’s EGPA and its relevance to the development of petitioner’s Ramsay Hunt syndrome.
Id. at 22-24. Respondent’s experts, Dr. Vinay Chaudhry and Dr. Arnold I. Levinson, disagree
that the flu vaccine can or did cause reactivation of petitioner’s Ramsay Hunt syndrome. Resp.
Post-Hearing Brief (“Br.”), filed Feb. 3, 2022, at 12-13 (ECF No. 257). Instead, respondent
asserts that petitioner’s Ramsay Hunt syndrome was caused by VZV infection reactivation. Id.

III. PROCEDURAL HISTORY

Petitioner filed a petition on January 4, 2016, along with medical records. Petition; Pet.
Exhibits (“Exs.”) 1-10. Petitioner filed additional medical records from April to August 2016.
Pet. Exs. 11-27. Respondent filed his Rule 4(c) Report on November 14, 2016, arguing against
compensation. Resp. Rept. at 1.

Petitioner filed medical records in March and May 2017 and an expert report from Dr.
Zamvil in September 2017. Pet. Exs. 28-30. On December 29, 2017, respondent filed
responsive expert reports from Drs. Levinson and Chaudhry. Resp. Exs. A, C. Petitioner filed a
responsive expert report from Dr. Zamvil on May 1, 2018 and an expert report from Dr.
Gershwin on May 31, 2018. Pet. Exs. 32-33. Petitioner also filed updated medical records in
July and August 2018. Pet. Exs. 35-36. In August 2018, respondent filed supplemental expert
reports from Dr. Chaudhry and Dr. Levinson. Resp. Exs. E-F.

The undersigned held a Rule 5 conference on September 21, 2018. Rule 5 Order dated
Sept. 21, 2018 (ECF No. 102). She was unable to provide her preliminary opinions, and
requested additional information from the parties. Id. at 1-2. Petitioner filed medical records
and declarations in October and November 2018. Pet. Exs. 37-40. The parties filed
supplemental expert reports from Dr. Levinson, Dr. Chaudhry, Dr. Gershwin, and Dr. Zamvil
from December 2018 to February 2019. Pet. Exs. 41, 43-44; Resp. Exs. G-H.

Petitioner filed updated medical records from June 2019 to November 2019. Pet. Exs.
45-52. During this time, the parties discussed informal resolution and began alternative dispute
resolution (“ADR”) proceedings in December 2019. Order Referring Case to ADR dated Dec.
30, 2019 (ECF No. 173). The case was unsuccessful in ADR and was removed on January 26,
2021. Order Removing Case from the ADR Process dated Jan. 26, 2021 (ECF No. 208).
Thereafter, petitioner filed medical records, medical literature, and photographs, and respondent
filed medical literature and medical literature summaries. Pet. Exs. 54-65; Resp. Exs. I-N.

An entitlement hearing was held on March 23 and 24, 2021. Transcript (“Tr.”) 1, 266.
Petitioner, Dr. Zamvil, Dr. Gershwin, Dr. Chaudhry, and Dr. Levinson testified. Tr. 3, 268.
Post-hearing briefs were ordered. Order dated Apr. 13, 2021 (ECF No. 245). Petitioner filed her
post-hearing brief on September 9, 2021, and respondent filed his responsive post-hearing brief
on February 3, 2022. Pet. Post-Hearing Br.; Resp. Post-Hearing Br. On April 21, 2022,
petitioner filed a reply brief. Pet. Reply to Resp. Post-Hearing Br. (“Pet. Post-Hearing Reply
Br.”), filed Apr. 21, 2022, at 2 (ECF No. 269).

3
 On April 20, 2022, petitioner filed a motion for leave to file a medical article authored by
Anjum et al.6 on the basis that respondent had asserted “petitioner relie[d] ‘upon a single case
report’ to establish causation,” and “[t]hus, [] placed the issue addressed by Anjum directly into
issue.” Pet. Motion for Leave to File Medical Literature - Exhibit 66, filed Apr. 20, 2022, at 1
(ECF No. 266); see also Pet. Ex. 66. Respondent filed his response and objection to the motion
and petitioner filed a reply on April 21, 2022. Resp. Response and Objection to Pet. Motion for
Leave to File New Medical Literature, filed Apr. 21, 2022 (ECF No. 267); Pet. Reply to Resp.
Response and Objection to Pet. Motion for Leave to File Medical Literature – Exhibit 66, filed
Apr. 21, 2022 (ECF No. 268). The undersigned granted petitioner’s motion and respondent filed
his response to the article on April 26, 2022. Order dated Apr. 26, 2022 (ECF No. 270); Resp.
Response to Pet. New Medical Literature, filed Apr. 26, 2022 (ECF No. 271).

This matter is now ripe for adjudication.

IV. MEDICAL TERMINOLOGY

Ramsay Hunt syndrome is a “peripheral facial nerve palsy accompanied by an
erythematous vesicular rash on the ear (zoster oticus) or in the mouth.” Pet. Ex. 30, Reference
(“Ref.”) 9 at 1.7 It is named for the physician who described the condition, Dr. James Ramsay
Hunt. Id. In addition to facial palsy and rash, other signs and symptoms may include “tinnitus,
hearing loss, nausea, vomiting, vertigo, and nystagmus.” Id.

Ramsay Hunt syndrome is caused by the reactivation of VZV. Pet. Ex. 30, Ref. 9 at 1.
“Primary VZV infection usually produces chickenpox after which the virus becomes latent in
neurons of cranial nerve ganglia (including the geniculate ganglia) and dorsal root ganglia along
the entire neuraxis.” Id. at 5. “VZV reactivation . . . occurs more frequently in
immunocompromised persons and in the elderly.” Pet. Ex. 32, Ref. 10 at 7.8 “The molecular
basis of reactivation is not known.” Id.

A similar type of facial paralysis that occurs without the zoster viral rash is Bell’s palsy.9
Pet. Ex. 30, Ref. 9 at 1. In fact, “Ramsay Hunt syndrome may initially be indistinguishable from

6
Rani Lill Anjum et al., Medical Scientists and Philosophers Worldwide Appeal to EMB to
Expand the Notion of ‘Evidence’, 25 EMJ Evidence-Based Med. 6 (2020).
7
C. J. Sweeney & D. H. Gilden, Ramsay Hunt Syndrome, 71 J. Neurology Neurosurgery
Psychiatry 149 (2001).
8
Jeffrey I. Cohen, VZV: Molecular Basis of Persistence (Latency and Reactivation), in Human
Herpesviruses: Biology, Therapy, and Immunoprophylaxis 689 (Ann Arvin et al. eds., 2007).
9
In petitioner’s medical records there are a number of references to Bell’s palsy, instead of
Ramsay Hunt syndrome. However, once petitioner had zoster vesicles noted in her ear, the
records generally reference Ramsay Hunt syndrome. Regardless of the references in petitioner’s
records to Bell’s palsy, her accurate diagnosis was Ramsay Hunt as agreed upon by the parties,
experts, and specialists who provided care to petitioner. See Joint Submission at 1-2.

4
Bell’s palsy,” at least until zoster virus vesicles are noted. Id. Patients with Ramsay Hunt
syndrome, however, usually “have more severe paralysis at onset and are less likely to recover
completely.” Id. Bell’s palsy is not caused by VZV reactivation, but may be “associated with
herpes simplex virus [] infection.” Id.

EGPA “is a multisystem disorder characterized by allergic rhinitis, asthma, and
prominent peripheral blood eosinophilia.” Pet. Ex. 62 at 1.10 It is “classified as a vasculitis of
the small and medium sized arteries, although the vasculitis is often not apparent in the initial
phases of the disease.” Id. The lungs are most commonly involved, but the disease can affect
the skin and other organs, including the heart, kidneys, and central nervous system (“CNS”). Id.
Antineutrophil cytoplasmic antibodies (“ANCA”)11 are found in 40 to 60% of patients. Id. at 2.

“Molecular mimicry is one of the leading mechanisms by which infectious or chemical
agents may induce autoimmunity. It occurs when similarities between foreign and self-peptides
favor an activation of autoreactive T or B cells by a foreign-derived antigen in a susceptible
individual.” Pet. Ex. 55 at 1.12 While “[f]our types of molecular mimicry have been proposed,”
the type most relevant here is “common or similar amino acid sequences or epitopes between the
microorganisms or environmental agent and its host.” Id. at 4, 4 tbl.1. An example is the shared
homology between polysaccharides on the membrane of the bacteria Campylobacter jejuni (“C.
jejuni”) and carbohydrate structures on the myelin sheath of peripheral nerve axons. Id. at 4
tbl.1. Animal studies have shown that “[m]ice inoculated with C. jejuni . . . induce the
development of flaccid limb weakness resembling [Guillain-Barré Syndrome (“GBS”)] and
confirming the role of molecular mimicry in [the] disease.” Id. at 3 fig.1.

V. FACTUAL SUMMARY

A. Summary of Medical Records

1. Pre-Vaccination Records

Petitioner was 38 years old when she received the flu vaccine at issue on January 4, 2013.
Pet. Ex. 1 at 20. Her past medical history was significant for childhood chickenpox, asthma,

10
Talmadge E. King, Epidemiology, Pathogenesis, and Pathology of Eosinophilic
Granulomatosis with Polyangiitis (Churg-Strauss), UpToDate, https://www.uptodate.com/
contents/epidemiology-pathogenesis-and-pathology-of-eosinophilic-granulomatosis-with-
polyangiitis-churg-strauss (last updated May 13, 2020).
11
ANCA is “an autoantibody to cytoplasmic constituents of monocytes and neutrophils, found in
increased amounts in some types of vasculitis. There are several different subtypes, each
characterized serologically by reactivity against particular cellular antigens; some are specific to
given disease states.” Antineutrophil Cytoplasmic Autoantibody, Dorland’s Med. Dictionary
Online, https://www.dorlandsonline.com/dorland/definition?id=59689 (last visited Apr. 14,
2022).
12
Manuel Rojas et al., Molecular Mimicry and Autoimmunity, 98 J. Autoimmunity 100 (2018).

5
mitral valve prolapse, acute ear pain and left otitis media on July 27, 2011, ear pain and right
acute otitis externa on August 6, 2012, acute pharyngitis, right anterior cruciate ligament tear in
the knee with surgery, and a C-section. Pet. Ex. 2 at 59, 63, 75, 78, 82; Pet. Ex. 7 at 4; Pet. Ex. 8
at 4; Pet. Ex. 12 at 5-7; Pet. Ex. 13 at 3; Pet. Ex. 18 at 1.

Of note, petitioner’s family history was significant for Bell’s palsy and autoimmune
illnesses. Petitioner’s father had Bell’s palsy (three times) and multiple myeloma. Pet. Ex. 18 at
2. She had a sister who also had Bell’s palsy, and another sister with diabetes and Crohn’s
disease. Id.; Pet. Ex. 35 at 25. Her mother had arthritis, which began when she was young, and
chronic Epstein Barr virus. Pet. Ex. 35 at 25.

Records dating back to 2010 note petitioner’s history of asthma. See Pet. Ex. 13. In
August 2010, petitioner had an upper respiratory infection with shortness of breath. Id. at 3, 5.
She was prescribed Albuterol, in addition to the Fluticasone (Advair Diskus) and Singulair she
was already prescribed. Id. at 4. In December 2010, she again had an upper respiratory
infection, and reported having very bad allergies. Id. at 7-8. Her asthma medications were
continued. Id. at 9. On January 18, 2011, she had fever, nasal congestion, and wheezing. Id. at
10. She was noted to be taking her asthma medication on a regular basis. Id. at 11. She tested
positive for flu A. Id. at 12-13. On March 31, 2011, petitioner’s medical records documented
that she was taking her asthma medication regularly, and was seeing an ear nose and throat
(“ENT”) physician for “chronic nasal congestion.” Id. at 14. Blood work drawn on March 31,
2011, revealed elevated eosinophils of 11% (range 0.0-5.0%). Id. at 20.

2. Post-Vaccination Records13

On January 10, 2013, about six days after her vaccination, petitioner developed left-sided
facial numbness. Pet. Ex. 2 at 39. She sought treatment at Urgent Care, where she was noted to
have subjective left-sided facial paresthesia and mild left-sided facial drooping. Id. at 41. A
head computerized tomography (“CT”) scan showed moderately severe opacification of the right
sphenoid sinus, with possible sinusitis. Id. at 87. Petitioner was diagnosed with Bell’s palsy,
and treatment was initiated with steroids, eye drops, and Valtrex. Id. at 42.

Petitioner returned to Urgent Care on January 13, 2013 with complaints of facial pain,
and was prescribed Percocet. Pet. Ex. 2 at 31, 35. Her diagnosis remained Bell’s palsy. Id. at
35. The next day, January 14, 2013, petitioner saw neurologist, Dr. Naomi T. Feuer. Pet. Ex. 6
at 11.14 Physical examination revealed complete left-sided facial weakness and two vesicles
were present in the left ear. Id. Due to the presence of zoster vesicles in her ear, petitioner’s

13
From 2013 forward, petitioner was seen by numerous physicians, and had repeated and
frequent laboratory and diagnostic testing and treatment, including numerous surgical
procedures. This summary includes relevant portions of her diagnostic studies and medical care
but is not exhaustive.
14
This record is from a visit with Dr. Feuer on August 28, 2013, but it contains notes from
petitioner’s prior visits with Dr. Feuer. See Pet. Ex. 6 at 11-13. It does not appear that full
records from visits prior to August 28, 2013 were filed.

6
diagnosis was changed to Ramsay Hunt syndrome. Id. Magnetic resonance imaging (“MRI”)
showed abnormal enhancement of the left facial nerve, consistent with her diagnosis. Id.

Subsequently, on January 16, 2013, petitioner was seen by neuro-ophthalmologist, Dr.
Cristiano Oliveira. Pet. Ex. 8 at 2. Examination revealed that petitioner was unable to close her
left eye with mild keratopathy in the left eye, but she had normal visual function. Id. at 7. Eye
drops and gabapentin were prescribed, and follow up with a corneal specialist was
recommended. Id. Petitioner was seen by Dr. Kevin Brown on January 17, 2013. Pet. Ex. 24 at
5. He confirmed the diagnosis of Ramsay Hunt syndrome, noted sensorineural hearing loss,
prescribed continuing steroid treatment, and recommended a repeat MRI. Id. at 6-7. The MRI
was performed on January 28, 2013, and it again showed abnormal enhancement of the facial
nerve. Pet. Ex. 6 at 38. Petitioner returned to Urgent Care on January 30, 2013 for sore throat,
headache, and earache. Pet. Ex. 2 at 16. She was given an antibiotic, Zithromax, and Percocet
for pain. Id. at 20. An audiogram performed on January 31, 2013 showed sensorineural hearing
loss in the left ear. Pet. Ex. 24 at 16.

On February 7, 2013, Dr. David M. Simpson diagnosed “severe facial paralysis
associated with Ramsay Hunt syndrome.” Pet. Ex. 18 at 2. He found “[v]ertigo and hearing
[symptoms] indicate[d] associated vestibular and auditory [nerve] involvement. MRI show[ed]
facial [nerve] enhancement, [consistent with] inflammation.” Id. Dr. Simpson observed that
petitioner had “received appropriate antiviral and corticosteroid [treatment]” and recommended
vestibular rehabilitation. Id. If she did not improve, facial nerve decompression could be
considered. Id. at 2-3.

On February 11, 2013, petitioner followed up with Dr. Feuer, who observed slight
improvement in petitioner’s facial strength. Pet. Ex. 6 at 11. Electromyography (“EMG”)
performed on February 14, 2013 was consistent with “[s]evere facial neuropathy with marked
axonal loss and denervation change.” Pet. Ex. 18 at 4-5. On February 22, 2013, petitioner was
seen by ophthalmologist Dr. Hilary J. Ronner. Pet. Ex. 3 at 1-2. Petitioner’s visual acuity had
decreased due to keratitis,15 paralytic lagophthalmos,16 and paralytic ectropion.17 Id. at 2-3; Pet.
Ex. 4 at 576. Dr. Ronner recommended procedures to address these problems, and on March 12,

15
Keratitis is “inflammation of the cornea.” Keratitis, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=26834 (last visited Apr. 14, 2022).
16
Lagophthalmos is “a condition in which the eye cannot be completely closed.”
Lagophthalmos, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=27482 (last visited Apr. 14, 2022).
17
Paralytic ectropion is “eversion of the margin of the lower eyelid as a result of paralysis of the
facial nerve, and loss of contractile power of the orbicularis oculi muscle.” Paralytic Ectropion,
Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=
72379 (last visited Apr. 14, 2022).

7
2013, petitioner had a bilateral brow lift, left lid load, and canthoplasty.18 Pet. Ex. 4 at 572, 576-
77.

Petitioner underwent acupuncture treatment in March and April 2013 with limited
improvement. Pet. Ex. 21 at 3-6, 8, 10-11. On March 24, 2013, she had approximately 5% of
movement in her left cheek and mouth, with prognosis for recovery fair to poor. Id. at 5-6. On
March 29, 2013, Dr. Adam R. Stracher documented that “probably avoiding flu vaccine in future
is reasonable.” Pet. Ex. 13 at 23.

On April 8, 2013, petitioner saw Dr. Feuer for follow up. Pet. Ex. 6 at 12. Petitioner
reported that she continued to have dizziness and anxiety, and that she also had agoraphobia and
photophobia. Id. Her medications included Valtrex, Cymbalta, and clonazepam. Id. Blood
work drawn on May 17, 2013 showed elevated eosinophils at 19.3% (range 0-7%) and elevated
absolute eosinophils at 1.2 (range < 0.7). Pet. Ex. 2 at 85.

Petitioner saw Dr. Feuer for follow up on June 20, 2013 with complaints of chronic
bilateral jaw pain and a blister in her right nostril for the past few weeks. Pet. Ex. 6 at 12. MRI
done on June 22, 2013 showed resolution of the left facial nerve enhancement.19 Id. at 42. On
June 27, 2013, petitioner was seen by otolaryngologist Dr. David I. Kutler, who documented that
she had a recurrence of her Ramsay Hunt syndrome, and that her facial nerve paralysis had
worsened. Pet. Ex. 11 at 29-30. Petitioner also had erosion of her nasal vestibule that was
attributed to Afrin and steroid nasal sprays. Id.

In July 2013, petitioner was diagnosed with post-herpetic neuralgia. Pet. Ex. 17 at 6.
She was treated with Norco and gabapentin. Id. She was seen several times in August 2013 with
complaints of facial pain. See Pet. Ex. 22 at 882, 889. She had another recurrence of Ramsay
Hunt documented by Dr. Feuer on August 28, 2013. Pet. Ex. 6 at 13, 16.

Petitioner was seen by her ENT physician, Dr. Joel M. Shugar, on September 19, 2013.
Pet. Ex. 16 at 12. He documented that her right nostril lesion had progressed to involve her right
upper lip. Id. He questioned whether petitioner had an immune deficiency disorder. Id. at 12-
14. Throughout September 2013, petitioner saw many different health care providers for
treatment of her nasal lesion. See, e.g., Pet. Ex. 13 at 27-29; Pet. Ex. 14 at 2. CT performed on
October 8, 2013 revealed a 1.3 cm nasal septal perforation. Pet. Ex. 16 at 31-32. Blood work
reported on October 24, 2013 documented that petitioner had elevated absolute eosinophils,

18
Canthoplasty is “plastic surgery of the medial and/or lateral canthus, especially section of the
lateral canthus to lengthen the palpebral fissure; also the surgical restoration of a defective
canthus.” Canthoplasty, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/
dorland/definition?id=7744 (last visited Apr. 14, 2022).
19
This MRI also showed an abnormality of the parotid gland, which was not related to
petitioner’s Ramsay Hunt syndrome. Pet. Ex. 6 at 42. As that finding is not relevant to this
Decision, it will not be discussed further.

8
Proteinase-3 antibodies, and C-reactive protein (“CRP”).20 Pet. Ex. 7 at 12, 15-16. Nasal biopsy
was performed on October 25, 2013 to “[r]ule out” Wegener’s granulomatosis21 [. . .].22 Pet. Ex.
16 at 39. Pathological diagnosis was “[n]ecrotic material and mucus with [] acute and chronic
inflammation” and “[u]lcerated granulation tissue.” Id.

On October 28, 2013, petitioner was admitted to the Emergency Department of Mount
Sinai Hospital with chief complaint of nasal cellulitis. Pet. Ex. 4 at 455-57. History of present
illness included petitioner’s history of Ramsay Hunt syndrome, a “pseudomonal facial abscess
for 1 mo[nth], [and] possible Weg[e]ner’s [g]ranulomatosis [presenting with] chronic facial
ulceration/abscess to [right] nares.” Id. at 459. Physical examination revealed a large cavitary
lesion with redness and purulent drainage of the right nostril. Id. at 460. She also had left eye
droop. Id. Admitting history was performed by Dr. Geena Varghese, who questioned whether
petitioner had Wegener’s granulomatosis, and noted that ANCA labs would be checked. Id. at
475. Blood work showed elevated eosinophils. Pet. Ex. 16 at 4.

Petitioner was admitted for IV antibiotics and seen by infectious disease specialist, Dr.
Jeffrey Gumprecht. Pet. Ex. 4 at 475. Dr. Gumprecht also questioned whether petitioner had
Wegener’s granulomatosis due to her nasal ulcer. Id. at 476. Petitioner was seen by
rheumatologist, Dr. Mark D. Horowitz on October 29, 2013, and he noted that petitioner’s CT
scan showed a “granulomatous process in [the] nasal septum and pansinusitis.” Id. at 481-82,
502-04. Petitioner was discharged on October 30, 2013, with the plan to have an outpatient
evaluation for Wegener’s granulomatosis. Id. at 483-89.

On November 2, 2013, laboratory results revealed that petitioner had a positive ANCA
screen, with elevated P-ANCA Titer of 1:160 (normal < 1:20) and C-ANCA Titer of 1:40
(normal < 1:20). Pet. Ex. 4 at 499. Comments explaining the results noted that “[t]he P-ANCA
pattern and autoantibodies to myeloperoxidase (MPO) are commonly associated with
microscopic polyangiitis, [and] [EGPA].” Id. Comments for C-ANCA explained that “[t]he C-
ANCA pattern and autoantibodies to Proteinase-3 (PR3) may be seen in most patients with

20
Absolute eosinophils were 1545 (range 15-500 cells/mcL). Pet. Ex. 7 at 12. Proteinase-3 AB
were > 8.0 (range < 1.0 AI). Id. at 15. The lab report states, “Autoantibodies to Proteinase-3 []
are accepted as characteristic for Wegener’s granulomatosis. They are detectable in 95 [percent]
of the histologically proven Wegener’s granulomatosis cases.” Id.
21
Wegener’s granulomatosis, or granulomatosis with polyangiitis, is “a multisystem disease . . .
characterized by necrotizing granulomatous vasculitis involving the upper and lower respiratory
tracts, glomerulonephritis, and variable degrees of the ANCA-associated type of small vessel
vasculitis.” Granulomatosis with Polyangiitis, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=79488 (last visited Apr. 14, 2022). It can
cause “necrotic lesions of the nose and ulcerations in the mouth due to vasculitis of larger
vessels.” Id.
22
[. . .] Potential complications associated with use of [. . .] include neutropenia, agranulocytosis,
arthralgias, . . . and skin necrosis.” Kachui C. Lee et al., Complications Associated with Use of
Levamisole-[. . .].

9
Wegener’s granulomatosis, but also in 30% of patients with microscopic polyangiitis and
[EGPA].” Id.

Blood work drawn on October 28 and November 22, 2013 revealed elevated Proteinase-3
autoantibodies. Pet. Ex. 16 at 1, 8. Comments explained that “[a]utoantibodies to Proteinase-3
(PR3) are accepted as characteristic for Wegener’s granulomatosis. They are detectable in 95
[percent] of the histologically proven Wegener’s granulomatosis cases.” Id. Petitioner’s
absolute eosinophils on November 22, 2013 were high at 718 (range 15-500 cells/mcL). Id. at 5.

On November 5, 2013, petitioner returned to Dr. Gumprecht, who concluded that
petitioner’s nasal breakdown and septal perforation were “[. . .] than Wegener’s
[granulomatosis].” Pet. Ex. 7 at 10. On November 22, 2013, Dr. Horowitz noted petitioner’s
abnormally elevated Proteinase-3 and eosinophils. Pet. Ex. 20 at 13. He documented that [. . .].
Id. Dr. Horowitz opined that the “entire presentation [was] consistent with [. . .] (“CIMDL”)
with secondary elevated antiProteinase-3 antibodies.”23 Id.

Biopsies of the upper lip and nose were done to rule out Wegener’s granulomatosis. Pet.
Ex. 20 at 6. December 3, 2013 pathology report showed “[u]lcerated mucosa with underlying
granulation tissue, skeletal muscle, acute and chronic inflammation with fibrosis, and marked
eosinophilic and histiocytic [] infiltration.” Id. No granulomas24 or vasculitis were seen. Id. A
right nasal cavity biopsy conducted on December 11, 2013 found “[u]lcerated, necrotic
respiratory tissue with granulation tissue and mixed acute and chronic inflammation composed of
predominantly plasma cells and eosinophils.” Pet. Ex. 16 at 77.

In January and June 2014, petitioner had facial reanimation and reconstructive surgical
procedures. Pet. Ex. 4 at 280-86, 410-13. The second of these procedures was followed by an
infection at the site where a tendon was harvested for use in the facial procedure. Pet. Ex. 7 at 4-
5. Petitioner began post-operative occupational therapy in July 2014. Pet. Ex. 27 at 6-7.

In April 2015, petitioner had additional facial reconstructive surgery, followed by Botox
injections for pain and facial spasms from June 2015 through January 2016. Pet. Ex. 4 at 45-47;
Pet. Ex. 26 at 6-9, 22, 31-32, 44-45. On February 22, 2016, petitioner sought treatment for left
ear pain. Pet. Ex. 15 at 36. No vesicles were seen in her left ear canal at that time. Id. at 38.

B. Dr. Arye Rubinstein’s Diagnosis of EGPA

Arye Rubinstein, M.D., Ph.D., is a Professor of Pediatrics, Microbiology, and
Immunology at the Albert Einstein College of Medicine at Montefiore Hospital. Pet. Ex. 28 at 2-
3. Dr. Rubinstein saw petitioner on December 15, 2016. Pet. Ex. 35 at 83. At that time, he

23
The undersigned notes that this record is handwritten and difficult to read.
24
Granuloma is “a small, nodular, delimited aggregation of mononuclear inflammatory cells or a
similar collection of epithelioid cells.” Granuloma, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=20934 (last visited Apr. 14, 2022).
“Some granulomas contain eosinophils and plasma cells . . . .” Id.

10
noted that petitioner’s eosinophilia was resolving. Id. He noted that petitioner’s sister had
eosinophilic esophagitis (“EoE”).25 Id. Dr. Rubinstein questioned whether petitioner had an
autoimmune disorder, noting her family history (sister with diabetes and Crohn’s disease, mother
with arthritis and chronic Epstein Barr virus, and father with multiple myeloma). Id. Based on
petitioner’s positive ANA26 and P-ANCA results, Dr. Rubinstein considered Wegener’s
granulomatosis and EGPA, noting that 50% of EGPA cases have elevated P-ANCA. Id. He
concluded that “[t]aken together[,] the most likely diagnosis is a variant of eosinophilic
granulomatosis.” Id.

After additional testing, Dr. Rubinstein summarized his findings and conclusions in a
“Letter of Medical Necessity” dated February 15, 2017. Pet. Ex. 28. The letter summarizes
petitioner’s past medical history, her evaluation for eosinophilia, and her diagnosis of EGPA.
See id. at 1-2. Dr. Rubinstein’s diagnoses included absence of antibody responses to
polysaccharide antigens,27 EGPA, recurrent shingles, recurrent Staphylococcus and
Pseudomonas infections, urticaria, histaminemia, and history of Ramsay Hunt syndrome. Id. at
1.

Dr. Rubinstein noted that in January 2014, petitioner developed Ramsay Hunt syndrome
on the left side. Pet. Ex. 28 at 1. Subsequently, she had corrective surgeries complicated by
infections and a nasal abscess. Id. She was “found to have [an] elevated [Immunoglobulin E
(“IgE”)][28] to > 18,000 and eosinophilia.” Id. Petitioner’s extensive rheumatology workups
from 2013 to 2015 were negative except for P-ANCA and C-ANCA. Id. She also had elevated
eosinophils at 17% (1,300), IgE was elevated at IU/mL > 5000.0 (range < 100.0), Proteinase-3
(PR3) Antibody Qualitative was positive with results of > 8.0 (range 0.0-0.9), histamine was
8.84 (high), and IL-6 was high at 27 (normal < 1.0). Id. at 1-2.

25
Eosinophilic esophagitis, or EoE, is “inflammation caused by eosinophilic infiltration of the
esophageal mucosa.” Eosinophilic Esophagitis, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=73847 (last visited Apr. 14, 2022). Other
records, including records from Dr. Rubinstein, state that petitioner’s daughter, not her sister, has
EoE. See Pet. Ex. 28 at 2; Pet. Ex. 35 at 25; Pet. Ex. 37 at 4.
26
The undersigned believes Dr. Rubinstein meant to write “ANCA,” and not “ANA.”
27
Specific or selective antibody deficiency (“SAD”) is a disorder that results in “an inability to
produce specific [Immunoglobulin G (“IgG”)] antibodies to polysaccharide antigens.” Tr. 374.
28
Immunoglobulins are “structurally related glycoproteins that function as antibodies.”
Immunoglobulin, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=24894 (last visited Apr. 14, 2022). Immunoglobulin E, or IgE, “has the unique
function of mediating immediate hypersensitivity [] reactions; it binds to specific receptors on
basophils and mast cells and triggers the release of mediators on contact with antigen.” Id.; see
also Peter. J. Delves, Acquired Immunity, Merck Manual, https://www.msdmanuals.com/home/
immune-disorders/biology-of-the-immune-system/acquired-immunity# (last reviewed Sept.
2021) (explaining how IgE antibodies trigger “immediate allergic reactions” when “[bound] to
basophils . . . in the bloodstream and to mast cells in tissues”).

11
 Dr. Rubinstein’s assessment was that petitioner’s “clinical picture [was] consistent with .
. . EGPA.” Pet. Ex. 28 at 2. He noted “[t]he disease usually appears in the 40s-50s.” Id. He
explained that

[EGPA] presents in [three] stages:

The allergic stage is reported by most patients presenting with allergic
rhinitis and asthma. It is followed by the hyper eosinophilia that is often
associated, as reported by [petitioner], with malaise, [fever of unknown origin],
cough, [and] abdominal pain. Many patients also develop high IgE levels by this
time. The vasculitic stage follows later. It is accompanied by severe pulmonary
granulomas, vascular complications with ulcerations, intestinal granulomas[,] and
often peritonitis.

Cytokines participate in this autoimmune process. Patients with [EGPA]
have markedly increased serum levels of interferon alpha and interleukin 2 (IL-2)
TNF-alpha and interleukin 1 beta (IL-1beta) and IL-6. IL-6, which is elevated in
[petitioner], is reported to be an important triggering factor of the autoimmune
process. At the same time IL-6 was shown to trigger mast cell replication, which
may explain the histaminemia in [petitioner].

The Ramsey Hunt syndrome and recurrent shingles may also be due to the
immune activation in [EGPA] leading to persistence of VZV infection and
suggest[ing] caution with immunosuppressive therapy as often used for [EGPA].

The family history of [petitioner], including EoE, Crohn’s disease,
arthritis, multiple myeloma, persisting EBV infection is intriguing.

Id. (emphasis omitted).

Petitioner continued to see Dr. Rubinstein for follow up and treatment of her EGPA with
Cinqair (reslizumab)29 intravenous infusions. See Pet. Exs. 35, 45, 54. On April 10, 2018, she
was noted to be taking levocetirizine for her allergies. Pet. Ex. 35 at 12. The only allergy noted
was to penicillin, which caused hives. Id. Dr. Rubinstein’s assessment was EGPA with lung
involvement (chronic). Id. at 13. At that visit, she received her routine infusion of reslizumab
and she also received the recombinant VZV vaccine. Id. Petitioner had no local reaction to the
vaccine, although she complained of feeling foggy several hours after vaccination. Id. This
problem resolved the next day. Id. At a previous visit, on March 28, 2017, she received the
pneumococcal polysaccharide PPSV23 vaccination. Id. at 59. There is no documentation to
suggest that she had any reaction to that vaccination. See id.

29
Cinqair is given to patients “whose asthma is not controlled with current asthma medicines and
who have high levels of eosinophils” to “reduce[] poorly controlled, severe eosinophilic asthma
symptoms and attacks.” About CINQAIR, Cinqair, https://www.cinqair.com/about-cinqair/ (last
visited Apr. 14, 2022).

12
 C. Petitioner’s Hearing Testimony and Declaration

Prior to January 4, 2013, petitioner was recovering from a knee surgery but was
otherwise in excellent health. Tr. 7. Petitioner explained that in her twenties, she suffered from
exercise-induced asthma when exercising outside, but she stated she never used her inhaler and
was never prescribed any medication for asthma. Tr. 7-8.

On cross-examination, petitioner was questioned about prescriptions for Singulair in
2011 and 2012, Nasonex in 2012, Advair in 2010 and 2011, and Albuterol in 2010. Tr. 63
(citing Pet. Ex. 1 at 30-31, 33-35; Pet. Ex. 13 at 4, 7-8). Petitioner did not dispute receiving
those prescriptions, but explained that “Nasonex [was not] something that [she] would have
taken for asthma,” and “Singulair is not necessarily an asthma medication” and “not something
that [she] would necessarily take for asthma.” Tr. 63-64. Regarding her Albuterol prescription,
she stated she always kept that prescription because that was her rescue inhaler. Tr. 64. And for
Advair, she agreed that it may have been prescribed, but “[t]hat doesn’t mean that [she]
necessarily used it.” Tr. 71.

Petitioner also testified that prior to the vaccination at issue, she had been treated for
allergies, including seasonal allergies, mold, and cats and dogs with fur, with Benadryl, Allegra,
or Claritin. Tr. 8-9. On cross-examination, she clarified that “[she] always had allergies,” but
“[did not] have asthma.” Tr. 65. She speculated that she “could have taken [Singulair] for
allergies, but [she] didn’t have asthma.” Tr. 69.

On August 6, 2012, petitioner stated that she was spending a lot of time in the pool and
developed right ear pain that she thought was swimmer’s ear. Tr. 11. She did not have an
infection and “[did not] believe that [she] was given medication or anything for it.” Id.
Sometime after August 2012, petitioner re-tore her anterior cruciate ligament in her right knee
for which she received surgery for in October 2012 and had physical therapy thereafter. Tr. 12.

After receiving the flu vaccine at issue here on January 4, 2013, petitioner stated that
“[her] legs started shaking” and “[she] felt extremely sick” that night.30 Tr. 14; see also Pet. Ex.
39 at ¶ 6. For the remainder of the weekend, petitioner remained in bed with flu-like symptoms.
Tr. 15. At that time, she had no facial pain or ear pain. Id. On Thursday morning, January 10,
petitioner had difficulty drinking her coffee and noticed “[her] face freeze.” Tr. 17; see also Pet.
Ex. 39 at ¶ 7 (noting the incorrect date of this occurrence). She thought she was having a stroke
and went to the local Urgent Care, where she was told she had Bell’s palsy. Tr. 17-18. She
continued to have difficulty closing her eye, keeping her eye shut, and blinking. Tr. 19-20. A
few days later, on January 13, she woke up with excruciating pain behind her left ear. Tr. 20-21;
see also Pet. Ex. 39 at ¶ 9. She returned to Urgent Care, where vesicles were seen in her ear. Tr.
20. It was recommended that she see a neurologist. Tr. 20-21.

Petitioner saw Dr. Feuer the following day, on January 14, 2013. Tr. 22. At the time of
that visit, petitioner’s “pain was overwhelming” and her “face was completely disfigured.” Id.

30
January 4, 2013 was a Friday.

13
Dr. Feuer saw vesicles in her ear and diagnosed her with Ramsay Hunt syndrome. Id. Petitioner
stated that Dr. Feuer told her it is “probable and likely that [] [petitioner] had a response to the
flu shot.” Id. Thereafter, petitioner saw other specialists, including an ophthalmologist and
audiologist, due to her difficulty closing her eye and ear pain. Tr. 22-23. Her pain with sound
and light continued to worsen, and she developed vertigo. Tr. 24-25. In February 2013,
petitioner continued to see specialists. Tr. 26-29. During this time, “[her] face looked
disfigured, and [she] had difficulty eating, speaking[,] and making normal facial expressions.”
Pet. Ex. 39 at ¶ 11.

In March 2013, she had platinum bars inserted in her eyelids to help with blinking and
eye closure and she had a brow lift to even out her face and help with her vertigo. Tr. 29-30, 34.
Petitioner continued to be in pain and her health was deteriorating. Tr. 35; Pet. Ex. 39 at ¶ 13.
She was on multiple pain medications and nerve blockers, she felt foggy, and she would not eat
or drink. Tr. 35-36; Pet. Ex. 29 at ¶ 14. She was depressed, suicidal, and paranoid. Tr. 36; Pet.
Ex. 39 at ¶¶ 14, 16. She “was not in a very good mental state” and “was [at] the lowest point in
[her] life.” Tr. 40; see also Pet. Ex. 39 at ¶ 14.

In March 2013, either in the weeks before or after her March 2013 facial surgery, [. . .].
Tr. 36-37, 97-101; Pet. Ex. 39 at ¶ 17. She believed she started using Afrin in 2013 to help with
the side effects of [. . .] Ramsay Hunt syndrome. See Tr. 107. From March to June 2013, she
“was still in a tremendous amount [of pain]” and she and her treating physicians could not
manage her pain. Tr. 39. During the summer of 2013, petitioner [. . .] to try prescribed
medications. Tr. 105-06; Pet. Ex. 39 at ¶ 20. By November 2013, before a surgery she had
scheduled, she permanently [. . .]. Tr. 39, 44; Pet. Ex. 39 at ¶¶ 23-24, 27. Prior to the January
2013 flu vaccination, petitioner did not use Afrin [. . .]. Tr. 13; Pet. Ex. 39 at ¶ 18.

Petitioner testified that by 2015, her allergies and asthma became unmanageable. Tr. 49-
50. She began seeing Dr. Rubinstein in 2016 for her allergies, asthma, fatigue, and urticaria. Tr.
48, 51. Dr. Rubinstein diagnosed her with EGPA, and she was given a new inhaler, which she
started using, and a EpiPen. Tr. 52. Since the EGPA diagnosis, her treatment includes Cinqair,
an intravenous medicine administered every three weeks at the hospital, and Hyqvia, a
subcutaneous IVIG plasma therapy she self-administers every two weeks for three hours a day.
Tr. 53.

The January 4, 2013 flu vaccination was not her first flu vaccination. Tr. 78-82.
Petitioner stated that she received a flu vaccine every year, and would normally get flu-like
symptoms for 24 hours after the vaccine. Tr. 57. She testified, however, that the January 2013
flu vaccination was different. Id. She never developed Ramsay Hunt syndrome or Bell’s palsy
after her prior flu vaccinations, but she has been diagnosed with the flu virus. Tr. 82. Petitioner
stated she has not received a flu vaccine since January 2013. Tr. 83. She testified that to her
knowledge, and based on what her treating physicians have told her, “there’s nothing else that . .
. should or could have caused this” other than her flu vaccination on January 4, 2013. Tr. 58.
Since January 2013, she has received shingles and pneumococcal vaccinations. Tr. 85-86.
Additionally, she received Covid-19 vaccines without incidence of Ramsay Hunt syndrome. Tr.
76.

14
 At the time of the hearing in March 2021, petitioner was appreciative that she could “get
up and move [her] body, and that [she was] not in the pain that [she] ha[d] been [in].” Tr. 43.
She still “[could not] drink without a straw[] [or] without things flying out of [her] mouth,” and
“still ha[d] extensive amount[s] of doctors’ visits,” but “[she was] grateful that [she was] able to
get up every day and move [her] body without pain.” Id. She suffers from synkinesis,31 which
she described as her facial nerves “learning to work again[] [but are] rewired the wrong way” so
her “brain tells the nerves to do the wrong thing.” Tr. 46. In addition to the Cinqair and Hyqvia
she received, petitioner takes two Benadryl pills every night and two Allegra pills every
morning. Tr. 53-54.

D. Declaration of Debra Kessler

Debra Kessler is petitioner’s friend. Pet. Ex. 40 at ¶ 1. She has known petitioner for
more than ten years and they used “see[] each other almost every day.” Id. at ¶¶ 2, 7. She has
“witnessed [petitioner’s] deteriorating physical condition” since January 2013. Id. at ¶ 3. Ms.
Kessler found “it difficult to understand [petitioner] when she spoke.” Id. She would often help
petitioner by feeding her and helping with her medications. Id. “[Petitioner] seemed to have lost
all senses and . . . her pain was severe.” Id. at ¶ 4. In July 2013, petitioner told Ms. Kessler [. .
.], but by December 2013, when their families spent the holidays together, petitioner was [. . .].
Id. at ¶¶ 7-8.

VI. EXPERT OPINIONS

A. Petitioner’s Expert, Scott S. Zamvil, M.D., Ph.D.32

1. Background and Qualifications

Dr. Zamvil is a board-certified neurologist with 19 years of experience and is currently
working as a Professor of Neurology at the University of California, San Francisco while
participating in active patient care as a Neurology Attending at University of California, San
Francisco, Moffett-Long Hospitals. Pet. Ex. 30 at 1-2; Pet. Ex. 31 at 1. After receiving his
Ph.D. and M.D. from Stanford Medical School, he completed an internship and residency before
beginning his teaching career at Harvard Medical School. Pet. Ex. 31 at 1. Since then, he has
“cared for hundreds of patients with neuroinflammatory conditions, including . . . acute and
recurrent [CNS] viral infections” such as shingles and Ramsay Hunt syndrome. Pet. Ex. 30 at 1.
Dr. Zamvil has “expertise in molecular mimicry” and focuses his research “on understanding
how antigen-presenting cells (APC) present CNS autoantigens for T cell recognition.” Id. at 2.
Throughout his career, Dr. Zamvil has served on various professional societies and committees
and had authored or co-authored over 150 publications. Pet. Ex. 31 at 2-3, 14-16.

31
Synkinesis is “an unintentional movement accompanying a volitional movement, such as the
facial contortions accompanying severe exertion.” Synkinesis, Dorland’s Med. Dictionary
Online, https://www.dorlandsonline.com/dorland/definition?id=48544 (last visited Apr. 14,
2022).
32
Petitioner filed three expert reports authored by Dr. Zamvil. See Pet. Exs. 30, 32, 44.

15
 2. Opinion

a. Althen Prong One

Dr. Zamvil opined that Ramsay Hunt syndrome is most commonly due to VZV
reactivation. Pet. Ex. 44 at 2. More specifically, he explained that Ramsay Hunt syndrome is
caused by “activation of herpes zoster, which is latent in the geniculate ganglion.” Pet. Ex. 30 at
7. The geniculate ganglion is the sensory ganglion (a group of nerve cell bodies) of the facial
nerve. Ganglion Geniculi Nervi Facialis, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=78055 (last visited Apr. 14, 2022).
Citing Sweeney and Gilden’s review article, Dr. Zamvil stated that VZV, the virus that causes
chickenpox, can remain dormant in the nerve ganglion after active infection. Pet. Ex. 30 at 9
(citing Pet. Ex. 30, Ref. 9 at 5). The virus remains dormant in the nerve until it is reactivated,
which can cause “paralysis of the facial nerve,” known as Ramsay Hunt syndrome. Id. Vesicles
seen in the outer portion of the ear canal can confirm the condition. Pet. Ex. 30, Ref. 9 at 1.

Dr. Zamvil agreed with respondent’s experts that “VZV is a well-documented cause of
Ramsay Hunt syndrome.” Pet. Ex. 32 at 2. He conceded that flu vaccination and wild flu
infection are not commonly known causes of Ramsay Hunt syndrome. Id. Although he agreed
that the flu vaccine is not a commonly known cause, Dr. Zamvil stated that it has been associated
with Ramsay Hunt syndrome. Pet. Ex. 44 at 1. He proffered “[s]everal possible mechanisms”
that could account for the development of petitioner’s initial episode of Ramsay Hunt syndrome
following her flu vaccination. Pet. Ex. 30 at 8. He explained that “[t]hese possibilities are not
mutually exclusive; each one could lead to reactivation of VZV.” Id.

The first “possible” mechanistic theory proposed by Dr. Zamvil is based on molecular
mimicry, specifically that the flu vaccine “could contain protein sequences (epitopes) that are
common with VZV.” Pet. Ex. 30 at 8. “Through molecular mimicry, vaccination with Fluvirin
could lead to a secondary (amplification) T cell or B cell (antibody) immune response in a person
that has had chicken pox.” Id. “T cells and antibodies that enter the geniculate ganglion [could]
cause paradoxical VZV reactivation, leading to facial weakness, pain[,] and vesicle formation.”
Id. Using a BLAST search,33 Dr. Zamvil identified a similar 13 amino acid sequence between
the flu A hemagglutinin in the vaccine and a protein in VZV (envelope glycoprotein H). Id. He
proposed this example of sequence homology as “one possibility” of how molecular mimicry
could occur. Tr. 139, 143.

Dr. Zamvil acknowledged that the finding of similar protein sequences did not “guarantee
T cell or antibody cross reactivity.” Pet. Ex. 30 at 8. After conceding this point, he suggested an
alternate theory, stating “that exposure to one virus can amplify CNS recruitment of CD8+ T

33
A BLAST (Basic Local Alignment Search Tool) search is an unbiased homology search
offered by the National Institute of Health, National Center for Biotechnology Information. Pet.
Ex. 30 at 8; Tr. 144. For a description of Dr. Zamvil’s process for conducting the BLAST
search, see Tr. 144.

16
cells[34] that recognize an unrelated virus, even when the unrelated virus is not detected in the
CNS.” Id. (citing Pet. Ex. 30, Ref. 14 at 1-2).35 Based on this observation, he opined that
“cross-reactivity may not be required” for reactivation to occur. Id. Instead, he testified that a
“virus may activate another virus.” Tr. 141. In support of this alternative idea, Dr. Zamvil
referenced the Matullo et al. paper. See Pet. Ex. 30, Ref. 14.

In Matullo et al., the authors studied “concurrent immune challenges.” Pet. Ex. 30, Ref.
14 at 1. Their “hypothesis [was] that viruses need not replicate in the tissue in which they cause
disease; specifically, [] a peripheral infection might trigger CNS pathology.” Id. In the study,
the CNS of mice were infected with the measles virus and their peripheral systems were infected
with the lymphocytic choriomeningitis virus. Id. They found infection with only one of the
viruses did not cause illness, however, “[c]o-infection resulted in a 12-fold increase in the
number of CD8+ T cells in the brain as compared to measles virus infection alone.” Id. Based
on the study, the authors suggested that the “recruitment of peripherally activated CD8+ T cells
to the CNS can potentiate neuroinflammation.” Id. at 2. The findings “raise[d] the possibility
that concomitant immune challenges may be an important cause of the neuroinflammation of
some human CNS diseases, perhaps accounting for the inability to identify a discrete pathogenic
trigger within affected brain tissues.” Id. They concluded that “a condition that compromises
and activates the blood-brain barrier and adjacent brain [tissue] can render the CNS susceptible
to [a] pathogen-independent immune attack.” Id. at 1. Dr. Zamvil used the study to illustrate the
point that even though the CD8+ T cells did not recognize the virus; they were able to activate
another virus in the CNS. Tr. 166-67.

Dr. Zamvil’s “second possibility” for how the flu vaccine could trigger reactivation of
VZV to cause Ramsay Hunt syndrome was based on “molecular mimicry between Fluvirin and
myelin or neuronal autoantigens.” Pet. Ex. 30 at 10; see also Tr. 139-40. He asserted that
“[h]omologies exist between [flu] A hemagglutinin and contactin-associated protein-1 and
neurofascin, two proteins associated with neuropathy.” Pet. Ex. 30 at 10. He also seemed to
suggest a variation on this theory, hypothesizing that the “[flu] vaccination cause[d] a T cell and
antibody response that elicit[ed] CNS inflammation (i.e. within or near the geniculate ganglion)
that promote[d] reactivation of latent VZV.”36 Id.

34
CD8+ T cells are “T lymphocytes that carry the CD8 antigen.” CD8 Cells, Dorland’s Med.
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=64001 (last visited
Apr. 14, 2022). T lymphocytes are “cells primarily responsible for cell-mediated immunity.” T
Lymphocytes, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=87562 (last visited Apr. 14, 2022). “When activated by antigen, T lymphocytes
proliferate and differentiate into T memory cells and the various types of regulatory and effector
T cells.” Id.
35
Christine M. Matullo et al., NCS Recruitment of CD8+ T Lymphocytes Specific for a
Peripheral Virus Infection Triggers Neuropathogenesis During Polymicrobial Challenge, 7 PLoS
e1002462 (2011).
36
It was not clear whether this variation was part of Dr. Zamvil’s theory based on the Matullo et
al. article, or a different theory.

17
 The third proposed mechanism posited by Dr. Zamvil is based on activation of the innate
immune response, in contrast to his first two theories that implicated the adaptive immune
response. Pet. Ex. 30 at 10. Dr. Zamvil opined that the flu vaccine “may trigger [the] innate
immune master regulator of inflammation, NF-κB.” Id. He explained that “[m]any infectious
organisms activate the immune system through Toll-like receptors (TLRs), a family of proteins
that are expressed on all nucleated cells.” Id. The NF-κB dependent pathway is activated by
TLRs, and is considered to be the “master regulator of inflammation.” Id. This pathway “leads
to production of type I interferon (IFN)-ß, which can have proinflammatory or anti-inflammatory
activities.” Id.; see also Tr. 184. Additionally, Dr. Zamvil stated that innate immune cells also
serve as “antigen presenting cells” that can “direct proinflammatory T cell differentiation.” Pet.
Ex. 30 at 11; see also Tr. 185. Dr. Zamvil explained that in this theory, he does not propose that
the innate immune system exclusively targeted the geniculate ganglion of the facial nerve. Tr.
186-88.

Although Dr. Zamvil stated that he offered three theories, in his reports and at the hearing
he discussed variations of his theories, two of which are described above. An additional
variation on a theory, described by Dr. Zamvil, was how the vaccine can activate an immune
response due to local damage created by the needle tract during vaccination. Tr. 164. This
causes innate cells to be activated, and they make T cells become proinflammatory. Id. The
innate cells make T cells “traffic” into the CNS where they cause myelin destruction.37 Id. The
response is called “epitope spreading.” Tr. 165. Dr. Zamvil also discussed the concept of
“bystander activation.” Tr. 167. He testified that “bystander activation is what leads to the
epitope spreading that can occur.” Id. His testimony on this point was somewhat confusing
because although he discussed the concept of epitope spreading, he also testified that he was not
suggesting that “epitope spreading occurred.” Id.

In support of his opinions that the flu vaccine can trigger reactivation of VZV and
thereafter cause Ramsay Hunt syndrome, Dr. Zamvil cited a 2010 case report by Gurbuz et al.38
See Pet. Ex. 30, Ref. 10. The Gurbuz et al. authors described the clinical course of a 66-year-old
female who presented to a health care provider “with complaints of weakness, running nose,
[and] headache.” Id. at 1. She had received a flu vaccination ten days earlier. Id. Antibiotics
were prescribed. Id. One week later, she had continued to have “dizziness, nausea[,] and
vomiting,” and was admitted to the hospital. Id. On day three of her hospitalization, she had
new symptoms of “hearing loss, earache[,] and itchy and painful vesicles on the right ear [and]
the right side . . . of [her] tongue. Id. Two days later, she had paralysis of the right side of her
face. Id. She was subsequently diagnosed with Ramsay Hunt syndrome. Id.

Gurbuz et al. provided background information about Ramsay Hunt syndrome,
explaining that VZV causes chickenpox, and afterward the “virus resides silent and inactive

37
Again, this aspect of his theory may have been related to Dr. Zamvil’s reliance on the Matullo
et al. article, but it was not entirely clear.
38
Melek Kezban Gurbuz et al., A Case of Ramsay Hunt Syndrome After Inactive Influenza
Vaccine, 6 J. Int’l Advanced Otology 419 (2010).

18
within the [CNS] for long years.” Pet. Ex. 30, Ref. 10 at 3. They noted that “[a]dvanced age,
chronic-systemic diseases, [and] immune deficiency conditions may cause reactivation.” Id.
Importantly, they did not reach any conclusion about whether the flu vaccine played a role in the
cause of the patient’s Ramsay Hunt syndrome. See id. They stated, “[i]n our case,
pathophysiology of [Ramsay Hunt syndrome] after seasonal [flu] vaccine is not clear. There is a
possibility that transient immune-deficient condition just after vaccination might have []
triggered reactivation of the inactive VZV.” Id. They also acknowledged there was no other
similar case of Ramsay Hunt syndrome reported after flu vaccination reported in the literature.
Id. While they questioned whether there was a “transient immune suppression” caused by
vaccination, they concluded that any causal mechanism associating vaccination and Ramsay
Hunt syndrome was “not explainable yet.” Id. The authors did not comment on the significance
of the patient’s symptoms of weakness, runny nose, or headache, for which she was prescribed
antibiotics. See id. at 1-3.

Dr. Zamvil cited a report by Rothova et al.,39 describing a case of reactivated VZV that
caused panuveitis40 following H1N1 flu vaccination. Pet. Ex. 32, Ref. 5 at 1. The authors
reported “a recurrence of bilateral VZV-associated panuveitis following vaccination against flu
H1N1 in a 60-year-old male patient with previous VZV-induced [acute retinal necrosis] after an
interval of 20 years of disease inactivity.” Id. The patient was diagnosed with bilateral
panuveitis seven days after vaccination. Id. Intraocular fluid tested positive for VZV. Id.
However, tests for CD4 and CD8 cells and immunoglobulins revealed normal levels. Id. The
authors suggested a hypothesis of causation which “might have been associated with a
(temporary) decrease in cellular immunity.” Id.

In addition, Dr. Zamvil cited an article by Walter et al.,41 who reported three cases of
reactivation of herpes virus infections after vaccinations. Pet. Ex. 32, Ref. 6 at 1. The first case
involved herpes zoster reactivation of the left T-10 dermatome following hepatitis A vaccine,
with a repeat episode of herpes zoster following the second dose of the hepatitis A vaccine. Id.
The second patient had reactivation of left thoracic herpes zoster after a flu vaccination in 1996.
Id. Of note, the patient had received flu vaccines in the two prior and two subsequent years
without incident. Id. The third patient had herpes zoster reactivation in the trigeminal nerve
after rabies and Japanese encephalitis vaccinations. Id. The authors questioned whether an
immunomodulation or immunosuppressive effect explained a “possible link between vaccination
and reactivation of herpesvirus infections.” Id.

39
Aniki Rothova et al., Reactivation of Acute Retinal Necrosis After Flu H1N1 Vaccination, 95
Brit. J. Ophthalmology 291 (2011).
40
Panuveitis is “inflammation of the entire uveal tract.” Panuveitis, Dorland’s Med. Dictionary
Online, https://www.dorlandsonline.com/dorland/definition?id=36655 (last visited Apr. 14,
2022). Uvea is the “vascular layer of [the] eyeball,” made of the iris, ciliary body, and choroid.
Tunica Vasculosa Bulbi, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/
dorland/definition?id=115933 (last visited Apr. 14, 2022).
41
Roland Walter et al., Reactivation of Herpesvirus Infections After Vaccinations?, 353 Lancet
810 (1999).

19
 On cross-examination, Dr. Zamvil agreed that Ramsay Hunt syndrome is not an
autoimmune disease. Tr. 194-95. He also agreed that there was no case report that established a
causal association between the flu vaccine and Ramsay Hunt syndrome. Tr. 198-99.
Additionally, Dr. Zamvil agreed that “VZV reactivation [] is the cause of Ramsay Hunt
syndrome.” Tr. at 171; see also Pet. Ex. 30 at 7.

b. Althen Prong Two

Regarding Althen Prong Two, a logical sequence of cause and effect, Dr. Zamvil stated
that petitioner “had latent herpes zoster in her geniculate ganglion.” Pet. Ex. 30 at 12. He
opined that the flu vaccine “trigger[ed] an adaptive immune response to [flu] determinants that
[led] to reactivation of VZV, likely by cross-reactivity to shared determinants with VZV, myelin
proteins[,] or axonal proteins.” Id. Alternatively, he opined that the flu vaccine “activate[d] an
innate immune response driven by NF-κB that [led] to damage in the geniculate ganglion.
Cytokines activate[d] the type 1 interferon pathway, which can also lead to transcription of genes
that activate herpes zoster.” Id. He found “[t]his sequence of events culminate[d] in an outbreak
of shingles in the facial nerve with paralysis and pain.” Id.

Petitioner had a number of recurrences of Ramsay Hunt syndrome that were not
temporally associated with her flu vaccination. Regarding her subsequent recurrences, Dr.
Zamvil made it clear that he “did not claim that there was a direct association between
[petitioner’s] January 4, 2013[] vaccination” and her recurrences of Ramsay Hunt syndrome.
Pet. Ex. 32 at 1. However, he believed “it [was] likely that once triggered by her [] 2013[] [flu]
vaccination, [petitioner] experienced increased susceptibility to VZV reactivation due to other
stressors.” Id.

Dr. Zamvil disagreed with respondent’s expert, Dr. Chaudhry, who opined that
petitioner’s VZV reactivation was caused by an altered immune competence related to pre-
existing EGPA. Pet. Ex. 32 at 3. Dr. Zamvil opined that there was “no significant evidence”
that petitioner’s eosinophilic illness pre-dated her January 4, 2013 vaccination. Id. While “[s]he
had eosinophilia, [and] high proteinase-3 Ab and CRP, [] her biopsy did not show
granulomatosis or polyangiitis to support diagnoses of Wegener’s [granulomatosis] or [EGPA].”
Pet. Ex. 30 at 12. Therefore, Dr. Zamvil did not consider an eosinophilic illness or EGPA to be
potential causes of petitioner’s Ramsay Hunt syndrome. See id. Moreover, Dr. Zamvil did not
believe that petitioner had any pre-exiting condition that contributed to her Ramsay Hunt
syndrome. Tr. 177-78.

Additionally, Dr. Zamvil did not believe that petitioner’s initial episode of Ramsay Hunt
syndrome was caused by [. . .] until after the vaccination at issue here. Pet. Ex. 32 at 3-4; Pet.
Ex. 44 at 1.

Dr. Zamvil agreed that none of petitioner’s treating physicians attributed her Ramsay
Hunt syndrome to her flu vaccination. Tr. 200-01.

20
 On cross-examination, Dr. Zamvil admitted that he did not know why the flu vaccine at
issue triggered petitioner’s Ramsay Hunt syndrome in January 2013, even though she had
received flu vaccinations in the past, and had previously been ill with the flu virus, and those
events did not trigger her Ramsay Hunt syndrome. Tr. 213. He suggested that there may have
been some unique reason related to the January 2013 vaccine, but when asked what that was, he
responded, “I don’t know.” Tr. 213-14.

c. Althen Prong Three

As for Althen Prong Three, Dr. Zamvil provided somewhat inconsistent opinions as to
the date of onset of petitioner’s Ramsay Hunt syndrome. In his first expert report, he opined that
petitioner’s onset was two weeks after vaccination and consistent with the case report by Gurbuz
et al. Pet. Ex. 30 at 12. The patient described by Gurbuz et al. developed painful vesicles in her
right ear approximately 20 days after vaccination and developed facial palsy two days later. Pet.
Ex. 30, Ref. 10 at 1.

At the hearing, however, Dr. Zamvil testified that petitioner’s onset was six days after
vaccination. Tr. 176. Specifically, the vaccine was administered on January 4, and onset of
symptoms was January 10. Id. He opined that petitioner likely had a “secondary immune
response here, meaning an amplification,” so the time frame from vaccination to onset was “very
short, within a matter of four to ten days,” with a “peak” around days five to six. Tr. 175. He
further testified that the onset of petitioner’s illness was appropriate based on his mechanistic
theories. Tr. 176.

B. Petitioner’s Expert, M. Eric Gershwin, M.D.42

1. Background and Qualifications

Dr. Gershwin is board certified in internal medicine, rheumatology, and allergy and
clinical immunology. Pet. Ex. 34 at 2. He completed his M.D. at Stanford University, after
which he completed an internship and residency at Tufts-New England Medical Center in
Boston, Massachusetts and worked as a clinical associate in immunology at the National
Institutes of Health in Bethesda, Maryland. Id. at 1-2. He currently works in the Division of
Rheumatology, Allergy, and Clinical Immunology at the University of California at Davis as a
professor and chief of the division. Id. Dr. Gershwin has been bestowed with numerous honors
and awards throughout his career, and he has held various editor and reviewer positions on
medical journals. Id. at 3, 5-7. He has authored or co-authored over 1,000 publications during
his career. Id. at 8-130.

2. Opinion

Dr. Gershwin did not opine on the cause of petitioner’s Ramsay Hunt syndrome or
address the issue of vaccine causation. Pet. Ex. 33 at 1. His opinions were limited to petitioner’s

42
Petitioner filed three expert reports authored by Dr. Gershwin. See Pet. Exs. 33, 41, 43.

21
diagnosis of EGPA, and specifically the question of whether she had EGPA prior to her
vaccination and the onset of her Ramsay Hunt syndrome. Id.

Dr. Gershwin first provided background information about the illness, and then opined as
to the onset of petitioner’s EGPA. He explained that EGPA is a rare condition with an incidence
rate “rang[ing] from approximately 0.5 to 7 per million people.” Pet. Ex. 33 at 1. It is a “small
vessel, necrotizing vasculitis,” with clinical characteristics including “allergic rhinitis, polyposis
of the sinuses[,] and asthma. Id. “It also includes systemic features, including fever and weight
loss,” but the primary “focus of immunopathology” is asthma. Id. at 1-2. The majority of
patients have lung infiltrates that are described as “transient and patchy.” Id. at 2. Criteria for
the diagnosis of EGPA include a history of asthma, eosinophilia, another organ involvement,
increased IgE, and positive ANCA results. Tr. 257.

From a biological point of view, the illness is characterized by elevated eosinophilia and
“nonspecific elevated [IgE] levels in the sera” of most patients. Pet. Ex. 33 at 2. Other abnormal
labs include ANCA. Id. Histologically, “small vessel angiitis and extravascular necrotizing
granulomas, usually containing eosinophilic infiltrates” may be seen. Id. at 3. Vasculitis
“typically involves both arteries and veins in pulmonary and systemic vessels.” Id. Lung tissue
may have “necrotizing vasculitis and areas resembling eosinophilic pneumonia.” Id. Other body
systems may be involved, including the skin and subcutaneous tissue. Id.

Regarding the onset of petitioner’s EGPA, Dr. Gershwin opined that she had “no
significant history of allergic rhinitis,” “no change in her asthma symptoms,” and “no evidence
of pulmonary infiltrates prior to [] vaccination.” Pet. Ex. 33 at 3. In his expert report, Dr.
Gershwin opined that petitioner did not have “clinically significant evidence of [EGPA] before
the acute clinical markers described by Dr. Rubenstein in 2017.” Id. He disagreed with
respondent’s expert, Dr. Levinson, who opined that petitioner had eosinophilia and EGPA prior
to her diagnosis of Ramsay Hunt syndrome. Id. Dr. Gershwin stated that Dr. Levinson used
outdated criteria from the American College of Rheumatology, and therefore, “misinterpreted the
laboratory report of March 31, 2011.” Id.

Dr. Gershwin explained that on March 31, 2011, petitioner’s “total eosinophil count was
only 700 and the 11.1% [was] [] the percentage of eosinophils in her total white cell count.” Pet.
Ex. 33 at 3 (citing Pet. Ex. 13 at 20). According to Dr. Gershwin, “[t]rue eosinophilia is defined
on the basis of the absolute number of cells, not the percentage.” Id. He opined that petitioner
did not have true eosinophilia until later in her clinical course. Id. For example, on July 16,
2014, petitioner’s “absolute eosinophil count was only 400,” which Dr. Gershwin characterized
as “well below the normal level.” Id. (citing Pet. Ex. 4 at 193). Dr. Gershwin opined petitioner
developed EGPA in 2017, four years after her vaccination, when she had a “dramatic elevation
of IgE to a level greater than 18,000 on February 16, 2017,” as well as a positive P-ANCA and
C-ANCA. Id. at 3-4.

22
 However, at the hearing, Dr. Gershwin testified that “in retrospect,” petitioner had
“clinical manifestations” of EGPA when she had a positive ANCA result in 2013.43 Tr. 253.
But he did not agree that onset of petitioner’s EGPA occurred prior to her vaccination on January
4, 2013, or that petitioner’s EGPA reactivated her latent VZV (Ramsay Hunt syndrome). Tr.
243-45.

Instead of attributing the cause of petitioner’s Ramsay Hunt syndrome to EGPA, Dr.
Gershwin opined that petitioner “had an autoimmune predisposition.” Pet. Ex. 33 at 4. He noted
that petitioner’s family members had autoimmune illnesses, including “[EoE], Crohn’s disease,
arthritis, and multiple myeloma,” and “[t]hese would in fact indicate an individual with a striking
genetic predisposition to immunopathology.” Id.

Dr. Gershwin emphasized that EGPA is an autoimmune illness, not an immune
deficiency. Pet. Ex. 43 at 1. He agreed that “immune suppression can result when immune
suppressive drugs are used to treat [EGPA] autoimmunity,” but there was “no evidence in the
medical records to suggest that [petitioner] had clinical immune suppression” that played a role
in the cause of her initial Ramsay Hunt episode. Id.

Dr. Gershwin also testified that the flu vaccine played no role in the development of
petitioner’s EGPA. Tr. 238-39. He believed that petitioner probably developed EGPA [. . .]. Tr.
239. He explained that [. . .], which is an irritant that causes inflammation and hypersensitivity
pneumonitis. Tr. 244.

In summary, Dr. Gershwin opined that petitioner’s EGPA was not relevant to the cause of
her Ramsay Hunt syndrome. Tr. 236. He stated that there are no reports of EGPA causing
Ramsay Hunt syndrome. Tr. 236-37. He opined that petitioner was not older, she did not have
recurrent infections, she had no weight loss, and she was not immunodeficient.44 Tr. 237-38. In
summary, Dr. Gershwin opined that petitioner’s EGPA did not present prior to her flu vaccine or
the onset of her Ramsay Hunt syndrome. Tr. 243-44.

C. Respondent’s Expert, Vinay Chaudhry, M.D.45

1. Background and Qualifications

Dr. Chaudhry is a neurology professor at Johns Hopkins University School of Medicine.
Resp. Ex. C at 1; Resp. Ex. D at 1. He is board certified in neurology, neuromuscular diseases,
electrodiagnostic medicine, and clinical neurophysiology. Resp. Ex. C at 1; Resp. Ex. D at 29.

Petitioner’s positive ANCA screen and elevated P-ANCA and C-ANCA were reported on
43

November 2, 2013. Pet. Ex. 4 at 499.
44
Petitioner was diagnosed with SAD by Dr. Rubenstein in 2017. Tr. 374; Pet. Ex. 28 at 1.
However, according to respondent’s expert Dr. Levinson, it did not play a role in the
development of her Ramsay Hunt syndrome. Tr. 374-76.
45
Respondent filed three expert reports authored by Dr. Chaudhry. See Resp. Exs. C, E, H.

23
After completing medical training in India, including a B.Sc., M.B., B.S., internship, and junior
residency, Dr. Chaudhry completed a neurology residency and fellowship in the United States.
Resp. Ex. D at 2. He “ha[s] an active clinical practice and evaluate[s] over 2000 patients a year
mostly related to peripheral nerve disease.” Resp. Ex. C at 1. Dr. Chaudhry has authored or co-
authored over 200 publications. Resp. Ex. D at 3-17. Given his experience over his career, “[he
is] considered an expert in evaluation and treatment of patients with peripheral neuropathies
including facial neuropathies.” Resp. Ex. C at 1.

2. Opinion

Dr. Chaudhry opined that petitioner “suffered from Ramsay Hunt [s]yndrome caused by
reactivation of VZV infection due to her underlying eosinophilic granulomatosis, a condition
known to reduce immune competence and [cause] VZV activation. [The] [f]lu vaccine didn’t
play a causative role.” Resp. Ex. C at 10. In his expert reports, Dr. Chaudhry discussed Ramsay
Hunt syndrome, recurrent zoster infections, EGPA, and the manifestation of these conditions in
petitioner’s case.

As described by Dr. Chaudhry, “Ramsay-Hunt syndrome is a peripheral facial nerve
palsy accompanied by an erythematous vesicular rash on the ear.” Resp. Ex. C at 8. Petitioner
developed “left sided facial nerve [] palsy with incomplete left eye closure, tearing in the left
eye, impaired chewing, [] dribbling, biting of the lips and inside of the cheeks[,] as well as
slurred speech.” Id. She had two vesicles in the left external ear. Id. Dr. Chaudhry opined that
“[t]he presence of facial palsy with vesicles in the ear is [a] rather typical presentation of
Ramsay-Hunt syndrome.” Id. He found petitioner was treated appropriately for the illness with
valacyclovir and prednisone. Id. Dr. Chaudhry noted that “[petitioner] had rather severe facial
palsy,” confirmed by her EMG that “showed severe left facial neuropathy.” Id. She had a
number of corrective surgical procedures and Botox injections, and her course was complicated
by infections. Id.

The etiology of Ramsay Hunt syndrome is reactivation of VZV infection “in the
geniculate ganglion of the facial nerve.” Resp. Ex. C at 8. Dr. Chaudhry explained the
mechanism of the illness as follows: once a person has chicken pox, the virus does not go away.
Tr. 284. After the initial infection, the virus resides in the ganglion in a latent form. Id. Ramsay
Hunt syndrome occurs when there is reactivation of the virus in the facial nerve ganglion. Tr.
284-85. It is not known why the virus becomes reactivated, but there are some risk factors or
triggers. Tr. 285. Often there is not a cause. Id. Triggers include age, seasonal variations, and
Wegener’s granulomatosis. Id. (citing, e.g., Resp. Ex. C, Tab 3).46 Dr. Chaudhry testified that
vaccination has not been identified as a trigger. Id.

Dr. Chaudhry further explained that the DNA of VZV “can be detected by polymerase
chain reaction in the trigeminal and geniculate ganglion confirming that VZV becomes latent in
these ganglion and that reactivation of the virus causes Ramsay Hunt syndrome.” Resp. Ex. C at

46
Peter K. Wung, Herpes Zoster in Immunocompromised Patients: Incidence, Timing, and Risk
Factors, 118 Am. J. Med. 1416.e9 (2005).

24
8 (citing Resp. Ex. O at 1-2).47 Dr. Chaudhry opined that “[t]here is no reason to additionally
invoke [f]lu vaccination . . . playing a causative role in [petitioner’s] Ramsay Hunt syndrome.”
Id.

Additionally, Dr. Chaudhry noted in his first expert report that petitioner’s treating
physicians agreed that VZV infection caused her condition. Resp. Ex. C at 8. He testified at the
hearing that there was no evidence in petitioner’s medical record to suggest that any of her
doctors attributed her Ramsay Hunt syndrome to her flu vaccination. Tr. 313, 332. There are
references in the records which state that petitioner has an allergy to the flu vaccine. Tr. 313,
332-34. However, Dr. Chaudhry testified that often an allergy noted in a patient’s records is
usually based on a subjective history provided by the patient. Tr. 335. Thus, he opined that a
record stating that petitioner had an allergy to the flu vaccine cannot be interpreted to suggest
that any of her treating physicians held an opinion that the flu vaccine played a causal role in her
Ramsay Hunt syndrome. Tr. 313, 335.

After her initial episode of Ramsay Hunt syndrome, petitioner had approximately four
recurrences, none of which were associated with vaccination. Tr. 293-94; Resp. Ex. C at 9. Dr.
Chaudhry explained that petitioner’s first recurrence was in June 2013. Tr. 293; Resp. Ex. C at
9. It was not related to vaccination. Tr. 293; Resp. Ex. C at 9. She may have had another
recurrence in August 2013, when lesions were seen in her left ear. Tr. 293; Resp. Ex. C at 9. Dr.
Chaudhry stated that this recurrence was also not associated with any vaccination. Tr. 293;
Resp. Ex. C at 9. He found her third recurrence was February 22, 2016, when one possible
vesicle was noted. Tr. 294. Petitioner’s fourth recurrence, according to Dr. Chaudhry, was
February 12, 2018, when petitioner again had left ear pain with vesicles in her left ear. Id. Dr.
Chaudhry observed that none of these episodes were associated with vaccination. Tr. 293; Resp.
Ex. C at 9.

Dr. Chaudhry disagreed with Dr. Zamvil’s opinion that “once triggered,” petitioner had
an “increased susceptibility to future reactivations.” Resp. Ex. E at 2. Instead of the vaccine
triggering petitioner’s Ramsay Hunt syndrome, Dr. Chaudhry agreed with petitioner’s treating
physician, Dr. Rubinstein, who stated in 2017 that petitioner’s “Ramsay Hunt syndrome and
recurrent shingles may [] be due to the immune activation in [EGPA] leading to persistence of
VZV infection.” Id. (quoting Pet. Ex. 28 at 2); see also Tr. 298-300.

Moreover, in October 2013, petitioner’s treating physicians questioned whether she had
Wegener’s granulomatosis with facial ulceration and an abscess to her right nose. Pet. Ex. 4 at
455-59. Dr. Chaudhry explained that subsequent diagnostic testing revealed abnormal lab
values48 and CT scan showed erosion of the nasal septum consistent with a granulomatous

47
Yasushi Furuta et al., Detection of Varicella-Zoster Virus DNA in Human Geniculate Ganglia
by Polymerase Chain Reaction, 166 J. Infectious Diseases 1157 (1992).
48
Dr. Chaudhry referenced the following abnormal diagnostic laboratory results: P-ANCA
1:160, C-ANCA 1:40, eosinophils 13%, Proteinase-3 antibodies >8.0, IgE 1:1800; CRP 5.03.
Resp. Ex. C at 9.

25
process, along with painful gums, jaw, and face, and fatigue, all consistent with EGPA. Resp.
Ex. C at 9.

Dr. Chaudhry opined that EGPA may have played a role in triggering petitioner’s
Ramsay Hunt syndrome. Tr. 340-41. He based his opinion on the fact that patients with
Wegener’s granulomatosis, a similar disease, have a twenty times higher incidence rate of
Ramsay Hunt syndrome. Tr. 341. “Wegener’s granulomatosis is a form of systemic vasculitis
characterized by necrotizing granulomatous inflammation.” Resp. Ex. C, Tab 3 at 2. Like
Ramsay Hunt syndrome, herpes zoster (shingles) is caused by reactivation of VZV, and also
occurs after a primary infection with the virus in childhood. Id. To illustrate the risk for
developing zoster reactivation in Wegener’s granulomatosis, Dr. Chaudhry cited Wung et al.
See id. Of a total of 180 patients with Wegener’s granulomatosis, eighteen “suffered a total of
19 herpes zoster episodes over a [] follow-up period of 27 months.” Id. at 1. Although the
majority of the patients had herpes zoster outbreaks while on immunosuppressive medication for
their Wegener’s granulomatosis, many patients had discontinued these medications when their
herpes zoster outbreaks occurred. Id. at 7. The two risk factors identified in the study were renal
dysfunction and female sex. Id. at 8.

Dr. Chaudhry explained EGPA is vasculitis of small and medium blood vessels. Tr. 301.
EGPA is an illness characterized by phases, and Dr. Chaudhry opined that petitioner’s records
showed that she experienced the phases known to occur with this condition. Resp. Ex. C at 9.
The first phase is the “[p]rodromal phase with asthma,” which generally occurs “in the second
and third decades of life.” Id.; Resp. Ex. E at 3; see also Resp. Ex. C, Tab 4 at 1.49 He explained
that petitioner had a history of asthma requiring treatment with Albuterol, Advair, and Singulair.
Resp. Ex. C at 9. She had seen a pulmonologist for at least three years prior to her initial episode
of Ramsay Hunt syndrome. Id. Dr. Chaudhry cited references to petitioner’s medical records
showing that in August and December 2010, she had upper respiratory infections. Resp. Ex. E at
6-7. On both occasions, petitioner was noted to have a history of asthma, and was taking
Albuterol, Fluticasone, and Montelukast (Singulair) for her asthma. Id. In January 2011,
petitioner had a sore throat, ear pain, nasal congestion, and wheezing. Id. at 7. Again, her
history of asthma was documented, and she was on the medications described above. Id. In
March 2011, she had nasal congestion, and again her history of asthma was noted. Id.

The second phase of EGPA is the “[e]osinophilic phase.” Resp. Ex. C at 9; Resp. Ex. C,
Tab 4 at 1. Dr. Chaudhry stated that this phase is characterized by malaise, fever of unknown
origin, cough, and abdominal pain. Resp. Ex. C at 9. Dr. Chaudhry stated that petitioner had
eosinophilia in 2011. Id. (citing Pet. Ex. 13 at 20). In March 2011, her eosinophils were
elevated at 11.1%, with an elevated absolute count of 700. Resp. Ex. E at 3 (citing Pet. Ex. 13 at
20).

49
Talmadge E. King, Clinical Features and Diagnosis of Eosinophilic Granulomatosis with
Polyangiitis (Churg-Strauss), UpToDate, https://www.uptodate.com/contents/clinical-features-
and-diagnosis-of-eosinophilic-granulomatosis-with-polyangiitis-churg-strauss (last updated Sept.
12, 2017).

26
 Based on the characteristic phases of EGPA, petitioner’s clinical course evidencing a
history of asthma and sinus issues back to 2010, and petitioner’s elevated eosinophils in March
2011, Dr. Chaudhry placed onset of petitioner’s EGPA in March 2011. Tr. 304-06.

Dr. Zamvil and Dr. Chaudhry disagreed about the significance of petitioner’s abnormal
eosinophilia levels in 2011, and specifically about whether an “absolute eosinophil count is more
reliable” than a percentage value. Resp. Ex. E at 3. Dr. Chaudhry cited to King, who noted
“peripheral blood eosinophilia absolute levels greater than 10 percent of the total leukocyte count
should prompt suspicion for EGPA.” Id. (citing Resp. Ex. C, Tab 4 at 4). Regardless of which
method is more reliable, percentage versus absolute count, Dr. Chaudhry concluded that
petitioner had elevated eosinophils in March 2011. Id.

Dr. Chaudhry prepared a chart demonstrating petitioner’s eosinophil levels from 2008
until 2017, as seen below:

Date % Eosinophils Absolute # Ref (%ULN/ Exhibit
(Abn- bolded) (abnl bolded) Absolute ULN)
12/31/08 2.7% 200 5/300 25-15
3/31/11 11/1%% 700 5/4.5 (should 13-20
be 0.45)

1/28/13 3.5% 300 5/450 (New 9-370
York Hospital
laboratories)
3/7/13 13% 1250 7/600 9-354
5/17/13 19.3% 1200 7/700 Exhibit 2 p 84-
significant
eosinophilia
probably allergies
10/24/13 15.3% 1545 8/500 7-12
10/28/13 13.1% 1200 6/600 4- 501
10/28/13 14.9% 1500 8/500 7-29
10/29/13 13.8% 1100 6/600 4-482
11/7/13 7.7% 547 8/500 20-016
11/19/13 12% 860 7/600 9-303
11/22/13 13.8% 718 8/500 7-23
12/8/13 9.6% 413 8/500 7-21
1/15/14 13/12% 1330/1330 7/600 9-307, 329
6/3/14 14% 860 7/600 19-11
7/11/14 3.4% 400 6/600 4 -201
7/12/14 3.6% 400 6/600 4-198
7/14/14 14.5% 700 6/600 4-197
7/15/14 1.5% 100 6/600 4-193
7/16/14 6.1% 400 5/600 4-193
7/17/14 8% 500 6/600 4-192
7/18/14 4.9% 400 6/600 4-192

27
 3/26/15 7% 470 6/600 9-92
4/27/16 13% 1200 8/500 15-40
2/15/17 17% 1300 28-01
3/28/17 9% 600 /300 29-6
3/28/17 11% 5% 29-10
5/4/17 6% 400 /300 29-4

Resp. Ex. E at 3-4.

The fact that petitioner’s eosinophils fluctuated, and were not always abnormal, is not
unusual according to Dr. Chaudhry. Resp. Ex. E at 4 (citing Resp. Ex. C at 4 (“Eosinophilia,
however, is occasionally missed because of rapid spontaneous, or glucocorticoid-induced
reductions or fluctuations in eosinophil counts.”)).

The next phase of EGPA is the vasculitis phase, characterized by “pulmonary
granulomas, vascular complications with ulcerations, intestinal granulomas[,] and peritonitis.”
Resp. Ex. C at 9; see also Resp. Ex. C, Tab 4 at 1. Dr. Chaudhry noted that petitioner had facial
ulcerations. Resp. Ex. C at 9. Ultimately blood tests were done that revealed eosinophilia and
ANCA antibodies, and Dr. Rubenstein made the diagnosis of EGPA. Id. Dr. Chaudhry
concluded that petitioner’s EGPA “played a critical role in reactivation of the VZV infection
leading to Ramsay Hunt syndrome.” Id. at 10. Dr. Chaudhry further opined that petitioner’s
EGPA was not caused by the flu vaccine. Id.

Next, Dr. Chaudhry discussed Gurbuz et al., a case report of a patient who developed
Ramsay Hunt syndrome following flu vaccine, referenced by Dr. Zamvil. Resp. Ex. C at 10
(citing Pet. Ex. 30, Ref. 10). Dr. Chaudhry noted that prior to the onset of Ramsay Hunt
syndrome, the patient complained of an illness (weakness, runny nose, and headache) and was
prescribed Amoxicillin, an antibiotic, presumably for a bacterial infection. Resp. Ex. C at 10;
Pet. Ex. 30, Ref. 10 at 1. Further, Dr. Chaudhry observed that the authors suggested that the flu
vaccine could cause “transient immunosuppression” but failed to provide any evidence to
support that proposition. Resp. Ex. C at 10.

Dr. Chaudhry also took issue with Dr. Gershwin’s opinion that the manifestation of
petitioner’s EGPA diagnosis did not become clear until “February 16, 2017, four years after . . .
vaccination.” Resp. Ex. E at 5. Dr. Chaudhry believed Dr. Gershwin failed to account for (1)
petitioner’s right nasal lesion in March 2013; (2) the reference to Wegener’s granulomatosis,
facial ulceration, and abscess of the right nose in October 2013; (3) elevated P-ANCA, C-
ANCA, and eosinophils in October 2013; (4) CT scan abnormalities in 2013; (5) autoantibodies
to Proteinase-3 in November 2013; and (6) abnormal eosinophils in July 2014. Id. at 5-6. Dr.
Chaudhry believed these abnormal findings suggested the diagnosis of EGPA between 2013 and
2017. Id. at 5. Moreover, when taking into account petitioner’s history of asthma, Dr. Chaudhry
believed petitioner may have had the illness as early as 2010. Id. at 5-7. And at the hearing, he
concluded that petitioner’s onset of EGPA was in 2011, when she had elevated eosinophils. Tr.
305-06.

28
 Regardless of when petitioner developed EGPA, Dr. Chaudhry opined that a trigger is not
needed for reactivation of VZV to occur. Tr. 340. “There is no reason to additionally invoke
[the] [f]lu vaccination . . . playing a causative role in [petitioner’s] Ramsay Hunt syndrome, a
syndrome well known to occur following reactivation of VZV infection.” Resp. Ex. C at 8.
Although he believed EGPA was a “possib[le] [] cause” for petitioner’s initial episode of VZV
reactivation, he did not hold this opinion to a probable or more likely than not standard. Tr. 340-
42.

In summary, Dr. Chaudhry disagreed that the flu vaccine can cause or did cause
petitioner’s VZV reactivation. Resp. Ex. C at 10. He opined that “latent VZV infection is
common with virtually all patients who have had chicken pox,” and “known risk factors for
reactivation are age, sex, race, seasonal variation, and altered immune competence such as with
hematological malignancies, stem cell transplants, HIV, inflammatory diseases (Wegener’s
[granulomatosis] and Crohn’s disease), use of immunosuppression[,] and diabetes.” Id. But he
emphasized that no infection or preceding vaccination is needed for VZV reactivation. Id.

D. Respondent’s Expert, Arnold I. Levinson, M.D.50

1. Background and Qualifications

Dr. Levinson is board certified in internal medicine and allergy and clinical immunology
and is an Emeritus Professor of Medicine and Neurology at the Perelman School of Medicine at
the University of Pennsylvania School of Medicine. Resp. Ex. A at 1; Resp. Ex. B at 2. He
received his M.D. from University of Maryland. Resp. Ex. B at 1. After completing an
internship and one year of residency, he was a fellow at Johns Hopkins Hospital, a postdoctoral
fellow in immunobiology at the University of Pennsylvania School of Medicine, a postdoctoral
fellow in immunology at the University of California San Francisco Medical Center, and an
allergy and clinical immunology fellow at the University of Pennsylvania School of Medicine.
Id. Over his career of more than 30 years, Dr. Levinson has “evaluated and treated patients with
a broad range of immune-mediated diseases including autoimmune, hypersensitivity and
immunodeficiency disorders.” Resp. Ex. A at 1. Dr. Levinson has held various editorial
positions and memberships in honorary, professional, and scientific societies, and has authored
or co-authored over 150 publications. Resp. Ex. B at 2-4, 10-21.

2. Opinion

Dr. Levinson’s opinions focused on Dr. Zamvil’s three causal mechanisms proffered to
explain how the flu vaccine could cause Ramsay Hunt syndrome. Resp. Ex. A at 5. He also
addressed the evolution of petitioner’s “nasal and sinus disease,” or EGPA, and its role in the
development of petitioner’s Ramsay Hunt syndrome. Id. at 6-8.

Before addressing Dr. Zamvil’s opinions, Dr. Levinson explained the cause of Ramsay
Hunt syndrome and described the mechanism of VZV reactivation. He explained that Ramsay
Hunt syndrome

50
Respondent filed three expert reports authored by Dr. Levinson. See Resp. Exs. A, F, G.

29
 is caused by reactivation of [VZV] in the geniculate ganglion. VZV is a
ubiquitous, human alpha herpesvirus that produces varicella on primary infection.
The virus then becomes latent in ganglionic neurons along the entire neuraxis.
With a decline in VZV-specific cell-mediated immunity in elderly and
immunocompromised individuals, defects in innate immunity or the presence of
anti-cytokine antibodies, the virus reactivates from one or more ganglia and
travels peripherally via the sensory nerve root, to the innervated target tissue
(skin, cornea, auditory canal, etc.). Typically, a single dermatome[51] is involved,
although two or three adjacent dermatomes may be affected. The lesions usually
do not cross the midline. Reactivation of VZV is often complicated by severe
pain, which may last indefinitely (post-herpetic neuralgia) as was the case [with
petitioner].

Resp. Ex. A at 6.

Dr. Levinson then analyzed each of Dr. Zamvil’s proposed causal mechanisms. He noted
that the first theory, that the “[flu] vaccination could trigger an adaptive immune response to
VZV . . . relies on three foundational principles.” Resp. Ex. A at 8. These principles are (1)
“that the [flu] viral antigens in the [flu] vaccine and VZV antigens share molecular motifs,” (2)
“that the [flu] vaccine induced a cross-reactive immune response to the shared antigens,” and (3)
“that said cross-reactive immune response led to VZV reactivation in the geniculate ganglion
which ultimately resulted in . . . clinical symptoms of Ramsay Hunt syndrome.” Id. at 8-9.

Dr. Levinson noted several problems with this theory.52 First, as conceded by Dr.
Zamvil, there is “no evidence that this putative example of molecular mimicry actually induces
any type of cross-reactive adaptive immune response to the VZV nucleocapsid molecule . . . or . .
. any other putative epitopes shared by [the flu vaccine] viral antigens and VZV antigens.” Resp.
Ex. A at 9.

The second problem Dr. Levinson identified was that there is no evidence that “cross-
reactive shared epitope specific T cells . . . enter the geniculate ganglion and . . . become
activated by resident latent VZV virus.” Resp. Ex. A at 9. “[I]n the latently infected geniculate
ganglion, . . . [one] can’t detect a peptide.” Tr. 387. Dr. Levinson explained that there is no
evidence to suggest that latent VZV produces nucleocapsid proteins. Resp. Ex. A at 9. “[T]he

51
Dermatome is “the area of skin supplied with [] nerve fibers by a single spinal nerve.”
Dermatome, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=13359 (last visited Apr. 14, 2022).
52
Although Dr. Levinson disagreed with Dr. Zamvil’s opinions, he prefaced his opinions at the
hearing by recognizing and acknowledging Dr. Zamvil’s “cutting-edge research,” which is
deserving of significant credit. Tr. 378.

30
putative shared epitope would likely not be expressed by cells in the geniculate ganglion due to
the . . . limited transcription[53] of DNA by latent VZV.” Id.

In support of this aspect of Dr. Levinson’s opinion, and the fact that molecular mimicry is
unlikely to play a role in VZV reactivation, respondent filed an article by Depledge et al.54 Resp.
Ex. M. The authors explained that after a primary infection (chickenpox), VZV infection
reactivates in approximately one-third of those infected, causing herpes zoster, which frequently
leads to neurological complications. Id. at 1. VZV is difficult to study because it is a human
pathogen that does not cause disease in animals, so experimental animal models have not been
helpful in researching the disease. Id. Because animal studies are not possible, researchers use
cadaver human ganglia naturally infected with VZV. Id. at 6. Research limitations have posed
significant difficulties in attempts to identify viral transcripts and their corresponding proteins.
Id. Based on available research, “VZV protein expression in human ganglia appears to be absent
or extremely rare.”55 Id. Two viral proteins (VLT and ORF63) have been identified, and while
they may have “the potential to be translated during latency, these viral proteins could not be
detected in latently infected human ganglia by immunohistochemistry.” Id. Based on existing
research, the reasons or causes of “VZV reactivation are poorly understood.” Id. at 10.

Thus, Dr. Levinson opined that there is no data to support Dr. Zamvil’s suggestion that T
cells would migrate to the geniculate ganglion and recognize presenting peptides, and then that
interaction would lead to reactivation. Tr. 388-89. Moreover, if such a theory were correct, Dr.
Levinson opined that he would expect patients who get zoster vaccines to develop VZV
reactivation, not protection, due to the potential for homology and molecular mimics between the
zoster vaccine and VZV, but that has not been seen or reported. Tr. 389.

Dr. Levinson noted that Dr. Zamvil conceded that his first theory could be improbable.
Resp. Ex. A at 9. Thus, Dr. Zamvil suggested an alternative theory, referencing an article he
suggested supported the idea that “concomitant infection with [] two viruses” could cause
neuropathology. Id. (citing Pet. Ex. 30, Ref. 14). However, Dr. Levinson observed that “this
outcome was only observed in animals,” where an active brain infection was induced. Id. (citing
Pet. Ex. 30, Ref. 14 at 11). Dr. Levinson distinguished the facts in Matullo et al. from those
here. Id. at 9-10. He explained that in the research reported by Matullo et al., there was
“concurrent active viral infection in the geniculate ganglion, which [c]ould promote the
immigration of . . . T cells and elicitation of tissue injury,” inconsistent with the facts of
petitioner’s case. Id.

53
Transcription is “RNA synthesis using a DNA template.” Illustrated Dictionary of
Immunology 713 (3d ed. 2009).
54
Daniel P. Depledge et al., Molecular Aspects of Varicella-Zoster Virus Latency, 10 Viruses 1
(2018).
55
For a more complete explanation, see Resp. Ex. M at 5, fig.2 (schematic illustration of the
reactivation of VZV).

31
 The second theory posited by Dr. Zamvil was “that molecular mimicry between [the flu
vaccine] and myelin or neuronal autoantigens could cause a T cell and antibody response that
elicit[ed] CNS inflammation [] within or near the geniculate ganglion[] that promote[d]
reactivation of latent VZV.” Resp. Ex. A at 10 (internal citations omitted). Dr. Zamvil gave an
example based on shared similar sequences between flu A hemagglutinin and contactin
associated protein 1 and neurofascin, proteins associated with neuropathy. Id. Because Dr.
Zamvil did not cite to any medical literature or studies in support of this example, Dr. Levinson
stated that he was unable to evaluate it. Id. Moreover, citing the National Academy of
Medicine, formerly called the Institute of Medicine, Dr. Levinson noted that many examples of
homology exist, but “the vast majority of these are not associated with biologically relevant
autoimmune phenomena or actual human disease.” Id. at 10 (citing Resp. Ex. A, Tab 12 at 3-
4).56

Dr. Zamvil’s third theory is “that by stimulating the activation of NFκ-B,” the flu vaccine
may trigger an immune reaction that causes VZV reactivation. Resp. Ex. A at 11. Dr. Zamvil
cited an article by Haralambieva et al.,57 that described a study on 159 adults, ages 50-74 years
old, who received a flu vaccine. Pet. Ex. 30, Ref. 18 at 1. The frame of reference for the study
was the lack of knowledge about “how age affects adaptive immunity and immune memory due
to vaccination, particularly in regard to [flu] response.” Id. Their goal was to “identify baseline,
early[,] and late transcriptional signatures []in peripheral blood mononuclear cells[]” following
vaccination. Id. at 2. One of their findings was the “involvement of known immune function-
related genes in the development of memory B cell response,” including “a member of the NF-
kappa-B inhibitor family[], which is involved in inflammatory response and apoptosis.” Id. at 3.
Dr. Zamvil opined that the study “found gene sets and genes . . . demonstrating significant
associations . . . with memory B cell response[s] [which] suggest[ed] the importance of . . . NF-
κB cell signaling . . . and transcriptional regulation gene signatures in the development of
memory B cell response after [flu] vaccination.” Pet. Ex. 30 at 11. Dr. Zamvil used this finding
to assert that “activation of innate immunity becomes a third mechanism that could contribute to
reactivation of VZ[V] following Fluvirin.” Id.

Dr. Levinson explained that the Haralambieva et al. study was not relevant because it
“did not investigate how innate immune activation following immunization with the trivalent
[flu] vaccine might lead to reactivation of VZV.” Resp. Ex. A at 11. While Dr. Levinson
acknowledged that “an early innate immune response [can] facilitate[] development of an
antigen-specific adaptive immune response,” he opined that “these observations in no way
provide a basis for claiming that vaccination with Fluvirin or any killed [flu] virus vaccine would
cause an innate immune reaction that causes reactivation of latent VZV.” Id. Moreover, Dr.
Levinson found it “difficult to understand how and why such a putative innate immune reaction
would exclusively target the geniculate ganglion.” Id.

56
Inst. of Med., Evaluating Biological Mechanisms of Adverse Events, in Adverse Effects of
Vaccines: Evidence and Causality 57, 70-71 (Kathleen Stratton et al. eds., 2012). Respondent
filed only two pages of this chapter; however, this text is well known to the undersigned.
57
Iana H. Haralambieva et al., Transcriptional Signatures of Influenza A/H1N1-Specific IgG
Memory-Like B Cell Response in Older Individuals, 34 Vaccine 3993 (2016).

32
 In addition to addressing Dr. Zamvil’s proposed causal mechanisms, Dr. Levinson also
discussed petitioner’s EGPA, and its relevance to her initial episode of Ramsay Hunt syndrome.
Resp. Ex. A at 6-8. Generally, Dr. Levinson agreed with the opinions of Dr. Rubenstein,
petitioner’s immunologist. Id. at 7. Dr. Levinson explained that EGPA is a “systemic vasculitis
[] characterized by granulomatous inflammation of small and medium arteries. It is typically
preceded by a history of asthma . . . . Other early clinical features include allergic rhinitis, nasal
polyps, and sinusitis.” Id. There are three phases of the disease, as previously explained above.
Id. These phases may “overlap and may not be clearly distinguishable.” Id. Petitioner had
“asthma, seasonal allergies, recurrent sinusitis, [] eosinophilia, and eosinophilic infiltrates on lip
biopsy, which “qualif[ied] her for the diagnosis of EGPA.” Id. at 7-8.

Dr. Levinson explained that the diagnosis of EGPA can be difficult to make, especially in
petitioner’s case, where she had symptoms that were thought to be [. . .]. Resp. Ex. A at 8.
Regardless, Dr. Levinson opined that her correct diagnosis was EGPA. Id. He believed that
“petitioner’s systemic inflammatory process” may have been “ongoing” when petitioner had her
initial Ramsay Hunt syndrome in January 2013, but that the “full clinical declaration of EGPA
may have been delayed by the corticosteroids she received as treatment” for Ramsay Hunt
syndrome. Id. Dr. Levinson noted that corticosteroids are also used to treat EGPA; and he
explained that “EGPA occurs in some patients with asthma after their treatment with []
corticosteroids is discontinued.” Id. He also opined that petitioner’s EGPA may have played a
role in the second episode of Ramsay Hunt syndrome, which petitioner had in June 2013. Id. at
12. However, Dr. Levinson clarified in a supplemental report that he did not hold these opinions
to a reasonable degree of medical probability. Resp. Ex. F at 3.

In summary, Dr. Levinson opined that petitioner’s flu vaccination did not cause
petitioner’s reactivation of VZV or the development of her Ramsay Hunt syndrome. Resp. Ex. A
at 12. He questioned whether petitioner may have had EGPA when she developed her initial
episode of Ramsay Hunt syndrome in January 2013, as well as the second episode in June 2013.
Id. at 8, 12.

VII. LEGAL AUTHORITY AND ANALYSIS

A. Standards for Adjudication

The Vaccine Act was established to compensate vaccine-related injuries and deaths. §
10(a). “Congress designed the Vaccine Program to supplement the state law civil tort system as
a simple, fair and expeditious means for compensating vaccine-related injured persons. The
Program was established to award ‘vaccine-injured persons quickly, easily, and with certainty
and generosity.’” Rooks v. Sec’y of Health & Hum. Servs., 35 Fed. Cl. 1, 7 (1996) (quoting
H.R. Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).

Petitioner’s burden of proof is by a preponderance of the evidence. § 13(a)(1). The
preponderance standard requires a petitioner to demonstrate that it is more likely than not that the
vaccine at issue caused the injury. Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315,
1322 n.2 (Fed. Cir. 2010). In particular, petitioner must prove that that the vaccine was “not only

33
[the] but-for cause of the injury but also a substantial factor in bringing about the injury.” Id. at
1321 (quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344, 1352-53 (Fed. Cir.
1999)); see also Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed. Cir.
2006). A petitioner who satisfies this burden is entitled to compensation unless respondent can
prove, by a preponderance of the evidence, that the vaccinee’s injury is “due to factors unrelated
to the administration of the vaccine.” § 13(a)(1)(B).

B. Factual Issues

A petitioner must prove, by a preponderance of the evidence, the factual circumstances
surrounding her claim. § 13(a)(1)(A). To resolve factual issues, the special master must weigh
the evidence presented, which may include contemporaneous medical records and testimony.
See Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (explaining that a
special master must decide what weight to give evidence including oral testimony and
contemporaneous medical records).

Medical records generally “warrant consideration as trustworthy evidence.” Cucuras v.
Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). However, greater weight
is typically given to contemporaneous records. Vergara v. Sec’y of Health & Hum. Servs., No.
08-882V, 2014 WL 2795491, at *4 (Fed. Cl. Spec. Mstr. May 15, 2014) (“Special Masters
frequently accord more weight to contemporaneously-recorded medical symptoms than those
recorded in later medical histories, affidavits, or trial testimony.”). Contemporaneous medical
records are presumed to be accurate. See Cucuras, 993 F.2d at 1528. The weight afforded to
contemporaneous records is due to the fact that they “contain information supplied to or by
health professionals to facilitate diagnosis and treatment of medical conditions. With proper
treatment hanging in the balance, accuracy has an extra premium.” Id. To overcome the
presumptive accuracy of medical records, a petitioner may present testimony which is
“consistent, clear, cogent, and compelling.” Sanchez v. Sec’y of Health & Hum. Servs., No. 11-
685V, 2013 WL 1880825, at *3 (Fed. Cl. Spec. Mstr. Apr. 10, 2013) (citing Blutstein v. Sec’y of
Health & Hum. Servs., No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30,
1998)), mot. for rev. denied, 142 Fed. Cl. 247 (2019), vacated on other grounds & remanded, 809
F. App’x 843 (Fed. Cir. 2020).

There are situations in which compelling testimony may be more persuasive than written
records, such as where records are deemed to be incomplete or inaccurate. Campbell v. Sec’y of
Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike any norm based upon common
sense and experience, this rule should not be treated as an absolute and must yield where the
factual predicates for its application are weak or lacking.”); Lowrie v. Sec’y of Health & Hum.
Servs., No. 03-1585V, 2005 WL 6117475, at *19 (Fed. Cl. Spec. Mstr. Dec. 12, 2005)
(“[W]ritten records which are, themselves, inconsistent, should be accorded less deference than
those which are internally consistent.” (quoting 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))). Ultimately, a
determination regarding a witness’s credibility is needed when determining the weight that such
testimony should be afforded. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1379
(Fed. Cir. 2009); Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d 1570, 1575 (Fed. Cir.
1993).

34
 Despite the weight afforded medical records, special masters are not bound rigidly by
those records in determining onset of a petitioner’s symptoms. Valenzuela v. Sec’y of Health &
Hum. Servs., No. 90-1002V, 1991 WL 182241, at *3 (Fed. Cl. Spec. Mstr. Aug. 30, 1991); see
also Eng v. Sec’y of Health & Hum. Servs., No. 90-1754V, 1994 WL 67704, at *3 (Fed. Cl.
Spec. Mstr. Feb. 18, 1994) (Section 13(b)(2) “must be construed so as to give effect also to §
13(b)(1) which directs the special master or court to consider the medical records (reports,
diagnosis, conclusions, medical judgment, test reports, etc.), but does not require the special
master or court to be bound by them”).

C. Causation

To receive compensation under the Program, petitioner must prove either: (1) that she
suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding to a
vaccine that she received, or (2) that she suffered an injury that was caused by a vaccination. See
§§ 11(c)(1), 13(a)(1)(A); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1319-20
(Fed. Cir. 2006). Petitioner must show that the vaccine was “not only a 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).

Because petitioner does not allege that she suffered a Table injury, she must prove that a
vaccine caused her injury. To do so, she must establish, by preponderant evidence: (1) a medical
theory causally connecting the vaccine and her injury (“Althen Prong One”); (2) a logical
sequence of cause and effect showing that the vaccine was the reason for her injury (“Althen
Prong Two”); and (3) a showing of a proximate temporal relationship between the vaccine and
her injury (“Althen Prong Three”). § 13(a)(1); Althen, 418 F.3d at 1278.

The causation theory must relate to the injury alleged. The petitioner must provide a
sound and reliable medical or scientific explanation that pertains specifically to this case,
although the explanation need only be “legally probable, not medically or scientifically certain.”
Knudsen, 35 F.3d at 548-49. Petitioner cannot establish entitlement to compensation based
solely on his assertions; rather, a vaccine claim must be supported either by medical records or
by the opinion of a medical doctor. § 13(a)(1). In determining whether petitioner is entitled to
compensation, the special master shall consider all material in the record, including “any . . .
conclusion, [or] medical judgment . . . which is contained in the record regarding . . . causation.”
§ 13(b)(1)(A). The undersigned must weigh the submitted evidence and the testimony of the
parties’ proffered experts and rule in petitioner’s favor when the evidence weighs in his favor.
See Moberly, 592 F.3d at 1325-26 (“Finders of fact are entitled—indeed, expected—to make
determinations as to the reliability of the evidence presented to them and, if appropriate, as to the
credibility of the persons presenting that evidence.”); Althen, 418 F.3d at 1280 (noting that
“close calls” are resolved in petitioner’s favor).

“Expert medical testimony which merely expresses the possibility—not the probability—
of the occurrence of a compensable injury is insufficient, by itself, to substantiate the claim that
such an injury occurred.” LaCour v. Sec’y of Health & Hum. Servs., No. 90-316V, 1991 WL
66579, at *5 (Fed. Cl. Spec. Mstr. Apr. 15, 1991); accord Burns v. Sec’y of Health & Hum.

35
Servs., No. 90-953V, 1992 WL 365410, at *6 (Fed. Cl. Spec. Mstr. Nov. 6, 1992), aff’d, 3 F.3d
415. The Federal Circuit has likewise made clear that the mere possibility of a link between a
vaccination and a petitioner’s injury is not sufficient to satisfy the preponderance standard.
Moberly, 592 F.3d at 1322 (emphasizing that “proof of a ‘plausible’ or ‘possible’ causal link
between the vaccine and the injury” does not equate to proof of causation by a preponderance of
the evidence); Waterman v. Sec’y of Health & Hum. Servs., 123 Fed. Cl. 564, 573-74 (2015)
(denying petitioner’s motion for review and noting that a possible causal link was not sufficient
to meet the preponderance standard); Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d
1351, 1359-60 (Fed. Cir. 2019). While certainty is by no means required, a possible mechanism
does not rise to the level of preponderance. Moberly, 592 F.3d at 1322; see also de Bazan v.
Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1351 (Fed. Cir. 2008).

D. Analysis

1. Althen Prong One: Petitioner’s Medical Theory

Under Althen Prong One, petitioner must set forth a medical theory explaining how her
vaccine could have caused her alleged injuries. Andreu, 569 F.3d at 1375; Pafford, 451 F.3d at
1355-56. Petitioner’s theory of causation must be informed by a “sound and reliable medical or
scientific explanation.” Knudsen, 35 F.3d at 548; see also Veryzer v. Sec’y of Health & Hum.
Servs., 98 Fed. Cl. 214, 223 (2011) (noting that special masters are bound by both § 13(b)(1) and
Vaccine Rule 8(b)(1) to consider only evidence that is both “relevant” and “reliable”). If
petitioner relies upon a medical opinion to support her theory, the basis for the opinion and the
reliability of that basis must be considered in the determination of how much weight to afford the
offered opinion. See Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed.
Cir. 2010) (“The special master’s decision often times is based on the credibility of the experts
and the relative persuasiveness of their competing theories.”); Perreira v. Sec’y of Health &
Hum. Servs., 33 F.3d 1375, 1377 n.6 (Fed. Cir. 1994) (stating that an “expert opinion is no better
than the soundness of the reasons supporting it” (citing Fehrs v. United States, 620 F.2d 255, 265
(Ct. Cl. 1980))).

The undersigned finds petitioner failed to prove by preponderant evidence that the flu
vaccination she received caused her Ramsay Hunt syndrome. There are several reasons for this
finding.

Petitioner proposed what appears to be a unique claim, that a flu vaccination can cause
reactivation of VZV so as to cause Ramsay Hunt syndrome. However, none of the articles filed
by petitioner offer support for any of the theories proffered by Dr. Zamvil. Generally, the
takeaway from the relevant medical literature is that while there are some triggers for VZV
reactivation, such as female sex, age, and immunosuppression, reactivation can occur in the
absence of any identifiable trigger.

36
 Additionally, the mechanism of VZV reactivation is not known. It has not been linked to
vaccinations. While petitioner did file a case report58 of Ramsay Hunt syndrome following flu
vaccination, that patient had been ill and an antibiotic had been prescribed for her illness. The
significance of the patient’s antecedent infection or its role in triggering reactivation was not
addressed. Further, the patient was older, and thus, her age may have been another risk factor for
VZV reactivation. And while the authors noted the temporal association of vaccination, they did
not conclude that the flu vaccine caused VZV reactivation.

Ramsay Hunt syndrome is not an autoimmune disease, a fact that Dr. Zamvil readily
acknowledged. However, two of his proposed causal mechanisms are based on molecular
mimicry, a mechanism associated with autoimmune illnesses. Molecular mimicry has been
accepted in the Vaccine Program as a sound and reliable mechanism for how the flu vaccine can
initiate an autoimmune process resulting in GBS. See, e.g., R.S. v Sec’y of Health & Hum.
Servs., No. 15-1207V, 2019 WL 7631017, at *32 (Fed. Cl. Spec. Mstr. Dec. 19, 2019), mot. for
rev. denied, 2020 WL 4049758 (Fed. Cl. 2020); Reichert v. Sec’y of Health & Hum. Servs., No.
16-697V, 2018 WL 4496561, at *15 (Fed. Cl. Spec. Mstr. Aug. 2, 2018). GBS is not thought to
be caused by reactivation of a prior virus that remains dormant in nerve ganglion. In contrast,
Ramsay Hunt syndrome is caused by reactivation of a prior VZV infection. Because Ramsay
Hunt syndrome is not an autoimmune disease, molecular mimicry is not a good theoretical fit.

Even if it were a good fit, there is no evidence to support the notion that VZV
reactivation is caused by molecular mimicry. The first molecular mimic suggested by Dr.
Zamvil is homology between flu A hemagglutinin in the vaccine and a protein in VZV. His
second proposed homology is between flu A hemagglutinin and contactin-associated protein
and/or neurofascin. The problems with these suggested homologies were identified by Dr.
Levinson, who showed that there is no evidence that either of the examples proposed by Dr.
Zamvil actually induce a cross-reactive adaptive immune response. Dr. Zamvil cited no
foundational evidence, medical literature, research, studies, or other evidence of any such cross-
reaction. Dr. Zamvil conceded that point.

Further, there is limited knowledge about the degree to which latent VZV is capable of
producing proteins that could be mimics of any similar amino acid sequence in the vaccine. As
explained in Depledge et al., “VZV protein expression in human ganglia appears to be absent or
extremely rare.” Resp. Ex. M at 6. Although Dr. Zamvil and Dr. Levinson disagree on this
point, the Depledge et al. study describes what is known about human ganglia infected with
latent VZV, and based on the research done in the study, there appears to be insufficient
evidence to support the theory of molecular mimicry. It also does not appear that any of the
literature filed suggests that molecular mimicry plays a role in VZV reactivation.

58
The undersigned acknowledges the Anjum et al. article filed by petitioner, in which the
authors recommend that “‘[c]ausal evidence’ should . . . include different types of evidence,
including case studies and cases reports, which can in some cases provide valuable information
for understanding causation and causal mechanisms. This is particularly important when dealing
with rare disorders.” Pet. Ex. 66 at 1. The undersigned agrees and has taken into account the
case report cited by petitioner. However, there are factual issues presented in the case report that
raise questions, including whether the patient may have had an antecedent infection.

37
 Dr. Zamvil’s theory based on concomitant viruses is also problematic. The Matullo et al.
study induced a “co-infection model,” but that model presents facts and circumstances that are
not present here. In Matullo et al., the CNS of mice were infected with measles virus and the
peripheral systems were infected with a different virus. A key finding was that peripherally
activated T cells potentiated neuroinflammation of the CNS. The study “raise[d] the possibility
that concomitant immune challenges may be an important cause of the neuroinflammation of
some human CNS diseases.” Pet. Ex. 30, Ref. 14 at 2. But this possibility is not applicable here
where there is no evidence that petitioner had an active infection in her brain. Dr. Zamvil did not
show that latent VZV in the geniculate ganglion is equivalent to an active measles infection of
the brain.

Dr. Zamvil’s theory based on the innate immune system and the Haralambieva et al.
study of older adults who received the flu vaccine also misses the mark. The findings of the
study broadly support the idea that early innate immune responses can facilitate the development
of adaptive immune responses. But, as explained by Dr. Levinson, the study does not explain
how the flu vaccine could cause reactivation of VZV. In a variation on the theory, Dr. Zamvil
suggested that T cells “traffic” into the CNS where they cause myelin destruction. Tr. 164. He
discussed the concepts of “epitope spreading” and “bystander activation.” Tr. 164-68. But then
Dr. Zamvil explained that he wasn’t proposing these concepts occurred in this case.59 Overall,
his theories based on the innate immune system were disjointed and confusing.

Another problem with Dr. Zamvil’s opinions arise from his use of the words “possible”
and “possibility” in his expert reports and at the hearing when describing his different
mechanistic theories. For example, in his first expert report, he opined that “[s]everal possible
mechanisms could account for the development of [petitioner’s] Ramsay Hunt [s]yndrome.” Pet.
Ex. 30 at 8. He stated that “[t]hese possibilities are not mutually exclusive.” Id. And when
referring to his second mechanism, he referred to it as “[a] second possibility.” Id. at 10. In his
second expert report, Dr. Zamvil stated, “I suggested possible mechanisms for the association of
Ramsay Hunt syndrome with [flu] vaccination.” Pet. Ex. 32 at 5. At the hearing, Dr. Zamvil
testified about “one possibility” and a “second possibility.” Tr. 139, 148. He also referred to his
proposed mechanisms at the hearing as “one possibility, the first possibility” and “the other
possibilities.” Tr. 159.

Opinions expressed as possibilities, however, are not sufficient to establish causation.
See, e.g., Garner v. Sec’y of Health & Hum. Servs., No. 15-063V, 2017 WL 1713184, at *16
(Fed. Cl. Spec. Mstr. Mar. 24, 2017) (providing the petitioner’s expert provided conclusory
reasoning for “possible” vaccine causation is “not sufficient”), mot. for rev. denied, 133 Fed. Cl.
140 (2017); LaCour, 1991 WL 66579, at *5 (“Expert medical testimony which merely expresses
the possibility—not the probability—of the occurrence of a compensable injury is insufficient,
by itself, to substantiate the claim that such an injury occurred.”); Moberly, 592 F.3d at 1322
(emphasizing that “proof of a ‘plausible’ or ‘possible’ causal link between the vaccine and the
injury” does not equate to proof of causation by a preponderance of the evidence); Waterman,

59
Specifically, Dr. Zamvil testified that “bystander activation . . . leads to the epitope spreading,”
but then clarified that “[he was] not saying that epitope spreading occurred.” Tr. 167.

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123 Fed. Cl. at 573-74 (denying petitioner’s motion for review and noting that a possible causal
link was not sufficient to meet the preponderance standard). While certainty is by no means
required, a possible mechanism does not rise to the level of preponderance. Moberly, 592 F.3d
at 1322.

In addition, in his second expert report, Dr. Zamvil declared, “I have made no ‘causality
claim’ in this case, as asserted by Dr. Levinson.” Pet. Ex. 32 at 8. This declaration is confusing
and seemingly inconsistent with the purpose of his expert reports and testimony, which was to
present casual theories about how vaccination could cause illness. This inconsistency is also
present when Dr. Zamvil uses the words “possible” and “possibilities,” alongside phrases like
“medical certainty” and “more likely than not.” He ultimately professed that he held his
opinions to the standard of, “more likely than not.” See id. Regardless, the undersigned found
Dr. Zamvil’s opinions to be less persuasive due to his inconsistent and confusing use of different
standards, two of which are not applicable here (possibility and medical certainty).

Overall, the hypotheses suggested by Dr. Zamvil were underdeveloped and unsupported
by evidence as they pertain to the cause of VZV reactivation. When evaluating whether
petitioners have carried their burden of proof, special masters consistently reject “conclusory
expert statements that are not themselves backed up with reliable scientific support.”
Kreizenbeck v. Sec’y of Health & Hum. Servs., No. 08-209V, 2018 WL 3679843, at *32 n.44
(Fed. Cl. Spec. Mstr. June 22, 2018), mot. for rev. denied, 141 Fed. Cl. 138 (2018), aff’d, 945
F.3d 1362 (Fed. Cir. 2020). “The undersigned will not rely on opinion evidence that is
connected to existing data only by the ipse dixit of the expert. Instead, special masters are
expected to carefully scrutinize the reliability of each expert report submitted.” Prokopeas v.
Sec’y of Health & Hum. Servs., No. 04-1717V, 2019 WL 2509626, at *19 (Fed. Cl. Spec. Mstr.
May 24, 2019) (internal quotations omitted).

In summary, petitioner has not offered a sound and reliable medical theory in support of
her claim. Thus, the undersigned finds petitioner has not met the preponderant evidentiary
standard with respect to the first Althen prong.

2. Althen Prong Two: Logical Sequence of Cause and Effect

Under Althen Prong Two, petitioner must prove by a preponderance of the evidence that
there is a “logical sequence of cause and effect showing that the vaccination was the reason for
the injury.” Capizzano, 440 F.3d at 1324 (quoting Althen, 418 F.3d at 1278). “Petitioner must
show that the vaccine was the ‘but for’ cause of the harm . . . or in other words, that the vaccine
was the ‘reason for the injury.’” Pafford, 451 F.3d at 1356 (internal citations omitted).

In evaluating whether this prong is satisfied, the opinions and views of the vaccinee’s
treating physicians are entitled to some weight. Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d
at 1326 (“[M]edical 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 trustworthy evidence, since they are
created contemporaneously with the treatment of the vaccinee. Cucuras, 993 F.2d at 1528. The

39
petitioner need not make a specific type of evidentiary showing, i.e., “epidemiologic studies,
rechallenge, the presence of pathological markers or genetic predisposition, or general
acceptance in the scientific or medical communities to establish a logical sequence of cause and
effect.” Capizzano, 440 F.3d at 1325. Instead, petitioner may satisfy his burden by presenting
circumstantial evidence and reliable medical opinions. Id. at 1325-26.

The central issue here is whether the flu vaccine caused petitioner’s Ramsay Hunt
syndrome. The undersigned finds petitioner has failed to prove by preponderant evidence that it
did for the following reasons.

Petitioner had chickenpox as a child. Thus, she had the requisite infection with varicella
zoster which must occur as a sort of condition precedent to reactivation of the virus. Petitioner’s
clinical course was consistent with Ramsay Hunt syndrome caused by VZV reactivation.
Petitioner had the characteristic vesicles, which confirmed the diagnosis of Ramsay Hunt
syndrome. Moreover, the medical literature shows VZV reactivation is the cause of Ramsay
Hunt syndrome. All of the experts agreed on this point.

The undersigned generally finds opinions of a treating physician to be persuasive evidence
of causation. While some of petitioner’s treating physicians noted the temporal association
between petitioner’s flu vaccine and the onset of her Ramsay Hunt syndrome, none of them
opined that her Ramsay Hunt syndrome was caused by her vaccination. This is particularly
important because she was seen by so many physicians and specialists.

One of petitioner’s treating physicians, Dr. Stracher, stated, “probably avoiding flu vaccine
in future is reasonable.” Pet. Ex. 13 at 23. This statement is minimally supportive, but not
persuasive evidence of causation in the context of all of the facts and circumstances here. The
statement suggests that Dr. Stracher supported petitioner’s request to avoid the flu vaccine in the
future. Similarly, a record identifying an allergy to the flu vaccine does not constitute evidence
of causation. Allergies are often reported by patients, and without additional supportive
evidence, notations of allergies may not provide persuasive evidence of causation.

The statement by Dr. Stracher is similar to that discussed in Austin. Austin v. Sec’y of
Health & Hum. Servs., No. 05-579V, 2018 WL 3238608 (Fed. Cl. Spec. Mstr. May 15, 2018),
mot. for rev. denied, 141 Fed. Cl. 268 (2018), aff’d, 818 Fed. App’x 1005 (Fed. Cir. 2020). In
Austin, a treating physician adjusted the child’s vaccination schedule due to concerns by the
parents about possible adverse side effects. Id. at *27. Chief Special Master Corcoran found
that the physician’s actions of changing the vaccination schedule, without more, was “not
sufficiently strong” evidence of causation. Id. While a “treating physician’s recommendation to
withhold a particular vaccination can be probative evidence of a causal link between the
vaccination and an injury sustained, special masters are less likely to find a causal link where the
treater does not seem to have a sound scientific rationale—or, as here, offers no explanation at
all.” Id.

While her treating physicians did not attribute her Ramsay Hunt syndrome to the flu
vaccine, Dr. Rubinstein did question whether petitioner’s Ramsay Hunt syndrome and
recurrences were due to EGPA. He stated, “[t]he Ramsay Hunt syndrome and recurrent shingles

40
may also be due to the immune activation in [EGPA] leading to persistence of VZV infection.”
Pet. Ex. 28 at 2. Because he did not evaluate petitioner until later in time, his opinions were
necessarily based on his review of medical records and/or a history provided by petitioner.
Moreover, he used the word “may,” which suggests that while he questioned the relationship
between petitioner’s EGPA and Ramsay Hunt syndrome, his opinion was not held to the
standard of “more likely than not.”

The experts devoted substantial time to the issue of whether petitioner’s eosinophilia or
undiagnosed EGPA played a role in the development of her Ramsay Hunt syndrome. Petitioner
received the flu vaccine at issue on January 4, 2013. Prior to her vaccination, she had a history
of asthma that was significant enough to require treatment with Albuterol, Advair, and Singulair.
In 2010, she had two episodes of upper respiratory infections. In January and March 2011, she
again had complaints of nasal congestion, sore throat, and symptoms consistent with upper
respiratory infections. She continued to take medications for her asthma. Notably, petitioner
had elevated eosinophils in March 2011.

Petitioner’s experts opined that there was no significant evidence that petitioner’s
eosinophilic illness pre-dated her vaccination on January 4, 2013. Dr. Zamvil did not consider
EGPA or an eosinophilic illness to be a potential cause of petitioner’s Ramsay Hunt syndrome.
He did not believe that petitioner had any pre-exiting condition that contributed to her Ramsay
Hunt syndrome. Dr. Gershwin concurred, although he agreed that in hindsight, the onset of
petitioner’s EGPA was when she had positive ANCA results, which occurred in November 2013.

Respondent’s expert, Dr. Chaudhry, opined that petitioner had EGPA prior to her flu
vaccine and Ramsay Hunt syndrome. Based on petitioner’s history of asthma, episodes of nasal
congestion in 2010 and early 2011, and elevated eosinophils in March 2011, he placed onset of
petitioner’s EGPA in March 2011. However, as he explained at the hearing, he did not hold this
opinion to the standard of more likely than not. Dr. Levinson, like Dr. Chaudhry, also
questioned whether petitioner’s underlying systemic vasculitis played a role in the development
of her Ramsay Hunt syndrome. But, like Dr. Chaudhry, Dr. Levinson also did not hold these
opinions to a reasonable degree of probability. In conclusion, they agreed with Dr. Rubinstein.

The undersigned acknowledges that petitioner is not required to eliminate other potential
causes in order to be entitled to compensation. See Walther v. Sec’y of Health & Hum. Servs.,
485 F.3d 1146, 1149-52 (Fed. Cir. 2007) (finding petitioner does not bear the burden of
eliminating alternative independent potential causes). However, she finds it reasonable to
consider “evidence of other possible sources of injury”—here, petitioner’s EGPA illness—in
determining “whether a prima facie showing has been made that the vaccine was a substantial
factor in causing the injury in question.”60 Stone v. Sec’y of Health & Hum. Servs., 676 F.3d
1373, 1379 (Fed. Cir. 2012). “[T]he presence of multiple potential causative agents makes it

60
In the parties’ joint submission, the parties identify a fact in dispute regarding the role, [. . .].
However, there was no evidence to suggest that [. . .] use caused or contributed to her
development of Ramsay Hunt syndrome. Thus, the undersigned finds that [. . .] is not relevant to
the issue of her alleged vaccine-related injury.

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difficult to attribute ‘but for’ causation to the vaccination.” Pafford, 451 F.3d at 1358-59; see
also Walther, 485 F.3d at 1151 n.4.

As to the recurrent episodes of Ramsay Hunt syndrome, Dr. Zamvil testified that he never
intended to argue that they were caused by the flu vaccine. His point was that once Ramsay
Hunt syndrome was triggered, it was more likely that petitioner would have recurrences.
However, the undersigned has found that petitioner has failed to prove that the flu vaccine can
cause Ramsay Hunt syndrome. Therefore, and for the reasons described above, the undersigned
finds that the petitioner has failed to prove that the flu vaccine caused her initial episode of
Ramsay Hunt syndrome.

Because the petitioner has not proven that the vaccination caused her initial episode of
Ramsay Hunt, it follows that petitioner has failed to prove that the vaccination caused any of
petitioner’s recurrences. This finding is consistent with petitioner’s clinical course described in
the medical records, and as described by Dr. Chaudhry.

Moreover, as testified to by Dr. Chaudhry, and supported by the medical literature, there
is no need to implicate any trigger in the development of petitioner’s Ramsay Hunt syndrome.
While there are some risk factors associated with VZV reactivation, it occurs in the absence of
any such risk factors. As Dr. Chaudhry opined, it is not necessary to invoke the flu vaccine as a
cause, when no trigger is necessary for VZV reactivation to occur.

For all of the reasons described above, the undersigned finds that petitioner has failed to
provide preponderant evidence of a logical sequence of cause and effect required under Althen
Prong Two.

3. Althen Prong Three: Proximate Temporal Relationship

Under Althen Prong Three, petitioner must provide “preponderant proof that the onset of
symptoms occurred within a time frame for which, given the understanding of the disorder’s
etiology, it is medically acceptable to infer causation-in-fact.” de Bazan, 539 F.3d at 1352. The
acceptable temporal association will vary according to the medical theory advanced in the case.
See Pafford, 451 F.3d at 1358. A temporal relationship between a vaccine and an injury,
standing alone, does not constitute preponderant evidence of vaccine causation. See, e.g.,
Veryzer, 100 Fed. Cl. at 356 (explaining that “a temporal relationship alone will not demonstrate
the requisite causal link and that petitioner must posit a medical theory causally connecting the
vaccine and injury”), aff’d, 475 F. App’x 765 (Fed. Cir. 2012).

Dr. Zamvil’s opinions as to onset were a bit inconsistent. In an expert report, he opined
that the onset of petitioner’s Ramsay Hunt syndrome two weeks after vaccination. He opined
that this time frame was consistent with the patient described by Gurbuz et al., who developed
painful vesicles in her right ear approximately 20 days after vaccination, and facial palsy two
days later. However, the Gurbuz et al. authors did not implicate the theory of molecular mimicry
as the causal mechanism of the patient’s Ramsay Hunt syndrome.

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 At the hearing, Dr. Zamvil testified that petitioner’s onset was six days. He opined that
she likely had a secondary immune response or amplification, and that the time frame from
vaccination to onset was “very short, within a matter of four to ten days,” although he also stated
that onset could occur up to a month after vaccination. Tr. 175. Dr. Zamvil opined that the onset
of petitioner’s illness was appropriate based on his mechanistic theories.

Respondent’s experts did not refute the fact that there was a temporal association
between petitioner’s flu vaccination and the onset of her Ramsay Hunt syndrome.

Regardless of the minor inconsistencies in Dr. Zamvil’s opinions as to Althen Prong
Three, the undersigned finds there was a temporal association between vaccination and the onset
of petitioner’s Ramsay Hunt syndrome. However, a temporal association alone is insufficient for
petitioner to show vaccine causation for her alleged injury, and thus, petitioner is not entitled to
compensation.

VIII. CONCLUSION

It is clear from the medical records and hearing testimony that petitioner has experienced
significant pain and suffering, and she has undergone extensive surgical procedures and
treatment for her Ramsay Hunt syndrome, as well as her other illnesses. The undersigned
extends her sympathy to petitioner for the tremendous hardships she has experienced. However,
the undersigned’s Decision cannot be based upon sympathy for the petitioner but rather an
analysis of the evidence and application of the law.

For the reasons discussed above, the undersigned finds that petitioner has not established
by preponderant evidence that she is entitled to compensation and her petition must be
dismissed. In the absence of a timely filed motion for review pursuant to Vaccine Rule 23, the
Clerk of Court SHALL ENTER JUDGMENT in accordance with this Decision.

IT IS SO ORDERED.

s/Nora Beth Dorsey
Nora Beth Dorsey
Special Master

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