# Knorr v. Secretary of Health and Human Services

> United States Court of Federal Claims · January 11, 2019

URL: https://www.frixlaw.com/law-library/cases/4358120

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** January 11, 2019
- **Precedential status:** Published
- **Opinion:** Opinion
- **Judges:** Brian H. Corcoran). (cr) Service on parties made
- **Cited by:** 0 later opinions in the Frix Law Library

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## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 15-1169V
(to be published)

************************* Special Master Corcoran
*
RAMONA KNORR, *
*
Petitioner, * Filed: December 7, 2018
*
v. * Decision; Influenza (“flu”)
* Vaccine; Microscopic Polyangiitis
SECRETARY OF HEALTH * (“MPA”); Granulomatosis with
AND HUMAN SERVICES, * Polyangiitis (“GPA”); Vasculitis
*
Respondent. *
*
*************************

Michael McLaren, Black McLaren Jones Ryland & Griffee, Memphis, TN, for Petitioner.

Sarah C. Duncan, U.S. Dep’t of Justice, Washington, DC, for Respondent.

DECISION DENYING ENTITLEMENT1

On October 9, 2015, Ramona Knorr filed a petition seeking compensation under the
National Vaccine Injury Compensation Program (“Vaccine Program”).2 Petitioner alleges that she
suffered from several injuries, including hearing loss, microscopic polyangiitis (“MPA”) (a form
of anti-neutrophil cytoplasmic antibody (“ANCA”)-positive vasculitis) with renal failure, and
polyneuropathy as a result of receiving doses of the influenza (“flu”) vaccine on November 7,
2012, and October 8, 2013, respectively.

1
This Decision has been formally designated “to be published,” and will be be posted on the Court of Federal Claims’s
website in accordance with the E-Government Act of 2002, 44 U.S.C. § 3501 (2012). This means the Decision will
be available to anyone with access to the internet. As provided by 42 U.S.C. § 300aa-12(d)(4)(B), however, the
parties may object to the Decision’s inclusion of certain kinds of confidential information. Specifically, under Vaccine
Rule 18(b), each party has fourteen days within which to request redaction “of any information furnished by that party:
(1) that is a trade secret or commercial or financial in substance and is privileged or confidential; or (2) that includes
medical files or similar files, the disclosure of which would constitute a clearly unwarranted invasion of privacy.”
Vaccine Rule 18(b). Otherwise, the Decision in its present form will be available. Id
2
The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,
100 Stat. 3758, codified as amended at 42 U.S.C. §§ 300aa-10 through 34 (2012) [hereinafter “Vaccine Act” or “the
Act”]. Individual section references hereafter will be to § 300aa of the Act (but will omit that statutory prefix).
An entitlement hearing was held on October 26-27, 2017. For the reasons stated below,
Petitioner has not demonstrated entitlement to compensation under the Vaccine Program.
Petitioner’s primary theory at hearing – that she began experiencing vaccine-induced symptoms
reflective of her vasculitis after the first dose of the flu vaccine in 2012 – relied on establishing
that those symptoms were in fact evidence of MPA, but Respondent effectively rebutted such
contentions, demonstrating that those symptoms were actually associated with a medically-
distinguishable form of vasculitis, granulomatosis with polyangiitis (“GPA”). Petitioner otherwise
has not demonstrated with reliable scientific and medical evidence that the second flu vaccine dose
she received in 2013 could be, or was, causative of her MPA, especially given the extent to which
her expert unpersuasively conflated that form of ANCA-positive vasculitis with GPA.

I. Factual Background

The record in this case consists of Ms. Knorr’s medical records, the testimony of multiple
experts, and one fact witness, plus the medical or scientific literature submitted by the parties in
support of their respective positions. I have reviewed the entire record as required by the Vaccine
Act.

November 2012 Flu Vaccination and Subsequent Symptoms

On November 7, 2012, Ms. Knorr received the flu vaccine at the office of her employer,
Presbyterian Homes of Tennessee, in Knoxville, Tennessee. Ex. 2 at 20. Prior to this time, it
appears that Mr. Knorr was relatively healthy, with no significant issues relevant herein – apart
from treatment for fluid in her right ear one year prior on October 17, 2011. Ex. 2 at 8. Earlier
records from July 2011 through September 2012 indicated unremarkable physical exams. See Ex.
2 at 1-2, 6-7, and 10-17 (detailing normal physical exams from July 2011 through September
2012). Ms. Knorr’s records also indicate a past history of attention deficit disorder (including
decreased concentration), depression, and stress. Ex. 2 at 6, 8, 11.

Five days post-vaccination, Ms. Knorr presented to her primary care physician (“PCP”),
Dr. Raye-Anne Ayo, with complaints of flu-like symptoms (including body aches, sore throat,
cough and congestion, nausea, and fever for one to two days). Id. Upon exam, Dr. Ayo found that
Ms. Knorr had enlarged tonsils and non-tender, enlarged lymph nodes. Id. Dr. Ayo also conducted
a lab screening for the flu virus, which was negative. Id. at 22. Dr. Ayo’s overall assessment
included flu-like symptoms, and she recommended that Ms. Knorr begin taking Tamiflu. Id. Office
notes from this visit make no mention of any hearing loss.

2
Hearing Loss in 2013 and Treatment

On January 19, 2013 (over two months post-vaccination), Ms. Knorr presented to the
Minute Clinic in Knoxville, Tennessee, complaining of bilateral ear pain with ear popping, and
that she had been experiencing such symptoms for approximately one month (or since the middle
of December). Ex. 3 at 1; Ex. 8 at 1-3. Ms. Knorr also complained of postnasal drainage,
congestion, and stuffiness. Ex. 8 at 1. Upon exam, her treating nurse practitioner, Mary Anne
Webster, noted that she had clear fluid in her left middle ear, and a bulging tympanic membrane
in her right ear. Id. at 2. The overall assessment included sinusitis and otitis media with effusion,
and Nurse Webster prescribed Amoxicillin. Id. Following this visit, Ms. Knorr returned to the
Minute Clinic roughly two weeks later on February 7, 2013, with continued complaints of bilateral
ear pain and nasal congestion. Ex. 3 at 2. Nurse Webster noted that Ms. Knorr now had red
eardrums with cloudy fluid on exam, and prescribed Augmentin. Consistent with Ms. Knorr’s visit
in January, the assessment remained acute otitis media, and included no mention of the flu vaccine
as having a connection. Id. at 3.

On February 25, 2013, Ms. Knorr took herself to Dr. Bond Almand, an ear, nose, and throat
(“ENT”) specialist at Blount Memorial Hospital in Maryville, Tennessee. Ex. 3 at 4. During this
visit, she reported a gradual, two-month history of hearing loss (with fullness and pressure) that
had not improved with antibiotics. Id. According to Ms. Knorr, her symptoms included occasional
ringing in the ear, as well as occasional pulsing, but no balance issues. Id. Upon examination, Dr.
Almand found no evidence of any ear infection or ear canal/drum injury, but an audiogram
conducted during the visit revealed profound mixed hearing loss in the right ear, and mild to severe
hearing loss in the left ear. Id. at 4. Dr. Almand’s overall assessment also included serous otitis
media and asymmetry in bone conduction threshold. Id. Following her visit with Dr. Almand, Ms.
Knorr presented to Blount Memorial for a follow-up MRI of the brain and ear canals. Id. at 6-7.
The treating radiologist noted no abnormalities in the brain, but did find “opacification of the
majority of the mastoids” in the ears, consistent with a combination of fluid and mucosal
thickening. Id. at 7.

Ms. Knorr next returned to her PCP, Dr. Ayo, on April 23, 2013, with continued complaints
of hearing loss (that she now reported began six months prior “with the flu”).3 Ex. 3 at 8. In
particular, Petitioner reported that she continued to experience congestion with general
improvement but no resolution, despite multiple rounds of antibiotic treatment. Id. Upon
examination, Dr. Ayo diagnosed Ms. Knorr with chronic otitis media (consistent with past
diagnoses), and chronic rhinitis. Id. at 9. Dr. Ayo also found evidence of fluid in the left ear and
Eustachian tube dysfunction in her right ear. Id. at 8-9. Allergy testing conducted during the visit

3
Notably, the record does not state whether the “flu” reference pertained to the vaccination or a wild virus infection.
See Ex. 3 at 8.
3
was positive for trees, weeds, and mold. These records contain no treater suggestions that the flu
vaccine Ms. Knorr received in November 2012 had any relationship with her hearing loss or related
symptoms.

Ms. Knorr subsequently presented to Dr. Elise Denneny, a second ENT specialist, on June
6, 2013, at Greater Knoxville Ear Nose & Throat Associates, in Knoxville, Tennessee, with
continued complaints of hearing loss in both ears. Ex. 3 at 18. Dr. Denneny’s notes reveal that Ms.
Knorr reported that she had experienced hearing loss after a “severe upper respiratory tract
infection,” rather than implicating the November 2012 vaccine. Id. at 19. Dr. Denneny observed
that Ms. Knorr’s audiogram (previously conducted by Dr. Almand) indicated bilateral hearing loss,
but her MRI (also conducted by Dr. Almand) showed no abnormalities in the cranial nerves. Id.
Dr. Denneny’s notes also indicated that Ms. Knorr reported “asymmetry in her smile[,]” although
the same notes do not set forth any diagnostic analysis of, or treatment recommendation for, this
symptom. Id. Dr. Denneny recommend that Ms. Knorr schedule a follow-up appointment for
placement of tympanostomy tubes4 to help with her hearing symptoms. Id.

Ms. Knorr’s next record is from July 2013, and primarily recounts her treatment for
seasonal allergies. Ms. Knorr began receiving allergy immunotherapy shots for allergic rhinitis on
July 29, 2013, at the Family Health Center in Knoxville, Tennessee. Ex. 3 at 20-26, 31-36.
Treatment records indicated that Ms. Knorr received approximately twenty injections during the
following two-month period. Id. No adverse reactions were noted in the accompanying office
notes.

In the interim, Ms. Knorr presented to her PCP, Dr. Ayo, on August 19, 2013, with
continued complaints of decreased hearing. Ex. 3 at 23. This record set forth Petitioner’s history
of hearing loss (via audiogram) and tube placement. Id. Ms. Knorr now reported that her tubes had
helped with draining fluid from the ears, but she also stated that her hearing loss had otherwise
worsened. Id. Upon examination, Dr. Ayo found that both ears were “clogged by cerumen[,]” or
wax, but her external auditory canals were normal. Id. Ms. Knorr’s overall assessment continued
to include decreased hearing loss and allergic rhinitis, pollen-induced (for which she was receiving
allergy shots). Id. at 24.

On September 27, 2013, Ms. Knorr presented (for a follow-up) to her ENT, Dr. Denneny
at Greater Knoxville Ear Nose & Throat. Ex. 3 at 28. According to this record, Ms. Knorr continued
to complain of hearing difficulties plus ear ringing, with onset of symptoms “gradual year(s) ago”

4
Tympanostomy tubes (or ear tubes) are used to prevent the accumulation of fluid behind the eardrum. Tympanostomy
tubes are typically surgically inserted into the eardrum using small, cylinder-shaped tubes made of plastic or metal.
See Tympanostomy Tubes, Mayo Clinic, https://www.mayoclinic.org/tests-procedures/ear-tubes/multimedia/img-
20199962 (last accessed on June 14, 2018).
4
and no known event preceded her hearing loss. Id. During this visit, Ms. Knorr described her
current state of hearing loss as “severe and unchanged” (and reported other new symptoms,
including ostalgia and light headedness). Id. Upon examination, Dr. Denneny noted bilateral gray
tympanic membranes in both ears and an occluded tympanostomy tube. Id. at 29. Overall, Dr.
Denneny’s follow-up assessment noted that Ms. Knorr was suffering from chronic serous otitis
media, bilateral hearing loss, and allergic rhinitis (consist with her overall health course and
statements of past treaters). Id. at 30.

October 2013 Flu Vaccine and Subsequent Symptoms

Ms. Knorr received a second flu vaccine on October 8, 2013, at her place of employment,
Presbyterian Homes of Tennessee, in Knoxville, Tennessee. Ex. 3 at 37. Specifically, Petitioner
was administered Fluarix – an inactivated, quadrivalent (meaning containing four wild flu virus
strains), and non-adjuvanted5 form of flu vaccine. Id.; see also Package Insert, FDA, May 2015,
filed as Court Ex. 1 (ECF No. 75-1). No adverse reactions were noted the day of vaccination.

Three days later, on October 11, 2013, Ms. Knorr returned to Greater Knoxville Ear Nose
& Throat, but this time presented to a different ear, nose, and throat (“ENT”) specialist, Dr. Richard
Desperio. Ex. 3 at 40. Consistent with her past statements, Ms. Knorr reported (for the second
time) a gradual onset of hearing loss beginning “year(s) ago,” without reference to any specific
prior event (such as vaccination), along with a worsening of symptoms since her last office visit.
Id. Dr. Desperio’s notes indicated that her latest audiogram showed a blocked right tube but no
fluid, along with an open left tube. Id. at 41. A hearing test returned decreased hearing levels. Id.
During this visit, Ms. Knorr also reported extreme tightness in her neck and tenderness/pain when
opening her mouth. Id. Dr. Desperio’s overall assessment remained chronic serous otitis media
(and also included cervicalgia6). Id. He advised Ms. Knorr to take Advil or Aleve for her pain, and
prescribed Xanax as well. Id. Office notes also indicated that Ms. Knorr scheduled a follow-up
appointment for six weeks later.

5
Adjuvants are used in some vaccines to create a stronger immune response to the disease being vaccinated against.
See Adjuvants Help Vaccines Work Better, CDC, https://www.cdc.gov/vaccinesafety/concerns/adjuvants.html (last
accessed on November 20, 2018). Aluminum salts, for example, have been used safely in vaccines since the 1930s.
Id. Not all vaccines contain adjuvants, however. Id. Typical non-adjuvanted vaccines include chickenpox, MMR,
rotavirus, seasonal flu, and yellow fever. Id.
6
“Cervical” is a general term used to describe the neck. Dorland’s Illustrated Medical Dictionary 333 (32nd ed. 2012)
(hereinafter Dorland’s). “Cervicalgia” refers to generalized neck pain. Symptoms can include muscle tightness,
spasms, headaches, and decreased ability to move the head. See Neck Pain, Mayo Clinic,
https://www.mayoclinic.org/diseases-conditions/neck-pain/symptoms-causes/syc-20375581 (last accessed on June
14, 2018).
5
One week post-vaccination, Mr. Knorr visited her PCP, Dr. Ayo, on October 15, 2013,
complaining of a four-day course of flu-like symptoms (including body aches, cough, subjective
fever, watery nasal discharge, and sore throat). Ex. 3 at 43. She specifically asserted that her
present symptoms were similar to those she experienced following her flu vaccine in November
2012. Id. Upon exam, however, Dr. Ayo noted that Ms. Knorr appeared healthy apart from
rhinorrhea and general malaise. Id. at 44. Her notes also indicated that Ms. Knorr was experiencing
temporomandibular joint dysfunction (“TMJ”) pain in the jaw and surrounding muscles. Id. Her
overall impression was that Ms. Knorr’s symptoms were flu-like and “seem[ed] related to
influenza vaccine.” Id. Dr. Ayo recommended that Ms. Knorr rest for a week and use a mouth
guard for her TMJ pain. Id.

On October 22, 2013, Ms. Knorr presented again to Dr. Ayo, now reporting a rash on her
neck, chest, and arms for the past week, plus a fever, arthralgia, and a dry cough (for two weeks).
Ex. 3 at 45. Dr. Ayo noted that Ms. Knorr received the flu vaccine earlier that month and had
reported flu-like symptoms a few days later, but she did not appear to opine as to any causal
connection between the vaccine and the present rash. Id. Dr. Ayo diagnosed Ms. Knorr with a
cough and rash, and prescribed antibiotics. Id. at 46. A lab workup conducted during the visit
showed increased platelets of 434 (reference range 130-400), but a normal erythematous
sedimentation rate (“ESR”) of 21 (reference range 0-32), which was not supportive of the
conclusion that she was at that time experiencing active inflammation. Id. at 51-52.

The lab results from October 2013, however, also revealed the presence of a number of
antibodies associated with the Epstein Barr virus (“EBV”). Ex. 3 at 50. Specifically, Petitioner
tested positive for Anti-Viral Capsid Antigen (“VCA”) IgM antibodies (3.9 on a reference range
of 0.0 to 0.8) and IgG antibodies (greater than 8 on the same range), and positive as well for the
EBV nuclear antigen (“EBNA”) antibody (also greater than 8 on the same range).7 Id. The
interpretation chart for this testing classified these results as most likely reflecting that Petitioner
was in the convalescent phase of a recent EBV infection (or mononucleosis). Id.

7
Immunoglobulin G (IgG) and Immunoglobulin M (IgM) are antibodies produced in response to infection, and their
titer levels can help monitor or detect immune deficiencies. IgM is an indicator of current infection, while IgG reflects
exposure to a past infection. Increased levels of IgG or IgM are indicia of hepatic diseases (including connective tissue
diseases and acute/chronic infections), while decreased levels are found in patients with primary/secondary immune
deficiencies. See Immunoglobulins (IgG, IgA, and IgM), Serum, Mayo Clinic Med. Laboratories,
https://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/8156 (last accessed June 14,
2018).

6
Worsening and Attempts to Diagnose Etiology of Symptoms

Ms. Knorr’s condition seemed to worsen in the weeks following her October 22nd
appointment. She presented to the emergency room at Parkwest Medical Center in Knoxville,
Tennessee, on November 4, 2013, complaining of a rash, fever, and bilateral pain in her upper
extremities. Ex. 3 at 54. She specifically recounted at this time that she had received the flu vaccine
roughly three weeks prior and developed flu-like symptoms four days post-vaccination. Id. Upon
intake, the treating physician noted that Ms. Knorr had some weakness, difficulty adducting her
thumb, calf pain, headaches, scalp tenderness, and dyspnea upon exertion. Id. Ms. Knorr also
reported subjective chills and decreased fever, weight loss, and an aching jaw. Id. Given her host
of symptoms, Mr. Knorr was admitted to Parkwest Hospital from November 4-5, 2013, with
concerns for systematic inflammatory response syndrome (“SIRS”), neuralgia, elevated liver
function tests (“LFTs”), and a possible vasculitis-type process. Id. Initial lab testing conducted
during her hospitalization now showed an elevated ESR of 106 (reference range 0-20) – a
significant change from the reading obtained two weeks prior - an elevated C-reactive protein of
32.5 (normal 0-0.5), and positive EBV-VCA IgG. Id. at 55, 67-69. Additional testing was also
notable for a positive p-ANCA antibody titer.8 Id. at 87.

During her stay at Parkwest Hospital, Ms. Knorr was evaluated by an infectious disease
physician, Dr. John Adams. Ex. 3 at 57. Dr. Adams observed Ms. Knorr to display generalized
weakness, numbness, calf pain, and reduced finger strength upon examination. Id. at 57-59. The
notes from his examination recount that Ms. Knorr had received a flu vaccine in October, but did
not opine as to a possible relationship between the vaccine and her current state. Id. at 57.
Following the consultation, Dr. Adams assessed Ms. Knorr with a “somewhat unusual syndrome
with an apparent initial viral syndrome which could have been Epstein-Barr virus reactivation”
followed by abnormal LFTs, although he expressed doubt that she was suffering from an active
infection, given her IgG and IgM measurements. Id. at 50, 59. Dr. Adams recommended a
neurological consultation. Id. While he opined that Ms. Knorr was suffering from a “clearly
evolving inflammatory process,” he was not convinced that her symptoms were related to
vasculitis, but more likely some form of acute demyelinating encephalomyelitis (or ADEM). Id.

Ms. Knorr was next seen by Dr. James Burns on November 4, 2013, for a neurology
consultation. Ex. 3 at 99. Dr. Burns recounted Ms. Knorr’s health course, noting that she reported
she was in excellent health prior to receiving a flu vaccine the prior year. Id. Thereafter, Ms. Knorr

8
Perinuclear antineutrophil cytoplasmic antibodies (“p-ANCA”) are used to evaluate patients suspected of having
autoimmune vasculitis (including GPA and MPA). See Test ID:ANCA, Mayo Clinic Med. Laboratories,
https://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/9441 (last accessed on June 14,
2018). P-ANCA antibodies are most closely associated with MPA, however. See A. Greco, et al., Microscopic
Polyangiitis: Advances in Diagnostic and Therapeutic Approaches, 14 Autoimm. Rev. 837, 840 (2015), filed as Ex.
C, Tab 2 (ECF No. 19-4).
7
had developed hearing loss (requiring tympanoplasty tubes) and a Bell’s palsy-type appearance
following vaccination, along with increased hearing loss following a second flu vaccination in
October 2013. Id. Similar to Dr. Adam’s evaluation, Dr. Burns noted that Ms. Knorr was
experiencing hand numbness and weakness (acute onset on day of admission), headaches, aching
in the calves/thighs/shoulders, rash, and elevated ESR. Id. Following the initial evaluation, Dr.
Burns ordered lab testing to measure Ms. Knorr’s anti-neutrophil cytoplasmic antibodies (or
ANCAs). Id. at 101. Ms. Knorr tested positive for p-ANCA antibodies and negative for c-ANCA
antibodies. Id. at 87. Dr. Burns ultimately raised concerns for the possibility of a vasculitis illness,
or a “neurologic reaction to vaccine such as an atypical Guillain-Barre-type presentation.” Id. at
101. He recommended that Ms. Knorr receive a full neurological evaluation at an alternate facility
with the appropriate capabilities. Id.

Ms. Knorr was transferred to Fort Sanders Regional Medical Center on November 5, 2013,
and remained hospitalized from November 5-12, 2013. Ex. 3 at 112. Upon discharge from
Parkwest, her overall assessment included a purpuric, balancing type rash, covering her upper
torso, arms, feet, and ankles. Id. at 112. The discharging physician indicated that her main
neurological abnormalities included decreased adduction of her thumb and index finger, decreased
flexion and extension strength in her forearms, as well as hyperflexivity in the upper and lower
extremities. Id. Lab testing noted in the record upon release indicated abnormal LFTs and elevated
platelet and white blood cell counts. Id. at 113.

During her stay at Fort Sanders, Ms. Knorr was seen by Dr. Darrell Thomas (a neurologist)
on November 5, 2013. Ex. 3 at 119. Dr. Thomas recounted a health history similar to that provided
to treaters at Parkwest. More specifically, Dr. Thomas noted that Ms. Knorr had presented to the
emergency room at Parkwest with acute onset pain and numbness in her arms and hands (along
with general sense of weakness, a rash, and history or hearing loss). Id. Upon exam, Dr. Thomas
found that Ms. Knorr displayed weakness in her fingers and wrist flexors, but no additional
concerning neurological symptoms. Id. at 119. Overall, Dr. Thomas assessed Ms. Knorr with
dysesthesias and weakness in the upper extremities, and described her condition “to be more of an
immune-mediated process probably precipitated by a flu shot.” Id. He excluded GBS as a possible
diagnosis (given Ms. Knorr’s normal reflexes and local distribution of weakness), but did not rule
out vasculitis or sarcoid. Id. Moving forward, Dr. Thomas ordered additional lab testing, an EMG,
and a lumbar puncture to test for infection or a carcinomatous-type process.

Ms. Knorr was seen by Dr. Amanda Miller for a rheumatology examination on November
6, 2013. Ex. 3 at 115. Similar to Dr. Thomas’s assessment, Dr. Miller indicated that Ms. Knorr had
experienced a systematic illness, “possibly a reaction to a flu vaccine, which would be the second
severe reaction . . . in two years.” Id. at 116. Dr. Miller suggested that Ms. Knorr might have some
form of vasculitis or other immunologic disease, but was not convinced her symptoms were
8
autoimmune in nature. Id. at 116. Dr. Miller found Ms. Knorr’s increased liver enzyme levels
(along with elevated platelet counts) to be significant and possibly a marker for an existing
inflammatory process. Id. Absent any identified infection or other cause (as indicated by Ms.
Knorr’s labs), Dr. Miller recommended a trial of high-dose steroids. Id.

An EMG/NCV conducted on November 7, 2013 was normal with no evidence of
neuropathy or plexopathy. Ex. 3 at 144. Spinal fluid studies also revealed no abnormalities. Id.
Upon discharge, Ms. Knorr’s treating physician diagnosed her with “weakness and dysesthesias
of the upper extremities following a flu vaccine, suspected inflammatory or autoimmune process.”
Id. at 145. Notes further indicated that “this appear[ed] to be the second serious reaction she has
had to flu vaccinations.” Id. The discharging physician recommended that Ms. Knorr begin therapy
for her physical symptoms and prescribed gabapentin. Id. at 147.

Vasculitis/MPA Diagnosis

Following her initial hospitalization, Ms. Knorr was seen in the rheumatology clinic at
Vanderbilt University Medical Center in Nashville, Tennessee, by Dr. Glenn Douglas on
November 19, 2013. Ex. 3 at 161. Ms. Knorr reported a health course similar to those referenced
above (including hospitalization for nerve pain and numbness beginning in October 2013). Id. Dr.
Douglas also included pneumonia, hearing loss, EBV infection, and a rash in her health history.
Id. Following an evaluation, Dr. Douglas diagnosed Ms. Knorr with ANCA-positive vasculitis
with possible renal involvement, as well as polyneuropathy (along with a rash). Id. He prescribed
Prednisone and Oxycodone (for pain), and recommended that Ms. Knorr schedule a follow-up
appointment in two weeks. Id.

Petitioner was subsequently hospitalized for vasculitis flares on three additional separate
occasions at Vanderbilt Medical Center in Nashville, from November 2013 through January 2014,
including: (1) November 27-December 1, 2013; (2) December 3-10, 2013; and (3) January 3-14,
2014. Ex. 3 at 164, 206; Ex. 4 at 27.

On November 27th, Ms. Knorr presented to Vanderbilt Medical Center with a history of
ANCA-positive vasculitis (including lower extremity swelling) and complaints of worsening
kidney involvement. Ex. 3 at 164. She was monitored and discharged with a diagnosis of lower
extremity swelling and blood in stool. Id. at 169. Ms. Knorr presented a second time on December
3rd with complaints of shortness of breath and fever related to her vasculitis diagnosis. Id. at 206.
Upon discharge on December 10, 2013, treating physicians concurred with prior determinations
that Ms. Knorr had ANCA-positive vasculitis with possible renal involvement – making the form
of vasculitis most likely MPA – and steroid induced-diabetes. Id. Following her December 2013
hospitalizations, Ms. Knorr presented a third time to Vanderbilt Medical Center after an
9
exacerbation of her vasculitis (including symptoms of pain, malaise, blurred vision, and
headaches). Ex. 4 at 27. Her diagnoses upon discharge continued to include MPA, renal failure,
neuropathic pain, and anemia of chronic disease. Id. Treaters recommended that she continue
physical therapy, and use Gabapentin and Cymbalta as needed. Id. at 28.

Mr. Knorr was hospitalized for a fourth flare-up from March 1-6, 2014, at the University
of Tennessee Medical Center in Knoxville, Tennessee. Ex. 4 at 192, 222. Her chief complaint
during this visit was fever and generalized weakness (associated with her MPA diagnosis roughly
four months prior). Id. at 192. Upon examination, the treating physician, Dr. Sahar Lotfi, noted
that Ms. Knorr displayed no acute distress (and stated she had been doing well overall), but
experienced an onset of lethargy and weakness two days prior. Id. Dr. Lotfi opined that Ms.
Knorr’s symptoms were related to her vasculitis diagnosis, steroid-induced hypoglycemia, and
renal failure (as well as the medication she was taking, including Prednisone). Id. In light of her
renal insufficiency, a right renal biopsy was conducted during her hospitalization which displayed
necrotizing and crescentic glomerulonephritis, consistent with ANCA-associated disease. Id. at
201, 222, 247. Ms. Knorr’s discharge summary indicated diagnoses of MPA, chronic kidney
disease, hypertension, and anemia. Id. at 222. Dr. Lofti also prescribed Cytoxan for her kidney
dysfunction.

Ms. Knorr next presented to a rheumatologist, Dr. Natalie Braggs, at Vanderbilt University
Medical Center on March 13, 2014. Ex. 4B at 15. Ms. Knorr recounted her recent diagnoses of
MPA and hospitalization for high fever and worsening kidney function. Id. Dr. Braggs noted that
Ms. Knorr reported that her kidney function had improved with IV Cytoxan. Id. According to Ms.
Knorr, she was still experiencing pain and numbness in her feet and hands, blurred vision, and
occasional shortness of breath (and cough). Id. at 15. Dr. Braggs’s overall assessment included
ANCA-vasculitis, steroid-induced diabetes, and neuropathy. Id. at 17. She recommended that Ms.
Knorr continue taking Prednisone (decreased to a lower dose), Cytoxan, and Gabapentin, and
follow-up as needed. Id. Relevant lab testing conducted during a lab follow-up showed a normal
C-reactive protein and ESR. Ex. 6 at 25-29.

During the following months, Ms. Knorr saw various additional treating physicians at
Vanderbilt Medical Center for follow-up appointments related to her vasculitis diagnosis and
kidney dysfunction (as well as additional on-going problems such as steroid-induced diabetes and
a vitamin D deficiency). See, e.g., Ex. 4B at 56-57 (4/15/2014 follow-up visit with Dr. William
Sullivan), 88 (5/20/2014 follow-up visit with Dr. Sullivan), 180 (6/17/2014 follow-up with Dr.
Williams). The records from these visits suggest that Ms. Knorr’s condition has seen steady
improvement with proper treatment and medication. See, e.g., Ex. 4B at 56, 87. Ms. Knorr has
continued to attend physical therapy for her hand/arm weakness. Id. at 118, 160; Ex. 6 at 2, 17-55.

10
II. Fact Witness Testimony

A. Ms. Ramona Knorr

Petitioner testified at hearing. Tr. at 6-59. Her testimony largely consisted of her own
recollections of her overall health history prior to receiving the flu vaccines on November 2012
and October 2013, respectively, as well as describing the symptoms that followed.

Ms. Knorr began by describing her overall condition prior to receiving her initial flu
vaccine in November 2012. At that time, she was extremely healthy, with no adverse health
problems or chronic ailments. Tr. at 12-13. She testified that she worked full-time as an
occupational therapist, attended school part-time, exercised occasionally, and cared for her three
children. Id. at 13.

Next, Ms. Knorr recounted her receipt of the flu vaccine on the day of November 7, 2012.
Tr. at 14. She noticed no adverse reaction to the vaccine the day it was administered. Id. Following
the vaccination, Ms. Knorr stated that she presented to her PCP, Dr. Ayo, four to five days later,
complaining of flu-like symptoms (including aches and pains). Id. at 15. However, she did not
recall experiencing hearing loss at that time. Id.

Ms. Knorr recalled going to a Minute Clinic at her local CVS roughly two months post-
vaccination, with worsening flu-like symptoms and ear pain/popping. Tr. at 16. Although she
categorized her symptoms as gradually increasing over the past months, she testified that she did
not return to her PCP or any other physician in the interim due to her busy schedule. Id. According
to Ms. Knorr, during this visit, she reported her hearing loss began shortly after her initial
presentation to Dr. Ayo on November 12, 2012 (likely around November 23rd-25th). Id. at 18.

Ms. Knorr expressed frustration that her hearing problems seemed to be getting worse,
despite her attempts to cure them (including antibiotics, and tube placement). Tr. at 19, 29-30. She
next recalled various appointments for hearing problems beginning in February 2013. Ms. Knorr
began with a February 2013 appointment with her ENT, Dr. Almand. Id. at 21. According to the
medical records, Ms. Knorr told Dr. Almand at this time that her symptoms began two-months (or
a “few” months) prior to her visit (which would place onset post-vaccination in December 2012).
Id. at 22-23. However, Petitioner characterized such statements to Dr. Almand as no more than
vague estimations. Id. at 23.

Ms. Knorr also discussed an appointment with a second ENT, Dr. Denneny, whose notes
indicated that her hearing loss symptoms actually began in June 2012 (pre-vaccination), and/or

11
followed a URI. Tr. at 32. Ms. Knorr disputed the accuracy of this record, but acknowledged that
statements concerning the URI were correct (which, according to Ms. Knorr, would place onset in
late November 2012). Id. Overall, despite the varying statements concerning the onset of hearing
problems, Ms. Knorr continued to maintain that her symptoms began in November 2012, a few
weeks following her initial flu vaccine on November 7th. Id. at 24.

By the summer of 2013, Ms. Knorr testified, she was having trouble working and keeping
up with her graduate school classes. Tr. at 26. She also recalled having an issue with her smile,
which she described as “like a Bell’s palsy sort of situation” or a “droopy smile.” Id. at 33, 34.
Despite these symptoms, no diagnosis of Bell’s palsy (or any other) was ever made, and Ms. Knorr
testified that these symptoms resolved on their own. Id. at 34.

Ms. Knorr next recalled her general health course following the October 2013 vaccination.
Tr. at 36. She presented to her PCP, Dr. Ayo, seven days post-vaccination with complaints of flu-
like symptoms (similar to her complaints with regard to her initial flu vaccination in November
2012. Ms. Knorr testified that Dr. Ayo prescribed Tamiflu and recommended that she get some
rest. Id. She was later diagnosed with Epstein Barr (or mono) in early November 2013 (although
she also noted she was diagnosed with mono as a teenager and did not feel as if she was
experiencing similar symptoms). Id. at 39. According to Ms. Knorr, her health course thereafter
continued to deteriorate during the following months, and she could no longer work. Id. at 38-39.

Finally, Ms. Knorr recounted her hospitalization for what now appears to be the early
manifestations of MPA. Ms. Knorr described her hospital course as “really, really rough.” Tr. at
43. She was in and out of Vanderbilt Hospital for four months with various symptomology and
flare-ups of MPA. Ms. Knorr testified that these flares ranged in severity and included symptoms
such as double vision, headaches, pain, and an inability to walk. Id. at 44. She also experienced
paralysis in her right hand, hair loss, and Prednisone-induced diabetes. Id. at 44, 46. According to
Ms. Knorr, her treatment course during this time included plasmapheresis, chemotherapy, spinal
taps, and rehab therapy. Id. at 44-45. To date, Ms. Knorr continues to have trouble walking, has
decreased sensation in her right hand, as well as balance issues and decreased fine motor skills. Id.
at 50-53. Ms. Knorr testified that she has not returned to work (given the general physical
demands), and continues to take azathioprine (immunosuppressant) and gabapentin (for nerve
pain). Id. at 48-50.

B. Petitioner’s Expert – Dr. Eric Gershwin

Dr. Gershwin is an immunologist who testified on behalf of Petitioner and offered three
expert reports in the case. Tr. 64-124, 156-58; Ex. 19, dated Feb. 17, 2016 (ECF No. 41)
(“Gershwin First Rep.”); Ex. 67, dated Aug. 11, 2016 (ECF No. 24-1) (“Gershwin Second Rep.”);

12
Ex. 96, dated Aug. 11, 2017 (ECF No. 42-1) (“Gershwin Third Rep.”). Dr. Gershwin opined that
Ms. Knorr’s initial flu vaccine in November 2012 (resulting in flu-like symptoms, hearing loss,
and Bell’s palsy-type symptoms), coupled with the second flu vaccine in October 2013
(exacerbating her hearing loss and resulting in additional flu-like symptoms), caused her MPA
vasculitis. Tr. at 93, 111, 153.

Dr. Gershwin received his bachelor's degree from Syracuse University in Syracuse, New
York, followed by his medical degree, which was completed at Stanford University in Stanford,
California. Ex. 66 at 1 (ECF No. 41) (“Gershwin CV”). He then completed his internship and
residency at Tufts–New England Medical Center in Boston, Massachusetts. Id. at 2. After
completing a fellowship in immunology with the National Institute of Health, Dr. Gershwin
became an assistant Professor in Rheumatology and Allergy at the University of California, School
of Medicine in Davis, California. Id. at 2. Along with maintaining a clinical practice, Dr. Gershwin
remains employed by the University of California, School of Medicine in Davis, California as the
Chief of the Division of Rheumatology/Allergy and Clinical Immunology. Gershwin CV at 1-2;
Tr. at 65. He currently serves as the editor-in-chief of the Journal of Autoimmunity as well as
several other publications focusing on autoimmunity. Tr. at 80; Gershwin CV at 5. Dr. Gershwin
also maintains a clinical practice (one day per week) at UC Davis and spends four to six weeks
conducting a rheumatology consult service. Tr. at 78.

To begin, Dr. Gershwin described vasculitis and provided a brief overview of its relevant
presenting symptoms. Tr. at 71. Dr. Gershwin defined vasculitis as “inflammation of the [blood]
vessel[s]” or an inflammatory response initiated by some injury. Id. at 72, 85. While Dr. Gershwin
acknowledged that genetic (or inherited) factors can play a role in its development, he opined that
vasculitis requires an environmental stimulus. Id. at 86. He characterized vasculitis as an all-
defining term, given the multiple types in existence, which he asserted differ mainly due to the
size of the vessel implicated, the presence of specific autoantibodies, as well as the presenting
location in the body (i.e. can be limited to the head and neck, for example, or spread through the
body). Id. at 72, 100, 102. It can also be associated with various environmental factors, including
viral illness or independent diseases such as lupus or rheumatoid arthritis. Id.

Dr. Gershwin went on to discuss some of the specific ANCA-associated vasculitis (or
“AAV”) sub-types (i.e. GPA and MPA), given their relevance in the present matter. Dr. Gershwin
defined ANCA-associated vasculitis as “a heterogeneous group of diseases that include the
presence of circulating ANCAs.” Gershwin First Rep. at 22. ANCAs are implicated in the
pathogenesis of AAV, although the process by which these antibodies are formed is not well-
understood (with genetic, environmental, or infection related-factors all considered possible
triggers). Id.; see R. Wijngaarden, et al., Hypotheses on the Etiology of Antineurtrophil
Cytoplasmic Autoantibody-Associated Vasculitis: The Cause Is Hidden, but the Result Is Known,
13
3 J. Am. Soc. Nephrol. 237, 237 (2008), filed as Ex. 53 (ECF No. 41) (“Wijngaarden”).
Wijngaarden discusses in depth some of the identified causes of ANCA-associated vasculitis,
including silica exposure, genetic predisposition, bacterial/viral infection (such as parvovirus
B19), and certain thyroid drugs. Wijngaarden at 237.

Dr. Gershwin defined Wegener’s granulomatosis (more accurately termed GPA) to be a
type of vasculitis mediated by a collection of white cells called granulomas9, or foreign body
reactions. Tr. at 72; see also Gershwin First Rep. at 22-23. GPA can be both acute (resulting in a
rapid onset), or indolent (resulting in a progression of symptoms over time). Tr. at 74-75. Dr.
Gershwin saw no reason to distinguish between GPA and Ms. Knorr’s MPA diagnosis given the
overlapping symptoms (although in so testifying he essentially acknowledged that some
differences existed), despite filing literature acknowledging expressly that MPA is
“distinguish[able] as a separate ANCA-associated vasculitis.” Wijngaarden at 237 (emphasis
added); see also Tr. at 308-09. He did, however, acknowledge that Petitioner’s MPA diagnosis
was medically accurate. Tr. at 74, 298.

For Petitioner’s causation theory, Dr. Gershwin maintained that Ms. Knorr’s vasculitis was
the result of immunological insult to her autonomic nervous system attributable to the flu vaccine,
occurring via the biologic mechanism of molecular mimicry and producing an inflammatory
response. Gershwin First Rep. at 22; Tr. at 143, 150. Dr. Gershwin described molecular mimicry
as an “antigen-specific phenomenon where there is activation of autoreactive B and T cells due to
antigen similarity between the host antigen and microbial antigen,” involving both amino acid
sequences as well as the secondary/tertiary structure of the presenting antigen (in this case, a
protein sequence from the flu vaccine). Gershwin First Rep. at 21-22. Antigens in the flu vaccine
mimicked self-structures in the body, producing a cross-reaction whereby antibodies produced in
response to the vaccine also attack those self-structures, resulting in an autoimmune illness. Tr. at
93-95, 143-44, 150-51. Dr. Gershwin’s opinion relied specifically on a lengthy block quote set
forth in a single cited item of literature. Gershwin First Rep. at 23 (citing T. Duggal, et al.,
Antineutrophil Cytoplasmic Antibody Vasculitis Associated with Influenza Vaccination, 38 Am. J.
Nephrology 174, 176-77 (2013), filed as Ex. 24 (ECF No. 41) (“Duggal”)); Tr. at 141.

To bulwark this proposed mechanism, Dr. Gershwin relied on various articles (not specific
to vasculitis) discussing molecular mimicry as a possible explanation for how infectious agents
can stimulate autoimmunity in an antigen-specific way. See, e.g., D. Wraith, et al., Vaccination
and Autoimmune Disease: What is the Evidence, 362 Lancet 1659 (2003), filed as Ex. 54 (ECF
No. 41); Y. Shoenfeld, et al., Vaccination and Autoimmune-‘Vaccinosis’: A Dangerous Liaison?,

9
Granulomas are areas of inflammation in the body tissue. See Granulomatosis with Polyangiitis, Mayo Clinic,
https://www.mayoclinic.org/diseases-conditions/granulomatosis-with-polyangiitis/symptoms-causes/syc-20351088
(last accessed on June 18, 2018).
14
14 J. Autoimm. 1 (2000), filed as Ex. 55 (ECF No. 41). Dr. Gershwin acknowledged, however,
that he could not identify homology (amino acid sequential similarity) between the viral
components of the version of the flu vaccine Petitioner received and a protein in the body that
would be the target of an autoantibody attack resulting in MPA, nor could he specify what
component of the vaccine was the antigenic mimic. Tr. at 119, 143, 151. At best, he could only
cite to an unspecified “ongoing NIH study” that implicates the importance of protein structure in
autoimmune cross-reactions (but did not file this study), and also opined the likely target antigen
to be the neutrophil cytoplasmic antigen, since it purportedly had such structural homology with a
flu vaccine component (again without filing anything in support). Id. at 143-45, 151; Gershwin
First Rep. at 22.

Alternatively, Dr. Gershwin proposed that viral RNA protein found in certain formulations
of the flu vaccine might contribute to the development of the ANCA autoantibodies. Tr. at 119,
143; Gershwin First Rep. at 23-24; see L. Jeffs, et al., Viral RNA in the Influenza Vaccine May
Have Contributed to the Development of ANCA-Associated Vasculitis in a Patient Following
Immunization, Clin. Rheumatol. (2015), doi 10.1007/s10067-015-3073-0, filed as Ex. 30 (ECF
No. 41) (“Jeffs I”). Jeffs I is a case control study involving a single patient (compared to eight
healthy controls and six ANCA controls) who developed ANCA-associated vasculitis two weeks
following receipt of a flu vaccine in Australia. Jeffs I at 1. In it, researchers isolated peripheral
blood samples from the fifteen patients and found evidence that the vaccinated index patient had
increased levels of PR3-ANCA in his blood, leading researchers to conclude that forms of the flu
vaccines also containing viral ribonucleic acid (RNA) might be able to stimulate production of this
particular ANCA autoantibody. Id. at 1-2, 8. Dr. Gershwin did not establish, however, that Fluarix
(the version of the vaccine Ms. Knorr received) is comparable to the tested versions of the flu
vaccine in Jeffs I, and Dr. Gershwin acknowledged in any event that he did not put much stock in
this mechanistic explanation for how ANCA production could be vaccine-stimulated. Tr. at 143
(“I think it’s less likely . . . [t]here is not likely to be much RNA there [in the vaccine], but I just
wanted to be complete”).

There are other problems with Jeffs I. First, it involved PR3-ANCA, an autoantibody more
commonly associated with GPA than MPA. See, e.g., A. Greco, et al., Microscopic Polyangiitis:
Advances in Diagnostic and Therapeutic Approaches, 14 Autoimm. Rev. 837, 840 (2015), filed
as Ex. C, Tab 2 (ECF No. 19-4) (“Greco”) (determining “PR3-ANCA usually cause a C-ANCA
pattern and are mainly associated with GPA[,]” while myeloperoxidase ANCA (“MPO-ANCA”)
are associated with MPA); L. Guillevin, et al., Microscopic Polyangiitis: Clinical Laboratory
Findings in Eighty-Five Patients, 42 Arthritis & Rheumatol. 421, 424, 428 (1999), filed as Ex. 50
(ECF No. 41) (“Guillevin”) (31 out of 51 MPA patients evaluated in study tested positive for anti-
MPO antibodies, where only 4 out of 51 tested positive for PR3). Second, an article with the same
primary author published in the same year as Jeffs I (and filed by Petitioner in this case) cautions
15
against overreliance on the possible implications of Jeffs I. See L. Jeffs, et al., Randomized Trial
Investigating the Safety and Efficacy of Influenza Vaccination in Patients with Antineutrophil
Cytoplasmic Antibody-Associated Vasculitis, 20 Nephrology 343, 345-51 (2015), filed as Exhibit
31 (ECF No. 41) (“Jeffs II”). Jeffs II specifically monitored thirty-one patients who already had
ANCA-associated vasculitis and concluded they were not likely to experience a relapse after
receipt of the flu vaccine. As part of its control grouping, the Jeffs II authors also analyzed 67
healthy patients and found no evidence that the flu vaccine could trigger the relevant ANCA-
associated antibodies necessary for disease onset. Id. at 343, 348-49. Since it is the Petitioner’s
theory that the earlier flu vaccine dose from 2012 played a role in causing her vasculitis after the
second dose, Jeffs II not only seems to limit the significance of Jeffs I, but calls into question the
entirety of the causation theory.10

In addition to molecular mimicry, Dr. Gershwin also suggested that the mechanism of
bystander activation could play a role in instigating an ANCA-associated vasculitis. As he
proposed, bystander activation results “in a release of previously sequestered self-antigens or
stimulat[ed] . . . innate immune response.” Gershwin First Rep. at 23; Tr. at 142. Dr. Gershwin’s
first report seems to define bystander activation (or what he also termed “polyclonal activation” at
hearing) as an immune mechanism initiated by a vaccine (or viral infection) which results in the
activation of T cells apart from any specific antigen stimulation directly caused by vaccination.
Gershwin First Rep. at 23; Tr. at 135, 149.

The literature ostensibly supporting this proposition, however, did not explain how
bystander activation could act as the predominant driver of an autoimmune process (as opposed to
a secondary process fueling an existing autoimmune reaction instigated by something else). See
M. Moro, et al., A Population Based Cohort Study to Assess the Safety of Pandemic Influenza
Vaccine Focetria in Emilia-Romagna, Italy—Part Two, 31 Vaccine 1438 (2013), filed as Ex. 35
(ECF No. 41); B. Ormen, et al., Attitudes and Side Effects Related to Pandemic Influenza A (H1N1)
Vaccination in Healthcare Personnel, 46 Mikrobiyol Bul. 57 (2012), filed as Ex. 36 (ECF No. 41)
(filed in Turkish language with English abstract); H. Reynolds, et al., A Prospective Observational

10
In addition, Jeffs I seems to possibly embrace a vaccine causation theory that has not been found scientifically
reliable (to date) in the Vaccine Program. Jeffs I noted that the examined case study reflected “another of the recently
proposed concepts of ‘Autoimmune/Inflammatory Syndrome Induced by Adjuvants’” or ASIA. Jeffs I at 8. But the
ASIA theory (which relies heavily on the proposition that adjuvants in a vaccine can overstimulate the immune system,
thereby precipitating an autoimmune reaction) has repeatedly been found to be unpersuasive and/or insufficiently
supported by present science to be reliable. See, e.g., Rowan v. Sec'y of Health & Human Servs., No. 10–272V, 2014
WL 7465661 (Fed. Cl. Spec. Mstr. Dec. 8, 2014); mot. for review den'd, 2015 WL 3562409 (Fed. Cl. 2015);
D'Angiolini v. Sec'y of Health & Human Servs., No 99–578V, 2014 WL 1678145 (Fed. Cl. Spec. Mstr. Mar. 27, 2014),
mot. for review den'd, 122 Fed. Cl. 86 (2015), aff'd, 645 F. App'x 1002 (Fed. Cir. 2016). More importantly, the version
of the flu vaccine Petitioner received does not contain an adjuvant – rendering ASIA completely irrelevant as a co-
explanatory mechanism. Dr. Gershwin himself specifically disavowed any faith in such a theory. Tr. at 141-42 (“I
personally do not believe that the adjuvants within a vaccine can cause an autoimmune disease”).

16
Safety Study on MF59 Adjuvanted Cell Culture-Derived Vaccine, Celtura During the A/H1N1
(2009) Influenza Pandemic, 30 Vaccine 6436 (2012), filed as Ex. 39 (ECF No. 41); Tr. at 143. At
hearing, Dr. Gershwin acknowledged that an existing autoimmune reaction (or infectious process)
must occur prior to the initiation of any polyclonal activation, but he did not identify what process
(if any) explained Ms. Knorr’s experience (unless it is assumed that Dr. Gershwin’s invocation of
bystander activation relied on his other mechanism of molecular mimicry occurring first). See Tr.
at 148-49.

Besides offering literature to support his theory, Dr. Gershwin cited reported cases of onset
of ANCA-associated vasculitis two to four weeks after receipt of the flu vaccine (and/or a flu wild
virus infection). Gershwin First Rep. at 23; Tr. at 112-13; Duggal (two cases of onset of ANCA-
associated vasculitis following flu vaccination, but concluding a causal role cannot be confirmed);
R. Birck, et al., ANCA-Associated Vasculitis Following Influenza Vaccination: Causal Association
or Mere Coincidence, 15 J. Clin. Rheumatol. 289-291 (2009), filed as Ex. 21 (ECF No. 41)
(“Birck”) (reporting three cases of onset of ANCA-associated vasculitis following flu vaccine, but
concluding that that it could not be determined if relationship was causal or due simply to chance);
B. Spaetgens, et al., Influenza Vaccination in ANCA-Associated Vasculitis, 24 Nephrol. Dial.
Transplant. 3258-59 (2009), filed as Ex. 44 (ECF No. 41) (“Spaetgens”) (case report detailing
temporal relapse of ANCA-associated vasculitis following flu vaccination); M. Uji, et al.,
Microscopic Polyangiits After Influenza Vaccination, 44 Intern. Med. 892-96 (2005), filed as Ex.
61 (ECF No. 41) (“Uji”) (case report detailing temporal onset of MPA in an 83-year-old patient
following flu vaccination); M. Konishi, et al., A Case of Microscopic Polyangiitis and Giant Cell
Arteritis after Influenza Vaccine, 34 Jpn. J. Clin. Immunol. 154 (2011), filed as Ex. 32 (ECF No.
41) (case report of 67-year-old patient who developed MPA and giant cell arteritis following a flu
vaccine); Wijngaarden at 2 (noting possible seasonal association between the flu wild virus and
MPA based on three case reports); see also T. Kwok, et al., Two Rare Cases of Retinal Vasculitis
Following Vaccination, 58 Scottish Med. J. E10-E12 (2013), filed as Ex. 34 (ECF No. 41)
(“Kwok”) (two case report study detailing onset of retinal vasculitis four weeks and two months
following flu vaccination).

Dr. Gershwin also noted the existence of reliable literature observing vasculitis relapse
following vaccination. See, e.g., J. Cannata, et al., Reactivation of Vasculitis After Influenza
Vaccination, 283 Br. Med. J. 526 (1981), filed as Ex. 63 (ECF No. 41); A. Kostianovsky, et al.,
Immunogenicity and Safety of Seasonal and 2009 Pandemic A/H1N1 Influenza Vaccines for
Patients with Autoimmune Diseases: A prospective, Moncentre Trial on 199 Patients, 30 Clin.
Exp. Rheumatol. S83 (2012), filed as Ex. 33 (ECF No. 41) (noting nineteen mild autoimmune
disease flares following flu vaccine administration); but see Jeffs II (flu vaccine likely safe for
existing cases of ANCA-associated vasculitis). He further submitted adverse event reports of
spontaneous vasculitis following immunizations across three international databases. See, e.g., P.
17
Felicetti, et al., Spontaneous Reports of Vasculitis as an Adverse Event Following Immunization,
34 Elsevier 6634, 6634-40 (2016), filed as Ex. 20 (ECF No. 41) (cataloging all reports of vasculitis
to EV,11 VAERS,12 and VigiBase13 between January 2003 and June 2014). Although Dr. Gershwin
categorized vasculitis as an uncommon or rare disease, he maintained that the literature cited above
supported a causal connection between the flu vaccine and vasculitis. Tr. at 112-13, 114, 121.

Dr. Gershwin next discussed the nature of autoimmune conditions and autoimmunity
generally, given the accepted principle that genetic and environmental factors can trigger
autoimmune disorders. Tr. at 94-96. He was unable to identify what specific suspected genetic
factors might be relevant to Ms. Knorr (beyond the somewhat conclusory assertion in his first
report that she likely had a “unique genetic predisposition”). Gershwin First Rep. at 24. Instead,
he emphasized possible environmental factors. Tr. at 96. Thus, given Ms. Knorr’s course of
symptoms (including hearing loss and Bell’s palsy) following the first flu vaccine, and then her
worsening hearing loss (and vasculitis diagnosis) following the second, a “striking” association
exists between Ms. Knorr’s vaccinations and her subsequent disease course. Id. at 97.

To bulwark his theory, Dr. Gershwin attempted to provide a close reading of Ms. Knorr’s
documented health course based upon the filed record. He concurred with her formal MPA
vasculitis diagnosis in November 2013, although he did point to a record suggesting a treater
expressed concerns about GPA. Tr. at 71, 88, 101, 117, 297; Gershwin Frist Rep. at 21; Ex. 18 at
666. Dr. Gershwin opined that Ms. Knorr experienced flu-like symptoms and hearing loss
following her receipt of the flu vaccine in November 2012, with additional flu-like symptoms and
a worsening of hearing loss following the second flu vaccine received in October 2013 – in turn
leading to the vasculitis diagnosis roughly a month later, in November 2013. Tr. at 89-91. The
second vaccine she received in October 2013 was essentially a “booster shot” that amplified her
aberrant immunologic reaction (already established as pathogenic in light of the first time she
received the flu vaccine), resulting in her “crescendo” of symptoms leading to her November

11
EudraVigilance (“EV”) is the European Medicines Agency (“EMA”) management system for reporting adverse
reactions to medications and drugs. EMA (along with the reporting system) is maintained by the European Union. The
database requires registration to access materials. As of June 15, 2018, the EMA’s website is currently under
construction (http://www.ema.europa.eu/).
12
The Vaccine Adverse Event Reporting System (“VAERS”) is a national warning system designed to detect safety
problems in U.S.-licensed vaccines. See About VAERS, VAERS, https://vaers hhs.gov/about html (last visited June
15, 2018). It is managed by both the CDC and the FDA. VAERS monitors and analyzes reports of vaccine related
injuries and side effects from both healthcare professionals and individuals.
13
VigiBase is a World Health Organization (WHO) database used to obtain case safety reports (ICSRs) of suspected
adverse effects of medicine, including vaccinations, collected between 1960-2017 from member countries. Currently,
110 contribute to the database. It is maintained by Uppsala Monitoring Centre in Uppsala, Sweden, on behalf of the
WHO. See What Is VigiBase?, UPS, https://www.who-umc.org/vigibase/vigibase/ (last accessed on June 15, 2018).

18
hospitalization and vasculitis diagnosis. Id. at 92, 99, 117. Thus, taking her health course as a
whole (including her symptoms following both vaccinations), Dr. Gershwin proposed that Ms.
Knorr’s onset of hearing loss following her first flu vaccine was the initial symptom of vasculitis
(given the indolent nature of the disease, its presenting limited location in the head and neck, and
its apparent stabilization following the placement of hearing tubes). Id. at 91, 115-17.

In support of these contentions, Dr. Gershwin cited a host of articles purporting to show a
connection between hearing loss and vasculitis. Gershwin Third Rep. at 2; see S. Bakthavachalam,
et al., Hearing Loss in Wegener’s Granulomatosis, 25 Otol. & Neurotol. 833, 833-34 (2004), filed
as Ex. 98 (ECF No. 42-3) (“Bakthavachalam”) (56 percent of GPA patients in a 36-person study
developed documented hearing loss); N. Rasmussen, et al., Management of the Ear, Nose, and
Throat Manifestations of Wegener’s Granulomatosis, 13 Curr. Opin. Rheumatol. 3, 4 (2001), filed
as Ex. 99 (ECF No. 42-4) (“Rasmussen”) (30 percent of GPA patients in 124-person study
developed new deafness); K. Devaney, et al., Wegener’s Granulomatosis of the Head and Neck,
107 Ann. Otol. Rhinol. 439, 440 (1998), filed as Ex. 100 (ECF No. 42-5) (“Devaney”) (ear pain,
edema, and hearing deficit are clinical manifestations of GPA); G. Hoffman, et al., Wegener’s
Granulomatosis: An Analysis of 158 Patients, 116 Ann. Intern. Med. 488, 489 (1992), filed as Ex.
101 (ECF No. 42-6) (“Hoffman”) (90 percent of GPA patients in a 159-patient study presented
with nasal, sinus, tracheal, or ear abnormalities during initial consultation for treatment). Dr.
Gershwin relied on the above articles despite the fact that they solely involved Wegener’s/GPA
(consistent with his view that MPA and GPA were largely congruent for purposes of present
analysis).14

Dr. Gershwin next discussed Ms. Knorr’s symptom progression over time, endeavoring to
pinpoint specific clinical evidence for a vaccine-induced vasculitis injury (or an inflammatory
process more generally). As mentioned earlier, Dr. Gershwin maintained that Ms. Knorr’s
November 2012 manifestation of hearing loss (and subsequent treatment with tubes) represented
the onset of her vasculitis. Tr. at 129, 152. He disputed the contention (raised by Respondent) that
Ms. Knorr’s hearing problems were attributable to a bacterial infection. Id. at 119, 127, 132;
Gershwin Third Rep. at 1. Rather, Dr. Gershwin opined that the medical record did not establish
the existence of a bacterial infection at the time (which would be evidenced by severe pain, pus,
and the treatment determination to make immediate placement of tubes or employ intensive
antibiotics). Tr. at 120.

14
Notably, one article cited by Dr. Gershwin (seeking to define the typical presenting clinical symptoms of MPA)
specifically excluded patients with ear, nose, and throat symptoms from inclusion in the study. See L. Guillevin, et al.,
Microscopic Polyangiitis, 42 Arthritis & Rheumatism 421, 422 (1999), filed as Ex. 50 (ECF No. 41).

19
Dr. Gershwin also mentioned Ms. Knorr’s ESR levels taken in October 2013, which he
asserted increased four-fold in the time period following her second vaccination and her
hospitalization (thereby establishing a rapidly-progressive inflammatory process). Tr. at 107, 120.
Although Dr. Gershwin argued that an elevated ESR can be evidence of systematic inflammation,
however, he could not explain Ms. Knorr’s course of up and down rates (as her October 2013 ESR
levels - taken two weeks post-vaccination – were normal, when compared with those taken during
her hospitalization in November). Id. at 140. He further admitted that proof of an elevated ESR
alone could not advance his overall theory. Id. at 107. At the same time, Dr. Gershwin asserted
that Ms. Knorr’s other lab results (like increased platelet levels) lent further support for his overall
opinion that Ms. Knorr was experiencing some inflammatory process that could be linked to her
vaccination (and earlier onset vasculitis) – even though her initial ESR findings, taken closer-in-
time to the second vaccination, were not elevated. Id. at 139-140, 155; Gershwin Third Rep. at 1.

In addition, Dr. Gershwin addressed Petitioner’s smile asymmetry that a June 2013 record
tangentially mentions as occurring in the time between the two vaccinations at issue herein. He
proposed that this could have been evidence of Bell’s palsy, a form of neuritis or neuropathy of
the face (although it was never formally diagnosed as such). Tr. at 92, 97; see Ex. 3 at 18, 99; Tr.
at 33-34. If so, Dr. Gershwin found this symptom to be an important potential inflammatory
marker, and thus an additional indicator of an ongoing vasculitis initiated by her initial receipt of
the flu vaccine in November 2012. Tr. at 93.

Besides offering support for his own theory, Dr. Gershwin made efforts to rebut
Respondent’s proposed alternate explanations for Ms. Knorr’s symptoms. Tr. at 104; Gershwin
Second Rep. at 1-2. He acknowledged that Ms. Knorr’s treaters had included a possible EBV
infection as an explanation for her condition in her differential diagnosis in 2013 (given relevant
testing as early as October 2013 revealed the presence of some form of EBV infection, as noted
by treaters in contemporaneous records). Tr. at 104-05, 300. Dr. Gershwin maintained, however,
that these elevated titer levels simply indicated that Ms. Knorr’s immune system had previously
been active against the EBV virus (consistent with her medical record, which revealed she had
experienced EBV-mediated mononucleosis earlier in life), rather than that she was experiencing a
new infection. Id. at 106, 147, 150. Accordingly, any EBV infection she was experiencing had
been reactivated by something else – most likely the ongoing autoimmune vasculitis, which Dr.
Gershwin maintained had begun the year before – rather than that the reactivated EBV infection
was causing her vasculitis.

To support this proposition, Dr. Gershwin emphasized literature discussing how EBV-
related antibody titer measurements should be clinically interpreted, citing an article released by
the Centers for Disease Control (the “CDC”). See Epstein-Barr Laboratory Testing, CDC,
https://www.cdc.gov/epstein-barr/laboratory-testing.html (last accessed on June 15, 2018), filed
20
as Ex. 103 (ECF No. 47-1) (“CDC Article”). The CDC Article discussed the lab testing helpful in
identifying not only whether a person suffers from an EBV infection, but also when the infection
may have begun. CDC Article at 1. To do so, it reviewed the different kinds of antibodies that will
be observed when an EBV infection exists. VCA IgM antibodies appear early in an active EBV
infection but soon disappear, whereas EBNA antibodies are not seen during the acute phase of
infection but instead arise slowly, up to two to four months after symptoms onset. Id. An individual
experiencing a current or ongoing EBV infection should test positive only for anti-VCA antigen
antibodies, whereas finding antibodies to both anti-VCA IgM and EBNA supports the conclusion
that the initiating EBV infection likely occurred several months to years earlier. Id. at 2. Because
Petitioner’s testing revealed the latter, she was more likely than not experiencing a reactivated
infection, rather than a new one that could have caused her subsequent vasculitis. Tr. at 300-01.
He added that irrespective of these results, no treater ultimately concluded that an EBV infection
was causative of her MPA. Id. at 135, 299-301, 311, 313.

Moreover, even if Ms. Knorr had been suffering from an intercurrent, recent EBV
infection, Dr. Gershwin did not deem that as undermining his theory, because the EBV infection
would at best be a secondary stimulus resulting from a pre-existing process initiated by the flu
vaccine. Tr. at 103, 135, 148; Gershwin Second Rep. at 1-2. Dr. Gershwin thus characterized EBV
as a “polyclonal B cell activator,” with the measured antibodies attributable to the autoimmune
process he alleged Petitioner was then experiencing. Gershwin Second Rep. at 1-2; Wijngaarden
at 241 (concluding there is not much support for a viral trigger for ANCA-associated vasculitis);
P. Xu, et al., Antineutrophil Cytoplasmic Antibody-Associated Vasculitis Associated with Epstein-
Barr Virus Infection: A Case Report and Review of the Literature, 42 Infection 591, 591-92 (2014),
filed as Ex. 85 (ECF No. 41) (“Xu”). Xu is a case report discussing the onset of ANCA-associated
vasculitis in a sixteen-year-old patient, where initial lab testing indicated a serum positive IgM
antibody against EBV, but concluding that more research is required before a causal association
could be determined. Id. at 594.15

Dr. Gershwin also attempted to rebut Respondent’s assertion that Ms. Knorr’s
immunotherapy allergy injections (or any diagnosed allergy for that matter) from the summer of
2013 may have played a role in her development of vasculitis, deeming the concept a “red herring.”
Tr. at 108, 130, 136, 315-16; Gershwin Second Rep. at 1. In his view, the relevant scientific
literature does not support the conclusion that allergy shots play any part in B cell immune system
stimulation, despite various submissions by Respondent proposing a possible association. Tr. at

15
Dr. Gershwin cited additional case reports similarly concluding that a causal relationship between EBV and
vasculitis-type diseases has yet to be determined. See P. Zoroquiain, et al., Leukocytoclastic Vasculitis as Early
Manifestation of Epstein-Barr Virus-Positive Diffuse Large B-Cell Lymphoma of the Elderly, 34 Am. J.
Dermatopathol. 330 (2012), filed as Ex. 87 (ECF No. 41); M. Yamazaki, et al., Transient Lupus Anticoagulant Induced
by Epstein-Barr Virus Infection, 2 Blood Coag. Fib. 771 (1991), filed as Ex. 88 (ECF No. 41).

21
110; see, e.g., A. Linneberg, et al., Allergen-Specific Immunotherapy and Risk of Autoimmune
Disease, 12 J. Allergy Clin. Iummonol. Pract. 161-67 (2012), filed as Ex. 69 (ECF No. 41)
(identifying case reports and concluding evidence to support idea that allergen-specific
immunotherapy as a trigger for autoimmune diseases is weak and speculative).16 On cross, Dr.
Gershwin asserted that he was the most qualified of the experts to opine on this particular topic,
given his background in allergy medicine. Tr. at 303. Relying on this expertise, he opined that
immunotherapy injections are not designed to stimulate the immune system, although he did allow
for the possibility that any antigen could itself be a stimulant. Id. at 304. Overall, however, he
testified that the literature suggests that immunotherapy-induced vasculitis is far too rare to be a
persuasive possible explanation for Petitioner’s MPA. Gershwin Second Rep. at 1.

Finally, Dr. Gershwin asserted that the onset of Ms. Knorr’s symptoms occurred three or
four days post-vaccination in November 2012, with it progressing thereafter in accordance with
the medical record. Tr. at 121, 125. He deemed her initial hearing loss to be the first manifesting
symptom, adding that it did not matter to his theory whether that loss was discovered at the time
he alleged or even in the winter of 2013. Id. at 306. He stressed, however, that his theory was
dependent on a finding that the autoimmune process in question began with the 2012 flu vaccine.
Id. at 153-54 (describing both vaccines as “integral” to his theory).

On rebuttal, Dr. Gershwin spent some time addressing distinctions drawn by Respondent’s
expert Dr. Oddis between MPA and GPA. In his view, the overlap between the two vasculitis
variants overshadowed any clinical or diagnostic differences (and therefore it did not matter if
some of the literature he relied upon to associate Ms. Knorr’s symptoms to her MPA, like hearing
loss, mostly related to GPA). Tr. at 296. He noted as well that some treaters had suggested
Petitioner was suffering from GPA/Wegener’s, as well as the fact that treatments for either variant
would be similar. Id. at 297-99; Ex. 18 at 740-42, 769 (internal medicine progress note indicating
that rheumatology consult suggested MPA diagnosis, but internist suggested possible
Wegener’s/GPA given renal laboratory abnormalities, and treated Petitioner the same given
similarities in treatment for both diseases).

16
Similarly, Dr. Gershwin offered a series of case reports concerning immunotherapy-induced vasculitis (indicating
the rarity of such a reaction) to bolster his assertions that Ms. Knorr’s injections did not causally contribute to her
symptoms. See, e.g., M. Branco-Ferreira, et al., Distal Digital Vasculitis Induced by Specific Immunotherapy, 53
Allergy 102 (1998), filed as Ex. 71 (ECF No. 41); G. Cabrera, et al., Digital Vasculitis Following Allergic
Desensitization Treatment, 20 J. Rheumatol. 1970 (1993), filed as Ex. 72 (ECF No. 41); L. Sanchez-Morillas, et al.,
Vasculitis During Immunotherapy Treatment in a Patient with Allergy to Cupressus Arizonica, 33 Allergol. &
Immunopathol. 333 (2005), filed as Ex. 75 (ECF No. 41); P. Phanuphak, et al., Onset of Polyarteritis Nodosa During
Allergic Hyposensitization Treatment, 68 Am. J. Med. 479 (1980), filed as Ex. 81 (ECF No. 41).

22
C. Respondent’s Experts

1. Dr. Lindsay Whitton

Respondent’s first expert, Dr. Whitton, submitted one written report and testified at
hearing, proposing that the flu vaccine has not been shown to cause vasculitis, and therefore
could not have caused Petitioner’s illness. See Whitton Expert Report, dated June 6, 2016, filed
as Ex. C (ECF No. 18-3) (“Whitton Rep.”); Tr. at 165-242. Dr. Whitton’s testimony mostly
pertained specifically to Petitioner’s causation theory as opposed to the veracity of her diagnosis
or its onset, although he did occasionally address the latter points.

Dr. Whitton is currently a professor in the Department of Immunology and Microbial
Science at the Scripps Institute in La Jolla, California, and has served in this capacity since 1998.
Tr. at 158. He received his medical degree from the University of Glasgow in Scotland. Tr. at
158-59; Whitton CV, filed as Ex. D (ECF No. 18-4) at 1. He also received a Ph.D. in molecular
biology from the University of Glasgow. Whitton CV at 1. His practice consists almost
exclusively of research related to viral immunology, although he also oversees a graduate
student program focused on virology and immunology. Tr. at 160-61. Eighty to ninety percent
of his research involves immune system responses to viruses, bacteria, and live virus vaccines.
Id. He has also served on the editorial board of various academic journals focused on virology.
Id. at 162. Dr. Whitton currently serves as an editor of Virology and has published roughly 35
papers on DNA vaccines. Id. Dr. Whitton does not see patients and is not currently licensed to
practice medicine in the United States. He does not hold any specialties in disease treatment.

With regard to Petitioner’s proffered medical theory, Dr. Whitton admitted that reliable
medical literature supports the existence of (rare) vaccine-induced injuries occurring via the
biologic mechanism of molecular mimicry. Tr. at 190, 204. However, Dr. Whitton took issue
with that mechanism’s applicability to this case, since it is so dependent on an adaptive immune
response (which typically requires a boosted or adjuvanted vaccine). Id. at 191-92. The Fluarix
form of the flu vaccine Petitioner received is not adjuvanted, diminishing the likelihood that
molecular mimicry would occur at all. Id. As a result, Ms. Knorr’s reliance on an innate immune-
mediated response in this case (Tr. at 126; Gershwin First Rep. at 23) rendered it even less likely
that the flu vaccine could have initiated an autoimmune process (even though he later admitted
an “adjuvant-free preparation[]” like the flu vaccine is still sufficiently immunogenic to
function). Id. at 236, 240. Despite his assertions, Dr. Whitton did acknowledge that an innate
response “may help facilitate or amplify the adaptive response[,]” although it does not appear
that this point altered his opinion in the instant case. See id. at 192.

23
Dr. Whitton was the first expert to note the importance of Petitioner’s specific diagnosis.
He stated that he agreed with Ms. Knorr’s final diagnosis of MPA, but disputed Dr. Gershwin’s
discussion of her diagnosis as interchangeable with Wegener’s granulomatosis (or GPA). Tr. at
166, 214, 241-42; Whitton Rep. at 5-6. Rather, in his view MPA is distinguishable from GPA,
given the presence of granulomatous inflammation specific to GPA. Tr. at 241. Head and neck
symptoms (as seen in Ms. Knorr’s case) are also more common in patients with GPA than MPA,
although hearing loss can precede both forms of the disease. Id. at 215. Dr. Whitton otherwise
agreed with Dr. Gershwin that the course of MPA can be indolent (and eventually progressive),
rather than strictly acute, and can be initiated by both genetic and environmental factors. Id. at
215. He also agreed that MPA is rare, although he disputed it was as uncommon as Dr. Gershwin
seemed to suggest. Id. at 206; Whitton Rep. at 9.

Based upon his review of Ms. Knorr’s health course, Dr. Whitton asserted that her
vasculitis was likely due to an alternate cause, such as a bacterial infection. At hearing, Dr.
Whitton also offered various explanations for a viral-induced trigger, including a pre-existing
ear infection or a reactivation of an EBV infection. Tr. at 165-70, 184-88; Whitton Rep. at 6.
Dr. Whitton further opined that Ms. Knorr’s onset of allergies and subsequent immunotherapy
injections could have played some role in her eventual MPA diagnosis, although he later
admitted her symptoms were not temporally congruent with the expected allergy season. Tr. at
174-75, 213; Whitton Rep. at 7.

To support the above, Dr. Whitton identified specific examples from the medical record.
Ms. Knorr reported an onset of hearing loss in January of 2013 (or possibly a few months prior
near the end of 2012). Tr. at 165-66. But in Dr. Whitton’s reading of the records, Petitioner was
likely experiencing a bacterial infection of the middle ear during this time. Id. at 167-69, 170;
Whitton Rep. at 8, 10. For support, he pointed to records from February 2013, indicating
complaints of ear pain, redness/cloudiness in the tympanic membrane, fluid in the ear, and
antibiotic treatment. Tr. at 167. The antibiotics she was prescribed likely eradicated the
infection, but she subsequently developed noninfectious serous otitis media causing her hearing
problems (and resulting the placement of tubes to equalize pressure in the ear). Id. at 170. Dr.
Whitton also took note of a medical record indicating that Ms. Knorr had been diagnosed with
fluid behind the ear pre-vaccination in 2011. Id. at 213. Taken together, Dr. Whitton attempted
to categorize Ms. Knorr’s hearing problems (or infection) as “chronic,” despite additional later
records indicating unremarkable findings. Id.

Moving to the summer of June 2013, Dr. Whitton addressed references to an undiagnosed
Bell’s palsy-type facial asymmetry. Tr. at 171, 173. In his view, the development of these
symptoms (along with the subsequent evidence from October 2013) suggested Ms. Knorr had
possibly experienced a “recurrence or reactivation” of an EBV infection she experienced earlier
24
in life. Id. at 172-73, 181-82, 320-324; Whitton Rep. at 6-7, 9; see B. Lazarus, et al., Recent
Advances in Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis, 28 Indian J. Neph.
86, 89 (2016) (“Lazarus”) (categorizing infections as a “second hit” inducer of autoimmunity in
the context of the pathogenesis of AAV). If so, then during such a reactivation, Ms. Knorr would
have developed anti-EBV IgM antibodies (which subsequent testing corroborated), making
them a plausible trigger for her MPA. Tr. at 188.

For support, Dr. Whitton cited case reports indicating an associative link between the
EBV virus and vasculitis, although he admitted he could not say for sure if EBV could actually
cause the disease or its relevant subtypes, given the state of the literature (and the speculation
inherent to case reports generally). Tr. at 188, 196; G. Teng, et al., Vasculitis Related to Viral
and Other Microbial Agents, 29 Best. Prac. Res. Clin. Rheumatol. 226, 236-37 (2015), filed as
Ex. C, Tab 3 (ECF No. 19-5) (“Teng”) (citing case reports); A. Schned, et al., Fatal Relapse of
ANCA-Associated Glomerulonephritis Triggered by Successive Epstein-Barr and Varicella
Zoster Virus Infections, 47 Am. J. Kidney Dis. 915-922 (2005), filed as Ex. C, Tab 8 (ECF No.
20-3) (“Schned”) (case report detailing relapse of GPA following EBV infection, but
determining that it cannot be stated with certainty that the EBV virus caused the relapse); C.
Casiraghi, et al., Epstein-Barr Virus and Autoimmunity: The Role of a Latent Viral Infection in
Multiple Sclerosis and Systematic Lupus Erythematosus Pathogenesis, 8 Future Virology 173
(2013), filed as Ex. C, Tab 5 (ECF No. 19-7) (attempting to link EBV to the development of
autoimmunity, but concluding that there is no clear evidence establishing EBV as a trigger).17

In making this argument, Dr. Whitton directly took on Dr. Gershwin’s assertions about the
significance of Petitioner’s EBV antibody titer test results, and whether they revealed her EBV
infection to be primary or a secondary/reactivated infection from some time in her prior medical
history. Tr. at 184-88, 196; Whitton Rep. at 2, 4, 6-7.18 Dr. Whitton admitted (as per the CDC
Article) that the testing at issue revealing presence of EBV antibodies was consistent with the

17
Dr. Whitton’s report also cited additional case reports acknowledging a possible association between the EBV virus
and vasculitis, but ultimately concluding that a causal relationship has yet to be determined. See Xu (filed by Petitioner
and Respondent); T. Daikeler, et al., Fever and Increasing cANCA Titre After Kidney and Autologous Stem Cell
Transplantation for Wegener’s Granulomatosis, 64 Ann. Rheum. Dis. 646 (2005), filed as Ex. C, Tab 7 (ECF No. 20-
2); R. Ranganath et al., Crescentic Glomerulonephritis and Leucocytoclastic Vasculitis Associated With Acute EBV
Infection, 16 Nephrology 617 (2001), filed as Ex. D (ECF No. 37-1); M. Yamaguchi et al., Anti-Neutrophil
Cytoplasmic Antibody-Associated Vasculitis Associated With Infectious Mononucleosis Due to Primary Epstein-Barr
Virus Infection: Report of Three Cases, 7 Clin. Kidney J. 45 (2014), filed as Ex. E (ECF No. 37-2).
18
Dr. Whitton also noted the contradiction between Dr. Gershwin’s embrace of bystander activation as a possible
mechanism under his causation theory and the actual facts of the case. If, he reasoned, bystander activation explained
the autoimmune process that allegedly caused Ms. Knorr’s MPA, then the same tests revealing the presence of
reactivated EBV antibodies should not have come out negative for the reactivation of other infections like
cytomegalovirus (a common infection that Ms. Knorr likely would have been exposed to in the past). Tr. at 186-87.

25
latter, although he maintained that convalescence for EBV can be prolonged (weeks to months),
thus allowing for the possibility that the EBV infection had begun sometime in 2013 (even if before
that October). Tr. at 217-18; see M. Paschale, et al., Serological Diagnosis of Epstein-Barr Virus
Infection: Problems and Solutions, 12 World J. Virol. 31, 31 (2012), filed as Ex. F (ECF No. 49-
1) (“Paschale”) (finding that the presence of VCA IgM and VCA IgG without EBNA-1 IgG
suggests an acute infection, while the presence of VCA IgG only and EBNA-1 IgG without VCA
IgM suggests a past infection, and the presence of all three may be detected simultaneously in a
recent infection or during a course of reactivation).19 He otherwise questioned Dr. Gershwin’s
view that a reactivated EBV viral infection could only induce expansion of pre-existing cells
responsible for creating ANCA antibodies (i.e., exacerbate an existing autoimmune process) – it
could just as easily directly cause the process in the first place. Tr. at 196.

Dr. Whitton also deemed significant Ms. Knorr’s receipt of immunotherapy allergy
injections during the summer of 2013, although he admitted that he was “not honestly utterly
certain about the composition of the . . . shots.” Tr. at 175; see also Whitton Rep. at 7. Such
allergy shots could be a possible trigger of vasculitis, via an adjuvant contained in the shots,
such as alum. Tr. at 175-76. (This argument was later greatly undercut when Dr. Whitton
admitted that immunotherapy injections are in fact not adjuvanted (Tr. at 249)). Dr. Whitton
further disputed Dr. Gershwin’s assertion that the injections were at best homeopathic in nature,
arguing that they could be dangerous because they involve “antibody-mediated disease,” and
could result in anaphylaxis. Id. at 176-77, 237. In support, Dr. Whitton cited to various case
reports purportedly evidencing an association between immunotherapy injections and vasculitis,
although he admitted he places little weight on case reports generally. Id. at 178; see, e.g., A.
Linneberg, et al., Allergen-Specific Immunotherapy and Risk of Autoimmune Disease, 12 Curr.
Opin. Allergy Clin. Immunol. 635-39 (2012), filed as Ex. C, Tab 10 (ECF No. 20-6) (evidence
to support immunotherapy-induced autoimmune diseases is weak and based on case reports).

Overall, Dr. Whitton could not opine for sure what caused Ms. Knorr’s vasculitis. Tr. at
207. Rather, he maintained that there were too many confounding factors in her health history
to conclude that the flu vaccines caused her injury. Id. Regardless, he insisted that Ms. Knorr’s

19
Respondent was later allowed to recall Dr. Whitton to clarify his views on the CDC Article – and specifically its
statements about what conclusions could be drawn about the nature of EBV antibody test results. See generally Tr. at
320-24. He claimed that these criteria (which Petitioner stressed suggested that the proper reading of her test results
revealing the presence of EBV antibodies was that the infection was resolved rather than intercurrent) had been
revisited – but in any event that he was not maintaining that Petitioner suffered from a primary/recent infection, but
rather that the antibodies had been reactivated due to prior exposure. Id.

26
vasculitis began no earlier than October 2013 (following her second vaccination), although he
somewhat revised this view in light of her Bell’s palsy-like symptoms, which he opined could
indicate onset of symptoms as early as June 2013. Id.

2. Dr. Chester Oddis

Respondent’s second expert, Dr. Oddis, submitted one written report and testified at
hearing. Similar to Dr. Whitton, Dr. Oddis proposed that the flu vaccine has not herein been shown
to cause Ms. Knorr’s vasculitis, but he also offered testimony illuminating the precise nature of
Petitioner’s illness that bears significantly on my ultimate determination of this case. See Oddis
Expert Report, dated July 1, 2016, filed as Ex. A (ECF No. 18-1) (“Oddis Rep.”).

Dr. Oddis is board-certified in internal medicine and rheumatology Tr. at 250; Oddis CV,
filed as Ex. B (ECF No. 18-2) (“Oddis CV”). He is presently a Professor of Medicine in the
Division of Rheumatology and Clinical Immunology in the School of Medicine at the University
of Pittsburgh. Tr. at 250. He received his undergraduate degree from the University of Pittsburgh
and his medical degree from Pennsylvania State University School of Medicine. Id. at 251. Dr.
Oddis specializes in the treatment of idiopathic inflammatory myopathies. Id. at 253-54. He has
also directed large clinical myositis trials and published extensively on the topic and its correlation
with autoantibodies. Id. at 254. In addition to his teaching duties, Dr. Oddis maintains a clinical
practice. Id. at 252. Dr. Oddis testified that he sees patients at the University of Pittsburgh clinic
weekly. Id. His clinical practice includes all rheumatologic diseases, including ANCA-vasculitis
and MPA. Id. at 253. At hearing, he estimated that he has treated roughly 100 patients with ANCA-
positive vasculitis (including MPA and GPA). Id.

Consistent with Drs. Gershwin and Whitton, Dr. Oddis agreed that Petitioner suffers from
MPA vasculitis. Tr. at 259; Oddis Rep. at 4. He did not, however, accept Dr. Gershwin’s assertion
that MPA and GPA (Wegener’s) were interchangeable, given important clinical distinctions
between the two, including the presenting antibody and evidence of granulomas in tissue –
distinctions born out in Petitioner’s presentation (since, as the record establishes above, Petitioner
did not have the antibodies associated with GPA, nor did she ever display granulomas). Tr. at 259-
60, 263.

To illustrate this point, Dr. Oddis embarked on an extended explanation of the distinctions
between the two ANCA-associated variants. He characterized MPA as a p-ANCA-antibody
disease targeting the myeloperoxidase antigen in the body; GPA, by contrast, is c-ANCA-mediated
and targets the proteinase 3 antigen. Tr. at 250, 289. With GPA, moreover, a tissue biopsy would
reveal the presence of immune-mediated granulomas, while MPA is not so characterized. Id. at
260-61. In addition, MPA typically presents in an “aggressive” and acute fashion, and is not
associated with a long progressive course. Id. at 289. Finally, while both GPA and MPA can
27
manifest adverse symptoms related to kidney and respiratory function, ENT dysfunction
(including hearing loss) is rarely associated with MPA. Id. at 261-62, 264, 295. This therefore
reduced the significance, in Dr. Oddis’s estimation, of the hearing loss evidence in the medical
record cited as proof that Petitioner suffered from MPA beginning sometime between the first and
second vaccinations (although he acknowledged that such symptoms could be secondary to
different forms of vasculitis regardless). Id. at 295.

Relying on this diagnostic distinction, Dr. Oddis maintained that Petitioner improperly
relied on literature specific to GPA to support her claim (due to the recognized clinical differences
between GPA and MPA, particularly with regard to ENT symptoms). See Guillevin at 422.
Guillevin in particular specifically studied patients with MPA, and in so doing excluded GPA
patients with ENT symptoms, such as the presence of granulomas in the ear. Id. at 291-93. Much
of the other literature cited by Dr. Gershwin as establishing a causal connection between vasculitis
and hearing loss related to patients diagnosed with GPA (not MPA). Tr. at 268; see generally
Bakthavachalam; Rasmussen; Hoffman. Ms. Knorr’s diagnosis, by contrast, clearly did not include
GPA, and the medical record revealed nothing that would support such an alternative diagnosis.
Tr. at 269.

Based on a review of Ms. Knorr’s health history, Dr. Oddis proposed that her hearing loss
likely began in early 2013, and could not be associated with any symptoms relating to her
subsequent 2013 MPA diagnosis. Tr. at 264, 267, 282, 295. He described her hearing loss as
unilateral, but allowed for the possibility that in some instances it presented as bilateral. Id. at 264,
283-84. Although he could not identify a specific cause of this hearing loss, Dr. Oddis opined that
the record suggested she likely had some form of an ear infection in early 2013. Id. at 266. In
addition, Ms. Knorr’s treaters diagnosed her with “serous otitis” in 2013, and proceeded as if the
otitis were infection-induced, despite a lack of record of evidence of pus or other more obvious
indicia of infection. Id. at 267, 284-85; Oddis Rep. at 5.

In addition (and consistent with Dr. Whitton’s testimony), Dr. Oddis opined that Ms.
Knorr’s health history included too many intervening factors to conclude that the flu vaccine was
casual of her vasculitis injury (such as chronic ear infection, allergies, and the allergy shots
treatment). Tr. at 267-68; Oddis Rep. at 5-6. Dr. Oddis specifically expressed concern with the
twenty-two immunotherapy injections Ms. Knorr received in the summer of 2013, which he opined
could not be discounted as a causal agent. Tr. at 267. Immunotherapy injections may stimulate the
immune system “in some fashion or form,” although Dr. Oddis later admitted that he could not say
what specifically the injections were meant to do. Id. at 269, 289. He also acknowledged that he
lacked sufficient expertise to opine on the topic. Id. at 289. Dr. Oddis did not, however, deem Ms.
Knorr’s Bell’s palsy-type symptoms (facial asymmetry) suggested in a June 2013 record to be of
any significance, given the lack of facial nerve involvement with MPA. Id. at 270.

28
With regard to Ms. Knorr’s October 2013 symptoms, Dr. Oddis observed the discrepancy
between her severe symptomology course and her “rock solid” ESR levels when first measured in
October 2013, not long after receipt of the second flu vaccine dose. Tr. at 271; Oddis Rep. at 5-6.
According to Dr. Oddis, a normal ESR is inconsistent with a typical MPA course unless the disease
process is “better under control.” Tr. at 272. As a result, he disputed that her vasculitis could have
begun close to the time of her vaccination. Id. Rather, he opined that early November 2013 – at
which time the record revealed her elevated ESR, coupled with a now “full blown phase” of
vasculitis (and pANCA-positive antibodies) – was the more likely onset date. Id. When cross-
examined, however, Dr. Oddis did allow for the possibility of MPA developing with an initially
normal ESR rate. Id.

Similar to Dr. Whitton, Dr. Oddis found significant the fact that Ms. Knorr’s lab results
revealed increased levels of EBV autoantibodies. Tr. at 274. Such results suggested to him that
Ms. Knorr had an active EBV infection in October 2013 that also may have played a causal role
in her development of MPA. Id. Dr. Oddis admitted that the literature cited by Respondent linking
an EBV infection to ANCA vasculitis consists mainly of case reports, although he opined that they
should be given some weight. Id. at 274-75; see also Xu. Even so, Dr. Oddis agreed that he lacked
the relevant expertise to opine as to an infectious disease alternative cause for Ms. Knorr’s injuries,
and he also declined to opine on the proper interpretation of the EBV antibody measurements set
in the CDC Article. Tr. at 287-88.

Dr. Oddis made some efforts to address the sufficiency of Petitioner’s “can cause”
showing. Tr. at 275. He testified that he knew of no evidence linking the flu vaccine to ANCA
vasculitis, and thus could not accept that the flu vaccine could have caused Ms. Knorr’s injuries
without more persuasive scientific and clinical evidence. Id. He did, however, admit that some
reliable literature suggested a seasonal correlation between the timing of flu vaccinations and onset
of MPA. Id. at 280-81; see Wijngaarden at 2. He again reiterated that overall he lacked the
expertise to opine on causation. Tr. at 279.

D. Post-Hearing Expert Reports

At my direction, the parties submitted post-hearing expert reports near the end of October
2018, to further clarify an issue I deemed to be inadequately addressed at hearing. In the process
of deciding the case, I had become concerned that Petitioner’s causation theory (which by Dr.
Gershwin’s admission relied heavily on linking the two flu vaccines to her MPA, with her
intervening ENT symptoms as proof of an initial vasculitis reaction) was deficient. However, the
obvious temporal association between the second vaccination and Petitioner’s MPA still allowed
for the possibility that her injuries were vaccine-caused – if the frame for considering her claim
were shrunk. I therefore asked them to address whether (and if so, how) the second flu vaccine

29
Petitioner received in October 2013 could be solely causal of her MPA. See Scheduling Order,
dated July 19, 2018 (ECF No. 66). Below is a brief summary of the filed responses.

1. Dr. Gershwin

Dr. Gershwin filed his supplemental report on August 30, 2018. See Post-Hearing Report,
dated August 11, 2018, filed as Ex. 104 (ECF No. 69-1) at 2-3 (“Gershwin Supp. Rep.”). Assuming
(as per my direction) that Ms. Knorr’s November 2012 vaccination played no role in the
developmental of her MPA symptoms, Dr. Gershwin opined that her second flu vaccine (received
on October 8, 2013) could alone be the trigger for her MPA.

In so maintaining, Dr. Gershwin again invoked the mechanism of molecular mimicry as
the most likely process for induction of Ms. Knorr’s MPA, with her symptoms progressing as
would be expected for a vaccine-induced reaction based on that process. Gershwin Supp. Rep. at
2. Under the assumed facts, Ms. Knorr’s symptom onset following her second vaccination
(approximately fourteen days) fell squarely within the timeframe he would expect for an immune
insult subsequent to a vaccine reaction, which in his opinion, could occur within thirty days
following vaccination. Id. at 2. For this conclusion Dr. Gershwin relied heavily on the documented
medical record, which he argued showed that Ms. Knorr had presented to treaters with concerns
for influenza-type symptoms on the 15th of October, which then progressed to more concerning
symptoms (including an increased SED rate and elevated C-reactive protein levels) between
October 22nd and her November 4th hospital presentation. Id. at 3.

Dr. Gershwin also offered two additional scientific articles in support of his opinion. See
R. Falk, et al., Clinical Manifestations and Diagnoses of Granulomatosis with Polyangiitis and
Microscopic Polyangiitis, Uptodate, filed as Ex. 105 (ECF No. 69-2); Y. Cao, et al., Polymorphism
and ANCA Disease Risk in White Populations: A Metaanalysis, 42 J. Rheumatology 292 (2015),
filed as Ex. 106 (ECF No. 69-3). These articles do not address how the flu vaccine can result in an
immunologic insult to the autonomic nervous system via Dr. Gershwin’s proposed mechanism,
however, or otherwise support causation as his prior testimony and reports proposed. Rather, they
seem to have been offered to supplement his argument that MPA and GPA are indistinguishable
for causation purposes.

Dr. Gershwin also offered a reply supplemental report aimed at further rebutting the
alternative cause based theories offered by Respondent’s experts (and revisited in their own post-
hearing reports). See Post-Hearing Report Reply, filed on Oct. 29, 2018 (ECF No. 73-1)
(“Gershwin Reply”). Consistent with earlier testimony, Dr. Gershwin again asserted that Ms.
Knorr’s EBV infection was best categorized as a “reactivation” of a prior resolved infection
(resulting from a non-specific activation of the immune system – presumably caused by the flu
vaccine). Gershwin Reply at 2. Dr. Gershwin relied on articles previously submitted with his
earlier reports, but also cited one new piece of literature. See N. Obel, et al., Serological Findings
30
in Patients with Serological Evidence of Reactivated Epstein-Barr Virus Infection, 104 APMIS
424 (1996), filed as Ex. 108 (ECF No. 73-2) (simultaneous positive results for IgM and IgG-EBNA
indicates a reactivation of latent EBV infection). He also again opined that Petitioner’s
immunotherapy injections played no role in her health course given the lack of scientific evidence
causally connecting immunotherapy with vasculitis. Gershwin Reply at 1.

2. Dr. Whitton

Dr. Whitton’s post-hearing report acknowledged that Ms. Knorr’s MPA likely began
between October and November 2013 (consistent with his earlier reports), but maintained that the
October 2013 flu vaccine she received was only temporally related to the onset of her MPA. See
Post-Hearing Report, filed as Ex. G (ECF No. 71-1) (“Whitton Post-Hearing Rep.”).

Dr. Whitton again contended that there is no verifiable scientific support for a causal
relationship between flu vaccines and any form of vasculitis. Whitton Post-Hearing Rep. at 4. He
also repeated his view that Ms. Knorr’s prior EBV infection was the more likely cause of her MPA,
characterizing the antibody titer test results as reflecting either a “late primary infection” or
“reactivation” of latent EBV. Id. at 2 (citing Ex. 3 at 50, 52); Paschale at 33. Moreover, Dr. Whitton
contented that the above conclusion is strengthened by the existence of case reports associating
the EBV virus with the onset of vasculitis (and other autoimmune diseases generally). Whitton
Post-Hearing Rep. at 3-4. He cited two case reports in support of EBV-induced vasculitis (both of
which had already been filed in the matter). See generally R. Ranganath, et al., Crescentic
Glomerulonephritis and Leucocytoclastic Vasculitis Associated with Acute EBV Infection, 16
Nephrology 617 (2011), filed as Ex. G, Tab 2 (ECF No. 71-3); M. Yamaguchi, et al., Anti-
Neutrophil Cytoplasmic Antibody-Associated Vasculitis Associated with Infectious Mononucleosis
Due to Primary Epstein-Barr Virus Infection: Report of Three Cases, 7 Clin. Kindney J. 45 (2014),
filed as Ex. G, Tab 3 (ECF No. 71-4).

3. Dr. Oddis

Respondent filed one final post-hearing report from Dr. Oddis. See Post-Hearing Report,
filed as Ex. H (ECF No. 71-5). In it, Dr. Oddis opined that flu vaccine Ms. Knorr received in
October 2013 played no role in her onset of MPA (either in isolation or in the context of her first
vaccination in 2012). Id. at 2. Similar to the post-hearing report offered by Dr. Whitton, Dr. Oddis’s
report attributed Ms. Knorr’s MPA to an EBV reactivation or even the multiple immunotherapy
injections (received between August and September 2013) as the more likely antecedent triggers.
Id. In support, Dr. Oddis cited to case reports (previously filed in the matter) revealing an
associative link between the EBV virus and onset of vasculitis, and contended that in most cases
of ANCA-associated vasculitis, there is no identifiable cause. Id. He otherwise asserted that Dr.
31
Gershwin had provided no additional evidence that the flu vaccine can cause ANCA-associated
vasculitis (or did so in this case). Id. at 1.

Procedural History

Ms. Knorr filed her Petition on October 9, 2015. Pet. at 1. Almost eight months later, after
most records in the case had been filed, on July 8, 2016, Respondent filed his Rule 4(c) report
denying that Ms. Knorr was entitled to compensation. ECF No. 17. The Statement of Completion
was then filed on February 8, 2016. ECF No. 11.

Thereafter, the parties began filing expert reports. Petitioner filed an initial expert report
from Dr. Gershwin on February 19, 2016. ECF No. 41. Respondent filed an initial expert report
from Dr. Whitton on June 6, 2016, 2016. ECF No. 18-3. Following a request to supplement the
record with additional expert support, Respondent filed a second expert report from Dr. Oddis on
July1, 2016 (ECF No. 18-1). Thereafter, Petitioner filed a supplemental report from Dr. Gershwin
on August 11, 2016. ECF No. 24-1. Given the issues identified the expert reports, I scheduled this
matter for hearing on October 26-27, 2017, to determine entitlement. ECF No. 23. Prior to the
hearing, Petitioner filed a second supplemental report by Dr. Gershwin on August 11, 2017. ECF
No. 96.

The entitlement hearing was held as scheduled on October 26-27, 2017. That hearing
included testimony from the experts identified above (along with testimony from Petitioner).
Following the hearing’s conclusion, the parties submitted post-hearing briefs on November 29,
2017, and December 6, 2017, respectively. ECF Nos. 56-57. Thereafter, as noted above I contacted
the parties and requested that they file supplemental expert reports addressing whether (were I to
find that the first flu vaccine dose was not causal of Petitioner’s MPA) the second dose from
October 2013 could be solely causal, and if so how. All experts weighed in on this topic, and the
parties also filed brief additional statements explaining their positions. ECF Nos. 72, 74. The
matter is ripe for adjudication.

Applicable Law

A. Petitioner’s Overall Burden in Vaccine Program Cases

To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
he suffered a “Table Injury” – i.e., an injury falling within the Vaccine Injury Table –
corresponding to one of the vaccinations in question within a statutorily prescribed period of time
or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table
Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §
11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1321 (Fed.
32
Cir. 2010); Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006).20
In this case, Petitioner does not assert a Table claim.

For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. Section 13(1)(a). That is, a petitioner must offer evidence that
leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence
before [he] may find in favor of the party who has the burden to persuade the judge of the fact’s
existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.
476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).
Proof of medical certainty is not required. Bunting v. Sec’y of Health & Human Servs., 931 F.2d
867, 873 (Fed. Cir. 1991). In particular, a petitioner must demonstrate that the vaccine was “not
only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.”
Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344,
1352-53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352, 1355 (Fed.
Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his assertions;
rather, the petition must be supported by either medical records or by the opinion of a competent
physician. Section 13(a)(1).

In attempting to establish entitlement to a Vaccine Program award of compensation for a
Non-Table claim, a petitioner must satisfy all three of the elements established by the Federal
Circuit in Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005): “(1)
a medical theory causally connecting the vaccination and the injury; (2) a logical sequence of cause
and effect showing that the vaccination was the reason for the injury; and (3) a showing of
proximate temporal relationship between vaccination and injury.” Althen, 418 F.3d at 1278.

Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners
must provide a “reputable medical theory,” demonstrating that the vaccine received can cause the
type of injury alleged. Pafford, 451 F.3d at 1355-56 (citations omitted). To satisfy this prong, a
petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”
Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such a theory
must only be “legally probable, not medically or scientifically certain.” Id. at 549.

Petitioners may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical

20
Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings
concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Human Servs., 59 Fed. Cl. 121,
124 (2003), aff’d 104 F. App’x 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Human Servs., No. 13-
159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).

33
theory. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009) (citing
Capizzano, 440 F.3d at 1325-26). Special masters, despite their expertise, are not empowered by
statute to conclusively resolve what are essentially thorny scientific and medical questions, and
thus scientific evidence offered to establish Althen prong one is viewed “not through the lens of
the laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant evidence
standard.” Id. at 1380. Accordingly, special masters must take care not to increase the burden
placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras v. Sec’y of
Health & Human Servs., 121 Fed. Cl. 230, 245 (2015) (“[p]lausibility . . . in many cases may be
enough to satisfy Althen prong one” (emphasis in original)), vacated on other grounds, 844 F.3d
1363 (Fed. Cir. 2017). But this does not negate or reduce a petitioner’s ultimate burden to establish
his overall entitlement to damages by preponderant evidence. W.C. v. Sec’y of Health & Human
Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted).21

The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Human Servs., 956
F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions
and views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 F.3d
at 1367; Capizzano, 440 F.3d at 1326 (“medical records and medical opinion testimony are favored
in vaccine cases, as treating physicians are likely to be in the best position to determine whether a
‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury’”)
(quoting Althen, 418 F.3d at 1280). Medical records are generally viewed as particularly
trustworthy evidence, since they are created contemporaneously with the treatment of the patient.
Cucuras v. Sec’y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).

However, medical records and/or statements of a treating physician’s views do not per se
bind the special master to adopt the conclusions of such an individual, even if they must be
considered and carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis,
conclusion, judgment, test result, report, or summary shall not be binding on the special master or
court”); Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is
nothing . . . that mandates that the testimony of a treating physician is sacrosanct – that it must be
accepted in its entirety and cannot be rebutted”). As with expert testimony offered to establish a
theory of causation, the opinions or diagnoses of treating physicians are only as trustworthy as the
reasonableness of their suppositions or bases. The views of treating physicians should also be

21
Although decisions like Contreras suggest that the burden of proof required to satisfy the first Althen prong is less
stringent than the other two, there is ample contrary authority for the more straightforward proposition that when
considering the first prong, the same preponderance standard used overall is also applied when evaluating if a reliable
and plausible causal theory has been established. Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339,
1350 (Fed. Cir. 2010).
34
weighed against other, contrary evidence also present in the record – including conflicting opinions
among such individuals. Hibbard v. Sec’y of Health & Human Servs., 100 Fed. Cl. 742, 749 (2011)
(not arbitrary or capricious for special master to weigh competing treating physicians’ conclusions
against each other), aff’d, 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec’y of Dept. of Health &
Human Servs., No. 06-522V, 2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot.
for review den’d, 100 Fed. Cl. 344, 356 (2011), aff’d without opinion, 475 Fed. App’x 765 (Fed.
Cir. 2012).

The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the
phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant
proof that the onset of symptoms occurred within a timeframe which, given the medical
understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan
v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for
what is a medically acceptable timeframe must also coincide with the theory of how the relevant
vaccine can cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of
Health & Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after remand, 105 Fed. Cl.
353 (2012), aff’d mem., 2013 WL 1896173 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Human
Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for review
den’d (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

B. Law Governing Analysis of Fact Evidence

The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 11(c)(2). The special master is required
to consider “all [] relevant medical and scientific evidence contained in the record,” including “any
diagnosis, conclusion, medical judgment, or autopsy or coroner’s report which is contained in the
record regarding the nature, causation, and aggravation of the petitioner’s illness, disability, injury,
condition, or death,” as well as the “results of any diagnostic or evaluative test which are contained
in the record and the summaries and conclusions.” Section 13(b)(1)(A). The special master is then
required to weigh the evidence presented, including contemporaneous medical records and
testimony. See Burns v. Sec’y of Health & Human Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (it is
within the special master’s discretion to determine whether to afford greater weight to
contemporaneous medical records than to other evidence, such as oral testimony surrounding the
events in question that was given at a later date, provided that such determination is evidenced by
a rational determination).

Medical records that are created contemporaneously with the events they describe are
presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s

35
health problems). Cucuras, 993 F.2d at 1528; Doe/70 v. Sec’y of Health & Human Servs., 95 Fed.
Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner’s testimony and his
contemporaneous medical records, the special master’s decision to rely on petitioner’s medical
records was rational and consistent with applicable law”), aff’d, Rickett v. Sec’y of Health &
Human Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption is
based on the linked propositions that (i) sick people visit medical professionals; (ii) sick people
honestly report their health problems to those professionals; and (iii) medical professionals record
what they are told or observe when examining their patients in as accurate a manner as possible,
so that they are aware of enough relevant facts to make appropriate treatment decisions. Sanchez
v. Sec’y of Health & Human Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr.
Apr. 10, 2013); Cucuras v. Sec’y of Health & Human Servs., 26 Cl. Ct. 537, 543 (1992), aff’d, 993
F.2d at 1525 (Fed. Cir. 1993) (“[i]t strains reason to conclude that petitioners would fail to
accurately report the onset of their daughter’s symptoms.”).

Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec’y of Health & Human Servs., No. 03-1585V, 2005
WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical
records are generally found to be deserving of greater evidentiary weight than oral testimony –
especially where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528;
see also Murphy v. Sec’y of Health & Human Servs., 23 Cl. Ct. 726, 733 (1991), aff’d per curiam,
968 F.2d 1226 (Fed. Cir. 1992), cert. den’d, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United
States v. United States Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that
oral testimony which is in conflict with contemporaneous documents is entitled to little evidentiary
weight.”)).

However, there are situations in which compelling oral testimony may be more persuasive
than written records, such as where records are deemed to be incomplete or inaccurate. Campbell
v. Sec’y of Health & Human Servs., 69 Fed. Cl. 775, 779 (2006) (“like any norm based upon
common sense and experience, this rule should not be treated as an absolute and must yield where
the factual predicates for its application are weak or lacking”); Lowrie, 2005 WL 6117475, at *19
(“[w]ritten records which are, themselves, inconsistent, should be accorded less deference than
those which are internally consistent”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a
determination regarding a witness’s credibility is needed when determining the weight that such
testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Human
Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

When witness testimony is offered to overcome the presumption of accuracy afforded to
contemporaneous medical records, such testimony must be “consistent, clear, cogent, and
compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec’y of Health & Human
36
Servs., No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In
determining the accuracy and completeness of medical records, the Court of Federal Claims has
listed four possible explanations for inconsistencies between contemporaneously created medical
records and later testimony: (1) a person’s failure to recount to the medical professional everything
that happened during the relevant time period; (2) the medical professional’s failure to document
everything reported to her or him; (3) a person’s faulty recollection of the events when presenting
testimony; or (4) a person’s purposeful recounting of symptoms that did not exist. La Londe v.
Sec’y of Health & Human Servs., 110 Fed. Cl. 184, 203-04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir.
2014). In making a determination regarding whether to afford greater weight to contemporaneous
medical records or other evidence, such as testimony at hearing, there must be evidence that this
decision was the result of a rational determination. Burns, 3 F.3d at 417.

C. Analysis of Expert Testimony

Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec’y of Health & Human Servs., 219 F.3d
1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to
the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509
U.S. 579, 594-96 (1993). See Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328, 1339
(Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir.
1999). “The Daubert factors for analyzing the reliability of testimony are: (1) whether a theory or
technique can be (and has been) tested; (2) whether the theory or technique has been subjected to
peer review and publication; (3) whether there is a known or potential rate of error and whether
there are standards for controlling the error; and (4) whether the theory or technique enjoys general
acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2 (citing Daubert,
509 U.S. at 592-95).

The Daubert factors play a slightly different role in Vaccine Program cases than they do
when applied in other federal judicial for a (such as the district courts). Daubert factors are usually
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors
are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health
& Human Servs., 94 Fed. Cl. 53, 66-67 (2010) (“uniquely in this Circuit, the Daubert factors have
been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of
expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the
persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88
Fed. Cl. at 742-45. In this matter (as in numerous other Vaccine Program cases), Daubert has not
been employed at the threshold, to determine what evidence should be admitted, but instead to
determine whether expert testimony offered is reliable and/or persuasive.

37
Respondent frequently offers one or more experts of his own in order to rebut a petitioner’s
case. Where both sides offer expert testimony, a special master’s decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe, 219 F.3d at 1362). However, nothing requires the acceptance of an expert’s conclusion
“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743
(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 91997)); see also Isaac v. Sec’y of Health &
Human Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot.
for review den’d, 108 Fed. Cl. 743 (2013), aff’d, 540 Fed. App’x 999 (Fed. Cir. 2013) (citing
Cedillo, 617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony,
based on a particular expert’s credibility, is part of the overall reliability analysis to which special
masters must subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d at 1325-26
(“[a]ssessments as to the reliability of expert testimony often turn on credibility determinations”);
see also Porter v. Sec’y of Health & Human Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this
court has unambiguously explained that special masters are expected to consider the credibility of
expert witnesses in evaluating petitions for compensation under the Vaccine Act”).

D. Consideration of Medical Literature

Both parties filed medical and scientific literature in this case – Petitioner a total of over
80 separate articles - but not every filed item factors into the outcome of this decision. While I
have reviewed all of the medical literature submitted in this case, I discuss only those articles that
are most relevant to my determination and/or are central to Petitioner’s case – just as I have not
exhaustively discussed every individual medical record filed. Moriarty v. Sec’y of Health &
Human Servs., No. 2015-5072, 2016 WL 1358616, at *5 (Fed. Cir. Apr. 6, 2016) (“[w]e generally
presume that a special master considered the relevant record evidence even though he does not
explicitly reference such evidence in his decision”) (citation om

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/4358120. Public record. Not legal advice.