VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_17-vv-00947
Package ID: USCOURTS-cofc-1_17-vv-00947
Petitioner: Erwin Casazza
Filed: 2017-07-14
Decided: 2023-09-25
Vaccine: influenza
Vaccination date: 2015-09-03
Condition: rheumatoid arthritis
Outcome: dismissed
Award amount USD: 

AI-assisted case summary:
Erwin Casazza, a 73-year-old man, filed a petition alleging that the influenza vaccine he received on September 3, 2015, caused him to suffer rheumatoid arthritis (RA). He later amended his petition to alternatively allege reactive arthritis. The case proceeded as an off-Table claim, meaning Mr. Casazza had to prove causation-in-fact. He presented expert testimony from Dr. M. Eric Gershwin, who initially opined that the vaccine caused reactive arthritis but later agreed with respondent's experts that Mr. Casazza had RA. Dr. Gershwin then proposed a theory that the flu vaccine could act as the final trigger for RA in predisposed individuals, citing post-vaccination cytokines and a bystander effect. Respondent presented expert testimony from rheumatologist Dr. Brendan Antiochos and immunologist Dr. Penelope Morel, who opined that the flu vaccine does not cause RA and that population studies show the flu vaccine is safe for RA patients. The court reviewed the evidence, including medical records and expert reports. The court found Dr. Gershwin's theory of causation to be vague and unsupported by substantial evidence, particularly when contrasted with numerous epidemiological studies presented by the respondent that indicated no link between the flu vaccine and RA. The court also noted that Mr. Casazza's treating physicians continued to recommend flu vaccinations, and he received them without incident. Furthermore, the court found the temporal relationship between the vaccination and the onset of RA to be unclear and not definitively established as proximate. Ultimately, the court concluded that Mr. Casazza had not met his burden of proof under the Althen test for causation-in-fact. Therefore, the petition was dismissed.

Theory of causation field:
Off-Table

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_17-vv-00947-0
Date issued/filed: 2023-09-25
Pages: 24
Docket text: PUBLIC DECISION (Originally filed: 8/30/2023) regarding 73 DECISION of Special Master Signed by Special Master Daniel T. Horner. (sh) Service on parties made.
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Case 1:17-vv-00947-UNJ Document 74 Filed 09/25/23 Page 1 of 24
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 17-947V
Filed: August 30, 2023
PUBLISHED
Special Master Horner
ERWIN CASAZZA,
Petitioner,
v.
SECRETARY OF HEALTH AND
HUMAN SERVICES,
Respondent.
Laura Levenberg, Muller Brazil, LLP, Dresher, PA, for petitioner.
Julia Marter Collison, U.S. Department of Justice, Washington, DC, for respondent.
DECISION1
On July 14, 2017, petitioner filed a petition under the National Childhood Vaccine
Injury Act, 42 U.S.C. § 300aa-10-34 (2012),2 alleging that the influenza (“flu”) vaccine
he received on September 3, 2015, caused him to suffer rheumatoid arthritis (“RA”).
(ECF No. 1, p. 1.) On October 9, 2019, petitioner filed an amended petition alternatively
alleging the same vaccine had instead caused reactive arthritis. (ECF No. 38.)
Ultimately, however, petitioner argues that he has met his burden with respect to RA.
(ECF No. 71.) For the reasons discussed below, I now find that petitioner is not entitled
to compensation.
1 Because this document contains a reasoned explanation for the action taken in this case, it must be
made publicly accessible and will be posted on the United States Court of Federal Claims' website, and/or
at https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government
Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic
Government Services). This means the document will be available to anyone with access to the
internet. In accordance with Vaccine Rule 18(b), Petitioner has 14 days to identify and move to redact
medical or other information, the disclosure of which would constitute an unwarranted invasion of privacy.
If, upon review, I agree that the identified material fits within this definition, I will redact such material from
public access.
2 Within this decision, all citations to § 300aa will be the relevant sections of the Vaccine Act at 42 U.S.C.
§ 300aa-10-34.
1

Case 1:17-vv-00947-UNJ Document 74 Filed 09/25/23 Page 2 of 24
I. Applicable Statutory Scheme
Under the National Vaccine Injury Compensation Program, compensation
awards are made to individuals who have suffered injuries after receiving vaccines. In
general, to gain an award, a petitioner must make a number of factual demonstrations,
including showing that an individual received a vaccination covered by the statute;
received it in the United States; suffered a serious, long-standing injury; and has
received no previous award or settlement on account of the injury. Finally – and the key
question in most cases under the Program – the petitioner must also establish a causal
link between the vaccination and the injury. In some cases, the petitioner may simply
demonstrate the occurrence of what has been called a “Table Injury.” That is, it may be
shown that the vaccine recipient suffered an injury of the type enumerated in the
“Vaccine Injury Table,” corresponding to the vaccination in question, within an
applicable time period following the vaccination also specified in the Table. If so, the
Table Injury is presumed to have been caused by the vaccination, and the petitioner is
automatically entitled to compensation, unless it is affirmatively shown that the injury
was caused by some factor other than the vaccination. § 300aa-13(a)(1)(A); § 300 aa-
11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B).
In many cases, however, the vaccine recipient may have suffered an injury not of
the type covered in the Vaccine Injury Table. In such instances, an alternative means
exists to demonstrate entitlement to a Program award. That is, the petitioner may gain
an award by showing that the recipient’s injury was “caused-in-fact” by the vaccination
in question. § 300aa-13(a)(1)(B); § 300aa-11(c)(1)(C)(ii). In such a situation, of course,
the presumptions available under the Vaccine Injury Table are inoperative. The burden
is on the petitioner to introduce evidence demonstrating that the vaccination actually
caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d
1274, 1278 (Fed. Cir. 2005); Hines v. Sec’y of Health & Human Servs., 940 F.2d 1518,
1525 (Fed. Cir. 1991).
The showing of “causation-in-fact” must satisfy the “preponderance of the
evidence” standard, the same standard ordinarily used in tort litigation. § 300aa-
13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 940 F.2d at 1525. Under that
standard, the petitioner must show that it is “more probable than not” that the
vaccination was the cause of the injury. Althen, 418 F.3d at 1279. The petitioner need
not show that the vaccination was the sole cause but must demonstrate that the
vaccination was at least a “substantial factor” in causing the condition, and was a “but
for” cause. Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344, 1352 (Fed. Cir.
1999). Thus, the petitioner must supply “proof of a logical sequence of cause and effect
showing that the vaccination was the reason for the injury[,]” with the logical sequence
being supported by “reputable medical or scientific explanation, i.e., evidence in the
form of scientific studies or expert medical testimony.” Althen, 418 F.3d at 1278; Grant
v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). A petitioner
may not receive a Vaccine Program award based solely on his or her assertions; rather,
the petition must be supported by either medical records or by the opinion of a
competent physician. § 300aa-13(a)(1).
2

Case 1:17-vv-00947-UNJ Document 74 Filed 09/25/23 Page 3 of 24
In what has become the predominant framing of this burden of proof, the Althen
court described the “causation-in-fact” standard, as follows:
Concisely stated, Althen’s burden is to show by preponderant evidence that
the vaccination brought about her injury by providing: (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. If Althen satisfies this burden, she is “entitled to
recover unless the [government] shows, also by a preponderance of the
evidence, that the injury was in fact caused by factors unrelated to the
vaccine.”
Althen, 418 F.3d at 1278 (citations omitted). The Althen court noted that a petitioner
need not necessarily supply evidence from medical literature supporting petitioner’s
causation contention, so long as the petitioner supplies the medical opinion of an
expert. Id. at 1279-80. The court also indicated that, in finding causation, a Program
factfinder may rely upon “circumstantial evidence,” which the court found to be
consistent with the “system created by Congress, in which close calls regarding
causation are resolved in favor of injured claimants.” Id. at 1280.
In this case, petitioner has variously alleged that the flu vaccine caused him to
suffer either RA or reactive arthritis. Since neither RA nor reactive arthritis is listed on
the Vaccine Injury Table relative to the flu vaccine, petitioner must satisfy the above-
described Althen test for establishing causation-in-fact.
II. Procedural History
This case was initially assigned to another special master. (ECF No. 4.)
Accompanying his petition, petitioner filed medical records marked as Exhibit 1-8 along
with an affidavit marked as Exhibit 9. (ECF No. 1.) Additional medical records marked
as Exhibits 10-12 were subsequently filed.3 (ECF Nos. 7, 11.) Respondent filed his
Rule 4 Report on May 7,2018. (ECF No. 15.) Respondent concluded that the case is
not appropriate for compensation.
Additional medical records marked as Exhibits 14-15 were subsequently filed.4
(ECF Nos. 19-20.) Petitioner then filed an expert report by rheumatologist/immunologist
M. Eric Gershwin, M.D. (ECF No. 21; Ex. 16.) Although petitioner had pleaded his
injury as RA, Dr. Gershwin disagreed with that diagnosis and instead opined that
petitioner suffered reactive arthritis. (Ex. 16, p. 2.) Dr. Gershwin then set forth a theory
as to how the flu vaccine can cause reactive arthritis. (Id. at 3-4.)
3 Exhibit 10 was later stricken and refiled on October 9, 2019. Accordingly, that exhibit is docketed at
ECF No. 42.
4 As with Exhibit 10, Exhibit 14 was later stricken and refiled on October 9, 2029. Accordingly, that exhibit
is docketed at ECF No. 42.
3

Case 1:17-vv-00947-UNJ Document 74 Filed 09/25/23 Page 4 of 24
Respondent responded with two expert reports by rheumatologist Brendan
Antiochos, M.D., and immunologist Penelope Morel, M.D. (ECF Nos. 24-27; Exs. A, C.)
Both of respondent’s experts opined that petitioner suffered RA rather than reactive
arthritis and discussed their opinions that there is insufficient evidence the flu vaccine
can cause RA. Petitioner then filed a responsive report by Dr. Gershwin shortly
thereafter. (ECF No. 28; Ex. 17.) Dr. Gershwin maintained his view that petitioner
suffered reactive arthritis and not RA and further stressed that he did not express any
opinion that vaccines can cause RA. (Id.)
On December 18, 2018, the special master issued an order noting the
discrepancy between petitioner’s pleading of RA and Dr. Gershwin’s opinion based on
reactive arthritis. (ECF No. 29.) Petitioner was ordered to clarify the nature of his claim.
(Id.) Petitioner later filed an amended petition alleging that his flu vaccine caused him to
suffer reactive arthritis, though he acknowledged that some of his medical records
indicated his diagnosis is RA.5 (ECF No. 38.) Petitioner also filed additional medical
records marked as Exhibits 18-23. (ECF Nos. 31, 34.) Respondent filed a further
report by Dr. Antiochos. (ECF No. 36; Ex. E.) Dr. Antiochos indicated that under the
relevant diagnostic standards, petitioner’s diagnosis of RA should be considered
“definite.” (Id.)
The special master then held a Rule 5 conference on October 8, 2019. (ECF No.
37.) She advised the parties that in her view the medical records “strongly support”
respondent’s experts’ opinion that petitioner suffers RA. The special master also
advised that her preliminary view was that a connection between the flu vaccine and RA
is unsupported. (Id.) Thereafter, petitioner again filed additional medical records (Ex.
24) and a third report by Dr. Gershwin (ECF Nos. 44-45; Exs. 25-26). In his third report,
Dr. Gershwin changed his view based on more recent laboratory testing and agreed
with Dr. Antiochos that petitioner has seropositive RA. (Ex. 25, p. 1.) In this report he
provided for the first time an explanation of how in his view the flu vaccine can cause (or
contribute to) RA. (Id. at 3.) Respondent filed responsive reports by both of his experts,
who both continued to opine that the flu vaccine cannot cause RA. (ECF No. 46; Exs.
F-G.)
On February 7, 2020, the special master issued an order reviewing the expert
reports filed to date and urging petitioner and Dr. Gershwin to review a prior case in
which she had found the petitioner had failed to prove that the flu vaccine can cause
RA. (ECF No. 47 (discussing C.P. v. Sec’y of Health & Human Servs., No. 14-917V,
2019 WL 5483624, at *28 (Fed Cl. Spec. Mstr. Aug. 21, 2019).) Petitioner then filed two
further reports by Dr. Gershwin, one responding to respondent’s most recent expert
reports and one responding to the special master’s reference to C.P. (ECF Nos. 49-50;
Exs. 27-29.)
5 Petitioner initially filed an amended petition on January 30, 2019, alleging that the flu vaccine caused
both RA and reactive arthritis. However, the special master ordered petitioner to strike and refile the
amended petition to clarify the injury alleged. The amended petition was refiled on October 9, 2019,
alleging reactive arthritis only.
4

Case 1:17-vv-00947-UNJ Document 74 Filed 09/25/23 Page 5 of 24
Petitioner then requested an entitlement hearing and also filed a final report by
Dr. Gershwin responding to specific points raised by the special master (Exs. 30-31)
and further medical records (Exs. 33-34.). (ECF Nos. 52-54, 59.) The special master
set an entitlement hearing to commence on May 10, 2022; however, the case was
subsequently reassigned to the undersigned on September 16, 2021. (ECF No. 61.)
The next day I issued a prehearing order and confirmed that the hearing would proceed
as previously scheduled. (ECF No. 62.)
However, petitioner subsequently advised on March 28, 2022, that both he and
his expert declined to testify. Specifically, petitioner refused to appear at the hearing
voluntarily and his expert in turn declined to appear voluntarily if petitioner did not
testify. (ECF No. 70.) On March 29, 2022, I issued a follow up order explaining to
petitioner that I remain amenable to holding the hearing if the parties choose, but that I
otherwise conclude the case is appropriate for resolution on the written record pursuant
to Vaccine Rule 8(d). Therefore, I advised that I did not see any need to sua sponte
compel testimony from petitioner or his expert.6 (ECF No. 69.) I ordered the parties to
confer regarding several points and to file a joint status report responding to my order.
(Id.) In a joint status report filed by petitioner on March 30, 2022, the parties confirmed
the following points as prompted by my order: that petitioner’s witnesses would not
appear voluntarily; that respondent does not intend to subpoena petitioner’s witnesses;
and that neither party objects to proceeding via a ruling on the written record. (ECF No.
70.)
Petitioner filed a motion for a ruling on the written record on June 21, 2022.
(ECF No. 71.) Respondent filed his response on August 22, 2022. (ECF No. 72.)
Petitioner filed no reply. Accordingly, this case is now ripe for resolution. I have
concluded that the parties have had a full and fair opportunity to develop the record and
that it is appropriate to resolve this case without an entitlement hearing. See
Kreizenbeck v. Sec’y of Health & Human Servs., 945 F.3d 1362, 1366 (Fed. Cir. 2020)
(citing Simanski v. Sec’y of Health & Human Servs., 671 F.3d 1368, 1385 (Fed. Cir.
2012); Jay v. Sec’y of Dept. of Health & Human Servs., 998 F.2d 979, 983 (Fed. Cir.
1993.)); see also Vaccine Rule 8(d); Vaccine Rule 3(b)(2).
III. Any Claim for Reactive Arthritis is Not Preponderantly Supported
Petitioner’s motion for a ruling on the written record advances an argument with
respect to RA only, as pleaded in his original petition, and does not argue that he has
met his burden of proof with respect to reactive arthritis, as pleaded in his amended
petition. (ECF No. 71.) However, there are some references to the possibility of
reactive arthritis in petitioner’s medical records and he never rescinded his amended
petition alleging reactive arthritis. Accordingly, I briefly confirm in the interest of
6 I also advised petitioner that his affidavit will be less compelling than oral testimony given the lack of
cross examination and further that if petitioner’s affidavit is silent as to any factual dispute of which
respondent has put him on notice, I would entertain a request from respondent for an adverse inference.
(ECF No. 70.)
5

Case 1:17-vv-00947-UNJ Document 74 Filed 09/25/23 Page 6 of 24
completeness that there is not preponderant evidence that petitioner suffered reactive
arthritis.
The expert opinions proffered in this case are unanimous in concluding that
petitioner suffered RA and not reactive arthritis.7 Additionally, as described in greater
detail in the Factual History below, although petitioner’s medical records include some
suspicion of reactive arthritis, he was never diagnosed by any of his treating physicians
as experiencing reactive arthritis and was instead diagnosed as having RA. For these
reasons, there is not preponderant evidence that petitioner suffered reactive arthritis
and it is therefore not necessary to further address that aspect of Dr. Gershwin’s opinion
that posits that the flu vaccine can cause reactive arthritis or that it did in this case.
Although reactive arthritis and RA are both immune-mediated inflammatory conditions
and can have overlapping clinical presentations, Dr. Gershwin has been very clear
throughout his reports in describing the conditions as involving two distinct disease
processes and the evidence presented with respect to the potential for vaccine-
causation of each condition is different.
Accordingly, the remainder of this decision will focus on petitioner’s claim of
vaccine-caused RA.8
7 As explained above, although Dr. Gershwin initially opined that petitioner suffered vaccine-caused
reactive arthritis, he reversed that opinion as of his third report and agreed that petitioner suffered RA.
(Ex. 25.) Although Dr. Gershwin did not explicitly disclaim his prior opinion as to reactive arthritis, it is
clear from Dr. Gershwin’s first three reports that he treats the two diagnoses as mutually exclusive
explanations of petitioner’s history. (Exs. 16-17, 25.) Nor does petitioner’s motion for a ruling on the
written record in any way suggest that Dr. Gershwin’s initial opinion regarding reactive arthritis remains an
active consideration in light of his subsequent opinion as to RA. Petitioner’s motion makes no request
that he be found entitled to compensation for an injury of reactive arthritis nor includes any argument that
would support such a finding. (ECF No. 71.)
8 The Federal Circuit has concluded that it is “appropriate for the special master to first determine what
injury, if any, [is] supported by the evidence presented in the record before applying the Althen test to
determine causation.” Lombardi v. Sec’y of Health & Human Servs., 656 F.3d 1343, 1351–53 (Fed. Cir.
2011). Importantly, “the function of a special master is not to ‘diagnose’ vaccine-related injuries, but
instead to determine ‘based on the record evidence as a whole and the totality of the case, whether it has
been shown by a preponderance of the evidence that a vaccine caused the [petitioner]’s injury.’” Andreu
ex rel. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1382 (Fed. Cir. 2009) (quoting
Knudsen ex rel. Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 549 (Fed. Cir. 1994)).
Petitioner must “specify his vaccine-related injury and shoulder the burden of proof on causation.”
Broekelschen v. Sec'y of Health & Human Servs., 618 F.3d 1339, 1346 (Fed. Cir. 2010). “Although the
Vaccine Act does not require absolute precision, it does require the petitioner to establish an injury – the
Act specifically creates a claim for compensation for ‘vaccine-related injury or death.’” Stillwell v. Sec'y of
Health & Human Servs., 118 Fed. Cl. 47, 56 (2014) (emphasis omitted) (quoting 42 U.S.C. § 300aa–
11(c)). And, in any event, a petitioner must prove by a preponderance of the evidence the factual
circumstances surrounding his claim. See 42 US.C. § 300aa–13(a)(1)(A).
6

Case 1:17-vv-00947-UNJ Document 74 Filed 09/25/23 Page 7 of 24
IV. Factual History
On September 3, 2015, petitioner received the flu vaccination at issue. (Ex. 1, p.
1.) He was 73 at the time and had a history of Type II diabetes, hyperlipidemia, and
hypertension. (Ex. 2, p. 6.) He was a heavy smoker until 1999. (Ex. 5, p. 8.)
In his affidavit, petitioner indicates that he began experiencing shoulder pain
immediately following his vaccination that increased in intensity over the next 24-hours
and that over the ensuing two months he “began to experience severe swelling in my
feet and the pain spread to my thumbs, the back of my head, shooting behind my right
ear, my abdomen, knees, hands, ankles, and jaw. By October of 2015, I began to
experience continuous excruciating pain throughout my whole body, as well as severe
weakness and the inability to get out of bed or a chair.” (Ex. 9, p. 1.)
On September 7, 2015, four days post-vaccination, petitioner presented to his
primary care provider complaining of chronic, intermittent thumb pain in both hands that
began more than two and a half years earlier after falling onto his hands. (Ex. 2, pp. 2-
7.) He was instructed to treat with over-the-counter pain medication along with warm
and cold compresses. (Id. at 3-7.) He returned the next day for treatment of pain
related to a contusion following an accidental jaw injury. X-rays were negative and
Ibuprofen and icing were the only treatment recommendations. (Id. at 8-12.) Two days
after that, petitioner presented for his annual physical. He was diagnosed with
osteoarthritis9 of the hands and referred to an orthopedist. (Ex. 3, pp. 50-54.)
On September 16, 2015, petitioner presented to an orthopedist. (Ex. 10, pp. 6-
7.) Petitioner complained of bilateral hand pain, mostly of the thumbs, but also over the
5th metacarpal (i.e. the pinky finger) of the right hand. (Ex. 10, p. 6.) He explained that
he had suffered a left side industrial accident in 1965 wherein his hand was crushed
and had also previously had right trigger thumb surgery performed. (Id.) X-rays
showed, inter alia, deformities consistent with prior fractures bilaterally as well as stage
four arthritis of both thumbs. (Id.) The orthopedist attributed petitioner’s symptoms to
his preexisting arthritis and deformities except for the right pinky finger pain for which
“his subjective complaints were out of proportion to objective findings.” (Id. at 7.) The
medical records do not identify whether the pain in petitioner’s pinky finger had any
separate date of onset.
On September 24, 2015, petitioner presented to the emergency department.
(Ex. 3, pp. 40-46.) He reported left arm pain, bilateral thumb pain, bilateral lower
extremity pain, and right-sided neck pain and stiffness. (Id. at 40.) Petitioner reported
that he had been feeling “progressively more sick” since receiving his flu vaccination.
(Id.) He complained of hand swelling and shortness of breath with exertion. (Id.) After
9 Distinct from the RA at issue in this case, osteoarthritis is “a noninflammatory degenerative joint disease
seen mainly in older persons, characterized by degeneration of the articular cartilage, hypertrophy of
bone at the margins, and changes in the synovial membrane.” Osteoarthritis, DORLAND’S MEDICAL
DICTIONARY ONLINE, https://www.dorlandsonline.com/dorland/definition?id=35780 (last visited August 15,
2023).
7

Case 1:17-vv-00947-UNJ Document 74 Filed 09/25/23 Page 8 of 24
ruling out any life-threatening conditions, he was discharged with a recommendation to
follow up with his primary care provider. (Id. at 43.) On October 5, 2015, petitioner
returned to his primary care provider complaining of neck pain and leg edema for four
weeks. (Ex. 3, p. 37.) He was diagnosed with venous insufficiency for which
compression stockings were recommended. He was instructed to follow up with an
orthopedist regarding the neck pain. (Id.)
On October 16, 2015, petitioner presented to a new orthopedist with a complaint
of neck pain radiating to his right ear following his flu shot. (Ex. 6, p. 1.) He also
complained of hand and foot swelling as well as stomach pain. (Id.) X-ray of his
cervical spine showed some degenerative changes and petitioner was diagnosed with
cervical strain with bridging osteophytes. (Id.) Physical therapy was recommended.
(Id.) On October 23, 2015, petitioner presented to a gastroenterologist. (Ex. 4, p. 7.)
He was diagnosed with abdominal pain of unclear etiology. A CT scan of the abdomen
was performed on November 4, 2015, and was unremarkable. (Id. at 3.)
Petitioner returned to the emergency department on November 30, 2015, and
was admitted to inpatient care. (Ex. 3, p. 28-30.) He complained of worsening body
aches, fatigue, generalized weakness, lower extremity edema, and difficulty standing.
He indicated onset was on September 9, 2015, following his flu vaccination. (Id.) Once
petitioner was admitted, he had a rheumatology workup.
At this point, petitioner tested positive for rheumatoid factor (“RF”). Additionally,
two markers of inflammation, ESR10 and CRP11, were also elevated. (Ex. 11, pp. 27,
58.) However, a further marker of RA – Cyclic Citrullinated Peptide antibodies
(“CCP”)12 – was negative. (Ex. 11, p. 155.) He was also negative for HLA-B27, a
genetic marker frequently found in RA patients. (Id.) Overall, petitioner’s history and
exam was “suggestive for inflammatory arthritis.” (Ex. 11, p. 58.) More specifically, it
was noted that “[c]linical symptoms [were] highly suspicious for relapsing rheumatoid
arthritis although reactive arthritis from viral infection versus reaction from flu vaccine
remains a possibility.” (Id.) An additional notation indicated “possibly RA must [rule out]
10 “Erythrocyte Sedimentation Rate (“ESR”) is the rate at which” red blood cells precipitate out from blood.
An elevated rate is evidence of an active inflammatory disease. Erythrocyte Sedimentation Rate,
DORLAND’S MEDICAL DICTIONARY ONLINE, https://www.dorlandsonline.com/dorland/definition?id=102146
(last visited August 15, 2023).
11 “C-Reactive Protein” (“CRP”) is “the most predominate of the acute-phase proteins.” C-Reactive
Protein, DORLAND’S MEDICAL DICTIONARY ONLINE,
https://www.dorlandsonline.com/dorland/definition?id=100489 (last visited August 15, 2023). Acute phase
proteins are “processes that occur after the onset of infection, trauma, inflammatory processes, and some
malignant conditions.” Acute Phase Response, DORLAND’S MEDICAL DICTIONARY ONLINE,
https://www.dorlandsonline.com/dorland/definition?id=103669 (last visited August 15, 2023).
12 “Cyclic Citrullinated Peptide” (“CCP”) is defined as “a synthetic, citrulline-containing peptide with a
cyclic structure, used in assays for rheumatoid arthritis; the presence of antibodies to this peptide is highly
specific for rheumatoid arthritis.” Cyclic Citrullinated Peptide, DORLAND’S MEDICAL DICTIONARY ONLINE,
https://www.dorlandsonline.com/dorland/definition?id=97140&searchterm=cyclic+citrullinated+peptide
(last visited August 24, 2023).
8

Case 1:17-vv-00947-UNJ Document 74 Filed 09/25/23 Page 9 of 24
reactive or post-infectious arthritis since [status post] flu shot.” (Id. at 62.) During his
hospitalization, he had consultation with rheumatologist James Paolino, M.D., who
similarly recorded an impression of “[a]cute polyarthritis x 6-8 weeks. Appearance of
RA, but the history of vaccine preceding onset. R/O Reactive or post-infectious arthritis.
Lab essential for differential dx.” (Id. at 70; see also Ex. 8, p. 9.) Petitioner experienced
“remarkable improvement” with steroid treatment and was discharged on December 3,
2015, with a diagnosis of “rheumatoid arthritis flare.” (Id. at 8.)
Petitioner has continued to treat his RA ever since. However, the subsequent
course of petitioner’s RA is mostly not germane to the issues presented by petitioner’s
motion or the parties’ experts and is therefore not summarized, except for two specific
considerations raised by the experts. First, petitioner was subsequently retested for RF
and CCP. Second, petitioner received several further flu vaccinations without incident.
Petitioner’s RF was rechecked on June 5, 2017, and was substantially higher than when
initially tested.13 (Ex. 8, p. 11.) Petitioner was retested for CCP on October 24, 2019.
At that time, he had 73 units where anything over 59 units was considered a “strong
positive.” (Ex. 24, pp. 3-4.) Petitioner received subsequent flu vaccinations on October
1, 2016, October 1, 2017, and October 1, 2018. (Ex. 22, pp. 13, 37.) It also does not
appear that Petitioner’s physicians connected any RA flare ups to these subsequent
vaccinations.
V. Expert Opinions
a. Petitioner’s Rheumatology/Immunology Expert, Dr. Gershwin14
In total, Dr. Gershwin provided six reports in this case. (Exs. 16, 17, 25, 27, 29,
30.) As discussed above, Dr. Gershwin’s first two reports addressed reactive arthritis
rather than RA. Additionally, Dr. Gershwin’s fifth report is dedicated to discussing the
theory presented in a different case. (Ex. 29.) Accordingly, these three reports are less
helpful and are not summarized, though they have been reviewed and considered in
full. (Exs. 16-17.)
In his third report, Dr. Gershwin agrees based upon the October 2019 finding of
CCP antibodies that petitioner has seropositive RA. (Ex. 25, p. 1.) However, even with
this change of opinion regarding diagnosis, he stands by his assertion from his prior
13 In June of 2017, petitioner’s RF measured 261 IU/mL where anything over 14 IU/mL was abnormal.
(Ex. 8, p. 11.) When RF was measured in December of 2015, it was 27 IU/mL. (Ex. 11, p. 58.)
14 Dr. Gershwin is currently a distinguished professor of medicine and the Jack and Donald Chia
Professor of Medicine in the Rheumatology/Allergy and Clinical Immunology division of the University of
California at Davis, where he previously served as chairperson of the Graduate Group in Immunology.
(Ex. 35, p. 1.) Dr. Gershwin received his bachelor’s degree from Syracuse University and his master’s
degree from the Centre for Astrophysics and Supercomputing. (Id.) He received his Doctor of Medicine
from Stanford University and is currently licensed to practice medicine in California. (Id. at 1-2.) Dr.
Gershwin is board certified in Internal Medicine with a subspecialty in Rheumatology and in Allergy and
Clinical Immunology. (Id. at 1-2.) In addition, he has published 72 books and monographs, 1039
experimental papers, 164 book chapters, 277 reviews, 40 guest editorials and book reviews, and five
letters to the editors. (Id. at 8-138.)
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reports that petitioner developed an acute inflammatory arthropathy that was not
present prior to vaccination. (Id.) Specifically, Dr. Gershwin asserts that, although
petitioner is an older individual with other musculoskeletal issues, he did not have any
clinical evidence of RA until December 1, 2015, when tests showed elevated
inflammatory markers of ESR and CRP.15 (Id. at 2 (citing Ex. 11, p. 27).) Further to
this, Dr. Gershwin indicates that petitioner’s later lab findings, including an increase in
RF and the first detection of CCP in October of 2019, show “significant maturation” or
“expansion” as compared to his December 1, 2015 evaluation. (Id. at 1-2.) Thus, Dr.
Gershwin opines that “one can trace backwards the origin of his antibodies to CCP to
the very beginning of his illness, which is shortly after his vaccination.” (Id. at 1-2.)
Although the mechanism is not known, Dr. Gershwin indicates that the presence of CCP
antibodies has been shown to correlate to disease severity and are likely related to
disease pathology. (Id. at 2.)
Dr. Gershwin acknowledges that petitioner was at increased risk of developing
RA due to his history of smoking. However, he explains that for at-risk individuals a pre-
clinical phase can occur in multiple stages up to the point where accumulating
environmental risk factors result in a breach of immune self-tolerance. (Id.) Dr.
Gershwin suggests that there is increasing evidence that rheumatoid factor is not
caused by a single environmental stimulus. Thus, he hypothesizes that “[t]he
immunization would be considered the final straw in the multi-step pathogenesis of
[RA].” (Id. at 3.) Dr. Gershwin cites prior publications discussing several case reports
as support for this specific proposition. (Id.) In fact, in his fourth report he further
stresses that he is not opining that petitioner’s RA is “solely” due to his vaccination. (Ex.
27, p. 1.) Dr. Gershwin’s fourth report further explains that cytokines produced post-
vaccination are pro-inflammatory and “would be key players in the differentiation and
expansion of the pathogenic antibodies.” (Id. at 2.) Dr. Gershwin cites several papers
for the proposition that the flu vaccine produces significant levels of cytokines and that
vaccination elicits a strong bystander effect. (Id.)
Dr. Gershwin stresses that petitioner had no evidence of CCP antibodies prior to
vaccination, had no evidence of clinical rheumatoid arthritis prior to vaccination, and
developed seropositive RA over the course of several years, with all inflammatory
markers dating back to December 1, 2015. (Ex. 25, pp. 2-3.) He also notes that onset
of RA at petitioner’s older age of 65 is relatively unusual. (Id. at 3.) All of this points to
the vaccination at issue being the environmental stimulus that broke self-tolerance in
petitioner’s case. (Id.) In his fourth report, Dr. Gershwin further stresses that
petitioner’s development of anti-CCP antibodies after clinical manifestation is unusual in
itself. (Ex. 27, p. 1.) Additionally, Dr. Gershwin suggests that smoking – the other
environmental factor implicated by petitioner’s medical history – directly produces
antibodies to CCP. Therefore, if smoking were the only environmental factor at issue,
one would have expected to see the CCP antibodies at the time of diagnosis. (Id. at 2.)
15 As discussed in greater detail under Althen prong three, Dr. Gershwin’s first report had identified a
period of onset for reactive arthritis as occurring between October 1 and October 15, 2015. (Ex. 16, p 4.)
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In his final report, Dr. Gershwin answers several specific questions prompted by
the special master. He opines that there is no significance in the fact that petitioner
later had additional vaccinations without any aggravation of his condition. (Ex. 30, p. 1.)
He suggests that the etiologies responsible for initiating a disease are not the same as
the etiologies that determine disease activity. He suggests that once self-tolerance is
broken, antibody levels do not correlate to the peptides that lead to synovitis and they
are not monitored as a biomarker of disease activity. (Id.) He further opines that it does
not matter whether the vaccine at issue is either live or adjuvanted and that “[t]he only
important feature is that it must be antigenic and induce an immune response.” (Id. at
2.) In response to the special master’s concern that large studies have shown the flu
vaccine to be safe for RA patients, Dr. Gershwin asserts that the variations in genetic
susceptibility, coupled with the need for multiple environmental factors needed to
produce disease, effectively place the issue beyond the reach of epidemiology absent
better biomarkers. (Id.)
b. Respondent’s Rheumatology Expert, Dr. Antiochos16
Dr. Antiochos provided three reports in this case. His first two reports need not
be belabored in light of Dr. Gershwin’s change of opinion. (Exs. A, E.) These reports
are largely dedicated to affirming the accuracy of petitioner’s RA diagnosis. Dr.
Antiochos opines that petitioner presented for care in late 2015 with an inflammatory
symmetric polyarthritis in a pattern consistent with RA. (Ex. A, p. 5.) Importantly,
however, Dr. Antiochos contends that this renders vaccine-causation less likely as
compared to Dr. Gershwin’s explanation relative to reactive arthritis. According to Dr.
Antiochos, the pathogenesis of RA is less established than for reactive arthritis. (Id.)
Additionally, he stresses that population-based studies have provided a “strong record”
with respect to the safety of the flu vaccine in patients with RA. (Id.) Accordingly, Dr.
Antiochos opines that [w]hile RA became clinically apparent at a date that followed the
administration of the influenza vaccine, I find no reason to believe that the influenza
vaccine played a causal role in RA development.” (Id. at 6.)
Dr. Antiochos’s third report disagrees with Dr. Gershwin’s theory that the flu
vaccine can cause RA. (Ex. G.) In short, Dr. Antiochos contends that any role for the
flu vaccine in causing RA is refuted by available epidemiologic data that shows no
increased risk of developing either incipient RA or enhanced RA disease activity
following influenza vaccination. (Id. at 1.) Dr. Antiochos stresses that vaccination is a
frequent event and RA is not a rare diagnosis. Accordingly, he notes that it is
“inevitable” that at least some cases of RA will have onset following vaccination by
chance alone. (Id. at 2.)
16 Dr. Antiochos is an assistant professor at John Hopkins University School of Medicine, Division of
Rheumatology. (Ex. B, p. 1.) He received his medical degree from Dartmouth Medical School. (Id.) He
completed his residency in internal medicine at Oregon Health and Science University and a fellowship in
rheumatology at Johns Hopkins. (Id.) He is currently certified in internal medicine by the Maryland
Medical Board. (Id. at 3.) In addition, he is board certified in internal medicine and rheumatology and
internal medicine by the American Board of Internal Medicine. (Id.) He has published 14 original
research articles, book chapters, and review articles. (Id. at 1-2.)
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c. Respondent’s Immunology Expert, Dr. Morel17
Dr. Morel provided two reports in this case. Despite Dr. Gershwin’s initial
reliance on reactive arthritis, Dr. Morel opined that a RA diagnosis is instead favored
because petitioner was RF positive, these RF factors have been increasing since
diagnosis, and in petitioner’s most recent recorded visit, he was experiencing a flare of
RA with elevated ESR and increased symptoms. (Ex. C, p. 5.) Thus, Dr. Morel’s first
report does include extensive discussion of the immunology underlying RA. She opines
that there is not sufficient evidence to implicate the flu vaccine as a cause of RA. (Ex.
C.) Dr. Morel’s second report revisited this subject in response to Dr. Gershwin’s later
assertion that the flu vaccine can cause RA. (Ex. F.)
Dr. Morel explains in her first report that the development of autoimmunity in RA
occurs in stages. (Ex. C, p. 3.) The first stage occurs when genetic and environmental
factors lead to the generation of auto-reactive T and B cells, often manifesting
circulating auto-antibodies. This represents a pre-clinical state that can last for months
to years. Thereafter, a further signal, such as micro-trauma, vascular events, or
infection, is likely required to initiate clinical RA during which inflammatory Th17 cells or
immune complexes initiate synovitis and joint damage. (Id.) Dr. Morel opines that
“close to 50% of the risk for developing RA is genetic.” (Id.) She notes that none of the
large studies available have supported the hypothesis that the influenza vaccine could
be one of the triggers of RA and season influenza vaccines are given to millions of
people and are considered extremely safe. (Id. at p. 4) She thus concludes that there
is no evidence to support the notion that season influenza vaccines could have caused
RA in petitioner’s case. (Id.)
In Dr. Morel’s supplemental report, she addresses Dr. Gershwin’s theory that
petitioner is indeed suffering from RA which was precipitated by the flu vaccine he
received in September 2015. (Ex. F, p. 1.) Dr. Morel rejects Dr. Gershwin’s view that
the vaccination was the final environmental stimulus that led to his RA. (Id.) While Dr.
Morel agrees that petitioner developed RA in December 2015, she disagrees that the
vaccine played a role in causing petitioner’s RA. (Id. at 2.) To support this conclusion,
Dr. Morel notes that there is no evidence in the literature to support the claim that the
influenza vaccine can cause RA and that the American College of Rheumatologists
recommends that all patients with RA receive influenza vaccines. (Id.) In addition, Dr.
Morel notes that petitioner has continued to receive annual influenza vaccines with no
additional adverse effects. (Id.) Therefore, Dr. Morel opines that Petitioner’s RA was
not caused by the influenza vaccine. (Id.)
17 Dr. Penelope A. Morel is a professor at the University of Pittsburgh in both the Department of
Immunology and Division of Rheumatology. (Ex. D, p. 3.) She received her doctorate degree from the
University of Geneva. (Id. at 1.) She has published 69 refereed articles, 93 published abstracts, and 38
other articles chapters, and reviews. (Id. at 4-21.)
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VI. Analysis
a. Althen Prong One
Under Althen prong one, petitioner must provide a “reputable medical theory,”
demonstrating that the vaccine received can cause the type of injury alleged. Pafford v.
Sec’y of Health & Human Servs., 451 F.3d 1352, 1355-56 (Fed. Cir. 2006) (citations
omitted). Such a theory must only be “legally probable, not medically or scientifically
certain.” Knudsen, 35 F.3d at 549. Petitioner may satisfy the first Althen prong without
resort to medical literature, epidemiological studies, demonstration of a specific
mechanism, or a generally accepted medical theory. Andreu, 569 F.3d at 1378-79
(citing Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1325-26 (Fed. Cir.
2006)). However, “[a] petitioner must provide a ‘reputable medical or scientific
explanation’ for [her] theory. While it does not require medical or scientific certainty, it
must still be ‘sound and reliable.’” Boatmon, 941 F.3d at 1359 (quoting Knudsen, 35
F.3d at 548-49).
In this case, there is no dispute that RA is an autoimmune condition of uncertain
cause that generally involves a combination of genetic and environmental factors or
stimuli progressively leading to autoimmunity over a prolonged preclinical phase. (Ex.
A, p. 5; Ex. C, p. 3; Ex. 25-2, p. 3.) Petitioner argues that Dr. Gershwin’s explanation of
how a flu vaccine can cause the final loss of autoimmune self-tolerance in RA carries
his burden of proof. (ECF No. 71, pp. 10-11.) Specifically, petitioner relies on Dr.
Gershwin’s explanation that the flu vaccine produces cytokines which contribute to the
expansion of pathogenic autoantibodies due to a strong bystander effect. (Id. at 11.)
Respondent counters that Dr. Gershwin’s explanation is both unsupported and too
vague, especially when contrasted against contrary epidemiology and the current views
of the relevant scientific community, which do not consider the flu vaccine to be among
the environmental stimuli capable of causing RA. (ECF No. 72, pp. 17-20.)
Respondent is far more persuasive on the whole. Very little on this record apart from
Dr. Gershwin’s say-so associates any vaccine with RA whereas much more purports to
refute Dr. Gershwin’s opinion.
Dr. Gershwin did present a 2007 review paper regarding the pathogenesis of RA
that indicates that vaccinations have been considered as a “possible” environmental
trigger of “various diseases,” but this is not specific to RA and stands in contrast to the
much firmer links the authors draw to other environmental triggers for RA. (Gourley &
Miller, Mechanisms of Disease: Environmental Factors in the Pathogenesis of
Rheumatic Disease, 3 NATURE CLINICAL PRACTICE RHEUMATOLOGY 172, 177 (2007) (Ex.
32, p. 6).) Otherwise, of all the literature Dr. Gershwin cites, only two papers from the
late 1980s and early 1990s discuss case reports and case series of RA developing post
vaccination. (DPM Symmons & K Chakravarty, Can Immunisation Trigger Rheumatoid
Arthritis?, 52 ANNALS RHEUMATIC DISEASES 843, (1993) (Ex. 26M); ASM Jawad & DGJ
Scott, Immunisation Triggering Rheumatoid Arthritis?, 48 ANNUALS RHEUMATIC DISEASES
174, (1989) (EX. 26N).) However, even those papers address different vaccines, mostly
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tetanus-containing vaccines.18 The Symmons paper cites a single case of reported
arthritis following flu vaccination, but specifies that the subject did not meet the criteria
for a diagnosis of RA. (Symmons & Charkravarty, supra, at Ex. 26M, p. 1.) Respondent
also filed several additional case reports of RA following vaccination, precisely because
Dr. Morel stresses that the limited number of available case reports stands in contrast to
much larger studies that have not supported the hypothesis. (Ex. C, p. 4; Gurjot Basra,
Praveen Jojoria, & Emilio Gonzalez, Rheumatoid Arthritis and Swine Influenza Vaccine:
A Case Report, 2012 CASE REPORTS IN RHEUMATOLOGY 1, (2012) (Ex. C, Tab 19); (Maria
Antonia Pou et al., Development of Autoimmune Diseases After Vaccination, 14 J.
CLINICAL RHEUMATOLOGY 243, (2008) (Ex. C, Tab 20); Tabache et al., Acute Polyarthritis
after Influenza A Immunization, 78 JOINT BONE SPINE 319, 321 (2011) (Ex. C, Tab 21, p.
3).)
Petitioners in this program often highlight the usefulness of case reports in cases
of rare diseases or unusual occurrences. E.g. Patton v. Sec’y of Health & Human
Servs., 157 Fed. Cl. 159, 166-67 (2021). However, case reports “‘do not purport to
establish causation definitively, and this deficiency does indeed reduce their evidentiary
value’. . . ,” even though they are not entirely devoid of evidentiary value. Paluck v.
Sec’y of Health & Human Servs., 104 Fed. Cl. 457, 475 (2012) (quoting Campbell v.
Sec’y of Health & Human Servs., 97 Fed. Cl. 650, 668 (2011), aff’d, 786 F.3d 1373
(Fed. Cir. 2015)); see also Crutchfield v. Sec’y of Health & Human Servs., No. 09-39V,
2014 WL 1665227, at *19 (Fed. Cl. Spec. Mstr. Apr. 7, 2014) (“single case reports of
Disease X occurring after Factor Y . . . do not offer strong evidence that the temporal
relationship is a causal one—the temporal relationship could be pure random chance”),
aff’d, 125 Fed. Cl. 251 (2014). In this case, neither the Jawad nor Symmons papers
cited by Dr. Gershwin are particularly strong evidence. Jawad presents a single
anecdotal case report. (Jawad & Scott, supra, at Ex. 26N.) Symmons discusses
several prior case series in brief but then discusses several significant reasons for
doubting any causal relationship. (Symmons & Charkravarty, supra, at Ex. 26M.) In
fact, Dr. Gershwin himself refers to the Symmons and Jawad paper as “not themselves
proof” but as “rais[ing] the specter of proof of principle.” (Ex. 25, p. 3.) However, this
mere “specter” must be considered in light of the fact that subsequent investigation, as
documented in numerous more recent papers filed in this case, has provided little that
would bear out the hypothesis.
Respondent’s experts have come forward with a number of more recent
epidemiologic studies of varying size that weigh against Dr. Gershwin’s theory.
Specifically: Carola Bardage et al., Neurological and Autoimmune Disorders After
Vaccination Against Pandemic Influenza A (H1N1) with a Monovalent Adjuvanted
Vaccine: Population Based Cohort Study in Stockholm, Sweden, 343 BRIT. MED. J. 1,
(2011) (Ex. A, Tab 1) (examined the risk of neurological and autoimmune disorders in
people vaccinated against influenza A in the population of those registered in Stockholm
county on October 1, 2009 who had lived in the region since January 1, 1998 and were
18 In his final report Dr. Gershwin does suggest that his theory would apply to any vaccine with “the only
requirement obviously [being] that it is antigenic and induces an immune response,” but this only
underscores respondent’s charge of vagueness as discussed further below. (Ex. 30, p. 2.)
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vaccinated against H1N1 and found no change in the risk for rheumatoid arthritis); F.
Milanetti et al., Safety and Immunogenicity of Co-Administered MF 59-Adjuvanted 2009
Pandemic and Plain 200-10 Seasonal Influenza Vaccines in Rheumatoid Arthritis
Patients on Biologicals, 177 CLINICAL AND EXPERIMENTAL IMMUNOLOGY 287, (2014) (Ex. A,
Tab 2) (seeking to determine the safety and immunogenicity of co-administered non-
adjuvated seasonal and pandemic influenza vaccines in 30 RA patients and concluded
that simultaneous administration of adjuvanted pandemic and non-adjuvated seasonal
influenza vaccines are safe and highly immunogenic in RA patients); Milomir Milanovic
et al., Influenza Vaccination in Autoimmune Rheumatic Disease Patients, 229 TOHOKU J.
EXPERIMENTAL MED. 29, (2013) (Ex. A, Tab 3) (studying the effect of vaccinating annually
for influenza using trivalent inactivated split vaccine during 2006-2010 on patients
suffering from autoimmune rheumatic diseases and found no exacerbation of the
underlying disease); Paula Ray et al., Risk of Rheumatoid Arthritis Following
Vaccination with Tetanus, Influenza and Hepatitis B Vaccines Among Persons 15-59
Years of Age, 29 VACCINE 6592, (2011) (Ex. A, Tab 5) (compared rates of new-onset RA
between one million vaccinated and unvaccinated Kaiser Permanente Northern
California members from 1997-1999 and found a possible association between RA and
the influenza vaccine in a smaller cohort analysis that was not borne out by the larger
case-control analysis); Ljudmila Stojanovich, Influenza Vaccination of Patients with
Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA), 13 CLINICAL AND
DEV. IMMUNOLOGY 373, (2006) (Ex. A, Tab 7) (studied 54 RA patients, half of which
received the influenza vaccine while the other half did not, and found the vaccine was
tolerated well in all cases and those RA patients who were vaccinated had fewer
occurrences of infections); Fabrizio Conti, Soheila Rezai, & Guido Valesini, Vaccination
and Autoimmune Rheumatic Diseases, 8 AUTOIMMUNITY REV. 124, 126(2008) (Ex. C,
Tab 29, p. 3) (RA patients immunization against the influenza can be considered safe
and immunogenic in most cases). The Federal Circuit has previously stressed that a
petitioner is not obligated to present an epidemiological case supporting his claim.
Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006).
However, “[n]othing in Althen or Capizzano requires the Special Master to ignore
probative epidemiological evidence that undermines petitioner’s theory.” D'Tiole v.
Sec’y of Health & Human Servs., 726 F. App’x 809, 811 (Fed. Cir. 2018) (citing Andreu,
569 F.3d at 1379 (“Although Althen and Capizzano make clear that a claimant need not
produce medical literature or epidemiological evidence to establish causation under the
Vaccine Act, where such evidence is submitted, the Special Master can consider it in
reaching an informed judgment as to whether a particular vaccination likely caused a
particular injury.”).
Dr. Gershwin offers no specific critique of any of the studies cited by
respondent’s experts, but urges more generally that the complicated relationship
between RA and its environmental factors makes it a poor fit for epidemiologic study.
(Ex. 30, p. 2.) While this might be a somewhat reasonable caveat, it is not enough to
cast substantial doubt on the value of the studies in this record without a more direct
discussion of study methodology and limitations. Dr. Gershwin cites a paper by Gourley
and Miller on this point, but that paper only suggests the epidemiology in this context is
challenging and requires a large population. (Gourley & Miller, supra, at Ex. 32.) It
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does not cast doubt on all epidemiology relative to RA and does not specifically address
prior studies regarding vaccination. Moreover, other literature cited by petitioner in this
case indicates that there are environmental factors such as smoking, air pollution, silica
exposure, and infection, that are accepted as having associations with RA despite the
issues raised by Dr. Gershwin. (E.g. V. Michael Holers et al., Rheumatoid Arthritis and
the Mucosal Origins Hypothesis: External Protection Becomes Internal Destruction, 14
NATURE REV. RHEUMATOLOGY 542, 546 (2018) (Ex. 28A, p. 5); Kevin D. Deane, Jill M.
Norris, & V. Michel Holers, Pre-Clinical Rheumatoid Arthritis: Identification, Evaluation
and Future Directions for Investigation, 36 RHEUMATOLOGY DISEASE CLINICS N. AM. 213,
216 (2010) (Ex. 28B, p. 4).) Even if one did entirely discount the epidemiologic studies
themselves, Dr. Gershwin’s theory also stands in contrast to the evidence of record
demonstrating that the relevant medical community recommends that RA patients
receive the flu vaccine. (Jasvinder A. Singh et al., 2015 American College of
Rheumatology Guideline for the Treatment of Rheumatoid Arthritis, 68 ARTHRITIS &
RHEUMATOLOGY 1, 18 (2015) (Ex A, Tab 6, p. 18); S van Assen, EULAR
Recommendations for Vaccination in Adult Patients with Autoimmune Inflammatory
Rheumatic Diseases, 40 ANNUALS RHEUMATOLOGY DISEASES 414, 416 (2011) (Ex. A, Tab
8, p. 3).)
None of this indicates that Dr. Gershwin’s theory should be viewed as
impossible. However, respondent is also persuasive in contending that, especially
when considering this overall context, Dr. Gershwin’s explanation is incredibly vague.
Much of what Dr. Gershwin discusses in his reports relates to the broader
understanding that RA is an autoimmune condition that develops in a stepwise process
in response to a combination of genetic and environmental factors. (Ex. 25, p. 3.) Little
in this broader discussion is disputed. Indeed, it is very similar to Dr. Morel’s discussion
of the immunology underlying RA. (Ex. C, pp. 3-4.) However, Dr. Gershwin’s broader
explanation of RA autoimmunity does not in itself implicate vaccines as one of the
environmental stimuli contributing to RA. Those aspects of Dr. Gershwin’s theory that
are vaccine-specific, namely his discussion of post-vaccinal cytokines and bystander
activation, lack any tether to RA and appear disjointed from the remainder of his causal
explanation.
With regard to the ability of the flu vaccine’s ability to generate pro-inflammatory
cytokines, Dr. Gershwin cites Talaat, et al. (Ex. 27, p. 2 (citing Talaat et al., supra, at
Ex. 28D).) In that study, 20 healthy subjects received a trivalent influenza vaccination
and serum cytokine levels were measured for up to two weeks post-vaccination.
Several cytokines were elevated post-vaccination; however, only mild adverse reactions
were reported.19 Nothing in this paper suggests that the observed cytokines would
cause or contribute to RA specifically or autoimmunity generally. Dr. Gershwin
combines the Talaat study with four additional papers he suggests show vaccines
generally have a “strong bystander effect.” (Ex. 27, p. 2 (citing Susan van Aaist et al.,
19 Ten subjects had generalized myalgia, eight reported injection site pain, two subjects reported
episodes of diaphoresis, one had sore throat, one experienced vomiting, and one had a vasovagal event
during a blood draw. (Talaat et al., Rapid Changes in Serum Cytokines and Chemokines in Response to
Inactivated Influenza Vaccination, 12 INFLUENZA AND OTHER RESPIRATORY VIRUSES 202 (2017) (Ex. 28D.))
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Bystander Activation of Irrelevant CD4+ T Cells Following Antigen-Specific Vaccination
Occurs in the Presence and Absence of Adjuvant, 12 PLOS ONE 1, (2017) (Ex. 28E);
Gianfranco Di Genova et al., Bystander Stimulation of Activated CD4+ T Cells of
Unrelated Specificity Following a Booster Vaccination with Tetanus Toxoid, 40 EUR. J.
IMMUNOLOGY 976, (2010) (Ex. 28F), Eleonora Li Causi et al., Vaccination Expands
Antigen-Specific CD4+ Memory T Cells and Mobilizes Bystander Central Memory T
Cells, 10 PLOS ONE 1, (2015) (Ex. 28G); Melody A. Swartz, Jeffrey A. Hubbell, & Sai T.
Reddy, Lymphatic Drainage Function and Its Immunological Implications: From
Dendritic Cell Homing to Vaccine Design, 20 SEMINARS IN IMMUNOLOGY 147, (2008) (Ex.
28H).) Dr. Gershwin suggests that following vaccination, proinflammatory cytokines
would “be key players in the differentiation and expansion of pathogenic
autoantibodies.” (Id.) Because Dr. Gershwin does not explain his reliance on any of
these specific studies, he has not substantiated how they support his opinion. Three of
these studies (Li Causi, et al., supra, at Ex. 28G; van Aaist, et al., supra, at Ex. 28E;
and Di Genova, et al., supra, at Ex. 28F) appear only to address the preliminary
question of whether vaccines induce bystander activation at all while the fourth (Swartz,
et al., supra, at Ex. 28H) is limited to discussing lymphatic drainage post-vaccination.
None of these studies involves RA specifically or otherwise demonstrate bystander
activation as leading to human disease more broadly.
Importantly, even if one accepts Dr. Gershwin’s explanation of cytokine-driven,
post-vaccination bystander activation as a generally useful concept, its particular
application to RA would still be unsupported. Dr. Morel agrees that transition to clinical
RA might involve a “second signal” that ultimately produces joint damage following an
inflammatory cascade. However, she explains that micro-trauma, vascular events, and
infectious events, but not vaccines, are suggested as viable possibilities. (Ex. C, p. 4.)
Additionally, the medical literature Dr. Gershwin himself relies upon in this case also
indicates that his underlying premise – that a distinct environmental stimulus acts as the
“final straw” in the multi-step process of transitioning from preclinical to clinical RA – is
unsettled. Specifically, the literature indicates that
[W]hile genetic and environmental factors have been associated with RA,
the exact role that these factors play in the development of RA-related
autoimmunity is not yet clear. Also, it is unclear whether these factors may
lead to initial RA related immune dysregulation or transition from
asymptomatic autoimmunity to clinically-apparent RA.
(Deane, Norris, & Holers, supra, at Ex. 28B, p. 4; see also Elizabeth W. Karlson & Kevin
Deane Environmental and Gene-Environment Interactions and Risk of Rheumatoid
Arthritis, 38 RHEUMATOLOGY DISEASE CLINICS N. AM. 405, 405 (2012) (Ex. 26I, p. 1) (“the
growing understanding of the prolonged period prior to the first onset of symptoms of
RA suggests that these environmental and genetic factors are likely acting to drive the
development of RA-related autoimmunity long before the appearance of the first joint
symptoms and clinical findings that are characteristic of RA.”); (Holers et al., supra, at
Ex. 28, p. 5) (“very few long-term prospective studies have been performed whose goal
would be to understand how stage-specific exposures influence the initial pre-clinical
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development of RA-related autoimmunity and subsequent clinical and/or immune
transitions.”) Thus, even if bystander activation showed that vaccines could be
considered capable of causing or contributing to the type of immune dysregulation
involved in the development of RA, it would still remain to be established that vaccines,
or in fact any environmental factor otherwise associated with RA, would act in the
manner of a “final straw” as Dr. Gershwin proposes.
Petitioner stresses in his motion that “[i]t is not necessary for a petitioner to point
to conclusive evidence in the medical literature linking a vaccine to the petitioner’s
injury, so long as the petitioner can show by a preponderance of the evidence that there
is a causal relationship between the vaccine and the injury, whatever the details of the
mechanism may be.” (ECF No. 71, pp. 11-12 (citing Moberly v Sec’y of Health &
Human Servs., 592 F.3d 1315, 1325 (Fed Cir. 2010).) 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 v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706,
743 (2009) (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)); 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 rev. denied, 108 Fed. Cl. 743 (2013), aff’d, 540 F.
Appx. 999 (Fed. Cir. 2013).
In this case, Dr. Gershwin has presented a description of the autoimmune
process involved in RA that does not itself implicate vaccines, a separate concept by
which any vaccine might in general contribute to autoimmunity without respect to any
specific context, and precious little that could tie the two together. This would at best
set the stage for the proposed causal relationship to be possible. (E.g. Gourley & Miller,
supra, at Ex. 32, p. 6 (RA review article discussing vaccine as only a “possible”
environmental trigger for “various diseases”).) Without more it simply does not add up
to preponderant evidence showing that the flu vaccine can cause or contribute to RA.
Boatmon, 941 F.3d at 1360 (explaining that “a ‘plausible’ or ‘possible’ theory does not
satisfy the standard”). Moreover, given that respondent has filed substantial literature
casting doubt on the idea that the flu vaccine causes or contributes to RA, and given
that both parties have filed literature demonstrating that vaccines are not generally
viewed as among the accepted environmental factors contributing to RA, even that
mere possibility would be at most a remote one. Accordingly, the analytic gap is simply
too great to allow for acceptance of Dr. Gershwin’s theory.
In light of all of the above, Dr. Gershwin has not presented a sound and reliable
theory of causation in this case and petitioner has not met his preponderant burden of
proof under Althen prong one.
a. Althen Prong Two
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,
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956 F.2d at 1148. 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 (quoting Althen, 418 F.3d at 1280) (stating
that “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’”). 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. See 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) (stating that “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”). Ultimately, petitioner may support his claim either through his
medical records or by expert opinion. § 300aa-13(a)(1).
There is no dispute in this case that petitioner’s RA first manifested clinically at
some point in the months following his vaccination, though there is a seeming inability to
pinpoint any precise onset. As discussed below under Althen prong three, Dr. Gershwin
provides a range of possibilities from late September to early December of 2015. Dr.
Antiochos agrees on respondent’s behalf that his condition first manifested in late 2015.
(Ex. A, p. 5.) Dr. Morel places onset in December of 2015. (Ex. F, p. 2.) However, for
all the reasons discussed separately under Althen prongs one and three, there is not
preponderant evidence supporting this post-vaccination onset of symptoms as medically
significant. And, in any event, temporality alone would not meet petitioner’s burden of
proof under Althen prong two. See, e.g. Bangerter v. Sec’y of Health and Human
Servs., No. 15-1186V, 2022 WL 439535, at *28 (Fed. Cl. Spec. Mstr. Jan. 18, 2022
(citing Veryzer v. Sec’y of Health and Human Servs., 100 Fed. Cl. 344, 356 (2011).
Petitioner’s treating physicians were largely silent as to causation. Petitioner
relies on the medical record of his treating rheumatologist (Dr. Paolino) as support for
the idea that there is a logical sequence of cause and effect between his vaccination
and onset of his RA, but misconstrues the record. (ECF No. 71, pp. 13-15 (citing Ex. 8,
p. 9.) Dr. Paolino’s impression on December 1, 2015 was “Acute polyarthritis x 6-8
weeks. Appearance of RA, but the history of vaccine preceding onset. R/O reactive or
post-infectious arthritis.” (Ex. 8, p. 9.) Petitioner quotes only the first part of this
impression, leaving out the language with respect to ruling out other conditions, and
interprets this record as an opinion that petitioner’s RA was vaccine-caused. (ECF No.
71, p. 13.) However, this record reflects that Dr. Paolino is engaging in differential
diagnosis based on petitioner’s history and presentation, not setting forth any opinion or
theory of causation. When read in full it is clear that Dr. Paolino is recording a
diagnostic suspicion for RA (the “appearance of RA”), but is also concerned that the
temporality to vaccination should point to another condition, such as the reactive
arthritis initially posited by petitioner’s own expert, that should be ruled out before
concluding that petitioner does suffer RA. Dr. Gershwin’s first two reports confirm that
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an opinion that vaccines can cause reactive arthritis is not equivalent to an opinion that
they can cause RA. (Exs. 16, 17.)
Additionally, as Dr. Morel has raised, petitioner’s physicians continued to
recommend flu vaccinations and petitioner continued to receive those vaccinations
without any adverse effects. (Ex. F, p. 1; Ex. 22, pp. 13, 37.) This is consistent with the
standard of care for RA. (Singh et al., supra, at Ex A, Tab 6, p. 18; van Assen et al.,
supra, at Ex. A, Tab 8, p. 3.) Although Dr. Gershwin indicates his hypothesis
distinguishes events that break self-tolerance from events that determine the course of
the disease (Ex. 30, p. 2), the fact that petitioner’s treating physicians felt administration
of the flu vaccine was safe and appropriate is some evidence in itself. “A treating
physician’s decision to administer or withhold a vaccination can be highly probative of
causation.” Tarsell v. United States, 133 Fed Cl. 782, 797 (2017) (citing Andreu, 569
F.3d at 1376).)
Dr. Gershwin asserts that the petitioner’s lab results show a progression over
time that allows for the markers of his disease to be traced back to onset and thereby
evidence vaccine causation. (Ex. 25 p. 1-2.) Specifically, petitioner’s second RF test of
261 U/mL showed an increase in RF after nearly two years and his CCP test of 73 units
was positive for the first time in October 2019, four years after onset, despite having
been previously negative at the time of onset. (Id. p. 2; Ex. 8, p. 11; Ex. 24, pp. 3-4.)
Although it is true that petitioner’s tests reflected these changes, Dr. Gershwin has not
substantiated that this is evidence meaningful to causation.
The literature filed in this case suggests that production of antibodies during the
pre-clinical phase does correlate to disease severity; however, the production of
antibodies is not in itself essential for clinical disease. (Markus M. J. Nielen et al.,
Specific Autoantibodies Precede the Symptoms of Rheumatoid Arthritis: A Study of
Serial Measurements in Blood Donors, 50 ARTHRITIS & RHEUMATISM 380, 385 (2004)
(Ex. 26D, p. 6.); Gary S. Firestein & Iain B. McInnes, Immunopathogenesis of
Rheumatoid Arthritis, 46 IMMUNITY 184, 184 (2017) (Ex. C, Tab 3, p. 1); V.F.A.M.
Derksen, T.W.J. Huizinga, & D. van der Woude, The Role of Autoantibodies in the
Pathophysiology of Rheumatoid Arthritis, 39 SEMINARS IMMUNOPATHOLOGY 437, 437
(2017) (Ex C, Tab 5, p. 1).) “[C]onversion to RF seropositivity continued after the onset
of symptoms and reached the commonly reported prevalence level of 67% after 6
years.” (Id.) In this case, petitioner was RF seropositive from the first time he was
tested. Although the same literature notes that “[i]n the majority of patients,
seropositivity, once established, is stable” (Nielen et al., supra, at Ex. 26D, p. 6.),
nothing on this record indicates that petitioner’s subsequent rise in RF is informative
with respect to either the timing of his initial seroconversion or the cause of his
condition. Additionally, the literature indicates that some studies have shown a subset
of subjects develop CCP antibodies after transitioning to clinical RA. (Lars Klareskog et
al., Mechanisms of Disease: Genetic Susceptibility and Environmental Triggers in the
Development of Rheumatoid Arthritis, 2 NATURE CLINICAL PRAC.: RHEUMATOLOGY 425,
428 (2006) (Ex. C, Tab 10, p. 4).) Dr. Gershwin has also filed literature explaining that
“the utility of anti-CCP retesting during the disease course in patients present with
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inflammatory arthritis is actually questionable and not recommended . . . the clinical
value of anti-CCP levels at disease onset and influence of titer changes over time on
disease outcome have not been fully clarified.” (Nicola Bizzaro et al., Anti-Cyclic
Citrullinated Peptide Antibody Titer Predicts Time to Rheumatoid Arthritis Onset in
Patients with Undifferentiated Arthritis: Results from a 2-Year Prospective Study, 15
ARTHRITIS RESEARCH AND THERAPY 1, 2 (2013) (Ex. 31, p. 2).)
Dr. Gershwin also relies on the fact that there is no other evidence of the cause
of petitioner’s RA, but this fails to account for petitioner’s history of smoking. Both
parties’ experts agree that smoking is well established as a factor contributing to the
development of RA. (Ex. 25, p. 2; Ex. C, p.2; Ex. F, p.1.) Given that Dr. Gershwin
agrees on this point, he has not adequately addressed why petitioner’s history of
smoking alone is not explanation enough for his RA. Dr. Gershwin suggests that
petitioner’s belated CCP finding is incompatible with smoking being the sole
environmental contributor because in that context CCP antibodies are expected at the
time of diagnosis. (Ex. 27, p. 2.) For this proposition he cites a review by Holers, et al.
(Id. (citing Holers et al., supra, at Ex. 28A).) However, this paper does not support Dr.
Gershwin’s assertion. Holers, et al., explain that a number of studies have associated
smoking with CCP antibodies and the eventual development of RA. (Holers et al.,
supra, at Ex. 28A, p. 5.) On the whole, these studies support a “well-accepted
association” between heavy smoking and the risk of developing seropositive RA. (Id.)
But none of the study findings discussed indicate that CCP antibodies are necessarily
present at the time of diagnosis. In fact, one of the cited studies found that smoking
was associated with both seropositive and seronegative RA. (Id.) Despite the
association, the authors indicate that “[t]he exact stage-specific timing of smoking
effects during the pre-clinical to classified arthritis natural history of RA is not well
understood.” (Id.)
In light of all of the above, petitioner has not met his preponderant burden of
proof under Althen prong two.
b. Althen Prong Three
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 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., 503 Fed. Appx. 952 (Fed. Cir. 2013); Koehn v. Sec’y of
Health & Human Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30,
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2013), mot. for review den’d (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir.
2014).
As discussed under Althen prong one, there is not agreement on whether the
environmental factors that contribute to clinical RA operate at earlier points within the
preclinical disease process or as the final set piece as Dr. Gershwin opines. (Compare
Ex. 27, p. 2 (proposing post-vaccination cytokines as “the final environmental block that
leads to the clinical onset of disease” and Deane, Norris, & Holers, supra, at Ex. 28B, p.
4; see also Holers et al., supra, at Ex. 28A, p. 5.) Thus, it does not even appear
possible to identify any clearly defined beginning point of a relevant latency period.
However, even accepting arguendo that a vaccine could be the “final straw” in the
development of RA, Dr. Gershwin’s opinion is still unpersuasive. Petitioner asserts that
onset of his RA began sometime between October 1, 2015, and October 15, 2015.
(ECF No. 71, p. 14.) He further contends that a latency of between four to six weeks
post-vaccination is appropriate to demonstrate a proximate temporal relationship
between the influenza vaccination and development of RA. (Id.) For both of these
points, petitioner cites the final page of Dr. Gershwin’s first report. (Id. (citing Ex. 16, p.
4.) However, petitioner’s reliance on this aspect of Dr. Gershwin’s opinion is not clear-
cut.
Initially, Dr. Gershwin identified the first concerning change in petitioner’s arthritic
symptoms as occurring on September 24, 2015, without respect to diagnosis. (Ex. 16,
p. 1.) Later in the same report, he specifically indicated that petitioner suffered onset of
reactive arthritis sometime between October 1 and October 15, 2015. (Id. 4.) These
two statements alone are difficult to reconcile, even accounting for Dr. Gershwin’s
suggestion that determining onset is more difficult due to other underlying medical
conditions. (Id.) It is not clear how Dr. Gershwin arrived at the specific October 1-
October 15 timeframe. However, in his third report, wherein he changed his diagnostic
opinion, Dr. Gershwin opined that “I do not believe [petitioner] had evidence of clinical
rheumatoid arthritis until the presence of the elevated inflammatory markers of ESR and
CRP on December 1, 2015.” (Ex. 25, p. 2 (emphasis added).) Dr. Morel then agreed
that this is the point at which petitioner developed clinical RA.20 (Ex. F, p. 1.)
Depending on which of Dr. Gershwin’s statements controls, the latency from vaccination
to injury is anywhere from three weeks to just shy of nine weeks. Yet, among all of his
reports, Dr. Gershwin only ever specifically endorses a period of four-to-six weeks as
consistent with any theory he has presented.
Further muddying the waters, while the clinical signs of RA and reactive arthritis
may overlap, Dr. Gershwin was very clear in describing two distinct causal mechanisms
for reactive arthritis and RA respectively. The full extent of Dr. Gershwin’s explanation
of the appropriate timing in any of his reports is that onset occurring four to six weeks
20 Dr. Gershwin does indicate that the presentations of reactive arthritis and RA can be confused, which
may suggest Dr. Gershwin intended to cite December 1 as the point by which RA could be diagnosed as
opposed to the date it became clinical RA. (Ex. 16, p.4.) However, this is not necessarily clear from the
report. Even granting that assumption, it would still not be clear how the specific diagnosis of RA
interplays with Dr. Gershwin’s stated inability to otherwise identify a precise onset of symptoms due to
other underlying conditions.
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post-vaccination is “consistent with the development of a T cell response.” (Ex. 16, p.
4.) But this was articulated relative to reactive arthritis specifically. (Id.) In his first
report, he explained that reactive arthritis is distinguished by the fact that it involves a
non-specific inflammatory T cell response that would occur de novo post-vaccination
and does not include a role for autoantibodies. (Ex. 16, p. 3.) In contrast, he explains in
his later reports that vaccine causation of RA would involve a necessary autoantibody
response, but in the context of an already smoldering autoimmune process. (Ex. 25, p.
2; Ex. 27, p. 2.) It is possible that these distinctions could ultimately have no net
significance to timing; however, there is no basis for making that assumption on this
record and Dr. Gershwin has provided no separate explanation regarding the timeframe
for the post-vaccination portion of the overall development of autoimmunity in RA.
Even looking beyond what Dr. Gershwin makes explicit, none of the limited
literature that Dr. Gershwin cites on this record with specific regard to suspected post-
vaccinal RA provides support for a four-to-six week latency for RA. The Jawad case
report had a latency of three weeks. (Jawad & Scott, supra, at Ex. 26N.) The
Symmons paper largely did not specify onset periods. The only case series with a
confirmed period of onset indicated that post-vaccination arthralgia occurred between 7-
10 days post-vaccination. (Symmons & Chakravarty, supra, at Ex. 26M, p. 1.) The
case reports filed by respondent had onset periods of between four days and one week
following H1N1 influenza vaccination and three days after a tetanus booster
vaccination. (Basra, Jajoria, & Gozalez, supra, at Ex. C, Tab 19; Maria Antonia Pou et
al., supra, at Ex. C, Tab 20; Tabache et al., supra, at Ex. C, Tab 21.) Even accounting
for the mechanistic aspects of Dr. Gershwin’s theory, the study he cited regarding post-
vaccination cytokines indicated that these cytokines peak at 24 hours post vaccination
and the study he cited with respect to bystander activation showed that in human
subjects T cell expansion peaked at one-week post-vaccination. (Talaat et al., supra, at
Ex. 28D; Causi et al., supra, at Ex. 28G, p. 5.) All of this implies a shorter latency than
what petitioner and Dr. Gershwin cite. None of it precludes a longer latency, but in the
absence of further explanation by Dr. Gershwin, it does not support one either.
In light of all of the above, petitioner has not met his preponderant burden under
Althen prong three.
VII. Conclusion
Petitioner has clearly suffered and he has my sympathy. However, for all the
reasons discussed herein, petitioner has not preponderantly demonstrated that he
actually suffered a vaccine-caused injury and is therefore not entitled to compensation.
Accordingly, this case is dismissed.21
21 In the absence of a timely-filed motion for review of this Decision, the Clerk of the Court shall enter
judgment accordingly.
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IT IS SO ORDERED.
s/Daniel T. Horner
Daniel T. Horner
Special Master
24