Powell v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

Filed: October 8, 2025

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

JENNIFER POWELL, * PUBLISHED

*

Petitioner, * No. 20-1726V

*

v. * Special Master Nora Beth Dorsey

*

SECRETARY OF HEALTH * Dismissal; Influenza (“Flu”) Vaccine;

AND HUMAN SERVICES, * Rheumatoid Arthritis (“RA”); Causation-in-

* Fact; Significant Aggravation.

Respondent. *

*

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

Sean Franks Greenwood, The Greenwood Law Firm, Houston, TX, for Petitioner.

Benjamin Patrick Warder, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION 1

On December 1, 2020, Jennifer Powell (“Petitioner”) filed a petition for compensation

under the National Vaccine Injury Compensation Program (“Vaccine Act” or “the Program”), 42

U.S.C. § 300aa-10 et seq. (2018). 2 Petitioner alleges that flu vaccinations administered on

December 1, 2017 and October 16, 2018 “were the cause-in-fact of and/or aggravated”

Petitioner’s chronic rheumatoid arthritis (“RA”). Petition at ¶¶ 4, 23, 31 (ECF No. 1).

Respondent argued against compensation, stating that “compensation is not appropriate in this

1

Because this Decision contains a reasoned explanation for the action in this case, the

undersigned is required to post it on the United States Court of Federal Claims’ website 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 Decision will be available to anyone with

access to the Internet. In accordance with Vaccine Rule 18(b), Petitioner has 14 days to

identify and move to redact medical or other information, the disclosure of which would

constitute an unwarranted invasion of privacy. If, upon review, the undersigned agrees that the

identified material fits within this definition, the undersigned will redact such material from

public access.

2

The National Vaccine Injury Compensation Program is set forth in Part 2 of the National

Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended,

42 U.S.C. §§ 300aa-10 to -34 (2018) (“Vaccine Act” or “the Act”). All citations in this Decision

to individual sections of the Vaccine Act are to 42 U.S.C.A. § 300aa.

case” and “this case should be dismissed.” Respondent’s Report (“Resp. Rept.”) at 1, 29 (ECF

No. 24).

After carefully analyzing and weighing the evidence presented in this case in accordance

with the applicable legal standards, 3 the undersigned finds that Petitioner has failed to provide

preponderant evidence that her flu vaccines caused her RA and thus has not satisfied her burden

of proof under Althen v. Secretary of Health & Human Services, 418 F.3d 1274, 1280 (Fed. Cir.

2005). Accordingly, the petition must be dismissed.

I. ISSUES TO BE DECIDED

Diagnosis is not at issue; the parties agree Petitioner has RA. Joint Pre-Entitlement

Submission (“Joint Sub.”), filed Aug. 12, 2024, at 1-2 (ECF No. 90). The parties stipulate that

Petitioner received flu vaccines on December 1, 2017 and October 16, 2018. Id. at 1. They

agree that on March 6, 2018, Petitioner’s rheumatologist noted “[i]mpression [n]o dramatic

swelling but her pattern is certainly consistent with RA.” Id. (quoting Pet. Ex. 4 at 34). Further,

they agree that on July 5, 2018, Petitioner’s rheumatologist diagnosed her with RA. Id.

Facts in dispute include the onset of Petitioner’s RA. Joint Sub. at 2. Causation is also in

dispute. Id. Specifically, the parties disagree as to whether the flu vaccine administered on

December 1, 2017 caused Petitioner to develop RA pursuant to the Althen prongs. Id.

The parties also dispute whether Petitioner had “a significant worsening of her RA

symptoms” after she received the flu vaccine on October 16, 2018, which they agree would be

governed by Loving. 4 Joint Sub. at 2; see Loving v. Sec’y of Health & Hum. Servs., 86 Fed. Cl.

3

While the undersigned has reviewed all the information filed in this case, only those filings and

records that are most relevant will be discussed. See Moriarty v. Sec’y of Health & Hum. Servs.,

844 F.3d 1322, 1328 (Fed. Cir. 2016) (“We generally presume that a special master considered

the relevant record evidence even though [s]he does not explicitly reference such evidence in

h[er] decision.”); Simanski v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 407, 436 (2014)

(“[A] Special Master is ‘not required to discuss every piece of evidence or testimony in her

decision.’” (citation omitted)), aff’d, 601 F. App’x 982 (Fed. Cir. 2015).

4

Loving sets forth six elements for an off-Table significant aggravation case:

(1) the person’s condition prior to administration of the vaccine, (2) the person’s

current condition (or the condition following the vaccination if that is also

pertinent), (3) whether the person’s current condition constitutes a ‘significant

aggravation’ of the person’s condition prior to vaccination, (4) a medical theory

causally connecting such a significant worsened condition to the vaccination, (5) a

logical sequence of cause and effect showing that the vaccination was the reason

for the significant aggravation, and (6) a showing of a proximate temporal

relationship between the vaccination and the significant aggravation.

Loving v. Sec’y of Health & Hum. Servs., 86 Fed. Cl. 135, 144 (2009).

2

135, 144 (2009). However, the parties’ experts do not address significant aggravation or the

Loving factors. 5 See Petitioner’s Exhibits (“Pet. Exs.”) 9, 37, 42 (failing to mention “significant

aggravation” or “Loving”); Resp. Exs. A, C, E-F (same). Therefore, the undersigned does not

undertake a Loving analysis or make any finding relative to whether the flu vaccine of October

16, 2018 caused a significant aggravation of Petitioner’s RA.

Even if the undersigned had addressed the question of significant aggravation, the

outcome here would have been the same since the Loving factors incorporate the Althen prongs. 6

See Loving, 86 Fed. Cl. at 143 (“[T]he appropriate framework for determining whether a

petitioner has made a prima facie showing that she has a compensable significant-aggravation

off-Table claim . . . [includes] the three-part test articulated in Althen.”); W.C. v. Sec’y of Health

& Hum. Servs., 704 F.3d 1352, 1357 (Fed. Cir. 2013) (holding that “the Loving case provides

the correct framework for evaluating off-table significant aggravation claims”); see also, e.g.,

Heller v. Sec’y of Health & Hum. Servs., 162 Fed. Cl. 621, 636 (2022) (“[T]he standards for

assessing Althen prongs 1-3 also apply to Loving prongs 4-6.”). 7 Therefore, because the

undersigned finds Petitioner failed to carry her burden as to Althen, Petitioner also cannot carry

her burden under Loving.

II. BACKGROUND

A. Medical Terminology

RA is a “chronic inflammatory joint disease characterized by a distinctive pattern of bone

and joint destruction.” Resp. Ex. A, Tab 2 at 2. 8 “The classic presentation of [RA] is a

5

Arguments by counsel, without expert opinion, does not constitute evidence and are

insufficient. The undersigned is unable to render findings relative to Loving in this case without

expert opinion evidence.

6

The three Althen prongs, which are also elements 4, 5, and 6 of Loving, require “(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 a

proximate temporal relationship between vaccination and injury.” Althen, 418 F.3d at 1278.

7

The parties agree. See Pet. Supportive Brief for Pet Mot. (“Pet. Br.”), filed Aug. 12, 2024, at 4

(ECF No. 88) (noting “Loving prong four is covered [by] [the] discussion concerning Althen

prong one,” “Loving prong five is covered [by] [the] discussion concerning Althen prong two,”

and “Loving prong six is covered [by] [the] discussion concerning Althen prong three”); Resp.

Response to Pet. Mot. (“Resp. Response”), filed Nov. 19, 2024 (ECF No. 95) (agreeing “[t]he

Loving test [] incorporates and requires a petitioner to prove the three Althen factors”).

8

Gabriel J. Tobón et al., The Environment, Geo-epidemiology, and Autoimmune Disease:

Rheumatoid Arthritis, 9 Autoimmun. Revs. A288 (2010).

3

symmetric small joint synovitis[9] of the hands and feet,” although the illness may present with

synovitis of the elbows and knees. Pet. Ex. 39 at 24. 10 Diagnostic criteria promulgated by the

American College of Rheumatology (“ACR”) and the European League Against Rheumatism

(“EULAR”) in 2010 assess points based on an algorithm which includes the following findings

or serology results: “active synovitis in at least one joint that cannot be better explained by

another diagnosis,” antibodies to citrullinated proteins, rheumatoid factor, abnormal

inflammatory markers (erythrocyte sedimentation rate (“ESR”) and C-reactive protein (“CRP”)),

and duration of symptoms of six weeks or greater. Id. at 24, 25 tbl.92.1.

The disease course can vary following onset and may be characterized as “progression,

stable course with or without flares, or remission.” Pet. Ex. 39 at 24. The disease incidence in

North America and Northern Europe “range[s] from 20-50 cases per 100,000 population.” Resp.

Ex. A, Tab 2 at 2. The cause is not known, although environmental and genetic risk factors may

play a role. Pet. Ex. 40 at 1. 11 These risk factors include genetics, age, gender, smoking,

infections, dietary factors, and genetic and environmental interactions. Resp. Ex. A, Tab 2 at 3-

4. Genetics “contribute 50% to 60% of the risk of developing RA.” Id. at 3. The two genes

most frequently associated with RA include HLA-DRB1, a “gene in the major histocompatibility

complex,” and PTPN22, a “tyrosine-phosphatase gene.” 12 Id. Relative to environmental factors,

“smoking has by far the strongest association with RA.” Id. There are a number of infections

that have been reported to induce RA, however, the question of whether infectious organisms

induce RA “remains controversial” because the evidence “remains inconclusive.” Id. at 3-4.

B. Procedural History

Petitioner filed her petition on December 1, 2020, along with an affidavit, and followed

by medical records 13 in March and April 2021. Petition; Pet. Exs. 1-7. This case was assigned

to the undersigned in September 2021. Notice of Reassignment dated Sept. 10, 2021 (ECF No.

16). Respondent filed his Rule 4(c) report, arguing against compensation, on February 7, 2022.

Resp. Rept. at 1.

9

Synovitis is “inflammation of a synovial membrane; it is usually painful, particularly on

motion, and is characterized by a fluctuating swelling due to effusion within a synovial sac.”

Synovitis, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/

definition?id=48576 (last visited Sept. 25, 2025).

10

Katherine P. Liao, Rheumatoid Arthritis: Classification and Epidemiology of Rheumatoid

Arthritis, in Rheumatology 747 (Marc C. Hochberg et al. eds., 7th ed. 2019).

11

Zahra Bagheri-Hosseinabadi et al., MTHFR Gene Polymorphisms and Susceptibility to

Rheumatoid Arthritis: A Meta-Analysis Based on 16 Studies, 39 Clin. Rheumatol. 2267 (2020).

12

For an explanation of these two genes, see Resp. Ex. A, Tab 2 at 3.

13

Medical records were filed throughout litigation.

4

On June 6, 2022, Petitioner filed an expert report from Dr. Omid Akbari. Pet. Ex. 9. On

October 4, 2022, Respondent filed expert reports from Dr. John T. Bates and Dr. Karen L Law.

Resp. Exs. A, C. Petitioner filed an expert report from Dr. David Axelrod on February 20, 2023.

Pet. Ex. 37.

Thereafter, pursuant to a request from the parties, the undersigned held a Rule 5

conference. Rule 5 Order dated June 21, 2023 (ECF No. 50). The undersigned preliminarily

found no dispute as to diagnosis (here, RA). Id. at 2. The undersigned noted issues with onset as

there was a conflict between Petitioner’s affidavit and medical records. Id. Lastly, the

undersigned indicted she was unable to provide her preliminary findings as to causation. Id.

Petitioner filed a supplemental expert report from Dr. Akbari on August 7, 2023. Pet. Ex.

43. On May 5, 2024, Respondent filed responsive expert reports from Dr. Bates and Dr. Law.

Resp. Exs. E-F.

The parties were unable to informally resolve this matter and requested to resolve

entitlement through a ruling on the record. Resp. Status Rept., filed Feb. 16, 2024 (ECF No. 70);

Joint Status Rept., filed June 4, 2024 (ECF No. 78). Petitioner filed his motion for a ruling on

the record along with a supporting brief on August 12, 2024. Pet. Motion for Ruling on the

Record (“Pet. Mot.”), filed Aug. 12, 2024 (ECF No. 87); 14 Pet. Br. Respondent filed his

response on November 19, 2024. Resp. Response. Petitioner did not file a reply.

This matter is now ripe for adjudication.

14

In Petitioner’s motion, counsel stated, “[w]ere the Special Master to opine that Petitioner is not

entitled to compensation for either the causation-in-fact or significant aggravation claim, the

Petitioner requests a live hearing before the Special Master.” Pet. Mot. at 1. However, the

parties requested to resolve entitlement through a ruling on the record. See Joint Status Rept.,

filed June 4, 2024. Further, the Vaccine Act and Rules encourage special masters to decide

petitions on the papers where (in the exercise of their discretion) they conclude that doing so will

properly and fairly resolve the case. § 12(d)(2)(D); Vaccine Rule 3(b)(2) (“The special master is

responsible for . . . endeavoring to make the proceedings expeditious, flexible, and less

adversarial, while at the same time affording each party a full and fair opportunity to present its

case and creating a record sufficient to allow review of the special master’s decision.”); Vaccine

Rule 8(d) (“The special master may decide a case on the basis of written submissions without

conducting an evidentiary hearing.”). The decision to rule on the record in lieu of hearing has

been affirmed on appeal. Kreizenbeck v. Sec’y of Health & Hum. Servs., 945 F.3d 1362, 1366

(Fed. Cir. 2020); see also Hooker v. Sec’y of Health & Hum. Servs., No. 02-472V, 2016 WL

3456435, at *21 n.19 (Fed. Cl. Spec. Mstr. May 19, 2016) (citing numerous cases where special

masters decided cases on the papers in lieu of hearing and that decision was upheld). The

undersigned is not required to hold a hearing in every matter, no matter the preferences of the

parties. And here, to hold a hearing after this case was submitted on the papers would not fairly

resolve this matter and would further prolong the proceedings.

5

C. Factual History

1. Medical History 15

Petitioner was thirty-five years old when she received the first flu vaccination at issue in

this case on December 1, 2017. Pet. Ex. 5 at 100.

a. Medical History Prior to December 1, 2017 Vaccination

Before her December 1, 2017 flu vaccination, Petitioner had a significant medical

history. On September 20, 2013, Petitioner presented to her primary care provider (“PCP”), Jane

Ragland, M.D. Pet. Ex. 7 at 21-24. Petitioner requested a prescription for antidepressants and

reported that she was prescribed Zoloft in the past, that she stopped taking it, and that she wanted

to start taking medication for depression again. Id. at 23. Petitioner also complained of neck

pain that began a few months prior that “ha[d] not gotten better” and occurred with movement.

Id. On examination, Dr. Ragland noted Petitioner had tenderness in her neck muscles and

decreased range of motion (“ROM”). Id. at 24. Dr. Ragland diagnosed Petitioner with

depression, neck muscle spasm, and a lip cyst. Id.

Petitioner returned to Dr. Ragland on September 28, 2013. Pet. Ex. 7 at 40. Petitioner

reported painful swelling in the back of her neck. Id. She also complained of feeling groggy in

the morning and reported taking muscle relaxants at night. Id. Examination revealed

Petitioner’s neck was not as tight as it had been during the previous visit, and there was no

swelling. Id.

On September 10, 2014, Petitioner received a flu vaccination in her right deltoid, with no

reported adverse effects. Pet. Ex. 3 at 65. From September 4, 2014 to April 2, 2015, Petitioner

presented for prenatal care. Id. at 12-56. Petitioner received a tetanus, diphtheria, and acellular

pertussis (“Tdap”) vaccination on February 25, 2015, with no reported adverse effects. Id. at 19,

64. Petitioner gave birth to a son via an elective caesarean section on April 7, 2015. Id. at 67-

70. Petitioner’s post-operative and postpartum courses were unremarkable. Id. Petitioner’s

15

This medical history is taken from Respondent’s Responsive Brief as the undersigned finds it

accurately reflects the medical records. See Resp. Response at 3-20. The undersigned has made

significant edits, deleted less relevant entries, and included additional information.

6

summary noted a prior history of methylenetetrahydrofolate reductase (“MTHFR”) deficiency. 16

Id.

On May 15, 2015, Petitioner saw Dr. Ragland complaining of pain from the middle-to-

lateral right side of her chest, with some radiation to her back. Pet. Ex. 7 at 120-23. Her pain

worsened with inspiration. Id. at 22. Dr. Ragland diagnosed Petitioner with pleurisy. Id. at 23.

The following year, on September 26, 2016, Petitioner called her PCP, reporting frequent

headaches, which sometimes improved with rest. Pet. Ex. 7 at 160-61. Tylenol and ibuprofen

were not alleviating the headaches. Id. at 161. Petitioner was instructed to keep a headache log

for a week. Id. at 160-61. Petitioner received a flu vaccination on October 4, 2016, with no

reported adverse effects. Pet. Ex. 2 at 1.

On October 28, 2016, Petitioner presented to Dr. Ragland. Pet. Ex. 7 at 169-72. She was

back at work and reported having anxiety issues and becoming upset easily. Id. at 170.

Petitioner shared her history of depression, explaining that she had taken Prozac in the past, but it

did not help her very much. Id. Petitioner also complained of heart palpitations, and she felt like

she was in a “constant state of crisis.” Id. She had been experiencing headaches intermittently

for the prior six months, and the headaches generally consisted of pain behind the right eye

occurring multiple times a week. Id. Petitioner also stated she was not sleeping well, and she

had “lots of stress with work.” Id.

Petitioner had a behavioral medicine consultation with psychiatrist Brandon Riley, M.D.,

on January 20, 2017. Pet. Ex. 5 at 180-83. Her history of depression and anxiety was noted, as

was her treatment with medication. Id. at 180. She had stopped taking her medication because

she started to feel better. Id. Petitioner reported that her anxiety had increased recently. Id.

Petitioner also described her belief that she had attention-deficit/hyperactivity disorder

(“ADHD”) when she was a child. Id. Dr. Riley’s impression was that Petitioner had generalized

anxiety disorder and panic disorder, and he prescribed Lexapro. Id. at 182. Petitioner returned

to see Dr. Riley monthly for follow-up visits. Id. at 146-79. Dr. Riley prescribed Adderall for

ADHD symptoms and adjusted the doses of her medications. Id.

16

MTHFR deficiency is “a common, autosomal recessive, inborn error of folate metabolism

caused by mutation in the MTHFR gene . . . , which encodes the enzyme. The chief biochemical

finding is homocystinuria with normal levels of plasma methionine.” Methylenetetrahydrofolate

Reductase (MTHFR) Deficiency, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=30976 (last visited Sept. 25, 2025). The

MFHFR enzyme “synthesises 5-methyl-tetrhydrofolate, which acts at the methyl donor for

remethylation of homocysteine to methionine.” Pet. Ex. 11 at 1 (Y. Berkun et al., Methotrexate

Related Adverse Effects in Patients with Rheumatoid Arthritis Are Associated with the A1298C

Polymorphism of the MTHFR Gene, 63 Ann. Rheum. Dis. 1227 (2004)). The C677T

polymorphism of this genetic mutation “results in decreased enzyme activity and

hyperhomocysteinaemia.” Id. Methotrexate, a drug given for RA, is contraindicated in those

who have the C677T polymorphism. Id.

7

On November 22, 2017, Petitioner saw Julie Haygood, M.D. Pet. Ex. 5 at 139-43. She

complained of a cough, sputum production, and shortness of breath, but she did not have any

wheezing. Id. at 140. Petitioner’s musculoskeletal examination was within normal limits. Id. at

141. Dr. Haygood diagnosed Petitioner with acute respiratory infection, and possible recurrent

pertussis, bronchitis, or atypical pneumonia. Id. at 142. A chest X-ray did not demonstrate any

acute disease. Id. at 199. Petitioner returned to Dr. Haygood November 30, 2017. Id. at 134-38.

She was still coughing a lot, especially at night, had chills, and a subjective fever. Id. at 135.

Petitioner also reported night sweats for several months and having unintentionally lost fifty

pounds in the previous few months. Id. Petitioner’s cough originally started in April 2017, but

had been lingering over the previous few weeks. Id. She reported tiring easily, heavy menses,

and that she was planning to have a uterine ablation in January 2018. Id. Dr. Haygood placed

Petitioner back on antibiotics and referred her to pulmonology. Id. at 137-38.

b. December 1, 2017 Flu Vaccination and Post-Vaccination

Medical History

As noted above, on December 1, 2017, Petitioner received a flu vaccination in her right

deltoid. Pet. Ex. 5 at 100.

Eleven days post-vaccination, on December 12, 2017, Petitioner presented to Dr.

Haygood. Pet. Ex. 5 at 123-27. She complained of several days of fever, chills, productive

cough, and facial pain associated with postnasal discharge, frontal headaches, and eye pain. Id.

at 124. Petitioner’s son had also been sick. Id. Petitioner was feeling fatigued and was dizzy

when standing. Id. Examination revealed cervical lymphadenopathy with redness and swelling

in her nasal passages. Id. at 125. Dr. Haygood diagnosed Petitioner with cough with fever, acute

sinusitis, normocytic anemia, and MTHFR heterozygous deficiency. Id. at 126-28. Dr. Haygood

ordered antibiotics and made referrals for pulmonology and hematology/oncology. Id. Chest X-

ray revealed no acute disease. Id. at 198.

Petitioner’s initial hematology/oncology consultation for complaints of bruising was on

December 13, 2017 with Kamran Shahid, M.D. Pet. Ex. 5 at 115-22. Petitioner’s review of

systems was positive for fatigue, weight loss, and easy bruising but no joint pain, swelling, or

redness. Id. at 116-17. She also denied decreased range of motion. Id. at 117. Examination

revealed palpable cervical lymph nodes on the right side of Petitioner’s neck. Id. at 118.

Musculoskeletal examination revealed no tenderness or swelling. Id. at 119. Dr. Shahid’s

impression was that Petitioner bruised easily but the cause was uncertain. Id. at 122. Laboratory

(“lab”) results revealed elevated white blood cell count, which was thought to be related to her

previous pertussis infection and her recent infection that was treated with azithromycin. Id. Dr.

Shahid directed Petitioner to follow up in four weeks. Id. A neck computed tomography (“CT”)

scan to evaluate Petitioner’s cervical lymph nodes was performed December 18, 2017. Id. at

196-97. The study did not identify any abnormally enlarged lymph nodes, but the right lobe of

her thyroid was enlarged and she had several low-density nodules typical of a multinodular

goiter. Id.

Petitioner had a pulmonology consult for her chronic cough on December 19, 2017 with

Richard Kronenberg, M.D. Pet. Ex. 5 at 109-12. Medical problems included acute respiratory

8

infection, and Petitioner was noted to be taking amoxicillin which had been prescribed by Dr.

Haygood on December 12, 2017. Id. at 109-110. Petitioner reported her cough had not gone

away, although there was no wheezing or whooping, but it was chronic and occurred throughout

the day. Id. at 110-11. Her pulmonary examination and pulmonary function tests were normal.

Id. at 111. Dr. Kronenberg noted that the etiology of Petitioner’s cough was “obscure,” but that

it may be due to irritation in her airways from her prior pertussis infection. Id. He prescribed

Symbicort and directed Petitioner to follow up in two weeks. Id. at 111-12. A chest X-ray did

not show any acute cardiopulmonary process. Id. at 195.

On December 21, 2017, Petitioner underwent an endometrial biopsy, which was positive

for hepatitis C virus antibody. Pet. Ex. 8 at 6-7.

One week later, on December 27, Petitioner reported that her entire household had a

stomach virus and she requested a prescription for Phenergan topical gel for nausea and

vomiting. Pet. Ex. 7 at 227.

Moving forward to 2018, Petitioner returned to see Dr. Kronenberg on January 2, 2018

for “[p]ossible flu.” Pet. Ex. 5 at 104-07. Since her visit two weeks prior, Petitioner had

“developed flu-like symptoms with fever[,] muscle aches[,] and malaise.” Id. at 105-06. Dr.

Kronenberg noted Petitioner appeared acutely ill. Id. at 106. His assessment was “[p]ossible

[flu]. Persistent nonproductive cough of uncertain etiology.” Id. Petitioner was prescribed

Tamiflu. Id.

In early January 2018, Petitioner discussed her positive hepatitis C virus antibody test at

length with Dr. Ragland. Pet. Ex. 7 at 229-30. On January 3, Petitioner emailed Dr. Ragland,

stating she did not fall into the risk category for hepatitis C and did not know how she could have

gotten hepatitis C, if she actually had it. Id. at 229. Dr. Ragland responded, stating she was

“hoping” for a false positive test. Id. On January 9, 2018, Petitioner emailed Dr. Ragland

advising that her hepatitis C viral load test was negative. Id. at 229-30. Petitioner sent the

negative result to Dr. Ragland on January 10, 2018. Id. at 230. Dr. Ragland stated that they

could consider that Petitioner had a false positive test. Id.

Petitioner returned to see Dr. Shahid for follow-up on January 11, 2018. Pet. Ex. 5 at 90-

99. During that appointment, Dr. Shahid reviewed the results of Petitioner’s lab testing and CT

scan. Id. at 90, 95-98. The CT showed an incidental finding of “[t]hyroid gland enlargement.”

Id. at 98. Based on Petitioner’s testing, Dr. Shahid ruled out lymphoproliferative or

myeloproliferative disorder. Id. at 90, 98. Due to the thyroid gland enlargement, the plan was

for Petitioner to have a thyroid ultrasound and thyroid function tests. Id. at 98. Petitioner did not

have any musculoskeletal complaints, and her musculoskeletal examination was within normal

limits. Id. at 92-93. A January 18, 2018 thyroid ultrasound showed a multinodular goiter in the

right lobe. Id. at 193-94.

To address her thyroid scan results, Petitioner saw endocrinologist Christina Bratcher,

M.D., on January 24, 2018. Pet. Ex. 5 at 65-69. Review of systems was positive for appetite

change, fatigue, fever, night sweats, weight loss, chills, diplopia without blurred vision, vertigo,

sore throat, cough, dysphagia, constipation, joint pain, headache, heat and cold intolerance, and

9

bruising. Id. at 67. On examination, Dr. Bratcher observed an enlarged thyroid. Id. at 68.

Musculoskeletal examination was not documented. See id. at 67-68. Dr. Bratcher noted the

thyroid ultrasound showed multinodular goiter of the right thyroid lobe. Id. at 66. Diagnoses

included thyroid nodule and nontoxic multinodular goiter. Id. at 69. Thyroid biopsy was

performed. Id.

Dr. Shahid saw Petitioner on January 25, 2018. Pet. Ex. 5 at 45-51. Review of

symptoms did not document complaints of joint pain, joint swelling, or decreased range of

motion. See id. at 47. Physical examination revealed no abnormalities of the musculoskeletal

system (no tenderness or swelling). Id. at 49. Dr. Shahid directed Petitioner to follow up with

him as needed and to continue seeing her endocrinologist, Dr. Bratcher. Id. at 50.

On January 29, 2018, Petitioner saw Dr. Riley. Pet. Ex. 5 at 52-55. During this visit, her

medication dosages were adjusted. Id. at 54. Dr. Riley diagnosed Petitioner with major

depressive disorder in full remission, generalized anxiety disorder, and ADHD. Id.

Also on January 29, 2018, Petitioner had an ultrasound-guided thyroid biopsy, which

revealed a benign nodule. Pet. Ex. 5 at 202.

On February 2, 2018, Petitioner saw Dr. Ragland. Pet. Ex. 7 at 243-46. Petitioner

reported that she had the flu one month earlier, had gotten better, and then she became sick again

the previous Wednesday night (January 31, 2018). Id. at 243. Petitioner had “fever, aches,

cough, [and] congestion” and “hurt[] all over.” Id. She was “more short[] of breath this time.

The max temp was 102. She fe[lt] worse than when she recently had [the] flu.” Id. Petitioner’s

rapid flu test and rapid strep test were both negative. Id. at 246. Review of systems was positive

for fever, sore throat, cough, and muscle problems. Id. at 244. She appeared ill, but had a

normal physical examination, including a normal musculoskeletal examination. Id. at 245. Dr.

Ragland opined Petitioner probably had a viral infection. Id. at 245-46. Also on February 2,

Petitioner sent an email to medical assistant, Amanda Westbrook, reporting that she had a

urinary tract infection. Id. at 256. Petitioner was asked to bring a urine sample to the office for

testing. Id. at 256-57.

In an addendum dated February 23, 2018, Dr. Haygood noted Petitioner requested Family

and Medical Leave Act (“FMLA”) paperwork to be completed because of her time off work

frequently due to illnesses. Pet. Ex. 5 at 128. Petitioner described her history of recent illnesses

and work up for health conditions, including her illness with pertussis the previous year and her

recent illness with acute bronchitis. Id. Dr. Haygood noted that she had referred Petitioner to

gastroenterology because of her positive hepatitis C antibody test result, but Dr. Haygood stated

that Petitioner’s ribonucleic acid (“RNA”) was normal. Id. Petitioner “also mentioned morning

stiffness/ joint aches” in her email. Id. Dr. Haygood ordered autoimmune testing, including

antinuclear antibody (“ANA”) and RA testing. Id.

On February 28, 2018, Petitioner had a urinalysis that was positive for Escherichia (“E.”)

coli. Pet. Ex. 5 at 41. Dr. Haygood referred Petitioner to rheumatology because she had a

positive rheumatoid factor. Id. at 41-42.

10

On March 6, 2018, Petitioner presented to rheumatologist Glen Graves, M.D. Pet. Ex. 4

at 31-34. Petitioner reported she was diagnosed with pertussis in May 2017, and since then, she

had “not felt well off and on.” Id. at 31. Petitioner further reported that she has gotten sick

every two weeks and has the MTHFR gene mutation. Id. She also complained of “joint pain in

bilateral hands, ankles, hip[s], and knees.” Id. “She state[d] [her] joint pain started a few years

ago and ha[d] increased.” Id. The prior week, “her hands were swollen and tingling,” and these

symptoms come and go. Id. Petitioner rated her daily joint pain as 4/10 in severity but noted

that at times it could increase to 10/10. Id. Petitioner indicated that over-the-counter ibuprofen

helped the pain “a little bit.” Id. She also had chronic fatigue that worsened in the evening. Id.

Adderall helped her fatigue, but when it wore off, she “c[ould] hardly stay awake.” Id.

Relevant family history indicated her maternal grandmother has RA and her mother has

osteoarthritis and fibromyalgia syndrome. Pet. Ex. 4 at 31. Review of systems was positive for

fever, weight loss, dry mouth, cool extremities, hair loss, back pain, bone/joint symptoms,

muscle pain, and neck stiffness. Id. at 33. Physical examination did not show active synovitis in

Petitioner’s upper or lower extremities, but she did have mild proximal interphalangeal

tenderness and fibromyalgia tender points. Id. Dr. Graves noted that a visual overview of all of

Petitioner’s extremities was normal; her shoulders, elbows, hips, ribs, pelvis, knees, ankles,

cervical spine, thoracic spine, and lumbar spine all appeared normal; and she did not have any

edema. Id. at 33-34.

Dr. Graves diagnosed Petitioner with “[p]ain in hand,” noting that although Petitioner did

not have dramatic swelling in her hands, the pattern of swelling was consistent with RA, and the

plan was to start Petitioner on prednisone. Pet. Ex. 4 at 34. Dr. Graves also diagnosed Petitioner

with “[s]tiffness of unspecified joint,” and noted that this was “certainly a clue to possible

inflammatory disease,” but that he would need check the results of Petitioner’s lab testing. Id.

Dr. Graves noted Petitioner’s positive hepatitis C antibody test but negative titer, and he added

that having hepatitis C could cause a false positive rheumatoid factor. Id.

On March 7, 2018, Petitioner saw Dr. Riley. Pet. Ex. 5 at 37-40. Dr. Riley noted that

Petitioner recently started prednisone, had an elevated rheumatoid factor, and exhibited some

signs of RA. Id. at 37. In the review of systems, Petitioner denied joint pain and muscle aches.

Id. at 38. Dr. Riley adjusted Petitioner’s Adderall dosage. Id. at 39-40.

Two weeks later, on March 23, 2018, Petitioner followed up with Dr. Haygood. Pet. Ex.

5 at 30-34. Petitioner reported that prednisone did not alleviate her joint pain or the swelling in

her hands and feet, it made her ADHD worse, and it caused anxiety and heart palpitations. Id. at

31. Petitioner had discontinued prednisone the prior week. Id. Petitioner reported that she had

developed nasal congestion and felt like her chest was “on fire.” Id. Petitioner also reported a

sore throat, increased fatigue, and nasal and postnasal drainage over the past week, but she

denied any facial or dental pain. Id. Petitioner reported having a fever of up to 101.4°F last

Wednesday and Thursday nights, which had resolved. Id. Petitioner also reported having a

cough with green sputum for the past week. Id. Petitioner’s review of systems was positive for

joint pain and swelling. Id. at 32. Dr. Haygood’s impression was an upper respiratory infection.

Id. at 34.

11

At her next visit with rheumatology, on April 3, 2018, Petitioner complained of morning

stiffness in both of her hands, with edema that lasted for three-to-four hours. Pet. Ex. 4 at 27.

Petitioner was not taking any medication for her stiffness currently, as she was unable to tolerate

prednisone due to heart palpitations. Id. Petitioner’s review of systems was now negative for

pain. Id. at 29. On examination, Petitioner did not have any active synovitis or edema. Id. Her

diagnosis remained “[p]ain in unspecified joint.” Id. Petitioner’s lab testing revealed an elevated

rheumatoid factor, and it was noted that she had a “rheumatoid pattern of pain.” Id. The plan

was to start Petitioner on sulfasalazine and for her to continue taking diclofenac. Id.

On April 5, 2018, Petitioner spoke by telephone with Dr. Haygood. Pet. Ex. 5 at 35.

Petitioner reported her right cervical lymphadenopathy had increased, but that she did not have

any pain. Id. It was further noted that Dr. Graves diagnosed Petitioner with RA, and that

Petitioner was having some improvement with the sulfasalazine. Id. Dr. Haygood advised that

she placed a consult with immunology to determine if a possible immunodeficiency was the

cause of Petitioner’s frequent infections. Id.

Petitioner returned to see her rheumatologist, Dr. Graves, on July 5, 2018. Pet. Ex. 4 at

22-26. Petitioner complained of increased pain in her neck, hands, hips, knees, feet, and ankles,

which had worsened over the previous week. Id. at 22. Petitioner also complained of swelling in

her hands and feet, for which she had been taking diclofenac, but it had not helped her pain. Id.

Petitioner’s review of systems was positive for fatigue, fever, generalized weakness, insomnia,

hair loss, bone/joint symptoms, and neck stiffness. Id. at 24. On examination, Petitioner did not

have active synovitis, fibromyalgia tender points, or edema. Id. at 25.

As of July 5, 2018, Petitioner’s diagnosis was listed as RA, and the plan was for her to

stop taking sulfasalazine and start taking methotrexate. Pet. Ex. 4 at 25. Hepatitis C was also

listed as one of Petitioner’s diagnoses, although Dr. Graves noted that her viral load was

negative. Id. Dr. Graves also noted that a positive hepatitis C antibody test could cause a false

positive rheumatoid factor, but that Petitioner’s levels were quite high with a negative cyclic

citrullinated peptide 17 antibody test. Id. Dr. Graves also diagnosed Petitioner with cervicalgia.

Id.

c. October 16, 2018 Flu Vaccination and Post-Vaccination

Medical History

On October 16, 2018, Petitioner received a flu vaccination in her left deltoid. Pet. Ex. 7

at 286.

On October 23, 2018, one week after vaccination, Petitioner presented for a follow-up

rheumatology appointment with Dr. Graves. Pet. Ex. 4 at 17-21. She complained of increased

bilateral pain in her hands, wrists, shoulders, ankles, and feet “for the past couple of weeks.” Id.

17

Cyclic citrullinated peptide is “a synthetic, citrulline-containing peptide with a cyclic structure,

used in assays for [RA]; the presence of antibodies to this peptide is highly specific for [RA].”

Cyclic Citrullinated Peptide, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=97140 (last visited Sept. 25, 2025).

12

at 17. Petitioner also complained of a productive cough, fever, chills, muscle pain,

gastrointestinal pain, and diarrhea for the past two days. Id. Examination revealed

metacarpophalangeal joint synovitis. Id. at 20. Dr. Graves’s impression was RA, and because

Petitioner was “doing poorly” on methotrexate, he changed her medication to Enbrel injections.

Id. Dr. Graves also prescribed azithromycin for Petitioner’s upper respiratory symptoms. Id.

On November 15, 2018, Petitioner saw PCP Alison Collins, D.O. Pet. Ex. 7 at 292-95.

Petitioner complained of swelling on the left side of her face. Id. at 292. Petitioner reported that

the swelling started as a small knot one week prior, and that it had been spreading since then. Id.

She further reported it hurt to swallow, that she could not open her mouth, and that the pain was

becoming severe and was starting to radiate down her neck. Id. Petitioner had started receiving

Enbrel injections three weeks earlier. Id. Petitioner had tenderness to palpation over the left

submandibular area and pain and swelling up to her left temple and under the left side of her

mandible. Id. at 295. Dr. Collins diagnosed Petitioner with sialadenitis 18 and directed her to go

to the emergency department (“ED”) for further evaluation and treatment. Id. Later that day,

Petitioner presented to the ED. Id. at 302-10. Examination showed that Petitioner had spasm of

the jaw muscle and tooth decay. Id. at 305. She was diagnosed with sialadenitis and prescribed

antibiotics. Id. at 309.

One week later, on November 21, 2018, Petitioner called her PCP reporting that she was

having a difficult time sitting because of pain due to shingles on her right buttock. Pet. Ex. 7 at

375. Dr. Collins recommended Petitioner present to urgent care to obtain a prescription for

antiviral medication. Id. Petitioner decided not to go to urgent care because she had a follow-up

appointment scheduled on November 23. Id. On November 23, Petitioner saw Dr. Collins. Id.

at 379. Petitioner complained of a rash on her right buttock that had been present for two days

with tingling pain and no itching. Id. It was noted that an ear, nose, and throat (“ENT”) doctor,

or otolaryngologist, believed that the etiology of Petitioner’s sialadenitis was Sjögren’s disease. 19

Id. Petitioner planned to follow up with ENT and rheumatology. Id. Dr. Collins’s assessment

was sialadenitis and herpes zoster without complication. Id. at 382.

Moving to 2019, Petitioner presented to the ED on January 14, 2019. Pet. Ex. 7 at 400.

Petitioner reported that she was assaulted the previous night by her ex-boyfriend. Id. Petitioner

lost consciousness for “‘seconds’ multiple times.” Id. Petitioner complained of neck pain, that it

hurt to swallow, headache, dizziness, visual changes, and nausea/vomiting. Id. On examination,

18

Sialadenitis is the “inflammation of a salivary gland.” Sialadenitis, Dorland’s Med. Dictionary

Online, https://www.dorlandsonline.com/dorland/definition?id=45680 (last visited Sept. 25,

2025).

19

Sjögren syndrome is “a symptom complex of unknown etiology, usually occurring in middle-

aged or older women, marked by the triad of keratoconjunctivitis sicca with or without lacrimal

gland enlargement, xerostomia with or without salivary gland enlargement, and the presence of a

connective tissue disease, usually [RA] but sometimes systemic lupus erythematosus,

scleroderma, or polymyositis. An abnormal immune response has been implicated.” Sjögren

Syndrome, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/

definition?id=111409 (last visited Sept. 25, 2025).

13

Petitioner had tenderness to her trachea and the paraspinal muscles around her neck, as well as

diffuse anterior wall tenderness. Id. at 401. Petitioner’s musculoskeletal examination revealed

normal ROM, no edema, and no tenderness. Id. at 402. She was diagnosed with a closed head

injury, anterior neck pain, and multiple thyroid nodules. Id. at 405.

On January 17, 2019, Petitioner saw Dr. Riley. Pet. Ex. 5 at 18-22. Petitioner stated that

she was diagnosed with RA in April 2018, and she felt like her depression and anxiety had

worsened since then. Id. at 19. Petitioner did not believe that her medications for her mental

health issues had been working for “some time.” Id. Petitioner also discussed her relationships,

noting that she had been involved in tumultuous relationships in the past. Id. Dr. Riley noted

Petitioner had “very significant mood lability,” physical and mental difficulties working, and that

she was currently working from home. Id. Dr. Riley adjusted Petitioner’s medication. Id. at 21.

On January 24, 2019, Petitioner saw rheumatology Nurse Practitioner Ranie Whatley.

Pet. Ex. 4 at 11-16. Petitioner complained of pain in all of her joints, muscle pain in her neck

and right shoulder, swelling in her hands and feet, and numbness and tingling in her hands and

toes. Id. at 11. She also reported hair loss since she started taking methotrexate. Id. Petitioner’s

diagnosis remained RA with a positive rheumatoid factor. Id. at 14. Petitioner was instructed to

continue receiving Enbrel injections because she had significant improvement while taking it.

Id. Petitioner was also diagnosed with right shoulder bursitis. Id. at 15.

On January 29, 2019, Petitioner exchanged emails with Dr. Ragland. Pet. Ex. 7 at 442.

Petitioner wrote that since November 2018, she had been unable to take her RA medications due

to repeat upper respiratory infections and other medical issues. Id. She also mentioned Dr.

Riley’s recent diagnoses and discussed the medications she was taking for those conditions. Id.

Petitioner reported that her ability to work had been negatively impacted because she had just

started retaking her RA medications the prior week and was now on new medications prescribed

by Dr. Riley. Id. Thus, Petitioner requested Dr. Ragland complete short-term disability

paperwork. Id. Dr. Ragland told Petitioner that she would complete the paperwork if she could

review records from Petitioner’s rheumatologist and psychiatrist since Dr. Ragland had not been

managing the issues for which Petitioner was trying to get short-term disability. Id.

Petitioner returned to see Dr. Riley on February 19, 2019. Pet. Ex. 5 at 14-17. Her mood

had stabilized, and she had less lability and anger. Id. at 15. She also reported sleeping better,

but did not feel refreshed, which Petitioner believed was due to her RA. Id. Work was her

largest stressor. Id. Petitioner was scheduled to start psychotherapy sessions. Id. at 17. Dr.

Riley noted that Petitioner’s ADHD was not controlled and that she would restart Adderall. Id.

Petitioner returned to see Dr. Riley on March 29, 2019. Id. at 7. Petitioner reported that she was

doing better, although she still had a lot of stressors, and she still felt that her medications wore

off before lunchtime. Id. at 8. Dr. Riley adjusted Petitioner’s medication. Id. at 10.

On October 28, 2019, Petitioner called her PCP, reporting a recent exposure to the flu.

Pet. Ex. 7 at 444-45. Petitioner’s niece tested positive for the flu, and Petitioner had cold-like

symptoms and fever that started the previous night. Id. at 445. Petitioner requested a

prescription for Tamiflu, which Dr. Ragland provided. Id.

14

At her next rheumatology appointment on June 24, 2020, Petitioner reported that she had

lost her health insurance, and because of that, had not had recent visits. Pet. Ex. 4 at 6. Her last

Enbrel injection was in October 2019. Id. Petitioner reported pain all over that was constant,

varied in severity, and worsened with increased activity. Id. Petitioner’s diagnosis remained RA

with a positive rheumatoid factor. Id. at 9. The plan was for Petitioner to restart Enbrel

injections after obtaining updated lab testing. Id.

Additional records have been filed but are not summarized, as they are not relevant to the

issues in dispute.

2. Petitioner’s Affidavit

Petitioner averred that “[w]ithin 45 minutes after receiving [her] flu shot” on December

1, 2017, she “began having trouble standing, and every joint in [her] body felt as though it [were]

on fire. [She] had difficulty moving and was unable to fully extend [her] joints.” Pet. Ex. 1 at ¶¶

2-3. And “[w]ithin several hours,” she developed a fever. Id. at ¶ 3. The following day, she was

unable to move or walk and called out of work. Id.

On December 12, 2017, Petitioner saw Dr. Haywood. Pet. Ex. 1 at ¶ 4. She “was still

struggling with pain in [her] body and a fever that had lasted several days.” Id. She also had “a

hard cough,” fatigue, and dizziness. Id. Petitioner was prescribed an antibiotic (Augmentin) and

hydrocodone cough syrup. Id. The next day, she saw Dr. Shahid complaining of night sweats

and easy bruising. Id. at ¶ 5. Testing was “negative for lymphoproliferative disorder, but

myelodysplastic disorders could not be ruled out.” Id. No complaints of joint pain were made at

these visits. See id. at ¶¶ 4-5; Pet. Ex. 5 at 115-27.

On December 18, 2017, Petitioner underwent a CT scan of her neck that revealed a

multinodular goiter. Pet. Ex. 1 at ¶ 6. The next day, she saw Dr. Kronenberg, complaining of a

cough that “had not subsided and was progressing.” Id. at ¶ 7. Joint pain was not mentioned at

this visit. See id.; Pet. Ex. 5 at 109-12.

The following month, on January 2, 2018, Petitioner returned to Dr. Kronenberg,

complaining of “mild fever, body aches, cough, and a general feeling of illness.” Pet. Ex. 1 at ¶

8. Later that month, on January 24, Petitioner reported “symptoms of diplopia, vertigo, sore

throat, tachycardia, worsening cough, dysphagia, worsening joint pain, headache, heat and cold

intolerance, worsening bruising, and anxiety.” Id. at ¶ 11. Petitioner began speaking to her

psychiatrist in January 2018 about her “heightened anxiety and depression due to [her]

symptoms.” Id. at ¶ 13.

In March 2018, Petitioner first saw rheumatologist Dr. Graves. Pet. Ex. 1 at ¶¶ 15, 17.

Petitioner complained of “bilateral joint pain in [her] hands, ankles, hips, and knees.” Id. at ¶ 17.

She also reported chronic fatigue and insomnia due to her severe pain. Id. At that visit, on

March 6, Dr. Graves stated Petitioner’s “pattern of pain was consistent with [RA] and possible

inflammatory disease.” Id. He prescribed prednisone; however, Petitioner discontinued this

medication due to side effects. Id. at ¶ 15. She returned to rheumatology on April 3, where it

was noted that she had elevated rheumatoid factor. Id. at ¶ 19.

15

Petitioner continued to see various health care professionals in 2018. Pet. Ex. 1 at ¶¶ 20-

31. On October 16, 2018, Petitioner received a flu vaccine. Id. at ¶ 26. She returned to

rheumatologist Dr. Graves on October 23, 2018, one week later, complaining of “increased joint

pain . . . over the past couple of weeks.” Id. at ¶ 27.

Petitioner maintained that she did not experience any of these symptoms prior to her

December 1, 2017 vaccination, and these symptoms continue as of the date she executed her

affidavit, December 1, 2020. Pet. Ex. 1 at ¶ 32, 8.

D. Expert Reports

1. Petitioner’s Expert, Dr. David Axelrod 20

a. Background and Qualifications

Dr. Axelrod is a clinical immunologist board certified in internal medicine, adult

rheumatology, and allergy and immunology. Pet. Ex. 37 at 1. He received his M.D. at the

University of Michigan Medical School and his M.S. in Clinical Research Design and Statistical

Analysis at the University of Michigan School of Public Health. Pet. Ex. 38 at 1. He then

completed an internal medicine residency at University of Toronto School of Medicine and

William Beaumont Hospital. Id. Dr. Axelrod completed a fellowship in clinical immunology,

which included adult rheumatology, allergy and immunology, and medical laboratory

immunology, at McGill University. Id. He also worked as a medical staff fellow in the clinical

immunology laboratory at the National Institutes of Health (“NIH”). Id. Dr. Axelrod held

academic appointments from 1982 to 2010, as well as other non-academic positions throughout

his career before retiring in January 2018. Id. at 2. Although he is currently retired from patient

care, as a clinician he was “involved with the diagnosis and treatment of individuals with drugs

reactions (including to vaccines).” Pet. Ex. 37 at 1. Dr. Axelrod has authored or co-authored

several publications. Pet. Ex. 38 at 3-4.

b. Opinion

Dr. Axelrod described RA as an “autoimmune disease that may result in destruction of

synovial joints, with resultant severe disability and premature mortality.” Pet. Ex. 37 at 9. He

explained that “[j]oint damage is rarely apparent in the early stages of disease and the

classification criteria tend to accumulate over time.” Id. Criteria for diagnosis include at least

one joint with “definite clinical synovitis (swelling)” that is “not better explained by another

disease.” Id.

20

Dr. Axelrod submitted one expert report. Pet. Ex. 37.

16

Citing the 2010 ACR/EULAR diagnostic criteria, 21 Dr. Axelrod explained that those

patients who have a score less than six out of ten do not have definite RA, but if the illness

worsens, reassessments may show that the criteria are “fulfilled cumulatively over time.” Pet.

Ex. 37 at 9-10 (citing Pet. Ex. 39 at 25 tbl.92.1). Reviewing Petitioner’s medical records, Dr.

Axelrod noted that Petitioner’s February 2018 lab studies showed a positive rheumatoid factor,

negative Immunoglobulin G (“IgG”) anti-cyclic citrullinated peptide antibody, negative ANA

screen, negative IgG antineutrophil antibody, and normal ESR. Id. at 6 (citing Pet. Ex. 5 at 228-

30, 242). When Petitioner first saw Dr. Graves on March 6, 2018, Dr. Graves noted that she did

not have active synovitis, but he documented proximal inter-phalangeal joint tenderness, and

thought her presentation was consistent with RA. Id. (citing Pet. Ex. 4 at 31-39). He also

prescribed prednisone for two weeks. Id. (citing Pet. Ex. 4 at 34).

Dr. Axelrod reviewed Petitioner’s visits to Dr. Graves on April 3, 2018 and July 5, 2018.

Pet. Ex. 37 at 7. On April 3, Dr. Graves documented Petitioner’s “increased pain in both hands,

with morning stiffness and swelling lasting [three-to-four] hours.” Id. (citing Pet. Ex. 4 at 27).

Again, he noted Petitioner had no active synovitis, but found Petitioner had a pattern of pain

consistent with RA and prescribed Sulfasalazine, “a treatment for mild to moderate [RA].” Id.

(citing Pet. Ex. 4 at 27-30). At the next appointment with Dr. Graves on July 5, 2018, he

documented “increased pain at her neck, hands, hips, knees, feet[,] and ankles, worse over the

previous week, with swelling of her hands and feet, despite Diclofenac and Sulfasalazine.” Id.

(citing Pet. Ex. 4 at 22-25). Again, he noted no active synovitis. Id. (citing Pet. Ex. 4 at 25). On

that date, “Dr. Graves diagnosed [Petitioner] with [RA].” Id. Dr. Axelrod opined that Petitioner

had joint pain in her hands, wrists, shoulders, ankles, and feet, a positive rheumatoid factor, and

symptoms lasting longer that six weeks, which satisfied the 2010 ACR/EULAR diagnostic

criteria for RA. Id. at 9-10.

He further explained that “[t]he cause of [RA] is not known.” Pet. Ex. 37 at 11. He

noted “a possible mechanism . . . is exposure to a pathogen,” although “no single pathogen or

group of pathogens ha[ve] been defined” as causal. Id. Infections thought “to cause or

contribute” to RA includes Epstein-Barr virus, Herpesvirus, Parvovirus, Retroviruses, Hepatitis

21

Dr. Axelrod included the criteria in his report:

Pet. Ex. 37 at 9 (citing Pet. Ex. 39 at 25, tbl.92.1).

17

B and C, and fungal infections, among others. Id. RA has also been associated with

parainfluenza virus, corona virus, and metapneumovirus. Id.

Regarding Petitioner’s history of infections and the question of alternative causes of her

RA, Dr. Axelrod noted that although she had a known history of Herpesvirus, Petitioner had not

had a “breakout” in the 12 years prior to the onset of morning stiffness and joint pain. 22 Pet. Ex.

37 at 11. As for other infections, Dr. Axelrod acknowledged Petitioner’s cough that was treated

with antibiotics on November 22, 2017, but he opined that if the etiology was bacterial, the

antibiotic would have “cleared the infection before she developed an immune response that

might have resulted in [RA].” Id. Further, he noted that testing for flu A and B and blood

cultures were negative. Id. at 12. Next, Dr. Axelrod addressed Petitioner’s cough documented

on November 30, 2017. Id. This time, Dr. Haygood did not prescribe an antibiotic or diagnose a

viral infection. Id. Further, Dr. Axelrod opined that in December 2017, Petitioner “did not have

evidence of Hepatitis C infection.” Id. In conclusion, Dr. Axelrod opined that there is no

evidence of an alternative cause, and that the only “new exposure” prior to the onset of RA was

the flu vaccination administered December 1, 2017. Id.

Petitioner filed an “evidentiary brief” on Dr. Axelrod’s medical literature. See Pet.

Evidentiary Brief Concerning Propositions of Medical Literature Utilized in Doctor Axelrod’s

Expert Report (“Pet. Axelrod Evidentiary Br.”), filed Aug. 12, 2024 (ECF No. 86). In it,

Petitioner stated that Dr. Axelrod cited to a textbook to “discuss the possibility for RA

development subsequent to exposure to a foreign pathogen, with the caveat that no single

pathogen or group of pathogens is definitively classified as a cause for RA.” Id. at 2 (emphasis

omitted) (citing Pet. Ex. 41). 23

Regarding all three Althen prongs, Dr. Axelrod deferred to Petitioner’s other expert, Dr.

Akbari. See Pet. Ex. 37 at 10, 12.

Dr. Axelrod did not offer opinions about whether the flu vaccine Petitioner received on

October 16, 2018 caused a significant aggravation of her RA. See Pet. Ex. 37.

In conclusion, Dr. Axelrod opined that Petitioner’s diagnosis is RA, and there is no

evidence of any other cause, other than the flu vaccination administered to her on December 1,

2017. Pet. Ex. 37 at 13.

22

Dr. Axelrod did not cite to the records or provide foundational support for the assertion that

Petitioner had not had an outbreak of Herpesvirus in the 12 years prior to onset of her RA. See

Pet. Ex. 37.

23

Andrew P. Cope, Rheumatoid Arthritis, in Clinical Immunology: Principles and Practice 705

(Robert R. Rich et al. eds., 5th ed. 2019).

18

2. Petitioner’s Expert, Dr. Omid Akbari 24

a. Background and Qualifications

Dr. Akbari is a professor of immunology and professor of medicine at the University of

Southern California, Keck School of Medicine. Pet. Ex. 33 at 2. He received a Ph.D. in cellular

and molecular immunology at the National Institute for Medical Research in London, United

Kingdom. Id. at 1. Thereafter, he completed a postdoctoral fellowship at Stanford University.

Id. Dr. Akbari’s research activities focus on the “[r]ole of [i]mmune cells in health and disease,”

including “[i]mmune tolerance and immune dysregulation” and the “[r]ole of [i]mmune cells in

viral and neurological disease.” Id. at 5-7. Dr. Akbari serves as an associate editor and reviewer

on several journals. Id. at 4-5. He has authored or co-authored numerous publications. Id. at 10-

17. None focus on RA. See id.

b. Opinion

i. Althen Prong One

Dr. Akbari purported to show “numerous ways in which the scientific evidence supports

the biological mechanism by which an immune stimulated response to the flu vaccination is able

to trigger immune cells that cause inflammatory disease such as RA.” Pet. Ex. 9 at 12. His

initial report generally discuss five topics, including the role of Th17 cells and regulatory T

lymphocytes (Tregs) in the induction of RA, inflammasome pathways triggered by adjuvants and

toxins, MTHFR mutations, and host susceptibility. 25 See id. at 3-11. In his second expert report,

Dr. Akbari also discussed molecular mimicry. See Pet. Ex. 43 at 9-11. Each of these subjects

are discussed in turn.

Dr. Akbari began with a general discussion of the role of T helper cells, or Th17 cells,

noting that these cells “secrete interleukin (IL)-17” which induces inflammation that plays a role

24

Dr. Akbari submitted two expert reports. Pet. Exs. 9, 43. Portions of Dr. Akbari’s reports

address concepts not related to the immediate question of whether the flu vaccine can cause RA

or the other Althen prongs. For example, in his second expert report, Dr. Akbari generally

discusses vaccine safety, the study of vaccine adverse reactions, the difficulty investigating rare

adverse effects of vaccines, etc. See Pet. Ex. 43 at 14-18. Due to lack of relevance, these

sections are not summarized.

25

The last subject discussed by Dr. Akbari in his first expert report relates to host susceptibility.

See Pet. Ex. 9 at 10-11. In his second expert report, he revisited this topic. See Pet. Ex. 43 at

20-21. His discussion of host susceptibility, and the papers cited, do not directly relate to the

issues here, and therefore, are not discussed.

19

in the cause of “many autoimmune diseases.” 26 Pet. Ex. 9 at 3-4. He asserted research of RA

patients has shown “increased levels of Th17 cells[] in their peripheral blood and joints.” Id. at

4. To support this proposition, he cited a paper by Zambrano-Zaragoza et al. 27 Id. (citing Pet.

Ex. 32). They stated that mice studies suggest that “Th17 cells may participate in the production

of autoantibodies that can induce arthritis.” Pet. Ex. 32 at 5. They also noted that Th17

“frequencies were found to be increased in patients compared to controls.” Id. While noting that

an increase in Th17 cells has been reported in RA patients, the authors did not discuss

vaccinations, or describe whether vaccinations generally, or the flu vaccination specifically,

played a role in causing RA in humans.

The next article cited by Dr. Akbari to support his comment that patients with RA have

increased levels of Th17 cells, Egan et al., 28 does not reference patients with RA. See Pet. Ex.

15. In its introductory paragraph, the authors stated that Th17 cells “have been shown to mediate

models of autoimmune diseases [], including . . . collagen-induced arthritis.” 29 Id. at 1. They

also stated that IL-17 has “potent proinflammatory effects that may promote the development of

inflammatory arthritis.” Id. But the article does not provide support for the proposition that

human patients with RA have increased levels of Th17 cells in their serum or joints.

26

In his second expert report, Dr. Akbari discussed pathogenetic and non-pathogenic Th17 cells,

asserting that “[p]athogenic Th17 cells are associated with inflammatory and autoimmune

diseases such as RA.” Pet. Ex. 43 at 7. He explained that the balance between the pathogenic

and non-pathogenic Th-17 cells is important for the maintenance of a healthy immune system.

Id.

27

José Francisco Zambrano-Zaragoza et al., Th17 Cells in Autoimmune and Infectious Diseases,

2014 Int’l J. Inflam. 1. This article is also cited as Petitioner’s Exhibit 74. Zambrano-Zaragoza

et al. provided the following frame of reference: CD4+ T cells initiate immune responses “by

providing help to other cells and taking on a variety of effector functions during immune

reactions.” Pet. Ex. 32 at 1. After stimulation with an antigen, “naïve CD4+ T cells activate,

expand, and differentiate into different effector subsets called T helpers.” Id. One of these

helpers is Th17, which is “characterized by the production of distinct cytokines and effector

functions. Th17 cells have been identified as one of the major pathogenic Th cell populations

underlying the development of many autoimmune diseases . . . .” Id. The IL-17 family includes

IL-17A and IL-17F, and these cytokines may be proinflammatory, but they also “perform diverse

immunoregulatory roles during infection.” Id. at 2. The focus of the discussion appears to be

infection. Vaccination was not mentioned.

28

Paul J. Egan et al., Promotion of the Local Differentiation of Murine Th17 Cells by Synovial

Macrophages During Acute Inflammatory Arthritis, 58 Arthritis & Rheum. 3720 (2008).

29

Collagen-induced arthritis is experimental form of arthritis induced in mice using complete

Freund’s adjuvant and type II collagen. David D. Brand et al., Collagen-Induced Arthritis, 2

Nat. Protocs. 1269 (2007), https://doi.org/10.1038/nprot.2007.173.

20

Egan et al. described an animal study where methylated bovine serum albumin 30 was

injected into knee joints to induce inflammatory arthritis. Pet. Ex. 15 at 1. Th17 cells were

found in the “inflamed synovium at the peak of disease.” Id. The researchers suggested that the

“differentiation of Th17 cells [was] maintained at the site of tissue inflammation by the local

cytokine milieu produced by synovial macrophages.” Id. at 2. However, they noted that “[t]he

ability of local antigen-presenting cells to induce Th17 cells may [] depend on the initial

stimulus, the cytokines produced, and the local environment.” Id. at 9. Thus, the authors

advised that the findings were limited to the methods employed in the study. See id. at 8-9. The

authors did not suggest the findings could be extrapolated to the effects of vaccination in

humans.

After asserting that Th17 and IL-17 play a role in inducing RA, Dr. Abkari then

suggested that the flu vaccine increases the levels of these T helper cells and related cytokines.

Pet. Ex. 9 at 6. Dr. Akbari explained that “flu infection or immunization with flu vaccine

increases the level of IL-17 and Th17 cells. This observation is supported by the fact that

significantly higher levels of IL-17 [were] detected in the serum, after flu infection or

administration of flu vaccine.” Id. In support, he cited two studies. Id. The first, by Bermejo-

Martin et al., 31 described the immune response following a severe pandemic flu infection, not

vaccination. See Pet. Ex. 48. Moreover, the notable findings in the study were that in flu

infections, Th17 cytokine responses were an “early distinctive hallmark[] of severe respiratory

compromise.” Id. at 8. The findings are not relevant to flu vaccination or to RA. The second

article, by Lin et al., 32 makes an introductory reference to IL-17 being associated with “tissue

destruction” in “models of autoimmune diseases such as arthritis;” however, the focus of the

paper is the protective role of IL-17 in vaccine-induced immunity against infections. Pet. Ex. 58

at 1.

Although Dr. Akbari referenced Th17 cells and their cytokine progeny (which he

identified as IL-17A, IL-17F, and IL-22), he did not offer medical literature or other foundational

evidence that flu vaccination increases these cells or that these cells play a role in triggering RA

after administration of a flu vaccination.

The second focus of Dr. Akbari’s opinions relates to regulatory T lymphocytes (Tregs).

See Pet. Ex. 9 at 7-8, 11; Pet. Ex. 43 at 11-13. Dr. Akbari explained that Tregs are “key in

preventing excessive immune responses and autoimmunity.” Pet. Ex. 9 at 7. “A balance in the

levels of Treg and T effector cells [Teffs] maintains the homeostatic and disease free state.” Id.

30

Methylated bovine serum albumin is used to induce arthritis in mouse models. See Pet. Ex.

15.

31

Jesus F. Bermejo-Martin et al., Th1 and Th17 Hypercytokinemia as Early Host Response

Signature in Severe Pandemic Influenza, 13 Crit. Care R201 (2009). This article was also filed

as Petitioner’s Exhibit 12.

32

Yinyao Lin et al., Th17 Cytokines and Vaccine-Induced Immunity, 21 Semin. Immunopathol.

79 (2010). This article was also cited as Petitioner’s Exhibit 24. Further discussion of this

article is below. See infra Section II.D.4.b.

21

at 7 fig.1. He opined that vaccines stimulate Teffs, which when induced, cause “protection or

pathology such as RA and joint inflammation.” Id. at 7-8; Pet. Ex. 43 at 12. Dr. Akbari further

opined that in those with a genetic predisposition (like Petitioner), vaccination causes

“pathogenic Teff cells . . . to differentiate further, exert robust effector function[,] and cause

severe injury.” Pet. Ex. 9 at 8; Pet. Ex. 43 at 12. He cited a paper by Herrero-Fernández et al. 33

purporting to show that Treg/Teff imbalance was associated with a “higher inflammatory status

in a cohort of elderly” vaccinees. Pet. Ex. 9 at 8; Pet. Ex. 43 at 12; Pet. Ex. 18 at 1.

The finding of the paper, however, was that “[a]ge related homeostatic dysregulation

involving the proliferation of . . . T-cell subsets, including Tregs, was related to a limited

responsiveness to the [flu] vaccination and a higher inflammatory status” in 60 subjects ages 61-

98. Pet. Ex. 18 at 1-2, 5 fig.1. There was a “higher baseline frequency of total-Tregs in non-

responders than responders,” and this higher baseline “impaired the response to vaccination.” Id.

at 5, 7. This same group also had “a tendency towards higher levels of [] inflammation-related

markers such as D-dimers, neutrophiles[,] or the NLR,” but the authors did not attribute this

finding to vaccination, (and it is not clear that these markers were only seen post-vaccination)

instead questioning whether it was related to thymic dysfunction, aging, conditions that cause

chronic systemic inflammation, or “the underlying mechanisms [related to] progression to death

in elderly people.” Id. at 7-8. The authors of the study do not suggest that lack of

responsiveness to the vaccine or the increase inflammatory markers seen in the non-responsive

group was caused by vaccination. Thus, the relevance of this paper is not clear.

The third subject discussed by Dr. Akbari related to adjuvants or toxins in vaccines and

how these initiate inflammasomes. 34 Pet. Ex. 9 at 5-6. However, there is no evidence that the

flu vaccination at issue here contained either adjuvants or toxins. See Pet. Ex. 43 at 2 n.1 (Dr.

Akbari agreeing the flu vaccine does not contain any adjuvant). Thus, Dr. Akbari’s opinions

about the effects of adjuvants or toxins, or their ability to trigger inflammasome pathways are not

discussed. In his second expert report, Dr. Akbari opined that even in the absence of adjuvants

or toxins, vaccines (viral peptides) can activate inflammasome pathways. Id. at 1-2. He cited

several articles in support of this opinion, but none support the conclusion that vaccine-induced

inflammasome activation (inflammasome dependent cytokines like IL-b and IL-1) can cause

RA. 35 See id.

33

I. Herrero-Fernández et al., Effect of Hemostatic T-Cell Proliferation in the Vaccine

Responsiveness Against Influenza in Elderly People, 16 Immun. & Ageing 1 (2019). This article

is also cited as Petitioner’s Exhibit 54.

34

Dr. Akbari explained that inflammasomes have three components: “a patterns recognition

receptor [], an adaptor protein, and an effector molecule called caspase-1.” Pet. Ex. 43 at 8. He

described the process by which inflammasomes trigger inflammation, noting their role in

neurological diseases, such as multiple sclerosis, and asserted they play a role in RA. See id. at

8-9.

35

Dr. Akbari noted one study examined the role of cytokines IL-1, IL-6, and TNF-α in the

induction of experimentally-induced demyelination; however, RA was not discussed. Pet. Ex. 43

at 5.

22

After discussing adjuvants and toxins, Dr. Akbari opined that the MTHFR genetic

mutation had a “possible role” in the “etiology of [RA].” Pet. Ex. 9 at 8-9; see also Pet. Ex. 43 at

13, 19. Dr. Akbari cited a paper by Berkun et al. as reporting a “two-fold increase in [the]

prevalence of RA in patients with MTHFR polymorphism.” Pet. Ex. 9 at 8 (citing Pet. Ex. 11).

This data point, however, does not appear to be referenced in the article. Even if the article did

offer the statistic cited by Dr. Akbari, the study is not relevant as to whether the flu vaccination

can cause RA.

In his discussion of the MTHFR genetic mutation and risk of disease following various

vaccinations, Dr. Akbari referenced a study by Reif et al. 36 Pet. Ex. 9 at 9 (citing Pet. Ex. 35).

In that study, a single nucleotide polymorphism of MTHFR (rs1801133) was associated with

adverse events after smallpox vaccination. Pet. Ex. 35 at 3. The adverse events included “fever,

rash, or reginal lymphadenopathy.” Id. at 1. There was no mention in the article of RA, or RA

as an adverse reaction to the smallpox vaccination.

Relative to the MTHFR mutation, Dr. Akbari explained that “the decreased number of

[Tregs] [is] most likely [] a main factor resulting in a person’s predisposition to develop

autoimmunity.” Pet. Ex. 9 at 11. He asserted that this “genetic variability may influence disease

progression or delay [] onset as strong Tregs are able to inhibit dysregulated immune responses

and control local pathogenic cells.” Id. He pointed out that “[t]hese observations [] explain why

some autoimmune diseases are acute whereas others [have] [] [a] more delayed onset.” Id.

These observations, however, do not appear to be relevant to explain how the flu vaccine can

cause RA. And Dr. Akbari does not explain the relevance to this case. 37 He cited an article by

Ohkura and Sakaguchi, 38 which described how genetic variations affecting Treg cell

development and function (called “Tregopathies”) can cause autoimmune diseases, including

36

David M. Reif et al., Genetic Basis for Adverse Events After Smallpox Vaccination, 198 J.

Infect. Dis. 16 (2008) (also filed as Petitioner’s Exhibit 27). In his expert report, Dr. Akbari

cited to an article by Rubini et al. about MTHFR polymorphism in Italian patients associated

with RA; however, this article was not filed. See Pet. Ex. 9 at 8; Pet. Ex. 27. Dr. Akbari also

discussed two other papers, but neither appear to be relevant and are therefore not discussed. See

Pet. Ex. 9 at 9 (citing Pet. Ex. 31 (Tomoyuki Yamaguchi et al., Control of Immune Responses by

Antigen-Specific Regulatory T Cells Expressing the Folate Receptor, 27 Immunity 145 (2007)

(also filed as Petitioner’s Exhibit 71)); Pet. Ex. 22 (Makoto Kinoshita et al., Dietary Folic Acid

Promotes Survival of Foxp3+ Regulatory T Cells in the Colon, 189 J. Immunol. 2869 (2012)

(also filed as Petitioner’s Exhibit 57))).

37

In this section of his expert report, Dr. Akbari cited two articles, one by Glatigny et al., which

does not appear to be relevant and is therefore not discussed. See Pet. Ex. 17 (Simon Glatigny et

al., Integrin Alpha L Controls the Homing of Regulatory T Cells During CNS Autoimmunity in

the Absence of Integrin Alpha 4, 5 Sci. Reps. 1 (2015)).

38

Naganari Ohkura & Shimon Sakaguchi, Transcriptional and Epigenetic Basis of Treg Cell

Development and Function: Its Genetic Anomalies or Variations in Autoimmune Diseases, 30

Cell Rsch. 465 (2020).

23

diabetes and RA. Pet. Ex. 25 at 1, 6. The article, however, does not address vaccine causation of

RA.

In his second expert report, Dr. Akbari, in response to Respondent’s expert, Dr. Law,

discussed the concepts of “[s]hared epitopes and molecular mimicry after inflammasome

induction.” 39 Pet. Ex. 43 at 9. Dr. Akbari opined shared epitopes and homology “play a crucial

role in the induction of inflammasomes . . . thereby triggering T cells capable of causing [RA].”

Id. He referenced a paper by Kanduc et al., 40 where the authors showed that “various viruses,

including the [flu] virus, share peptides with the human proteome.” Id. (citing Pet. Ex. 56). He

surmised that “if a vaccine contains peptides that mimic human autoantigens, administering that

vaccine has the potential to induce an autoimmune disorder, such as [RA], particularly in

susceptible individuals.” Id. Even acknowledging potential homologies, Dr. Akbari agreed that

“most people do not develop autoimmune diseases.” Id. at 10. Further, he explained that

“molecular mimicry alone is insufficient to induce autoimmunity” due to immune regulatory

factors, including Tregs. Id.

Dr. Akbari cited Yoshida et al. 41 as “evidence” of homology in the context of RA. Pet.

Ex. 43 at 11 (citing Pet. Ex. 73). Yoshida et al. sampled the serum of 130 patients with RA and

found that 78.5% had autoantibodies to citrullinated type II collagen. 42 Pet. Ex. 73 at 1. The

authors concluded that “involvement of these autoantibodies in RA pathogenesis remains

unclear.” Id. Yoshida et al. did not discuss the flu vaccine or provide evidence suggesting the

flu vaccine caused RA by triggering autoantibodies to type II collagen.

He also cited a paper by Frankild et al. 43 to suggest that “amino acid similarity [] is a

predictive measure of cross-reactivity, as observed in [flu]-induced autoimmune diseases like

[RA] resulting from molecular mimicry.” Pet. Ex. 43 at 10 (citing Pet. Ex. 52). However, Dr.

39

Dr. Akbari also cited a paper by Rojas et al. related to “autoimmune tautology” and molecular

mimicry. Pet. Ex. 43 at 10. He cited the paper for the proposition that the “[flu] vaccination has

been associated with an approximately [three]-fold increase in the risk of [RA] following

immunization with the H1N1 [flu] vaccine;” however, he did not provide a citation to the article,

nor is it filed or identified in Petitioner’s list of exhibits. Id.

40

Darja Kanduc et al., Massive Peptide Sharing Between Viral and Human Proteomes, 29

Peptides 1755 (2008).

41

Mamoru Yoshida et al., Autoimmunity to Citrullinated Type II Collagen in Rheumatoid

Arthritis, 16 Mod. Rheumatol. 276 (2006).

42

The authors explained that “[RA] is associated with citrullination, which is the conversion of

arginine residues into citrulline residues. . . . Citrullinated proteins have been found in the

synovium of RA patients.” Pet. Ex. 73 at 1. Of note, Petitioner had a negative cyclic

citrullinated peptide antibody test. See Pet. Ex. 4 at 25.

43

Sune Frankild et al., Amino Acid Similarity Accounts for T Cell Cross-Reactivity and for

“Holes” in the T Cell Repertoire, 3 PLoS ONE e1831 (2008).

24

Akbari’s reliance on the article is misplaced as it does not support the conclusion that RA is

induced by flu infection or vaccination. The authors studied cytotoxic T cell cross reactivity.

See Pet. Ex. 52. RA was not discussed. See id. The authors did not study RA, did not address

whether T cell cross-reactivity was applicable to RA, or otherwise suggest that the flu infection

or the flu vaccine plays any role in causing RA.

In further support of causation, Petitioner submitted an “evidentiary brief” on Dr.

Akbari’s medical literature. Pet. Evidentiary Br. Concerning Propositions of Medical Literature

Utilized in Doctor Akbari’s Expert Reports (“Pet. Akbari Evidentiary Br.”), filed Aug. 12, 2024

(ECF No. 85). In this supporting brief, Petitioner explained her supporting medical literature,

using the word “might” 16 times. See id. For example, citing to Symmons and Chakravarty, 44

Petitioner stated that “[i]n genetically susceptible individuals, the immune stimulation induced

by a vaccine might cause a disruption in immune regulation, leading to the activation of

inflammatory pathways that contribute to RA.” Id. at 16 (citing Pet. Ex. 28). Describing

MTHFR mutations, Petitioner cited the study by Bermejo-Martin et al. and stated that while the

study describes the immune response to flu infection, “it provides insights relevant to

understanding how similar responses might be triggered by vaccines.” Id. at 24 (citing Pet. Ex.

48). Next, Petitioner stated that the study by Frankild et al. is “relevant for understanding how

[flu] vaccines might trigger autoimmune reactions through molecular mimicry.” Id. at 29 (citing

Pet. Ex. 52). Lastly, by way of example, referring the paper by Tang et al., 45 Petitioner stated

that “[t]he authors investigated how the components of the flu vaccine might activate the

inflammasome.” Id. at 38 (citing Pet. Ex. 66).

ii. Althen Prongs Two and Three

Regarding Althen prong two, Dr. Akbari opined that Petitioner “developed RA[] as a

result of the flu vaccination administered on December 1, 2017.” Pet. Ex. 9 at 1. He further

opined that Petitioner’s “onset of symptoms following the flu vaccine support that the most

logical sequence of cause and effect . . . is that the flu vaccine administered on December 1, 2017

resulted in the onset of RA.” Id. at 12.

Dr. Akbari also opined that the time frame between Petitioner’s flu vaccination and onset

of her RA is consistent with the literature. Pet. Ex. 9 at 12; Pet. Ex. 43 at 23. In reaching this

conclusion, he noted that 11 days after vaccination, on December 12, 2017, Petitioner saw Dr.

Haygood, and complained of “fever, chills, cough, facial pain, and fatigue for several days.” Pet.

Ex. 43 at 23 (citing Pet. Ex. 5 at 123-27). Dr. Akbari also noted that Dr. Haygood diagnosed

cough and fever and prescribed antibiotics. Id. Approximately two months later, on February

27, 2018, Petitioner tested positive for rheumatoid factor and was referred to rheumatology. Id.

According to Dr. Akbari, most adverse reactions begin with “a type of hypersensitivity

associated with the induction of inflammasome” which “increase[] over time.” Id. He opined

44

D.P.M. Symmons & K. Chakravarty, Can Immunisation Trigger Rheumatoid Arthritis?, 52

Ann. Rheum. Dis. 843 (1993). This article was also filed as Petitioner’s Exhibit 65.

45

Weichun Tang et al., Post-Vaccination Serum Cytokines Levels Correlate with Breakthrough

Influenza Infections, 13 Sci. Reps. 1 (2023).

25

that “[t]he timing between receipt of the vaccine and development of inflammasome related

reaction and subsequent development of RA by molecular mimicry is an appropriate timeframe

for the immune-mediated mechanism described” in his reports. Id.

In support of the temporal association between vaccination and onset, Dr. Akbari cited

Basra et al., 46 a case report of a patient who “developed symptoms of RA shortly after receiving

the swine flu vaccine.” Pet. Akbari Evidentiary Br. at 1 (citing Pet. Ex. 10). “This temporal

association suggests that the vaccine might have played a role in triggering the autoimmune

response.” Id. at 2.

Dr. Akbari did not offer opinions in support of the question of whether Petitioner

experienced any significant aggravation of her RA after her flu vaccination on October 16, 2018.

See Pet. Exs. 9, 43.

3. Respondent’s Expert, Dr. Karen L. Law 47

a. Background and Qualifications

Dr. Law is board certified in rheumatology and internal medicine. Resp. Ex. C at 1;

Resp. Ex. D at 2. She received her M.S. from Brown University. Resp. Ex. D at 2. Thereafter,

she completed an internal medicine residency and a fellowship in rheumatology at Emory. Id.

She is a clinical rheumatologist and a professor of medicine in the rheumatology division at

Emory University School of Medicine, as well as the associate vice chair of education and

program director for the internal medicine residency at Emory. Id.; Resp. Ex. C at 1. Dr. Law

“ha[s] experience in evaluating a spectrum of rheumatic diseases, including [RA], and [she] ha[s]

published in the areas of [RA] and other rheumatic diseases.” Resp. Ex. C at 1. She “estimates

that [she] ha[s] treated over 500 [] patients with [RA] over the course of [her] career.” Id. Dr.

Law is also the editor and author of the 2014 textbook, Rheumatology Board Review, and she has

authored or co-authored other publications on rheumatology. Id.; Resp. Ex. D at 15-17.

b. Opinion

i. Althen Prong One

Dr. Law opined that there is “no confirmed causal relationship” between the flu vaccine

and RA. Resp. Ex. C at 9. Further, she explained that Dr. Akbari’s mechanistic theory is not

supported by published data and “presents an overly simplified version of possible causality”

based on “one potential pathway of inflammation,” without regard to multiple other “cell

signaling pathways” of the immune system. Id.

46

Gurjot Basra et al., Rheumatoid Arthritis and Swine Influenza Vaccine: A Case Report, 2012

Case Reps. Rheumatol. 1. This article was also filed as Petitioner’s Exhibit 47.

47

Dr. Law submitted two expert reports. Resp. Exs. C, F.

26

She explained that RA is a common type of “inflammatory, autoimmune arthritis,”

affecting 1% of the population. Resp. Ex. C at 5. RA occurs more commonly in women with

onset between the ages of 35 to 50. Id. The typical clinical presentation is greater than six

weeks of “inflammatory arthritis in the wrists” and joints of the fingers, in a symmetrical pattern,

progressing to morning stiffness, swelling, redness, warmth, decrease range of motion, and pain.

Id. Without treatment, the process can lead to destruction of the joints along with systemic

symptoms. Id. Diagnosis is made after a physical examination and positive laboratory studies

evidencing inflammation, including elevated rheumatoid factor, anticyclic citrullinated antibody,

and inflammatory markers. Id. Although RA is “mediated by immune complex deposition and

inflammation in the lining of the small and medium-sized joints,” the cause is not known. Id.

Dr. Law noted “many genetic and environmental factors may contribute” to the disease. Id. She

also emphasized that many of the genetic mutations relevant to RA have not been identified.

Resp. Ex. F at 3. Similarly, there are “multiple unknown molecular mechanisms that contribute

to the development of [RA].” Id.

Next, Dr. Law critiqued the causal theories advanced by Dr. Akbari. First, as for the

“shared epitope” theory 48 advanced by Dr. Akbari, Dr. Law criticized his reliance on Basra et al.

Resp. Ex. C at 5 (citing Pet. Ex. 10). As Dr. Law noted, Basra et al. specifically explained that a

“causal relationship has not been confirmed.” Id. (quoting Pet. Ex. 10 at 2). However, Dr.

Akbari cited the article for the reported “temporal association,” and thus, it does not appear that

he inappropriately characterized this particular paper. See Pet. Ex. 9 at 6.

Regarding the role of Th17 and Tregs in RA, Dr. Law explained that Dr. Akbari

“present[ed] widely accepted data” about the finding of elevated Th17 cells in synovial

macrophages in animal and human models of RA. Resp. Ex. C at 6. While Dr. Law agreed

these cells play a role in RA, she disagreed that there is any “specific pathway leading directly

from vaccination to the development of [RA]” implicating these cells. Id. She opined Dr.

Akbari’s opinions “deliberately ignore[] the varied roles these cells play in . . . autoimmunity” as

well as their other responses to “many environmental stimuli, including vaccination.” Id.

Dr. Akbari also opined that Petitioner’s MTHFR gene mutation increased her risk for RA

post-vaccination, which Dr. Law observed is unsupported by any published studies. Resp. Ex. C

at 7; see Pet. Ex. 9 at 8-12. Dr. Law explained MTHFR mutations have only noted a “possible

link” and such link is “independent of any exposure to vaccination.” Resp. Ex. C at 7. She gave

an example of Dr. Akbari improperly citing an article (Reif et al.) for the general proposition that

systemic adverse effects of vaccination in individuals with the MTHFR mutation may include

RA, where the article did not mention RA. Id. (citing Pet. Ex. 35). Instead of RA, the adverse

reactions after the smallpox vaccine in that study were identified as fever, lymphadenopathy, and

rash. Id. (citing Pet. Ex. 35 at 1).

Dr. Law further criticized Dr. Akbari’s discussion of alum adjuvants in vaccines, since

there is “no published data supporting the hypothesis that alum adjuvant stimulation of the

48

Dr. Law referred to this theory as the “shared epitope” theory, but the Basra et al. authors

referred to it as an “antigen specific” process whereby the “vaccine products share epitope

mimicry.” Pet. Ex. 10 at 2.

27

immune system” causes unfavorable outcomes after vaccination in RA patients or that it is

associated with the development of RA. 49 Resp. Ex. C at 7.

Lastly, Dr. Law observed that it does not appear that Dr. Akbari has any particular

experience related to RA and “its pathogenesis or immunologic basis, nor has he had experience

diagnosing or treating [RA] or associated rheumatic conditions.” Resp. Ex. C at 8.

In summary, Dr. Law opined that Dr. Akbari’s theory is not supported by published data.

Resp. Ex. C at 9; Resp. Ex. F at 4. “No vaccine safety events linking the [flu] vaccine and RA

have been reported or confirmed by vaccine surveillance programs to date.” Resp. Ex. F at 4.

Further, Dr. Law noted that Dr. Akbari’s theory of “inflammasome-mediated pathogenesis”

conflicts with “decades of scientific research suggesting multiple genetic and environmental

factors, rather than one specific exposure” as the cause of RA. Id. The idea that one specific

exposure could induce RA is inconsistent with “current scientific opinion” which views the case

of RA to be based on a “multifactorial model of pathogenesis.” Id.

ii. Althen Prongs Two and Three

Dr. Law opined that Dr. Akbari failed to provide any “logical sequence of cause and

effect for the development of [RA] following [flu] vaccination [] supported by established data.”

Resp. Ex. C at 8. That is, he failed to identify any “specific biological mechanism connecting

[the] [flu] vaccination to [RA].” Id.

Further, while the cause of RA is not known, Dr. Law agreed that Petitioner’s MTHFR

gene mutation does “increase [her] likelihood of developing [RA], independent of vaccination

status.” Resp. Ex. C at 9. Dr. Law did not opine that the increased risk posed by the MTHFR

mutation, more likely than not, caused Petitioner’s RA. See id. Instead, she explained that

“many genetic and environmental factors may contribute” to the cause of RA. Id.

Regarding a temporal association, Dr. Law explained that the onset of Petitioner’s joint

symptoms is not clear. Resp. Ex. C at 6 n.1. Although Petitioner reported joint pain on January

24, 2018, she also reported that her joint pain began “a few years ago” during her first visit to her

rheumatologist on March 6, 2018. Id. (quoting Pet. Ex. 4 at 31) (citing Pet. Ex. 5 at 65-69). In

her affidavit, she averred that her joints felt like they were “on fire” within 45 minutes of

vaccination. Id. (quoting Pet. Ex. 1 at ¶ 3). And in the weeks following vaccination, Petitioner

described “fever, myalgia, and fatigue, but she did not specifically report joint pain, swelling,

[or] morning stiffness,” symptoms characteristic of RA. Id. at 8. Dr. Law noted the first

documented complaint of joint pain was on January 24, 2018, “more than [seven] weeks after

vaccination.” Id.

Dr. Akbari referenced only one published report of RA following the flu vaccination,

from Basra et al., where onset occurred one week after vaccination. Resp. Ex. C at 5-6, 8 (citing

Pet. Ex. 10). Here, the records first note joint pain on January 24, 2018, seven weeks after

vaccination. Id. at 6, 8. Dr. Law opined that seven weeks “is far beyond a medically appropriate

49

There is no foundational evidence that the flu vaccine at issue in this matter contained alum.

28

timeframe to infer causation.” Id. at 8. Although Dr. Akbari opined that Petitioner’s symptoms

occurred within “an appropriate timeframe,” Dr. Law observed that he failed to provide

supportive evidence to support an onset of seven weeks, especially given his theory based on an

“inflammasome-related reaction.” Resp. Ex. F at 2-3.

4. Respondent’s Expert, Dr. John T. Bates 50

a. Background and Qualifications

Dr. Bates is a “broadly trained immunologist” working as an assistant professor in the

Department of Cell and Molecular Biology and in the Department of Medicine at the University

of Mississippi Medical Center. Resp. Ex. A at 1; Resp. Ex. B at 2. He received his Ph.D. in

microbiology from the University of Alabama. Resp. Ex. B at 1. Thereafter, he completed two

post-doctoral fellowships, the first at Wake Forrest University School of Medicine, where he

studied “the innate immune response to vaccine adjuvants, namely flagellin,” and the second at

Vanderbilt University School of Medicine, “where [he] worked on a number of B-cell and

antibody-related projects ranging from design of vaccine immunogens to testing anti-viral

vaccines in non-human primate models.” Resp. Ex. A at 1; see also Resp. Ex. B at 1. Dr. Bates

is a member of professional organizations, including the American Association of Immunologists

and International Society for Vaccines, he has reviewed various manuscripts for journals, he has

served as an ad hoc member of four different NIH study sections related to vaccines and

immunology, and he has authored or co-authored numerous publications. Resp. Ex. A at 1;

Resp. Ex. B at 2-8.

b. Opinion

Dr. Bates opined that the essence of Dr. Akbari’s theory is that the flu immunization

administered to Petitioner on December 1, 2017, “triggered an imbalance in [Petitioner’s]

immune system which compromised the function of immunoregulatory cells of her immune

system.” Resp. Ex. A at 5. He further opined “Dr. Akbari speculate[d] that such immunological

imbalances are the product of inflammasome activation and a subsequent Th17-skewed CD4+ T

cell response, confounded by a shortage of regulatory CD4+ T cells.” Id. Although Dr. Bates

agreed that Th17 CD4+ T cells are involved in inflammatory and autoimmune conditions, he

noted that many details of Petitioner’s RA do not support Dr. Akbari’s causal injury. Id.

First, Dr. Bates disagreed that induction of inflammasome pathways by adjuvants or

components of viruses (in the vaccine) result in the production of cytokines that contribute to

the manifestation of RA. Resp. Ex. A at 5 (citing Pet. Ex. 9 at 6). Dr. Bates explained that

fever and lassitude often “accompany vigorous immune responses that have no association with

RA.” Id. Further, most people who experience these symptoms do not develop RA. Id.

Instead, the symptoms of fever and lassitude are “self-resolving and characteristic of a normal,

vigorous innate immune response.” Id.

50

Dr. Bates submitted two expert reports in this matter. Resp. Exs. A, E.

29

Next, regarding Dr. Akbari’s theory that adjuvants and toxins played a casual role, Dr.

Bates researched the vaccine given to Petitioner, and based on the lot number, determined she

received the Fluzone Quadrivalent seasonal flu vaccine, which does not contain adjuvants or

toxins. Resp. Ex. A at 5-6. In response, Dr. Akbari opined that even if the flu vaccine did not

contain an adjuvant, it could still stimulate inflammasomes. Resp. Ex. E at 1 (citing Pet. Ex. 43

at 1-4). In support of this opinion, Dr. Akbari cited Crooke et al. 51 Id. (citing Pet. Ex. 43 at 1-4;

Pet. Ex. 51).

Dr. Bates distinguished Crooke et al., explaining that the “paper does not directly

address [Dr. Akbari’s] point.” Resp. Ex. E at 1 (citing Pet. Ex. 51). Dr. Bates stated that in

Crooke et al., the authors “measured the production of inflammasome-dependent cytokines in

cultured human cells, which is not the same as measuring in vivo activation of the

inflammasome following vaccination.” Id. (citing Pet. Ex. 51). Further, Dr. Bates noted that

the Crooke et al. paper was “confusing” because the authors discussed cell response after

vaccination and cell response in vitro at the same time. Id. (citing Pet. Ex. 51). Another point

made by Dr. Bates was that Crooke et al. found that post-vaccination cytokine levels were

similar to baseline levels, and thus, they did not seem to have any immediate effect on

inflammasome activity. Id. (citing Pet. Ex. 51 at 4). Due to this lack of response, an

experimental adjuvant, Resiquimod (R848) 52 was used. Id. Based on these reasons, Dr. Bates

concluded that flu vaccines without an adjuvant does not stimulate inflammasome-dependent

cytokines. Id. at 2.

Dr. Bates also discussed Chatziandreou et al., 53 another article cited by Dr. Akbari to

support his opinion that the flu vaccination activated the inflammasome pathway. Resp. Ex. E

at 3-4 (citing Pet. Ex. 43 at 3-4; Pet. Ex. 49). Dr. Bates explained that while cytokine IL-1α

levels were elevated, this cytokine is not considered to be dependent on inflammasome. Id. at 3.

The authors stated they were studying “an ‘inflammasome-independent’ event,” which Dr.

Bates noted was a “signaling pathway that does not involve the inflammasome.” Id. at 3-4

(quoting Pet. Ex. 49 at 2). For these reasons, Dr. Bates concluded that Dr. Akbari’s opinion that

the “flu vaccine [] activates the inflammasome” is not supported by the literature in this case.

Id. at 4.

51

Stephen N. Crooke et al., Inflammasome Activity in Response to Influenza Vaccination Is

Maintained in Monocyte-Derived Peripheral Blood Macrophages in Older Adults, 2 Front.

Aging 1 (2021).

52

Resiquimod has “potential immune response modifying activity;” “[d]ue to its

immunostimulatory activity, this agent may potentially be useful as a vaccine adjuvant.”

Resiquimod, PubChem, Nat’l Ctr. for Biotech. Info., Nat’l Libr. Med.,

https://pubchem.ncbi.nlm.nih.gov/compound/Resiquimod (last visited Oct. 6, 2025).

53

Nikolaos Chatziandreou et al., Macrophage Death Following Influenza Vaccination Initiates

the Inflammatory Response that Promotes Dendritic Cell Function in the Draining Lymph Node,

18 Cell Reps. 2427 (2017).

30

Next, Dr. Bates examined Dr. Akbari’s assertion that patients with RA have “increased

levels of Th17 cells[] in their peripheral blood and joints,” and “[t]his increase in Th17 cells “is

believed to be involved in the pathogenesis of RA.” Pet. Ex. 9 at 4. In response, Dr. Bates

explained that Dr. Akbari failed to show that the flu vaccination is associated with “detrimental

levels of IL-17.” Resp. Ex. A at 6. He noted Bermejo-Martin et al., an article cited by Dr.

Akbari to support his opinion, reported IL-17 levels following the 2009 pandemic flu virus

infection, not vaccination. 54 Id. (citing Pet. Ex. 48). Dr. Bates explained that an immune

response to active infection is “significantly different” than the response following vaccination

with an inactivated flu virus. Id. Dr. Bates noted that Dr. Akbari’s theory, when “considered in

light of . . . the Bermejo-Martin paper, may be applicable to [Petitioner’s] [flu] infection in

January 2018. However, it is not applicable to [Petitioner’s] vaccination against [flu] in

December 2017.” Id.

Moreover, Dr. Bates opined that Dr. Akbari’s reliance on Lin et al. is also problematic.

Resp. Ex. A at 6 (citing Pet. Ex. 58). Lin et al. described the role of Th17 cells in producing

cytokine IL-17 after flu vaccination. 55 Pet. Ex. 58 at 1. The authors acknowledged that IL-17

plays a role “in tissue destruction associated with models of autoimmune diseases such as

arthritis, multiple sclerosis, and colitis.” Id. However, the focus of the paper was on how Th17

cells, and their progeny, including IL-17, work to create vaccine-induced immunity against

infectious diseases. Id. Lin et al. reviewed relevant studies and stated that “[c]ollectively, []

these reports [] demonstrate that IL-17 has a critical role in vaccine-induced immunity against

bacterial infections . . . . Therefore, targeting IL-17 is an area of active research and likely to

impact future vaccine design against bacterial infections.” Id. at 4. In addition to bacteria, the

authors examined the potential for Th17 vaccine-induced immunity against fungus, viruses, and

parasites as well as how to use Th17 cytokines in conjunction with adjuvants. Id. at 4-7. The

authors do not discuss the flu vaccine at issue here, nor whether it can induce production of

Th17 cells that cause or contribute to the induction of RA.

Further, Dr. Bates noted that the vaccine described in Lin et al. is an “experimental

DNA-based vaccine,” 56 which he opined is “fundamentally different” from the seasonal flu

vaccine because the nature of the immune responses is different in DNA vaccines. Resp. Ex. A

at 6 (citing Pet. Ex. 58). Dr. Bates explained that the seasonal flu vaccine uses inactivated viral

54

As noted by Dr. Bates, this paper examined Th1 and Th17 cytokines following infection with

the pandemic flu virus. See Pet. Ex. 48. The study did not examine cytokines following

vaccination or after the seasonal flu vaccination. See id.

55

In Lin et al., the authors suggested IL-17 plays a critical role in “protective vaccine-induced

immunity against infectious diseases” and may be “a good predictor of vaccination success.”

Pet. Ex. 58 at 1-2.

56

Lin et al. described “DNA booster vaccines expressing M. tuberculosis Ag85A in the adjuvant

vaxfectin induced higher levels of IL-17 . . . when compared to unvaccinated . . . groups.” Pet.

Ex. 58 at 6-8. This vaccine was a DNA vaccine that contained an adjuvant. See id. at 4 tbl.1.

The undersigned agrees with Dr. Bates that Dr. Akbari’s reliance on this information is

misplaced.

31

antigens to induce an immune response, whereas DNA vaccines stimulate production of

“antigens by cells of the immunized individual.” Id. Due to the differences between the

vaccines, Dr. Bates asserted Dr. Akbari’s comments about the vaccine in Lin et al. cannot be

extrapolated to this case. Id.

Dr. Bates next noted another paper cited by Dr. Akbari, from Symmons and

Chakravarty, suffered from a similar lack of relevance problem. Resp. Ex. A at 6 (citing Pet. Ex.

28). Symmons and Chakravarty (1993) conducted a literature review of post-vaccination

arthritis cases and concluded that the Rubella live virus vaccine was associated with arthritis.

Pet. Ex. 28 at 1-2. The authors suggested a prospective study was warranted to explore an

association between tetanus toxoid and RA. Id. As noted by Dr. Bates, the authors did not

reach any such conclusions about the seasonal flu vaccine at issue here. Resp. Ex. A at 6.

In contrast, Dr. Bates cited Ray et al., 57 a large study of one million Kaiser patients that

found no association between hepatitis B, tetanus, and flu vaccinations and RA. Resp. Ex. A at

7 (citing Resp. Ex. A, Tab 1). The study employed a retrospective chart review with cohort and

case-control analysis of ages 15 to 59 from 1997 to 1999. Resp. Ex. A, Tab 1 at 1. A “possible

association” between the flu vaccination and RA was seen in the ranges of 180 and 365 days of

vaccination in the cohort analysis, but in the larger case-control analysis this association was not

seen. Id.

In addition to distinguishing the medical literature cited by Dr. Akbari based on a lack of

relevance, Dr. Bates identified facts that weigh against Dr. Akbari’s theories. Resp. Ex. A at 7.

For example, Dr. Bates explained that Petitioner received numerous vaccinations prior to her

receipt of the flu vaccination on December 1, 2017, and Petitioner did not experience any

adverse effects even though she has a MTHFR mutation. Id. Citing Reif et al., Dr. Akbari

opined that Petitioner’s MTHFR mutation increased her risk of adverse reactions to vaccination.

Pet. Ex. 9 at 9 (citing Pet. Ex. 35). But the Reif et al. study involved the smallpox vaccine,

which contained a live virus, unlike the flu vaccine here. Resp. Ex. A at 7; Pet. Ex. 35. Dr.

Bates explained that a live virus vaccine may be contraindicated in those who are able to receive

inactivated viral vaccines, like the flu vaccine at issue here. Resp. Ex. A at 7. Moreover, Dr.

Bates noted that Petitioner received the smallpox vaccine in 2006, and there was no mention of

any adverse reaction to it, or any other vaccines she received, in her records. Id. (citing Pet. Ex.

5 at 59).

In addition to the risk factor associated with Petitioner’s MTHFR mutation, both Dr.

Akbari and Dr. Bates agreed that there are other contributing risk factors for RA, including

57

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).

32

infectious triggers, 58 such as infection with the flu virus. Resp. Ex. A at 7-8; Pet. Ex. 9 at 11.

Other risk factors include family history, female gender, history of smoking, and depression.

Resp. Ex. A at 8. Given her many risk factors, Dr. Bates opined it was not surprising that she

developed RA at age 35. Id. He especially noted Petitioner’s history of chronic infections,

including Fifth’s disease (documented in a February 2018 addendum) and flu infection

(documented on January 2, 2018). Id. (citing Pet. Ex. 5 at 104-07, 128).

Specific to Fifth’s disease, Dr. Bates noted that it is caused by Parvovirus B19, which is

“one of the most frequent causes of viral arthritis.” Resp. Ex. A at 8 (citing Resp. Ex. A, Tab 7

(noting “[i]nfection with parvovirus B19 causes several clinical syndrome [including []fifth

disease” and listing RA as a complication post-parvovirus B19 infection during pregnancy); 59

Resp. Ex. A, Tab 8 (“Parvovirus B19 . . . [is] among the most common causative agents of viral

arthritis.”)); 60 see also Pet. Ex. 28 at 2 (“Parvoviruses are [] capable of inducing both an acute

and a chronic arthritis. . . . Some patients with early RA have serological evidence of recent

parvovirus infection.”).

Dr. Akbari also opined that the flu virus can be a trigger for RA, which suggested to Dr.

Bates that Petitioner’s flu illness in January 2018 was “a potential cause of her RA.” Resp. Ex.

A at 8 (citing Pet. Ex. 9 at 11). However, Dr. Bates observed that Dr. Akbari did not address

Petitioner’s “intervening infection with [flu] on January 2, 2018” as “an infectious potential

trigger for RA,” despite identifying the flu virus as a trigger. Id. (citing Pet. Ex. 9 at 11).

Regarding the time frame between vaccination and onset of RA, Dr. Bates raised several

concerns. Resp. Ex. A at 7-9. At her initial visit March 6, 2018 with her rheumatologist Dr.

Graves, Petitioner reported that her joint pain began “a few years ago and ha[d] increased.” Id.

at 7 (quoting Pet. Ex. 4 at 31). She also reported that she had not felt well since her pertussis

58

Dr. Bates discussed the infections suffered by Petitioner prior to her vaccination. See Resp.

Ex. A at 2-4. Of note, Dr. Bates summarized

In February [2017], [Petitioner] suffered from a urinary tract infection ([Pet.] Ex.

5 at 208). In May [2017], [Petitioner] tested positive for antibodies against

Bordetella pertussis ([Pet.] Ex. 5 at 162). In October, [Petitioner] presented with

a “left labial abscess” ([Pet.] Ex. 7 at 196-200). On November 22, 2017,

[Petitioner] was diagnosed with “[a]cute respiratory infection-possible recurrent

pertussis, bronchitis or atypical pneumonia,” and she had an elevated white blood

cell count ([Pet.] Ex. 5 at 142 and [Pet.] Ex. 5 at 213). On November 30, 2017,

one day prior to her immunization, [Petitioner’s] review of systems included

“fever, night sweats, weight loss, chills, [and] nosebleed.” ([Pet.] Ex. 5 at 136).

Id. at 4.

59

L.D. Rogo et al., Human Parvovirus B19: A Review, 58 Acta Virologica 199 (2014).

60

Vikas Sharma & Aman Sharma, Infectious Mimics of Rheumatoid Arthritis, 36 Best Prac. &

Rsch. Clin. Rheumatol. 101736 (2022).

33

infection in May 2017. Id. (citing Pet. Ex. 4 at 31). Dr. Bates opined that if Petitioner’s

symptoms began years or months before her December 2017 flu vaccination, then her RA was

not caused by her flu vaccination. Id. He also referenced a medical record from 2013, where

Petitioner complained of “arthralgia” in her review of systems and neck joint pain that had been

“waxing and waning.” Id. at 8 (quoting Pet. Ex. 7 at 40). Dr. Bates opined that these entries in

Petitioner’s medical records, especially Dr. Graves’ March 2018 note reporting that her joint

pain began a few years earlier, did not support a temporal association between her flu

vaccination and the onset of her RA. Id. at 8-9.

In conclusion, Dr. Bates opined that Dr. Akbari failed to provide a “credible medical

theory” associating the flu vaccination with Petitioner’s RA. Resp. Ex. E at 5. Dr. Bates opined

“it is highly unlikely” that Petitioner’s flu vaccination on December 1, 2017 caused her to

develop RA. Resp. Ex. A at 8; Resp. Ex. E at 5.

III. DISCUSSION

A. Standards for Adjudication

The Vaccine Act was established to compensate vaccine-related injuries and deaths. §

10(a). “Congress designed the Vaccine Program to supplement the state law civil tort system as

a simple, fair and expeditious means for compensating vaccine-related injured persons. The

Program was established to award ‘vaccine-injured persons quickly, easily, and with certainty

and generosity.’” Rooks v. Sec’y of Health & Hum. Servs., 35 Fed. Cl. 1, 7 (1996) (quoting

H.R. Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).

Petitioner’s burden of proof is by a preponderance of the evidence. § 13(a)(1). The

preponderance standard requires a petitioner to demonstrate that it is more likely than not that the

vaccine at issue caused the injury. Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315,

1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y of Health

& Hum. Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). Petitioner need not make a specific type of

evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of pathological

markers or genetic predisposition, or general acceptance in the scientific or medical communities

to establish a logical sequence of cause and effect.” Capizzano v. Sec’y of Health & Hum.

Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006). Instead, Petitioner may satisfy her burden by

presenting circumstantial evidence and reliable medical opinions. Id. at 1325-26.

In particular, Petitioner must prove that the vaccine was “not only [the] but-for cause of

the injury but also a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321

(quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999));

see also Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). The

received vaccine, however, need not be the predominant cause of the injury. Shyface, 165 F.3d

at 1351. A petitioner who satisfies this burden is entitled to compensation unless Respondent

can prove, by a preponderance of the evidence, that the vaccinee’s injury is “due to factors

unrelated to the administration of the vaccine.” § 13(a)(1)(B). However, if a petitioner fails to

establish a prima facie case, the burden does not shift. Bradley v. Sec’y of Health & Hum.

Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

34

“Regardless of whether the burden ever shifts to the [R]espondent, the special master

may consider the evidence presented by the [R]espondent in determining whether the [P]etitioner

has established a prima facie case.” Flores v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 157,

162-63 (2014); see also Stone v. Sec’y of Health & Hum. Servs., 676 F.3d 1373, 1379 (Fed. Cir.

2012) (“[E]vidence of other possible sources of injury can be relevant not only to the ‘factors

unrelated’ defense, but also to whether a prima facie showing has been made that the vaccine

was a substantial factor in causing the injury in question.”); de Bazan v. Sec’y of Health & Hum.

Servs., 539 F.3d 1347, 1353 (Fed. Cir. 2008) (“The government, like any defendant, is permitted

to offer evidence to demonstrate the inadequacy of the [P]etitioner’s evidence on a requisite

element of the [P]etitioner’s case-in-chief.”); Pafford, 451 F.3d at 1358-59 (“[T]he presence of

multiple potential causative agents makes it difficult to attribute ‘but for’ causation to the

vaccination. . . . [T]he Special Master properly introduced the presence of the other unrelated

contemporaneous events as just as likely to have been the triggering event as the vaccinations.”).

B. Factual Issues

A petitioner must prove, by a preponderance of the evidence, the factual circumstances

surrounding his claim. § 13(a)(1)(A). To resolve factual issues, the special master must weigh

the evidence presented, which may include contemporaneous medical records and testimony.

See Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (explaining that a

special master must decide what weight to give evidence including oral testimony and

contemporaneous medical records). 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.” § 13(b)(1)(A).

Contemporaneous medical records, “in general, warrant consideration as trustworthy

evidence.” Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).

But see Kirby v. Sec’y of Health & Hum. Servs., 997 F.3d 1378, 1382 (Fed. Cir. 2021) (rejecting

the presumption that “medical records are accurate and complete as to all the patient’s physical

conditions”); Shapiro v. Sec’y of Health & Hum. Servs., 101 Fed. Cl. 532, 538 (2011) (“[T]he

absence of a reference to a condition or circumstance is much less significant than a reference

which negates the existence of the condition or circumstance.” (quoting Murphy v. Sec’y of

Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff’d per curiam, 968 F.2d 1226 (Fed. Cir.

1992))), recons. den’d after remand, 105 Fed. Cl. 353 (2012), aff’d mem., 503 F. App’x 952

(Fed. Cir. 2013).

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 & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike

any norm based upon common sense and experience, this rule should not be treated as an

absolute and must yield where the factual predicates for its application are weak or lacking.”);

Lowrie v. Sec’y of Health & Hum. Servs., No. 03-1585V, 2005 WL 6117475, at *19 (Fed. Cl.

35

Spec. Mstr. Dec. 12, 2005) (“Written 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 v. Sec’y of Health &

Hum. Servs., 569 F.3d 1367, 1379 (Fed. Cir. 2009); Bradley, 991 F.2d at 1575.

Despite the weight afforded to medical records, special masters are not rigidly bound by

those records in determining onset of a petitioner’s symptoms. Valenzuela v. Sec’y of Health &

Hum. Servs., No. 90-1002V, 1991 WL 182241, at *3 (Fed. Cl. Spec. Mstr. Aug. 30, 1991); see

also Eng v. Sec’y of Health & Hum. Servs., No. 90-1754V, 1994 WL 67704, at *3 (Fed. Cl.

Spec. Mstr. Feb. 18, 1994) (noting Section 13(b)(2) “must be construed so as to give effect also

to § 13(b)(1) which directs the special master or court to consider the medical records (reports,

diagnosis, conclusions, medical judgment, test reports, etc.), but does not require the special

master or court to be bound by them”).

C. Causation

To receive compensation through the Program, Petitioner must prove either (1) that she

suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding to a

vaccine that she received, or (2) that she suffered an injury that was actually caused by a

vaccination. See §§ 11(c)(1), 13(a)(1)(A); Capizzano, 440 F.3d at 1319-20. Petitioner must

show that the vaccine was “not only a but-for cause of the injury but also a substantial factor in

bringing about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface, 165 F.3d at 1352-53).

Because Petitioner does not allege she suffered a Table Injury, she must prove a vaccine

he received caused her injury. To do so, Petitioner must establish, by preponderant evidence:

“(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 a proximate temporal relationship between vaccination and injury.” Althen, 418 F.3d at 1278.

The causation theory must relate to the injury alleged. Petitioner must provide a sound

and reliable medical or scientific explanation that pertains specifically to this case, although the

explanation need only be “legally probable, not medically or scientifically certain.” Knudsen v.

Sec’y of Health & Hum. Servs., 35 F.3d. 543, 548-49 (Fed. Cir. 1994). Petitioner cannot

establish entitlement to compensation based solely on her assertions; rather, a vaccine claim must

be supported either by medical records or by the opinion of a medical doctor. § 13(a)(1). In

determining whether a petitioner is entitled to compensation, the special master shall consider all

material in the record, including “any . . . conclusion, [or] medical judgment . . . which is

contained in the record regarding . . . causation.” § 13(b)(1)(A). The undersigned must weigh

the submitted evidence and the testimony of the parties’ proffered experts and rule in Petitioner’s

favor when the evidence weighs in her favor. See Moberly, 592 F.3d at 1325-26 (“Finders of

fact are entitled—indeed, expected—to make determinations as to the reliability of the evidence

presented to them and, if appropriate, as to the credibility of the persons presenting that

evidence.”); Althen, 418 F.3d at 1280 (noting that “close calls” are resolved in Petitioner’s

favor).

36

Testimony that merely expresses the possibility—not the probability—is insufficient, by

itself, to substantiate a claim that such an injury occurred. See Waterman v. Sec’y of Health &

Hum. Servs., 123 Fed. Cl. 564, 573-74 (2015) (denying Petitioner’s motion for review and

noting that a possible causal link was not sufficient to meet the preponderance standard). The

Federal Circuit has made clear that the mere possibility of a link between a vaccination and a

petitioner’s injury is not sufficient to satisfy the preponderance standard. Moberly, 592 F.3d at

1322 (emphasizing that “proof of a ‘plausible’ or ‘possible’ causal link between the vaccine and

the injury” does not equate to proof of causation by a preponderance of the evidence); Boatmon

v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359-60 (Fed. Cir. 2019). While certainty is

by no means required, a possible mechanism does not rise to the level of preponderance.

Moberly, 592 F.3d at 1322; see also de Bazan, 539 F.3d at 1351.

IV. ANALYSIS

A. Onset

Petitioner received the flu vaccination on December 1, 2017. The first mention of joint

pain in her medical records was January 24, 2018, when she saw Dr. Bratcher. Review of

systems was positive for “joint pain.” Pet. Ex. 5 at 67. Although joint pain was documented,

there was no description of the location of the pain, whether it was in symmetric joints, and

swelling of the joints was not documented on physical examination (musculoskeletal

examination was not documented). The following day, January 25, Petitioner saw Dr. Shahid.

Dr. Shahid did not document joint pain in the review of systems. Physical examination did not

reveal abnormalities of the musculoskeletal system, and no joint pain or swelling was noted at

this visit. Petitioner’s musculoskeletal examination was also normal when documented by Dr.

Ragland on February 2, 2018.

An addendum, dated February 23, 2018, from Dr. Haygood, 61 referenced an email she

received from Petitioner, presumably that day. Dr. Haygood noted Petitioner had complained of

“morning stiffness/ joint aches.” Pet. Ex. 5 at 128. Dr. Haygood ordered lab work for RA that

day, and Petitioner’s lab results dated February 27, 2018 revealed a positive rheumatoid factor

test.

When Petitioner saw rheumatologist Dr. Graves on March 6, 2018, he took a very

thorough history. Petitioner reported that her joint pain began “a few years ago.” Pet. Ex. 4 at

31. At that visit, Petitioner reported bilaterial joint pain in her “hands, ankles, hip[s], and knees.”

Id. The prior week, “her hands were swollen” and she reported pain levels of 4/10 up to 10/10.

61

Dr. Axelrod interprets Dr. Haygood’s addendum to be an addition to the note referable to

Petitioner’s visit on December 12, 2017. The undersigned does not agree with Dr. Axelrod’s’

interpretation, and instead, finds that Dr. Haygood’s addendum reflects receipt of an email, on or

about February 23, 2018, from Petitioner requesting paperwork for her FMLA form.

Presumably, in that email, Petitioner complained of morning stiffness and joint aches. This

interpretation is consistent Petitioner’s affidavit which states that on February 23, 2018, she sent

an email to Dr. Haygood. Dr. Haygood responded to Petitioner’s email and ordered autoimmune

labs, which were done February 27, 2018.

37

Id. Dr. Graves observed that Petitioner did not have dramatic swelling in her hands, or active

synovitis, but that her presentation was consistent with RA.

Petitioner executed an affidavit on December 1, 2020, which was filed with her petition

on December 1, 2020. In it, Petitioner avers that “[w]ithin 45 minutes after receiving [the] flu

shot” on December 1, 2017, “every joint in [her] body felt as though it [were] on fire. [She] had

difficulty moving and was unable to fully extend [her] joints.” Pet. Ex. 1 at ¶¶ 2-3. Petitioner’s

first reference in her affidavit to bilateral joint pain was on March 6, 2018, when she stated she

complained of “bilateral joint pain in [her] hands, ankles, hips, and knees.” Id. at ¶ 17. And Dr.

Graves told her that her “pattern of pain was consistent with [RA] and possible inflammatory

disease.” Id.

In his explanation of the ACR/EULAR diagnostic criteria, Dr. Axelrod explained that

patients can initially present with symptoms that do not fulfill the diagnostic criteria, but over

time may show that the criteria are met through additional reassessments. Dr. Axelrod noted that

at Petitioner’s first visit to Dr. Graves on March 6, 2018, her February 27, 2018 lab studies

included a positive rheumatoid factor, negative cyclic citrullinated peptide antibodies, and

normal ESR. When she saw Dr. Graves on March 6, 2018, he noted that she did not have active

synovitis, but he documented proximal inter-phalangeal joint tenderness, he thought her

presentation was consistent with RA, and he prescribed prednisone for two weeks. Dr. Graves

reached a “diagnosis” of RA on July 5, 2018, when Petitioner complained of “increased pain at

her neck, hands, hips, knees, feet[,] and ankles, worse over the previous week, with swelling of

her hands and feet, despite Diclofenac and Sulfasalazine.” Pet. Ex. 4 at 22-25.

Regarding Petitioner’s affidavit testimony about having a response 45 minutes after

vaccination, feeling like “her joints were on fire,” the undesigned notes that none of the experts

opined that this response was a manifestation of the onset of her RA. Without an opinion by a

treating physician or expert that Petitioner’s response was a manifestation of RA, the

undersigned does not find it evidences the onset of RA. Further, Petitioner’s medical records do

not document this response. After her flu vaccination, Petitioner was seen by many different

health care providers over the course of the following months, and none of these providers

documented the response she described in her affidavit as occurring 45 minutes after vaccination.

Medical records generally “warrant consideration as trustworthy evidence.” Cucuras,

993 F.2d at 1528. However, greater weight is typically given to contemporaneous records.

Vergara v. Sec’y of Health & Hum. Servs., No. 08-882V, 2014 WL 2795491, at *4 (Fed. Cl.

Spec. Mstr. May 15, 2014) (“Special Masters frequently accord more weight to

contemporaneously-recorded medical symptoms than those recorded in later medical histories,

affidavits, or trial testimony.”); see also Doe/70 v. Sec’y of Health & Hum. Servs., 95 Fed. Cl.

598, 608 (2010). The weight afforded to contemporaneous records is due to the fact that they

“contain information supplied to or by health professionals to facilitate diagnosis and treatment

of medical conditions. With proper treatment hanging in the balance, accuracy has an extra

premium.” Cucuras, 993 F.2d at 1528. Here, the contemporaneous records are silent regarding

any signs or symptoms described by Petitioner in her affidavit.

38

Therefore, the undersigned does not find Petitioner’s affidavit testimony regarding her

recitation of the events on the day of vaccination to be persuasive evidence. See Vergara, 2014

WL 2795491, at *4 (“[T]estimony which is in conflict with contemporaneous documents is

entitled to little evidentiary weight.” (quoting Murphy, 23 Cl. Ct. at 733)); see also Doe/70, 95

Fed. Cl. at 608 (“Given 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.”).

Taking the whole of Petitioner’s clinical course into account, the undersigned finds that

she had joint pain for “a few years” before she saw Dr. Graves on March 6, 2018. A reasonable

interpretation of the phrase “a few years” is more than one year, but maybe two or three years.

The records again noted joint pain on January 24, 2018. However, joint pain on review of

systems, without more, is not preponderant evidence of RA. More specific to RA, and based on

the opinions of Dr. Axelrod, as well as the medical records of Dr. Haygood and Dr. Graves, the

undersigned finds that Petitioner complained of morning stiffness and joint pain in an email to

Dr. Haygood on February 23, 2018. She had a positive rheumatoid factor serology on February

27, 2018. On March 6, 2018, she reported involvement of her hands, hips, knees, feet, and

ankles. As explained by Dr. Axelrod, and documented by Dr. Graves, these symptoms are

consistent with RA. Therefore, the undersigned finds the first manifestation specific to RA

occurred on February 23, 2018, when she complained of morning stiffness and joint pain in an

email to Dr. Haygood, which caused Dr. Haygood to order lab work up for autoimmune

conditions, including RA.

B. Causation

1. Althen Prong One

Under Althen Prong One, Petitioner must set forth a medical theory explaining how the

received vaccine could have caused the sustained injury. Andreu, 569 F.3d at 1375; Pafford, 451

F.3d at 1355-56. Petitioner’s theory of causation need not be medically or scientifically certain,

but it must be informed by a “sound and reliable” medical or scientific explanation. Boatmon,

941 F.3d at 1359; see also Knudsen, 35 F.3d at 548; Veryzer v. Sec’y of Health & Hum. Servs.,

98 Fed. Cl. 214, 223 (2011) (noting that special masters are bound by both § 13(b)(1) and

Vaccine Rule 8(b)(1) to consider only evidence that is both “relevant” and “reliable”). If

Petitioner relies upon a medical opinion to support his theory, the basis for the opinion and the

reliability of that basis must be considered in the determination of how much weight to afford the

offered opinion. See Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed.

Cir. 2010) (“The special master’s decision often times is based on the credibility of the experts

and the relative persuasiveness of their competing theories.”); Perreira v. Sec’y of Health &

Hum. Servs., 33 F.3d 1375, 1377 n.6 (Fed. Cir. 1994) (stating that an “expert opinion is no better

than the soundness of the reasons supporting it” (citing Fehrs v. United States, 620 F.2d 255, 265

(Ct. Cl. 1980))).

The undersigned finds Petitioner failed to provide preponderant evidence of a sound and

reliable theory to explain how the flu vaccination can cause RA. There are several reasons for

this finding.

39

First, Dr. Akbari describes six immunological concepts, drawn from general immunology

principles and various clinical studies, but none of the concepts individually or when joined

together constitute a mechanism to explain how the flu vaccine can cause RA. For example, his

discussion about Th17 cells and IL-17 does not address basic questions relevant to the

pathogenesis of RA. Dr. Akbari provides an overview of Th17 cells, explaining that these cells

produce cytokines, induce inflammation, and assiss in the maintenance of immune system

homeostasis. But he does not explain from start to finish what and how the flu vaccine induces

Th17 cells upon vaccination, what happens after vaccination in the body relative to these cells,

how these cells travel to the joints, what part of the joints are affected, or how these cells induce

joint pain and destruction. He also does not explain how this process becomes chronic. In

summary, he introduces concepts pulled from the literature but does not build the framework

required to support a mechanism of causation.

In the conclusion of his first expert report, Dr. Akbari writes that he has “shown

numerous ways in which the scientific evidence supports the biological mechanism by which an

immune stimulated response to the flu vaccination is able to trigger immune cells that cause

inflammatory disease such as RA.” Pet. Ex. 9 at 12. While it may not be inappropriate to

explore six alternative ways that a vaccine could cause RA, Petitioner’s approach of identifying a

handful of theories unsupported by literature or other evidence reduces the persuasiveness of the

opinions offered. See, e.g., Baron v. Sec’y of Health & Hum. Servs., No. 14-341V, 2019 WL

2273484, at *17 (Fed. Cl. Spec. Mstr. Mar. 18, 2019) (“Although Petitioners . . . do not need to

provide the specific components of the mechanism by which the vaccine[] at issue can cause [the

alleged injury], they do need to propose something more than taking a vague ‘kitchen sink’

approach and listing eleven mechanisms that have been previously submitted in the Program for

claims of vaccine-caused injury with various degrees of success. Petitioners have listed many

possibilities but have not identified a sound and reliable explanation that can be applied to the

vaccines and injury in this case.”).

Second, Dr. Akbari offered an erroneous opinion which the undersigned finds also

undermined his credibility and persuasiveness. In his initial report, he discussed the addition of

adjuvants and toxins to the vaccine. However, the flu vaccine at issue here does not contain

adjuvants or toxins, which Dr. Akbari agreed with in this second expert report after Dr. Bates

pointed this out. See Pet. Ex. 43 at 1-2, 2 n.1 (Dr. Akbari agreeing the flu vaccine does not

contain any adjuvant). Thus, it appears Dr. Akbari was not aware of the components of the flu

vaccine when he issued his first report. An immunology expert who offers opinions about

vaccine causation is expected to have a working knowledge of vaccines in general, as well as the

vaccine at issue. This includes a general understanding of the components of the vaccine,

including whether it contains an adjuvant to induce an immune response. Dr. Akbari’s

discussion of adjuvants in his first expert report suggests that he did not know that the vaccine

did not contain an adjuvant. This lack of knowledge diminishes the persuasiveness of his

opinions.

Third, Dr. Akbari mischaracterizes the medical literature he cites which further adversely

affects his credibility and the reliability of his opinions. A number of examples are cited above,

during the summary of his expert opinions and discussion of the medical articles. See supra

40

Section II.D.2.b. Without reviewing all of the examples set forth above, several are summarized

here. He cited Egan et al. for the proposition that Th17 cells play a role in inducing RA. Egan et

al., however, discusses experimental collagen-induced arthritis in animal models and describes a

study where methylated bovine serum albumin is used in animals to induce inflammatory

arthritis. While the study does offer important information about Th17 cells in acute

inflammatory arthritis in the context of animal models, the authors do not suggest that its

findings are comparable to the effects of the flu vaccination in humans or that their study

simulates vaccination. Dr. Akbari failed to identify the distinction between the study and the

context at hand.

Another illustration is Dr. Akbari’s use of Bermejo-Martin et al. to support his opinion

that the flu vaccination increases the Th17 and IL-17 levels. Bermejo-Martin et al. described an

immune response to a severe pandemic form of flu infection, not vaccination. Further, the Th17

response was described as severe respiratory distress, not an inflammatory response of the joints

that occurs in RA. Again, in his discussion, Dr. Akbari did not describe the limitations of the

study.

Next, Dr. Akbari cited to papers related to infections, not vaccinations, suggesting that

the immune responses to both were the same. See Pet. Ex. 9 at 6 (“[F]lu infection or

immunization with flu vaccine increases the level IL-17 and Th17 cells”). Dr. Akbari did not

acknowledge or identify the limitations of the studies he cited, differentiate between infection

and vaccination, or provide foundational evidence to bridge the gap between experimentation

and preponderant proof of causation. “An expert may ‘extrapolate from existing data,’ and use

‘circumstantial evidence,’ [b]ut the reasons for the extrapolation should be transparent and

persuasive.” K.O. v. Sec’y of Health & Hum. Servs., No. 13-472V, 2016 WL 7634491, at *12

(Fed. Cl. Spec. Mstr. July 7, 2016) (internal citations omitted) (first quoting Snyder v. Sec’y of

Health & Human Servs., 88 Fed. Cl. 706, 743 (2009); and then quoting Althen, 418 F.3d at

1280).

Fourth, there is a lack of evidence that the flu vaccine can cause RA. Petitioner cites only

one case report (Basra et al.) of RA following the flu vaccination. While case reports merit some

evidentiary weight, they do not constitute strong supportive evidence of vaccine causation, and

alone cannot meet the preponderance of the evidence standard. See Campbell v. Sec’y of Health

& Hum. Servs., 97 Fed. Cl. 650, 668 (2011); Caves v. Sec’y of Health & Hum. Servs., No. 07-

443V, 2010 WL 5557542, at *14 (Fed. Cl. Spec. Mstr. Nov. 29, 2010) (finding a petitioner’s

“reference to case reports [did] not help her meet her burden of demonstrating a persuasive and

reliable theory causally connecting the [] vaccine to [the injury]”), mot. for review den’d, 100

Fed. Cl. 119 (2011), aff’d, 463 F. App’x 932 (Fed. Cir. 2012); Muchnik ex rel. Muchnik v. Sec’y

of Health & Hum. Servs., No. 90-703V, 1991 WL 217673, at *4 (Fed. Cl. Spec. Mstr. Oct. 10,

1991) (“For the petitioner to establish causation in fact by a preponderance of the evidence in

any given case requires something more than case reports . . . .”).

Additionally, Respondent filed several large studies which do not show an association

between the flu vaccine and RA. For example, in Ray et al., the authors conducted a study

involving medical chart review of approximately one million patients with RA from 1997 to

1999. The authors found a “possible association” between flu vaccination and RA with onset

41

periods between six months and one year (180 days to 365 days) in their cohort analysis, but in

their larger case-control analysis, no association was seen.

Although a petitioner need not make a specific type of evidential showing (i.e.,

epidemiologic studies) to satisfy her burden, special masters shall still consider and weigh the

evidence in the record, including the epidemiological studies filed. See § 13(b)(1) (indicating the

special master shall consider all materials in the record); Capizzano, 440 F.3d at 1325-26; Grant

v. Sec’y of Health & Hum. Servs., 956 F.2d 1144, 1149 (Fed. Cir. 1992) (finding

“epidemiological studies are probative medical evidence relevant to causation” and

“considerable weight [is] due to epidemiological studies in the absence of direct evidence of

actual causation”). And after weighing the submitted evidence, the undersigned finds the

evidence does not preponderate in Petitioner’s favor. See Moberly, 592 F.3d at 1325-26

(“Finders of fact are entitled—indeed, expected—to make determinations as to the reliability of

the evidence presented to them and, if appropriate, as to the credibility of the persons presenting

that evidence.”). The undersigned finds the totality of the evidence presented demonstrates no

association between the flu vaccine and the development of RA.

Fifth, in support of causation, Petitioner submitted an evidentiary brief regarding the

medical literature cited by Dr. Akbari. In this brief, Petitioner repeatedly used the word “might”

in relation to causation. According to Merriam-Webster dictionary, “might” is “used to say

something is possible.” Might, Merriam-Webster Dictionary, https://www.merriam-

webster.com/dictionary/might (last visited Oct. 7, 2025). Similarly, Cambridge Dictionary

indicates “might” is “used to express the possibility that something will happen or be done, or

that something is true although not very likely.” Might, Cambridge Dictionary,

https://dictionary.cambridge.org/us/dictionary/english/might (last visited Oct. 7, 2025).

Counsel’s interpretation of the medical literature is consistent with that of the undersigned. The

articles offer possible concepts which might be relevant. Possibilities, however, are insufficient.

See Waterman, 123 Fed. Cl. 564, 573-74; Moberly, 592 F.3d at 1322; de Bazan, 539 F.3d at

1351.

Lastly, the undersigned’s finding that Petitioner has failed to provide preponderant

evidence of causation is consistent with case law regarding vaccination (including but not limited

to the flu vaccine) and RA. See, e.g., Hock v. Sec’y of Health & Hum. Servs., No. 17-168V,

2020 WL 6392770, at *23-25 (Fed. Cl. Spec. Mstr. Sept. 30, 2020) (discussing numerous

reasoned Program decisions that have dismissed petitions alleging the flu vaccine can cause RA);

Aultman v. Sec’y of Health & Hum. Servs., No. 21-1802V, 2025 WL 2401983, at *22 (Fed. Cl.

Spec. Mstr. July 11, 2025) (listing reasoned decisions that have not found any covered vaccine

can cause RA); Maxwell v. Sec’y of Health & Hum. Servs., No. 17-1367V, 2025 WL 1291642,

at *29-30 (Fed. Cl. Spec. Mstr. Mar. 26, 2025) (discussing reasoned decisions that have rejected

petitioners’ theories that a vaccine can cause RA).

In Hock, for example, the Chief Special Master found the petitioner’s theory was not

“sufficiently reliable” to show that the flu vaccine can cause RA. Hock, 2020 WL 6392770, at

*1. There, petitioner’s expert proposed a three-phase theory: an initial innate response with rapid

secretion of cytokines, followed by “bystander activation,” and ending with molecular mimicry.

Id. at *5-7.

42

The special master in Moran rejected the petitioner’s theory that the flu vaccine can cause

RA via molecular mimicry, finding it was not a sound and reliable theory. Moran v. Sec’y of

Health & Hum. Servs., No. 16-538V, 2021 WL 4853544, at *22-30 (Fed. Cl. Spec. Mstr. Oct. 4,

2021).

And more recently, the special master in Maxwell found the petitioner did not provide

preponderant evidence to support his theory that the flu vaccine can cause an abnormal innate

immune response in the joints. Maxwell, 2025 WL 1291642, at *23-27.

The undersigned acknowledges there is one case where a petitioner was found entitled to

compensation in a flu vaccine/RA case; however, the undersigned finds this case is not

instructive because it applies a different standard (plausibility) and the facts and circumstances

are distinct from this present case. See Campbell v. Sec’y of Health & Hum. Servs., 97 Fed. Cl.

650 (2011).

Although decisions of other special masters are not binding, the undersigned finds these

cases instructive. See Boatmon, 941 F.3d at 1358; Hanlon v. Sec’y of Health & Hum. Servs., 40

Fed. Cl. 625, 630 (1998), aff’d, 191 F.3d 1344 (Fed. Cir. 1999).

Overall, the undersigned finds that here, Petitioner’s proffered concepts do not constitute

sound and reliable causal theories supported by medical or scientific facts, research, or any other

reliable evidence. Moreover, the concepts are not developed and are speculative and conclusory

in nature. When evaluating whether petitioners have carried their burden of proof, special

masters consistently reject “conclusory expert statements that are not themselves backed up with

reliable scientific support.” Kreizenbeck v. Sec’y of Health & Hum. Servs., No. 08-209V, 2018

WL 3679843, at *31 (Fed. Cl. Spec. Mstr. June 22, 2018), mot. for rev. denied, decision aff’d,

141 Fed. Cl. 138, aff’d, 945 F.3d 1362 (Fed. Cir. 2020). The undersigned will not rely on

“opinion evidence that is connected to existing data only by the ipse dixit of the expert.”

Prokopeas v. Sec’y of Health & Hum. Servs., No. 04-1717V, 2019 WL 2509626, at *19 (Fed.

Cl. Spec. Mstr. May 24, 2019) (quoting Moberly, 592 F.3d at 1315). Instead, special masters are

expected to carefully scrutinize the reliability of each expert report submitted. See id.

In summary, Petitioner has failed to offer a sound and reliable medical theory in support

of her claim. Thus, the undersigned finds Petitioner has failed to provide preponderant evidence

with respect to the first Althen prong.

2. Althen Prong Two

Under Althen Prong Two, Petitioner must prove by a preponderance of the evidence that

there is a “logical sequence of cause and effect showing that the vaccination was the reason for

the injury.” Capizzano, 440 F.3d at 1324 (quoting Althen, 418 F.3d at 1278). “Petitioner must

show that the vaccine was the ‘but for’ cause of the harm . . . or in other words, that the vaccine

was the ‘reason for the injury.’” Pafford, 451 F.3d at 1356 (internal citations omitted).

43

In evaluating whether this prong is satisfied, the opinions and views of the vaccinee’s

treating physicians are entitled to some weight. Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d

at 1326 (“[M]edical records and medical opinion testimony are favored in vaccine cases, as

treating physicians are likely to be in the best position to determine whether a ‘logical sequence

of cause and effect show[s] that the vaccination was the reason for the injury.’” (quoting Althen,

418 F.3d at 1280)). Medical records are generally viewed as trustworthy evidence, since they are

created contemporaneously with the treatment of the vaccinee. Cucuras, 993 F.2d at 1528.

Petitioner need not make a specific type of evidentiary showing, i.e., “epidemiologic studies,

rechallenge, the presence of pathological markers or genetic predisposition, or general

acceptance in the scientific or medical communities to establish a logical sequence of cause and

effect.” Capizzano, 440 F.3d at 1325. Instead, Petitioner may satisfy her burden by presenting

circumstantial evidence and reliable medical opinions. Id. at 1325-26.

Since Petitioner failed to prove Althen prong one, it follows that she cannot prove Althen

prong two. However, even if Petitioner had proven Althen prong one, the undersigned finds

Petitioner has failed to provide preponderant evidence that there is a logical sequence of cause

and effect showing Petitioner’s flu vaccine caused her RA.

First, Petitioner’s treating physicians did not offer opinions in her medical records

associating her RA with her flu vaccinations. In cases with such evidence, it can be considered

in an analysis of Althen prong two. See Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d at 1326

(“[M]edical records and medical opinion testimony are favored in vaccine cases, as treating

physicians are likely to be in the best position to determine whether a ‘logical sequence of cause

and effect show[s] that the vaccination was the reason for the injury.’” (quoting Althen, 418 F.3d

at 1280)). Here, there is no such supportive evidence.

Second, there is evidence of risk factors and alternative causes for Petitioner’s RA.

Petitioner’s most significant risk factor was her MTHFR mutation. The experts generally agreed

that this risk factor made Petitioner more susceptible to developing the disease, though they did

not opine that the risk factor alone more likely than not caused her RA. See Pet. Ex. 9 at 8-9 (Dr.

Akbari discussing the “possible role” of the MTHFR genetic mutation in the “etiology of [RA]”);

Resp. Ex. A at 7-8 (Dr. Bates listing numerous risk factors Petitioner had for developing RA,

including the MTHFR polymorphism); Resp. Ex. C at 7, 9 (Dr. Law agreeing that Petitioner’s

MTHFR gene mutation does “increase [her] likelihood of developing [RA], independent of

vaccination status,” but not opining that the increased risk was more likely than not the cause of

Petitioner’s RA).

Regarding an alternative cause, however, Dr. Bates identified parvovirus and flu

infections as potential causes of Petitioner’s RA. Both Dr. Bates and Dr. Akbari cited literature

supporting parvovirus as a common cause of arthritis; however, Dr. Akbari did not discuss

parvovirus, or its relation to Fifth’s disease. See Resp. Ex. A, Tabs 7-8; Pet. Exs. 9, 28, 43. Dr.

Akbari agreed that the flu infection can be a trigger for the illness. See Pet. Ex. 9 at 11

(“Additional infectious potential triggers include . . . [flu] virus.”). But he failed to discuss or

acknowledge Petitioner’s flu infection in January 2018. See Pet. Exs. 9, 43.

44

The undersigned acknowledges that Petitioner is not required to eliminate other potential

causes in order to be entitled to compensation. See Walther v. Sec’y of Health & Hum. Servs.,

485 F.3d 1146, 1149-52 (Fed. Cir. 2007) (finding petitioner does not bear the burden of

eliminating alternative independent potential causes). However, it is reasonable to consider

“evidence of other possible sources of injury” in determining “whether a prima facie showing

has been made that the vaccine was a substantial factor in causing the injury in question.” Stone,

676 F.3d at 1379; see also Winkler v. Sec’y of Health & Hum. Servs., 88 F.4th 958, 963 (Fed.

Cir. 2023) (“Such contemplation of a potential causative agent when evaluating whether or not a

petitioner has established a prima facie case is in accordance with the law.”); Flores, 115 Fed. Cl.

at 162-63 (“[T]he special master may consider the evidence presented by the [R]espondent in

determining whether the [P]etitioner has established a prima facie case.”). Here the record

indicates two other causes, parvovirus and flu illnesses. The undersigned finds it reasonable to

consider these potential causes of Petitioner’s condition in determining that Petitioner has failed

to provide preponderant evidence of prong two.

Accordingly, the undersigned finds that Petitioner failed to satisfy her burden under

Althen prong two.

3. Althen Prong Three

Althen prong three requires Petitioner to establish a “proximate temporal relationship”

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

defined as a “medically acceptable temporal relationship.” Id. The Petitioner must offer

“preponderant proof that the onset of symptoms occurred within a time frame for which, given

the medical understanding of the disorder’s etiology, it is medically acceptable to infer

causation-in-fact.” de Bazan, 539 F.3d at 1352. The explanation for what is a medically

acceptable time frame must also coincide with the theory of how the relevant vaccine can cause

the injury alleged (under Althen Prong One). Id.; Koehn v. Sec’y of Health & Hum. Servs., 773

F.3d 1239, 1243 (Fed. Cir. 2014); Shapiro, 101 Fed. Cl. at 542; see also Pafford, 451 F.3d at

1358. A temporal relationship between a vaccine and an injury, standing alone, does not

constitute preponderant evidence of vaccine causation. See, e.g., Veryzer, 100 Fed. Cl. at 356

(explaining that “a temporal relationship alone will not demonstrate the requisite causal link and

that [P]etitioner must posit a medical theory causally connecting the vaccine and injury”).

Petitioner, through Dr. Akbari, offered six different theories of causation, describing how

“the flu vaccine can provoke innate and adaptive immunity.” Pet. Ex. 9 at 1. But Dr. Akbari did

not provide an appropriate timeframe relative to each of his theories. As a general principle,

innate immune responses occur more quickly than adaptive immune responses. 62 However,

Petitioner did not provide such time periods here.

For example, Dr. Akbari did not opine as to an appropriate onset timeframe for his theory

about the role of inflammasome and Th17 cells in the induction of RA. But see Resp. Ex. F at 2-

3 (Dr. Law opining that Dr. Akbari failed to provide supportive evidence to support an onset of

62

See Inst. of Med., Evaluating Biological Mechanisms of Adverse Events, in Adverse Effects of

Vaccines: Evidence and Causality 57, 57-58 (Kathleen Stratton et al. eds., 2012).

45

seven weeks here, especially given his theory based on an “inflammasome-related reaction,”

when the only supportive literature was Basra et al., who documented a case report of an onset of

one week) (citing Pet. Ex. 10)). The same is true for Dr. Akbari’s other five theories. Instead,

Dr. Akbari opined that “onset of disease occurred within an appropriate time period after

vaccination to implicate the vaccination as a cause of her illness.” Pet. Ex. 9 at 1-2. He

concluded that Petitioner’s development of RA was consistent with the “cause and effect” of the

flu vaccination. Id. at 12.

To the extent that Dr. Akbari opines Petitioner’s onset was 11 days post-vaccination

because this was her first health care appointment after her December 1, 2017 flu vaccination,

the undersigned does not agree. As Dr. Akbari documents, Petitioner complained of “fever,

chills, cough, facial pain, and fatigue for several days” during this visit and was diagnosed with a

cough and fever. Pet. Ex. 43 at 23. No complaints of joint pain were made during this visit. Nor

were physical examination findings consistent with RA documented. According to Dr. Akbari,

most adverse reactions begin with “a type of hypersensitivity associated with the induction of

inflammasome” which “increase[] over time.” Id. However, neither of his reports discuss this

“hypersensitivity” reaction, or mention “hypersensitivity” again.

In summary, Petitioner offered no expert opinions as to the specific onset or range of

onset of her RA. Nor did Petitioner provide expert opinions explaining how the causal theories

offered were consistent with that time frame.

Therefore, the undersigned finds that Petitioner failed to provide preponderant evidence

of Althen prong three.

V. CONCLUSION 63

The undersigned extends her sympathy to Petitioner for the pain and suffering that she

experienced due to her illness. The undersigned’s Decision, however, cannot be decided based

upon sympathy, but rather on the evidence and law.

For the reasons discussed above, the undersigned finds that Petitioner has failed to

establish by preponderant evidence that her flu vaccine caused her RA. Therefore, Petitioner is

not entitled to compensation and the petition must be dismissed.

In the absence of a timely filed motion for review pursuant to Vaccine Rule 23, the Clerk

of Court SHALL ENTER JUDGMENT in accordance with this Decision.

IT IS SO ORDERED.

s/Nora Beth Dorsey

Nora Beth Dorsey

Special Master

63

Due to the sensitive nature of Petitioner’s medical and psychiatric history, Petitioner is

encouraged to seek redaction of her name to her initials in accordance with Vaccine Rule 18(c).

46