Hunt v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 20-1455V

Filed: May 23, 2024

Special Master Horner

JULIA HUNT,

Petitioner,

v.

SECRETARY OF HEALTH AND

HUMAN SERVICES,

Respondent.

Amy A. Senerth, Muller Brazil, LLP, Dresher, PA, for petitioner.

Meghan Murphy, U.S. Department of Justice, Washington, DC, for respondent.

DECISION1

On October 23, 2020, petitioner filed a petition under the National Childhood

Vaccine Injury Act, 42 U.S.C. § 300aa-10, et seq. (2012),2 alleging that she suffered

dermatomyositis following an influenza (“flu”) vaccination that she received on

November 14, 2017. (ECF No. 1.) Petitioner alleged her injury was caused-in-fact by

her vaccination. (Id. at 4.) For the reasons set forth below, I conclude that petitioner is

not entitled to compensation and the petition is dismissed.

I. Applicable Statutory Scheme

Under the National Vaccine Injury Compensation Program, compensation

awards are made to individuals who have suffered injuries after receiving vaccines. In

1 Because this document contains a reasoned explanation for the action taken in this case, it must be

made publicly accessible and will be posted on the United States Court of Federal Claims' website, and/or

at https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government

Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic

Government Services). This means the document will be available to anyone with access to the

internet. In accordance with Vaccine Rule 18(b), Petitioner has 14 days to identify and move to redact

medical or other information, the disclosure of which would constitute an unwarranted invasion of privacy.

If, upon review, I agree that the identified material fits within this definition, I will redact such material from

public access.

2 Within this decision, all citations to § 300aa will be the relevant sections of the Vaccine Act at 42 U.S.C.

§ 300aa-10, et seq.

1

general, to gain an award, a petitioner must make a number of factual demonstrations,

including showing that an individual received a vaccination covered by the statute;

received it in the United States; suffered a serious, long-standing injury; and has

received no previous award or settlement on account of the injury. Finally – and the key

question in most cases under the Program – the petitioner must also establish a causal

link between the vaccination and the injury. In some cases, the petitioner may simply

demonstrate the occurrence of what has been called a “Table Injury.” That is, it may be

shown that the vaccine recipient suffered an injury of the type enumerated in the

“Vaccine Injury Table,” corresponding to the vaccination in question, within an

applicable time period following the vaccination also specified in the Table. If so, the

Table Injury is presumed to have been caused by the vaccination, and the petitioner is

automatically entitled to compensation, unless it is affirmatively shown that the injury

was caused by some factor other than the vaccination. §§ 300aa-13(a)(1)(A), (B); §

300 aa-11(c)(1)(C)(i); § 300aa-14(a).

In many cases, however, the vaccine recipient may have suffered an injury not of

the type covered in the Vaccine Injury Table. In such instances, an alternative means

exists to demonstrate entitlement to a Program award. That is, the petitioner may gain

an award by showing that the recipient’s injury was “caused-in-fact” by the vaccination

in question. § 300aa-13(a)(1)(B); § 300aa-11(c)(1)(C)(ii). In such a situation the

presumptions available under the Vaccine Injury Table are inoperative. The burden is

on the petitioner to introduce evidence demonstrating that the vaccination actually

caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d

1274, 1278 (Fed. Cir. 2005); Hines ex rel. Sevier v. Sec’y of Health & Human Servs.,

940 F.2d 1518, 1524-25 (Fed. Cir. 1991). Because petitioner’s injury is not listed on the

Vaccine Injury Table, petitioner must satisfy this burden of proof.

The showing of “causation-in-fact” must satisfy the “preponderance of the

evidence” standard, the same standard ordinarily used in tort litigation. § 300aa-

13(a)(1)(A); see also Althen, 418 F.3d at 1278; Hines, 940 F.2d at 1525. Under that

standard, the petitioner must show that it is “more probable than not” that the

vaccination was the cause of the injury. Althen, 418 F.3d at 1279. The petitioner need

not show that the vaccination was the sole cause of the injury or condition but must

demonstrate that the vaccination was at least a “substantial factor” in causing the

condition and was a “but for” cause. Shyface v. Sec’y of Health & Human Servs., 165

F.3d 1344, 1352 (Fed. Cir. 1999). Thus, the petitioner must supply “proof of a logical

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

injury;” the logical sequence must be supported by “reputable medical or scientific

explanation, i.e., evidence in the form of scientific studies or expert medical testimony.”

Althen, 418 F.3d at 1278; Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144,

1148 (Fed. Cir. 1992). A petitioner may not receive a Vaccine Program award based

solely on his or her assertions; rather, the petition must be supported by either medical

records or by the opinion of a competent physician. § 300aa-13(a)(1).

In what has become the predominant framing of this burden of proof, the Althen

court described the “causation-in-fact” standard, as follows:

2

Concisely stated, Althen’s burden is to show by preponderant evidence that

the vaccination brought about her injury by providing: (1) a medical theory

causally connecting the vaccination and the injury; (2) a logical sequence

of cause and effect showing that the vaccination was the reason for the

injury; and (3) a showing of proximate temporal relationship between

vaccination and injury. If Althen satisfies this burden, she is entitled to

recover unless the [government] shows, also by a preponderance of the

evidence, that the injury was in fact caused by factors unrelated to the

vaccine.

Althen, 418 F.3d at 1278 (citations omitted). The Althen court noted that a petitioner

need not necessarily supply evidence from medical literature supporting petitioner’s

causation contention, so long as the petitioner supplies the medical opinion of an

expert. Id. at 1279-80. However, that expert’s opinion must be based upon “sound and

reliable” scientific explanation. Boatmon v. Sec’y of Health & Human Servs., 941 F.3d

1351, 1359 (Fed. Cir. 2019) (quoting Knudsen ex rel. Knudsen v. Sec’y of Health &

Human Servs., 35 F.3d 543, 548-49 (Fed. Cir. 1994)). The Althen court also indicated

that, in finding causation, a Program factfinder may rely upon “circumstantial evidence,”

which the court found to be consistent with the “system created by Congress, in which

close calls regarding causation are resolved in favor of injured claimants.” 418 F.3d at

1280.

II. Procedural History

Initially petitioner filed medical records and an affidavit marked as Exhibits 1-12.

(ECF Nos. 1, 16.) She filed her Statement of Completion in January of 2021. (ECF No.

17.) After completion of a Pre-Assignment Review, the case was assigned to the

undersigned in February of 2021. (ECF No. 19.) Respondent filed his Rule 4 Report

recommending against compensation in June of 2021. (ECF No. 24.) Respondent

contended that the medical records were inadequate to support petitioner’s burden of

proof under the Althen test. (Id. at 11-14.)

Subsequently, petitioner filed an expert report by rheumatologist/immunologist M.

Eric Gershwin, M.D., and accompanying literature. (ECF No. 25; Exs. 13-54.)

Respondent filed responsive reports by rheumatologist Christopher Mecoli, M.D., and

immunologist James Moy, M.D. (ECF Nos. 31-32; Exs. A-D.) Thereafter, the parties

confirmed during a status conference held June 24, 2022, that the case is ripe for

resolution on the written record. (ECF No. 34.)

Petitioner filed her motion for a ruling on the written record in December of 2022.

(ECF No. 38.) Respondent filed his response in May of 2023 and petitioner filed her

reply in July of 2023. (ECF Nos. 43-45.)

In light of the above, I have determined that the parties have had a full and fair

opportunity to present their cases and that it is appropriate to resolve entitlement on the

3

existing record. See Vaccine Rule 8(d); Vaccine Rule 3(b)(2); see also Kreizenbeck ex

rel. C.J.K. v. Sec’y of Health & Human Servs., 945 F.3d 1362, 1366 (Fed. Cir. 2020)

(noting that “special masters must determine that the record is comprehensive and fully

developed before ruling on the record”). Accordingly, this matter is now ripe for

resolution.

III. Factual History

The details of petitioner’s medical history are not disputed. Accordingly, only an

abbreviated history is provided. However, I have reviewed the medical records in full.

Petitioner received the flu vaccination at issue during a routine exam on

November 14, 2017. (Ex. 1, p. 2.) At that time she had no prior history of

dermatomyositis, though she did have a history of thyroid nodules, vitamin D deficiency,

prediabetes, and elevated cholesterol. (Ex. 4, pp. 74-75, 86-87.) Six days post-

vaccination she presented to her endocrinologist for her thyroid nodules and reported

no symptoms of joint or muscle pain or weakness. (Ex. 5, pp. 476-79.)

On December 5, 2017, she presented for care with joint and muscle pain, which

she indicated had begun the day she received the flu vaccine. (Ex. 4, p. 59.) Petitioner

did not have fever or chills at the time of this medical encounter. (Id.) She was

diagnosed with muscle pain and prescribed naprosyn. (Id. at 60.)

On December 15, 2017, she presented to the emergency department with

complaints of shortness of breath and swelling of her face and upper extremities, as

well as malaise and dizziness. (Ex. 3, p. 12.) She indicated her symptoms had been

present for three weeks. (Id.) She also stated that she “started having joint aches,

fevers, chills, night sweats, facial swelling around her eyes, hand swelling and arm

weakness, leg swelling and thigh weakness [two] days after [receiving her flu

vaccination]. She said she thought it was a reaction to the flu shot, so when it didn’t go

away after [two] weeks, she went to go see her doctor. Her doctor prescribed her

naproxen for a week, which did improve her symptoms except for thigh weakness.” (Id.

at 83.) Petitioner was admitted with a differential diagnosis of lupus flare versus

polymyositis versus dermatomyositis and rheumatologist was consulted. (Id. at 14.)

Petitioner had elevated CK, AST, and ALT, which was concerning for

inflammatory myositis. (Ex. 3, p. 16.) She was also positive for ANA and Anti-Jo-1

antibodies. (Id.) An MRI of petitioner’s bilateral thighs showed diffuse myositis and a

biopsy showed “[e]xtensive myofiber necrosis and regeneration, focal limited

inflammation and a positive HLA Class 1 immunohistochemistry study, most consistent

with an immune-mediated (inflammatory) myopathy.” (Ex. 2, p. 30.) During

hospitalization, IV fluids improved her symptoms and her CK trended downward. (Ex. 3,

p.16.) At discharge she was instructed to continue on prednisone at 60 mg and to

follow up with rheumatology. (Id.)

4

Petitioner then saw rheumatologist David Ozeri, M.D., on January 8, 2019. (Ex.

5, pp. 49-53.)3 It was noted that petitioner had self-tapered her prednisone to 40 mg.

(Ex. 5, p. 51.) Petitioner reported a history of symptoms arising post-vaccination and it

was noted that “[s]he is suspicious that the flu vaccine triggered her polymyositis.” (Id.)

Petitioner was doing well with “no significant proximal muscle weakness” and Dr. Ozeri

agreed to further taper prednisone to 30mg in light of petitioner’s anxiety regarding

insomnia from the prednisone. (Id. at 52-53.) Dr. Ozeri’s impression was biopsy-

proven myositis consistent with polymyositis. (Id. at 52.) He instructed petitioner to

follow up with her primary care provider to rule out age-appropriate malignancies given

high incidences of paraneoplastic immune mediated myopathy. (Id. at 52-53.)

Petitioner continued to follow up with Dr. Ozeri. (Ex. 5, pp. 83-88, 133-38, Ex.

12, pp. 4-8.) As of March 12, 2018, petitioner’s lab work showed resolution of her

myositis. (Ex. 5, p. 105.) Dr. Ozeri concluded that petitioner had been suffering Jo1

idiopathic inflammatory myopathy (“IIM”) and remarked that it “may have been triggered

by a flu vaccine suggesting possible autoimmune/autoinflammatory disease induced by

adjuvants.” (Id.) By June 4, 2018, petitioner had been tapered down to 4 mg of

prednisone and was still doing well. (Ex. 12, p. 4.) Dr. Ozeri concluded she had

“recovered fully.” (Id. at 7.) He noted that “[m]y overall impression is that she has

autoimmune syndrome induced by adjuvants . . . [and] she has been counseled to avoid

flu vaccine in future.” (Id.) His ultimate diagnoses were dermatomyositis and reaction

to influenza immunization. (Id. at 7.)

Petitioner would subsequently see two different rheumatologists in management

of her condition who diagnosed CPK with polymyositis (Ex. 5, p. 353) and inflammatory

myositis (Ex. 2, p. 7). However, the initiating cause of her condition was not revisited.

IV. Expert Reports

a. Petitioner’s rheumatology/immunology expert, M. Eric Gershwin,

M.D.4

According to Dr. Gershwin, classification of inflammatory muscle diseases,

including dermatomyositis, is “crude and enigmatic.” (Ex. 13, p. 3.) “Causes leading to

inflammation in idiopathic inflammatory myopathies (IIMs) are enigmatic, but

autoimmune mechanisms are strongly involved with an inappropriate activation of the

3 She had other encounters in the interim. (Ex. 4, pp. 44-49, 50-54.)

4 Dr. Gershwin is currently a distinguished professor of medicine and the Jack and Donald Chia Professor

of Medicine in the Rheumatology/Allergy and Clinical Immunology division of the University of California

at Davis, where he previously served as chairperson of the Graduate Group in Immunology. (Ex. 14, p.

1.) Dr. Gershwin received his bachelor’s degree from Syracuse University and his master’s degree from

the Centre for Astrophysics and Supercomputing. (Id.) He received his Doctor of Medicine from Stanford

University and is currently licensed to practice medicine in California. (Id. at 1-2.) Dr. Gershwin is board

certified in Internal Medicine with a subspecialty in Rheumatology and Allergy and Clinical Immunology.

(Id. at 2.) In addition, he has published 72 books and monographs, 1039 experimental papers, 164 book

chapters, 277 reviews, 40 guest editorials and book reviews, and five letters to the editors. (Id. at 8-138.)

5

innate immune system leading to the secondary dysregulation of the adaptive immune

response that is now considered to be a central pathogenic feature of IIMs.” (Id. (citing

Thorsten Hornung & Joerg Wenzel, Innate Immune-Response Mechanisms in

Dermatomyositis: An Update on Pathogenesis, Diagnosis and Treatment, 74 DRUGS

981 (2014) (Ex. 15); Sahil Khanna & Ann M. Reed, Immunopathogenesis of Juvenile

Dermatomyositis, 41 MUSCLE NERVE 581 (2010) (Ex. 16); Kanneboyina Nagaraju &

Ingrid E. Lundberg, Polymyositis and Dermatomyositis: Pathophysiology, 37 RHEUMATIC

DISEASE CLINICS N. AM. 159 (2011) (Ex. 17)).) Dr. Gershwin indicates that

dermatomyositis is a rare disease – too rare to be detected by epidemiologic study –

that requires both a genetic predisposition and environmental factors to develop. (Id. at

2-3.)

Dermatomyositis is a disease of excessive activation of the innate immune

system with strong expression of interferon (IFN)-regulated proteins directed to muscle

and skin. (Ex. 13, p. 3 (citing J. Wenzel et al., Evidence for a Role of Type I Interferons

in the Pathogenesis of Dermatomyositis, 156 BRIT. J. DERMATOLOGY 462 (2005) (Ex. 22);

Steven A. Greenberg et al., Interferon-α/β-Mediated Innate Immune Mechanisms in

Dermatomyositis, 57 ANNALS NEUROLOGY 664 (2005) (Ex. 23)).) Skin biopsies have

shown mature CD4+ T cells producing IL-2, IFN-γ, and IL-4. (Id. (citing M. Caproni et

al., Infiltrating cells, Related Cytokines and Chemokine Receptors in Lesional Skin of

Patients with Dermatomyositis, 151 BRIT. J. DERMATOLOGY 784 (2004) (Ex. 26)).)

Intermediate-sized vessels are affected by a compliment cascade leading to

microangiopathy. (Id. (citing Marinos C. Dalakas, Pathogenesis and Therapies of

Immune-Mediated Myopathies, 11 AUTOIMMUNITY REVS. 203 (2012) (Ex. 28)).)

Antibodies directed against endothelial cells ultimately cause swelling, vacuolization,

capillary necrosis, perivascular inflammation, ischemia, and ultimately destruction of

muscle fiber. (Id. (citing Marinos C. Dalakas & Reinhard Hohlfeld, Polymyositis and

Dermatomyositis, 362 LANCET 971 (2003) (Ex. 30)).) In this process, cytokines and

chemokines released following the compliment activation recruit vascular cell adhesion

molecules and activated T cells to the site of inflammation. (Id. at 3-4 (citing Dalakas &

Hohlfeld, supra, at Ex. 30).) “Key cytokines in IIM are produced by Th1 (i.e. IFN-γ, IL-2,

IL-12, TNF-α), TH2 (i.e. IL-4 and IL-13), Th17 (IL-17, IL-22, IL-23, IL-6), and Treg (i.e.

IL-10, TGF-β) cells. IL-1 family cytokines such as Il-1 α and β are also altered in IIM

sera and tissues.” (Id. at 4 (citing E. M. Moran & F. L. Mastaglia, Cytokines in Immune-

Mediated Inflammatory Myopathies: Cellular Sources, Multiple Actions and Therapeutic

Implications, 178 BRIT. SOC’Y IMMUNOLOGY, CLINICAL & EXPERIMENTAL IMMUNOLOGY 405

(2014) (Ex. 33)).)

Regarding environmental factors, infectious agents are the most commonly

associated with the induction of dermatomyositis. (Ex. 13, p. 4.) Dr. Gershwin suggests

there are several proposed mechanisms. (Id. at 4-5.) First, the infectious agent could

cause self-proteins to become novel neo-antigens. (Id. at 4.) Second, the infectious

agent may expose an otherwise sequestered antigen to an immune response. (Id.)

Third, there may be cross-reaction between the infectious agent and muscle antigens or

other low affinity autoreactive cells. (Id. at 4-5.) Additionally, an aberrant cytokine

response may facilitate a loss of tolerance in a genetically susceptible host. (Id. at 5.)

6

He stresses that “[a] vaccination is designed to fool the body into thinking it is

responding to an infection.” (Id.)

Dr. Gershwin acknowledges that there are no reports in the literature of

increased incidences of dermatomyositis after any large vaccination campaigns. (Ex.

13, p. 4.) However, he stresses that this is not surprising given the rarity of the

condition, which he indicates has an estimated annual incidence of only 2 per million.

(Id. (citing Peter N. Malleson et al., The Incidence of Pediatric Rheumatic Diseases:

Results from the Canadian Pediatric Rheumatology Association Disease Registry, 23 J.

RHEUMATOLOGY 1981 (1996) (Ex. 39)).) However, a mouse model study by Katsumata,

et al., has shown that when genetically susceptible mice are immunized with the muscle

autoantigen found in myositis – histidyl-tRNA synthase or “Jo-1” – they have auto

antibodies 14 days post immunization that continue to increase for eight weeks and

their muscle histopathology at eight weeks demonstrates inflammatory cells. (Id. at 5-6

(citing Yasuhiro Katsumata et al., Species-Specific Immune Responses Generated by

Histidyl-tRNA Synthetase Immunization are Associated with Muscle and Lung

Inflammation, 29 J. AUTOIMMUNITY 174 (2007) (Ex. 43)).) Further, he notes that the

response to flu vaccination would have included production of interferons and, in

particular, plasmacytoid dendritic cells. (Id. at 5-6 (citing Marie Wahren-Herlenius &

Thomas Dorner, Immunopathogenic Mechanisms of Systemic Autoimmune Disease,

382 LANCET 819 (2013) (Ex. 45)).) He quotes Wahren-Herlenius, et al., for the further

proposition that “[w]ith activation of dendritic cells, an autoimmune self-amplification

loop would produce more interferon, promising and sustaining autoreactive responses,

keeping activated T cells and B cells in a vicious cycle, and producing more

autoantibodies.” (Id. at 7 (quoting Wahren-Herlenius & Dorner, supra, at Ex. 45, p. 6).)

Dr. Gershwin cites seven papers that he indicates demonstrate the plausibility of a

linkage between vaccination and dermatomyositis. (Id. (citing (Arie Altman et al., HBV

Vaccine and Dermatomyositis: Is There an Association?, 28 RHEUMATOLOGY INT’L 609

(2008) (Ex. 48); Clodoveo Ferri et al., Polymyositis Following Pandemic Influenza A

(H1N1) and 2009-10 Seasonal Trivalent Vaccines, 2012 CASE REPORTS RHEUMATOLOGY

1 (2012) (Ex. 49); F.M. Jani et al., Influenza Vaccine and Dermatomyositis, 4

NEUROEPIDEMIOLOGY 125 (1985) (Ex. 50); Hedi Orbach et al., Vaccines and Autoimmune

Diseases of the Adult, 9 DISCOVERY MED. 90 (2010) (Ex. 51); K. Perdan-Pirkmajer et al.,

Autoimmune Response Following Influenza Vaccination in Patients with Autoimmune

Inflammatory Rheumatic Disease, 21 LUPUS 175 (2012) (Ex. 52); Natasa Toplak &

Tadeg Avcin, Influenza and Autoimmunity, 1173 CONTEMP. CHALLENGES AUTOIMMUNITY

619 (2009) (Ex. 53); David C. Wraith et al., Vaccination and Autoimmune Disease: What

is the Evidence?, 362 LANCET 1659 (2003) (Ex. 54)).)

Regarding petitioner’s case, Dr. Gershwin proposes that she was genetically

predisposed to dermatomyositis. (Ex. 13, p. 6.) However, he does not cite any

evidence to support this suspicion apart from the fact that she developed

dermatomyositis. In fact, he acknowledges that the medical records do not identify any

underlying autoimmune or immunologic disease or infection that would have left her

susceptible to development of dermatomyositis. (Id. at 1-2.) He does note, however,

7

that petitioner had a vitamin D deficiency, which he suggests is thought to be a

predisposition to autoimmunity. (Id. at 1.)

Dr. Gershwin emphasizes that petitioner developed dermatomyositis post-

vaccination without any evidence of any prior muscle disease and without any evidence

of a viral infection at the time of onset. (Ex. 13, p. 1.) He interprets petitioner’s biopsy

as consistent with autoimmune myositis. (Id. at 2.) However, although petitioner had

Anti-Jo-1 antibodies, Dr. Gershwin opines that “her disease was initiated by her innate

immune system and there does not yet appear to be a clinically significant role for

adaptive immunity.” (Id. at 4 (citing Ann M. Reed & Floranne Ernste, The Inflammatory

Milieu in Idiopathic Inflammatory Myositis, 11 CURRENT RHEUMATOLOGY REPORTS 295

(2009) (Ex. 35)).) Nonetheless, he proposes that the above-discussed Katsumata, et

al., study, finding Jo-1 antibodies in mice by 14 days post-immunization, supports an

appropriate temporal relationship because it is “similar to what occurred herein.” (Id. at

5-6 (citing Katsumata et al., supra, at Ex. 43).)

b. Respondent’s rheumatology expert, Christopher Mecoli, M.D.5

Dr. Mecoli agrees that petitioner has a form of IIM and more specifically

concludes that petitioner has “anti-Jo1-positive idiopathic inflammatory myositis.” (Ex.

B, p. 3.) He notes that her medical records variously reference her condition as

“myositis,” “polymyositis,” dermatomyositis,” and “anti-synthase syndrome,” but explains

that all of these conditions fall under the larger umbrella of IIM. (Id.)

Dr. Mecoli stresses that the cause of IIM is unknown. (Ex. B, p. 4.) However, he

agrees that infectious agents (bacteria, parasites, and viruses) are among the most

commonly proposed causal agents, along with medications, ultraviolet light, and cancer.

(Id. (citing C. Thompson et al., The Pathogenesis of Dermatomyositis, 179 BRIT. J.

DERMATOLOGY 1256 (2018) (Ex. B, Tab 1); Brittany L. Adler & Lisa Cristopher-Stine,

Triggers of Inflammatory Myopathy: Insights into Pathogenesis, 25 DISCOVERY MED. 75

(2018) (Ex. B, Tab 2)).) In light of the difficulties in studying IIM, causal assessments

generally place an emphasis on temporality. (Id. at 4.) “Given the focus on infection,

vaccines inevitably are considered as a potential environmental trigger.” (Id.) However,

this consideration has largely been limited to case reports, which should not be

interpreted as proof of causation. (Id. (citing Joerg-Patrick Stubgen, A Review on the

Association Between Inflammatory Myopathies and Vaccination, 13 AUTOIMMUNITY

REVS. 31 (2014) (Ex. 41)).)

5 Dr. Mecoli is a board certified rheumatologist. (Ex. A, p. 6.) He received his undergraduate degree from

the College of New Jersey and his medical degree from Rutgers University. (Id. at 1.) He completed an

internship and a residency at the University of Pennsylvania, and a fellowship in rheumatology at Johns

Hopkins Hospital. (Id.) Dr. Mecoli is currently the Director of Research Operations at Johns Hopkins

Myositis Center, the Director of Myositis at Precision Medicine Center Initiative, an assistant professor in

the Division of Rheumatology at Johns Hopkins University, and an attending physician at Johns Hopkins

Medical Center. (Id.) He has published 31 original research papers, a book chapter, and has been

invited to review seven articles. (Id. at 1-4.)

8

Dr. Mecoli does not disagree with Dr. Gershwin regarding the general

background of IIM but does not agree that his theory of causation is reliably supported.

He suggests that “[t]he main argument appears to be that vaccines can elicit many of

the same immunologic perturbations that are observed in patients with IIM, and

therefore, given IIM occurred in close temporal proximity to the petitioner’s influenza

vaccination, there is likely a causal association.” (Ex. B, pp. 4-5.) He disagrees that the

Katsumata, et al., study cited by Dr. Gershwin is valuable, both because it is merely a

mouse model and also because it did not involve the flu vaccine. (Id. at 5.) Dr. Mecoli

indicates that the crux of his disagreement is Dr. Gershwin’s suggestion that petitioner

would have had a “unique” interferon signature that would have facilitated antigen

presentation of her autoantigens to plasmacytoid dendritic populations leading to an

inflammatory response in the skin and muscle. (Id. (quoting Ex. 13, p. 7).) While Dr.

Mecoli agrees an interferon response to vaccination is a desired outcome, he stresses

there is no evidence this happened in petitioner’s case and no evidence this has led to

IIM in any other patient. (Id.) Further, Dr. Mecoli stresses that, if vaccines could trigger

this autoimmunity in susceptible individuals, then one might expect IIM patients to

experience relapses or “flares” after vaccination; however, such flares have not been

demonstrated. (Id. (citing Carla G. S. Saad et al., Immunogenicity and Safety of the

2009 Non-Adjuvanted Influenza A/H1N1 Vaccine in a Large Cohort of Autoimmune

Rheumatic Diseases, 70 ANNALS RHEUMATIC DISEASES 1068 (2011) (Ex. B, Tab 5)).)

Although he agrees the rarity of IIM complicates epidemiology, he notes that at least

one study has purported to find no statistically significant evidence of increased

incidences of post-vaccination dermatomyositis or polymyositis. (Id. at 6 (citing H.

Orbach & A. Tanay, Vaccines as a Trigger for Myopathies, 18 LUPUS 1213 (2009) (Ex.

B, Tab 6)).)

c. Respondent’s immunology expert, James Moy, M.D.6

Dr. Moy asserts that Dr. Gershwin “has not given any specific medical theory on

mechanisms” as to how the flu vaccine can cause dermatomyositis. (Ex. D, p. 3.)

Regarding Dr. Gershwin’s observation that the response to the flu vaccine leads to

production of interferons, Dr. Moy characterizes this as a “broad, general statement”

that does not explain how the flu vaccine would lead to dermatomyositis. (Id.) Dr. Moy

indicates that the Wahren-Herlenius publication Dr. Gershwin quotes addresses

environmental factors including drugs, chemicals, infectious agents, cigarettes, and

6

Dr. Moy is a board certified in allergy and immunology and pediatrics. (Ex. C, p. 2.) He received his

undergraduate degree from Northwestern University and his medical degree from the University of Illinois

College of Medicine. (Id. at 1.) He completed a residency in pediatrics at the University of Minnesota and

a fellowship in allergy and immunology at Rush-Presbyterian-St. Luke’s Medical Center. (Id.) Dr. Moy is

currently an associate professor of Immunology/Microbiology, Pediatrics, and Internal Medicine, an

associate program director of the Allergy and Immunology Fellowship, and an associate director of

Immunology Discipline at Rush Medical College. (Id. at 1-2.) He has “evaluated and managed over 300

pediatric, adolescent and young adult patients with autoimmune diseases and disorders” including “lupus

erythematosus, juvenile idiopathic arthritis, . . . juvenile dermatomyositis, Kawasaki disease, scleroderma,

inflammatory bowel diseases, . . . and celiac disease.” (Ex. D, p. 1.) At the time he submitted his CV, he

had authored 53 publications, 43 abstracts, and 8 book chapters. (Ex. C, pp. 7-17.)

9

ultraviolet radiation, can precipitate autoimmunity, but not vaccinations. (Id. at 4 (citing

Wahren-Herlenius & Dorner, supra, at Ex. 45, pp. 6 (Figure 5), 8 (Table 2)).)

Dr. Moy agrees with Dr. Gershwin’s general discussion of the roles of both the

innate and adaptive immune responses in autoimmune disease but finds the proposed

link to the flu vaccine lacking any reliable or persuasive evidence. (Ex. D, p. 4.)

Regarding the seven specific citations Dr. Gershwin cited to demonstrate the plausibility

of this purported link, Dr. Moy addresses each in turn and observes the following: Three

of Dr. Gershwin’s citations (Altman et al., supra, at Ex. 48; Ferri et al., supra, at Ex. 49;

Jani et al., supra, at Ex. 50) are merely case reports, which “are not scientific evidence

of cause and result.” (Id. (citing Trygve Nissen & Rolf Wynn, The Clinical Case Report:

A Review of its Merits and Limitations, 7 BIOMED. CENT. RSCH NOTES 1 (2014) (Ex. D,

Tab 2)).) Moreover, the case report at Exhibit 48 involves a different vaccine, further

reducing its significance. (Id. (citing Altman et al., supra, at Ex. 48).) Petitioner’s Exhibit

51 is a study from which the authors concluded that no statistically significant increase

in polymyositis or dermatomyositis was observed after mass vaccination. (Id. (citing

Orbach et al., supra, at Ex. 51, p. 3).) Petitioner’s Exhibit 52 is a study that found only

“transient changed in antibody production” in both autoimmune patients and healthy

subjects following flu vaccination, but no exacerbation of disease in autoimmune

patients or new onset of autoimmune disease in healthy patients. (Id. at 5 (citing

Perdan-Pirkmajer et al., supra, at Ex. 52).) Petitioner’s Exhibits 53 and 54 discuss the

flu vaccine as a cause of autoimmunity in the context of GBS and Henoch-Schoenlein

purpura, but not dermatomyositis. (Id. (citing Toplak & Avcin, supra, at Ex. 53; Wraith et

al., supra, at 54).)

Regarding the details of this petitioner’s history, Dr. Moy places onset of

petitioner’s dermatomyositis on November 17, 2017, about three days post-vaccination.

(Ex. D, p. 5.) He therefore contends that the Katsumata, et al., mouse study, which

observed autoantibodies at 14 days, does not support medically appropriate timing of

onset in this case. (Id. (citing Katsumata et al., supra, at Ex. 43).) Dr. Moy also asserts

that Dr. Gershwin is inconsistent in suggesting that there was no significant clinical role

for petitioner’s adaptive immune response given that petitioner did have anti-Jo-1

antibodies. (Id.) This implies that her condition was at least in part a consequence of

her adaptive immune response. (Id.) Dr. Moy opines that there is not reliable evidence

that the flu vaccine did cause petitioner’s dermatomyositis and further that the timing of

onset is too soon after vaccination to implicate her vaccination. (Id. at 6.)

V. Discussion

a. Althen prong one

Under Althen prong one, petitioner must provide a “reputable medical theory,”

demonstrating that the vaccine received can cause the type of injury alleged. Pafford

ex rel. Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352, 1355-56 (Fed. Cir.

2006) (quoting Pafford ex rel. Pafford v. Sec’y of Health & Human Servs., No. 01-

0165V, 2004 WL 1717359, at *4 (Fed. Cl. Spec. Mstr. July 16, 2004)). Such a theory

10

must only be “legally probable, not medically or scientifically certain.” Knudsen, 35 F.3d

at 548-49. Petitioner may satisfy the first Althen prong without resort to medical

literature, epidemiological studies, demonstration of a specific mechanism, or a

generally accepted medical theory. See Andreu ex rel. Andreu v. Sec’y of Health &

Human Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009) (citing Capizzano v. Sec’y of

Health & Human Servs., 440 F.3d 1317, 1325-26 (Fed. Cir. 2006)). However, “[a]

petitioner must provide a ‘reputable medical or scientific explanation’ for [her] theory.

While it does not require medical or scientific certainty, it must still be ‘sound and

reliable.’” Boatmon, 941 F.3d at 1359 (quoting Moberly ex rel. Moberly, 592 F.3d 1315,

1322 (Fed. Cir. 2010); Knudsen, 35 F.3d at 548-49).

In this case, the parties’ experts all effectively agree regarding the pathogenesis

of IIM generally. That is, both parties agree that IMMs are likely autoimmune conditions

involving a combination of genetic and environmental factors, but for which specific

causes are unknown or, as Dr. Gershwin puts it, “enigmatic.” (Ex. 13, p. 3; see also Ex.

B, pp. 3-4; Ex. D, p. 2, 3.) There is also no dispute that infectious antigens are among

the suspected causes and that anti-Jo-1 antibodies can be implicated as the

autoimmune pathway as Dr. Gershwin asserts. (Ex. 13, pp. 4-5; see also Ex. B, p. 3-4;

Ex. D, pp. 2-3.) However, none of this implicates vaccinations as a cause of IMMs.

Thus, the crux of Dr. Gershwin’s theory is his juxtaposition of two concepts: (1) that the

initial inflammatory aspect of IMMs is mediated by interferons and (2) that the flu

vaccine is known to stimulate interferons. (Ex. 13.) Combining these two concepts, Dr.

Gershwin asserts that it is plausible to link the flu vaccine to IMM. (Ex. 13, p. 7.)

However, as Dr. Moy submits, even accepting both concepts as true, this latter

assertion is a broad and generic statement that merely invokes the immune response

that the flu vaccine is intended to have. (Ex. D, pp. 3-4.) Prior decisions have

concluded that this type of reasoning is not persuasive, without more, as a theory of

causation. E.g. Cordova v. Sec’y of Health & Human Servs., No. 17-1282V, 2021 WL

3285367, at *17 (Fed. Cl. Spec. Mstr. June 23, 2021) (observing that “[e]vidence that a

vaccine causes an immune response – the intended function of any vaccine – does not

amount to a showing that this response is, or can become, pathologic, absent additional

proof linking to evidence of the vaccine . . .”). Accordingly, petitioner’s Althen one

presentation turns on the evidence underlying Dr. Gershwin’s statement that a link

between dermatomyositis and the flu vaccine is plausible and how effectively Dr.

Gershwin marries the largely undisputed general understanding of interferon-mediated

inflammation leading to autoimmunity and IIM with the very modest evidence implicating

vaccines in that process. Respondent’s experts persuasively assert that on this record,

Dr. Gershwin’s assertion that the flu vaccine has been plausibly linked to IMMs is

virtually unsupported.

As discussed above, Dr. Gershwin has cited seven specific publications that he

asserts support the plausibility of the flu vaccine as a cause of IIMs, each of which

respondent’s experts, and in particular Dr. Moy, have sought to rebut. (Compare Ex.

13, pp. 6-7 and Ex. D, pp. 4-5.) In addition to several case reports (by Altman, et al,

Ferri, et al, and Jani, et al, respectively), Dr. Gershwin cites two review papers, one by

Orbach et al., and one by Wraith, et al., addressing vaccines as a potential cause of

11

autoimmunity more broadly (Orbach et al., supra, at Ex. 51, Wraith et al., supra, at 54),

a paper by Toplak and Avcin addressing influenza infection and autoimmunity (Toplak &

Avcin, supra, at Ex. 53), and a study by Perdan-Pirkmajer, et al., addressing the flu

vaccine and inflammatory rheumatic diseases (Perdan-Pirkmajer et al., supra, at Ex.

52). However, apart from the case reports, none of these publications purport to directly

implicate the flu vaccine as a cause of IIMs. To the extent they could theoretically

provide circumstantial support even without being facially relevant, Dr. Gershwin has

not actually explained what in these papers actually supports his opinion. (See Ex. 13,

p. 7.) In fact, his report seems to acknowledge that the proposed link is asserted

without yet being supported. Specifically, Dr. Gershwin indicates in reference to these

citations that “[t]he plausibility of a linkage between vaccination and [dermatomyositis] is

also noted from a variety of literature that has attempted to show causation and [] which

discusses the theoretical basis to link an association, albeit with the limitations of power

calculations discussed above.” (Id.)

Upon my own review, neither Orbach, et al., nor Wraith, et al., implicate

vaccinations as a cause of IIMs. Wraith, et al., lists dermatomyositis as a confirmed

autoimmune condition, but not as an autoimmune condition known to be caused by

vaccinations. (Wraith et al., supra, at Ex. 54, pp. 2-3 (Compare Panel 1 and Panel 3).)

Orbach, et al., explain that there have been “sporadic” case reports reporting post-

vaccination myopathies, but stressed that “[t]here is no statistically significant increase

in the incidence of polymyositis or dermatomyositis after any mass vaccination.”

(Orbach et al., supra, at Ex. 51, p. 3.) Toplak and Avcin do not discuss IMMs at all.

(Toplak & Avcin, supra, at Ex. 53.) Perdan-Pirkmajer examined potential autoimmune

responses following seasonal flu vaccination among 218 patients already suffering

rheumatologic conditions. (Perdan-Pirkmajer et al., supra, at Ex. 52, pp. 1-2.) The

study reported transient changes in autoantibodies post-vaccination, especially ANA.

(Id. at 1.) However, the study did not correlate these findings to clinical outcomes.

Moreover, out of a study population of 218 patient with rheumatologic conditions, only

one patient had dermatopolymyositis. (Id. at 2.) Although the authors note having

screened some patients for anti-Jo-1 antibodies, no findings were reported relative to

that antibody. (Id. at 3.) Although a specific autoantibody has not been definitively

identified for dermatomyositis (Hornung & Wenzel, supra, at Ex. 15, p. 3; Khanna &

Reed, supra, at Ex. 16, p. 6 (Table 1)), Dr. Gershwin specifically singled out the anti-Jo-

1 antibody as having been experimentally supported as leading to the development of

dermatomyositis. (Ex. 13, pp. 5-6 (citing Katsumata et al., supra, at Ex. 43).) Moreover,

he cited literature indicating that the anti-Jo-1 antibody is “strongly associated” with the

interferon pathway to autoimmunity he has advanced in this case. (Nagaraju &

Lundberg, supra, at Ex. 17, p. 5.)

This leaves only the case reports as support for Dr. Gershwin’s theory. However,

as Dr. Moy explains, case reports “are not scientific evidence of cause and result.” (Ex.

D, p. 4 (citing Nissen & Wynn, supra, at Ex. D, Tab 2).) Although case reports are not

entirely without evidentiary value, they are not strong evidence without more. E.g.

Crutchfield v. Sec’y of Health & Human Servs., No. 09-39V, 2014 WL 1665227, at *19

(Fed. Cl. Spec. Mstr. Apr. 7, 2014) (“single case reports of Disease X occurring after

12

Factor Y . . . do not offer strong evidence that the temporal relationship is a causal

one—the temporal relationship could be pure random chance”), aff’d, 125 Fed. Cl. 251

(2014); see also Paluck v. Sec’y of Health & Human Servs., 104 Fed. Cl. 457, 475

(2012) (indicating that case reports “‘do not purport to establish causation definitively,

and this deficiency does indeed reduce their evidentiary value’. . . [but] ‘the fact that

case reports can by their nature only present indicia of causation does not deprive them

of all evidentiary weight.”), aff’d, 786 F.3d 1373 (Fed. Cir. 2015)). Additionally, one of

the case reports cited by petitioner involves a different vaccine, further reducing its

significance. (Altman et al., supra, at Ex. 48).)

To be clear, both parties have filed literature that acknowledges that vaccines

have been hypothesized as a cause of IIM in at least some rare instances. (Orbach &

Tanay, supra, at Ex. B, Tab 6; Stubgen, supra, at Ex. 41.) However, when considering

this literature holistically, it is apparent from these discussions that the purported link

has not been substantiated. In that regard, Dr. Gershwin asserts that dermatomyositis

is too rare to reasonably expect it to be detected by epidemiology. (Ex. 13, pp. 2-3.)

Respondent’s experts likewise agree that dermatomyositis is a rare enough condition

that epidemiology must be approached with caution. (Ex. B, p. 3.) That is, both parties’

experts conclude would be very challenging to develop a study sufficiently powered to

detect post-vaccination incidences of dermatomyositis. (Id. at 4; Ex. 13, pp. 2-3.) And,

of course, petitioners in this program are not obligated to come forward with

epidemiologic support in order to meet Althen prong one. See Andreu, 569 F.3d at

1378-79 (citing Capizzano, 440 F.3d at 1325-26).

However, that is not to say that all epidemiology is irrelevant. Special masters

may consider whether available epidemiology undermines a petitioner’s claim. D'Tiole

v. Sec’y of Health & Human Servs., 726 F. App’x 809, 811 (Fed. Cir. 2018) (citing

Andreu, 569 F.3d at 1379 (“Although Althen and Capizzano make clear that a claimant

need not produce medical literature or epidemiological evidence to establish causation

under the Vaccine Act, where such evidence is submitted, the Special Master can

consider it in reaching an informed judgment as to whether a particular vaccination likely

caused a particular injury.”). In this case, Dr. Gershwin has cited a review paper that

discusses two types of studies that are not affected by the issue of the rarity of

dermatomyositis in the general population. First, retrospective study has examined

whether patients diagnosed with dermatomyositis had had recent immunizations.

(Stubgen, supra, at Ex. 41, p. 3.) Vaccination was not identified as an important trigger

for dermatomyositis. (Id.) Second, a prospective study also looked at the effects of the

flu vaccination on individuals already suffering dermatomyositis. (Id. at 6.) This study

determined that the flu vaccine has no short-term effect on the disease course of those

already suffering dermatomyositis. (Id.) While these types of studies obviously still

have limitations, they do not depend on having a large enough scale to overcome the

rarity of dermatomyositis in the general population, overcoming the specific issue raised

by Dr. Gershwin to discount epidemiologic study of dermatomyositis. Accordingly, I find

it reasonable to consider these studies as some evidence weighing against petitioner’s

theory.

13

Notably, prior petitioners have failed to come forward with preponderant evidence

demonstrating that the flu vaccine can cause dermatomyositis. Whelan v. Sec’y of

Health & Human Servs., No. 16-1174V, 2019 WL 1061473 (Fed. Cl. Spec. Mstr. Jan.

28, 2019); McDaniel v. Sec’y of Health & Human Servs., No. 17-1322V, 2023 WL

4678688 (Fed. Cl. Spec. Mstr. June 26, 2023). However, I am also aware of one prior

case in which a petitioner was found entitled to compensation for dermatomyositis

caused-in-fact by a flu vaccine based on a theory similar to the one presented in this

case.7 Ulysse v. Sec’y of Health & Human Servs., No. 15-451V, 2022 WL 2115248

(Fed. Cl. Spec. Mstr. May 19, 2022). A critical factor in the resolution of that case was

the degree to which the petitioner’s theory of causation was unchallenged by

respondent. Id. at 19. The special master noted in conclusion that “[i]n a different case,

with a more substantive opposition marshaled by Respondent, the outcome would likely

have been different.” Id. at 20. An additional case found a petitioner entitled to

compensation for a minor child’s juvenile dermatomyositis caused by a simultaneous

administration of DTaP, MMR, Polio, and varicella vaccinations. Rodriguez ex rel. C.R.

v. Sec’y of Health & Human Servs., No. 13-253V, 2017 WL 5563419 (Fed Cl. Spec.

Mstr. Oct. 26, 2017). However, that case involved different vaccines and other cases

have suggested that juvenile dermatomyositis is a distinguishable condition. Id.;

McDaniel, 2023 WL 4678688, at *32 n. 62.

Thus, considering all of the above and the record as a whole, the record of this

case best reflects the conclusion that it may be possible, but not preponderantly

established, that the flu vaccine could be a cause of dermatomyositis. Thus, petitioner

has not met her burden of proof under Althen prong one. Under Althen prong one,

petitioner must come forward with more than a merely possible theory of causation.8

Boatmon, 941 F.3d at 1360.

a. Althen prong two

The second Althen prong requires proof of a logical sequence of cause and

effect, usually supported by facts derived from a petitioner's medical records. Althen,

418 F.3d at 1278; Andreu, 569 F.3d at 1375–77; Capizzano, 440 F.3d at 1326; Grant,

956 F.2d at 1148. Medical records are generally viewed as particularly trustworthy

evidence. Cucuras v. Sec'y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir.

7 Myositis is also sometimes raised as part of an overlapping presentation inclusive of other

rheumatologic conditions. These cases have also been resolved to mixed results for petitioners.

Compare Rodd v. Sec’y of Health & Human Servs., No. 13-122V, 2015 WL 8489035 (Fed. Cl. Spec. Mstr.

Nov. 13, 2015) (implicating the flu vaccine in an overlap syndrome inclusive of Sjogren’s Syndrome,

carpal tunnel syndrome, polymyositis, and inflammatory arthritis) and Suliman v. Sec’y of Health &

Human Servs., 13-993V, 2018 WL 6803697 (Fed. Cl. Spec. Mstr. Nov. 27, 2018) (finding against the

petitioner in case involving polymyalgia rheumatica (“PMR”) and myositis allegedly caused by a Tdap

vaccine). These other types of cases are not easily compared to the instant case given the interplay of

the different conditions and diagnoses.

8 In his motion response, respondent stresses Dr. Gershwin’s use of the word “plausible” to describe the

link between the flu vaccine and dermatomyositis. (ECF No. 43, p. 16.) Although respondent is correct,

my conclusion that petitioner’s theory is merely plausible derives from my own review of the record

evidence. It does not turn on Dr. Gershwin’s specific use of the term plausible in his report.

14

1993). However, medical records and/or statements of a treating physician's views do

not per se bind the special master. See § 300aa-13(b)(1) (providing that “[a]ny such

diagnosis, conclusion, judgment, test result, report, or summary shall not be binding on

the special master or court”); Snyder ex rel. Snyder v. Sec'y of Health & Human Servs.,

88 Fed. Cl. 706, 746 n. 67 (2009) (“there is nothing ... that mandates that the testimony

of a treating physician is sacrosanct—that it must be accepted in its entirety and cannot

be rebutted.”) A petitioner may support a cause-in-fact claim through either medical

records or expert medical opinion. § 300aa-13(a). The special master is required to

consider all the relevant evidence of record, draw plausible inferences and articulate a

rational basis for the decision. Winkler v. Sec’y of Health & Human Servs., 88 F.4th

958, 963 (Fed. Cir. 2023) (citing Hines, 940 F.2d at 1528).

Although Dr. Ozeri opined that petitioner’s condition was vaccine caused, his

stated rationale for so opining was the concept of autoimmune syndrome induced by

adjuvants or “ASIA.” (See Ex. 5, p. 105.) ASIA has been the subject of substantial

criticism and has been repeatedly rejected as a viable theory of causation in this

program. See J.F. v. Sec’y of Health & Human Servs., No. 13-799V, 2022 WL 5434214

(Fed. Cl. Spec. Mstr. Sept. 9, 2022); D’Angiolini, v. Sec’y of Health & Human Servs.,

No. 99-578V, 2014 WL 1678145 (Fed. Cl. Spec. Mstr. Mar. 27, 2014), mot. for rev.

denied, 122 Fed. Cl. 86 (2015); Rowan v. Sec’y of Health & Human Servs., No. 10-

272V, 2014 WL 7465661 (Fed. Cl. Spec. Mstr. Dec. 8, 2014), aff’d, 2015 WL 3562409

(Fed. Cl. May 18, 2015). In fact, ASIA has specifically been rejected as a theory

purporting to link myositis to vaccination. Suliman, 2018 WL 6803697, at *25-28.

Although treating physician opinions are often given significant weight, such opinions

are only as sound as their bases. See Isaac v. Sec’y of Health & Human Servs., No.

08-601V, 2012 WL 3609993, at *24 (Fed. Cl. Spec. Mstr. July 30, 2012). Moreover,

respondent stresses that the flu vaccine petitioner received was not adjuvanted. (ECF

No. 43, p. 22.) Accordingly, without further elaboration or substantiation of his opinion,

Dr. Ozeri’s mere invocation of ASIA does not preponderantly support petitioner’s claim.

Conspicuously, petitioner’s expert, Dr. Gershwin, did not rely on ASIA in formulating his

own theory of causation even though some of the literature he cited does discuss the

ASIA hypothesis with respect to post-vaccination autoimmunity more broadly. (E.g.

Stubgen, supra, at Ex. 41, p. 6; Perdan-Pirkmajer et al., supra, at 52, p. 8.)

Dr. Gershwin’s causal assessment also faulters insofar as he has not

preponderantly established that the flu vaccine can cause dermatomyositis at all.

Additionally, his opinion suffers due to internal inconsistency. As Dr. Moy points out,

despite explaining dermatomyositis as involving an inflammatory response leading to an

autoimmune response involving anti-Jo-1 antibodies, Dr. Gershwin puzzlingly

disclaimed any role for petitioner’s documented anti-Jo-1 antibodies in her own disease

process. (Ex. D, p. 5.) This appears likely to be an effort to sidestep any need to

substantiate a more direct causal relationship between petitioner’s vaccination and her

ultimate antibody response. Dr. Gershwin was never more specific than to assert that

vaccinations mimic infections and that there are a variety of theories to suggest how an

infectious agent may induce dermatomyositis. (Ex. 13, pp. 4-5.) However,

respondent’s experts reasonably concluded that petitioner’s anti-Jo-1 antibodies likely

15

suggest her condition was least partly the result of an adaptive immune response. (Ex.

D, p. 5.) Especially given the nature of the evidence Dr. Gershwin presented to support

his theory of causation, which among other things “strongly associated” anti-Jo-1

antibodies to the interferon pathway to autoimmunity in dermatomyositis, this

sidestepping by Dr. Gershwin reduces his causal opinion to one merely recognizing the

presence of timing coincident to vaccination. Such opinions do not preponderantly

support a cause-in-fact claim. Althen, 418 F.3d at 1278 (citing Grant, 956 F.2d at

1149).

For all these reasons, petitioner has not met her preponderant burden of proof

under Althen prong two.

a. Althen prong three

The third Althen prong requires establishing a “proximate temporal relationship”

between the vaccination and the injury alleged. Althen, 418 F.3d at 1278. A petitioner

must offer “preponderant proof that the onset of symptoms occurred within a timeframe

for which, given the medical understanding of the disorder's etiology, it is medically

acceptable to infer causation.” de Bazan v. Sec'y of Health & Human Servs., 539 F.3d

1347, 1352 (Fed. Cir. 2008).

Petitioner has submitted three publications that include five case reports of

individual patients experiencing IIM subsequent to vaccination. Among those five case

reports, one patient initially had a fever and cough a “few” days post-vaccination and

then later developed additional symptoms of IIM such as muscle weakness two weeks

later. (Ferri et al., supra, at Ex. 49, p. 1.) Otherwise, the remaining four cases identify

onset ranging from one week to one-month post-vaccination. (Id.; Altman et al., supra,

at 48; Jani et al., supra, at 50.) Similarly, the review paper cited by Dr. Gershwin

identifies two case reports of either dermatomyositis or polymyositis occurring within two

days of vaccination, but otherwise lists 20 other case reports placing onset at between

five days and six weeks post-vaccination. (Stubgen, supra, at Ex. 41, p. 3 (Table 1).)

Thus, these case reports on the whole tend to suggest that onset of vaccine-caused

dermatomyositis – if such a thing were to exist – would likely occur at least one-week

post-vaccination. In this case, however, Dr. Gershwin asserts that onset of petitioner’s

own condition arose just two days post-vaccination.

In seeking to assert that onset of petitioner’s dermatomyositis occurred during a

timeframe within which it is reasonable to infer vaccine causation, Dr. Gershwin relies

on a mouse model study by Katsumata, et al., that found Jo-1 antibodies in mice by 14

days post-immunization. (Ex. 13, pp. 5-6 (citing Katsumata et al., supra, at Ex. 43).)

There are two issues with this reliance. First, as discussed under Althen prong two,

above, Dr. Gershwin disclaimed any causal role for petitioner’s own documented anti-

Jo-1 antibodies. (Ex. 13, pp. 6-7.) Accordingly, Dr. Gershwin has not substantiated that

this antibody finding by Katsumata, et al., has any relevance to the timing of onset

based on Dr. Gershwin’s own assessment of the cause of petitioner’s condition.

Second, the Katsumata study authors appear to indicate that it is the difference in

16

antibody response between ten days and eight weeks that permits them to conclude

that a cross-reactive antibody response had developed during that period. (Katsumata

et al., supra, at Ex. 43, pp. 6, 16 (Fig. 4).) Indeed, Dr. Gershwin cites this progression

and corresponding findings on muscle histopathology, as the basis for opining that a

disease process has set in. (Ex. 13, pp. 5-6.) However, the study authors confirm that

in the course of the study subject mice were sacrificed for sample harvesting after ten

days at the earliest. (Katsumata et al., supra, at Ex. 43, pp. 3-4.) Thus, it is not

apparent that the Katsumata study has any ability in itself to suggest what, if any,

disease process occurred prior to ten days. These study results remain consistent with

the great majority of the above-discussed case reports that generally place onset

between one-week and six-weeks post vaccination.

None of this evidence necessarily rules out a two to three-day latency as

medically appropriate to infer vaccine-causation. However, it does not preponderantly

support a temporal relationship between petitioner’s vaccination and onset of her

dermatomyositis. For his part, respondent’s immunology expert, Dr. Moy, did opine that

petitioner’s condition arose too soon after vaccination to implicate her vaccine as a

cause. (Ex. D, p. 6.)

For all these reasons, petitioner has not met her preponderant burden of proof

under Althen prong three.

VI. Conclusion

After weighing the evidence of record within the context of this program, and for

all the reasons discussed herein, petitioner has not demonstrated by preponderant

evidence that her condition was caused by her November 14, 2017 flu vaccination.

Accordingly, this case is dismissed.9

IT IS SO ORDERED.

s/Daniel T. Horner

Daniel T. Horner

Special Master

9

In the absence of a timely-filed motion for review of this Decision, the Clerk of the Court shall enter

judgment accordingly.

17