VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_18-vv-00769
Package ID: USCOURTS-cofc-1_18-vv-00769
Petitioner: Kathleen Cooper-Loher
Filed: 2018-05-31
Decided: 2023-08-01
Vaccine: influenza
Vaccination date: 2015-11-09
Condition: granuloma annulare
Outcome: dismissed
Award amount USD: 

AI-assisted case summary:
Kathleen Cooper-Loher filed a petition alleging that her November 9, 2015 influenza vaccine caused her to develop granuloma annulare (GA), and that a subsequent influenza vaccine on November 7, 2016, significantly aggravated her condition. Petitioner, an operating room registered nurse, had a history of skin conditions, including GA noted in 2010 and possibly earlier. She alleged that following the 2015 vaccine, she experienced severe itching that progressed to a rash in early 2016, which she attributed to the vaccine. However, medical records indicated the rash appeared approximately five months after the 2015 vaccination and was preceded by a viral upper respiratory infection (URI). Petitioner's expert, Dr. Rostad, theorized a delayed-type hypersensitivity (DTH) reaction to the vaccine caused the GA. Respondent's expert, Dr. Boos, argued that GA is rare, Petitioner's condition predated the vaccinations, and the timing of her rash was more consistent with a viral infection than the vaccine. Dr. Knierim, Petitioner's second expert, initially opined the GA was vaccine-triggered but later conceded in a supplemental report that GA was present years prior to the vaccinations, significantly weakening Petitioner's claim. The court found that Petitioner's GA was present before the vaccinations, and the evidence did not establish a clear causal link or significant aggravation directly attributable to the vaccines, especially given the intervening viral infections and the significant time lapse between vaccination and symptom onset. Therefore, the petition was dismissed.

Theory of causation field:
Off-Table

Public staged source text:

================================================================================
DOCUMENT 1: USCOURTS-cofc-1_18-vv-00769-1
Date issued/filed: 2023-08-01
Pages: 34
Docket text: PUBLIC DECISION (Originally filed: 05/18/2023) regarding 66 DECISION of Special Master. Signed by Special Master Herbrina Sanders. (rig) Service on parties made.
--------------------------------------------------------------------------------
Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 1 of 34
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: May 18, 2023
* * * * * * * * * * * * * * * * * *
KATHLEEN COOPER-LOHER, * No. 18-769v
*
Petitioner, * Special Master Sanders
*
v. *
*
SECRETARY OF HEALTH * Ruling on the Record; Dismissal;
AND HUMAN SERVICES, * Influenza (“Flu”) Vaccine; Granuloma
* Annulare (“GA”); Significant Aggravation
Respondent. *
* * * * * * * * * * * * * * * * * *
Carol L. Gallagher, Carol L. Gallagher, Esquire, LLC, Somers Point, NJ, for Petitioner.
Debra A. Filteau Begley, United States Department of Justice, Washington, DC, for Respondent.
DECISION ON ENTITLEMENT1
On May 31, 2018, Kathleen Cooper-Loher (“Petitioner”) filed a petition pursuant to the
National Vaccine Injury Compensation Program (“Program” or “Vaccine Program”).2 Petitioner
alleges that she received the influenza vaccine on November 9, 2015, “causing her to suffer with
granuloma annulare” (“GA”).3 Pet. at 1, ECF No. 1. Petitioner further alleges her GA was
exacerbated “following a mandated influenza vaccine administered on November 7, 2016.” Id.
1 Because this Decision 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 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, I agree that
the identified material fits within this definition, I will redact such material from public access.
2 National Childhood Vaccine Injury Act of 1986, Pub.L. No. 99–660, 100 Stat. 3755. Hereinafter, for ease
of citation, all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. § 300aa
(2012).
3 Granuloma annulare is “a group of benign, usually self-limited granulomatous diseases of unknown
etiology with both localized and disseminated varieties, most often seen in children and young adults. The
lesions chiefly involve the dermis and are perforating papules or subcutaneous nodules grouped in rings.
Histopathologic findings include palisading macrophages surrounding foci of necrobiosis of the dermis.”
Dorland’s Illustrated Medical Dictionary 1, 803 (32nd ed. 2012) [hereinafter “Dorland’s”]. A papule is “a
small circumscribed, superficial, solid elevation of the skin less than 1 cm (0.5 cm according to some
authorities) in diameter.” Id. at 1373. Necrobiosis is “swelling, basophilia, and distortion of collagen
bundles in the dermis, sometimes with obliteration of normal structure, but without actual necrosis[.]” Id.
at 1234.

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 2 of 34
Petitioner filed a motion for a ruling on the record on June 9, 2022. Pet’r’s Mot. for Ruling
[hereinafter “Pet’r’s Mot.”], ECF No. 62. For the reasons stated below, Petitioner’s case is hereby
DISMISSED.
I. Procedural History
Over the next several months after filing her petition on May 31, 2018, Petitioner filed
seven medical record exhibits in support of her claim, an affidavit, and her first statement of
completion. Pet’r’s Exs. 1–8, ECF Nos. 7, 9–11, 13. Thereafter, on November 19, 2018,
Respondent filed a status report, in which he identified outstanding medical records needed to
evaluate Petitioner’s claim. ECF No. 14. These records included pre-vaccination health records,
post-vaccination records, and photos of Petitioner’s rash that were referenced in prior documents.
See id.
In response, on November 30, 2018, Petitioner filed photos and a pre-vaccination medical
record. Pet’r’s Exs. 9–10, ECF No. 16. She filed employment records and an amended statement
of completion on January 3, 2019. Pet’r’s Ex. 11, ECF Nos. 17–18. On April 9, 2019, Petitioner
filed an additional medical record. Pet’r’s Ex. 12, ECF No. 22. Respondent filed his Rule 4(c)
report on May 6, 2019, in which he recommended against compensation. Resp’t’s Report at 8–9,
ECF No. 24. Respondent argued that Petitioner is unlikely to satisfy her burden for compensation
because “it is not clear when [P]etitioner developed GA.” Id. at 6. Respondent continued that
“Petitioner’s records document that she had chronic skin issues before her 2015 and 2016 flu
vaccinations, and there are no records documenting any rash on [P]etitioner’s skin until seven
months after her 2016 flu vaccination.” Id. Therefore, Respondent maintained that Petitioner’s
medical records do “not document either the onset or a flare of GA in association with either of
her vaccines.” Id. at 7. Petitioner filed an affidavit in response to Respondent’s assertions on May
21, 2019. Pet’r’s Ex. 13, ECF No. 25.
The same day, I ordered Petitioner to submit an expert report by July 22, 2019. Sched.
Order, docketed May 21, 2019. Petitioner filed an expert report from Dr. Steven Rostad, his
curriculum vitae, and supporting literature on July 22 and 23, 2019. Pet’r’s Exs. 14–48, ECF Nos.
27–31. Additionally, Petitioner submitted two affidavits: one on her own behalf and another from
a co-worker. Pet’r’s Exs. 49–50, ECF Nos. 32–33. Based on these filings, I held a status conference
with the parties on August 22, 2019. Min. Entry, docketed Aug. 22, 2019. During the conference,
Respondent raised specific factual issues within Petitioner’s expert report relating to the
development and timing of her symptoms. Sched. Order, ECF No. 35. As such, Respondent
indicated he did not “feel that a rebuttal expert report was necessary to demonstrate that the case
should not proceed.” Id. at 1. I awarded Petitioner thirty days to determine whether she could
provide evidence corroborating the post-vaccination onset of her symptoms or to otherwise
indicate how she wished to proceed. Id. She filed an additional medical record on September 24,
2019. Pet’r’s Ex. 52, ECF No. 41.
Petitioner submitted an additional expert report and status report that were ultimately
stricken from the record “because the filings d[id] not clarify issues in the case.” See Sched. Order,
ECF No. 42. The decision to strike these filings came following an agreement by the parties during
a status conference held on September 25, 2019. See id.; see also Min. Entry, docketed Sept. 25,
2

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 3 of 34
2019. During the conference, Respondent stated his intention to file a motion to dismiss and I gave
Respondent thirty days to do so. Sched. Order, docketed Sept. 25, 2019.
Respondent filed his motion to dismiss on October 28, 2019. Resp’t’s Mot. to Dismiss,
ECF No. 47. Respondent reiterated his position articulated in his Rule 4(c) report. Id. He added
that Dr. Rostad’s expert “report is based on an incorrect timeline, excludes relevant pre-vaccination
facts, assumes facts contradicted by the medical records, and relies on speculation.” Id. at 8 (citing
Pet’r’s Ex. 14 at 3–4). Petitioner filed medical literature and a response to Respondent’s motion
on November 5, 2019. Pet’r’s Ex. 53, ECF No. 48; Pet’r’s Resp., ECF No. 49. In Petitioner’s
response, she noted that “there remain genuine issues of material facts in the instant case.” Pet’r’s
Resp. at 1. Therefore, a dismissal would not be appropriate, given the procedural posture of the
claim. Id.
Although Respondent styled his motion as a motion to dismiss, it was more akin to a motion
for summary judgment. In ruling on such a motion, “special masters must draw on every inference
concerning disputed facts in favor of the nonmoving party.” See Order at 4, ECF No. 50 (internal
citations omitted). Further, “if to dispose of the case[,] the special master must resolve conflicts of
fact or weigh conflicting evidence,” summary judgment is inappropriate. Id. I denied Respondent’s
motion to dismiss and noted that the onset date of Petitioner’s GA is a material fact in dispute. Id.
I further noted that Petitioner’s theory of causation was also contested. Id. Therefore, I was unable
to resolve the case or make the necessary credibility findings, resolve conflicts of fact, and weigh
conflicting evidence in favor of or against Petitioner without a complete evidentiary record. Id. at
5. I then ordered Petitioner to file an expert report including a detailed discussion on symptom
onset and but-for causation. Order at 1, ECF No. 50-1.
After one motion for extension of time, Petitioner filed the expert report and curriculum
vitae of Dr. Richard Knierim on June 4, 2021, followed by supporting medical literature on June
8, 2021. Pet’r’s Exs. 54–55, ECF No. 52; Pet’r’s Exs. 56–60, ECF No. 53. Respondent filed the
responsive expert report and curriculum vitae of Dr. Markus Boos on October 8, 2021, along with
supporting medical literature. Resp’t’s Exs. A, A Tabs 1–14, B, ECF No. 56. Petitioner filed a
supplemental report from Dr. Knierim on November 18, 2021. Pet’r’s Ex. 61, ECF No. 57.
Following a status conference to discuss further proceedings, Petitioner filed a motion for ruling
on the record on June 9, 2022. Pet’r’s Mot., ECF No. 62. Respondent responded on July 13, 2022.
Resp’t’s Resp., ECF No. 64. Petitioner filed a reply on July 20, 2022. Pet’r’s Reply, ECF No. 65.
This matter is now ripe for consideration.
II. Evidence
a. Medical Records
i. Pre vaccination
Petitioner’s pre-vaccination history is significant for asthma and several skin-related
conditions. Pet’r’s Ex. 11 at 243, ECF No. 17-1. Her medical records include summaries from
annual physicals conducted over several years from 2010 through 2014. See generally Pet’r’s Ex.
9, ECF No. 16-1. Janet Bowen, a board-certified advanced registered nurse practitioner
3

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 4 of 34
[hereinafter “NP Bowen”], recorded assessments from Petitioner’s physical exams that often
included a skin evaluation. Id. The note from Petitioner’s December 15, 2010 exam, showed that
her “lower legs [presented] with granuloma annularis [sic], otherwise without suspicious lesions.”
Id. at 4. The physical the following year, on November 9, 2011, had no notation for a skin
evaluation. Id. During the exam, however, Petitioner reported “chronic skin problems and rashes
that pop[ped] up here and there due to eczema4 and dermatitis.”5 Id. at 5. She stated that
triamcinolone cream6 “seem[ed] to take care of it quite well[,]” and NP Bowen prescribed
Petitioner betamethasone dipropionate.7 Id. On November 21, 2012, NP Bowen noted Petitioner’s
“forearms and upper left arm [appeared] with several areas of red, flat, macular-type8 lesions,
otherwise grossly without suspicious lesions.” Id. at 3. NP Bowen renewed Petitioner’s
betamethasone dipropionate prescription. Id. There is no record for a physical conducted in 2013,
but Petitioner’s May 20, 2014 physical notes indicated that her skin was “grossly without
suspicious lesions.” Id. at 2. NP Bowen renewed Petitioner’s betamethasone dipropionate cream.
Id. Petitioner did not file records documenting any care between May 21, 2014, and November 8,
2015. She received the first flu vaccine at issue on November 9, 2015. Pet’r’s Ex. 1 at 1, ECF No.
7-1.
ii. Post vaccination
There are no filed medical records documenting any treatment for Petitioner between
November 10, 2015, and April 14, 2016. Petitioner’s first post-vaccination medical visit occurred
on April 15, 2016. Pet’r’s Ex. 3 at 15, ECF No. 7-3. Petitioner presented to urgent care that day
“with a rash mainly over [her] trunk, arms[,] and legs.” Id. She disclosed “an upper respiratory
illness [(“URI”)] starting about [two] weeks [prior].” Id. Petitioner reported the URI “symptoms
including sinus congestion, cough and chest heaviness seemed better [after] about [one] week[;]
however, [the following week], she also developed a pruritic9 rash starting more so on the trunk
and then subsequently spreading down the legs and arms.” Id. This rash, according to Petitioner,
was unlike previous hive-like irritations she has had. Id. An examination revealed a “very
4 Eczema is “any of various pruritic, papulovesicular types of dermatitis occurring as reactions to
endogenous or exogenous agents. In acute types there may be erythema, edema, inflammatory infiltrates in
the dermis, vesiculation, crusting, and scaling. In chronic types there may be lichenification, skin
thickening, signs of excoriation; and areas of hyperpigmentation or hypopigmentation.” Dorland’s at 592.
Pruritic means itchy. Id. at 1540. Dermatitis is generally, “inflammation of the skin.” Id. at 494.
Lichenification is “hypertrophy of the epidermis, with thickening and toughening of the skin to give it a
leathery appearance, and exaggeration of its normal markings; this is caused by prolonged rubbing or
scratching and may be on seemingly normal skin or on skin that has a pruritic disorder.” Id. at 1034.
5 See id.
6 Triamcinolone cream is a “synthetic glucocorticoid used in replacement therapy for adrenocortical
insufficiency and as an anti-inflammatory and immunosuppressant in a wide variety of disorders.”
Dorland’s at 1959.
7 Betamethasone dipropionate is “used topically for the relief of inflammation and pruritus in corticosteroid-
responsive dermatoses.” Dorland’s at 211.
8 Macular pertains to “macules.” A macule is “a discolored skin lesion that is not elevated above the
surface.” Dorland’s at 1094.
9 See supra, note 4 (defining pruritic).
4

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 5 of 34
minimally raised, erythematous,10 maculopapular11 rash.” Id. at 16. The visit record noted that the
areas on Petitioner’s abdomen and back were “more coalesced into a larger collection of lesions.”
Id. There were smaller, more isolated patches on her legs. Id. Petitioner was diagnosed with
“likely” viral exanthem12 and prescribed hydroxyzine13 and prednisone.14 Id. Petitioner indicated
that she had used hydroxyzine in the past and was more comfortable with it than prednisone, which
she would “hold off on.” Id. There are no filed medical records documenting any treatment for
Petitioner between April 16, 2016, and August 28, 2016.
On August 29, 2016, Petitioner sought treatment from dermatologist Dr. Robert
Aylesworth and his physician’s assistant, Stephanie Keller, for a five-month history of “a rash to
the chest and flanks.” Pet’r’s Ex. 4 at 1, ECF No. 7-4. Petitioner reported that her symptoms
“started out with a viral URI that her entire family had[,] and many family members ended up with
a rash.” Id. Her family members’ rashes quickly resolved, but hers lasted “[six to eight] weeks,
[went] away, then [came] back,” though “[e]ach recurrence [wa]s less bothersome than the
previous.” Id. Petitioner had self-treated unsuccessfully with topical steroids, Benadryl,15 and
Atarax.16 Id. She reported a history of psoriasis.17 Id. Dr. Aylesworth assessed Petitioner with
dermographism18 and recommended a biopsy. Id. Petitioner refused the procedure and wanted to
rely on Zyrtec.19 Id. Dr. Aylesworth prescribed 10 mg tablets, twice daily. Id.
On November 7, 2016, Petitioner received another flu vaccine, mandated by her employer.
Pet’r’s Ex. 1 at 1. Petitioner did not file records documenting any care between November 8, 2016,
and June 14, 2017.
10 Erythematous refers to skin reddening due to the accumulation of blood in dilated capillaries, as in
inflammation; a rash. Dorland’s at 643.
11 Maculopapular is “characterized by both macules and papules.” Dorland’s at 1095.
12 Viral exanthem is a skin rash related to a viral infection. Dorland’s at 656.
13 Hydroxyzine is an antihistamine. Dorland’s at 884. The term “antihistamine” can “broadly include any
agent that blocks any histamine receptor, in practice it is usually used to denote those blocking H receptors
1
(H1 receptor antagonists), which are the drugs conventionally used to treat allergic reactions and are also
components of many cough and cold preparations.” Id. at 107.
14 Prednisone is a “synthetic glucocorticoid derived from cortisone; used as an anti-inflammatory and
immunosuppressant in a wide variety of disorders.” Dorland’s at 1509.
15 Benadryl is the trademark preparation of diphenhydramine hydrochloride, which is “used for the
symptomatic treatment of allergic symptoms[.]” Dorland’s at 208, 523.
16 Atarax is the trademark preparation of hydroxyzine hydrochloride. Dorland’s at 170. Hydroxyzine
hydrochloride is an antianxiety agent used in the manifestations of allergic dermatoses. Id. at 884.
17 Psoriasis refers to “any of a group of common chronic, squamous dermatoses with variable symptoms
and courses; some are inherited. Principal histologic findings are [] microabscesses and [] pustules; also
seen are rounded, circumscribed, erythematous, dry, scaling patches of various sizes, covered by gray,
silvery, or white, umbilicated, lamellar scales. The most common sites are extensor surfaces, nails, scalp,
genitalia, and the lumbosacral region.” Dorland’s at 1547.
18 Dermographism is “a type of physical urticaria in which moderately firm stroking or scratching of the
skin with a dull instrument produces a wheal with a red flare on each side.” Dorland’s at 499.
19 Zyrtec is the “trademark for preparations of cetirizine hydrochloride.” Dorland’s at 2097. Cetirizine
hydrochloride is a nonsedating antihistamine used in the treatment of allergies. Id. at 334.
5

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 6 of 34
Petitioner returned to Dr. Aylesworth on June 15, 2017, complaining of “itchy, red bumps
all over her entire body,” and she explained that topical steroids and antihistamines had not been
helpful. Pet’r’s Ex. 4 at 2. Petitioner stated that her “condition ha[d] been present since Fall [of]
2015, and her current flare ha[d] been present since Feb[ruary of] 2017.” Id. She continued that it
“ha[d] become more severe each time she ha[d] a flu shot and when she has gotten a cold.” Id.
Petitioner reported that the rash had changed from “a fine, faint rash and is now multiplied and
increased in size. It bleeds from scratching.” Id. Petitioner rarely used Zyrtec because it “made her
very sleepy.” Id. She stated that she used “betamethasone [dipropionate] twice daily which
help[ed] a bit.” Id. Upon exam, Dr. Aylesworth noted “[s]oft, small[,] enlarged nodes to axilla and
crural folds[, and r]ed, eroded papules20 up to 1.5cm in size . . . scattered to [Petitioner’s] chest,
axilla, arms, and legs.” Id. Dr. Aylesworth listed Petitioner’s clinical diagnosis as “[n]eoplasm21
of uncertain behavior” and noted to “[rule out pityriasis lichenoides et varioliformis acuta
(“PLEVA”)22 versus cutaneous T-cell lymphoma].”23 Id. He prescribed triamcinolone cream. Id.
The same day, Dr. Aylesworth ordered a skin biopsy. Id. at 3. Dermatopathologist Dr. Seun
L. Kim performed a biopsy on June 17, 2017. Id. at 31. The biopsy results revealed “mild compact
hyperkeratosis24 and mild mounding parakeratosis[.]”25 Id. at 30. There was evidence of
“equivocal focal spongiosis26 with associated occasional intraepidermal lymphocytes.” Id. Tissue
staining showed numerous small T-cells that “favor[ed] a reactive pattern.” Id. at 6, 30. Dr. Kim’s
surgical pathology report listed Petitioner’s diagnosis as “[p]alisaded interstitial histiocytic
dermatitis27 with increased dermal mucin.”28 Id. at 31. He added in the comments that “[t]he
histology is favored to represent a palisaded and necrobiotic granulomatous dermatitis,29 most
likely [GA] given the associated increased mucin.” Id.
20 See supra, note 3 (defining papules).
21 Neoplasm is “any new and abnormal growth; specifically[,] a new growth of tissue in which the growth
is uncontrolled and progressive[.]” Dorland’s at 1239.
22 PLEVA is “an acute or subacute, sometimes relapsing, widespread macular, papular, or vesicular eruption
that tends to crusting, necrosis, and hemorrhage, which heals to leave pigmented depressed scars, followed
by a new crop of lesions.” Dorland’s at 1451.
23 Cutaneous T-cell lymphoma is “a group of lymphomas including a spectrum of disorders, all of which
exhibit both clonal expansion of malignant T lymphocytes and malignant infiltration of the skin. The
lymphocytes have been arrested at varying stages of differentiation into helper cells, and skin infiltration is
often the chief or only manifestation of disease.” Dorland’s at 1086. Lymphoma is any neoplastic disorder
of the lymphoid tissue; also called a malignancy. Id.
24 Hyperkeratosis is also known as a callus. Dorland’s at 890.
25 Parakeratosis refers to the “persistence of the nuclei of the keratinocytes into the stratum corneum[.]”
Dorland’s at 1376. A keratinocyte is an epidermal cell that synthesizes keratin. Id. at 979. Keratin is a
scleroprotein that makes up the constituents of the epidermis, hair, nails, and other tissues. Id. The stratum
corneum is the outermost layer of the epidermis, consisting of cells that are dead. Id. at 1779.
26 Spongiosis refers to the “intercellular edema of the epidermis, giving the tissue a spongelike appearance
due to the formation of microvesicles.” Dorland’s at 1755.
27 Palisaded interstitial histiocytic dermatitis can be defined as follows: palisaded refers to “the arrangement
of cells or cellular structures side by side in rows, like pickets in a fence[.]” Dorland’s at 1365. Interstitial
dermatitis or interstitial granulomatous dermatitis is “a rare skin condition that presents with erythematous
and violaceous plaques, and may be associated with pruritus and pain.” See Z. Ahmed et al., Interstitial
granulomatous dermatitis successfully treated with etanercept, 15 AM. J. CASE REP. 94–96 (2014).
28 Dermal mucin refers to the most abundant macromolecules in mucus. Dorland’s at 1185.
29 See supra, notes 3, 27 (defining necrobiosis and palisaded and granulomatous dermatitis).
6

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 7 of 34
On June 30, 2017, Petitioner returned to Dr. Aylesworth and explained that she had a “flu
vaccine and viral illness since [her] last visit and feels much worse now. The condition remains
unchanged.” Id. at 6. An examination revealed red papules with erosions on Petitioner’s back and
chest. Id. Dr. Aylesworth diagnosed Petitioner with GA, administered a Kenalog injection,30 and
ordered testing for an underlying autoimmune disease. Id. Testing for rheumatoid factor,31 Lyme
disease,32 and Sjögrens antibodies33 was negative. Id. at 28. An anti-nuclear antibody (“ANA”)34
screening was also negative. Id. During a return visit to Dr. Aylesworth on July 19, 2017, Petitioner
reported improvement following the Kenalog injection, and she was prescribed methotrexate.35 Id.
at 8. Petitioner’s records show that she improved with methotrexate but suffered a flare whenever
she became ill with a viral infection. See id. at 9–10. In October of 2017, Petitioner obtained a note
from Dr. Aylesworth that stated a flu vaccine can induce a flare of GA, and this was “likely to be
the case w[ith] this patient.” Pet’r’s Ex. 5 at 3, ECF No. 7-5.
Thereafter, Petitioner continued to take methotrexate for her skin condition through
October of 2018. Pet’r’s Ex. 12 at 1, ECF No. 22-1. During a visit with Dr. Aylesworth on January
4, 2019, Petitioner stated that when she stopped her medication, her condition “worsened a bit,”
but that she did not feel the need to restart any medication and was only rarely applying steroid
cream. Id. During a return visit to Dr. Aylesworth on March 27, 2019, Petitioner was noted to be
stable with only occasional “red spots” that she treated with steroid cream. Id. at 2. Petitioner has
not filed additional medical records.
30 A Kenalog injection refers to the trademark preparation of triamcinolone acetonide, which is used “as an
antiinflammatory and immunosuppressant in a wide variety of disorders[,]” including allergies and asthma.
Dorland’s at 978, 1959.
31 Rheumatoid factor refers to “antibodies directed against antigenic determinants, i.e., Gm, in the Fc region
of the IgG class of immunoglobulins . . . . Rheumatoid factors may be of the IgM, IgG, or IgA classes of
immunoglobulins[.]” Dorland’s at 676.
32 Lyme disease is “a recurrent, multisystemic disorder caused by the spirochete Borrelia burgdorferi;
vectors for human infection are the ticks Ixodes scapularis and I. pacificus. It begins in most cases with
erythema chronicum migrans (at least 5 cm in diameter), often accompanied by fatigue, malaise, chills,
fever, headache, and regional lymphadenopathy, followed after several weeks or months by highly variable
manifestations that may include musculoskeletal pain, involvement of the heart and the nervous system,
and conjunctivitis and other eye abnormalities. Persistent infection, which may last for months or years, is
characterized by arthritis of large joints and, in some cases, neurologic manifestations, including chronic
axonal polyneuropathy, ataxia, and spastic paraparesis.” Dorland’s at 538.
33 Sjögren’s antibodies are immunoglobulins specific to that disease. Dorland’s at 100. Sjögren’s 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 rheumatoid
arthritis but sometimes systemic lupus erythematosus, scleroderma, or polymyositis. An abnormal immune
response has been implicated.” Id. at 1848.
34 ANAs are “antibodies directed against nuclear antigens; ones against a variety of different antigens are
almost invariably found in systemic lupus erythematosus and are frequently found in rheumatoid arthritis,
scleroderma (systemic sclerosis), Sjögren syndrome, and mixed connective tissue disease. Antinuclear
antibodies may be detected by immunofluorescent staining. Serologic tests are also used to determine
antibody titers against specific antigens.” Dorland’s at 101.
35 Methotrexate is a folic acid antagonist used as an “antipsoriatic and antiarthritic in the treatment of severe,
recalcitrant, disabling psoriasis and severe rheumatoid and psoriatic arthritis.” Dorland’s at 1151.
7

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 8 of 34
b. Affidavits
i. Petitioner’s First Affidavit
Petitioner filed her first affidavit on June 5, 2018, and provided a chronology of the
progression of her condition post vaccination. Pet’r’s Ex. 2 at 1, ECF No. 7-2. At the time of both
flu vaccinations at issue, Petitioner was employed as an operating room registered nurse. Id.
Seasonal flu vaccinations were a mandatory condition for her continued employment. Id. Petitioner
stated that “gradually beginning approximately two to three weeks” following her November 9,
2015 flu vaccination, Petitioner “notice[d] that [her] skin had become very pruritic.” Id. The
itching “worsened to the point that [Petitioner] could not wear anything tight.” Id. She added that
“scratching made the itching worse,” although she “did not notice any rashes or lesions.” Id. In
March of 2016, Petitioner “contracted a cold and [her] skin erupted in a fine, extremely itchy rash.”
Id.
The itching continued, and Petitioner “could[ not] sleep at night.” Id. at 2. She stated that
“[a]nything that touched [her] skin would exacerbate [the itching] to the point [she] would be in
tears.” Id. at 1. Petitioner used home remedies, including “baking soda baths, oatmeal baths, topical
steroids, Benadryl, hydroxyzine, Claritin,36 elimination diets, calamine lotion, and aloe vera[,]”
without success. Id. at 2. Approximately one month later, Petitioner went to seek medical treatment
at urgent care and was prescribed hydroxyzine and oral prednisone. Id. She “did not take the
prednisone at first, and the hydroxyzine did not help with either the rash or the itching.” Id.
Petitioner did not see a dermatologist until August of 2016, noting that “there [wa]s only
one dermatologist covering the entire northern Wisconsin region, and appointments [we]re booked
out for months.” Id. At that time, according to Petitioner, her “rash was in remission, although
there were still some small affected areas.” Id. Petitioner noticed that her “skin would break out
whenever [she] contracted a virus.” Id.
Petitioner stated that at the time of her November 7, 2016 flu vaccination, she “was
recovering from a virus, and [her] skin was badly broken out and very pruritic.” Id. at 1–2. Despite
her condition, Petitioner was ordered to “take the vaccine or [she would] get fired.” Id. at 3. She
stated that following her vaccination, she “again broke out worse than [she] ever had[,]” including
with lesions that “have not abated[.]” Id. Eventually, the lesions “became disfiguring, leaving
scars.” Id. Petitioner noted that her “coworkers were shocked at the state of [her] skin.” Id. She
continued that she “never missed work,” but “[t]here were many times that [she] had to be excused
from [her] duties because [she] was so miserable that [she] would dissolve into tears.” Id.
When medical treatment did nothing to alleviate the itching, Petitioner “tried alternative
methods, such as acupressure, acupuncture, a vegan diet, tanning, and again did not receive any
relief.” Id. Petitioner sought out another dermatologist and was diagnosed with “interstitial
granulomatous dermatitis, a form of [GA].” Id. After steroids did not help, Petitioner stated that
she was prescribed methotrexate, which “did help to mitigate the symptoms, [but did] not
alleviat[e] them all together.” Id.
36 Claritin refers to the trademark preparation of loratadine, which is a nonsedating antihistamine. Dorland’s
at 368, 1074.
8

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 9 of 34
This condition has affected Petitioner’s ability to show affection to family members
because physical contact is “unbearable.” Id. at 4. Her hair is thinning, and she takes uncomfortably
cold showers to relieve the itching. Id. In an unsuccessful effort to reduce stress and achieve
remission, Petitioner retired from her job in January of 2018. Id. Petitioner “realized that this very
well may be a lifelong condition.” Id. She stated in her affidavit that she “truly believe[s] that the
flu vaccine [she] received on November 9, 2015, caused [her] injuries.” Id. at 5.
ii. Petitioner’s Second Affidavit
Petitioner filed a second affidavit “as a response to the Respondent’s Rule 4(c) Report.”
Pet’r’s Ex. 13 at 1. Petitioner acknowledged that she “had skin issues in the past, but never of the
severity that [she] had after the [November 9, 2015] flu vaccine, and not the same type.” Id. She
identified those “previous skin issues [as] eczema or contact dermatitis that were easily treated
with topical creams.” Id. She explained that “[t]he lesions [she] developed after the flu vaccines
were entirely different and debilitating, and nothing worked to treat it except methotrexate and
time.” Id.
Petitioner acknowledged that there were long periods of time during which she did not seek
medical treatment, even as her itching was described as “unbearable” and “bringing her to tears.”
Id.; see also Pet’r’s Ex. 2 at 1–2. Petitioner blamed her high insurance deductibles and copays as
contributing factors to her delay in seeking treatment. Pet’r’s Ex. 13 at 1. She explained that
“[a]nother factor that contributed to the lag in the early symptoms and the [first post-vaccination]
office visits” was a lack of dermatologists in the area and that she had “an excruciatingly long wait
to receive an appointment.” Id. at 2. Petitioner asserted that treaters at the urgent clinic also
misdiagnosed her condition when she sought treatment there “in the spring of 2016.” Id. Petitioner
noted “[t]hey were not doctors, they were physicians’ assistants.” Id. Petitioner maintained that
she was healthy pre vaccination and asserted “[t]he absence of medical records for long periods of
time indicates that [she] indeed did have an abrupt change in condition after the [November 9,
2015] flu vaccine.” Id. at 1.
Petitioner stated that the reaction that she had following her receipt of the flu vaccination
in November of 2016 is what helped her realize “the [November 2015] flu vaccine had caused
[her] problem.” Id. at 2. Petitioner asserted that “in autoimmune disorders of this type, sometimes
at the beginning of the symptoms, no one really knows what caused it.” Id. at 3. She admitted that
“she did not [know] either until [she] received the second flu vaccine [in November of 2016] and
[her symptoms] became so much worse and she thought back and remembered the timeline of
[her] symptoms[]” as dating back to her November 9, 2015 flu vaccine. Id.
iii. Affidavit of Peggy Bessette
Ms. Bessette was a colleague of Petitioner’s who provided an affidavit describing
Petitioner’s symptoms following her November 9, 2015 vaccination. Pet’r’s Ex. 50, ECF No. 33-
1. Ms. Bessette stated that Petitioner “developed a rash covering a large portion of her torso and
upper and lower extremities.” Id. at 1. Ms. Bessette noted that the rash “appeared as small,
reddened, raised bumps and was so numerous in number that in places it appeared as large[,]
reddened blotches.” Id. Petitioner reported to Ms. Bessette that the rash was “extremely
9

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 10 of 34
uncomfortable,” and that Petitioner “would have long scratch marks on her body that would be
open and bleeding” from the itching. Id. According to Ms. Bessette, the rash “lasted well over a
year and was still present when [Ms. Bessette] terminated [her] employment.” Id. She noted that
“[n]othing [Petitioner] tried brought her relief from this debilitating rash and itch.” Id.
c. Additional Filed Evidence37
i. Emailed Communications
On November 14, 2016, Petitioner sent an email to Cynthia Vogelsang, her employee
health and safety nurse. Pet’r’s Ex. 5 at 1. Petitioner wanted it “on record that [she] had a severe
reaction after the influenza vaccine [she] received on Monday, November 7[, 2016].” Id. Petitioner
noted that she “already had an existing viral rash from a recent URI, and after the vaccine it [was]
exacerbated to the point that the itching was agonizing for the rest of the week and weekend.” Id.
She described unbearable itching but explained she “ha[d] not seen anyone about it, because [she
would] not be working [at the same medical facility] next year when the vaccines are being given,
so that ma[de] it a waste of time.” Id.
ii. Employee Records
On August 3, 2017, Petitioner filed an injury/illness report with her employer claiming that
she suffered a reaction to the flu vaccine in 2015. Pet’r’s Ex. 11 at 312. Petitioner admitted that
she did not initially realize the cause of her condition. Id. She stated that she developed an itchy
rash that “got worse with each exposure to a virus.” Id. Following another flu vaccine in 2016,
Petitioner stated that she got worse because “she was thereafter misdiagnosed by two doctors and
now sees Dr. Aylesworth.” Id. She explained that she has a rare skin condition and that while little
is known about her condition, it is triggered by vaccines. Id.
Petitioner’s employer denied her request for a medical exemption to the mandatory
seasonal flu vaccination on September 28, 2017. Pet’r’s Ex. 5 at 4. The employee health manager
explained that “[i]nfluenza exemptions are reviewed using the [CDC] guidelines for
contraindications.” Id. After review, “it [was] determined that [Petitioner did] not have a
contraindication to receiving the influenza vaccine.” Id. Petitioner submitted a letter of resignation
on November 6, 2017, and stated that her last day would be January 3, 2018. Pet’r’s Ex. 11 at 12.
iii. Photographs
37 Petitioner filed medical and scientific literature in this case, but not every filed item factors into the
outcome of this Decision. While I have reviewed all the medical literature submitted in this case, I refer
only to those articles that are most relevant to my determination and/or are central to Petitioner’s case—
just as I have not exhaustively discussed every individual medical record filed. Moriarty v. Sec’y of Health
& Hum. Servs., 844 F.3d 1322, 1328 (Fed. Cir. 2016) (“We generally presume that a special master
considered the relevant record evidence even though he does not explicitly reference such evidence in his
decision.”) (citation omitted); see also Paterek v. Sec’y of Health & Hum. Servs., 527 F. App’x. 875, 884
(Fed. Cir. 2013) (“Finding certain information not relevant does not lead to—and likely undermines—the
conclusion that it was not considered.”).
10

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 11 of 34
On November 30, 2018, Petitioner filed three sets of photos with hand-written notations
that they were taken in April 2016, May 2017, and March 2018, respectively. See Pet’r’s Ex. 11.
The first two photos depict one extremity (not identified) and the lower abdomen. Id. The
annotations are the same on both and state, “taken in April of 2016,” and “skin after flu vaccine in
2015.” Id. at 1–2. The clarity is poor, but there appears to be some discoloration on the skin
consistent with a rash that is maculopapular. Id. The next three photos are of Petitioner’s abdomen
and a side view of her torso. Id. at 3–5. The notations on these photos state they were “taken in
May of 2017” and depict “skin after flu vaccine in 2016.” Id. These images better illustrate the
redness of the rash and the individual nodules, which were widespread. Id. The last two photos are
of the front and back of Petitioner’s torso taken of the “skin in [March of] 2018 after halving
[Petitioner’s] dose of methotrexate.” Id. at 6–7. The notes accompanying these photos also state
that the lesions had returned and that there was scarring. Id. There is a marked lessening in severity
in these last two photos. See id.
d. Expert Reports
i. Petitioner’s Expert, Dr. Steven Rostad
Petitioner filed an expert report authored by Dr. Steven Rostad. Pet’r’s Ex. 14, ECF No.
27-1. Dr. Rostad is “a pathologist, board-certified in anatomic and neuropathology and a Fellow
of the College of American Pathologists.” Id. at 1. He received his B.A., magna cum laude, from
Harvard College in 1978 and his medical degree from the University of Washington in 1983.
Pet’r’s Ex. 15 at 1–2, ECF No. 28-1. Dr. Rostad completed a fellowship in neuropathology,
followed by a residency in anatomical pathology at the University of Washington. Id. at 1. He then
began his thirty-year practice as a neuropathologist with Swedish Medical Center and as an
anatomic pathologist with CellNetix Pathology. Id. Retired since 2018, Dr. Rostad “currently
review[s] consultations predominantly of a medical-legal nature.” Pet’r’s Ex. 14 at 1. In the past
five years, he has “provided expert testimony in approximately [twelve] cases,” including
“approximately [six] medico-legal cases and given testimony in [three].” Id. at 2. Dr. Rostad
admitted that he has “not directly treated patients with skin problems,” but he “routinely . . .
evaluated tissue samples for skin issues, including inflammatory problems.” Id. at 1. He has seen
hundreds of GA cases over his career and “is qualified to address the pathologic criteria.” Id. Dr.
Rostad also noted that he has not published on GA but has “attended multiple conferences, which
have discussed skin disorders in general and this topic in particular, along with its differential
diagnosis.” Id. He has published in topics including temporal lobe seizures, the varicella-zoster
virus, with a focus in AIDS patients, pituitary adenoma pathogenesis, and breast tissue DNA.
Pet’r’s Ex. 15 at 3–6.
After a discussion of Petitioner’s medical history, Dr. Rostad “concu[rred] with the
excellent workup, [GA] diagnosis[,] and comments outlined in Dr. Kim’s [surgical pathology]
report.” Pet’r’s Ex. 14 at 7. In support of Petitioner’s GA diagnosis, Dr. Rostad highlighted “the
presence of palisading dermal histocytes/macrophages (granulomas) with associated necrobiosis.”
Id. He also thought Dr. Kim’s “concern for an infectious etiology” was appropriate. Id. According
to Dr. Rostad, a review of Petitioner’s histologic evaluation showed a “reduce[d] possibilit[y] of
acid-fast and fungal infections.” Id. He opined that “[t]he histologic findings are not those of a
contact or allergic dermatitis, which had been considered in her past medical history.” Id. Also,
11

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 12 of 34
Dr. Rostad concluded that PLEVA was adequately considered but not diagnosed. Id. Without
further comment, Dr. Rostad added that other rheumatological conditions “were apparently not
considered likely as they were not discussed” by Petitioner’s treaters. Id.
Dr. Rostad defined GA as a “noninfectious granulomatous disease of the skin . . . typically
characterized by an annular38 arrangement of erythematous to flesh-colored papules.” Id. This is
supported by Dr. Peggy Cyr’s article, Diagnosis and Management of Granuloma Annulare.39
Pet’r’s Ex. 17, ECF No. 28-3. Dr. Cyr noted that “[d]espite the dramatic appearance of this
cutaneous eruption, it generally is asymptomatic; however, there may be some mild pruritus.” Id.
at 1. Petitioner filed Pruritus40 by Dr. Scott Moses, which describes the symptom as “a common
manifestation of dermatologic disease.” Pet’r’s Ex. 24 at 1, ECF No. 28-10. Dr. Moses explained
that “[a] single mechanism cannot explain all causes of pruritus.” Id. However, he listed several
dermatological causes, exposure-related causes, and pregnancy-related causes. See generally id.
Dr. Moses also identified systemic causes of pruritus, including lymphoma,41 HIV, anemia,42
cancers, parasitic infections, viral infections, neuropathy,43 and scleroderma.44 Id. at 4.
Dr. Rostad continued that GA can be generalized, patchy/macular, subcutaneous, or
perforating. Pet’r’s Ex. 14 at 8. He opined that Petitioner developed generalized granuloma
annulare (“GGA”), “consisting of hundreds of papules that are either discrete or confluent, but
typically do not show any annular arrangement.” Id. Dr. Cyr explained in her article that GA is
most commonly localized and self-limited, while disseminated GGA is widespread. Pet’r’s Ex. 17
at 1. Dr. Cyr also noted that “[t]he cause of [GA] is unknown but it has been reported to follow
trauma, malignancy, viral infections,45 insect bites, and tuberculosis skin46 tests.” Id. In these
cases, “a delayed-type hypersensitivity reaction and cell-mediated immune response are
hypothesized.” Id. Dr. Rostad expanded on Dr. Cyr’s list and asserted that GA “has been linked to
trauma, animal or insect bites, vaccinations, drugs, sun exposure, tuberculosis, various viral
infections[,] and chronic stress.” Pet’r’s Ex. 14 at 8.
38 Annular means shaped like a ring; circular. Dorland’s at 94.
39 P. R. Cyr, Diagnosis and Management of Granuloma Annulare, 74(10) AM. FAM. PHYS. 1729–35 (2006).
40 S. Moses, Pruritis, 68(6) AM. FAM. PHYS. 1135–43 (2003).
41 See supra, note 23 (defining lymphoma).
42 Anemia is “a reduction below normal in the concentration of erythrocytes or hemoglobin in the blood,
measured per mm3 or by volume of packed red cells per 100 mL of blood; it occurs when the equilibrium
is disturbed between blood loss (through bleeding or destruction) and blood production.” Dorland’s at 78.
43 Neuropathy is “a functional disturbance or pathologic change in the peripheral nervous system,
sometimes limited to noninflammatory lesions as opposed to those of neuritis[.]” Dorland’s at 1268.
44 Scleroderma is “chronic hardening and thickening of the skin[.]” Dorland’s at 1679.
45 Dr. Cyr listed HIV, Epstein-Barr virus, and herpes zoster as viruses that have been associated with the
development of GA. Pet’r’s Ex. 17 at 1.
46 Tuberculosis refers to “any of the infectious diseases caused by species of Mycobacterium and
characterized by tubercle formation with caseous necrosis in the tissues . . . . Any organ may be affected,
but in humans the lung is the major seat of the disease [] and is the usual portal of entry into the body.”
Dorland’s at 1979.
12

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 13 of 34
Petitioner filed several articles that discussed GA generally and its pathology. The De Paola
et al.47 article described GA as one of “a broad group of distinct reactive inflammatory conditions.”
Pet’r’s Ex. 16 at 1, ECF No. 28-2. The authors noted that GA “is a benign, self-limiting, relatively
common dermatosis” and has “significant associations with systemic diseases.” Id. The cause is
unknown, but GA “has been reported following traumas, malignancy, viral infections, insect bites,
and tuberculosis skin tests.” Id. Although the authors reiterated that “[t]he pathogenesis of GA
remains still obscure[, p]ossible pathogenetic factors suggested include humoral and delayed type
hypersensitivity, vascular damage, metabolic disorder, or primary collagen48 and/or elastin49
alteration mediated through an immunologic mechanism.” Id. Piette and Rosenbach50 began their
article by noting that there are “a number of hypotheses regarding the underlying etiology of GA;
however, most of these hypotheses are supported by relatively limited evidence.” Pet’r’s Ex. 57 at
1, ECF No. 53-2; see also Resp’t’s Ex. A, Tab 12, ECF No. 56-13. The authors acknowledged
associations between GA and some systemic diseases and vaccinations. Pet’r’s Ex. 57 at 5.
Specifically, they identified case studies involving the Bacillus Calmette-Guérin (“BCG”)51
vaccine, hepatitis B, tetanus, and diphtheria vaccines. Id.
While acknowledging that “[t]he trigger for the development of GA is unknown,” Dr.
Rostad stated it is one of three types of abnormal immune responses: “overactive (i.e.
hypersensitivities), ineffective (immunodeficiency)[,] and inappropriate (autoimmunity).” Pet’r’s
Ex. 14 at 8. Specifically, he explained that GA is “a lymphocyte-mediated hypersensitivity type
IV mechanism, or delayed type hypersensitivity (“DTH”) reaction.” Id. The Vaillant and
Ramphul52 article explained that a “[g]ranulomatous-type hypersensitivity results from the
persistence within macrophages of intracellular pathogens or other substances that the cell is
unable to process or destroy.” Pet’r’s Ex. 23 at 2, ECF No. 28-9. The “histology shows a typical
epithelioid-cell granuloma” with visible, giant cells “in the center of the lesion, [and] surrounded
by a cuff of lymphocytes.” Id. at 3. Dr. Rostad asserted that the presence of activated CD4+ T-
helper cells is evidence of an immune process. Pet’r’s Ex. 14 at 8. He noted that “[i]t is thought
that GA is a DTH reaction to primary collagen or elastin destruction.” Id. Collagen destruction
occurs when macrophages within the lesions release proinflammatory cytokines. Id. The most
important cytokines being “[tumor necrosis factor (“TNF”)]-alpha and beta IL-2, and
[granulocyte-macrophage colony-stimulating factor] (“GM-CSF”).” Id.
Dr. Rostad cited the Lynch and Barrett53 study that explains this phenomenon. Pet’r’s Ex.
22, ECF No. 28-8. The study stated that altered collagen is thought to be an antigenic trigger that
47 M. De Paola et al., Granuloma Annulare, Autoimmune Thyroiditis, and Lichen Sclerosus in a Woman:
Randomness or Significant Association?, 2013 CASE REP. DERMATOL. MED. 1–4 (2013).
48 Collagen is “any of a family of extracellular, closely related proteins occurring as a major component of
connective tissue, giving it strength and flexibility.” Dorland’s at 384.
49 Elastin is “a scleroprotein that is the essential constituent of elastic connective tissue.” Dorland’s at 598.
50 E.W. Piette & M. Rosenbach, Granuloma annulare: Pathogenesis, disease associations and triggers,
and therapeutic options, 75 J. AM. ACAD. DERMATOL. 467–79 (2016).
51 The Bacillus Calmette-Guérin vaccine “is administered by scarification or intradermal or intracutaneous
injection to tuberculin-negative individuals for prevention of tuberculosis.” Dorland’s at 190.
52 ANGEL A. JUSTIZ VAILLANT & KAMLESHUN RAMPHUL, DELAYED HYPERSENSITIVTY REACTIONS 1–8
(StatPearls eds., 2022).
53 J. M. Lynch & T.L. Barrett, Collagenolytic (necrobiotic) granulomas: part 1 – the ‘blue’ granulomas,
31 J. CUTAN. PATHOL. 353–61 (2004).
13

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 14 of 34
attracts T-helper (“Th”) cells, which then release proinflammatory cytokines. Id. at 3. The Th cells
“also secrete macrophage-inhibiting factors, causing macrophages to persist in the area.” Id. The
authors contend that the apoptotic54 macrophages in the lesion are evidence of a DTH reaction that
incites macrophages. Id. The lesions are self-limiting because cell destruction “is controlled by
activation-induced apoptosis in lymphocytes and macrophages.” Id. In GGA cases, “lesions have
palisading granulomas” with “[t]hick and multilayered basal lamina around lesional capillaries
[that suggest] a more pronounced immune reaction is responsible.” Id. at 4. In Vaccine-associated
Hypersensitivity,55 authors McNeil and DeStefano discussed the effects of this type of immune
system stimulus. Pet’r’s Ex. 48, ECF No. 31-4. They noted that “[l]arge local vaccine reactions
secondary to T-cell infiltration are often associated with prolonged and very effective immunity.”
Id. at 2. The reactions are described as “self-limiting conditions that do not contraindicate
administration of future doses (e.g., booster doses) of the same vaccine.” Id.
Other biological mechanisms for GA following cancer treatment mentioned briefly in Dr.
Rostad’s report include a “reaction to a vaccine immunotherapy for metastatic melanoma,” and
check point inhibitors that “block the inhibitory signal of CD4+ Th1 cells.” Pet’r’s Ex. 14 at 13
(citing Pet’r’s Exs. 43–44, ECF Nos. 30-9–30-10).56 This disruption “subsequently lead[s] to T
cell activation and proliferation, resulting in aggregation and activation of macrophages, i.e.[,]
granuloma formation.” Id.
Dr. Rostad further relied on the Vaillant and Ramphul article in support of his assertion
that this type of DTH reaction (granulomatous) would appear approximately 21–28 days following
contact with the inducing antigen, as opposed to a contact or tuberculin reaction that would both
appear within 48 to 72 hours. Id. at 8 (citing Pet’r’s Ex. 23 at 1). He explained that the “[d]iseases
caused by DTH responses tend to be chronic, such as with leprosy,57 tuberculosis,
schistosomiasis,58 sarcoidosis[,]59 and Crohn’s disease.”60 Id. The McNeil and DeStefano article
also provided an appropriate temporal relationship between a vaccine and DTH reaction. See
Pet’r’s Ex. 48. The authors stated that “[d]elayed-type reactions occur commonly within hours or
days after exposure, although symptom onset can be delayed up to [two to three] weeks.” Id. at 2.
54 Apoptotic or apoptosis refers to the “morphologic pattern of cell death affecting single cells,” marked by
shrinkage of the cell; “a mechanism for cell deletion in the regulation of cell populations[.]” Dorland’s at
118.
55 M. McNeil & F. DeStefano, Vaccine-associated hypersensitivity, 141 J. ALLERGY CLIN. IMMUNOL. 463–
72 (2018).
56 A. Aria et al., Chronic granulomatous reaction in patients receiving vaccine immunotherapy for
metastatic melanoma, 4 JAAD CASE REPS. 87–90 (2018); J. Wu et al., Granuloma annulare associated
with immune checkpoint inhibitors, 32(4) J. EUR. ACAD. DERMATOL. VENEREOL. 124–30 (2018).
57 Leprosy is “a slowly progressive, chronic infectious disease caused by Mycobacterium leprae and
characterized by granulomatous or neurotrophic lesions in the skin, mucous membranes, nerves, bones, and
viscera, with a broad spectrum of clinical symptoms.” Dorland’s at 1022.
58 Schistosomiasis is an acute and chronic parasitic disease caused by blood flukes (trematode worms) “of
the genus Schistosoma.” Dorland’s at 1675.
59 Sarcoidosis is “a chronic, progressive, systemic granulomatous reticulosis of unknown etiology,
characterized by hard tubercles . . . . It can affect almost any organ or tissue, including the skin, lungs,
lymph nodes, liver, spleen, eyes, and small bones of the hands and feet.” Dorland’s at 1668.
60 Crohn’s disease is “one of the principal forms of inflammatory bowel disease, a chronic granulomatous
disease of the gastrointestinal tract of unknown etiology[.]” Dorland’s at 531.
14

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 15 of 34
According to Dr. Rostad, Petitioner’s “symptoms occurr[ed] within two-three weeks of the
November 2015 influenza [vaccine].” Pet’r’s Ex. 14 at 15. Dr. Rostad continued, “GGA or DTH
eventually presented [four] months post vaccination,” and “[t]his interval fits with more recent
experience with DTH reactions.” Id. He concluded that “[t]he 2016 flu vaccination caused
acceleration of [Petitioner’s] disease.” Id.
The logical sequence of cause and effect for Petitioner’s GA is summarized by Dr. Rostad
in five parts:
1) Petitioner’s health had been stable up until she received the 2015–2016 influenza
vaccination on November 9, 2015,
2) Antigen stimulation caused an immune response, noted within two-three weeks [post
vaccination], which most likely started locally, eventually became systemic in the form
of relentless itching,
3) The flu vaccine immune response, which began near the injection site, eventually
triggered a delayed systemic lymphocyte-mediated hypersensitivity type IV or DTH
response in the form of GA,
4) The GA and related symptoms progressed and were retriggered following additional
immune challenges, including upper respiratory infections and the 2016–2017 flu
vaccination,
5) Once powerful immune suppression and antigen containment were instituted, her
condition improved considerably.
Id. at 9. Dr. Rostad stated that his “theory is based on knowledge of the pathogenesis of DTH and
GA.” Id. at 15.
Dr. Rostad illustrated how Petitioner’s clinical presentation was consistent with his theory.
He noted that Petitioner’s first symptom (itching) “began gradually approximately two to three
weeks after receiving the November 2015 vaccine.” Id. at 9. Dr. Rostad noted that itchiness “is a
nonspecific clinical symptom, sometimes reported following vaccination.” Id. He added that “it is
a common finding with GA” but acknowledged that “[a] formal medical evaluation for her pruritus
was not obtained.” Id. He characterized Petitioner’s URI that occurred four months later, in March
of 2016, as an immune challenge causing her pruritic condition to progress to a rash. Id. He asserted
that “the rash and pruritus showed correlation with the initial vaccination and appeared to change
in relative intensity together[, meaning] it is most likely that they are manifestations of the same
disease, namely DTH (GA).” Id. Petitioner’s “more intense reactivation of her symptoms and DTH
(GA)” followed her November 7, 2016 vaccination. Id. His conclusion that Petitioner suffered “[a]
DTH-like reaction [] was supported by the histopathology and immunocytochemical biopsy
results.” Id. at 15.
A significant section of Dr. Rostad’s report then provided a detailed explanation of
“autoimmune diseases or autoimmune syndromes induced by adjuvants [(“ASIA”)].” Id. at 10. He
opined that “[v]accine antigens or adjuvants could have caused [ P]etitioner’s condition.” Id. He
stated that “the aluminum adjuvant literature shows overlap to those in [ P]etitioner’s case,
including the granulomatous, DTH-like histopathology, potential delayed time intervals between
vaccination and development of lesions, a weak association with autoimmune disease (as with
15

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 16 of 34
GA)[,] and the presence of systemic symptoms.”61 Id. Dr. Rostad admitted that “[t]he exact
allergen that triggered the proposed DTH reaction in [Petitioner] is unknown.” Id.
Dr. Rostad acknowledged that the “number of reports relating vaccines and GA is limited.”
Id. at 13. Dr. Rostad asserted, however, that GA “has been associated with vaccination and other
immune reactions.” Id. In support of this contention, Dr. Rostad noted “one case of GA following
influenza vaccination[]” and “[eleven] previous cases of GA following other vaccines.” Id. The
Suzuki et al.62 study examined the case of a 76-year-old woman “suffering from a tender
subcutaneous nodule on her left upper arm,” one month following an influenza vaccination in the
same arm. Pet’r’s Ex. 38 at 1, ECF No. 30-4. The authors suggested that a specific, unidentified
“vaccine antigen may evoke a T cell-mediated, granuloma-inducing immune reaction in
predisposed individuals.” Id. at 2. The patient in that case study had “diabetes mellitus,63 a disease
potentially promoting granuloma formation, such as necrobiosis lipoidica64 and GA[; therefore,
the patient] might [have] be[en] susceptible to vaccine-induced GA.” Id. The eleven cases that do
not involve the influenza vaccine include patients that range from infancy to 58 years old and
include hepatitis B, BCG, tetanus, diphtheria, and rubella vaccinations. Pet’r’s Ex. 40 at 3, ECF
No. 30-6.65 Three of the eleven patients were adults and experienced long-term skin rashes
following hepatitis B booster vaccinations. Id. The three adult patients included a 51-year-old with
resolution at four years and a 20-year-old that still had symptoms after one year. Id.
61 Petitioner’s expert spent several pages of his initial report explaining ASIA and asserting that ASIA was
the biological mechanism for Petitioner’s GA. In her reply brief to her motion for a ruling on the record,
however, Petitioner stated “adjuvants were not [P]etitioner’s expert’s theory in this case.” Pet’r’s Reply at
3. Furthermore, the ASIA theory has never been successfully asserted in the Program. See D’Angiolini v.
Sec’y of Health & Hum. Servs., 122 Fed. Cl. 86, 102 (2015) (upholding special master’s “determin[ation]
that ASIA does not provide[] a biologically plausible theory for recovery”), aff’d, 645 F. A'ppx. 1002 (Fed.
Cir. 2016); Garner v. Sec’y of Health & Hum. Servs., No. 15-063V, 2017 WL 1713184, at *8 (Fed. Cl.
Spec. Mstr. Mar. 24, 2017) (observing that the ASIA theory “is, at a minimum, incomplete and
preliminary—and therefore unreliable from an evidentiary standpoint”); Rowan v. Sec’y of Health &
Hum. Servs., No. 10-272V, 2014 WL 7465661, at *12 (Fed. Cl. Spec. Mstr. Dec. 8, 2014) (rejecting the
ASIA theory because it “is not a proven theory” and no “persuasive or reliable evidence” supports
it); Johnson v. Sec’y of Health & Hum. Servs., No. 10-578V, 2016 WL 4917548, at *7–*9 (Fed. Cl.
Spec. Mstr. Aug. 18, 2016) (rejecting a theory that “any adjuvant [is] capable of causing any autoimmune
disease,” finding it “overbroad, generalized, and vague, to the point that it could apply to virtually everyone
in the world who received a vaccine containing an adjuvant and then at some time in their lives developed
an autoimmune disease”). Therefore, a detailed discussion of this mechanism is not included in this
Decision.
62 T. Suzuki et al., Subcutaneous granuloma annulare following influenza vaccination in a patient with
diabetes mellitus, 32 DERMATOL. SINICA 55–57 (2014).
63 Diabetes mellitus is “an autoimmune disease that results in the destruction of beta cells of the pancreas,
leading to loss of the ability to secrete insulin.” Dorland’s at 506.
64 Necrobiosis lipoidica is “a degenerative disease of dermal connective tissue, characterized by
erythematous papules or nodules in the lower leg and sometimes elsewhere, forming shiny yellow to red
plaques that are covered with telangiectatic vessels and have a depressed center. More than half of affected
patients have diabetes mellitus, although the condition appears the same in both diabetic and nondiabetic
patients.” Dorland’s at 1234.
65 T. Nomiyama et al., Granuloma annulare-like reaction to the bacillus Calmette-Guerin vaccination, 54
AUSTRAL. J. DERMATOL. 4–7 (2013).
16

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 17 of 34
The Yang,66 Nomiyama et al.,67 and Lee et al.68 studies all contemplated GA following
receipt of the BCG vaccination. Pet’r’s Exs. 39–41, ECF Nos. 30-5–30-7. The Yang et al. study
involved a three-month-old infant “who developed a bacilli-containing granuloma over the
vaccination site and subsequent granuloma annulare-like eruptions over the arm and back.” Pet’r’s
Ex. 39 at 1. One month post vaccination, “[a] reddish papule” was noted at the injection site and
“gradually became an indurated nodule.” Id. The following month, “several scattered
erythematous papules and annular plaques developed.” Id. The patient’s “lesions came and went
for another [four] weeks and finally resolved completely with no further relapse over an 18-month
follow-up period.” Id. The other two articles also described infants who experienced a reaction at
the injection site, approximately one month post vaccination, followed by an eruption of lesions
all “over the body” during the second month post vaccination. Pet’r’s Ex. 40 at 1; Pet’r’s Ex. 41
at 1. With corticosteroid treatment, the lesions resolved after three and one months, respectively.
Pet’r’s Ex. 40 at 3; Pet’r’s Ex. 41 at 1. The multiple “reports of GA as a complication of BCG
vaccination” suggested to Dr. Rostad “that GA might occur in relation to the physical trauma of
vaccination or a cell-mediated delayed hypersensitivity reaction against a certain antigen of the
vaccine.” Pet’r’s Ex. 14 at 13. Dr. Rostad also referenced “extensive cutaneous granulomas”
following a live rubella virus vaccination. Id. (citing Pet’r’s Ex. 42, ECF No. 30-8).69
ii. Petitioner’s Expert, Dr. Richard Knierim
Dr. Knierim received his B.A., magna cum laude, from Columbia Union College in 1966,
and his medical degree from Loma Linda University in 1970. Pet’r’s Ex. 55 at 3, ECF No. 52-2.
He completed a residency in anatomic and clinical pathology at University of Washington
Affiliated Hospitals. Id. at 5. Up until approximately 2020, Dr. Knierim held board certifications
in both specialties. Id. He has also been board certified in cytopathology and dermatology. Pet’r’s
Ex. 54 at 2, ECF No. 52-1. Dr. Knierim has been a pathologist for Swedish Medical Center since
1990. Pet’r’s Ex. 55 at 1. He has also worked for CellNetix as a dermatopathologist and as a clinical
associate professor of pathology at the University of Washington School of Medicine. Id. He was
the chief of anatomic pathology for the Madigan Army Medical Center and the United States Army
Hospital in Okinawa, Japan. Id. at 3. Dr. Knierim stated in his written expert report that he “has
been mostly retired from the practice of pathology” since 2018. Pet’r’s Ex. 54 at 2. Dr. Knierim
noted that he has “not directly treated patients with skin problems.” Id. He expressed that he has
qualifications “to address the pathologic criteria of [GA], and ha[s] reviewed triggers associated
with the onset of GA.” Id.
In his report dated June 4, 2021, Dr. Knierim stated that he had reviewed Petitioner’s
medical records and sample slides, filed evidence, Dr. Rostad’s expert report, and Respondent’s
Rule 4(c) Report. Id. at 2–4. Dr. Knierim noted that Petitioner’s “skin lesions prior to November
2015 [are] not relevant.” Id. at 5. He opined that “[i]t is not at all surprising that a correct diagnosis
66 S. Yang & C. Chang, Bacilli-containing granuloma with subsequent granuloma annulare-like eruptions
following Bacillus Calmette-Guérin vaccination, 59 PED. & NEONATOL. 525–26 (2018).
67 See T. Nomiyama et al., supra note 65.
68 S. Lee et al., Generalized Granuloma Annulare in Infancy Following Bacillus Calmette-Guerin
Vaccination, 23(3) ANN. DERMATOL. 319–22 (2011).
69 C. Bodemer et al., Live rubella virus vaccine long-term persistence as an antigenic trigger of cutaneous
granulomas in patients with primary immunodeficiency, 20 CLIN. MICROBIOL. INFECT. 656–63 (2014).
17

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 18 of 34
of disseminated [GA] was made by a pathologist and dermatologist months after the second
immunization.” Id. To support the length of time between the onset of Petitioner’s skin condition
and her proper diagnosis, Dr. Knierim stated that he had “seen important diagnoses made only at
autopsy.” Id. He concluded “that it is more probable than not that a serious form of [GA], the
disseminated form, was triggered in [Petitioner] by [her] influenza immunizations.” Id. at 6.
Dr. Knierim conceded in his November 15, 2021 report, that GA “was present in
[Petitioner] years prior to the 2015 and 2016 influenza vaccinations.” Pet’r’s Ex. 61 at 1, ECF No.
57-1. In Dr. Knierim’s supplemental report he quoted a communication from Petitioner he received
in October of 2021. Id. at 2. It was not filed in this case, but the relevant excerpt from Dr. Knierim’s
report is copied here:
I had granuloma annulare healing on my legs in 2010. I did, only it was a much
more benign form that caused small non itchy bumps in a circular pattern in my
legs and much purplish discoloration. In 2010, when they were noted by my nurse
practitioner, I had had the healing lesions for a couple of years (hence annulare, it
takes years to heal). They had started appearing AFTER A FLU SHOT I
RECEIVED IN 2007. I didn't put two and two together when it happened, but I did
once I got the same thing, only in a much more virulent form, after the other flu
shots. I had even asked Dr. Aylesworth, (whom I had seen around 2008 or so,
because of the mysterious lesions on my legs) if he still had records that far back,
and he said no, they had been destroyed. It could prove a relation with the flu
vaccine, and the autoimmune response resulting in the granuloma annulare skin
lesions.
Id. After he received this additional information, Dr. Knierim changed his opinion from his first
report and asserted that Petitioner’s GA “was significantly exacerbated by mandated influenza
vaccine[s she] received [on] November 9, 2015[,] and November 7, 2016.” Id. In support of his
position, Dr. Knierim noted Dr. Aylesworth’s October 11, 2017 contention that Petitioner “ha[d]
disseminated [GA] and vaccination can induce flaring of this disorder and this is likely to be the
case with this patient.” Id. (citing Pet’r’s Ex. 5 at 3). According to Dr. Knierim, the decision to use
a more aggressive treatment, methotrexate, in July 2017 “is evidence of GA which at that time was
severe and difficult to treat.” Id. at 3. Dr. Knierim also cited Petitioner’s affidavit and her filed,
post-vaccination “photographs70 [to] support the diagnosis of a quite severe case of disseminated
GA.” Id. at 2. Dr. Knierim concluded that there is “[a] possibility that [an] influenza vaccine
received by [Petitioner] in 2006 was a factor [in the development of her condition that] cannot be
excluded.” Id. at 3.
e. Respondent’s Expert, Dr. Markus Boos
Dr. Markus Boos received his B.A. degree, summa cum laude, with a double major in
biology and economics from Kalamazoo College in 2000. Resp’t’s Ex. B at 1, ECF No. 56-16.
After completing a Ph.D. program in immunology at the University of Chicago, he received his
70 Handwritten notes on the photos state that they were taken in April of 2016 after the flu vaccine in 2015;
in May of 2017 after the flu vaccine in 2016; and in March of 2018 “after halving [her] dose of methotrexate
– lesions returned.” See generally Pet’r’s Ex. 10.
18

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 19 of 34
medical degree from the same institution with honors in 2010. Id. Dr. Boos completed his
residency in dermatology and served as the chief resident at the University of Pennsylvania. Id.
He currently serves as an associate professor of dermatology and pediatric dermatology at the
University of Washington and Seattle Children’s Hospital. Id. at 1–2. He is board certified in
dermatology and pediatric dermatology. Resp’t’s Ex. A at 1, ECF No. 56-1. Dr. Boos noted that
he has seen “a wide spectrum of inflammatory skin diseases, including [approximately fifty to
sixty pediatric and adult cases of GA].” Id. Dr. Boos further noted his doctoral research in
immunology. Id. He asserted that his “background in immunology informs [his] understanding of
the molecular pathogenesis of many skin conditions that are driven by immune processes.” Id.
Dr. Boos used the Bolognia’s Dermatology reference text to define GA as “a benign,
usually self-limited, cutaneous disease that classically presents a[n] arciform to annular plaques
located on the extremities of young people.” Id. at 6 (citing Resp’t’s Ex. A, Tab 3 at 1, ECF No.
56-4).71 Continuing his reliance on the Bolognia definition, he noted that the plaques may range
from skin colored to purple and “are usually asymptomatic.” Id. While GGA is a less common
form, it “has a later age of onset, poorer response to therapy, and increased prevalence [in patients
with] the HLABw35 allele.” Id. (citing Resp’t’s Ex. A, Tab 3 at 2). Dr. Boos noted that various
diseases, including diabetes, hyperlipidemia,72 and “less commonly[,]” cancers and viral
infections, were comorbidities in some patients, but “a plurality of patients had no identifiable
associated diseases or triggers.” Id. (citing Resp’t’s Ex. A, Tab 10 at 1, ECF No. 56-11).73 He also
noted that “the pathogenesis of [GA] is unknown,” although “it has been proposed that GA
represents a delayed-type hypersensitivity reaction.” Id. at 7.
In Petitioner’s case, Dr. Boos wrote, “it is not at all clear that [Petitioner’s post-vaccination
GA] was a new diagnosis.” Id. at 9. He referenced her December 15, 2010 annual exam, during
which GA was observed and noted. Id. (citing Pet’r’s Ex. 9 at 4–5). He explained that GA is “a
relatively rare diagnosis.” Id. Furthermore, “it is extremely unlikely that a non-dermatologist
would use this term without a patient having received this diagnosis previously.” Id. at 9–10. Dr.
Boos stated that Petitioner “described waxing and waning of her skin condition in accordance with
her stress levels,” but he noted that “we have no further context/record from before 2010 to confirm
this.” Id. at 10.
When Petitioner’s pruritus appeared post vaccination in 2015, “she did not develop any
sort of a skin eruption at that time.” Id. Dr. Boos explained that “[i]tchy skin alone, without any
evidence of a rash, is not consistent with a GA flare[,] and itch is not recognized as a prodromal
symptom of GA.” Id. Petitioner’s April 2016 complaint of a rash occurred “following an [URI
two] weeks prior,” and approximately “[four to five] months” post vaccination. Id. Although Dr.
Boos did not review the photos of Petitioner’s April 2016 rash, he assumed the rash was a
manifestation of her GA for the sake of argument. Id. Without citing to a particular article or case
study, Dr. Boos asserted that “every reported case described onset of GA from within [one] week
to [two] months of receiving said vaccination.” Id. In his experience, “non-specific flares of
71 JEAN BOLOGNIA, BOLOGNIA’S DERMATOLOGY 2 (Joe Jorizzo et al. eds., 3rd ed. 2012).
72 Hyperlipidemia is “a general term for elevated concentrations of any or all of the lipids (fats) in the
plasma.” Dorland’s at 891.
73 T.M. Nordmann et al., A Monocentric, Retrospective Analysis of 61 Patients with Generalized
Granuloma Annulare, 236(4) DERMATOL. 369–74 (2020).
19

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 20 of 34
inflammatory skin disorders can be triggered by viral infections or vaccination, but typically do so
within approximately a week of stimulation[.]” Id. Therefore, Petitioner’s “URI present
immediately preceding the eruption is more likely to have triggered [her] rash” in April of 2016.
Id.
Dr. Boos also pointed to inconsistencies between Petitioner’s statement and that of her
former colleague, Ms. Bessette. Id. He noted Ms. Bessette’s statement that Petitioner, “[f]ollowing
the injection of a flu shot on November 9, 2015, . . . developed a rash covering a large portion of
her torso and upper and lower extremities [that] . . . caused an exceptionally itchy sensation.” Id.
(quoting Pet’r’s Ex. 50 at 1). He then highlighted that “not even [P]etitioner state[d] that she
developed a rash immediately after that vaccination.” Id. at 11. The fact that Ms. Bessette’s
affidavit was completed “nearly [four] years after the incident in question” also caused Dr. Boos
to question its accuracy. Id. Instead, Dr. Boos opined that “no cutaneous findings were present
until [five] months after [Petitioner received] the influenza vaccine in November [of] 2015 and[,]
in fact[,] the initial eruption in March/April 2016 was temporally associated with a viral URI[.]”
Id. He continued, “attributing the development of GA to [Petitioner’s November 9, 2015 flu]
vaccination therefore strains plausibility.” Id. Petitioner’s account of rash onset to Dr. Aylesworth
on August 29, 2016, as beginning “five months earlier[,] puts the onset in late March or early April
[of] 2016.” Id. Dr. Boos also noted Petitioner’s report that her rash had resolved at the time of her
August 2016 visit with Dr. Aylesworth, but that “it continued to flare every [six to eight] weeks.”
Id. (citing Pet’r’s Ex. 4 at 1). Dr. Boos stated that Petitioner “did not have a rash during her August
29, 2016 exam, and [P]etitioner did not return to Dr. Aylesworth until June 15, 2017, despite her
claim that she developed a significantly worsened rash in November 2016.” Id. These facts, Dr.
Boos asserted, are evidence of GA flares more likely exacerbated by illness and stress without
“any particular events surrounding her vaccinations.” Id.
Petitioner’s GA, in “presentation and overall course[,] is very consistent with idiopathic
generalized GA[.]” Id. Dr. Boos noted that “[Petitioner’s] age and the fact that her condition was
treatment resistant and recurrent, with resolution only over [three] years, is more commonly seen
in generalized GA as a whole.” Id. Quoting Bolognia, Dr. Boos explained that “GA is estimated
to resolve spontaneously ‘within [two] years in 50% of patients, but there is a 40% recurrence rate.
The duration of untreated lesions has been reported to range from a week to several decades.’” Id.
(citing Resp’t’s Ex. A, Tab 3 at 3). He characterized Petitioner’s GA as idiopathic that was “present
years before vaccination[, with] flares associated with immune stimulation—including [URIs],
stress or vaccination.” Id. While Dr. Boos identified vaccination as a potential catalyst for flares,
he hypothesized that “[i]f [Petitioner] did, in fact, suffer [] flares around the time of her
vaccination[s],” these flares were minor and resolved without treatment, “in a waxing and waning
pattern.” Id. at 12.
Furthermore, “[w]ith respect to [Petitioner’s] second vaccination in November 2016, she
endorse[d] that she already had a flare of her condition secondary to a URI that was present at the
time of vaccination.” Id. Dr. Boos noted that Petitioner’s next medical visit following this
vaccination occurred in June of 2017. Id. During that visit, Petitioner stated that a “flare [was still]
present at that time [after first] appear[ing] in February [of] 2017[.]” Id. at 13 (citing Pet’r’s Ex. 4
at 2). Dr. Boos continued that this “again demonstrat[ed] months between [Petitioner’s]
20

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 21 of 34
vaccination and a severe flare of her skin condition that warranted mention and [for her to seek]
treatment.” Id.
III. Summary of the Parties’ Arguments
a. Petitioner’s Motion for Ruling on the Record and Reply
In her motion for a ruling on the record, Petitioner alleged that her November 9, 2015 flu
“vaccine triggered a skin condition, [GA], and that this condition was exacerbated by a subsequent
mandated influenza vaccine administered to her on November 7, 2016.” Pet’r’s Mot. at 1. In
support of her argument, she described the appearance of a pruritic rash that appeared “within a
couple of weeks of the [2015 vaccination].” Id. Petitioner asserted that at the time of her November
7, 2016 vaccination, “her GA had not been formally diagnosed.” Id. at 2. Petitioner reiterated in
her reply brief that “Dr. Aylesworth diagnosed [her] with GA following a skin biopsy performed
on June 17, 2017.” Pet’r’s Reply at 1.
She highlighted the qualifications of her expert, Dr. Rostad, noting he is a board-certified
pathologist that “has reviewed over 80,000 cases within surgical, autopsy, neuropathology,
cytology, forensic, medical-legal[,] and pediatric specialties, including skin pathology.” Pet. Mot.
at 3. Notably, Petitioner mentioned that “Dr. Rostad graduated from Harvard[,] magna cum laude,”
and “[h]is curriculum vitae speaks for itself.” Pet’r’s Reply at 4. Petitioner stated that her expert is
therefore well qualified to opine that “the appearance of the skin lesions ‘[was] not inconsistent
with GA,’” that was “due to a vaccine DTH reaction.” Pet’r’s Mot. at 4. Petitioner argued that Dr.
Knierim, her second expert, provided further support for her claim. Id. Petitioner highlighted Dr.
Knierim’s work as “a major in the medical corp. of the United States Army and a pathologist in
the United States Army Hospital in Okinawa, Japan[.]” Pet’r’s Reply at 4. Petitioner argued that
her experts’ theories are clearly explained in their respective reports, and they are both well
qualified to form those opinions. Id.
Petitioner stated that the Loving factors are relevant to her claim that the 2016 flu vaccine
significantly aggravated her GA that was initially caused by the 2015 vaccination. Id. at 2 (citing
Loving v. Sec’y of Health & Hum. Servs., 86 Fed. Cl. 135 (2009)). She also explained that she did
not receive an adjuvanted flu vaccine in 2015 or 2016 and therefore, “adjuvants were not
[P]etitioner’s experts’ theory in this case.” Id. at 3. Petitioner concluded that her sixty exhibits,
including “[three] expert reports and [thirty-eight] exhibits of medical literature” support her claim
of entitlement to compensation. Pet’r’s Mot. at 5. She contended that Respondent’s expert,
however, “has given no alternative explanation as to what could have caused [P]etitioner’s GA.”
Id.
b. Respondent’s Response
Respondent did not dispute Petitioner’s GA diagnosis in his response to Petitioner’s
motion. Resp’t’s Resp. at 1. Indeed, Respondent first argued that Petitioner’s condition predates
her vaccination, according to a 2010 medical record that mentions the condition. Id. at 12 (citing
Pet’r’s Ex. 9 at 4). This, according to Respondent, is confirmed by Petitioner’s admission to Dr.
Knierim in October of 2021, that she “had [GA] healing on her [her] legs in 2010” and that those
21

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 22 of 34
lesions “started appearing after a flu shot [she] received in 2007.” Id. at 12 n.6 (citing Pet’r’s Ex.
61 at 2) (emphasis omitted). Petitioner also noted within that same communication with Dr.
Knierim that she was diagnosed with GA by Dr. Aylesworth in 2008. See id. Respondent noted
that aside from her assertions, Petitioner has not filed evidence that she received the 2007 flu
vaccination, a contemporaneous adverse reaction, or a 2008 GA diagnosis by Dr. Aylesworth. Id.
Secondly, Respondent argued that Petitioner did not experience a GA flare after her 2015
vaccination, as her symptoms were not consistent with GA at that time. Id. at 14.
Because Petitioner’s GA predated her vaccinations, Respondent argued that Petitioner “is
limited to a significant aggravation claim.” Id. at 16. He continued that she cannot establish,
pursuant to the factors set out in Loving, that she experienced worsening of her GA, “which
result[ed] in markedly greater disability, pain or illness, accompanied by substantial deterioration
of health” post vaccination. Id. (citing Loving, 86 Fed. Cl. at 136; 42 U.S.C. § 300aa-33(4)).
Respondent also argued that Petitioner did not provide preponderant evidence pursuant to the
Althen causation factors. Id. at 18–21 (citing Althen v. Sec’y of the Dept. of Health & Hum. Servs.,
418 F.3d 1274, 1278 (Fed. Cir. 2005)). He criticized Petitioner’s reliance on the Suzuki et al. study
of a single case involving a patient with a GA-associated comorbidity that predated her influenza
vaccination. Id. at 20 (citing Pet’r’s Ex. 38). He argued that Petitioner offered no evidence of a GA
case with an onset and manifestation similar to her clinical presentation. Id. at 23. He further
argued that Petitioner’s asserted biological mechanism, a DTH reaction, is not consistent with her
clinical presentation revealed in her medical records and affidavits. Id. at 22. Discounting the
timeline relied on by Petitioner’s experts, Respondent argued that Petitioner did not establish that
the flu vaccine can cause or aggravate GA generally, or that it did in this specific case. Id. at 24.
IV. Applicable Law
I am resolving Petitioner’s claim on the filed record. The Vaccine Act and Rules not only
contemplate but 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. See 42
U.S.C. § 12(d)(2)(D); Vaccine Rule 8(d). The decision to rule on the record in lieu of a 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 those decisions were upheld). I am
simply not required to hold a hearing in every matter, no matter the preferences of the parties.
Hovey v. Sec’y of Health & Hum. Servs., 38 Fed. Cl. 397, 402–03 (1997) (determining that the
special master acted within his discretion in denying an evidentiary hearing); Burns v. Sec’y of
Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993); Murphy v. Sec’y of Health & Hum. Servs.,
No. 90-882V, 1991 WL 71500, at *2 (Fed. Cl. Spec. Mstr. Apr. 19, 1991).
To receive compensation under the Vaccine Act, a petitioner must demonstrate either that:
(1) the petitioner suffered a “Table injury” by receiving a covered vaccine and subsequently
developing a listed injury within the time frame prescribed by the Vaccine Injury Table set forth
at 42 U.S.C. § 300aa-14, as amended by 42 C.F.R. § 100.3; or (2) the petitioner suffered an “off-
Table injury,” one not listed on the Table, as a result of his receiving a covered vaccine. See 42
U.S.C. §§ 300aa-11(c)(1)(C); Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321
22

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 23 of 34
(Fed. Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1319–20 (Fed. Cir.
2006). Petitioner did not allege a Table injury in this case; thus, she must prove that her injury was
caused-in-fact by a Table vaccine or was significantly aggravated by a Table vaccine.
In the seminal case of Althen v. Sec’y of the Dept. of Health & Hum. Servs., the Federal
Circuit set forth a three-pronged test used to determine whether a petitioner has established a causal
link between a vaccine and the claimed injury. See 418 F.3d at 1278–79. The Althen test requires
petitioners to set forth: “(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.”
Id. at 1278.
Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners
must provide a “reputable medical theory” demonstrating that the vaccine received can cause the
type of injury alleged. Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355–56 (Fed.
Cir. 2006) (citations omitted). To satisfy this prong, a petitioner’s theory must be based on a “sound
and reliable medical or scientific explanation.” Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d
543, 548 (Fed. Cir. 1994). Such a theory must only be “legally probable, not medically or
scientifically certain.” Knudsen, 35 F.3d at 549.
Petitioner may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1378–79 (Fed. Cir. 2009) (citing
Capizzano, 440 F.3d at 1325–26). This may be accomplished in a number of ways. “Reliability
and plausibility of . . . pathogenesis can be bolstered by providing evidence that at least a sufficient
minority in the medical community has accepted the theory, so as to render it credible.” See Pafford
v. Sec’y of Health & Hum. Servs., No. 01-0165V, 2004 WL 1717359, at *4 (Fed. Cl. Spec. Mstr.
July 16, 2004). Special masters, despite their expertise, are not empowered by statute to
conclusively resolve what are complex scientific and medical questions, and thus scientific
evidence offered to establish Althen prong one is viewed “not through the lens of the laboratorian,
but instead from the vantage point of the Vaccine Act’s preponderant evidence standard.” Andreu,
569 F.3d at 1380. The special master essentially must weigh and evaluate opposing evidence in
deciding whether a petitioner has met their burden of proof. See id.; see also Grant v. Sec’y of
Health & Hum. Servs., 956 F.2d 1144, 1149 (Fed. Cir. 1992).
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. The third Althen prong requires establishing a “proximate temporal
relationship” between the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term
has been equated to the phrase “medically-acceptable temporal relationship.” Id. A petitioner must
offer “preponderant proof that the onset of symptoms occurred within a timeframe which, given
the medical understanding of the disorder’s etiology, it is medically acceptable to infer causation.”
de Bazan v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation
for what is a medically acceptable timeframe must also coincide with the theory of how the relevant
vaccine can cause an injury (Althen prong one’s requirement). de Bazan, 539 F.3d at 1352; Shapiro
v. Sec’y of Health & Hum. Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after remand on
23

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 24 of 34
other grounds, 105 Fed. Cl. 353 (2012), aff’d without op., 503 F. App’x. 952 (Fed. Cir. 2013);
Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr.
May 30, 2013), mot. for review denied (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir.
2014). The special master cannot infer causation from temporal proximity alone. See Thibaudeau
v. Sec'y of Health & Hum. Servs., 24 Cl. Ct. 400, 403–04 (1991); see also Grant, 956 F.2d at 1148.
A petitioner who satisfies all three prongs of the Althen test has established a prima facie
showing of causation. Hammitt v. Sec’y of Health & Hum. Servs., 98 Fed. Cl. 719, 726 (2011).
When and if a petitioner establishes a prima facie case, the burden then shifts to the government
to prove that an alternative cause, unrelated to the administration of the vaccine, was the “sole
substantial factor” in causing the alleged injury. de Bazan, 539 F.3d at 1354; see also Hammitt, 98
Fed. Cl. at 726 (explaining that the respondent’s burden is to show that the “factor unrelated” was
the “sole substantial factor” in causing the injury). Additionally, a factor unrelated “may not
include ‘any idiopathic, unexplained, unknown, hypothetical, or undocumentable cause, factor,
injury, illness or condition.’” 42 U.S.C. § 300aa-13(a)(2).
This case also presents a signification aggravation claim. The Vaccine Act defines
significant aggravation as “any change for the worse in a preexisting condition which results in
markedly greater disability, pain, or illness accompanied by substantial deterioration of health.” §
300aa-33(4). In Loving, the United States Court of Federal Claims established the governing six-
part test for off-Table significant aggravation claims. Petitioner must show by a preponderance of
the evidence:
(1) the p erson’s condition prior to administration of the vaccine, (2) the person’s current
c ondition (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, 86 Fed. Cl. at 144; se e also W.C. v. Sec’y of Health & Hum. Servs., 704 F.3d 1352, 1357
(Fed. Cir. 2013) (adopting this as the proper legal standard for significant aggravation claims
brought under the Vaccine Act).
The first two prongs of L oving are preliminary steps that are necessary to “evaluate the
p erson’s pre-vaccination condition and current, post-vaccination condition.” Whitecotton v. Sec’y
of Health & Hum. Servs., 81 F.3d 1099, 1107 (Fed. Cir. 1996). Indeed, “these two steps are
practically inherent in the term ‘aggravation.’” Id. In Sharpe, the Federal Circuit clarified
the Loving prongs and what is required by petitioners to successfully demonstrate a causation-in-
fact significant aggravation claim. Sharpe v. Sec’y of Health & Hum. Servs., 964 F.3d 1072 (Fed.
Cir. 2020). Loving prong three requires only a comparison of a petitioner’s current, post-
vaccination condition, with her pre-existing, pre-vaccination condition. Sharpe, 964 F.3d at
1082; Whitecotton, 81 F.3d at 1099. A petitioner is not required to demonstrate an expected
24

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 25 of 34
outcome or that her post-vaccination condition was worse than such an expected outcome. Sharpe,
964 F.3d at 1081.
Loving pro ngs four, five, and six are derived from the Federal Circuit’s test for off-Table
a ctual causation cases. See Althen, 418 F.3d at 1281. Under Loving prong four, a petitioner need
only provide a “medical theory causally connecting [the petitioner’s] significantly worsened
condition to the vaccination.” See Sharpe, 964 F.3d at 1083; see also Loving, 86 Fed. Cl. at 144.
In other words, a petitioner is required to present a medically reliable theory demonstrating that a
vaccine “can cause a significant worsening” of the condition. Sharpe, 964 F.3d at 1083 (citing
Pafford ex. rel. Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1356–57 (Fed. Cir.
2006)).
L oving prong five requires a petitioner to show “a logical sequence of cause and effect
s howing that the vaccination was the reason for the significant aggravation.” Loving, 86 Fed. Cl.
at 144. In other words, a petitioner must show that the vaccination “did cause a worsening of [a
petitioner’s underlying disorder].” Id. The sixth prong of Loving is an adaptation of Althen prong
three’s requirement of a medically-acceptable temporal relationship. Id. A petitioner may be able
to establish a prima facie case under Loving without eliminating a pre-existing condition as the
cause of her significantly aggravated injury. Id. (citing Walther v. Sec’y of Health & Hum.
Servs., 485 F.3d 1146, 1151 (Fed. Cir. 2007) (noting that “the government bears the burden of
establishing alterative causation . . . once petitioner has established a prima facie case”)).
In Program cases, contemporaneous medical records and the opinions of treating
p hysicians are favored. Capizzano, 440 F.3d at 1326 (citing Althen, 418 F.3d at 1280). This is
because “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.’” Id. In
addition, “[m]edical records, in general, warrant consideration as trustworthy evidence. The
records 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. These records are also generally contemporaneous to the medical
events.” Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). While
a special master must consider these opinions and records, they are not “binding on the special
master or court.” § 13(b)(1). Rather, when “evaluating the weight to be afforded to any such . . .
[evidence], the special master . . . shall consider the entire record . . . .” Id. There is no presumption
that medical records are accurate and complete as to all the patient’s physical conditions. Kirby v.
Sec’y of Health & Hum. Servs., 997 F.3d 1378, 1383 (Fed. Cir. 2021) (finding that “[b]ecause a
reasonable fact finder could conclude that [the petitioner’s] testimony [wa]s not inconsistent with
her medical records . . . it was not arbitrary and capricious for the special master to credit [the
petitioner’s] testimony” over her medical records). Where there are inconsistencies, special
masters are within their discretion to award contemporaneous medical records greater weight than
later conflicting testimony. See Cucuras, 993 F.2d at 1528 (holding that the special master’s
reliance on contemporaneous medical records over conflicting oral testimony given after the fact
was not arbitrary or capricious); see also Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417
(Fed. Cir. 1993) (holding that the decision of whether to accord greater weight to contemporaneous
medical records or later given testimony is “uniquely within the purview of the special master”).
In determining whether a petitioner is entitled to compensation, a special master must consider the
25

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 26 of 34
entire record and is not bound by any particular piece of evidence. § 13(b)(1) (stating that a special
master is not bound by any “diagnosis, conclusion, judgment, test result, report, or summary”
contained in the record).
V. Analysis
a. Experts
I will comment on Petitioner’s experts because Petitioner curiously highlighted certain
aspects of her experts’ backgrounds in her briefings. For example, Petitioner noted Dr. Rostad’s
undergraduate degree from Harvard (with honors) and proclaimed his curriculum vitae as res ipsa
loquitur. Pet’r’s Reply at 4. It is true, as is the case with most of the medical experts we see in the
Program, that both of Petitioner’s experts are esteemed physicians with exemplary backgrounds.
However, and more importantly, neither is an authority in GA. In fact, Dr. Rostad’s curriculum
vitae does not list any training, experience, or expertise in dermatology. See generally Pet’r’s Ex.
15. Dr. Knierim was board certified in dermatology but is mostly retired from his practice in
pathology. Furthermore, both physicians conceded that they have “not directly treated patients
with skin problems.” Pet’r’s Ex. 14 at 1; Pet’r’s Ex. 54 at 2. Nothing requires the acceptance of an
expert’s conclusion “connected to existing data only by the ipse dixit of the expert,” especially if
“there is simply too great an analytical gap between the data and the opinion proffered.” Snyder v.
Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen. Elec. Co. v. Joiner, 522
U.S. 136, 146 (1997)); see also Isaac v. Sec’y of Health & Hum. Servs., No. 08-601V, 2012 WL
3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. for review den’d, 108 Fed. Cl. 743
(2013), aff’d, 540 F. App’x. 999 (Fed. Cir. 2013). The Federal Circuit has clearly stated that special
masters, as 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.” Moberly, 592 F.3d at 1326. When assessing the reliability of expert
testimony, special masters may consider factors such as “the qualifications, training, and
experience of the expert witnesses; the extent to which their proffered opinions are supported by
reliable medical research and other testimony; and the factual basis for their opinions[.]” Lehner
v. Sec’y of Health & Hum. Servs., No. 08-554V, 2015 WL 5443461, at *5 (Fed. Cl. Spec. Mstr.
July 22, 2015) (citing LaLonde v. Sec’y of Health & Hum. Servs., 746 F.3d 1334, 1340 (Fed. Cir.
2014)).
Petitioner’s experts had different views on the onset and development of Petitioner’s
disease. Because of this fundamental disagreement, and their lack of subject-matter expertise, I do
not find their arguments on such issues persuasive. Instead, I am more persuaded by their
explanations, opinions, and conclusions made with support in the factual record or medical
literature. Accordingly, I will award assertions without citations to the record or supporting
authority less weight.
b. Granuloma Annulare Symptom Onset
Petitioner’s GA diagnosis is not in dispute, but the initial onset is a main point of
contention. Petitioner asserted in her petition that her GA initially presented as unrelenting and
26

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 27 of 34
incurable itching in November of 2015 and developed into a rash in early 2016.74 According to
Petitioner’s affidavits and medical records, the itching presented first, approximately two to three
weeks following her November 9, 2015 vaccination. Ultimately, Petitioner developed a rash that
she first reported during her April 15, 2016 visit to urgent care. However, the record shows
Petitioner’s pruritus predated her rash by several months.
Dr. Rostad also identified Petitioner’s first symptom of GA as itching that “began gradually
approximately two to three weeks after receiving the November 2015 vaccine.” Pet’r’s Ex. 14 at
9. Experts from both parties described the clinical presentation of GA in their reports. Dr. Rostad
described GA as erythematous papules. Pet’r’s Ex. 14 at 7. He cited medical literature and Dr.
Cyr’s definition indicating that GA can be localized or generalized. Pet’r’s Ex. 17 at 1. Dr. Boos’s
definition was similar, and he wrote that GA presents as “arciform to annular plaques that can
range from skin colored to purple.” Resp’t’s Ex. A at 6. Dr. Boos characterized the condition as
asymptomatic. Id. Dr. Cyr also noted that GA is generally asymptomatic but may be accompanied
by mild pruritus. Pet’r’s Ex. 17 at 1. Dr. Rostad agreed that itching has an association with GA but
acknowledged that pruritus “is a nonspecific clinical symptom.” Pet’r’s Ex. 14 at 9. Neither of the
experts nor the filed medical literature includes severe itching as a diagnostic symptom or even
common characteristic of GA. In one of Petitioner’s filed articles, Dr. Moses noted that pruritus
occurs with several diseases, but he did not mention GA. Pet’r’s Ex. 24 at 4.
It is unclear why Dr. Rostad identified Petitioner’s itching as the onset symptom of her
GA. The five-month time lapse between the pruritis onset and the appearance of the rash further
undermines any argument that the two are related or indicative of the same condition. Given that
itching is not identified by the experts or the medical literature as a diagnostic symptom of GA;
that Petitioner’s itching was described as severe and not the mild pruritis that has been seen with
GA; and that Petitioner’s itching and her rash manifested months apart, there is not preponderant
evidence that Petitioner’s itching is connected to her GA. Therefore, there is not preponderant
evidence that Petitioner’s GA manifested with her pruritus, two-to-three weeks after her 2015 flu
vaccination.
Petitioner’s first post-vaccination, telltale GA rash, consistent with the medical literature
and expert testimony, appeared in late March/early April of 2016. A medical record from April
15, 2016, described an erythematous, maculopapular rash on Petitioner’s abdomen and legs that
was pruritic. Pet’r’s Ex. 3 at 16. Petitioner’s complete medical records and statements provide
consistent evidence of the approximate five-month gap between her 2015 flu vaccination and the
appearance of the rash. During this time, Petitioner suffered from a known intervening cause of
GA. Indeed, Petitioner was diagnosed with viral exanthem in April of 2016, and the medical
literature filed by both parties identifies viruses as potential causes of GA. See Pet’r’s Ex. 58;
Resp’t’s Ex. A, Tab 12. Petitioner’s own accounts are also consistent with her treater’s ultimate
74 Within Dr. Knierim’s supplemental expert report, there is an account of a statement wherein Petitioner
stated that she was first treated for GA by Dr. Aylesworth in 2008. Pet’r’s Ex. 61 at 2. Dr. Knierim relied
on this statement to argue that Petitioner’s flu vaccinations in 2015 and 2016 significantly aggravated her
preexisting GA. Despite filing this report, Petitioner did not assert this specific significant aggravation
claim. Likewise, she did not acknowledge in her motion for a ruling on the record that her GA predated her
2015 vaccination. See generally Pet’r’s Mot.
27

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 28 of 34
opinion that Petitioner’s rash flared whenever she had a virus. Pet’r’s Ex. 2 at 1; Pet’r’s Ex. 4 at 2,
9–10.
Petitioner continued to complain of red bumps on her chest and flanks in August of 2016
and described a history of psoriasis to her treater during a visit that month. Pet’r’s Ex. 4 at 1.
Following Petitioner’s November 7, 2016 flu shot, however, there is another extended period
without medical records. She stated in her affidavit that at the time of her 2016 vaccination, she
was recovering from a viral infection and covered in an itchy rash. Pet’r’s Ex. 2 at 1–2. Again, in
June of 2017, Petitioner sought treatment for itchy, red bumps all over her entire body, present
since February of 2017. Pet’r’s Ex. 4 at 2. Her treater observed red, eroded papules on her chest,
axilla, arms, and legs. Id. at 6. Petitioner told her treater that her symptoms get worse following a
flu shot or cold. All of these descriptions are similar. Petitioner argued these flares are all
manifestations of her GA that was only diagnosed by Dr. Aylesworth following her June 17, 2017
biopsy. Id. at 3. However, there is preponderant evidence that these flares followed viral infections
that were closer in time to Petitioner’s reactions than the vaccines in question.
In Dr. Knierim’s first expert report, he reiterated Petitioner’s argument that her GA began
post vaccination and opined that “other skin lesions prior to November 2015 [are] not relevant.”
Pet’r’s Ex. 54 at 5. Notably, in his second expert report, Dr. Knierim rescinded his prior assertion
and admitted that GA “was present in [Petitioner] years prior to the 2015 and 2016 influenza
vaccinations.” Pet’r’s Ex. 61 at 1. At no point in any of Petitioner’s filings does she address Dr.
Knierim’s reversal or the basis for his change in opinion. Petitioner’s gross omission undermines
the general credibility of her entire claim, and specifically her causation-in-fact theory.
Furthermore, Petitioner’s medical records are consistent with Dr. Knierim’s reversal and
document symptoms consistent with GA on several occasions pre vaccination, as early as 2010
and thereafter. Most notably, Petitioner’s 2010 annual exam documented that her “lower legs
[presented] with granuloma annularis [sic].” Pet’r’s Ex. 9 at 4. Indeed, Petitioner admitted to Dr.
Knierim that she was diagnosed with GA by 2008 after lesions developed on her legs in 2007.
Pet’r’s Ex. 61 at 2. Respondent’s expert, Dr. Boos, noted that GA is rare, and “it is extremely
unlikely that a non-dermatologist [(such as the treater conducting Petitioner’s annual exam in
2010)] would use this term without a patient having received this diagnosis previously.” Resp’t’s
Ex. A at 9–10. I agree. This argument is further supported by Dr. Knierim’s assertion that a
pathologist and dermatologist were necessary to identify Petitioner’s correct diagnosis of
disseminated GA in 2017. Pet’r’s Ex. 54 at 5. Furthermore, in 2011, Petitioner described “chronic
skin problems and rashes that pop[ped] up here and there” although she described them as “eczema
and dermatitis.” Pet’r’s Ex. 9 at 5. A November 21, 2012 record, from Petitioner’s annual exam,
noted Petitioner’s “forearms and upper left arm are with several areas of red, flat, macular-type
lesions.” Id. at 3. Given Petitioner’s clinical course, it appears more likely than not that she was
properly diagnosed with GA years prior to the flu vaccines at issue.
In her second affidavit, Petitioner explained that she “had skin issues in the past,” but they
were “not the same type” as her post-vaccination injury. Pet’r’s Ex. 13 at 1. She continued that her
previous diagnoses included “eczema or contact dermatitis that were easily treated with topical
creams.” Id. However, Petitioner did not submit medical records that clarify the nature of her pre-
vaccination skin conditions. The catalyst for Petitioner’s skin conditions, including her GA, has
28

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 29 of 34
varied from stress to a viral infection. The descriptions of her physical manifestations and rashes,
however, have remained consistent. Petitioner has not presented preponderant evidence that her
GA developed after her 2015 flu vaccine. The medical records provide evidence that Petitioner
suffered from GA as early as 2010.
c. Pre-vaccination Condition: Loving prong one
Petitioner has maintained throughout the course of this claim that she developed GA as a
result of her 2015 flu vaccination. In her first affidavit, she stated her belief that her November 9,
2015 vaccination was the cause of her injuries. Pet’r’s Ex. 2 at 5. Furthermore, Petitioner asserted
in her motion for a ruling on the record that “her GA had not been formally diagnosed” prior to
her 2016 flu vaccination. Pet’r’s Mot. at 2. As previously discussed, however, Dr. Knierim
acknowledged that Petitioner suffered from GA pre vaccination. Also as previously noted,
Petitioner’s filings support Dr. Knierim’s opinion and provide some evidence to assess her pre-
vaccination condition pursuant to Loving prong one. Petitioner noted in her affidavit that she has
a history of skin conditions that she could treat with topical creams. Petitioner’s medical records
document pre-vaccination rashes on her lower legs, forearms, and upper left arm. She regularly
filled a prescription for betamethasone dipropionate, a glucocorticoid steroid, for such rashes
characterized as chronic eczema and dermatitis, that would “pop up here and there.” Id. Dorland’s
explains that this ointment is used to relieve inflammation and pruritus in varied dermatological
conditions.75 Dr. Cyr noted in her article on the diagnosis and management of GA that “treatment
is usually not necessary,” but some patients that insist on treatment receive topical corticosteroids.
Pet’r’s Ex. 17 at 4. Petitioner has established with preponderant evidence that her pre-vaccination
skin conditions were reasonably controlled with her prescribed medication and home remedies,
including calamine lotion and aloe vera.
d. Post-vaccination Condition/ Significant Aggravation: Loving prong two
Petitioner argued in her motion for a ruling on the record that her claim is primarily a but-
for causation claim specific to her 2015 vaccination. Her secondary significant aggravation claim
alleges that the condition she developed in 2015 was exacerbated by her 2016 vaccination. This
claim stands in direct contrast to Dr. Knierim’s argument that Petitioner’s 2015 vaccination
significantly aggravated her pre-existing GA. Despite Petitioner’s insistence that her significant
aggravation claim is limited only to the 2016 vaccine, I will consider her expert’s argument and
any supporting evidence to decide entitlement. Petitioner’s condition during the time between her
vaccinations (November 9, 2015 – November 7, 2016) will therefore be assessed for: 1) a
significant aggravation of her pre-existing GA following her 2015 vaccination and 2) a significant
aggravation of her GA condition following her 2016 vaccination.
i. Pre-existing GA aggravated by 2015 vaccination
Petitioner did not present evidence of an immediate reaction following her 2015
vaccination. She did not seek treatment and does not have contemporaneous medical records that
document the extent and specific onset of itching. In her affidavit, she described the gradual
development of an increasingly worsening pruritus, approximately two to three weeks following
75 See supra, note 7 (defining betamethasone dipropionate).
29

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 30 of 34
her November 9, 2015 flu vaccination. Petitioner also described a rash that developed in March of
2016. This rash appeared several months after the 2015 vaccine and, per Petitioner, followed a
cold. Petitioner noted that the topical treatments and home remedies she used for previous skin
conditions were ineffective on this rash. Medical records from treatment in April of 2016 revealed
a rash on Petitioner’s trunk and limbs that was diagnosed as viral exanthem. Petitioner also filed
photographs that she asserts depict the rash on her abdomen and one of her extremities in April of
2016. The clarity of the images is poor, but some discoloration of the skin is visible. Petitioner’s
former colleague, Ms. Bessette, stated in her affidavit that Petitioner’s rash following her 2015
vaccination was red and blotchy with bleeding scratch marks. Petitioner was prescribed an
antihistamine and steroids, but she told treaters that she would continue to use medications
previously prescribed to treat her pre-vaccination skin issues. When Petitioner sought
dermatological treatment in August of 2016, her rash was in remission but not completely gone.
She disclosed occasional, recurring break outs following viral illnesses.
Without photos, dermatological records, or additional medical records from 2010 through
2015, or from the months immediately following her November 9, 2015 vaccine, it is difficult to
compare the severity of Petitioner’s skin condition pre vaccination to post vaccination. However,
Petitioner asserted that her GA worsened in March of 2016, and medical records document an
extensive rash in April of 2016. The increased severity during that timeframe is supported by her
ultimate decision to seek professional medical treatment in April of 2016. This worsening more
likely than not occurred after her November 2015 vaccination. Therefore, Petitioner has presented
preponderant evidence that her skin condition worsened after her 2015 flu vaccination.
ii. 2015 GA aggravated by 2016 vaccine
At the time that Petitioner received her November 2016 flu vaccination, she was already
suffering from an itchy rash. Petitioner admitted that this rash appeared in the wake of a viral
infection. Post vaccination, Petitioner reported persistent unbearable itching, disfiguring, and
scarring lesions present since February 2017, that did not respond to treatment. See, e.g., Pet’r’s
Ex. 2 at 3; Pet’r’s Ex. 4 at 2. Petitioner’s submitted photos dated May of 2017, provide clearer
images of the extent of the rash and nodules consistent with the descriptions in the expert reports
and medical literature as characteristic of GA. Dr. Aylesworth observed this rash and ordered a
skin biopsy in June of 2017. Pet’r’s Ex. 4 at 2. The biopsy revealed thickening of the skin and
underdevelopment of the top layer skin cells. This is consistent with Petitioner’s statement that she
had multiple skin irritations that bled from her scratching around that time. Petitioner was
prescribed methotrexate from July 2017 through 2019, and she reported that it effectively treated
her flares. By January of 2019, Petitioner told Dr. Aylesworth that she used steroid cream rarely
and did not need further treatment.
Petitioner asserted that the itching and the rashes she experienced following her November
2016 vaccination were worse than she had ever experienced. Pet’r’s Ex. 2 at 3. However, her
description of the rash that appeared in March of 2016 (before her 2016 vaccination) is similar to
her description of other rashes that developed at the time of her 2016 vaccination and thereafter.
For instance:
30

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 31 of 34
1. Petitioner presented to urgent care on April 15, 2016, complaining of a rash following an
URI in March, one month earlier. She described the itching as tear-inducing and noted that
none of her usual remedies worked. She sought treatment from a dermatologist in August
of 2016, with continued complaints of a rash recurring every six-to-eight-weeks since her
URI five months prior.
2. At the time of her flu vaccine in November of 2016, Petitioner asserted that she had already
developed a rash following another URI. Petitioner did not say how long this flare lasted,
and there are no medical records during this time. In an email to her employer two weeks
post vaccination, Petitioner described the rash and agonizing itching, but indicated she
would not seek treatment.
3. In June of 2017, seven months later, Petitioner saw Dr. Aylesworth and complained of a
rash present since February of 2017. She reported that the rash increased in severity
following her flu shots and colds. Petitioner stated the pruritus drove her to scratch until
she bled with no relief from medication or home remedies.
Petitioner described her rash as having an unbearable itching, red bumps, and a resistance to topical
treatments in all instances. See, e.g., Pet’r’s Ex. 3 at 15; Pet’r’s Ex. 5 at 1; Pet’r’s Ex. 2 at 2; Pet’r’s
Ex. 4 at 2. These three documented instances of Petitioner’s skin condition reveal a history of
flares before and after her 2016 vaccination that are similar in severity. I do not find preponderant
evidence that Petitioner’s flares changed for the worse following her 2016 vaccination, or resulted
“in markedly greater disability, pain, or illness accompanied by substantial deterioration of health.”
§ 300aa-33(4).
e. General Causation: Althen prong one / Loving prong four
Petitioner’s expert Dr. Rostad acknowledged that the trigger for GA is unknown; however,
he hypothesized that GA is the result of an abnormal immune response triggered by vaccines. I
must note that Dr. Rostad, like Petitioner, maintained that Petitioner did not suffer a significant
aggravation until her 2016 flu vaccine. His proposed biological mechanism involves an initial
manifestation of the disease caused by the 2015 flu vaccine and not a significant aggravation.
Despite my findings with respect to Loving factors one through three, to ensure complete
consideration of Petitioner’s claim, I will analyze her cause-in-fact mechanism.
Dr. Rostad identified GA as a lymphocyte-mediated hypersensitivity type IV or DTH
reaction caused by an antigen trigger. Dr. Rostad continued that GA is a manifestation of a DTH
reaction to collagen or elastin destruction. Respondent’s expert, Dr. Boos, agreed that “it has been
proposed that GA represents a [DTH] reaction.” Resp’t’s Ex. A at 7. Dr. Rostad explained that the
antigen incites the immune system, including macrophages that release proinflammatory
cytokines, and that this release causes damage to collagen or elastin in the lesions. Petitioner filed
articles that explain this DTH pathology. Pet’r’s Exs. 22–23.
While Petitioner provided evidence that GA can be caused by a DTH reaction, she did not,
however, file articles that explain the pathogenesis of a flu-vaccine induced DTH. Dr. Rostad
identified the flu vaccine (or one of its components) as an example of a triggering antigen, but he
did not explain his basis for this assertion or file any supporting literature. Aside from his
discussion of adjuvants, which will be addressed in more detail below, Dr. Rostad did not identify
31

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 32 of 34
any flu vaccine component that would result in a local DTH reaction. Petitioner does not have to
provide a specific mechanism, but it must be detailed enough to apply to the specific vaccine and
injury in this case. Otherwise, any vaccination, by nature of its purpose to illicit an immune
response, could be asserted as the cause of any autoimmune disease that later developed in an
individual. Indeed, this reasoning would nullify but-for causation in its entirety. See W.C. v. Sec’y
of Health & Hum. Servs., 704 F.3d 1352, 1360 (2013) (finding that a petitioner cannot prevail by
simply invoking a biological term, or by showing that the mechanism is a valid theory to explain
how other triggers may have induced other diseases and determining that a petitioner must produce
additional evidence that the mechanism can cause that vaccine to cause a specific disease); Caves
v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 119, 135 (2011), aff’d, 463 F. App’x. 932 (2012);
McKown v. Sec’y of Health & Hum. Servs., No. 15-1451, 2019 WL 4072113, at *50 (Fed. Cl.
Spec. Mstr. July 15, 2019).
Of the filed medical literature, only one case study discussed the development of GA
following the flu vaccine. The Suzuki et al. article revealed that the patient also suffered from
diabetes mellitus, a disease the author suggested promotes granuloma formation. Pet’r’s Ex. 38 at
1. Other articles filed by both Petitioner and Respondent discuss GA following other vaccinations,
including tetanus, live rubella, and several following the BCG vaccine. Dr. Rostad did not explain
how these vaccines are analogous to the flu vaccine, such that the articles would be instructive for
a case involving the flu vaccine. I must stress that the filing of medical literature is not a
requirement in order to establish causation in the Program. However, to the extent it is filed and
relied upon, the authors’ opinions, suggestions, and omissions may be considered. See Knudsen,
35 F.3d at 549; Andreu, 569 F.3d at 1378–79 (citing Capizzano, 440 F.3d at 1325–26).
To the extent that Dr. Rostad presented a biological mechanism specific to the flu vaccine,
it was limited to the ASIA theory that Petitioner ultimately disavowed. Petitioner did not receive
an adjuvanted vaccine in this case, and that argument is therefore rightly characterized by
Petitioner as irrelevant. Indeed, as stated previously in this Decision, Petitioner stated in no
uncertain terms, that ASIA was not her asserted theory of causation. This is likely an informed
choice, given the breadth of claims in the Program’s history that have unsuccessfully relied on
ASIA, also previously cited.76
Dr. Rostad did not present any evidence of a biological mechanism for the alleged 2016
significant aggravation. If he had, it may also have been applicable to Petitioner’s symptoms
following the 2015 vaccination. Dr. Knierim likewise did not identify any biological mechanism.
Petitioner has not provided preponderant evidence that the flu vaccine can cause or significantly
aggravate GA.
f. Specific Causation: Althen prong two / Loving prong five
I have already explained that Petitioner has not presented preponderant evidence that her
GA first manifested after her 2015 vaccination. Indeed, the preponderant evidence of her GA prior
to the first vaccination at issue precludes a successful but-for causation claim. Shalala v.
Whitecotton, 514 U.S. 268, 274–75 (1995) (a Vaccine Act claimant who demonstrates she
experienced symptoms of injury after receipt of vaccination does not succeed in her claim if the
76 See supra, note 61.
32

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 33 of 34
evidence indicates that she had symptoms of injury before her vaccination); Locane v. Sec'y of
Health & Hum. Servs., 99 Fed. Cl. 715, 727 (2011), aff'd, 685 F.3d 1375 (Fed. Cir. 2012) (finding
that the petitioner's Crohn's disease began prior to her vaccinations and therefore vaccine causation
could not be established). Furthermore, Petitioner has not submitted preponderant evidence of a
viable mechanism to establish that a flu vaccination can cause or significantly aggravate GA. The
lack of preponderant evidence of worsening symptoms following the second vaccination at issue
in this case also precludes Petitioner’s asserted secondary claim of significant aggravation.
Petitioner has, however, been able to establish by preponderant evidence that her pre-existing GA
worsened following her 2015 flu vaccination. Therefore, despite the lack of a significant
aggravation mechanism, I will complete consideration of the record to determine if Petitioner
provided preponderant evidence that her November 9, 2015 flu vaccine significantly aggravated
her preexisting GA. A comparison of Petitioner’s clinical presentation to her expert Dr. Rostad’s
hypothesis further illustrates the incongruity of his argument. Dr. Rostad began by noting that
Petitioner’s health had been stable up to November 9, 2015. It is correct that Petitioner’s filed
medical records do not include a formal diagnosis of GA or any other severe skin conditions prior
to her 2015 vaccination. However, Petitioner’s records do not include dermatological records that
could provide context for the December 15, 2010 GA notation from her physical exam. Also,
Petitioner has had a continuous prescription for a corticosteroid for many years and reported skin
conditions exacerbated by stress and illness. While it can be stated that Petitioner did not suffer
from severe medical conditions, the health of her skin was only stable insofar as she maintained
her steroid treatments and avoided her self-identified triggers, including stress and viral illness.
Dr. Rostad then opined that some unknown antigen stimulated Petitioner’s immune system,
first locally, and that the reaction expanded within two-to-three weeks into systemic itching. In her
affidavits and reports to medical professionals, however, Petitioner never described a localized
reaction to either vaccine. She described itching all over her upper body, noting that she could not
wear tight clothing. As explained previously, this itching predated Petitioner’s rash by several
months, and Petitioner has not presented preponderant evidence to connect the symptoms. Five
months following her November 2015 vaccination, medical records document a rash covering
Petitioner’s abdomen, back, and legs. Petitioner, at the time, identified the ‘unknown’ antigen as a
URI that had infected her entire family. In fact, her diagnosis at that time, viral exanthem, is
consistent with a viral pathology rather than an adverse reaction to vaccination.
Despite no evidence of a localized, immune response at the injection site, Dr. Rostad
asserted that this occurrence triggered a DTH reaction in the form of GA. He offered in support
that his “theory is based on knowledge of the pathogenesis of DTH and GA.” Pet’r’s Ex. 14 at 15.
This assertion is unhelpful, as Dr. Rostad acknowledged that the pathogenesis of GA is unknown.
Id. at 8. Furthermore, Petitioner’s clinical presentation is uncharacteristic of even Dr. Rostad’s
descriptions of localized GA following the flu vaccine. The McNeil and DeStefano article
identified rashes as the most common sign of a vaccine-induced DTH reaction; however, the
authors asserted that DTH reactions “are often self-limiting conditions that do not contraindicate
administration of future doses.” Pet’r’s Ex. 48 at 2. This statement is contrary to Petitioner’s claim
that her condition “has become more severe each time she has had a flu shot.” Pet’r’s Ex. 4 at 2.
The initial pruritic symptoms, delayed symptom onset, and the presence of intervening viral
antigens all overwhelmingly disrupt any logical sequence of cause and effect in Petitioner’s case.
33

Case 1:18-vv-00769-UNJ Document 73 Filed 08/01/23 Page 34 of 34
Petitioner is therefore unable to establish by preponderant evidence that her 2015 flu vaccination
significantly aggravated her GA.
g. Timing: Althen prong three / Loving prong six
Although Petitioner has been unable to establish by a preponderant standard that her GA
was aggravated by her 2015 flu vaccine, I will complete the Loving analysis and determine if there
is an appropriate temporal relationship between Petitioner’s 2015 flu vaccination and the
manifestation of the worsening of her GA flares. Dr. Rostad filed literature on DTH reactions that
noted occurrences within days and up to two to three weeks following exposure. Pet’r’s Ex. 48 at
2. He also asserted that a GA DTH reaction could occur approximately 21–28 days following
contact with the offending antigen, which in this case would be an unknown component of the flu
vaccine. Even assuming that approximately one month is an acceptable temporal relationship
between vaccination and symptom onset, Petitioner’s case does not fall within those parameters.
Petitioner’s alleged post-vaccination injury, GA, did not manifest until five months following her
2015 vaccination. This lapse is simply too long to fit within Petitioner’s asserted mechanism.
Petitioner has not presented preponderant evidence of an appropriate temporal relationship
between her November 9, 2015 flu vaccine and GA flare in March of 2016.
VI. Conclusion
Petitioner has undergone a frustrating and trying experience, and I have reviewed the entire
record in an effort to understand what happened to her. After careful consideration, I find that
Petitioner has not provided evidence that her 2015 and/or 2016 flu vaccinations caused her to
develop or significantly aggravate her GA. Therefore, her claim must be DISMISSED.77
IT IS SO ORDERED.
s/Herbrina D. Sanders
Herbrina D. Sanders
Special Master
77 Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint filing of a notice
renouncing the right to seek review.
34