Guzman v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 15-736V

(To be Published)

************************* Special Master Corcoran

GLADYS GUZMAN, *

* Filed: May 14, 2019

Petitioner, *

* Decision; Influenza (“flu”)

v. * Vaccine; Chronic Urticaria;

* Urticarial Vasculitis; Cutaneous

SECRETARY OF HEALTH AND * Vasculitis

HUMAN SERVICES, *

*

Respondent. *

*

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

Virginia E. Anello, Douglas & London, P.C., New York, NY, for Petitioner.

Debra Filteau Begley, U.S. Dep’t of Justice, Washington, DC, for Respondent.

DECISION DENYING ENTITLEMENT1

On July 16, 2015, Ms. Gladys Guzman filed a petition seeking compensation under the

National Vaccine Injury Compensation Program (“Vaccine Program”).2 Petitioner alleges that she

experienced cutaneous vasculitis (“CV”) due to her receipt of the influenza (“flu”) vaccine on

February 18, 2014. An entitlement hearing was held on October 25, 2018, in New York, New

York. For the reasons stated in more detail below, Petitioner has not demonstrated entitlement to

compensation under the Vaccine Program.

1

This Decision has been formally designated “to be published,” and will be posted on the Court of Federal Claims’s

website in accordance with the E-Government Act of 2002, 44 U.S.C. § 3501 (2012). This means the Decision will

be available to anyone with access to the internet. As provided by 42 U.S.C. § 300aa-12(d)(4)(B), however, the

parties may object to the Decision’s inclusion of certain kinds of confidential information. Specifically, under Vaccine

Rule 18(b), each party has fourteen days within which to request redaction “of any information furnished by that party:

(1) that is a trade secret or commercial or financial in substance and is privileged or confidential; or (2) that includes

medical files or similar files, the disclosure of which would constitute a clearly unwarranted invasion of privacy.”

Vaccine Rule 18(b). Otherwise, the Decision in its present form will be available. Id

2

The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,

100 Stat. 3758, codified as amended at 42 U.S.C. §§ 300aa-10 through 34 (2012) [hereinafter “Vaccine Act” or “the

Act”]. Individual section references hereafter will be to § 300aa of the Act (but will omit that statutory prefix).

I. Factual Background – Medical Record

Although Petitioner’s pre-vaccination history does not bear significantly on the outcome

of this case, it does reveal that she previously experienced allergies or allergic-like symptoms that

could be associated with her post-vaccination condition. For example, on May 3, 2013 (the year

before the vaccination at issue), Ms. Guzman sought treatment for a reported fever, loss of appetite,

sneezing, a runny nose, and eye discharge, and treaters assessed her with allergic rhinitis and poor

appetite. Ex. 1 at 173, 175. A few days later, on May 8, 2013, she sought treatment for a one-day

history of pain on her right side and was diagnosed with post-herpetic neuralgia. Id. at 185-87.

Then, at a September 2013 appointment, Petitioner reported that she had developed a rash in

association with a new medication (Famotidine) she had recently started taking, although the

records do not indicate that this was an ongoing concern for which additional treatment was sought.

Id. at 487. Ms. Guzman also received the flu vaccine in April 2013 (over a year before the

vaccination in question) without recorded incident. Id. at 21-22.

On February 18, 2014, Ms. Guzman received a flu vaccine at the walk-in clinic of New

York Presbyterian Hospital after seeking treatment for possible heart palpitations. Ex. 1 at 526-27,

534. There is no immediate record evidence in the subsequent time period of any reaction. Id.

Eight days later, on February 26, 2014, she went to an urgent care clinic for treatment of an itchy

rash, which she stated had begun “about 48h after flu shot (2/18/14),” with more pressing

symptoms developing over the prior four days. Id. at 493. She also reported a similar reaction

following receipt of the flu vaccine in 2013 (although as noted above the filed records from 2013

do not memorialize such a reaction). Id. The records from this February 2014 visit describe the

rash as a “diffuse[,] fine, erythematous,3 maculopapular4 rash” present everywhere on her body

except for her face and lower legs. Id. at 494.

Ms. Guzman was assessed with a “recurrence of rash 48h after flu shot without other clear

exposures.” Ex. 1 at 494. The treating physician noted her rash was most consistent with a

“systemic allergic reaction; allergen not yet known,” prescribed hydrocortisone cream (topical

steroids) and an allergy medication (Loratadine5), and recommended she see an allergist. Id.

Ms. Guzman sought additional treatment at the New York Presbyterian walk-in clinic less

than a week later, on March 1, 2014, for the same rash which she again identified as having begun

3

Erythema is defined as “redness of the skin produced by congestion of the capillaries.” Dorland’s Illustrated Medical

Dictionary 643 (32nd ed. 2012) (hereinafter Dorland’s).

4

Macules are discolored skin lesions that are not elevated above the surface of the skin. Dorland’s at 1094. Papules

are small circumscribed, superficial, solid elevations of the skin (which are no larger than one centimeter in diameter).

Id. at 1373.

5

Loratadine is an antihistamine used to relieve or prevent symptoms associated with allergies by mitigating the effects

of histamine – a substance in the body that causes itching, sneezing, runny nose, and watery eyes. See Antihistamine

(Oral Route), Mayo Clinic, https://www mayoclinic.org/drugs-supplements/antihistamine-oral-route-parenteral-

route-rectal-route/description/drg-20070373 (last accessed on April 16, 2019).

2

within two days of her receipt of the flu vaccine. Ex. 1 at 497. She was, as before, assessed with a

possible allergic reaction and prescribed a short course of oral steroids. Id. at 499. She next sought

treatment on March 24, 2014, because the rash remained (although her overall symptoms had

subsided somewhat in severity). Id. at 501-02. The examining physician observed a “macular

erythematous rash over arms and esp[ecially] trunk, blanching, improving from prior

documentation.” Id. at 502. Ms. Guzman was assessed with “allergic/drug rash” and directed to

follow-up with an allergist. Id. The following month, on April 15, 2014, Petitioner returned to New

York Presbyterian to see her internist, Dr. Amanda Westlake. Id. at 503-05. She informed Dr.

Westlake that her “[r]ash ha[d] completely resolved,” but that she was nevertheless “intermittently

using steroid cream” and taking Loratadine. Id. at 503.

Over the next eleven months, Ms. Guzman sought medical treatment multiple times for a

variety of conditions, but she did not report a rash at any such time, and no rash was ever observed

on any examination. Ex. 1 at 507-52; Ex. 4 at 1. Of note, on August 29, 2014, Petitioner was treated

by an ear, nose, and throat specialist, Dr. Jeffery Ahn, for allergic rhinitis and ear wax removal.

Ex. 4 at 1-6. Notes from the visit indicated that Petitioner was still taking Loratadine and using

hydrocortisone cream as needed (though the notes do not reveal any specific health problems

related to the medication use). Id. at 1. No mention was made of a current rash at that time.

The following year, in March 2015, Petitioner saw an allergist, Dr. Stephen Canfield, at

New York Presbyterian. Ex. 1 at 555-57. She repeated her prior assertion that she had developed

a rash within two days of the February 2014 flu vaccine, but now added as well that she had also

experienced a “fever, burning sensation, headaches, weak[ness], + nausea, swelling of breasts.”

Id. at 555. Significantly, however, although she complained of a number of symptoms she had

purportedly experienced since that time (and which she associated with exposure to deodorant,

detergents, perfumes, lipstick, and Clorox), she made no mention of a persisting rash over the

intervening period, and did not display one on exam. Id. at 555-56. Based upon the history provided

above, Dr. Canfield concluded that it was “unlikely” that Ms. Guzman had experienced an allergic

reaction to the flu vaccine. Id. at 556. He also offered to test Petitioner’s possible vaccine allergy

with a challenge test to the flu vaccine next year. Id.

Over the next four months, Ms. Guzman sought care many times for a myriad of

complaints, but she did not mention to any treaters that she had a rash. Ex. 1 at 557-67. Later that

summer, in July 2015 she returned to Dr. Canfield, again reporting a one-year history of myalgias

and fatigue following her February 2014 flu vaccine, but not mentioning an ongoing rash. Id. at

576. Her exam did, however, reveal that she had a rash on her inner elbow that was described as

“erythema” or “erythematous rash with papules, not itchy.” Id. at 576-77. Dr. Canfield assessed

Ms. Guzman with “unclear etiology for diffuse myalgias and fatigue” and determined it was

“unlikely for symptoms to be secondary to previous flu vaccine . . . due to [the] persistence of

symptoms.” Id. at 577. He recommended that Ms. Guzman be tested for Lyme disease and a

vitamin D deficiency. Id. Testing thereafter revealed a negative Lyme’s disease titer, as well as a

normal IgE level, and normal inflammatory markers. Id. at 593-95.

3

Since the middle of 2015, the record establishes several instances in which Petitioner has

sought medical care but has not complained of a persistent or concerning rash – nor do medical

treaters seem to have observed one. Ex. 2 at 1-20. At most, at a visit to Dr. Canfield on April 7,

2016 (after this action had been initiated), Petitioner again complained of a history of an

“erythematous rash with papules, not itchy,” adding that the rash improved when she applied

hydrocortisone cream or other over-the-counter lotions or ointments. Id. at 27. Her exam, however,

did not reveal a rash, and Dr. Canfield maintained his view that Ms. Guzman’s ongoing,

intermittent symptoms were probably not related to her 2014 flu vaccination. Id. at 28. Petitioner

saw Dr. Canfield the following month, at which time she again reported a history of a

“erythematous rash with papules[.]” Id. at 42. She did not, however, display any rash on exam,

and a skin test for allergens produced results termed “equivocal.” Id. at 43. Petitioner has not filed

any medical records for subsequent time periods.6

II. Witness Testimony

A. Gladys Guzman

Petitioner testified at hearing via Spanish translator and filed an affidavit in support of her

claim. Tr. at 6-56; see also Affidavit, filed as Ex. 3 (ECF No. 20-1). Her testimony largely

consisted of her own recollection of her overall health history post-vaccination, with some

additional explanation of disputed issues relevant to certain medical records.

Consistent the with medical record detailed above, Ms. Guzman testified that she received

the flu vaccine on February 18, 2014, at the New York Presbyterian office of her primary care

treaters. Tr. at 8. She did not recall experiencing any adverse reaction or symptoms immediately

following vaccine administration. Id. at 9.

Within forty-eight hours thereafter, however, Ms. Guzman represented, she began to

experience weakness, nausea, headaches, a burning sensation, and a rash extending to the back,

thighs, upper torso, and arms. Tr. at 9, 11, 37. The skin on her back appeared red and she began to

put water on it in hopes it would help alleviate her symptoms. Id. at 10.

Due to the above concerns, Ms. Guzman presented to the hospital at New York

Presbyterian on February 26, 2014 (roughly one week following her receipt of the vaccine). Tr. at

11. She recalled being examined by multiple physicians. Id. She represented that one such treater

advised her that she had experienced an adverse reaction to the flu vaccine, and prescribed

Loratadine and hydrocortisone cream to treat her symptoms (two medications she had not taken

prior to that date). Id. Ibuprofen was recommended for her headaches. Id. at 12. Ms. Guzman also

recalled that hospital treaters advised her to schedule an appointment with an allergist, but she

6

Exhibit 5 contains Ms. Guzman’s relevant pharmacy records, and Exhibit 6 contains photos of Ms. Guzman’s hands

(dated July 30, 2015), which are discussed below.

4

maintained that the appointment could not be scheduled until March 2015 (as the attending

allergist was on maternity leave). Id.

Ms. Guzman returned to the New York Presbyterian office of her primary care provider

the next day to refill her prescriptions. Tr. at 13-14. The office was closed, however, so Ms.

Guzman instead went to a local urgent care clinic. Id. at 14. The urgent care physician examined

Ms. Guzman and prescribed Prednisone (along with refills of Loratadine and hydrocortisone

cream). Id. The physician also advised her to return to the hospital if her symptoms did not

improve. Id.

Ms. Guzman testified that she took Prednisone for “several days” thereafter, but could not

specify for how long. Tr. at 16. She recalled returning to the office of her primary care provider

thereafter because of her persistent symptoms. Id. Ms. Guzman continued to take Loratadine and

hydrocortisone cream with some improvement, though she maintained that her rash never cleared

fully (despite record evidence to the contrary). Id. at 17, see Ex. 1 at 503.7 At times, however, Ms.

Guzman recalled that she would stop taking Loratadine due to adverse side effects (i.e., sleepiness),

at which time the rash would reappear on her palms, arms, legs, chest, and upper torso. Tr. at 17-

18. Ms. Guzman otherwise testified that she continues to take Loratadine at present (as well as use

various over-the-counter medications and lotions). Id. at 18, 22.8

Given her perception that she could not see the allergist at New York Presbyterian for

several months, Ms. Guzman began to search for another specialist.9 On August 29, 2014, she

presented to Dr. Jeffrey Ahn. Tr. at 19. Upon arrival, Ms. Guzman realized that Dr. Ahn’s specialty

(ear, nose, and throat) meant that he did not treat patients with the condition she was experiencing,

but she went through with the examination regardless. Id. She recalled that Dr. Ahn examined her

eyes, nose, and throat, and also cleaned her ear canals. Id.

Thereafter, Ms. Guzman was seen by an allergist, Dr. Canfield, at Columbia University

Medical Center. Tr. at 20. Ms. Guzman maintained that her rash was still present at this time

(despite a normal examination), though it had improved somewhat. Id. at 45-46, 47. She recalled

that Dr. Canfield concluded she had experienced an adverse reaction to the flu vaccine, and wanted

to complete testing to confirm this. Id. at 43.10 She explained that Dr. Canfield also suggested the

7

Ex. 1 at 503, for example, indicates that Ms. Guzman told her internist, Dr. Westlake, the rash had “completely

resolved” as of April 15, 2014. Tr. at 37-38, 49-50. Ms. Guzman maintained at hearing, however, that she showed Dr.

Westlake the rash and was prescribed the same medications. Id. at 37-38.

8

Although Ms. Guzman maintained she used hydrocortisone cream routinely in 2014, her pharmacy records suggest

that between April 2014 and July 2015 the prescription was not refilled. Tr. at 39-40.

9

As noted earlier, Petitioner maintained that she could not see the allergist at New York Presbyterian until 2015 (due

to the treater’s scheduled maternity leave). Tr. at 30-32. She acknowledged at hearing, however, that she did not

attempt to schedule an appointment with a different allergist at the same hospital as an alternative. Id. at 34.

10

On cross, Respondent pointed out that the medical record reveals that Dr. Canfield suggested that the flu vaccine

likely played no role in Petitioner’s onset of rash (or other symptoms). Tr. at 43; see Ex. 1 at 577 (“[u]nlikely for

5

vaccine had compromised her immune system and lowered her “defenses.” Id. at 23. According to

Ms. Guzman, Dr. Canfield recommended that she continue taking Loratadine and using

hydrocortisone (and prescribed Tamiflu). Id. at 23, 40-42.11

At present, Ms. Guzman continues to see Dr. Canfield, but only as needed (as she has found

his treatment to be unhelpful in resolving her symptoms). Tr. at 23. The Loratadine helps at times,

but as she testified earlier, her rash returns when she stops taking the medication. Id. at 35. Ms.

Guzman described her rash as “more spotty today” than when it initially began. Id. at 37.

On cross, Petitioner maintained that she truthfully reported her symptoms to her treaters

over the course of her illness. Tr. at 28. Ms. Guzman also submitted photographs of the palms of

her hands (taken in July 2015 – at the time of the filing of this action, and thus almost eighteen

months post-vaccination), which in her view corroborated her claims of a vaccine reaction. Id. at

51-53; see Ex. 6 (ECF No. 21-1).12 She otherwise maintained that she continues to suffer from a

rash at present (though she described it as a “subcutaneous” problem), despite the lack of

contemporaneous medical record support. Tr. at 53.

Ms. Guzman acknowledged at hearing that she had experienced certain seasonal allergies

prior to receiving the vaccine at issue in this matter. Tr. at 28-29. She attributed these allergies to

“certain medications” and “detergents” which caused only “watery eyes.” Id. at 29. She also

acknowledged taking medication for these allergies, though she maintained the symptoms at the

heart of her petition occurred only after receipt of the flu vaccine. Id. at 29-30, 53-54.13

B. Petitioner’s Expert – Dr. David Axelrod

Dr. Axelrod prepared two written reports for this case and testified at hearing. Tr. at 66-

120; Expert Report, dated Aug. 19, 2015 (ECF No. 31-1) (“First Axelrod Rep”); Expert Report,

symptoms to be secondary to previous flu vaccine given last year due to persistence of symptoms”). Petitioner,

however, insisted that Dr. Canfield advised her that she should not receive the flu vaccine in the future. Tr. at 43.

11

Respondent pointed out, however, that Ms. Guzman submitted no record evidencing a prescription for Tamiflu. Tr.

at 45.

12

The filed color photograph does not suggest the presence of a rash to the untrained eye. At best, the photo reveals

some skin redness in the bottom corners of both palms. Otherwise, Ms. Guzman’s hands appear to look normal. As

discussed in greater detail below, Respondent’s expert posited that this photographic evidence was not consistent with

vasculitis or chronic urticarial lesions (as Petitioner’s expert suggests). Tr. at 154. Dr. Levinson’s first expert report

characterizes the rash as showing “macular erythema on the palms” or “a totally non-specific eruption . . . not

emblematic of a vasculitis process in both appearance and location.” See Expert Report, dated Dec. 2, 2016 (ECF No.

22-1) (“First Levinson Rep.”) at 9.

13

Ms. Guzman could not recall how long she had taken at least one of the allergy medications, but was unable to deny

on cross-examination that the record suggested she had filled prescriptions for the medication since 2004. Tr. at 29-

30.

6

dated Feb. 15, 2017 (ECF No. 64-1) (“Second Axelrod Rep.”). He offered the opinion that the flu

vaccine Petitioner received caused her to suffer from “chronic urticaria,” which he deemed a subset

of cutaneous vasculitis. Tr. at 64, 69, 98, 101.14

Dr. Axelrod graduated from the University of Michigan Medical School in 1974 (after

obtaining his bachelor’s degree at Michigan as well). See Curriculum Vitae, filed as Ex. 40 (ECF

No. 38-16) (“Axelrod CV”) at 1. He completed two residencies in internal medicine, one at the

University of Toronto and one at William Beaumont Hospital, followed by additional fellowships

in allergy, immunology, and rheumatology at McGill University. Id. He then served as a fellow

for the National Institutes of Health in the Clinical Immunology Laboratory. Id. Dr. Axelrod holds

board certifications in allergy and immunology, adult rheumatology, and medical laboratory

immunology. Id. He currently works in private practice, with the vast majority of his patients

having allergies, immunologic conditions, or autoimmune rheumatic diseases. Tr. at 59-61. Dr.

Axelrod testified at hearing that he has treated patients with vasculitic and urticarial conditions

in his rheumatology and immunology practices. Id. at 64-67. He does not appear, however, to

have ever conducted research or published on immunologic matters relevant to urticarial

vasculitis (or vasculitic conditions generally). Axelrod CV at 2-4; Tr. at 90.

To begin, Dr. Axelrod defined vasculitis and provided a brief overview of its relevant

presenting symptoms. Tr. at 63. In his view, vasculitis is best described as “inflammation of the

blood vessels.” Id. The relevant literature filed by Dr. Axelrod indicates that vasculitis causes cell

destruction or narrowing of the blood vessel wall, in which blood flow is restricted, thereby

resulting in organ or tissue damage. See N. Kluger, et al., Cutaneous Vasculitis and Their

Differential Diagnoses, 27 Clin. Exp. Rheum. 124 (2009), filed as Ex. 9 (ECF No. 21-4)

(“Kluger”).

Dr. Axelrod characterized Petitioner’s injury as “cutaneous,” or a form of vasculitis

isolated to the skin (and thus, not systemic in nature). Tr. at 64; Second Axelrod Rep. at 1.

Cutaneous vasculitis is an all-defining term, given the multiple types in existence, which Dr.

Axelrod asserted vary depending on the type and size of the blood vessel involved (i.e., arterial

or venial, for example15). Tr. at 63-64. Dr. Axelrod offered cutaneous leukocytoclastic vasculitis16

– an idiopathic inflammation in the smaller arterial blood vessels – as an example of a cutaneous

14

Notably, Dr. Axelrod’s first expert report identified Petitioner’s injury as “isolated cutaneous vasculitis,” not chronic

urticaria. First Axelrod Rep. at 2-3, 5. His second report similarly only discusses vasculitis with an emphasis on

cutaneous involvement. Second Axelrod Rep. at 1-3. The term “chronic urticaria” appears in none of his expert reports

as a descriptor of Petitioner’s condition.

15

An arterial vasculitis, in Dr. Axelrod’s view, would be more severe in terms of the patient’s overall health course.

Tr. at 103.

16

At hearing, Dr. Axelrod acknowledged that Ms. Guzman did not have cutaneous leukocytoclastic vasculitis given

the absence of any palpable purpura evidenced in her records. Tr. at 71-72. He appears to have used the condition only

as an example, and he later admitted it does not bear on his opinion in this case. Id. at 77.

7

vasculitis. Id. at 64. It presents with “palpable purpura,” or “nonblanching lesions,” and typically

does not respond to antihistamines. Id. at 64, 72-73, 94. Pathologic evidence is used to confirm a

cutaneous vasculitis diagnosis. Id. at 99; see Kluger at 124 (“histology is mandatory to confirm

the diagnosis of vasculitis”) (emphasis added).

Chronic urticaria, Dr. Axelrod maintained, is also a subset of cutaneous vasculitis17 and

involves inflammation of the venules or “the other side of the capillaries.” Tr. at 64, 98, 101.18 It

does not have specific diagnostic criteria apart from the presence of hives and persistence (i.e,

lasting for six weeks or more). Id. at 95-96; see A. Kaplan, Chronic Spontaneous Urticaria:

Pathogenesis and Treatment Considerations, 9 Allergy Asthma Immunol. Res. 477 (2017), filed

as Ex. 27 (ECF No. 38-3) (“Kaplan”). Symptoms of chronic urticaria typically manifest as post-

inflammatory hyperpigmentation lesions affecting all areas of the body (including the feet and

palms), and it can be diagnosed without evidence of palpable purpura. Tr. at 96. Relying on his

own treatment experience, Dr. Axelrod posited that the vast majority of patients with chronic

urticaria also congruently experience vasculitis. Id. at 103, 111-12. Literature he filed in support,

however, does not support this assertion. Id. at 100; see Kluger at 129 (“[urticarial vasculitis] is

a rare . . . condition, that affects 5 to 10% of the patients with chronic urticaria”).

Based on his review of the record, Dr. Axelrod opined that Ms. Guzman developed

autoimmune “chronic urticaria”19 as the result of her receipt of the flu vaccine in February 2014.

Tr. at 69, 75-76, 87-88. In forming his opinion regarding her proposed diagnosis, Dr. Axelrod

relied primarily on Ms. Guzman’s medical records (which notably evidenced no treater support

for such a diagnosis), his own treatment experience, and Ms. Guzman’s testimony (along with

the photographic evidence from July 2015) tending to suggest that her rash presented close-in-

time to the vaccine and thereafter persisted for quite some time. Id. at 104-05, 119.

The sole medical record references Dr. Axelrod relied upon (from late February to March

2014) reveal that Ms. Guzman’s initial rash was noted to be “maculopapular” or “branching.” Tr.

17

Notably, literature filed by Petitioner in support of her claim directly contradicts the assertion that chronic urticaria

is a form of vasculitis. See, e.g., I. Jauregui, et al., Antihistamines in the Treatment of Chronic Urticaria, 17 J. Investig.

Allergol. Clin. Immunol. 41, 43 (2007), filed as Ex. 26 (ECF No. 38-2) (“[Chronic urticaria] is characterized by a

perivascular infiltrate around the venules, without vasculitis or immune complex deposits”) (emphasis added).

18

Throughout his hearing testimony, Dr. Axelrod equated chronic urticaria with “urticarial vasculitis.” Tr. at 67

(noting both terms refer to “urticaria . . . in the skin”). At times, however, he also suggested the two differed in some

respects. Id. at 67 (noting urticarial vasculitis can be associated with low complement levels in the blood); 101

(“urticarial vasculitis is inflammation maybe in the arterials and the venules . . . we mostly see venules with chronic

urticaria”). On cross, he seemingly clarified that he merely intended to reference urticarial vasculitis as an additional

example of cutaneous vasculitis, in order to underscore that palpable purpura is not required to make a chronic urticaria

diagnosis. Id. at 91-96.

19

Dr. Axelrod distinguished autoimmune chronic urticaria from urticaria related to allergies. Tr. at 88. In his view,

urticaria related to an allergy is an acute, monophasic event. Id. Otherwise, if the reaction is chronic, it is deemed

autoimmune. Id.

8

at 69, 77, 86; see Ex. 1 at 492-94, 502. That same record, however, included no treater speculation

that Ms. Guzman’s rash was consistent with urticarial lesions. Tr. at 91-92, 104. Dr. Axelrod

nonetheless posited that a maculopapular eruption of the sort Petitioner displayed at the time is

common in patients presenting with autoimmune urticaria. Id. at 69-70, 93, 104-06.20 Ms.

Guzman’s symptoms also responded well to antihistamine treatment (as well as topical steroids),

which he deemed significant. Id. at 70, 72-73, 103-04, 112; see I. Jauregui, et al., Antihistamines

in the Treatment of Chronic Urticaria, 17 J. Investig. Allergol. Clin. Immunol. 41, 43-44 (2007),

filed as Ex. 26 (ECF No. 38-2) (discussing the beneficial effects of antihistamines in treating

urticarial lesions); A. Ellingsen, et al., Treatment of Chronic Idiopathic Urticaria with Topical

Steroids, 76 Acta. Derm. Venereol. 43 (1996), filed as Ex. 42 (ECF No. 38-18) (stating the same).

Moreover, Ms. Guzman’s rash persisted for more than six weeks, rendering it “chronic”

in nature. Tr. at 69-70, 105. Indeed, Dr. Axelrod noted, Ms. Guzman herself claimed to have

experienced the effects of her rash for months following her vaccination (despite the long gap

noted in the record where Petitioner did not appear to complain of adverse symptoms, or display

them on examination). Id. at 105. He also emphasized that Petitioner used various medications to

treat her symptoms over a seventeen-month period, and those treatments may have masked her

overall state. Id.; see also Second Axelrod Rep. at 2.

Dr. Axelrod could not, however, point to any other record tending to support his

diagnostic findings as a whole. Tr. at 107. Rather, he posited that relevant photographic evidence

submitted by Ms. Guzman confirmed his suspicion that she was still experiencing urticaria

symptoms into July 2015. Id. at 107-08; Second Axelrod Rep. at 2. In his view, the photo of

Petitioner’s hands evidenced a “macular” rash, but nothing palpable or purpuric, which as noted

earlier, would not in his opinion be uncommon in the typical urticaria presentation. Tr. at 107.

Dr. Axelrod agreed, however, that the photograph alone was insufficient to confirm an ongoing

process. Id. at 108.

Apart from the above, Dr. Axelrod acknowledged that the relevant medical record lacked

any other evidence to support a chronic urticaria or vasculitic diagnosis. Indeed, Ms. Guzman

never underwent skin biopsy testing for her condition (which relevant literature suggests is

required for diagnostic confirmation of cutaneous vasculitis). Tr. at 73-74, 101-02; Second

Axelrod Rep. at 1; Kluger at 124. But Dr. Axelrod suggested that physicians typically only

perform urticarial biopsies if the patient has not responded well to antihistamines or to rule out

20

In support of his opinion that a maculopapular rash could be a symptom associated with vasculitis (and chronic

urticaria more specifically), Dr. Axelrod referenced one item of literature. Tr. at 93; see L. Calabrese, et al., The

American College of Rheumatology 1990 Criteria for the Classification of Hypersensitivity Vasculitis, 33 Arthritis &

Rheum. 1108 (1990), filed as Ex. 8 (ECF No. 21-3) (“Calabrese”). But Calabrese defines the diagnostic criteria for

hypersensitivity vasculitis (a vasculitis induced due to some “over reacti[on]” to a drug, for example), which Dr.

Axelrod acknowledged at hearing was not entirely relevant to his opinion in his case (as he was not suggesting

Petitioner had hypersensitivity vasculitis). Tr. at 77-76. On cross, Dr. Axelrod emphasized that he offered Calabrese

only to show that certain forms of vasculitis could manifest symptoms consistent with a maculopapular rash (as

evidenced in Ms. Guzman’s records), without purpura. Id. at 91-93, 94-95.

9

other conditions. Tr. at 73-74. Given that Ms. Guzman’s symptoms were alleviated by

antihistamines, Dr. Axelrod did not find it concerning that a biopsy was never conducted. Id. He

also agreed that he could not definitively state that Ms. Guzman had any form of cutaneous

vasculitis absent a biopsy. Id. at 102. Nonetheless, Dr. Axelrod opined that a majority of biopsied

patients (who do not respond well to medication) typically would have evidence of some form of

inflammation around the venules in any event – thus, the presence or absence of biopsy results

did not weight heavily against his opinion. Id.

Dr. Axelrod similarly acknowledged that none of Ms. Guzman’s treaters proposed chronic

urticaria (or any other form of cutaneous vasculitis) as an appropriate diagnosis for Ms. Guzman’s

symptoms. Tr. at 105. And Dr. Axelrod agreed that there was no evidence in the record to suggest

that Ms. Guzman tested positive for the relevant antibodies associated with cutaneous vasculitis

(or any form of vasculitis for that matter). Id. at 105, 117-18. He nevertheless maintained that no

other possible explanation (i.e., chronic liver disease, infection, pregnancy, or similar condition)

existed for Ms. Guzman’s post-vaccination symptoms. Id. at 70-71; First Axelrod Rep. at 2, 5.

He thus concluded that the vaccine was the most likely cause of the condition, given its close

temporal relationship to her reported onset of rash and other symptoms. Tr. at 109.

Dr. Axelrod next proposed a mechanism by which the flu vaccine could have caused Ms.

Guzman’s chronic urticaria: an idiotype network theory, coupled with a secondary immune

response due to prior vaccine exposure. Tr. at 78-79, 80-83, 86; First Axelrod Rep. at 5-6.

According to Dr. Axelrod, the formation of idiopathic networks (or “lattice[s]”) occurs when the

initial antibodies produced in response to a vaccine cause the body’s immune cells to produce

additional antibodies that bind with vaccine antigens – thereby producing idiotype immune

complexes. Tr. at 83; First Axelrod Rep. at 5-6; Second Axelrod Rep. at 1-2; see N. Jerne,

Towards A Network Theory of the Immune System, 125 Ann. Immunol. 373 (1974), filed as Ex.

14 (ECF No. 21-9). In Ms. Guzman’s case, Dr. Axelrod theorized, upon receipt of the flu vaccine

idiotype immune complexes were formed, transported, and “deposit[ed]” into the blood vessel

wall – therein “recruit[ing]” an overproduction of lymphocytes to the area – and resulting in

urticaria. Tr. at 82-83; Second Axelrod Rep. at 1-2.21

In support of Petitioner’s proffered medical theory, Dr. Axelrod offered various scientific

studies purportedly showing how idiotype immune complexes can both form and expand post-

vaccination, resulting in a pathologic process capable of producing chronic urticaria. See C.

Brozek, et al., Crossreactivity and Inheritance of Idiotype Restricted to Human Anti-Tetanus

Toxoid Antibodies, 79 J. Clin. Invest. 1242 (1987), filed as Ex. 16 (ECF No. 21-11) (“Brozek”).

Brozek, for example, suggests that tetanus toxoid antigens can bind with human IgG antibodies

and produce idiotype determinants. Another article described a mouse model study in which the

21

The same concept, Dr. Axelrod maintained, could apply to leukocytoclastic vasculitis, in which case the immune

complexes would “fix complement” instead of depositing/recruiting lymphocytes. Tr. at 83-84, 86.

10

flu virus was found to result in a major idiotype having specificity for virus hemagglutinin.22 See

A. Brown, In Situ Detection of Autoanti-Idiotype Anti-Body Forming Cells Induced by Influenza

Virus Infection, 139 Cellular Immunol. 162 (1992), filed as Ex. 41 (ECF No. 38-17) (“Brown”).

Dr. Axelrod also referenced literature suggesting that vaccines can be used to treat patients

with certain types of cancer or parasitic illnesses by promoting idiotype antibody/antigen

formation. See M. Warnke, et al., Control of the Specificity of T Cell-Mediated Anti-Idiotype

Immunity by Natural Regulatory T Cells, 60 Ctr. Immunol. Immunother. 49 (2011), filed as Ex.

25 (ECF No. 38-1); M. Bhattacharya-Chatterjee, et al., Anti-Idiotype Antibody Vaccine Therapy

for Cancer, 2 Exp. Op. Biol. Ther. 870 (2001), filed as Ex. 18 (ECF No. 21-13) (“Bhattacharya-

Chatterjee”); M. Phillips, et al., The Regulation of Resistance to Schistosoma Mansoni by Auto-

Anti-Idiotype Immunity, 145 J. Immunol. 2272 (1990), filed as Ex. 17 (ECF No. 21-12)

(“Phillips”). All in all, however, none of the above-described studies suggest that a vaccine can

initiate immune complex formation in the context of a pathologic process resulting in cutaneous

vasculitis.

To account for the quick onset of Ms. Guzman’s symptoms (two days following

administration of the flu vaccine), Dr. Axelrod proposed that Ms. Guzman likely experienced a

“secondary adaptive response” – or a reaction to a subsequent exposure to the same antigen –

connected to her receipt of the flu vaccine the year before the vaccination at issue, which resulted

in an amplified or inherently more rapid cellular response. Tr. at 79, 81-82; First Axelrod Rep. at

4-5. In contrast to a primary immune response23 that may not peak for a period of weeks after

vaccination or antigen exposure, a secondary response to an antigen to which an individual has

been previously exposed can begin within two to four days thereafter. Tr. at 79-81; First Axelrod

Rep. at 4. Given the similarities in strains of the two vaccines Petitioner received, Ms. Guzman’s

2014 exposure to the flu vaccine (after having received a flu vaccination in 2013) likely

contributed to her development of chronic urticaria thereafter, which would be consistent with a

“challenge-rechallenge” response.24 Tr. at 81; First Axelrod Rep. at 5.

22

Influenza viruses are divided into subtypes based on two viral proteins located on the surface of the virus: the

hemagglutinin and the neuraminidase. See Types of Influenza Viruses, CDC, https://www.cdc.gov

/flu/about/viruses/types htm (last accessed on May 6, 2019). Hemagglutinin proteins enable the flu virus to bind to

surfaces cells in the host. Dorland’s at 830.

23

Dr. Axelrod acknowledged that Petitioner’s manifestation of symptoms was too soon after vaccination to be

primary. Tr. at 81.

24

Challenge-rechallenge is “a paradigm for exploring whether one substance caused an adverse reaction. Under this

model, an individual who has had an adverse reaction to the initial vaccine dose (the challenge event) suffers a

worsening of symptoms after a second or third injection (the rechallenge event.)” Viscontini v. Sec'y of Health &

Human Servs., No. 98-619V, 2011 WL 5842577, at *22 (Fed. Cl. Spec. Mstr. Oct. 21, 2011) (quoting Doe/70 v. Sec'y

of Health & Human Servs., 95 Fed. Cl. 598, 603 (2010) (quotations omitted)), mot. for review den'd, 103 Fed. Cl. 600

(2012).

11

In support of his opinion, Dr. Axelrod cited to two studies exploring the concept of

immunologic memory as it relates to the body’s ability to respond more quickly upon re-exposure

to a foreign antigen. See A. Abbas, Cellular and Molecular Immunology 10 (8th ed. 2015), filed

as Ex. 12 (ECF No. 21-7) (“Abbas”); J. Miller, et al., The Speed of the Second Immune Response

to Tetanus Toxoid With a Review of War Reports and Observations on Simultaneous Injections

of Toxoid and Antitoxin, 3 Pediatrics 64 (1949), filed as Ex. 13 (ECF No. 21-8) (“Miller”). Neither

Miller or Abbas, however, supports Dr. Axelrod’s theory that a vaccine can initiate a secondary

pathologic response resulting in any disease process (let alone vasculitis or one of its subtypes),

or that a second event response would be expected to occur even in the absence of an identifiable

initial event response (since, as noted above, Ms. Guzman’s medical records do not suggest she

experienced any reaction at all to her 2013 flu vaccination).

Dr. Axelrod also proposed a mechanism for the ongoing destruction or perpetuation of

Petitioner’s chronic urticaria that might account for the chronic nature of her alleged symptoms.

Tr. at 84; First Axelrod Rep. at 5-6; Second Axelrod Rep. at 2. The antibody response to the

vaccine (i.e, the formed immune complexes) could cause damage to the surrounding tissue and

allow for a secondary damaging immune response to other structures of the skin. Second Axelrod

Rep. at 2. This could theoretically happen through the mechanism of epitope spreading, a process

in which invading agents accelerate an ongoing autoimmune process by local activation of

antigens presenting as a result of the existence of immune complexes. Id.; see B. McRae et al.,

Functional Evidence for Epitope Spreading in the Relapsing Pathology of Experimental

Autoimmune Encephalomyelitis, 182 J. Exp. Med. 75 (1995), filed as Ex. 22 (ECF No. 25-3); A.

Vojdani, A Potential Link between Environmental Triggers and Autoimmunity, 2014

Autoimmune Diseases 1 (2014), filed as Ex. 15 (ECF No. 21-10).

Beyond the generalities of his causation theory, Dr. Axelrod referenced various case

reports of cutaneous vasculitis with onset following flu vaccine administration – although many

involved leukocytoclastic vasculitis, a condition he admitted (as noted above) did not bear upon

Ms. Guzman’s actual condition. Tr. at 71-72, 77, 84.25 One case report involved urticarial

25

See S. Chen, et al., Cutaneous Leukocytoclastic Vasculitis Following Influenza Vaccination in Older Adults: Report

of Bullous Purpura in an Octogenarian after Influenza Vaccine Administration, 10 Cureus E2323 (2018), filed as Ex.

28 (ECF No. 38-4); S. Cao, et al., Leukocytoclastic Vasculitis Following Influenza Vaccination, BMJ Case Rep.

(2017), doi:10.1136/bcr-2016-217755, filed as Ex. 29 (ECF No. 38-5); S. Ulm, et al., Leukocytoclastic Vasculitis and

Acute Renal Failure after Influenza Vaccination in an Elderly Patient with Myelodysplastic Syndrome, 29 Onkologie

470 (2006), filed as Ex. 31 (ECF No. 38-7); S. Walker, et al., Leukocytoclastic Vasculitis and Influenza Immunization,

29 Clin. Exp. Derma. 91 (2004), filed as Ex. 32 (ECF No. 38-8); N. Yanai-Berar, et al., Influenza Vaccination Induced

Leukocytoclastic Vasculitis and Pauci-Immune Crescentic Glomerulonephritis, 58 Clin. Nephrol. 220 (2002), filed as

Ex. 33 (ECF No. 38-9); S. Tavadia, et al., Leukocytoclastic Vasculitis and Influenza Vaccination, 28 Clin. Exp. Derma.

154 (2003), filed as Ex. 34 (ECF No. 38-10); S. Monjazeb, et al., A Case of Leukocytoclastic Vasculitis Following

Influenza Vaccination, 2 JAAD Case Rep. 340 (2016), filed as Ex. 35 (ECF No. 38-11); F. Giuseppe, et al.,

Leukocytoclastic Vasculitis After Influenza Vaccination, 12 J. Clin. Rheumatol. 48 (2006), filed as Ex. 36 (ECF No.

38-12); P. Liu, et al., Cutaneous Vasculitis Following Influenza Vaccination, 49 Int. Med. 2187 (2010), filed as Ex.

30 (ECF No. 38-6).

12

vasculitis post-vaccination (and notably involved various symptomatology distinguishable from

that Petitioner experienced). See R. Hughes, et al., Urticarial Vasculitis Secondary to H1N1

Vaccination, 90 Acta. Derm. Venereol. 1 (2010), filed as Ex. 37 (ECF No. 38-13). The subject

discussed in this case report was a twenty-one-year-old woman who presented with wide-spread

pruritis and fixed urticarial plaques (along with purpura and peripheral pallor) six days following

vaccination with the H1N1 influenza A vaccine. Id. at 1. A biopsy of the affected area of skin

confirmed the diagnosis. Id. The patient was prescribed antihistamine treatment for ten days, and

the urticarial rash resolved over a two-week period thereafter. Id.

Dr. Axelrod also spent some time at hearing analogizing Ms. Guzman’s condition to drug-

induced vasculitis. Tr. at 77-78, 85; First Axelrod Rep. at 2-3; Second Axelrod Rep. at 1; M.

Radic, et al., Drug-Induced Vasculitis: A Clinical and Pathological Review, 70 J. Med. 12 (2012),

filed as Ex. 10 (ECF No. 21-5) (“Radic”). Radic is a review article aimed at distinguishing drug-

induced vasculitis from those originating due to idiopathic autoimmune syndromes. Radic at 12.

Notably, Radic does not discuss vaccines in the context of drug-induced triggers, nor do the

authors attempt to analogize vaccines to the various drugs considered to be causal (i.e.,

antibiotics, anti-tumor drugs, psychoactive agents). Dr. Axelrod posited, however, that the flu

vaccine is a drug that could initiate a vasculitic process akin to one developed after taking oral

medication. Tr. at 77-78. In so stating, Dr. Axelrod acknowledged that Ms. Guzman’s records

revealed she was taking multiple medications prior to her receipt of the flu vaccine. Id. at 78. He

maintained, however, that when compared to the pre-existing prescription medications, the flu

vaccine was newly-introduced, and thus the more likely cause of Ms. Guzman’s urticaria given

the temporal relationship between the two. Id.

Regarding onset, Dr. Axelrod posited that the timing of Ms. Guzman’s injury supported

his contention that her chronic urticaria was indeed vaccine-caused. Ms. Guzman received the flu

vaccine and within two days experienced a secondary adaptive immune response, resulting in her

physical manifestation of symptoms. Tr. at 80, 87.26 In his view, a two to four-day onset of

symptoms would be reasonable for onset of a vaccine injury based on Miller. Id. at 80, 87, 110;

Second Axelrod Rep. at 2. As noted earlier, Miller suggests that re-exposure to a vaccine (or

“booster”) can amplify an immune response with subsequent injections – thereby enhancing a

host’s immunity to a particular infectious agent (specifically, the tetanus toxoid) in measurable

titer quantities within a period of two to seven of days following reimmunization. Miller at 68-

71. Dr. Axelrod admitted on cross, however, that two days would be on the “lower end” of what

would be considered medically appropriate for a secondary immune response. Tr. at 110. He did

not, however, offer literature supporting such a timeframe as it would relate to a vaccine-induced

pathologic process (as opposed to the typical booster response).

26

Dr. Axelrod’s filed expert reports, however, placed symptom onset at four days post-vaccination. First Axelrod Rep.

at 6; Second Axelrod Rep. at 1.

13

C. Respondent’s Expert – Dr. Arnold Levinson

Dr. Levinson was Respondent’s expert. He filed two written reports in the matter and

testified at hearing. Tr. at 121-231; Expert Report, dated Nov. 28, 2016, filed as Ex. A (ECF No.

22-1) (“First Levinson Rep.”); Expert Report, dated Sept. 6, 2017, filed as Ex. B (ECF No. 27-1)

(“Second Levinson Rep.”). Dr. Levinson opined that Ms. Guzman did not suffer from any form of

cutaneous vasculitis and did not have chronic urticaria – and any inflammatory reaction that might

otherwise characterize her post-vaccination symptoms was not caused by the flu vaccine. Tr. at

139-40; First Levinson Rep. at 5; Second Levison Rep. at 3-4.

Dr. Levinson currently serves as Emeritus Professor of Medicine and Neurology at the

Perelman School of Medicine at the University of Pennsylvania (in addition also being a consultant

to other biotech and pharmaceutical companies). See Curriculum Vitae, filed as Ex. A, Tab 1 (ECF

No. 22-2) (“Levinson CV”) at 2-5; Tr. at 121-23. During his career with the Perelman School, Dr.

Levinson held a number of positions: Chief of the Allergy and Immunology Section, Director of

the Fellowship Training Program in Allergy and Immunology, and Director of the Center for

Clinical Immunology. Levinson CV at 1-2; Tr. at 122-25. He received his undergraduate degree

and medical degrees from the University of Maryland. Levinson CV at 1. He is also currently

board certified in internal medicine and allergy and clinical immunology, and holds a medical

license in the state of Pennsylvania. Id. at 2-3.

Over the course of his career, Dr. Levinson conducted a clinical practice where he

evaluated and treated patients with immune-mediated diseases, including autoimmune, neurologic

system disorders, and vasculitic conditions. Tr. at 124-25. During his tenure at the Perelman

School, Dr. Levinson estimated that he spent ten percent of his time in a clinical allergy and

immunology teaching role. Id. at 128. Seventy percent of his time was devoted to research focused

on IgE-mediated hypersensitivity disorders, and immunodeficiency with an emphasis on

autoimmunity. Id. at 129. Dr. Levinson testified that he has treated five to ten patients with

urticarial vasculitis, but many more with chronic urticaria and/or leukocytoclastic vasculitis. Id. at

126.

Dr. Levinson has served on the editorial board of multiple journals, including the Journal

of Allergy and Clinical Immunology. Levinson CV at 4. He has published peer-reviewed articles

centering on immune-mediated diseases skin diseases (including vasculitis syndromes that impact

the neurologic system), drug reactions, and anaphylaxis EAE models. Id. at 10-21; Tr. at 123-24,

130-32. Dr. Levinson has also published a textbook chapter on vasculitis. Tr. at 131-32. At hearing,

he testified that much of his career has centered on studying “prototypic” autoimmune diseases,

specifically myasthenia gravis (including the antibody/antigen mechanism for the disease). Id. at

133. Although, Dr. Levinson does not currently see patients, he consults on complex

hypersensitivity cases or cases suggestive of immunodeficiency. Id. at 125-26.

14

Dr. Levinson began his testimony by defining vasculitis as well as the relevant subtypes

offered by Petitioner in support of her claim. Tr. at 140. In his view, vasculitis refers to

inflammation of the blood vessels, along with resulting destruction or injury to the vessels (and

other organ systems) brought about by the inflammation. Id.; see also First Levinson Rep. at 6. He

defined this inflammatory process as “fibrinoid necrosis,” which involves the deposition of fiber-

looking material into the vessel wall, and results in tissue ischemia, skin lesions, and/or injury to

other organs in the body that are supplied by the targeted vessel. Tr. at 140; First Levinson Rep. at

6. Vasculitic disorders can be primary (i.e., with no identifiable cause) or secondary to some other

disease process or microbial trigger. First Levinson Rep. at 6.27 The subtypes vary in severity,

ranging from involvement of small to large vessels (with emphasis also placed on any associated

inflammatory/systemic process), and are distinguishable based on clinical and histopathological

features (as well as therapeutic response). Id.; see also J. Jennette, et al., 2012 Revised

International Chapel Hill Consensus Conference Nomenclature of Vasculitides, 65 Arth. &

Rheumat. 1 (2013), filed as Ex. A, Tab 3 (ECF No. 23-2).

Although vasculitis might be immune-mediated, Dr. Levinson maintained that it is not

necessarily an autoimmune disease, because in most vasculitic conditions antibodies typically

attack “exogenous” antigens (i.e., drugs or microbial organisms) rather than self structures. Tr. at

176, 178 (vasculitis is not always “a product of an autoimmune response against a self-antigen”);

see also C. Langford, Vasculitis, 125 J. Allergy & Clin. Immunol. 216, 216-17 (2010), filed as Ex.

A, Tab 2 (ECF No. 23-1) (discussing the various antibodies associated with the vasculitic variants

and their roles). A vasculitic injury occurs when antibodies produced in response to some foreign

antigen bind to that antigen, forming immune complexes. Tr. at 176; First Levinson Rep. at 6.

Those complexes are then deposited in the vasculature and result in damage to the vessel wall. Tr.

at 176; First Levinson Rep. at 6. The type and severity of the vasculitis is determined by the

location of deposit (i.e., whether in the venules, capillaries, or arterials). Tr. at 176.

Dr. Levinson next considered the purported vasculitis subtypes referenced by Dr. Axelrod

on direct: leukocytoclastic vasculitis, urticarial vasculitis, and chronic urticaria. Tr. at 141-44. He

described leukocytoclastic vasculitis as a “histopathological description” of a type of vasculitis

largely associated with inflammation and destruction of post-capillary venules, and which results

in direct infiltration of the vessel wall. Id. at 141. Leukocytoclastic vasculitis is neutrophil-driven

– meaning neutrophils28 undergo cell death in the vessel wall – causing necrosis or wall

obstruction. Id. at 142-43. Symptoms can include palpable purpura (i.e., raised lesions/bruising

27

Dr. Levinson agreed that vasculitis can be drug-induced or manifest as a result of other therapeutic agents. Tr. at

152-53. He did not, however, accept Dr. Axelrod’s opinion that Ms. Guzman’s symptoms were indicative of drug-

induced vasculitis (or any vasculitis for that matter) for the reasons discussed herein. Id. at 153; see also Second

Levinson Rep. at 1.

28

Neutrophils are white blood cells that aid the body in fighting off infections. See Neutropenia, Mayo Clinic, https://

www mayoclinic.org/symptoms/neutropenia/basics/definition/sym-20050854 (last accessed on May 2, 2019).

15

associated with accumulation of red blood cells in the dermis tissue) or petechia (i.e., smaller

lesions that occur when red blood cells/other blood products are released into the skin). Id. at 155-

56; First Levinson Rep. at 6. Dr. Levinson admitted that leukocytoclastic vasculitis is the

consequence of an immune reaction, but disputed that it occurs via an autoimmune mechanism

(i.e., in which an antibody attacks a self-antigen or structure in the body). Tr. at 175-76.

Urticarial vasculitis is a rare subtype of leukocytoclastic vasculitis in which patients have

chronic urticaria or angioedema reflected in individual lesions and localized pain. Tr. at 143, 178-

79; First Levinson Rep. at 7; Kluger at 126, 139. It is often seen in patients with serum sickness,

connective-tissue disorder, infections, or physical urticarias. First Levinson Rep. at 7. Seventy

percent of cases are idiopathic, and many times its onset points to the existence of some form of

underlying systemic disease. Tr. at 148, 152. It is considered to be a chronic condition (i.e., lasting

six weeks or more). Id. at 156. Symptoms are limited to urticaria and pain – thus, urticarial

vasculitis patients do not present with palpable purpura or petechia. Id. In Dr. Levinson’s view, an

urticarial vasculitic condition cannot be diagnosed without a biopsy. Id. at 174; First Levinson

Rep. at 7. It also usually does not respond well to antihistamine treatment.29 Tr. at 143, 178-79.

Dr. Levison was firm in opining that chronic urticaria is not equivalent to urticarial

vasculitis. Tr. at 141. Although symptoms associated with urticarial vasculitis can involve chronic

urticaria, the urticarial vasculitic clinical course is more severe, and involves other distinguishable

symptoms. Id. at 144. For example, urticarial vasculitic lesions “linger” for a period of twenty-

four to forty-eight hours (i.e., they do not come and go rapidly like regular hives). Id. at 144, 184-

85, 214; Kluger at 126. Lesions related to urticarial vasculitis are also typically accompanied by

pain and pruritis (i.e., itching), unlike lesions associated with chronic urticaria (which are usually

erythematous with a blanching, pale center). Tr. at 144-45, 150-52. In addition, urticarial vasculitic

lesions typically involve hyperpigmentation – a process wherein red blood cells have escaped from

the lesion – thereby leaving visible marks or “footprints” on the skin. Id. at 145, 184-85, 214;

Kluger at 126. Maculopapular-type rashes (as described in Petitioner’s records) are not indicative

of urticarial lesions (i.e., a hive or welt), but are more likely associated with an alternate condition

(such as a drug reaction or prior infection, for example). Tr. at 151-52. As noted earlier, the two

are also pathologically distinguishable, as cutaneous vasculitis, histologically, is associated with

29

On cross, Petitioner referenced literature suggesting that vasculitis could in fact be successfully treated with

antihistamines. Tr. at 181-83; see C. Langford, Vasculitis, 125 J. Allergy & Clin. Immunol. 216, 223 (2010), filed as

Ex. A, Tab 2 (ECF No. 23-1). Dr. Levinson, however, countered that patients who present with some form of a

rash/urticaria might first try an antihistamine for a couple of weeks to see if the treatment alleviated the symptoms

and/or assisted the treater determine the etiology of the rash. Tr. at 183, 213. But, by in large, the antihistamine

treatment would later (in his experience) prove ineffective in successfully resolving any form of vasculitis. Id. at 183.

16

distinct patterns (typically evidenced as eosinophilia30 or granulomas31). Id. at 146-47; see Kluger

at 133.

Dr. Levinson asserted that the two conditions are also distinguishable based on the

appropriate treatment protocol (and in fact attempts to identify the most effective treatment can

aid in determining the nature of the patient’s condition). Tr. at 147-49. Patients presenting with

acute urticaria are typically treated initially with antihistamines but not corticosteroids. Id. at 147.

Urticarial vasculitis, on the other hand, is more often associated with systemic disease in which

aggressive corticoid steroids/anti-inflammatory/immunosuppressive drugs are deemed necessary.

Id. at 148. Moreover, topical corticosteroid creams are typically not used to treat urticarial

vasculitis (if the lesions are disseminated) since they could have an adverse effect on the patient if

the steroid is widely absorbed. Id. at 148-49; see J. Ference, et al., Choosing Topical

Corticosteroids, 79 Am. Family Phys. 135, 137 (2009), filed as Ex. C (ECF No. 35-1) (“Ference”).

Dr. Levinson otherwise posited that patients with chronic urticaria rarely also experience vasculitis

at the same time, and pointed to literature confirming that only five to ten percent of patients

present with both conditions. Id. at 141; Kluger at 129.

Based on his review of the literature coupled with relevant medical records, Dr. Levinson

concluded that Ms. Guzman did not likely have any form of vasculitis or chronic urticaria. Tr. at

153, 164-65, 199. He acknowledged that Petitioner presented to treaters in late February 2014 with

a blanching, maculopapular rash on exam roughly two weeks post-vaccination, and that the rash

persisted until late March or mid-April 2014. Id. at 155-56, 161-62, 163-64, 196-97; see Ex. 1 at

502-03 (4/15/2014 visit note indicating rash had completely resolved). But in Dr. Levinson’s

understanding, blanching, maculopapular lesions (absent palpable purpura or petechia) are not

indicative of either vasculitis or chronic urticaria. Tr. at 155. Those same records also did not

suggest that Ms. Guzman was experiencing chronic hives (or any hives at all for that matter) at the

time of those visits. Id. at 156. Dr. Levinson acknowledged that visit notes from August 2014 did

suggest that Ms. Guzman was still using Loratadine and hydrocortisone cream (even though no

rash was seen on exam). Id. at 201-02. Even so, the fact that Ms. Guzman may have been

successfully treating her symptoms in this manner further supported his opinion – given that

vasculitic conditions would not likely respond well to antihistamine treatment. Id. at 162-63, 198.

Petitioner’s visit with Dr. Canfield thereafter in March 2015 revealed no rash on exam. Tr.

at 204-05. Dr. Levinson admitted that this record made some reference to a vaccine reaction (or

allergy to the flu vaccine), but he proposed it was unclear who authored the note, which could

30

Eosinophilia is a higher than normal level of eosinophils (or disease-fighting white blood cells). The condition is

most often associated with a parasitic infection, allergic reaction, or cancer. See Eosinophilia, Mayo Clinic, https://

www mayoclinic.org/symptoms/eosinophilia/basics/definition/sym-20050752 (last accessed on May 2, 2019).

31

Granuloma annulare is a skin condition that causes raised reddish or skin-colored lesions (or bumps) in a ring pattern

on the skin. See Granuloma Annulare, Mayo Clinic, https://www mayoclinic.org/diseases-conditions/granuloma-

annulare/symptoms-causes/syc-20351319 (last accessed on May 2, 2019). It typically presents on the hands or feet.

Id.

17

merely reflect the history recounted by Petitioner. Id. at 206-07. Dr. Canfield did continue to

prescribe Loratadine and hydrocortisone cream, but Dr. Levinson attributed those medications as

needed to treat other allergies. Id. at 208. Dr. Levinson also acknowledged that a subsequent visit

record from July 2015 indicated that Ms. Guzman had some erythema (or “red patch of skin”) on

the inner elbow. Id. at 208-09; see Ex. 1 at 576-77. He agreed that his could be evidence of an

active skin rash, but asserted that such a rash was likely different from the maculopapular rash

described in February 2014. Tr. at 210-12.32 Overall, however, Dr. Levinson maintained that no

treater ever diagnosed Ms. Guzman with chronic urticaria/hives or vasculitis, and he found no

evidence in the medical record of such lesions on exam over the course of her treatment. Id. at 157,

186-87.

The July 2015 photo submitted by Ms. Guzman similarly did not alter Dr. Levinson’s

opinion. Tr. at 154. In his view, it revealed no evidence of vasculitis or chronic urticaria. Id.

Moreover, based on his review of the medical literature, lesions associated with either condition

almost never appear on the palms (as the photograph purports to show) or soles of feet. Id. at 151.

He thus found this evidence more supportive of his opinion that Petitioner did not suffer from

either condition.

Dr. Levinson next discussed the biologic mechanism offered by Dr. Axelrod in support of

Petitioner’s causation theory. Tr. at 165-66. In his view, Dr. Axelrod accurately explained the

workings of an idiotype/anti-idiotype network, a process that regulates the adaptive immune

system in responding to certain foreign stimulants like infection. Id. at 166-67; Second Levinson

Rep. at 2. Petitioner was also arguing, accurately, that the initial antibodies produced in an adaptive

immune response caused additional T cells/B cells to produce additional antibodies (specific to the

original antigen/antibody response) – which thereafter bind to the insulting antigen and form an

“idiotype” or mosaic complex. Tr. at 167-68.

But Dr. Levinson did not, however, find Dr. Axelrod’s application of the theory in this case

to be credible – because the mechanism had not been shown to be pathogenic in nature. Tr. at 169,

170; First Levinson Rep. at 9-10. Rather, Dr. Axelrod was describing a “physiologic” response

that (even if vaccine-triggered) has never been demonstrated to be capable of producing immune

complexes resulting in pathology akin to what Petitioner had allegedly experienced. Tr. at 169-70.

Dr. Levinson posited that the literature offered by Dr. Axelrod on this point suggested that no

animal (or human) experimental models have indicated that these complexes can actually (as

opposed to theoretically) form from the above-described antibody interaction. Id. at 169. And in

any event, none of the literature cited by Petitioner (i.e., Jerne, Phillips, Bhattacharya-Chatterjee,

32

Dr. Levinson also found it significant that Dr. Canfield did not choose to biopsy the rash noted on exam at this visit.

In his view, Dr. Canfield is a well-credentialed and experienced allergist would request a biopsy be performed if he

felt Ms. Guzman had any form of vasculitis. Tr. at 146-47. Since there was no record evidence of a biopsy, Dr.

Levinson felt this weighed against concluding Petitioner’s condition included vascular involvement in any way.

18

Brown, Brozek) suggested that these complexes could be vaccine-induced, or result in vasculitis

or chronic urticaria. First Levinson Rep. at 10; Second Levinson Rep. at 2.

Dr. Levinson further critiqued Dr. Axelrod’s theory that the concept of epitope spreading

could accurately account for how the alleged initial vaccine-induced response could produce a

chronic condition. Tr. at 170. In his view, that theory could only be credibly linked to autoimmune

diseases already known to be mediated by autoreactive T cells or B cells (or autoantibodies). Id.;

see also First Levinson Rep. at 10. In the context of the present case, however, Dr. Levinson

posited, there is no evidence of an autoimmune reaction in the proffered medical records – thereby

rendering the concept inapplicable, given that epitope spreading depends on initial tissue damage

due to a primary autoimmune reaction that then in turn causes secondary expression of other

autoantibodies to “spread” damage. Tr. at 170-71; First Levinson Rep. at 10; Second Levison Rep.

at 2-3; see C. Vanderlugt, et al., Epitope Spreading in Immune-Mediated Disease: Implications for

Immunotherapy, 2 Immunol. 85, 86-91 (2002), filed as Ex. A, Tab 9 (ECF No. 23-8). Vasculitis,

by contrast, is simply “autoreactive” from the outset – and thus would not present in this manner.

Tr. at 171.

Ultimately, Dr. Levinson maintained that vaccines cannot cause urticarial vasculitis or

chronic urticaria. Tr. at 215. At best, some formulations of the flu vaccine (specifically those

containing the allergen ovalbumin) could theoretically cause an individual with an egg allergy to

develop urticarial lesions immediately post-vaccination, but such a reaction would only lead to

acute urticaria, not a chronic form. Id. at 215-26. Dr. Levinson did allow for the hypothetical

possibility that chronic hives could manifest post-vaccination, but he doubted that a plausible

biologic scientific or medical mechanism exists to explain such a reaction. Id. at 216-17. He also

seemingly conceded that Ms. Guzman’s initial maculopapular rash could have been associated

with the flu vaccine (given that she complained of other symptoms commonly associated with

vaccination, like nausea, headache, etc.). Id. at 219. But despite the above, Dr. Levinson

maintained that facts of this case and the testimony offered (both by Petitioner and Dr. Axelrod)

in support could not credibly establish that Petitioner’s own symptoms could be so explained. Id.

at 217-19.

Instead of vaccination, Dr. Levinson suggested that Ms. Guzman’s symptoms could be

more reliably attributed to various chemical hypersensitivities (for example, cleaning detergents,

perfumes, lipstick, etc.). Tr. at 218; First Levinson Rep. at 8. He referenced medical records

suggesting that Ms. Guzman had reported experiencing allergies and/or skin reactions following

exposure to these agents (as well as documented diagnosis of allergic rhinitis). Tr. at 218; see, e.g.,

Ex. 1 at 173, 175. In his view, these agents could not be ruled out as potential causes for her

symptoms – although he admitted that no treater had conducted an allergic evaluation to determine

if her skin rash symptoms could be attributed to these sensitivities. First Levinson Rep. at 8.

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III. Procedural History

Ms. Guzman filed her Petition on July 16, 2015. Pet. at 1. Following the filing of pertinent

medical records, Respondent filed the Rule 4(c) Report on April 11, 2016 (ECF No. 15), contesting

Ms. Guzman’s right to an entitlement award. Updated medical records were filed thereafter. See

ECF No. 17.

Due to the issues identified in the Rule 4(c) Report, I ordered the parties to file expert

reports in support of their respective positions. Petitioner filed an initial report for Dr. Axelrod on

September 9, 2016 (ECF No. 21-2). Respondent’s initial report from Dr. Levinson was filed

thereafter on December 2, 2016 (ECF No. 22-1). Supplemental expert reports were filed on May

10, 2017 (ECF No. 25-1) and September 8, 2017 (ECF No. 27), respectively.

I set the matter for hearing on October 25, 2018 (ECF No. 29). The hearing took place as

scheduled, and included testimony from the experts identified above (along with testimony from

Petitioner). Following the hearing’s conclusion, the parties did not submit post-hearing briefs. The

matter is ripe for adjudication.

IV. Applicable Law

A. Petitioner’s Overall Burden in Vaccine Program Cases

To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that

he suffered a “Table Injury” – i.e., an injury falling within the Vaccine Injury Table –

corresponding to one of the vaccinations in question within a statutorily prescribed period of time

or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table

Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §

11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1321 (Fed.

Cir. 2010); Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006).

In this case, Petitioner does not assert a Table claim.

For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance

of the evidence” burden of proof. Section 13(1)(a). That is, a petitioner must offer evidence that

leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence

before [he] may find in favor of the party who has the burden to persuade the judge of the fact’s

existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.

476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).

Proof of medical certainty is not required. Bunting v. Sec’y of Health & Human Servs., 931 F.2d

867, 873 (Fed. Cir. 1991). In particular, a petitioner must demonstrate that the vaccine was “not

only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.”

Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344,

1352-53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352, 1355 (Fed.

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Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his assertions;

rather, the petition must be supported by either medical records or by the opinion of a competent

physician. Section 13(a)(1).

In attempting to establish entitlement to a Vaccine Program award of compensation for a

Non-Table claim, a petitioner must satisfy all three of the elements established by the Federal

Circuit in Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005): “(1)

a medical theory causally connecting the vaccination and the injury; (2) a logical sequence of cause

and effect showing that the vaccination was the reason for the injury; and (3) a showing of

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

Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners

must provide a “reputable medical theory,” demonstrating that the vaccine received can cause the

type of injury alleged. Pafford, 451 F.3d at 1355-56 (citations omitted). To satisfy this prong, a

petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”

Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such a theory

must only be “legally probable, not medically or scientifically certain.” Id. at 549.

Petitioners may satisfy the first Althen prong without resort to medical literature,

epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical

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

Capizzano, 440 F.3d at 1325-26). Special masters, despite their expertise, are not empowered by

statute to conclusively resolve what are essentially thorny scientific and medical questions, and

thus scientific evidence offered to establish Althen prong one is viewed “not through the lens of

the laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant evidence

standard.” Id. at 1380. Accordingly, special masters must take care not to increase the burden

placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras v. Sec’y of

Health & Human Servs., 121 Fed. Cl. 230, 245 (2015) (“[p]lausibility . . . in many cases may be

enough to satisfy Althen prong one” (emphasis in original)), vacated on other grounds, 844 F.3d

1363 (Fed. Cir. 2017). But this does not negate or reduce a petitioner’s ultimate burden to establish

his overall entitlement to damages by preponderant evidence. W.C. v. Sec’y of Health & Human

Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted).

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

supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,

569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Human Servs., 956

F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions

and views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 F.3d

at 1367; Capizzano, 440 F.3d at 1326 (“medical records and medical opinion testimony are favored

in vaccine cases, as treating physicians are likely to be in the best position to determine whether a

‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury’”)

(quoting Althen, 418 F.3d at 1280). Medical records are generally viewed as particularly

21

trustworthy evidence, since they are created contemporaneously with the treatment of the patient.

Cucuras v. Sec’y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).

However, medical records and/or statements of a treating physician’s views do not per se

bind the special master to adopt the conclusions of such an individual, even if they must be

considered and carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis,

conclusion, judgment, test result, report, or summary shall not be binding on the special master or

court”); Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is

nothing . . . that mandates that the testimony of a treating physician is sacrosanct – that it must be

accepted in its entirety and cannot be rebutted”). As with expert testimony offered to establish a

theory of causation, the opinions or diagnoses of treating physicians are only as trustworthy as the

reasonableness of their suppositions or bases. The views of treating physicians should also be

weighed against other, contrary evidence also present in the record – including conflicting opinions

among such individuals. Hibbard v. Sec’y of Health & Human Servs., 100 Fed. Cl. 742, 749 (2011)

(not arbitrary or capricious for special master to weigh competing treating physicians’ conclusions

against each other), aff’d, 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec’y of Health & Human

Servs., 100 Fed. Cl. 119, 136 (2011), aff'd, 463 F. App'x 932 (Fed. Cir. 2012); Veryzer v. Sec’y of

Health & Human Servs., No. 06-522V, 2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29,

2011), mot. for review den’d, 100 Fed. Cl. 344, 356 (2011), aff’d without opinion, 475 F. App’x

765 (Fed. Cir. 2012).

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

the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the

phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant

proof that the onset of symptoms occurred within a timeframe which, given the medical

understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan

v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for

what is a medically acceptable timeframe must also coincide with the theory of how the relevant

vaccine can cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of

Health & Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after remand, 105 Fed. Cl.

353 (2012), aff’d mem., 2013 WL 1896173 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Human

Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for review

den’d (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

B. Law Governing Analysis of Fact Evidence

The process for making determinations in Vaccine Program cases regarding factual issues

begins with consideration of the medical records. Section 11(c)(2). The special master is required

to consider “all [] relevant medical and scientific evidence contained in the record,” including “any

diagnosis, conclusion, medical judgment, or autopsy or coroner’s report which is contained in the

record regarding the nature, causation, and aggravation of the petitioner’s illness, disability, injury,

condition, or death,” as well as the “results of any diagnostic or evaluative test which are contained

22

in the record and the summaries and conclusions.” Section 13(b)(1)(A). The special master is then

required to weigh the evidence presented, including contemporaneous medical records and

testimony. See Burns v. Sec’y of Health & Human Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (it is

within the special master’s discretion to determine whether to afford greater weight to

contemporaneous medical records than to other evidence, such as oral testimony surrounding the

events in question that was given at a later date, provided that such determination is evidenced by

a rational determination).

Medical records that are created contemporaneously with the events they describe are

presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s

health problems). Cucuras, 993 F.2d at 1528; Doe/70 v. Sec’y of Health & Human Servs., 95 Fed.

Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner’s testimony and his

contemporaneous medical records, the special master’s decision to rely on petitioner’s medical

records was rational and consistent with applicable law”), aff’d, Rickett v. Sec’y of Health &

Human Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption is

based on the linked propositions that (i) sick people visit medical professionals; (ii) sick people

honestly report their health problems to those professionals; and (iii) medical professionals record

what they are told or observe when examining their patients in as accurate a manner as possible,

so that they are aware of enough relevant facts to make appropriate treatment decisions. Sanchez

v. Sec’y of Health & Human Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr.

Apr. 10, 2013); Cucuras v. Sec’y of Health & Human Servs., 26 Cl. Ct. 537, 543 (1992), aff’d, 993

F.2d at 1525 (Fed. Cir. 1993) (“[i]t strains reason to conclude that petitioners would fail to

accurately report the onset of their daughter’s symptoms.”).

Accordingly, if the medical records are clear, consistent, and complete, then they should

be afforded substantial weight. Lowrie v. Sec’y of Health & Human Servs., No. 03-1585V, 2005

WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical

records are generally found to be deserving of greater evidentiary weight than oral testimony –

especially where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528;

see also Murphy v. Sec’y of Health & Human Servs., 23 Cl. Ct. 726, 733 (1991), aff’d per curiam,

968 F.2d 1226 (Fed. Cir. 1992), cert. den’d, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United

States v. United States Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that

oral testimony which is in conflict with contemporaneous documents is entitled to little evidentiary

weight.”)).

However, there are situations in which compelling oral testimony may be more persuasive

than written records, such as where records are deemed to be incomplete or inaccurate. Campbell

v. Sec’y of Health & Human Servs., 69 Fed. Cl. 775, 779 (2006) (“like any norm based upon

common sense and experience, this rule should not be treated as an absolute and must yield where

the factual predicates for its application are weak or lacking”); Lowrie, 2005 WL 6117475, at *19

(“[w]ritten records which are, themselves, inconsistent, should be accorded less deference than

those which are internally consistent”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a

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determination regarding a witness’s credibility is needed when determining the weight that such

testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Human

Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

When witness testimony is offered to overcome the presumption of accuracy afforded to

contemporaneous medical records, such testimony must be “consistent, clear, cogent, and

compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec’y of Health & Human

Servs., No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In

determining the accuracy and completeness of medical records, the Court of Federal Claims has

listed four possible explanations for inconsistencies between contemporaneously created medical

records and later testimony: (1) a person’s failure to recount to the medical professional everything

that happened during the relevant time period; (2) the medical professional’s failure to document

everything reported to her or him; (3) a person’s faulty recollection of the events when presenting

testimony; or (4) a person’s purposeful recounting of symptoms that did not exist. La Londe v.

Sec’y of Health & Human Servs., 110 Fed. Cl. 184, 203-04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir.

2014). In making a determination regarding whether to afford greater weight to contemporaneous

medical records or other evidence, such as testimony at hearing, there must be evidence that this

decision was the result of a rational determination. Burns, 3 F.3d at 417.

C. Analysis of Expert Testimony

Establishing a sound and reliable medical theory often requires a petitioner to present

expert testimony in support of his claim. Lampe v. Sec’y of Health & Human Servs., 219 F.3d

1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to

the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509

U.S. 579, 594-96 (1993). See Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328, 1339

(Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir.

1999). “The Daubert factors for analyzing the reliability of testimony are: (1) whether a theory or

technique can be (and has been) tested; (2) whether the theory or technique has been subjected to

peer review and publication; (3) whether there is a known or potential rate of error and whether

there are standards for controlling the error; and (4) whether the theory or technique enjoys general

acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2 (citing Daubert,

509 U.S. at 592-95).

The Daubert factors play a slightly different role in Vaccine Program cases than they do

when applied in other federal judicial for a (such as the district courts). Daubert factors are usually

employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence

that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors

are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health

& Human Servs., 94 Fed. Cl. 53, 66-67 (2010) (“uniquely in this Circuit, the Daubert factors have

been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of

expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the

24

persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88

Fed. Cl. at 742-45. In this matter (as in numerous other Vaccine Program cases), Daubert has not

been employed at the threshold, to determine what evidence should be admitted, but instead to

determine whether expert testimony offered is reliable and/or persuasive.

Respondent frequently offers one or more experts of his own in order to rebut a petitioner’s

case. Where both sides offer expert testimony, a special master’s decision may be “based on the

credibility of the experts and the relative persuasiveness of their competing theories.”

Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing

Lampe, 219 F.3d at 1362). However, nothing requires the acceptance of an expert’s conclusion

“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too

great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743

(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 91997)); see also Isaac v. Sec’y of Health &

Human Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot.

for review den’d, 108 Fed. Cl. 743 (2013), aff’d, 540 Fed. App’x 999 (Fed. Cir. 2013) (citing

Cedillo, 617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony,

based on a particular expert’s credibility, is part of the overall reliability analysis to which special

masters must subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d at 1325-26

(“[a]ssessments as to the reliability of expert testimony often turn on credibility determinations”);

see also Porter v. Sec’y of Health & Human Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this

court has unambiguously explained that special masters are expected to consider the credibility of

expert witnesses in evaluating petitions for compensation under the Vaccine Act”).

D. Consideration of Medical Literature

Both parties filed medical and scientific literature in this case, but not every filed item

factors into the outcome of this decision. While I have reviewed all of the medical literature

submitted in this case, I discuss only those articles that are most relevant to my determination

and/or are central to Petitioner’s case – just as I have not exhaustively discussed every individual

medical record filed. Moriarty v. Sec’y of Health & Human Servs., 844 F.3d 1322, 1328 (Fed. Cir.

2016) (“[w]e generally presume that a special master considered the relevant record evidence even

though he does not explicitly reference such evidence in his decision”) (citation omitted); see also

Paterek v. Sec’y of Health & Human Servs., 527 F. App’x 875, 884 (Fed. Cir. 2013) (“[f]inding

certain information not relevant does not lead to – and likely undermines – the conclusion that it

was not considered”).

ANALYSIS

I. Overview of Relevant Medical Terms and Prior Relevant Decisions

As noted above, Respondent argues that the diagnoses proffered by Petitioner (whether

cutaneous vasculitis or chronic urticaria) are unsupported by the medical record in light of

25

scientific/medical understanding of these conditions. Because Petitioner’s causation theory turns

on the determination that Dr. Axelrod properly characterized her condition, I will briefly discuss

what the expert testimony and filed literature says about the two most relevant proposed diagnoses.

The literature filed in the present matter unquestionably defines vasculitis as inflammation

of the blood vessels. Kluger at 125. The various vasculitic subtypes differ according to a spectrum

of severity (generally dependent upon the type of blood vessel affected and the underlying

inflammatory/systemic effect on the body), and are further distinguishable based on the clinical

and histopathologic features (as well as the extent of the damage caused to the body’s organ

systems). As noted earlier, cutaneous vasculitis is isolated to the skin. It displays a wide variety

of elementary lesions including urticaria, purpura, infiltrated erythema, hemorrhagic vesicles,

ulcers, nodules, livedo, infarcts, and digital gangrene. Kluger at 125. The urticaria associated with

vasculitis, however, is considered “atypical” with “distinct features from common urticaria.” Id.

at 126. Typically, urticarial lesions associated with vasculitis linger for a period longer than

twenty-four hours, and are routinely accompanied by purpura, postinflammtatory pigmentation,

and symptoms of burning. Id. Palpable purpura is by far the most frequent manifestation. Id. at

125. A skin biopsy is required to confirm the diagnosis and subtype, and treatment typically

includes anti-inflammatory agents and/or stronger immunosuppressive drugs (depending on the

severity of disease course). Id. at 128, 137.

Chronic urticaria is defined as “urticaria that is present for greater than [six] weeks.”

Kaplan at 477. Histologically, it is characterized by a “perivascular infiltrate around the venules,

without vasculitis or immune complex deposits.” Jauregui at 43 (emphasis added). Triggering

events include identifiable agents like an allergic reaction to a food/drug or a viral illness. Kaplan

at 477. There are two subtypes associated with chronic urticaria: inducible urticaria and

spontaneous urticaria. Id. Inducible urticarial lesions appear as often as the host interacts with an

identified stimulus, and typically last for more than an hour – but less than twenty-four to thirty-

six hours, thereby distinguishing chronic urticaria from urticarial-related vasculitis. Jauregui at 42;

Kaplan at 477. Spontaneous urticarial lesions are unpredictable, but appear in similar fashion –

though they can present for multiple days at a time. Kaplan at 477. Antihistamines and

corticosteroids can be used to treat both types (though antihistamine is considered the treatment

option of choice). Id.; see also Jauregui at 41. Chronic urticaria usually does not involve systemic

manifestations. Jauregui at 43.

Urticarial vasculitis is a rare, chronic, subtype of cutaneous vasculitis that affects five to

ten percent of patients with chronic urticaria. Kluger at 129. In most cases, the disease is idiopathic

in nature. Id. Two subtypes have been identified: hypocomplementemic (HUV) and

nonhypocomplementemic (NUV). HUV can be associated with certain illnesses (including

connective tissue disease, systemic lupus, cryoglobulinemia, hepatitis C infection, drugs, and viral

infections. Id. Pathologically, HUV is also associated with elevated anti-C1q antibodies or

antinuclear antibodies. Id. It is also typically accompanied by an elevated ESR. Id. NUV is usually

26

idiopathic, limited to the skin, and self-resolving (but can be associated with elevated eosinophil

levels). Id. As with vasculitis generally, a biopsy is required to confirm the diagnosis. Id. at 137.

Cutaneous vasculitis has been deemed a compensable injury in the Program in other cases.

See, e.g., McElroy v. Sec’y of Health & Human Servs., No. 11-679, 2012 WL 1739873, at *4 (Fed.

Cl. Spec. Mstr. Apr. 13, 2012) (awarding entitlement where biopsy-confirmed urticarial vasculitis

presented within a “few” days following the flu vaccine). Chronic urticaria has also been alleged

as an injury, but with varying degrees of success. Waterman v. Sec’y of Health & Human Servs.,

No. 13-44V, 2016 WL 761173, at *8 (Fed. Cl. Spec. Mstr. Feb. 5, 2016) (physician-diagnosed

chronic urticaria with two-week onset found to be caused by HPV vaccine); but compare Warfle

v. Sec’y of Health & Human Servs., No. 05-1399V, 2010 WL 2671504, at *32 (Fed. Cl. Spec.

Mstr. June 15, 2010) (DTap vaccine not causal of chronic urticaria, where Petitioner failed to

preponderantly establish the injury alleged and ultimately the first Althen prong – due primarily to

the lack of evidence establishing the ability of the vaccine to cause persistent, month-long

symptoms).

II. Petitioner Has Not Satisfied the Althen Prongs.

I am addressing the Althen prongs in order of their significance to my determination, rather

than consistent with their sequential presentation in the underlying Federal Circuit decision.

A. Althen Prong Two

1. Petitioner Did Not Have Vasculitis or Chronic Urticaria

Assuming for sake of argument that Petitioner could establish that the flu vaccine can cause

cutaneous vasculitis and/or chronic urticaria, I would still be unable to conclude (based on the

records filed in this case) that it likely caused Ms. Guzman’s symptoms – because it does not

appear she suffered from either condition. The failure to establish a claimed injury can be fatal to

a petitioner’s claim. See, e.g., Lombardi v. Sec'y of Health & Human Servs., 656 F.3d 1343, 1353

(Fed. Cir. 2011). This is especially true in this case, as Petitioner’s causation theory largely

depended on my finding that Petitioner suffered some kind of vasculitis, with her rash-like

symptoms being the condition’s primary manifestation.

Nowhere in the record is there clear evidence that Ms. Guzman was ever diagnosed with

vasculitis or chronic urticaria. See Ex. 1 at 494, 497-99, 501-02, 503-05, 555-57. 576-77; Ex. 2 at

27, 42-43. No treater documented urticarial lesions on exam, and the record is otherwise void of

any concern for a vasculitic condition. No test results (i.e., a biopsy) of any kind can be credibly

pointed to in this case that could suggest Petitioner experienced some vasculitic injury (or urticarial

lesions).

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Moreover, the record otherwise does not contain sufficient evidence from which it could

be concluded that Petitioner more likely than not did have vasculitis or urticarial lesions, regardless

of whether she was so diagnosed. The treaters most competent to weigh in on the topic of such a

condition, such as Dr. Canfield, never reached any conclusions about her complaints that could be

deemed consistent with vasculitis or urticaria in a meaningful sense. At best, the records close-in-

time to her receipt of the vaccine in February 2014 reveal that Ms. Guzman was assessed with a

maculopapular or erythematous rash consistent with a possible allergic reaction that mostly

resolved within two months thereafter (or by mid-April 2014). Ex. 1 at 493, 497-99, 501-03.

Ms. Guzman’s testimony at hearing similarly did not reliably establish that she experienced

any additional adverse symptoms (that could arguably be associated with vasculitis) other than the

initial rash documented in the record between February 2014 and mid-April of that year (and the

inner elbow rash noted on exam in July 2015). Her statements at hearing were generally consistent

with the medical records, apart from her assertion that she experienced the documented rash on

and off consistently since late February 2014 (and even at the time of hearing – in October 2018).

Tr. at 23, 40-42, 37, 53. Indeed, the records filed in the case reference multiple visits where no

rash was found on exam following mid-April 2014. See, e.g., Ex. 1 at 503-05, 508-52, 555-56; Ex.

4 at 1-6; Ex. 2 at 27, 43. To the extent Petitioner attempted to vary what the record stated, she

failed to establish grounds for so doing. See, e.g., Cucuras, 993 F.2d at 1528.

Petitioner also points to the fact that she was continuously taking, or being prescribed,

certain medications that were successfully treating her condition (and thus presumably tempering

her overall presentation, and thereby allowing the inference that her condition was more than

regular hives). Yet, as discussed above, literature filed by both parties indicates that true vasculitis

does not respond to antihistamine treatment – and topical creams would be used with simple

urticaria rather than a vasculitis (for which, Dr. Levinson stated, such a treatment would in fact be

contraindicated). See, e.g., Ference; Tr. at 72-74, 148-49. Accordingly, the effectiveness of these

treatments is equally supportive of the conclusion that Petitioner’s condition was not an immune-

mediated vasculitis, but instead something more benign.33

Dr. Axelrod acknowledged all of the above, but maintained that Petitioner’s records were

consistent with a vasculitic condition, with symptoms manifesting as chronic urticaria. In so

opining, however, he relied primarily on Ms. Guzman’s testimony and the photographic evidence

submitted in support (which, as Dr. Levinson credibly established, was not particularly probative).

Since he could not point to a contemporaneous record documenting concerns for a vasculitic

condition (or urticarial lesions), Dr. Axelrod insisted that notations in the record revealing the

presence of a maculopapular rash were consistent with an urticarial presentation. Tr. at 69-70, 93,

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The literature does suggest that antihistamines can be beneficial in treating chronic urticaria (see, e.g., Jauregui;

Ellingsen), but (for the reasons discussed herein) the record does not support such a diagnosis – and Petitioner’s overall

causation theory relies on the determination that her condition was vasculitic.

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104-06. To support this assertion, Dr. Axelrod cited to Calabrese – a study he acknowledged at

hearing discussed a form of vasculitis distinguishable from the one proffered in the present case

(hypersensitivity vasculitis). Calabrese at 1110. Calabrese does include maculopapular rash as one

criteria relevant to the urticarial vasculitis diagnosis, but adds that the diagnosis requires

satisfaction of three out of five criteria (including: age at onset > 16 years, medication use at onset,

palpable purpura on exam, and/or biopsy evidence consistence with that typical for a vasculitis

injury) for confirmation. Id. I thus could not conclude from the above that Ms. Guzman’s rash was

by itself suggestive of a vasculitic condition without evidence of additional criteria, which in this

case (beyond Petitioner’s age) are absent. Otherwise, none of the scientific literature referenced in

connection with chronic urticaria indicates that a maculopapular rash is a presenting symptom.

See, e.g., Kaplan; Kluger.

Dr. Levinson by contrast, offered scientific literature discussing the relevant

symptomatology course associated with both vasculitis and chronic urticaria, and persuasively

distinguished the conditions from the maculopapular rash revealed occasionally in Ms. Guzman’s

medical record. Relying on Kluger, Dr. Levinson posited that urticarial lesions associated with

cutaneous vasculitis would present in a lingering form (i.e., lasting twenty-four to forty-eight

hours) and would be accompanied by pain, itching, and hyperpigmentation of the skin (non-

blanching). Tr. at 144, 184-85, 214; Kluger at 126. A biopsy would also be required to confirm the

diagnosis (although one was never performed in this case). Tr. at 146-49; Kluger at 133. Lesions

associated with chronic urticaria, by contrast, would typically manifest as an acute, erythematous,

blanching, lesion with a pale center – and require standard antihistamine treatment. Tr. at 144-45,

150-52. No such lesions were noted in the medical record at any time.

Also harming Petitioner’s showing on this front were limitations in Dr. Axelrod’s expertise

to testify on the injury in question. Although it is not uncommon in the Program for testifying

experts to propose a diagnosis that no contemporaneous treater has considered or embraced,

experts are only persuasive in doing so when their opinion arises from time-tested experience

treating or studying the injury in question. Despite his immunologic qualifications, and although

he may have some treatment familiarity with the proposed injuries, Dr. Axelrod did not

demonstrate personal expertise in the study or treatment of vasculitis-oriented conditions, and

certainly was less qualified to opine on such matters than Dr. Levinson (even taking into account

that the latter does not regularly treat patients anymore). Petitioner therefore could not obtain from

Dr. Axelrod’s testimony what the record and the filed medical and scientific literature did not

provide to her in support of the proposed diagnoses.

2. The Record Does Not Suggest the Flu Vaccine Injured the Petitioner

Petitioner’s obligation under the second Althen prong is to demonstrate a logical sequence

of cause and effect connecting the particular facts of her case to his medical theory. Sturdivant v.

Sec’y of Health & Human Servs., No. 07-788V, 2016 WL 552529, at *18 (Fed. Cl. Spec. Mstr.

Jan. 21, 2016) (discussing Althen prong two). But even if my focus is limited to those post-

29

vaccination symptoms and reactions that are reflected in the medical record, preponderant

evidence has not been offered establishing that the flu vaccine is likely responsible for Petitioner’s

symptoms.

The medical record in this case does not establish that Ms. Guzman was experiencing any

kind of chronic vaccine-caused injury in the months after vaccination. Rather – and contrary to

testimony at hearing regarding the “chronic” nature of her symptoms – that record suggests that

her rash largely resolved within a two- to three-month period post-vaccination (apart from the one

notation of erythema in July 2015 well after).34 The photographic evidence offered in support (also

dated over one year from onset) similarly does not represent clear evidence that her rash persisted

beyond that timeframe (and in fact is not particularly persuasive evidence of anything other than

some nonspecific redness on the palms that cannot be credibly linked to Petitioner’s alleged

symptoms course). See Tr. at 154; First Levinson Rep. at 9. And qualified specialist treaters like

Dr. Canfield, who did in July 2015 report observing some rash, directly disputed any causal

connection between the flu vaccine and Petitioner’s complained-of symptoms. See Ex. 1 at 577.

Moreover, there is no evidence in the record that suggests the existence of an undercurrent

of autoimmunity of the kind often seen in other Program cases, such as ongoing inflammation or

some other subclinical, pathologic process. Dr. Axelrod proposed that Ms. Guzman responded

well to antihistamine and topical steroid treatment – which allegedly prompted her treaters to

forego any biopsy testing that would have confirmed the nature of her injury. See Tr. at 73-74. But

the medical record reveals that relevant testing for the typical inflammatory marks (including IgE

and CRP) returned normal results. See Ex. 1 at 593-98. I give such facts greater weight than

Petitioner's explanations for why certain testing evidence might be absent from the record (which

can just as credibly be attributed to the fact that Ms. Guzman’s existing treaters saw no reason,

based upon her presentation, even to suspect that vasculitis might explain her symptoms).

I also take note of the fact that Respondent’s expert identified an alternative explanation

for Petitioner’s symptoms that was inadequately countered by Petitioner. Dr. Levinson pointed to

evidence in the record suggesting that Petitioner’s symptoms could be attributable to various pre-

existing hypersensitivities (i.e., cleaning detergents, perfumes, and lipsticks) or allergic rhinitis.

Tr. at 218. Petitioner herself acknowledged that she complained of problems associated with these

allergic agents. Id. at 28-29. Program case law recognizes that clearly-identified alternative

diagnoses can call into question a petitioner’s allegations that a vaccine caused their onset of

adverse symptoms thereafter. See, e.g., Pafford v. Sec’y of Health & Human Servs., 64 Fed. Cl.

34

For this reason, even if it were conceded that Petitioner had experienced an initial allergic reaction to the flu vaccine,

manifesting in the form of a rash (as evidenced by the maculopapular rash and related symptoms noted in the record

from late February 2014), that reaction was transient, resolving well before the six-month period required under the

Vaccine Act’s severity requirement. 42 U.S.C. § 300aa-11(c)(1)(D)(i); see e.g., Hinnefeld v. Sec'y of Health & Human

Servs., No. 11-328V, 2012 WL 1608839, at *4-5 (Fed. Cl. Spec. Mstr. Mar. 30, 2012) (dismissing case where medical

history revealed that petitioner's injury resolved less than two months after onset). And regardless, this is not the theory

presented by Petitioner herein.

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19, 31 (2005) (“the Special Master may look to other facts apparent in the record, including

potential alternative causes that may undermine the petitioner’s case . . . .”), aff’d, 451 F.3d 1352

(Fed. Cir. 2006). The proposal that allergies caused Ms. Guzman’s symptoms (while plausible)

was certainly not established by Respondent with preponderant evidence, but it further served to

undercut the overall sufficiency of Petitioner’s showing on the “did cause” Althen prong.

B. Althen Prong One

Petitioner has not offered sufficient reliable scientific or medical evidence to meet her

burden of establishing a reliable theory for how the flu vaccine could cause vasculitis or urticarial

lesions. As described herein, Dr. Axelrod proposed that the flu vaccine can induce the production

of immune complexes, thereby causing inflammation sufficient to create a favorable environment

for the development of cutaneous vasculitis or chronic urticaria. But this theory has several

deficiencies.

First, a significant component of Petitioner’s theory unsuccessfully attempts to leverage

what is known about the proper functioning of the immune system (and specifically what causes

the creation of immune complexes) into proof that these anticipated processes can also be

pathogenic. Petitioner has referenced reliable literature establishing that certain immune

complexes can form in reaction to infection with a wild virus (see, e.g., Brown; Brozek), and that

these same complexes may play a role in various disease processes. But the theory lacks similar

support for its connecting proposition – that immune complex formation leads to or causes

vasculitis or urticarial lesions (even if those conditions involve such complexes) – as well as the

linchpin concept that vaccination can instigate such an entire disease process. It is not enough to

note that immune complexes have been measured in the context of certain injuries or illnesses (or

are involved in the body’s reaction to those illnesses). Dr. Axelrod otherwise does not have enough

demonstrated expertise studying these unsupported elements of the theory to give them ballast,

and no persuasive or reliable literature was offered on such points. There remain too many

unsupported, but vital, planks in Petitioner’s causation theory to deem it to have been

preponderantly established.

Another mechanism proposed by Dr. Axelrod – that Ms. Guzman’s subsequent re-exposure

to antigens in the flu vaccine (administered over a year prior) resulted in an amplified and

inherently more rapid cellular response, resulting in her alleged vasculitis – fails for similar

reasons. As the record indicates, Petitioner’s complained-of symptoms presented within two days

following her receipt of the vaccine. Ex. 1 at 493. And, Dr. Axelrod acknowledged at hearing that

he could not rely solely on a primary adaptive response to explain Petitioner’s onset of symptoms.

Tr. at 79-81. He therefore attempted to establish the February 2014 vaccination as a secondary

response attributable to priming that Petitioner’s immune system received from a vaccination

administered a year earlier (and with no documented evidence of a reaction to the initial

vaccination). To support this argument, Dr. Axelrod offered literature describing the concept of a

vaccine booster response intended to assist the body in developing immunologic memory to certain

31

vaccine antigens. See, e.g., Abbas; Miller. Neither Abbas nor Miller, however, provide any

evidence that a cumulative effect or response to a prior vaccine can produce an adverse pathologic

process (let alone one that results in vasculitis or urticarial lesions). The facts of this case otherwise

do not fit the paradigm of “challenge-rechallenge,” whereby a demonstrated initial reaction to a

prior vaccine is followed up with a demonstrably more robust reaction (thereby implicating the

vaccine). See, e.g., Viscontini v. Sec’y of Health & Human Servs., No. 98-619V, 2011 WL

5842577, at *22-24 (Fed. Cl. Spec. Mstr. Oct. 21, 2011), mot. for review den’d, 103 Fed. Cl. 600

(2012). The mere fact Petitioner received a flu vaccine before, without apparent incident, cannot

be transmuted into an explanation for a purported reaction to a second flu vaccination.

Petitioner’s invocation of epitope spreading to explain the seventeen month-long, chronic

character of her rash and related alleged symptoms following her receipt of the vaccine in February

2014 is also generally inconsistent with what is known about autoimmune disease processes (given

the facts of Petitioner’s case). As Dr. Levinson posited, epitope spreading can only occur

secondary to an initial autoimmune process – in which case tissue damage could occur and spread

after the initial process has already been triggered. The concept of epitope spreading (as it applies

to this set of facts) is thus not applicable, given Petitioner’s inability to establish a reliable theory

providing an explanation for her primary alleged vaccine reaction.

Petitioner otherwise heavily relied on case reports associating forms of the flu vaccine with

different types of vasculitis. See, e.g., Hughes; Chen; Liu. It is well recognized in the Program that

case reports are deserving of some evidentiary weight. Paluck v. Sec’y of Health & Human Servs.,

104 Fed. Cl. 457, 475 (2012) (noting that although “case reports ‘do not purport to establish

causation definitively, and this deficiency does indeed reduce their evidentiary value’ . . . ‘the fact

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

evidentiary weight’”) (quoting Campbell v. Sec’y of Health & Human Servs., 97 Fed. Cl. 650, 668

(2011)). However, case reports are not robust evidence favoring causation (even under the

Program’s comparatively lenient preponderance evidentiary standard). W.C. v. Sec’y of Health &

Human Servs., No. 07-456V, 2011 WL 4537887, at *13 (Fed. Cl. Spec. Mstr. Feb. 22, 2011) (“case

reports are generally weak evidence of causation because case reports cannot distinguish a

temporal relationship from a causal relationship”), mot. for review den’d, 100 Fed. Cl. 440 (2011),

aff’d, 704 F.3d 1352 (Fed. Cir. 2013). Moreover, the case reports offered either involved vasculitic

conditions that (as I note above) the record does not establish Petitioner had, or involved drug-

induced disease distinguishable from vaccination (see, e.g., Radic).

At bottom, Petitioner’s theory (by Dr. Axelrod’s admission) places great emphasis on the

injury’s close temporal association to vaccination (see, e.g., Tr. at 74, 88, 115-17) – a factual

connection well understood to be insufficient to meet a claimant’s burden. See, e.g., LaLonde v.

Sec’y of Health & Human Servs., 746 F.3d 1334, 1341 (Fed. Cir. 2014) (“a temporal correlation

alone is not enough to demonstrate causation”). She otherwise has not fleshed the theory out with

reliable and persuasive literature establishing that the flu vaccine could instigate vasculitis. And

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Dr. Axelrod’s expertise, while somewhat sufficient to explain aspects of the theory, was not

enough to fill in its many gaps. Petitioner has not met the Program’s preponderant evidentiary

standard with respect to the first Althen prong.

C. Althen Prong Three

The record in this case, as interpreted by Dr. Axelrod, does support the conclusion that

Petitioner's injury (assuming that it was vasculitis and/or chronic urticaria and that the flu vaccine

could indeed produce such a reaction) occurred in a medically acceptable timeframe consistent

with her theory. As noted above, Petitioner asserts that her symptoms began two days after her

receipt of the flu vaccine, and she offered reliable evidence supporting the contention that the

immune response to a vaccine would still be underway at that time. See, e.g., Abbas; Miller.

Notably, however, as discussed above, Petitioner’s causation theory in this case is not sufficiently

supported with preponderant evidence. Accordingly, the consistency of the onset timing in this

case with Petitioner’s theory does not aid Petitioner, when that same theory has been found to lack

reliability.

CONCLUSION

The evidentiary record does not support Petitioner’s contention that the flu vaccine she

received in February 2014 caused her to develop cutaneous vasculitis and/or chronic urticaria, or

that it could have done so. Petitioner has not established entitlement to a damages award, and

therefore I must DISMISS her claim.

In the absence of a timely-filed motion for review (see Appendix B to the Rules of the Court),

the Clerk shall enter judgment in accordance with this decision.

IT IS SO ORDERED.

/s/ Brian H. Corcoran

Brian H. Corcoran

Special Master

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