McKown v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 15-1451V

(to be published)

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

* Special Master Corcoran

*

CAILEN MCKOWN, *

* Filed: July 15, 2019

Petitioners, *

* Entitlement Decision; Human

v. * Papillomavirus (“HPV”) Vaccine;

* Postural Orthostatic Tachycardia

SECRETARY OF HEALTH AND * Syndrome (“POTS”); Eczema;

HUMAN SERVICES, * Autoimmune Diseases

*

Respondent. *

*

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

Clifford J. Shoemaker, Shoemaker, Gentry & Knickelbein, Vienna, VA, for Petitioner.

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

DECISION DENYING ENTITLEMENT1

On December 1, 2015, Cailen McKown filed a Petition under the National Vaccine Injury

Compensation Program (the “Vaccine Program”2), alleging that two doses of the Human

Papillomavirus (“HPV”) vaccine she received on March 20, 2013, and September 3, 2013,

respectively, along with a Hepatitis A vaccine received on March 20, 2013, caused her to suffer

postural orthostatic tachycardia syndrome (“POTS”) and skin rashes (including eczema). Petition

(ECF No. 1) (“Pet.”) at 1-2.

1

This Decision will be posted on the United States Court of Federal Claims’ 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 published

Decision’s inclusion of certain kinds of confidential information. Specifically, under Vaccine Rule 18(b), each party

has fourteen (14) 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 entire Decision will be available to the public in its current form. Id.

2

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

100 Stat. 3755 (codified as amended at 42 U.S.C. §§ 300aa-10–34 (2012)) (hereinafter “Vaccine Act” or “the Act”).

All subsequent references to sections of the Vaccine Act shall be to the pertinent subparagraph of 42 U.S.C. § 300aa.

A hearing in this matter was held on September 26-27, 2018. After consideration of the

record and testimony provided at hearing, I find that Petitioner is not entitled to a compensation

award. As discussed in more detail below, Petitioner has not demonstrated with reliable scientific

and medical evidence that the HPV or Hep A vaccines could be, or were, causative of her POTS

(or worsening of POTS or her preexisting eczema/skin symptoms). Petitioner’s experts failed to

offer a persuasive, reliable medical theory in support of her claim, and were unpersuasive in their

attempt to establish that Petitioner’s POTS was the rare neuropathic variant that could be

autoimmune in nature.

I. Factual Background

Pre-Vaccine Health History

Ms. McKown was born on January 14, 2000, and received routine vaccinations throughout

her childhood without any reported adverse events. Ex. 1 at 13-14. Her medical history was

significant for eczema (treated with Elidil), diffuse dry skin, and recurrent fever blisters, which

she experienced one to three times per month since the age of six months. Id. at 32-34 (12/1/2010

ten-year-old well-adolescent visit), 36 (2/25/2011 eleven-year-old well-adolescent visit), 38.

Around the time Petitioner received the first dose of the HPV vaccine, she had already

displayed symptoms pertaining to the injuries at issue in this case, in addition to eczema. Thus, on

March 20, 2013, at Petitioner’s thirteen-year-old well-child visit, her mother, Mrs. Tabatha

McKown, reported to treaters that Petitioner had recently experienced lightheadedness with

position changes and two episodes of syncope in the prior three months, both associated with

position changes and without heart palpitations. Ex. 1 at 44. Ms. McKown’s history of dry skin

was also noted, but she was otherwise deemed to be well. Id. The pediatrician’s impression was

neurocardiogenic syncope, and Petitioner was told to increase fluids and salt in her diet, with a

referral to a cardiologist to follow up on the possible cause of these symptoms. Id.

Receipt of HPV Vaccine Doses

Petitioner received the first HPV vaccine dose (along with the Hep A vaccine) on March

20, 2013, at the aforementioned well-child visit. Ex. 1 at 14, 44. No adverse reaction was noted at

the time, and there is no recorded instance of any reaction to the first HPV dose within a month of

its administration. Then, on April 26, 2013 (about five weeks following vaccination), emergency

medical service providers transported Ms. McKown to the emergency room at Eastside Medical

Center in Snellville, Georgia, from a local yogurt shop, where, following an upset stomach, she

had stood up and then immediately began feeling lightheaded, along with a severe headache. Ex.

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8 at 6-16. Petitioner passed in and out of consciousness for brief intervals several times, and she

was hyperventilating when EMS responders arrived. Id. at 6, 12.

At Eastside Medical Center, the treating ER physician noted that Ms. McKown had

reportedly experienced similar symptoms in the past, observing that she had been recently advised

by her primary care physician (“PCP”) to follow up with a cardiologist. Ex. 8 at 6, 12. Laboratory

results, an EKG,3 and a head CT scan4 were normal, with the exception of revealing left sphenoid

sinus disease. Id. at 8-10, 24-25. The ER physician diagnosed Petitioner with sinusitis (which he

noted could explain her headaches and dizziness), and vasovagal syncope, discharging her that

same day. Id. at 10.

Three days later Ms. McKown followed up with her PCP, Dr. Melissa Magill. Ex. 1 at 47.

Petitioner’s mother recounted Petitioner’s recent syncope symptoms at the yogurt shop, noting that

she had been “lightheaded” and “woozy,” and “trembly,” but not jerking, drifting in and out of

consciousness for five to ten minutes. Id. Following an exam, Dr. Magill assessed Petitioner with

a “known history of neurocardiogenic syncope[,]” and recommended that she increase fluid and

salt intake. Id.

Cardiology Assessment

On May 1, 2013, Ms. McKown saw Dr. Kenneth Dooley, a cardiologist at Sibley Heart

Center in Atlanta. Ex. 7 at 5-7. Dr. Dooley noted that Petitioner reported having passed out a total

of two to five times previously, most recently the week before. Id. Petitioner provided some

additional details about the circumstances of three of the times she had experienced syncope: first,

three years prior after her father had reprimanded her for poor behavior; second, approximately

six months prior while watching a veterinary procedure; and third, five days prior, in the yogurt

shop incident. Id. at 5. She also stated that she felt that her symptoms were worsening. Id. Upon

exam, Dr. Dooley noted that Petitioner almost passed out when asked to sit up. Id. at 6. Her supine

blood pressure was noted to be 104/64 (heart rate: 68), and her standing blood pressure was 90/52

3

An EKG (or “electrocardiogram”) is a noninvasive graphic tracing that records the electrical activity of the heart

muscle. Dorland’s Illustrated Medical Dictionary 597, 599 (32nd ed. 2012) (hereinafter Dorland’s). Each beat of the

heart is triggered by an electrical impulse (generated from cells in the heart), and the EKG records the timing and

strength of these signals. See Electrocardiogram, Mayo Clinic, https://www.mayoclinic.org/tests-

procedures/ekg/about/pac-20384983 (last accessed on June 19, 2019). EKGs are used to detect or diagnose common

heart problems (including irregular heart rhythm, blocked arteries, structural problems, heart attacks, or heart disease).

Id.

4

A CT (or “computerized tomography”) scan combines a series of X-rays taken from different angles around the body

and uses computer processing to create cross-sectional images of the bones, blood vessels, and soft tissues inside the

body. See CT Scan, Mayo Clinic, https://www.mayoclinic.org/tests-procedures/ct-scan/about/pac-20393675 (last

accessed on July 19, 2019). CT images are more detailed than a plain X-ray. Id. This type of scan is used to quickly

examine patients who may have wide-spread internal injuries, and can be used to diagnose or monitor diseases such

as cancer, heart disease, lung nodules, and liver masses. Id.

3

with a pulse of 100. Id. Dr. Dooley diagnosed her with “syncope, possibly vasovagal in origin[,]”

noting that her history and symptoms were most suggestive of simple fainting. Id. He scheduled

Petitioner for a tilt table test5 and recommended she be screened for epilepsy as well. Id.

Petitioner had a follow up appointment with Dr. Dooley two months later, on July 1, 2013.

Dr. Dooley noted that the tilt table test conducted in late May 2013 had been positive for POTS.

Ex. 7 at 8-9; see also Ex. 55. Orthostatic readings taken in conjunction with the test revealed a

significant increase in heartrate (when tilted from the supine position to the standing position),

followed by complaints of dizziness and blurry vision (after approximately eight minutes at

standing). Ex. 55 at 5. Ms. McKown’s blood pressure then dropped significantly (minimum cuff

pressure of 57/32) and her heartrate slowed significantly (into the low fifties) as the tilt returned

to flat. Id. Within five minutes after returning to the supine position, her rates returned to normal.

Id. Dr. Dooley discussed the results of the test, and noted that Petitioner continued to have short

syncopal episodes. Ex. 7 at 8-9. He prescribed Fludrocortisone (0.1 mg, once daily) in addition to

the Valtrex she was currently taking. Id. Dr. Dooley also advised Petitioner to return in six months

(or sooner if the medication did not work), and to have her mother notify him if she experienced

additional episodes. Id.

Repeated Skin-Related Symptoms

A week later, on July 8, 2013, Petitioner’s mother called Dr. Dooley’s office to report that

Petitioner had stopped taking Fludrocortisone, thinking it had caused her to develop a rash and

hives, although these symptoms resolved on their own after treatment with Benadryl. Ex. 7 at 33.

A week later, Petitioner’s mother called again to report that her hives had returned after she drank

a large glass of milk, causing Petitioner’s PCP to diagnose her with a dairy allergy. Id. at 31. Notes

from the telephone call also indicated that Ms. McKown’s PCP suspected her pre-existing eczema

may have been a manifestation of her dairy allergy. Id. Petitioner thereafter restarted

Fludrocortisone, with no initial notable problems at that time. Id. On July 23, 2013, however, her

mother called a third time to report that Petitioner was now suffering from worsening headaches,

and was not “feel[ing] like herself” (i.e., “feeling very tense”), although without any repeat

syncopal episodes. Id. at 30. Dr. Dooley recommended that Ms. McKown start Midodrine as an

alternative to Fludrocortisone. Id.

Petitioner went back to her PCP at Lawrenceville Pediatrics on July 25, 2013, now

complaining of worsening eczema, a rash on her neck, back, and arms, and insect bites. Ex. 1 at

5

A tilt table test is used to evaluate syncope by measuring heart rate and blood pressure in response to the body’s

change in position. Tilt Table Test, Mayo Clinic, https://www mayoclinic.org/tests-procedures/tilt-tabletest/about/pac-

20395124 (last accessed July 5, 2019). The patient begins by lying flat on a table for around 15 minutes. Id. The table

is then quickly tilted upright to change the body’s position from lying down to standing up. Id. The table generally

remains upright for 45 minutes to allow the doctor to monitor the patient's cardiovascular response. Id.

4

50. The pediatric nurse practitioner noted that Ms. McKown’s eczema flared when the weather

was hot, causing her to feel itchy and scratch her skin. Id. It was also noted that Petitioner had been

diagnosed with POTS recently and was waiting to see an electrophysiologist. Id. The nurse

practitioner advised Petitioner to see an allergist, and recommended treatment with various over-

the-counter antihistamines and ointments. Id. A few weeks later, on September 3, 2013, Petitioner

presented again to Lawrenceville Pediatrics with complaints relating to a sore throat and

congestion. Id. at 15-17. She was diagnosed with sinusitis, and now received her second HPV

vaccine dose, with no noted adverse reaction. Id. at 17.

Progression of Skin Symptoms and Efforts to Treat Them

In the ensuing months in the fall of 2013, Ms. McKown’s skin condition continued to

worsen. In November 2013, she had four dermatology appointments at Georgia Skin Cancer and

Aesthetic Dermatology in Athens, Georgia, for treatment of an itchy rash all over her body that

was reported to have been present for months. Ex. 2 at 11-12, 13-16, 20, 25-26. Following

examination, the treating dermatologist (Dr. Jeffrey Moulton) diagnosed her with atopic and

contact dermatitis and eczema. Id. at 25-26. Dr. Moulton recommended that Petitioner take

Clobetasol and/or Vaseline to mitigate her symptoms (in addition to avoiding strong cleansers,

scented detergents, and excessive hand washing). Id. at 25. Patch testing was also performed,

which was positive for numerous chemicals. Id. at 11-12, 13-16, 20. No instances of syncope or

POTS-related symptoms are reported in the medical records from this time period, however, and

Ms. McKown was noted to be alert, oriented, and in “no acute distress.” Id. at 11, 13, 25-26.

One month later, on December 4, 2013, Ms. McKown sought yet another opinion regarding

her skin condition. She presented to Dr. Deidre Crocker, at the Allergy & Asthma Center of

Conyers in Monroe, Georgia, complaining of worsening eczema and a rash. Ex. 3 at 2-4. At this

visit, Petitioner informed Dr. Crocker that she had always had mild eczema, but that her symptoms

had worsened in May 2013 – around the same time she was diagnosed with POTS. Id. at 2. The

rash was aggravated by hot water and sweat, and a variety of treatments (steroid injections,

Benadryl, and changes in shampoos/lotions) had proven ineffective. Id. Increased itching was also

noted with ingestion of wheat products. Id.

On exam, Petitioner displayed multiple scaly, red eczema patches on the neck, arms, and

trunk. Ex. 3 at 2-3. Her diagnosis remained “contact dermatitis and other eczema, due to

unspecified cause.” Id. at 3. Dr. Crocker expressed the view, however, that Ms. McKown’s skin

condition was likely not related to POTS. Id. at 4 (“POTS is not an immune disease so do not feel

that is triggering eczema but possible she has had some st[r]essors contributing to increased

eczema . . . [a]lso possible she may have developed some allergic sensitivities triggering her

eczema”). Id. She advised Petitioner to avoid a number of dermatitis allergens, and prescribed

Mometasone cream. Id.

5

Ms. McKown had a follow-up appointment with Dr. Crocker two weeks later, on

December 19, 2013. It was reported at this time that her eczema had improved, but she still was

experiencing significant itching and a rash. Ex. 3 at 5-6. Her food diary also revealed that every

time she ingested corn products she broke out in hives, with a milder reaction to wheat and other

products. Id. at 5. Blood work conducted on the following day was negative for celiac disease, but

allergy testing was positive for several foods and environmental substances, including fruits, oat,

carrot, barley, sweet potato, corn, and wheat. Id. at 11-13. During this blood testing, Ms. McKown

also had an episode of hypotension, hypoxia, and tachycardia during the blood draw. Ex. 1 at 18;

Ex. 20 at 1. She was reported to have passed in and out for ten minutes until her vitals came back

to normal. Ex. 20 at 1. But this reaction to the testing did not result in any further medical treatment,

emergency or otherwise.

2014 Treatment of Skin and POTS-related Symptoms

On January 2, 2014, Petitioner saw Dr. Crocker again, now reporting that the steroidal

treatment she had been prescribed the prior month had cleared her skin over the holiday, but that

she had experienced flares after playing with dogs and ingesting a wheat cracker. Ex. 3 at 8-9. Her

physical exam was normal but for multiple scaly, erythematous patches of eczema on the face,

neck, elbows, knees and legs. Id. at 9. Additional testing showed strong positives to cat, dust mites,

tree pollen, and grass pollen (as well as certain foods including wheat, corn, and soy). Id. Ms.

McKown was again prescribed oral Prednisone. Id. at 9.

One week later Ms. McKown presented to Dr. Seth Marcus, at GI Care for Kids in Atlanta

for treatment of abdominal pain (with specific concern for possible “allergic gut”), syncope, and

food allergies. Ex. 12 at 5-9; Ex. 1 at 18-21, 75. Similar to the health course described above, Dr.

Marcus noted that Petitioner had experienced minor syncopal episodes in the past, culminating in

her May 2013 complete loss of consciousness for twenty to thirty minutes along with other

associated symptoms. Ex. 12 at 5-6. He noted that these episodes usually arose with stressful or

exciting events, appeared to be more frequent during her menstrual cycle, and generally occurred

two to three times per month. Id. at 5-6. A history of eczema was also noted, along with intermittent

hives and worsening of her eczema in May 2013 (although the contemporaneous record does not

really record increased complaints of eczema before July 2013). Id. at 6. Consistent with Dr.

Crocker, Dr. Marcus expressed uncertainty as to whether Petitioner’s syncopal episodes could be

related to her atopic disease or were an independent phenomenon. Id. at 8-9 (“I am unaware of a

known relationship between POTS and atopy, histamine release, hypereosinophilic syndrome or

eosinophilic gastrointestinal disease”). Id. at 9. He did however opine that her syncope was likely

unrelated to dietary exposures, with the exception of her most recent event that had occurred one

day after exposure to wheat. Id. Labs again ruled out celiac disease. Ex. 5 at 85.

6

On January 27, 2014, Ms. McKown had a follow-up visit with her cardiologist, Dr. Dooley,

seeking clearance for her upcoming colonoscopy and endoscopy to help assess the cause of her

ongoing GI symptoms. Ex. 7 at 10-11, 34. Petitioner now stated she was having one to two

episodes of syncope per month, the last of which was on December 29, 2013, lasting around

twenty-five minutes and resulting in stiffness and eye-rolling (although this incident is not

reflected in any immediately contemporaneous record). Id. Dr. Dooley noted, however, that

Petitioner had not been taking her POTS medication for months, out of the concern that it

exacerbated her rash. Id. The colonoscopy and upper GI endoscopy were performed by Dr. Marcus

on January 31, 2014. Ex. 12 at 19-20. Biopsies showed no significant abnormalities except for

mild esophagitis with rare eosinophils in the distal and mid esophagus. Ex. 5 at 79-84.

On February 21, 2014, Petitioner saw another immunologist, Dr. Karen Freedle, at Emory

Children’s Center in Atlanta for a secondary evaluation of her skin condition. Ex. 1 at 76-79, 85-

87; Ex. 5 at 42-72. Consistent with past treaters, Dr. Freedle’s impression was atopic dermatitis,

chronic urticaria of unclear etiology, chronic nasal and ocular symptoms, intermittent GI

complaints, and multiple food allergies. Ex. 1 at 76. Laboratory results conducted during the visit

were also normal, with the exception of a mildly elevated sedimentation rate and positive ANA at

1:40 with a homogeneous pattern. Ex. 5 at 76-78.

On March 5, 2014, telephonic records establish that Petitioner’s mother called Dr. Dooley

about a recent study in a journal indicating that POTS could be caused by an autoimmune disorder,

and asked whether Petitioner’s treatment would change in light of such findings. Ex. 6 at 25. She

reported that Ms. McKown had been tested for lupus and many allergies, her last syncopal episode

was in December, and that most of her other medications had been eliminated. Id. Dr. Dooley

noted that he had not heard POTS was autoimmune, but that he could refer Petitioner to a

neurologist to explore this concern. Id.

Over the course of the next few months, Ms. McKown’s adverse skin symptoms continued

to worsen. On April 7, 2014, Petitioner again saw her PCP, Dr. Magill, complaining of the same

rash, but with concerns for possible staph infection. Ex. 1 at 22-24. On examination, Petitioner had

diffuse dry skin with “punched out” lesions to the forehead, elbow, wrists, ankles, and knees. Id.

at 23. Her diagnosis remained eczema, and Dr. Magill recommended that she continue taking

clindamycin and acyclovir. Id. That same month Petitioner had a follow-up with Dr. Freedle on

April 21, 2014. Ex. 5 at 35-37. Her examination was normal except for open, excoriated areas of

skin. Id. at 36. A skin biopsy taken at this visit from her right arm revealed subacute spongiotic

dermatitis. Ex. 1 at 93-96.

On May 12, 2014, Ms. McKown saw a different dermatologist, Dr. Zakiya Rice of

Children’s Healthcare of Atlanta, regarding her rash and sores. Ex. 4 at 65-70. The history from

this visit again identified onset as May 2013, with heat causing aggravation of symptoms. Id. at

7

65-66. The examination revealed eczematous papules with excoriations, but well-hydrated skin.

Id. at 68. Dr. Rice assessed Petitioner with “spongiotic dermatitis, steroid responsive,” and

recommended that she restart topical steroids and taper oral Prednisone. Id. At a follow-up

appointment on June 2, 2014, Dr. Rice noted that Petitioner continued to use Prednisone due to

her persist rash. Id. at 50-57. A biopsy taken during the visit was consistent with eczema. Id. at 55.

The following month, Petitioner saw her PCP, Dr. Magill, for her fourteen-year-old well

visit on June 4, 2014. Ex. 1 at 25-30. She now reported that she had been experiencing joint pain

in the shoulders, upper back, wrists, and fingers since October 2013 (in addition to the skin

rashes/eczema and syncopal episodes described above) – although, as the somewhat exhaustive

record review above reveals, no prior treaters had been informed of these newly-reported

symptoms. Id. at 25. Her examination was positive for persistent diffuse dry skin with

lichenification on the elbows and an erythematous rash on the face (consistent with her ongoing

skin symptoms). Id. at 27. Hives were also reported as a current problem (attributable to

overheating, embarrassment, and emotion), but were not noted on exam. Id. at 25, 27. By June 12,

2014, Ms. McKown had completed steroid treatment, but her skin was reportedly still red and

burning, the hives and sores were becoming more severe, and her joints were reported to be

throbbing. Ex. 4 at 32-33; Ex. 5 at 137-38.

Treatment of Joint Pain

On June 30, 2014, Ms. McKown saw a rheumatologist, Dr. Kelly Rouster-Stevens, at

Children’s Healthcare of Atlanta, for evaluation of her joint complaints. Ex. 21 at 1-3; Ex. 23 at

21-24. Dr. Rouster-Stevens noted that Petitioner had been diagnosed with POTS in May 2013, and

then a few months later developed a rash associated with pruritus and burning. Ex. 21 at 1. The

medical history from this visit also states that since her last syncopal episode in December 2013,

Petitioner had experienced some improvement in her POTS symptoms, but had developed joint

pain, and the persistence of her skin rash (initially thought to be related to allergies) was proposed

to possibly have some alternative explanation. Id. On examination, Ms. McKown displayed

eczema patches and multiple tender trigger points in her back and extremities, but no joint swelling

or warmth. Id. at 3. Dr. Rouster-Stevens opined that Petitioner likely did not have lupus, arthritis,

myositis, or any other chronic rheumatologic process, suggesting instead that her exam was most

consistent with amplified musculoskeletal pain syndrome. Id. Lab tests performed at this time did

not support a diagnosis of lupus or other autoimmune connective tissue disease. Id. at 4, 7-8. Dr.

Rouster-Stevens ultimately recommended that Petitioner be evaluated in the pain clinic. Id. at 10.

Roughly one month later, Ms. McKown had follow-up appointments with Drs. Freedle and

Rice on July 21, 2014. Ex. 5 at 20-22; Ex. 4 at 16-21. Dr. Freedle noted that Petitioner’s rash

responded well to steroids, but that she stopped taking them due to how they made her feel

mentally, and that overall she felt she was not experiencing true improvement on this treatment

8

course. Ex. 5 at 20. Her visit with Dr. Rice revealed the same persistent symptoms noted above.

Ex. 4 at 16-21. At this visit, Petitioner and her mother also reported they “worried about this

startign [sic] with Gardasil vaccination 3/2013 and 9/2013[,]” but Dr. Rice offered no opinion

regarding vaccine causation. See id. Otherwise, Dr. Rice noted that a naturopathic consult had been

scheduled for July of that year – at which time Petitioner planned to seek further treatment. Id.6

Cleveland Clinic Evaluation

In mid-August 2014, Petitioner obtained multiple evaluations at the Cleveland Clinic in

Ohio in an attempt to ascertain the etiology for her constellation of symptoms. None of these

Cleveland Clinic treaters concluded that her symptoms were vaccine-related, and few saw any

relationship between the different symptoms she was experiencing.

First, on August 13, 2014, Ms. McKown saw dermatologist Dr. Joan Tamburro, D.O. Ex.

11 at 5-11. The health history taken during the visit indicated that Petitioner reported she had been

itchy with sores all over her body since October 2013, shortly after receiving a second HPV

vaccine dose. Id. at 5. Her POTS diagnosis and joint pain were also noted. Id. at 6. After

examination and consideration of Petitioner’s history, Dr. Tamburro diagnosed her with atopic

dermatitis (consistent with the diagnosis of past treaters) which had not been adequately treated.

Id. at 7. Dr. Tamburro found no evidence to support a diagnosis of connective tissue disease,

determining only that Petitioner likely had an “angry back” (based on previous patch testing)

which explained the numerous allergy positives. Id. Exam notes also indicated that Dr. Tamburro

discussed with Petitioner and her mother that a “persistent rash from Gardasil [wa]s unlikely.” Id.

Lidex and topical ointments were prescribed for her symptoms. Id.

Second, on the following day Petitioner saw two Cleveland Clinic allergists, Drs. Maria

Blanch and Velma Paschall, for an alternative evaluation of what appeared to possibly be chronic

urticaria. Ex. 11 at 12-23. Both physicians noted that Petitioner had a history of eczema since

childhood that had become more severe beginning the summer of 2013. Id. at 12. Episodes of hives

(or urticaria) were also noted to be triggered by heat, stress, showers, and animals. Id. Upon exam,

it was determined that Petitioner’s symptoms were most consistent with severe, chronic urticaria

that was resistant to standard antihistamine treatment, recommending instead an alternative,

newly-approved treatment (Xolair). Id. at 14. Following lab testing, Dr. Paschall sent a letter to

6

In late July 2014, Ms. McKown sought naturopathic care for her persistent symptoms described herein (including

skin rashes, hives, dizziness, and joint pain). See Ex. 19 at 6-8 (visit to Oconee Natural Healthcare Center in

Watkinsville, GA). Ms. McKown’s treater, Dr. Wyler Hecht, reviewed her health history and recommended treatment

with various supplements including Sea Cure (a white-fish dietary supplement), Immuno PRP spray (an immune-

balancing spray), Immuno PRP powder (immune-balancing vitamin supplement), and Curacel (a plant-based vitamin

for cell growth) to aid her symptoms. Id. at 8. Dr. Hecht’s notes also indicated that Petitioner’s mother felt “as though

the Gardasil vaccine triggered the reaction in her daughter[,]” but he offered no opinion regarding causation. See id.

at 6.

9

Petitioner’s mother (dated September 19, 2014) in which she expressed the view that it was

“unlikely that [Petitioner] has autoimmune chronic urticaria” because both her anti-IgE and anti-

IgE receptor antibody tests were negative. Ex. 22 at 1.

Third, on August 15, 2014, Petitioner saw Cleveland Clinic rheumatologist Dr. Andrew

Zeft for a second evaluation for onset of joint symptoms and persistent rash. Ex. 11 at 24-28. The

examination revealed no objective evidence of arthritis. Id. at 28. Dr. Zeft opined that her arthralgia

was mechanical in etiology, and that she had amplified pain from muscle spasm and trigger of

muscle spasm secondarily due to pain and itching from her skin lesions. Id. He thus recommended

treatment of her primary skin lesions, and knee stretching and strengthening exercises. Id.

Subsequent Treatment

The following September through November 2014, Ms. McKown began treatment with

Dr. Phillip DeMio7 in Worthington, Ohio. Ex. 14 at 12. At this time, Petitioner’s mother reported

to Dr. DeMio that she had received a diagnosis of “Gardasil Syndrome (recently spoke with Lloyd

to confirm and Dr. Hitch in Athens),” along with POTS, chronic hives, and dermatitis. Id. She also

specifically told Dr. DeMio that Dr. Rice (the dermatologist Petitioner saw in the spring of 2014)

had determined that “Gardasil triggered all this but . . . won’t go on record to say so.” Id. at 22.

(As noted above, however, the official records from Petitioner’s visits to Dr. Rice do not

corroborate this assertion – and, if anything, undermine it).

Petitioner’s first visit with Dr. DeMio included a discussion of her health history and a

physical exam. Ms. McKown was noted to be “calm and “coop[erative]” on exam. Ex. 14 at 12.

Eczema and hives were present at the time of the visit, and her POTS diagnosis was noted. Id. at

12, 25. Dr. DeMio assessed Petitioner with “adverse rxn to [G]ardasil,” noting that she had

“reported this to many prior practitioners” in the past (albeit ones who wouldn’t “stand for any

suggestion of va[ccine] injury”). Id. at 25, 27. Dr. DeMio recommended that Ms. McKown begin

self-administered vitamin B-12 injections to treat her symptoms. Id. at 59-60. Lab testing revealed

a positive IgM titer for Lyme western blot (but negative IgG), and normal results for toxic/essential

elements and metals. Id. at 36-37, 38-52.

On November 4 through 6, 2014, Mrs. McKown called to report a decline in Petitioner’s

condition, but noted that the B-12 injections had helped “tremendously” to give her more energy.

Ex. 14 at 30. In a handwritten note, Dr. DeMio indicated a “Dx: “Lyme [disease], [and] what

components of current [symptoms] are directly from Lyme: based at least in part on index’s

response.” Id. at 31. Notes taken during the phone consultation reveal that Dr. DeMio

7

Dr. DeMio’s website indicates that his practice focuses on medical testing and treatment for autism, AD/HD

disorders, and Lyme disease. See About Dr. DeMio, http://drdemio.com/dr-phillip-demio/ (last accessed on June 19,

2019).

10

recommended that Petitioner continue with the B-12 injections. Id. He also prescribed ultra-low

dose Naltrexone capsules, Hydroxychloroquine, Doxycycline, Cefdenir, and Valtrex. Id. at 53-58.

At a follow up visit in May 2015, Dr. DeMio ordered blood work relating to static encephalopathy,

metabolic disorder, mineral deficiency, and autoimmune disorder. Ex. 9 at 5-6. The results,

however (including sedimentation rate, iron, c-reactive protein, ammonia, ANA, and lupus), were

normal and negative for autoimmune disorders. Id. at 7-12.

From August 2014 to April 2015, Ms. McKown began attending counseling and started

physical therapy for her joint pain. A counseling note from September 2014 indicated that she had

“learned she no longer has a POTS diagnosis” but rather her symptoms were “actually a part of

the illness related to Gardasil.” Ex. 18 at 7. Notes from October of that year also report that the B-

12 injections were having a positive effect, causing Petitioner to feel much better. Id. at 16-17, 19-

20. In November 2014, her counselor noted that she had been diagnosed with Lyme disease

(presumably on Dr. DeMio’s suspicion), and had started antibiotic treatment in response. Id. at 20-

23. Petitioner’s physical therapy notes from the following April indicated that she reported her

joint and muscles aches were caused by “Gardasil vaccine/Lyme disease.” Ex. 15 at 6. Her health

history included concerns for “Gardasil syndrome[,]” Lyme disease, and POTS. Id. at 7.

Over the next few months, Ms. McKown’s health course began to improve. The following

year, on March 4, 2016, she returned to her PCP for a sixteen-year-old well-adolescent visit at

Lawrenceville Pediatrics. Ex. 24 at 2-8. The evaluating nurse practitioner noted that Ms.

McKown’s mother reported that Petitioner was “still recovering” (presumably from the symptoms

discussed herein), but no current illnesses or chronic problems were noted, with a normal exam.

Id. at 2, 4. The only current medication reported was Mometasone ointment, and Petitioner was

not on any supplements at the time of the appointment. Id. at 2. An additional PCP visit on March

17, 2016, indicated that Ms. McKown presented with complaints of flu-like symptoms, fever, and

moderate nasal congestion (though no medications were prescribed). Id. at 9-11. No further

medical records have been filed.

II. Fact and Expert Witnesses

A. Petitioner’s Witnesses and Hearing Evidence

1. Mrs. Tabitha McKown

Mrs. McKown, Petitioner’s mother, testified about her health history and symptomatology

course following receipt of doses of the vaccines at issue herein. Tr. at 11-97; see also Ex. 63

(narrative statement). Prior to receiving doses of the HPV vaccine, Petitioner was healthy, active,

and energetic. Tr. at 12. She was training for a triathlon, and enjoyed biking, swimming, and

running. Id. In support, Mrs. McKown offered multiple photographs of Petitioner (between in

11

September 2012 and January 2013) showing her interacting with friends and enjoying the above-

noted activities. Id. at 13-15.8

As noted above, Petitioner had multiple pre-existing medical conditions which bear on the

injuries alleged in the present matter (specifically, dry skin and eczema). Mrs. McKown

acknowledged this fact but maintained that her daughter’s symptoms were exacerbated after her

receipt of doses of the HPV vaccine. Tr. at 15, 61; see also Ex. 7 at 31 (dated July 15, 2013). She

described Petitioner’s childhood eczema as mild to moderate (consisting of dry patches on the

folds of the arms and backs of the legs). Tr. at 15, 60-61. Following the administration of Vaseline

or steroid cream, the patches would resolve rather quickly, and before vaccination Petitioner never

experienced eczema on the face, chest, or back. Id. at 15-16.

Mrs. McKown also acknowledged that Petitioner had experienced syncopal episodes (and

lightheadedness with position change) in the past. Tr. at 15-16. She attributed such instances of

lightheadedness to Ms. McKown’s triathlon training, dehydration, and low blood pressure. Id. at

16. Mrs. McKown disputed the accuracy of a record from March 2013 indicating that Dr. Magill

had noted that Petitioner experienced two syncopal episodes in the last three months, maintaining

that she had reported to Dr. Magill the episodes of syncope had occurred over a three-year period

(consistent with reports made to Dr. Dooley), and were triggered in ways distinguishable from

other instances (e.g., following a reprimand for poor behavior or the sight of blood). Id. at 16-17.

According to Mrs. McKown, Petitioner’s overall health began to decline rapidly following

her first dose of the HPV vaccine on March 20, 2013. Tr. at 17.9 She experienced a “pretty quick[]”

onset of migraines thereafter, though Mrs. McKown could not recall the exact date they started.

Id. Five weeks later, Petitioner experienced a syncopal episode while at a yogurt shop with friends.

Id. at 17-18. The event resulted in EMS transporting Petitioner to the local emergency room. Id. at

17. Mrs. McKown recalled that her daughter was diagnosed with POTS within weeks of the yogurt

shop episode. Id. Thereafter, her syncopal episodes became more severe (i.e., lasting anywhere

from a few seconds to thirty minutes) and occurred more frequently. Id. at 17-18.

8

The photographs offered in support of Ms. McKown’s pre-vaccine health (as well as a number also purporting to

demonstrate the progression of her skin-related symptoms) were not filed prior to hearing. Tr. at 12-13. On direct

examination of Mrs. McKown, Respondent objected to the photographs being entered into evidence. Id. at 29-31. I

permitted their admission over this objection, although I cautioned counsel that the evidence had to be properly

authenticated once filed. Petitioner’s counsel filed the photographs on October 31, 2018 (roughly one month following

the hearing), but has not authenticated them. See Exs. 73-74. The photos are also undated.

9

At hearing, Mrs. McKown testified that she initially declined to have her daughter vaccinated against HPV, due to

her age. Tr. at 35. At eleven years old, she felt Petitioner was not highly at risk for HPV, especially given her personal

circumstances (i.e., she was homeschooled and not sexually active). Id.

12

Petitioner subsequently developed new allergies, dramatic exacerbation of her skin

condition (including hives and oozing sores that would cover her body), and joint pain after the

second HPV dose. Tr. at 18-19, 27. Her migraines became more intense, and there were days when

her leg pain was so severe she could not get out of bed. Id. at 19.10 Treaters tested her for multiple

conditions including lupus. Id. at 27. Her syncopal episodes continued through the remainder of

2013. Mrs. McKown recalled an episode of syncope that required a trip to the emergency room at

Clearview Medical Center in December 2013. Id. at 92-93. During this episode, Petitioner’s pulse

and oxygen levels dropped low enough to (in her words) trigger a “code blue” alert, although the

source of this characterization of the incident was the phlebotomist responsible for drawing

Petitioner’s blood. Id. at 92-93.11

Mrs. McKown further posited that Petitioner’s symptoms worsened in January 2014. Tr.

at 28, 54. Her joint pain and fatigue escalated, she could not concentrate on her school work, and

she had no energy and had trouble sleeping at night. Id. The pain triggered by her skin symptoms

and joint pain required morphine treatment (which was ineffective). Id. She also needed assistance

with various personal care tasks (including ambulating and bathing). Id. Petitioner would also wear

long-sleeved clothing to hide the affected areas of skin and hide her face in photographs. Id. at 38-

39, 54.

Next, Mrs. McKown recalled the cardiology appointment with Dr. Dooley that she attended

with Petitioner in May 2013 (around the time she was tested for POTS). Tr. at 64-65. At that time,

Petitioner had reported an episode of syncope lasting twenty-five minutes. Id. at 64-65. Mrs.

McKown testified that these syncopal episodes occurred “dozens” of times. Id. at 65. During the

episodes, Petitioner would experience feelings of cold, her eyes would roll back in her head, and

at times she would convulse. Id. at 66. Mrs. McKown acknowledged that Dr. Dooley (along with

Dr. Magill) recommend that Petitioner schedule an appointment with a neurologist. Id. at 67-68.

But Mrs. McKown decided against a neurology consult because she believed POTS to be strictly

a cardiac condition, fearful that it could be misdiagnosed as “epilepsy” and other conditions. Id. at

67.12 She also did not want to subject her daughter to endless testing. Id. at 69-71.13

10

Notably, however, Respondent submitted evidence revealing that Ms. McKown participated in a 5K race on

November 16, 2013. Tr. at 58.

11

On cross, Respondent pointed out that Ms. McKown had submitted no records memorializing this allegedly drastic

drop in her vitals apart from a hand-written note (filed as Ex. 20 and dated October 9, 2014) prepared by the

phlebotomist responsible for the blood test that immediately triggered the purported reaction. Tr. at 92-93. The only

other documentation in the medical record noting a significant change in vitals is Ex. 55 (her tilt table test results from

May 2013). Id. at 93.

12

Mrs. McKown also testified that she did not recall Dr. Dooley suggesting that Petitioner’s POTS was not

autoimmune in nature (despite the suggestion in the medical record to the contrary). Tr. at 68-69; but see Ex. 7 at 25.

13

According to Mrs. McKown, Petitioner’s treaters at the Cleveland Clinic also did not consider neurology testing to

be necessary for further evaluation of her condition. Tr. at 68. She did, however, admit later in her testimony that she

13

As Mrs. McKown recalled, Petitioner’s skin condition continued to worsen during June

2014. Tr. at 59-60. At this point, Mrs. McKown posited that her daughter was taking six to eight

Zyrtec daily in attempts to combat the rashes and sores. Id. at 59-60. According to Mrs. McKown,

Petitioner’s treaters even suggested that she begin six weeks of chemotherapy (given the persistent

nature of the symptoms) – which prompted her to seek out second opinions regarding the cause of

her condition (and appropriate treatment). Id. at 24-25, 60. (There is no record support for this

recollection, however).

In July 2014, Petitioner was examined by a rheumatologist, Dr. Rouster-Stevens, at Atlanta

Children’s for evaluation of her joint pain, and assessed with “amplified musculoskeletal pain

syndrome.” Tr. at 71-72. Lupus and other autoimmune tissue disease were both ruled out based on

lab results. Id. at 74.14 Mrs. McKown testified, however, that she could not recall the particular

diagnostic opinion offered at this visit, remembering only that Dr. Rouster-Stevens advised

Petitioner to “go back to immunology” (presumably given her skin condition and congruent allergy

testing) or seek treatment at a pain clinic. Id. at 72. As she recalled, Petitioner’s diagnosis often

varied depending on what type of specialist evaluated her symptoms, leading her to feel as if the

family was being shuffled from specialist to specialist with no resulting concrete explanation for

her condition. Id. at 74-75.

Mrs. McKown also testified about the Cleveland Clinic evaluations, starting with

rheumatologist Dr. Zeft in August 2014. Tr. at 76-77. Dr. Zeft diagnosed Petitioner with amplified

musculoskeletal pain (consistent with Dr. Rouster-Stevens) for which he recommended

specialized exercises and pain management. Id. at 76-78. Ultimately, Mrs. McKown

acknowledged these recommendations, but decided against scheduling a pain clinic evaluation. Id.

at 75. Petitioner did, however, participate in some exercises (such as yoga, for example) to help

with her joint pain. Id. at 77.

Mrs. McKown next discussed Petitioner’s appointment with allergist Dr. Paschall. Tr. at

78, 80. Records from this visit indicate that Dr. Paschall assessed Ms. McKown with “chronic

idiopathic urticaria” and discussed the appropriate treatment protocol for the illness, ruling out

autoimmune chronic urticaria. Id. at 84. Despite the record evidence, Mrs. McKown could not

recall any treater opining that Petitioner had chronic urticaria. Id. at 78. She also could not

remember if her daughter took any of the medications prescribed for such a condition, though she

requested a neurologic evaluation at the Cleveland Clinic (along with testing relating to aluminum levels in the blood),

but was rebuffed. Id. at 69-71.

14

Despite the lack of testing evidencing typical autoimmunity markers, Mrs. McKown maintained that Petitioner’s

treaters informed her that her elevated ANA levels indicated she had some form of autoimmune disease. Tr. at 74 (“I

was told that a positive ANA means there is some type of autoimmune somewhere”).

14

allowed for the possibility (given the multitude of treatments that were recommended to treat her

symptoms). Id. at 79-80. She also admitted that Petitioner had tried multiple topical steroid creams

(along with oral steroids) intermittently in the past to assist with her symptoms. Id. at 59-60, 83-

84. She could not recall if Petitioner was currently using any ointments at the time of her Cleveland

Clinic evaluation. Id.

According to Mrs. McKown, it was at the Cleveland Clinic that Petitioner’s treaters first

proposed a connection between the HPV doses she received and her onset of POTS (despite record

evidence to the contrary). Tr. at 22, 24-25.15 Later on in her testimony, Mrs. McKown

acknowledged that she and she daughter learned of the term “Gardasil syndrome” through online

research, and that they began to discuss the concept with treaters – although, as the medical record

reveals, the idea was generally not embraced. Id. at 31-32, 89. Two treaters in particular – Dr. Rice

(Ms. McKown’s dermatologist at Emory) and Dr. Freedle – refused to treat Petitioner further after

the suggestion was made that her HPV doses had resulted in her condition. Id. at 31-32, 85, 87-88.

When confronted with medical records evidencing treater opinions that the HPV vaccine was

likely not the cause for her condition, Mrs. McKown posited that these treaters were simply

unwilling to admit the possibility that the vaccine could have caused Petitioner’s symptoms. Id. at

85, 86-88.

Mrs. McKown also testified about Petitioner’s treatment with Dr. DeMio. Tr. at 32, 85.

She indicated that Dr. DeMio was one of the only physicians who shared her suspicion that her

daughter’s symptoms were caused by the HPV vaccine. Id. at 85-86, 90.16 He started Petitioner on

a “recovery protocol” which included the paleo diet, antibiotics, and various supplements, and

which Mrs. McKown alleged had resulted in a “slow improvement” of Petitioner’s symptoms. Id.

at 32, 85. Over a period of months thereafter, Petitioner’s skin cleared (though Mrs. McKown

testified that she continues to experience flares presently). Id. at 33. Her syncopal episodes were

controlled (i.e., she experienced only one every few months or so). Id. She was also able to compete

in 5K races by April of that year. Id. at 58. As of 2018, Petitioner was successfully attending

college, although she purportedly continues to experience syncopal episodes three to four times

per week that can last up to thirty minutes. Id. at 33. Stress continues to trigger flare-ups of her

skin condition and her headaches continue to be severe. Id. at 33-34.

15

Notes from the Cleveland Clinic evaluations actually suggest that Ms. McKown was able to control her POTS

symptoms through behavior modifications (including physical movements like squeezing her hands or completing

exercises to help with blood flow). Tr. at 90-91.

16

At hearing, Mrs. McKown also testified that one of Petitioner’s pediatricians at Lawrenceville Pediatrics, “Tammie,”

allowed for the possibility that the HPV vaccine caused her condition, but could not recall this treater’s full name. Tr.

at 87-88. Respondent pointed out that at the time of the hearing, Petitioner had submitted no records evidencing an

evaluation from a physician with that first name. Id. Given the discrepancy, counsel indicated that Petitioner would

filed update records following the conclusion of the hearing. Id. at 88-89. However, no additional information has

been filed.

15

2. Photographic and Social Media Evidence

To illustrate her contentions about the course of Petitioner’s skin-related symptoms, Mrs.

McKown offered photographs purportedly taken on various dates ranging from 2013 through

2015, many of which had been posted to social media. Tr. at 21-26; see Ex. 74. As she described,

one photo was taken close-in-time to Ms. McKown’s receipt of the second dose of HPV (in

September 2013), and showed redness and hives scattered over the arms and trunk following

exposure to water. Tr. at 26; see Ex. 74 at 9. Multiple filed photos were taken around December

2013 during the Cleveland Clinic consultations (and showed inflamed patches of skin on the face

and neck). Tr. at 22-23; see Ex. 74 at 3-8. Yet another photo from (mid-April or May 2015)

evidenced a skin eruption after spending time in the sun. Tr. at 21; see Ex. 74 at 1.17

In reaction, Respondent produced additional photographic evidence (spanning the length

of the relevant time period), all of which tended to show that Petitioner’s skin appeared to be

relatively clear at various points throughout 2013 through 2018. Tr. at 41-52; see Exs. P and Q.18

These photographs were taken from Ms. McKown’s Facebook account, with timestamps revealing

that they were posted on various dates between April 2013 and 2018 (although this obviously does

not establish when a particular photo was actually taken). For example, in a photo posted in mid-

November 2013 (or two months following Petitioner’s receipt of the second dose of HPV), Ms.

McKown’s skin appears to be clear and she was not wearing any long-sleeved or high-necked

clothing to cover her skin. Tr. at 41-42. Mrs. McKown explained, however, that her daughter

would routinely repost photos to Facebook that were taken pre-vaccination (and likely did so in

November of that year). Id. at 41-42. Three photos taken in August 2014 and January 2015 also

appear to show Petitioner wearing short-sleeved clothing (with no noticeable skin rashes on her

face or arms). Id. at 42-43. In response, Mrs. McKown testified that Petitioner often edited photos

she posted to social media during her illness in order to remove any evidence of a rash (a practice

Mrs. McKown witnessed her doing throughout 2014). Id. at 43-44, 93-94.

Respondent also offered photos posted on various dates in late 2015 through early 2018, at

which time Petitioner’s skin symptoms began to subside. Tr. at 45-48. A photo dated from April

2018 depicted Ms. McKown on the beach with family members. Id. at 49. Her skin appears to be

17

As previously stated, the photographs (filed as Ex. 74) were not filed prior to hearing, although Petitioner’s counsel

indicated that they would be filed following the hearing (with evidence confirming the dates they were taken). Counsel

did so, but did not offer evidence to confirm the dates upon which they were taken. See generally Ex. 74. I can thus

only rely on the testimony offered by Mrs. McKown (which tends to suggest they were taken following Petitioner’s

receipt of the second dose of HPV in September 2013 through mid-2015). I largely do not, however, find that the

photos do more than illustrate vaguely the existence of eczema flares in this period – a contention not fully disputed,

and one that even if deemed correct does not aid Petitioner in establishing that the HPV vaccine caused the flares.

18

Respondent also filed evidence that Petitioner participated in 5K races in November 2013 and April 2015. See Ex.

R.

16

clear in the photo, and Mrs. McKown admitted at hearing that the sores her daughter had

experienced previously were no longer a problem at this time. Id. She did, however, maintain that

the photograph showed evidence of a rash or “redness” on her hands and back. Id. Overall, after

late 2015, Mrs. McKown posited that Petitioner would have “good days” where her skin remained

clear, but she continued to experience breakouts on and off for the last three years. Id. at 50-54.

3. Dr. Carlo Tornatore

Dr. Tornatore authored one expert report and also testified at the entitlement hearing on

Petitioner’s behalf. See Ex. 56, filed on July 31, 2018 (ECF No. 42-2) (“Tornatore Rep.”). He

opined that Petitioner developed POTS (along with a significant aggravation of preexisting

eczema) following her receipt of HPV vaccine doses on March 20, 2013, and September 3, 2013.

Tr. at 120-21, 135; Tornatore Rep. at 14. In the alternative, if Petitioner’s POTS preexisted her

vaccinations, then the vaccines likely significantly aggravated that condition. Tr. at 135; Tornatore

Rep. at 14.19

Dr. Tornatore is a board-certified neurologist. See Exhibit 57, dated July 31, 2018 (ECF

No. 42-3) (“Tornatore CV”). He graduated from Cornell University with a Bachelor of Arts in

Neurobiology, and attended Georgetown University, where he received a Master of Science in

Physiology. Tr. at 98; Tornatore CV at 2. He subsequently graduated from medical school at

Georgetown University School of Medicine, completing a residency in the Department of

Neurology at Georgetown University Hospital. Tr. at 98; Tornatore CV at 2. He also completed a

fellowship in molecular virology and genetics at the National Institute of Health in Bethesda,

Maryland. Tr. at 98; Tornatore CV at 2. Dr. Tornatore has published multiple articles addressing

cell biology and pathology of demyelinating disorders. Tornatore CV at 8-20. Currently, he serves

as the Chair of the Department of Neurology at Georgetown University Medical Center, and

Interim Chair of the Department of Neurology at Medstar Georgetown University Hospital. Tr. at

98-99; Tornatore CV at 3. He also serves as a director of the neurology clerkship program at

Georgetown University Hospital (which is responsible for training roughly 200 medical students

per year). Tr. at 99; Tornatore CV at 3. During his tenure at Georgetown, Dr. Tornatore also

developed the Neuroimmunology and Multiple Sclerosis Center. Tr. at 99; Tornatore CV at 3. He

also serves as an ad hoc reviewer for several neurology journals. Tr. at 102; Tornatore CV at 7.

Dr. Tornatore is not board certified in immunology or dermatology. Tr. at 133, 139. His

CV also does not evidence any subspecialty in autonomics (or reference any publications or

memberships associated with such a specialty). Id. at 133-34, 135. In his current practice, he

primarily treats multiple sclerosis (“MS”) patients (some of whom have congruent autonomic

19

Upon questioning by the Court, Dr. Tornatore stated that his opinions herein (along with those contained in his

expert reports) were wholly independent from those offered by Drs. Mikovits and Ruscetti. Tr. at 188.

17

issues). Id. at 100, 103. Dr. Tornatore estimated that roughly 600 of his MS patients have POTS

(attributable to various primary illnesses, including deconditioning, cardiovascular issues, or

autonomic problems). Id. at 137-38. He acknowledged, however, that he is not an expert in POTS

or the autonomic nervous system. Id. at 137-38. He also has not performed any testing related to

POTS (i.e., a title table test), but does have some familiarity with orthostatic reading measures. Id.

at 138. In addition, Dr. Tornatore has not treated any MS/POTS patients with dermatologic

problems similar to those describe herein. Id. at 103, 136-37, 140.

Dr. Tornatore characterized POTS as dysfunction of the autonomic nervous system20

resulting from dysregulation of the blood vessels responsible for adjusting the heart rate when the

body changes position. Tr. at 103. Patients suffering from POTS typically experience increased

heart rate, accompanied by a drop in blood pressure, due to the heart’s attempt to compensate for

lack of blood supply to the brain (which can result in dizziness when moving from a lying down

position to a standing one, for example – as evidenced by tilt table testing). Id. POTS can also

present secondarily to central nervous system disorders (like MS, for example). Id. Other

symptoms can include lightheadedness, syncope, and dizziness (something Dr. Tornatore deemed

characteristic of the disease, but not evidence of it). Id. at 156-58. The filed literature suggests

several different triggers can cause an individual to develop POTS, including viruses, bacteria,

deconditioning, and genetics. See C. Gibbons, et al., Structural and Functional Small Fiber

Abnormalities in the Neuropathic Postural Tachycardia Syndrome, PlosOne (2013),

https://doi.org/10.1371/journal.pone/0084716, filed as Ex. 61 (ECF No. 47-5) (“Gibbons”).

In addition, Dr. Tornatore proposed that POTS can be autoimmune in origin. Tr. at 103-

04. An autoimmune disease or disorder features an individual’s immune system reacting

hyperactively, attacking self antigens (at the same time it is reacting to foreign infectious agents).

Dr. Tornatore relied on the presence of certain autoantibodies in patients diagnosed with POTS as

evidence of its autoimmune nature, offering literature (including that authored by Respondent’s

expert, Dr. Gibbons) that he said established this finding. See generally Gibbons at 1-10. The

Gibbons paper analyzed twenty-four POTS patients (along with ten healthy controls) to define the

neuropathology and clinical parameters of neuropathic POTS (as compared to the non-neuropathic

variants). Gibbons at 1. While Gibbons concluded that various subtypes of POTS display

overlapping symptoms, neuropathic POTS patients (experiencing “sudomotor dysfunction”) could

also exhibit symptoms similar to those seen in post-ganglionic dysautonomia. Id. at 6-7. Based on

the above, Dr. Tornatore concluded that there is a specific target antigen associated with

neuropathic POTS) – the “postganglionic proteins” or “ganglia” (which have shown to be virally-

associated with “postganglionic cholinergic dysautonomia”). Tr. at 122-23.

20

Dr. Tornatore defined the autonomic nervous system as the primary regulator of involuntary physiologic processes

(i.e., sweating, bowels, bladder, and respiratory functions). Tr. at 103.

18

In Dr. Tornatore’s opinion, POTS can also be associated with the onset of various skin

eruptions (including eczema and atopic dermatitis). Tr. at 119-20, 181. Dysfunction in the

autonomic nervous system can, he proposed, also cause dysregulation (or inflammation) in the

somatosensory nerves in the skin. Id. at 117-18, 119. Specifically, neural signaling by the sensory

nerves (or “neuroimmune signaling”) can produce neurogenic inflammation, thereby resulting in

the nervous system playing an “active role in inflammation” – attacking the skin directly, and

leading to eczema and atopic dermatitis. Id. at 118-19. He claimed that Ms. McKown’s skin biopsy

from April 2014 (which evidenced markers for inflammation) supported his conclusion. Id. at 152-

53.

On cross, Dr. Tornatore admitted that he had offered no literature directly supporting his

proposition that eczema could be autoimmune in derivation instigated by vaccination. Tr. at 120-

21, 153-54. He nonetheless emphasized that it was reasonable to associate a skin eruption (or

outbreak) with other evidence of autoimmune disease, given that both occur congruently with an

underlying inflammatory process. Id. at 124, 154-55. In support, Dr. Tornatore referenced a single

piece of literature, which he posited shows that eczema can be induced by certain antibodies. Id.

at 153; see T. Voisin, et al., Neuro-Immune Interactions in Allergic Diseases: Novel Targets for

Therapeutics, 29 Int’l Immnol. 247 (2017), filed as Ex. 72 (ECF No. 55-4) (“Voisin”).21 Voisin,

however, discussed allergic inflammation and the interplay between immune cells/inflammatory

mediators as “neurotransmitters” or signalers (which, by way of “cross-talk,” mediate the immune

response to allergens). Voisin at 1. It also made no mention of POTS (nor does it attempt to relate

autoimmune disease to allergies, or connect POTS to eczema). Dr. Tornatore otherwise offered no

evidence that the autoantibodies he discussed as associated with a neuropathic form of POTS could

also be implicated in causing eczema. Tr. at 153-54.

Dr. Tornatore went on to discuss what Petitioner’s actual medical records revealed, in an

effort to bulwark the reasonableness of his theory. First, he noted that Petitioner’s tilt table testing

(completed in May 2013) confirmed she suffers from POTS. Tr. at 169-70, 180. Her subsequent

episodes of prolonged unconsciousness22 (i.e., anywhere from ten to thirty minutes) thereafter were

also in his view likely related. Id. at 165-67, 168-70. Dr. Tornatore could not confirm, however,

which POTS variant best described Petitioner’s specific symptoms. Id. He theorized that Ms.

McKown likely had a form of autoimmune “neurogenic” or “neuropathic” POTS (despite any

treater evidence so opining). Id. at 180-81. In support of this determination, Dr. Tornatore pointed

to Petitioner’s worsening eczema flares (in conjunction with accompanying “skin color changes”)

as evidence of this finding. Id. at 181. He maintained as well that the Voisin article supported his

21

Voisin was filed the day before the hearing. ECF No. 55 (confirming Voisin was filed on September 25, 2018).

22

The fact that one of these prolonged episodes was observed only by a phlebotomist did not alter Dr. Tornatore’s

opinion. Tr. at 165-68. Respondent also noted that these observed episodes were not contemporaneously recorded in

the record (but rather were dictated in letters thereafter or described by Petitioner’s mother only). Id. at 165-68.

19

opinion (given the association of neuroimmune signaling with the pathophysiology of allergic

diseases, such as forms of eczema). Id.

On cross, Dr. Tornatore also posited that “acrocyanosis” – which he described as bluish-

colored limbs – is a “hallmark” of neurogenic POTS. Tr. at 549-50. As he explained, bluish

coloring in the limbs is evidence of some “neurogenic issue” by which the nerves compress the

capillaries. Id. at 549-50. Dr. Tornatore pointed to an instance in the record where one of

Petitioner’s treaters noted such an occurrence. Id. at 550 (citing Ex. 21 at 1), 556. In so maintaining,

he again invoked Voisin, which discussed a 1901 study revealing that nerve stimulation could

result in “vasodilation” (or a change in limb color). Id. at 554; Voisin at 3. As discussed earlier,

however, Voisin makes no mention of POTS at all (and it thus does not consider whether limb

discoloration is a hallmark of neuropathic POTS). Nonetheless, Dr. Tornatore maintained that

evidence of nerve stimulation (and the resulting bluish coloring or “flushing” of the limbs noted

in the medical records) was enough to conclude the best diagnosis was likely

neurogenic/neuropathic POTS. Tr. at 556.23

In reaction to Respondent’s argument that Petitioner’s POTS was more likely attributable

to “hypovolemia” or dehydration, Dr. Tornatore referenced various lab reports in Petitioner’s

records tending to suggest that the relevant markers for hypovolemia were documented as normal

over the course of her illness. Tr. at 556-59. Hypovolemia (or dehydration caused by low blood

volume), he posited, is best evidenced by an elevated BUN24 to creatinine measurement25 (i.e.,

evidence of blood volume depletion). Id. at 559. But, based on his own understanding of the

science, Dr. Tornatore suggested that low levels of creatinine could “falsely elevate” the BUN-

creatinine ration (due to diet or GI issues) – thereby rendering the marker somewhat unreliable at

times as a diagnostic tool. Id. at 558-59. Even so, absent any irregular BUN-creatinine ratio, a

diagnosis of chronic dehydration (associated with POTS) could not be reliably supported in his

reading of the record. Id. at 559-60.

Dr. Tornatore next maintained there was a plausible biologic mechanism by which the HPV

vaccine could cause POTS: molecular mimicry. Tornatore Rep. at 13-14. Molecular mimicry

23

Apart from the above, Dr. Tornatore posited that Respondent’s expert, Dr. Gibbons, offered some evidence that a

“lack of sympathetic tone” in the limbs could result in blood vessel constriction and pooling – thereby causing some

discoloration similar to that noted above. Tr. at 556-57. He could not, however, point to any literature cited by

Respondent relating this specific symptom to POTS. Id. at 557-58.

24

A BUN (or “blood urea nitrogen”) test is a blood test used to measure the amount of urea nitrogen in the blood. See

Blood Urea Nitrogen (BUN) Test, Mayo Clinic, https://www.mayoclinic.org/tests-procedures/blood-urea-

nitrogen/about/pac-20384821 (last accessed on June 19, 2019). Urea nitrogen is a chemical waste product that is

typically removed from the body through the kidneys. Id. A higher than normal BUN test can suggest that the kidneys

or liver may not be working properly. Id.

25

Creatinine is a chemical waste product produced by muscle metabolism. See Creatine Test, Mayo Clinic,

https://www.mayoclinic.org/tests-procedures/creatinine-test/about/pac-20384646 (last accessed on June 19, 2019).

Properly functioning kidneys filter creatine from the blood. Id. A creatine test – which measures the level of creatinine

in the blood – can thus indicate kidney irregularities. Id.

20

occurs when the body is exposed to an environmental factor (such as a vaccine or infection) which

results in a cross-reaction between autoantibodies (produced by the body in response to that

external factor) and a self structure in the body that the foreign antigen has mimicked. In so

proposing, Dr. Tornatore relied on scientific literature establishing homology between protein

components of the HPV vaccine and certain human protein structures. Tr. at 170-71, 547-49; D.

Kanduc & Y. Shoenfeld, Inter-Pathogen Peptide Sharing and the Original Antigenic Sin: Solving

Paradox, 8 Open Immunol. J. 16 (2018), filed as Ex. 69 (ECF No. 53-3) (“Kanduc”).26 Kanduc

examined a nine-protein sequence from HPV16, and recorded amino acid sequence similarities to

the human proteome at the pentapeptide level, concluding that the proteome contains twenty-nine

pentapeptides also found in the HPV16 vaccine – and thus ample mimics for molecular mimicry

to have occurred. Kanduc at 16.

Dr. Tornatore struggled, however, to specify where in the body this autoimmune cross-

reaction was purportedly occurring. At most, he proposed that the immune response triggered by

receipt of the HPV vaccine caused a cross reaction directed at the body’s peripheral nerves (or

some “neuronal element” or epitope). Tr. at 120-21, 171. He also made some suggestion that

Kanduc supported a conclusion that the triggered autoimmune response could be directed against

the human septin-9 protein. Id. at 171; Kanduc at 21. He did not, however, offer literature

evidencing homology between the HPV vaccine components and any specific tissues in the

autonomic nervous system. Tr. at 172. And Kanduc referenced no studies or models indicating

such a cross reaction could occur (in the context of either target). Dr. Tornatore nonetheless

admitted at hearing that he relied solely on Kanduc to establish that components of the HPV

vaccine could interact with septin-9 (or some other “crossreactive target”) and result in POTS

(though, he posited that he could offer more support if given additional time).27 Id. at 171-72, 173,

548; see Kanduc at 21. He maintained, however, the Kanduc paper provided enough support to

conclude such a similarities existed (given the Program’s “more probable than not” preponderance

standard). Tr. at 172.28

26

On cross, Respondent raised concerns regarding the reliability of Kanduc (given that it was published in the Open

Immunology Journal, which Respondent proposed was a disreputable, “predatory” journal). Tr. at 174. Dr. Tornatore,

however, posited that the circumstances of Kanduc’s publication (or the reputation of the authors) did not weigh

heavily on his assessment of the findings discussed in the article. Id. at 175. In his view, the authors simply performed

proteomic searchers (which he deemed “totally objective”), confirming the possibility of homology between the HPV

vaccine components and self structures. Id. at 175-76.

27

Kanduc, like Voisin, was filed the night before the hearing. See ECF No. 53 (confirming Kanduc was filed on

September 25, 2018).

28

In so stating, Dr. Tornatore stepped outside of his demonstrated medical expertise and into the shoes of the person

designated to determine the law in this proceeding – here, the special master. But it is inadvisable for medical or

scientific experts to so comment on the relevant legal standard, as I have noted in other cases. See, e.g., Chinea v.

Sec’y of Health & Human Servs., No. 15-95V, 2019 WL 1873322, at *19, 31 n.42 (Fed. Cl. Spec. Mstr. Mar. 15,

2019), appeal docketed, No. 15-95V (Fed. Cl. Apr. 15, 2019).

21

This inability to establish more than vague contours of how homology between the HPV

vaccine and self proteins might explain a putative autoimmune attack went beyond this narrow

issue, however. Dr. Tornatore offered little in the way of evidence suggesting that the HPV vaccine

has ever been shown from a reliable experiment or study to be pathogenic in the manner proposed

(i.e., to trigger an autoimmune process sufficient to produce the symptoms relevant to this case).

Rather, he relied solely on the fact that Kanduc supported a finding of “human homology” between

HPV vaccine protein components and host proteins – without evidence suggesting the alleged

cross-reactivity could result in an adverse disease process. At most, Dr. Tornatore referenced

Sydenham’s chorea (a known autoimmune disease characterized by rapid, jerking movements) to

explain how an immune response directed against a bacterial infection can “overshoot” and also

lead to different illnesses (rheumatic heart disease, for example). Tr. at 110. As he described, in

the case of Sydenham’s chorea, the body develops an immune response to strep bacteria – and the

autoantibodies produced in response cross-react with host proteins – thus, causing direct damage

to the heart and brain. Id.

Along those same lines, and as another mechanistic explanation in the alternative to

molecular mimicry, Dr. Tornatore briefly discussed the concept of “T cell receptor degeneracy.”

Tr. at 105-07, 189-90; Tornatore Rep. at 14. According to Dr. Tornatore, the body lacks an “army

of T cells” capable of defending against the “millions, if not billions” of antigens it is exposed to

on a regular basis. Id. Thus, it would be impossible for one specific T cell to be directed at one

single antigen. Id. at 105, 566. Rather, T cells are “degenerate” – meaning they can recognize

several different antigens (and mount an immune response against those antigens) without having

to have identifiable homology to every possible foreign antigen, including amino acid chains

whether associated with a particular virus or vaccine. Id. at 105, 546.

Dr. Tornatore characterized the degeneracy concept as either a primary or secondary

adaptive response, but distinguished it from the more typical underlying mechanisms offered in

the Program (i.e., bystander activation and epitope spreading). Tr. at 189. In his view, T cell

degeneracy involves antigen stimulation the of the “same identical T cell clone[,]” rather than by

acceleration of an ongoing immune process by local activation of antigens presenting as a result

of the cross-reactivity. Id. But he stressed that because Kanduc established that the HPV vaccine

has specific homology with self-protein sequences, T cell degeneracy was not a necessary

mechanistic explanation for his theory in this case. Id. at 189 (“we have that specificity for HPV

protein sequence and human sequences to say . . . you don’t need the T cell degeneracy”), 546.

Though, upon further questioning, Dr. Tornatore posited it was possible that both had occurred in

this case – protein cross-reactivity led to the onset of POTS, while T cell degeneracy contributed

to the exacerbation of Ms. McKown’s skin symptoms (in which case it is possible the eczema

worsening was either directly aggravated by the nervous system or stimulated by the underlying

adaptive process attributable to POTS). Id. at 547.

Dr. Tornatore further suggested that Petitioner’s subsequent re-exposure to antigens in the

second dose of the HPV vaccine could have played some role in the molecular mimicry process.

22

Tr. at 107-09. Because of the homology identified between components in the HPV vaccine and

self sequences, nonspecific T cells could attack self structures/amino acid sequences (following

immune system stimulation by the vaccine) in addition to those cells responding specifically to the

vaccine – thereby resulting in a more amplified and inherently more rapid cellular response. Id. at

107-08. Just as a vaccine booster response is intended to assist the body in developing

immunologic memory to certain antigens, Dr. Tornatore posited that memory developed from

exposure to a second dose of HPV could cause the cross-reactivity to occur at a much faster pace.

Id. at 108-09; see Kanduc at 21.

Admittedly, Dr. Tornatore conceded, Kanduc offered multiple possible sequence mimics

that could share homology with numerous self proteins in the entire human genome. Tr. at 112,

552. To account for such a large amount of protein sequence similarities, Dr. Tornatore posited

that genetic risk factors also play a part in how the immune system “overshoot[s]” or reacts in

response to vaccine-induced autoantibodies. Id. at 112-13. Dr. Tornatore offered rheumatologic

disorders as a pertinent illustration. Id. Patients with spondyloarthropathies, for example, have

elevated levels of HLAB-27 (an abnormal haplotype protein located on the immune cells). Id.

These proteins (produced as a result of a genetic rheumatologic disorder) inhibit the body’s ability

to regulate the immune system – thereby resulting in an increased risk for autoimmunity. Id. at

113. Thus, regardless of the number of possible shared sequences, Dr. Tornatore seemed to suggest

that a patient’s genetics will always play some role in susceptibility to develop an autoimmune

disorder. Id. at 190-91, 552-53. He did not indicate, however, what (if any) genetic abnormality

contributed to Petitioner’s onset of symptoms. Id. at 552.

Dr. Tornatore next discussed the evidence (or “combination of things”) in the medical

records that he maintained supported the conclusion that Petitioner likely experienced chronic

inflammation (and resulting immune dysfunction) post-vaccination. Tr. at 127, 179-80. First, Dr.

Tornatore pointed to Petitioner’s POTS – a disease which (as discussed above) “can be

autoimmune” in some circumstances. Id. at 177, 180. He also asserted that eczema “is

inflammatory in nature” which further evidenced some systemic involvement. Id. at 177. Indeed,

Petitioner’s biopsy from April 2014 revealed inflammation in the skin. Id. at 153, 178, 180.

Otherwise, Dr. Tornatore referenced allergy testing – which revealed elevated levels of IgE to

various food and outdoor allergens. Id. at 179 (citing Ex. 1 at 65-66), 180. Even so, Dr. Tornatore

admitted on cross that elevated IgE is not specific to autoimmunity directly, but could suggest a

patient has a “propensity for a hyperimmune state.” Id. at 179. He also agreed that Petitioner’s

records contained no test results establishing the existence of any specific antibodies to neuronal

antigens – though he deemed such testing insignificant. Id.

Apart from the above, Dr. Tornatore concluded that the HPV vaccine doses Petitioner

received were likely responsible for instigating her condition given their close temporal

relationship to her reported onset (and/or worsening) of syncope and rash symptoms. Tr. at 125,

127, 177, 553. In his view, Petitioner’s health course and the “tempo” of her symptoms “changed

dramatically after vaccination, particularly the second vaccination in September.” Id. at 125. She

23

at most experienced situational syncope before her receipt of the HPV vaccine doses, with worse

and longer instances thereafter. Id. at 125-26. Her preexisting eczema also worsened following her

second dose of HPV (as evidenced by the multiple doctor visits she attended over the course of

her illness). Id. at 125-27. Dr. Tornatore also cited to various treater statements indicating their

recognition that Petitioner’s symptoms had worsened in the months following her vaccine doses.

Id. at 125 (citing Ex. 1 at 49), 129 (citing Ex. 3 at 2-4).

While stressing the significance of the above, Dr. Tornatore was dismissive of the fact that

testing performed on Petitioner did not reveal other common, objective indicators of systemic

inflammation (including the CRP29 and ESR30 rates). Tr. at 110-11. In his view, such

measurements are not always elevated in autoimmune disease patients because not all immune

responses result in protein production detectable in the blood. Id. at 110-11. In multiple sclerosis

and myasthenia gravis, for example, inflammation is directed at the nervous system tissue – and

the CRP and ESR testing typically reveal normal results for its patient population (given that

antibodies produced in response to such immune-mediated conditions are deposited in the tissue,

not the blood). Id. at 111-12.31 In addition, Petitioner experienced worsening eczema at the same

time that her CRP and ESR rates were normal (a point conceded by Respondent’s expert). Id. at

111. Thus, as Dr. Tornatore posited, the underlying pathogenesis of an autoimmune disease

process could not be discredited in this case even if some classic tests for inflammation had not

been satisfied. Id. at 177-78.

Dr. Tornatore also acknowledged that Ms. McKown’s medical records evidenced a pre-

vaccination history of two syncopal episodes – but he deemed them “situational” or “vasovagal”

in nature, and thus distinguishable. Tr. at 128, 161-63; see also Tornatore Rep. at 14. In his view,

both instances of past syncope were accompanied by a “significant emotional” component (i.e., a

reprimand for bad behavior and exposure to blood). Tr. at 162. They were therefore not likely

associated with her subsequent autoimmune-instigated POTS, given the above-noted situational

components, the rarity of such occurrences, and lack of other evidence suggest a preexisting

underlying autonomic problem. Id. at 128, 162, 163 (noting “these episodes were 2 ½ years apart”).

By contrast, Ms. McKown clearly experienced more syncopal episodes following her receipt of

two HPV vaccine doses. Id. at 129, 162-63. However, if her pre-vaccine syncopal episodes could

29

CRP is a test used to measure inflammation in the body. C-Reactive Protein Test, Mayo Clinic,

https://www.mayoclinic.org/tests-procedures/c-reactive-protein-test/about/pac-20385228 (last accessed June 20,

2019). It measures the amount of C-reactive protein in the blood via a simple blood test. Id. The results can indicate a

patient's risk for infection or heart disease, for example. Id.

30

ESR is a blood test used to show inflammatory activity in the body. Sed Rate (Erythrocyte Sedimentation Rate),

Mayo Clinic, https://www mayoclinic.org/tests-procedures/sed-rate/about/pac-20384797 (last accessed June 20,

2019). It measures the distance red blood cells fall in a test tube in one hour. Id. The further the cells descend in the

tube, the greater evidence of an existing inflammatory response of the immune system. Id.

31

For further support, Dr. Tornatore posited that the best indicator of a multiple sclerosis diagnosis is an MRI. Tr. at

179. Bloodwork for multiple sclerosis patients is typically normal and does not reveal the presence of systemic

inflammation. Id.

24

be related to POTS, then Dr. Tornatore proposed that the HPV vaccine doses likely aggravated it

given the increased incidence of post-vaccination symptoms. Id. at 128-29, 161-62; Tornatore Rep.

at 14.

As to the timing of the onset of Petitioner’s POTS symptoms, Dr. Tornatore maintained

that she had experienced her first “true” symptoms of syncope on April 26, 2013 (or four to five

weeks post vaccination) at the yogurt shop, and that such timing was medically reasonable. Tr. at

155, 164; Tornatore Rep. at 14. For support, he relied solely on a single epidemiologic study –

involving a totally different disease. See L. Schonberger, et al., Guillain-Barré Syndrome

Following Vaccination in the National Influenza Immunization Program, United States, 1976-

1977, 110 Am. J. Epidem. 105 (1979), filed as Ex. 60 (ECF No. 47-4) (“Schonberger”).

Schonberger’s authors studied the incidence of onset of GBS following receipt of the swine flu

vaccine, concluding that such an increase had occurred mostly within a five-week period thereafter

(although it was possible the risk interval could extend nine to ten weeks). Schonberger at 110.

By contrast, Dr. Tornatore acknowledged outright that Petitioner’s eczema most likely

began pre-vaccination. Tr. at 142. But he felt the symptoms she experienced in this time period

were less recurrent or “episodic” – with the “tempo” of incidents increasing after the second HPV

vaccine dose in September 2013. Id. at 149-50, 151. Despite record evidence suggesting that

Petitioner’s eczema had actually been deemed “recurrent” or “severe” in the past, Dr. Tornatore

maintained that records from close-in-time to her receipt of the vaccine clearly described an

exacerbation of symptoms. Id. at 144-45, 146, 148-49. Dr. Tornatore also pointed to instances in

the record where other treaters categorized Petitioner’s skin condition as “coming and going” (or

at times normal). Id. at 146-48. Ultimately, Dr. Tornatore could not pinpoint the exact day and

time Ms. McKown’s skin symptoms worsened, but maintained that the skin rashes progressively

worsened over a six-month period (beginning in June or July 2013 and later resulting in an

exacerbation or flare-up in September). Id. at 151.

For support on the reasonableness of the eczema exacerbation timeframe, Dr. Tornatore

again referenced Schonberger. Tr. at 116-17. He posited that literature on the topic of ADEM also

supported a conclusion that autoimmune diseases can occur between forty-eight hours and thirty

days following vaccine administration (though, he offered no literature directly addressing eczema

in this context, or why literature pertaining to GBS or some other clearly neuropathic condition

could also be applied to eczema). Id. at 117. Based on Schonberger, Dr. Tornatore also explained

that an initial immune response mediated by T cells could be quick (especially in the context of an

anamnestic response), but could also linger for a period of two months or even longer. Id. at 116.

Given the amount of time it takes to develop immune memory, Dr. Tornatore posited that an

autoimmune response would occur in a similar timeframe (i.e., within a sixty-day period or earlier

if the patient has previous exposure to the same vaccine antigens). Id. at 116-17.

25

2. Drs. Judy Mikovits and Francis Ruscetti

Drs. Mikovits and Ruscetti32 prepared two reports in support of Petitioner’s claim. See

Expert Report, dated Dec. 2, 2016, filed as Ex. 25 (ECF No. 18-2) (“First Mikovits Rep.”); Expert

Report, dated July 19, 2017, filed as Ex. 51 (ECF No. 30-2) (“Second Mikovits Rep.”). Only Dr.

Mikovits testified at hearing, however.33 Dr. Mikovits offered the opinion that the two doses of

HPV, in conjunction with the Hep A vaccine, caused Petitioner to develop POTS and atopic

dermatitis. Contrary to Dr. Tornatore, however, Dr. Mikovits posited that Ms. McKown’s medical

records did not offer persuasive evidence that she indeed suffered from recurrent skin rashes

(characterized as atopic dermatitis) prior to her receipt of the above-noted vaccines – thus, her

opinion does not appear to implicate a significant aggravation theory (at least as it applies to

Petitioner’s skin condition).

Dr. Mikovits is a consultant with MAR Consulting Inc., a group she co-founded, and serves

as an advisor for a private equity investment company. Curriculum Vitae, filed as Ex. 26 (ECF

No. 18-3) (“Mikovits CV”) at 1. She received her undergraduate degree in biology from the

University of Virginia, and a Ph.D. in molecular biology and biochemistry from George

Washington University. Id. at 4. Dr. Mikovits did not attend medical school, however, and is not

a licensed medical doctor. Tr. at 247. She thus has no direct experience treating skin diseases or

autonomic disorders.

From 1992 to 1994, Dr. Mikovits was a post-doctoral fellow in molecular virology at the

National Cancer Institute, Lab of Genomic Diversity, subsequently serving as a staff scientist at

the National Cancer Institute, Lab of Leukocyte Biology, from 1994 to 1998. Mikovits CV at 1-2.

Thereafter, from 1999 to 2001, she served as a Lab Director at the Laboratory of Antiviral Drug

Mechanisms, a division of the National Cancer Institute. Id. at 3. Dr. Mikovits worked in various

capacities at several biotechnology start-up companies from 2002 to 2006, and conducted research

at the Whittemore Peterson Institute for Neuroimmune Disease (“Whittemore”) from 2006 to

2011, studying diseases with inflammatory components and environmentally acquired immune

32

At hearing, Dr. Mikovits testified that both she and Dr. Ruscetti separately reviewed the medical records and case

filings prior to preparing their joint expert report. Tr. at 224. They assumed the factual assertions contained in

Respondent’s Rule 4(c) Report were correct. Id. at 225. She further stated that she and Dr. Ruscetti worked together

to prepare the report, relying on their respective areas of expertise in substance (for Dr. Ruscetti: dendritic cells and

the adaptive immune system; for Dr. Mikovits: mast cells and microglia involvement in disease pathology). Id.

33

According to his CV, Dr. Ruscetti received his B.S. in biology from Boston University, followed by a Ph.D. in

microbiology from the University of Pittsburgh. See Curriculum Vitae, filed as Ex. 27 (ECF No. 18-4) at 1. From

1972 to 1975, Dr. Ruscetti served as a research instructor at the University of Pittsburgh School of Medicine. Id. He

worked for Litton Bionetics as a cell biologist from 1975 to 1978. Id. In 1978, he joined the National Cancer Institute,

and presently serves as Principal Investigator for the Leukocyte Biology Section. Id. at 1-2. He is also an Adjunct

Professor of Biochemistry and Molecular Biology at George Washington University. Id. at 2. Dr. Ruscetti serves on

the editorial board of Stem Cells, and his CV lists multiple authored publications. Id. at 2-33.

26

deficiency. Mikovits CV at 2; Tr. at 221. She has not conducted research since 2012, but now

works as a consultant. Mikovits CV at 1.

Significant and alarming elements of Dr. Mikovits’s professional history were pointed out

at hearing that greatly diminished her credibility as an expert. In particular, while at Whittemore

Dr. Mikovits was accused of stealing laboratory materials, arrested, and fired from her position.

Tr. at 218, 265-66. In addition, a paper Dr. Mikovits published in Science was later retracted

because the results could not be replicated, causing the journal to lose confidence in the report and

the validity of its conclusions. Id. at 216, 258-59. Dr. Mikovits nevertheless has continued to

reference the article on her consulting website without disclosing its retraction. Id. at 265. Dr.

Mikovits has also published works and given presentations which dispute the safety and value of

vaccines, imply a link between vaccines and autism, and/or recommend a moratorium on vaccine

administration generally. Id. at 250-51, 255, 256-58. She has collaborated with an anti-vaccination

publisher and co-author, and regularly speaks at the “AutismOne” conference. Id. She has also

supported a ban on all HPV vaccines and attacked the Vaccine Program as biased. Id. at 255.

Like Dr. Tornatore, Dr. Mikovits testified about Petitioner’s claimed vaccine-caused

diagnoses of POTS and atopic dermatitis, as well the possible causal connection between the HPV

vaccine (and Hep A) and her disease onset. Although the opinions she offered regarding the

vaccines at issue in the case and the appropriate causal mechanism differed from those offered by

Dr. Tornatore, she similarly opined that Ms. McKown’s onset of POTS and atopic dermatitis flares

were caused by an autoimmune process (or reaction) that was likely vaccine-induced.

Dr. Mikovits began by discussing Petitioner’s May 2013 POTS diagnosis. Although Dr.

Mikovits has never treated POTS patients, she filed literature defining POTS as a heterogeneous

disorder characterized by abnormal increments in heart rate upon assumption of the upright

posture, accompanied by orthostatic intolerance and other secondary symptoms. See, e.g., L.

Brinth, et al., Orthostatic Intolerance and Postural Tachycardia Syndrome as Suspected Adverse

Effects of Vaccination Against Human Papilloma Virus, 33 Vaccine 2602 (2015), filed as Ex. 42

(ECF No. 20-7) (“Brinth”).34 Though the cause of POTS is unknown, the onset of its symptoms

can occur following febrile illness, pregnancy, immunization, sepsis, surgery, or trauma. Brinth at

2603; see also E. Benarroch, Postural Tachycardia Syndrome: A Heterogenous and Multifactorial

Disorder, 87 Mayo Clin. Proc. 1214 (2012), filed as Ex. 28 (ECF No. 19-2) (“Benarroch”) (50

percent of POTS cases have an antecedent viral infection, and 25 percent have prior familial

34

Dr. Mikovits expert report stated – incorrectly – that lightheadedness and syncope were not associated with POTS.

Second Mikovits Rep. at 2. She also cited literature positing the same. See S. Blitshteyn, Postural Tachycardia

Syndrome Is Not Caused by Deconditioning, 6 Pulm. Circ. 401 (2016), filed as Ex. 66 (ECF No.49-4) (letter to the

editor). At hearing, she corrected herself and stated she should have said those symptoms were simply not “diagnostic”

of the condition. Tr. at 271.

27

history); First Mikovits Rep. at 5-6.35 Dr. Mikovits also suggested that POTS could be related to a

genetic susceptibility. Tr. at 280-81.36

Dr. Mikovits also characterized POTS as an autoimmune disease. Tr. at 243-44. As she

broadly posited, the “heterogeneity” of the disease suggests it is neuroinflammatory in nature. Id.

at 229; see also S. Blitshteyn, Autoimmune Markers and Autoimmune Disorders In Patients With

Postural Tachycardia Syndrome (POTS), 24 Lupus 1364 (2015), filed as Ex. 64 (ECF No. 49-2)

(“Blitshteyn”). In support, Dr. Mikovits cited to instances in the medical records where various

treaters noted that Petitioner had, post-vaccination, experienced symptoms often associated with

an underlying inflammatory process (including pain, brain fog, weakness, and skin eruptions). Tr.

at 287, 292.37 And she pointed to lab results from December 201338 (revealing increased levels of

IgE and Lyme disease) as evidence of ongoing inflammation. Id. at 287-88. She did, however,

acknowledge that the more traditional biomarkers for inflammation – which she defined as “mast

cell mediators” – were either documented as normal (i.e., CRP and ESR) or never tested (i.e.,

cytokine levels). Id. at 287-88.

Dr. Mikovits went on to argue that relevant literature establishes that at least “half” of all

POTS cases have some neuropathic basis. Tr. at 276-77; M. Thieben, et al., Postural Orthostatic

Tachycardia Syndrome: The Mayo Clinic Experience, 82 Mayo Clin. Proc. 308 (2007), filed as

Ex. 54 (ECF No. 30-5) (“Thieben”); Benarroch at 1215-16. Thieben was a retrospective study of

152 POTS patients seen at the Mayo Clinic over eleven years, and considered the data and test

results obtained during treatment. Thieben at 308. It hypothesized that a particular autoantibody

(the ganglionic acetylcholine receptor) was associated with neuropathic cases of POTS, although

by its own terms the article does not propose or embrace the contention that POTS is in all (or

even most) cases an autoimmune disease. Id. Indeed, as observed in Benarroch (a review article

aimed at cataloging the pathophysiology and subtypes of POTS, including the neuropathic and

hyperadrenergic variants), Thieben only found that fourteen percent of all POTS patients

considered in the study presented with evidence of a ganglionic acetylcholine receptor antibody

35

During her testimony, Dr. Mikovits asserted that POTS is not caused by deconditioning (a contention directly

contrary to what the medical community better versed in POTS understands to be the case in many instances). Tr. at

245; compare Benarroch at 1216-17.

36

Dr. Mikovits spent some time at hearing discussing the MTHFR methylation defect (which she suggested was

present in Petitioner’s family history). Tr. at 280-81. But she could not point to a medical record confirming that Ms.

McKown possessed this particular defect, nor did she offer evidence associating it with POTS. Id. at 281.

37

Upon further questioning, Dr. Mikovits admitted that she relied heavily on the fact of the POTS diagnosis as proof

that Petitioner had experienced post-vaccination neuroinflammation. Tr. at 292.

38

Presumably, Dr. Mikovits is referring to Ex. 1 at 65-66 (dated from December 2013) – which is consistent with Dr.

Tornatore’s testimony. Dr. Mikovits did not reference a particular date during her testimony, however. See Tr. at 287-

88.

28

(which could indicate an immune cause of neuropathic POTS in some cases, but hardly even close

to half. Benarroch at 1215-16.

Dr. Mikovits further relied on various studies associating POTS with other autoimmune

conditions, such as autoimmune inflammatory syndrome induced by adjuvants (“ASIA”)), and

chronic fatigue syndrome (“CFS”). Tr. at 243-45; see, e.g., S. Dahan, et al., Postural Orthostatic

Tachycardia Syndrome (POTS) – A Novel Member of the Autoimmune Family, 25 Lupus 339

(2016), filed as Ex. 65 (ECF No. 49-3) (“Dahan”); S. Cerpa-Cruz, et al., Adverse Events Following

Immunization With Vaccines Containing Adjuvants, 56 Immuno. Res. 299 (2013), filed as Ex. 30

(ECF No. 19-4) (“Cerpa-Cruz”); G. Giannotta, et al., Vaccines and Neuroinflammation, 3 Int’l J.

Public Health Safety 1 (2018), filed as Ex. 68 (ECF No. 53-2) (“Giannotta”). Dr. Mikovits posited

that forty percent of POTS patients congruently suffer from other autoimmune conditions (like

those noted above) – though no specific piece of literature directly supports such an assertion. Tr.

at 272.

In addition, Dr. Mikovits referenced various review articles that “reported” occurrence of

“severe somatoform dysautonomic and neuropathic syndromes” following receipt of the HPV

vaccine, all of which she posited result in symptoms consistent with or overlapping POTS. Tr. at

228-29; First Mikovits Rep. at 7; see B. Palmieri, et al., Severe Somatoform and Dysautonomia

Syndromes After HPV Vaccination: Case Series and Review of Literature, SpringerOnline (2016),

doi 10.1007/s12026-016-8820-z, filed as Ex. 32 (ECF No. 19-6)39; S. Aratani, et al., Murine

Hypothalamic Destruction With Vascular Cell Apoptosis Subsequent to Combined Administration

of Human Papilloma Virus Vaccine and Pertussis Toxin, Scientific Reports (2016),

doi:10.1038/srep36943, filed as Ex. 43 (ECF No. 20-8); M. Martinez-Lavin, Hypothesis: Human

Papillomavirus Vaccination Syndrome—Small Fiber Neuropathy and Dysautonomia Could be Its

Underlying Pathogenesis, Clin. Rheum. (2015), doi:10.1007/s10067-015-2969-z, filed as Ex. 34

(ECF No. 19-8); Brinth at 2602.

Dr. Mikovits next discussed the purported association between Petitioner’s skin symptoms,

which she characterized as atopic dermatitis, and an autoimmune process. Tr. at 277-79. Atopic

dermatitis, in her view, is also immune-mediated – and thus distinct from eczema, for example. Id.

at 230, 277-78. While both conditions are of the same disease family, atopic dermatitis is a

subgroup that is inflammatory in nature, while eczema is not. Id. at 278. To support the purported

neuropathic connection between Petitioner’s skin symptoms and POTS, Dr. Mikovits referenced

Voisin (discussed earlier by Dr. Tornatore), which concluded that immune cells/inflammatory

mediators can act as “neurotransmitters” or signalers (by way of “cross-talk,”), and thereby

mediate allergic inflammation. Id. at 230; Voisin at 1. Dr. Mikovits concluded that “cross-talk”

between neuronal receptors and immune cells can cause skin inflammation – as evidenced by an

onset of itching. Tr. at 230.

39

Exhibit 33 is a corrected version of this article.

29

Based on her review of the record and scientific literature filed in support, Dr. Mikovits

posited that the biologic process responsible for Ms. McKown’s onset of symptoms post-

vaccination likely originated with dysregulation or “overstimulation” of the innate immune system

(which she defined as comprising the body’s “first responders” during an immune response). Tr.

at 196, 227, 289; First Mikovits Rep. at 8. Autoimmunity, in her view, is initiated by an “overactive

immune system” in which various innate immune mediators (including dendritic cells, mast cells,

and microglia) respond to some “perceived threat” (or foreign agent), thereby causing excessive

inflammation in the body. Tr. at 237-38; see also First Mikovits Rep. at 8. The innate system is

capable of recognizing foreign antigens quickly and building a memory response. First Mikovits

Rep. at 8.

Dr. Mikovits next turned to the role a vaccine could play in causing such innate system

overactivity. As. Dr. Mikovits explained, the components of the HPV and Hep A vaccines (both

of which contain aluminum as an adjuvant) dysregulate brain microglia (and mast/dendritic cells

at the mucosal cell surface) – thereby causing chronic neuroinflammation in a genetically

susceptible patient. Tr. at 226-27, 233, 281-82; First Mikovits Rep. at 8-9. After stimulation by a

vaccine, the innate system triggers the overproduction of inflammatory cytokines. Tr. at 227, 233.

Such an overproduction of cytokines could thereafter become chronic, when microglia – non-

neuronal glial cells located in the brain that also play an immune defense role – are primed to

become a source of excess cytokine production, often in reaction some prior insult (such as

vaccination). First Mikovits Rep. at 8-9. In most cases, patients confronted with a cascade of

proinflammatory cytokines can self-regulate the overproduction via a normal immune system

response (with the help of T cells). Tr. at 230-40. Those who experience dysregulation, however,

typically have some form of a genetic susceptibility to autoimmunity (though puberty and/or a

traumatic injury could also spur on such a response). Id. at 240-41.

Dr. Mikovits specifically implicated the IL-1 beta cytokine (which she stated “controls the

local pro-inflammatory cascade”) as responsible for preventing protective immunity from

becoming destructive. Tr. at 230-31. Dr. Mikovits posited that scientific literature on the topic

shows that inhibiting IL-1 beta production can prevent adverse cardiac events from occurring

(though, she did not file any to corroborate her statements). Id. at 231. Based on the above, Dr.

Mikovits concluded that POTS (which is cardiac driven) is likely caused by an inflammatory

response brought about by the overproduction of IL-1 beta. Id.

The receipt of multiple vaccines, Dr. Mikovits maintained, could amount to “damage at a

distance” whereby the immune system cannot adequately respond to the above and properly self-

regulate. Tr. at 232, 295. Inflammatory cytokines can thus more quickly cross from the periphery

(where they originate) and into the central nervous system (thereby interacting with brain

microglia), breaching the blood-brain barrier with the help of macrophages. Id. at 295. Dr.

30

Mikovits posited that histidine and polysorbate 80 (both HPV vaccine ingredients) were also likely

responsible for this breach. Id. at 233. And she allowed for the possibility that “virus-like particles”

contained in the vaccines can “package pieces and parts of other DNA and other retroviruses”

could contribute to the breach, but she could not be more specific as to how (or even what literature

existed that reliably could support such a contention). Id. at 234; see also First Mikovits Rep. at

10.

Along those same lines, Dr. Mikovits discussed the various “excipient[]” components (i.e.,

preservatives or adjuvants) contained in the HPV and Hep A vaccines – which she deemed

responsible for such as response. Tr. at 231-32; First Mikovits at 10-11. In particular, Dr. Mikovits

implicated the aluminum adjuvant40 (which is present in both the HPV and Hep A vaccines) as

causative of the dysregulation of the cytokine balance discussed above. Tr. at 232; R. Gherardi, et

al., Aluminum Adjuvants of Vaccines Injected Into the Muscle: Normal Fate, Pathology, and

Associated Disease, 100 Morphologie 85 (2016), filed as Ex. 49 (ECF No. 21-5); F. Liang & K.

Lore, Local Innate Immune Response in the Vaccine Adjuvant-Injected Muscle, 5 Clin. & Trans.

Immunol. 74 (2016), filed as Ex. 41 (ECF No. 20-6); C. Exley, et al., When an Aluminum Adjuvant

Is Not an Aluminum Adjuvant Used in Human Vaccination Programmes, 30 Vaccine 2042 (2012),

filed as Ex. 39 (ECF No. 20-4) (Letter to the Editor); C. Exley, et al., Aluminum-Based Adjuvants

Should Not Be Used as Placebos In Clinical Trials, 29 Vaccine 9289 (2011), filed as Ex. 38 (ECF

No. 20-3) (Letter to the Editor).

She also referenced literature discussing the concept of ASIA41 (even though Petitioner has

explicitly indicated it is not part of her causation theory)42, and mast cell activation disorder –

which, in her view, establishes that merely 400 micrograms of alum is enough to “cripple[e]” the

microglia – thereby resulting in a disease state characterized by ongoing inflammation. Tr. at 232,

281, 289-90; First Mikovits Rep. at 11; see L. Tomlijenovic, et al., Postural Orthostatic

Tachycardia With Chronic Fatigue After HPV Vaccination as Part of the “Autoimmune/Auto-

Inflammatory Syndrome Induce By Adjuvants”: Case Report and Literature Review, J. Invest.

Med. (2014), doi:10.1177/2324709614527812, filed as Ex. 29 (ECF No. 19-3); M. Frieri, et al.,

Mast Cell Activation Syndrome: A Review, 13 Curr. Allergy Asthma Rep. 27 (2013), filed as Ex.

40 (ECF No. 20-5). The chronic aspect of such a response is attributable to the alum “stay[ing] in

40

At hearing, Dr. Mikovits asserted that the specific aluminum adjuvant present in the HPV and Hep A vaccines has

never been tested for safety despite being used in vaccines for over 80 years. Tr. at 281.

41

On cross, Respondent pointed out that ASIA is not recognized by the World Health Organization as playing a role

in the causation of adverse events related to vaccination. Tr. at 272-73. Dr. Mikovits acknowledged the finding, but

maintained that the ASIA is consistent with the theory that an autoimmune disease can be triggered by various external

agents. Id. at 273.

42

See Pre-Hearing Reply, dated Sept. 21, 2018 (ECF No. 52) (“Respondent spends a good portion of their Pre-Hearing

memorandum addressing the ASIA theory. However, while Drs. Mikovits and Ruscetti reference ASIA, neither they

nor Dr. Tornatore assert ASIA as their theory of causation.”).

31

the macrophage” for “more than one year.” Tr. at 289.43 This interaction (coupled with the

components of her theory discussed below) helps to create the overall autonomic dysfunction

Petitioner alleges to have experienced post-vaccination. Id. at 289-91.44

While maintaining that the autoimmune process resulting in Ms. McKown’s injuries

originated from an innate immune response, Dr. Mikovits posited that the adaptive system (via

molecular mimicry) also likely plays a role in the overall cascade of autoimmune dysfunction. In

addition to sequential homology (between vaccine-induced autoantibodies and self proteins), Dr.

Mikovits explained that “conformational epitope[s]” expressed on the cell surface (in response to

the insulting foreign antigen) are actually responsible for the cross-reactivity. Tr. at 234-35. For

example, the Hep A vaccine contains a “cell line” called MRC-5 (a human cell line from aborted

fetal tissue) that shares homology with endogenous human retroviruses. Id. at 231. The

overlapping mimicry thus stimulates neuroinflammatory pathways and results in some adverse

disease process. Id. In the context of the HPV vaccine doses, Dr. Mikovits posited that the Kanduc

paper (also referenced by Dr. Tornatore) establishes 200 potential immunogenic and cross-reactive

epitopes to HPV vaccine antigens. Id. at 235. This process can also be hastened by subsequent

exposure to the same vaccine antigens, which would be consistent with a “challenge-rechallenge”

response. Id. at 235-36.

B. Respondent’s Witnesses

1. Dr. Christopher Gibbons

Dr. Gibbons filed one written report in this matter and testified at hearing. Tr. at 303-443;

Expert Report, dated May 4, 2018, filed as Ex. D (ECF No. 35-1) (“Gibbons Rep.”). Based upon

the record as a whole and his review of the scientific literature, Dr. Gibbons posited that vaccines

do not cause POTS (nor did they do so in this case).

Dr. Gibbons currently serves as a staff neurologist at Beth Israel Deaconess Medical Center

in Boston, Massachusetts. Curriculum Vitae, filed as Ex. O (ECF No. 54-1) (“Gibbons CV”); Tr.

at 303. In addition to the above, he holds a number of clinical and teaching positions: Associate

43

Dr. Mikovits also made some suggestion that the chronic inflammation (or driver of the “disease engine”) associated

with immune system disorders can also be caused by “oxidative stress” or “reactive nitrogen species”. Tr. at 244. Such

concepts were not discussed in depth – but have been offered in prior Program cases without success. See, e.g., Bast

v. Sec’y of Health & Human Servs., No. 01-565V, 2012 WL 6858040, at *6 (Fed. Cl. Spec. Mstr. Dec. 20, 2012)

(rejecting theory that seizures resulted from vaccine-induced mitochondrial dysfunction associated with oxidative

stress), mot. for review den’d, 117 Fed. Cl. 104 (2014).

44

On cross, when confronted with evidence that humans ingest far more aluminum per day than the considerably

smaller amounts contained in a vaccine, Dr. Mikovits posited that ingesting is not comparable in effect to injecting

cells directly with the adjuvant. Tr. at 282. She did not offer any scientific or medical evidence to corroborate the

assertion, however.

32

Professor of Neurology, Director of the Neurocutaneous Laboratory, Associate Director of the

Autonomic Laboratory, and Director of the Neuropathy Clinic at Beth Israel’s Joslin Diabetes

Center. Tr. at 303. He received his undergraduate degree from Dartmouth College, followed by a

and medical degree from Albert Einstein College of Medicine. Gibbons CV at 1; Tr. at 309. He

completed a neurology residency at Johns Hopkins Hospital in Baltimore, Maryland, and a

fellowship thereafter in clinical neurophysiology (with a subspecialty in autonomic disorders) from

Beth Israel. Tr. at 309.

Over the course of his career, in his clinical practice Dr. Gibbons has repeatedly evaluated

and treated patients with immune-mediated conditions, including autonomic disorders, peripheral

nerve disease, neuropathies, and small fiber neuropathies. Tr. at 303-04. Due to the overlap

between the autonomic and peripheral nervous systems, his treatment focus has been in patients

with Parkinson’s disease (who also display dysautonomia), multiple system atrophy, and diabetic

neuropathy. Id. at 304-05. He also oversees a neurocutaneous skin biopsy lab in which he (and his

students) evaluate biopsy results to determine nerve involvement. Id. at 305. He treats patients

with POTS (and routinely conducts tilt tabling testing). Id. at 306-07, 340. In addition, Dr. Gibbons

serves on the board of various journals focused on autonomic issues, including Autonomic

Neuroscience: Basics and Clinical. Id. at 308. Dr. Gibbons estimated that he spends roughly half

of his time treating patients (while the remaining half is used for teaching and research). Id. at 305-

06, 311. He does not have specialty training in the fields of immunology, dermatology, or

epidemiology, however. Id. at 399.

Dr. Gibbons began his testimony by describing the primary functions of the autonomic

nervous system (along with defining descriptive terms used to describe autonomic nervous system

irregularities, such as “dysautonomia” and “autonomic damage”). Tr. at 315. Dr. Gibbons defined

the autonomic system as the “subconscious” part of the nervous system responsible for controlling

or regulating the body’s involuntary functions (including breathing, heart rate, blood pressure,

sweating, urination, and defecation). Id. “Dysautonomia” or “autonomic dysfunction,” he posited,

is a vague term used in the literature to refer to a “perceived problem” with the autonomic system,

which may or may not be associated with some function in the autonomic system itself. Id. at 315-

16.

In contrast, “autonomic damage” refers to a specific, identifiable injury to the autonomic

system. Tr. at 316-17. For example, Parkinson’s disease is a condition linked to autonomic

damage. Id. at 317. As Dr. Gibbons explained, Parkinson’s can be attributed to a particular protein

in the body (“alpha-synuclein”), the presence of which is identifiable by both microscopic imaging

and testing, and which causes direct damage to the autonomic system. Id. Vasovagal syncope (or

presyncope symptoms: dizziness, lightheadedness, palpitations, or blacking/greying out), on the

other hand, does not necessarily reflect the existence of damage to the autonomic system, but can

33

instead constitute a “normal, completely physiologic, typical response” by an otherwise-healthy

autonomic nervous system. Id. at 316, 336-37.

Dr. Gibbons next defined POTS and its usual symptoms and course. POTS is characterized

by a “heart rate increase that goes up over time beyond what we would consider normal,” resulting

in a number of symptoms (lightheadedness, dizziness, palpitations, tremulousness, feelings of

presyncope, and vasovagal syncope). Tr. at 317-18, 322; see also R. Freeman, et al., Consensus

Statement on the Definition of Orthostatic Hypotension, Neurally Mediated Syncope and the

Postural Tachycardia Syndrome, 161 Autonomic Neurosci. 46 (2011), filed as Ex. D, Tab 1 (ECF

No. 35-2); Gibbons Rep. at 3-4. Skin rashes, in his view, are typically not a presenting symptom

of POTS. Tr. at 436-37.45 In addition, vasovagal syncope is not by itself diagnostic of POTS (or

its inevitable result). Id. at 322, 414, 416 (“people with POTS don’t have to faint”).

POTS is classified as a “syndrome” due to the various etiologies (some of which can be

autoimmune) associated with its onset, including deconditioning, chronic illness, and/or

autonomic neuropathy. Tr. at 317; Gibbons Rep. at 3-4.46 As Dr. Gibbons explained, POTS can be

an “end result of many potential avenues,” including a secondary reaction to a variety of diseases,

like diabetes, thyroid dysfunction, renal dysfunction, or multiple sclerosis. Tr. at 318. The

diagnostic criteria for POTS require (a) an increase in the heart rate of more than 30 bmp or more

from the supine to standing position (or 40 bmp or more if under twenty years of age), (b)

symptoms that are consistent with such a diagnosis (as describe above), and (c) a continuation of

symptoms for greater than six months. Id. at 318-19. POTS is most common in young women

(generally teenagers up to their twenties). Id. at 319.

POTS can be divided into various subgroups with overlapping symptoms (Tr. at 402),

including hypovolemic, hyperadrenergic, and neuropathic. As Dr. Gibbons explained, all the

variants are distinguishable based on laboratory or clinical testing. Tr. at 322, 402. Hypovolemic

POTS is characterized as POTS “related to low blood pressure” (occurring, for example, when an

individual exercises excessively without proper fluid intake). Id. at 320-21. The hypovolemic

variant can also present secondarily to various illnesses associated with deconditioning (including

myalgic encephalomyelitis and CFS). Id. at 419-20. Hyperadrenergic POTS is related to an

adrenaline response (i.e., an increase in norepinephrine). Id. at 321. According to Dr. Gibbons, this

45

As already noted, Petitioner’s experts relied on Voisin as establishing “cross talk” between nerves resulting in onset

of skin rashes that could in turn demonstrate how skin conditions like eczema were the product of the same

autoimmune process that allegedly was causing a person to experience POTS. Tr. at 423-25. In response, Dr. Gibbons

deemed the theory “interesting” but claimed that it did not stand as reliable evidence establishing a reliable medical

association between such conditions (nor evidence that the nerves were indeed damaged in the process). Id. at 423,

433.

46

At hearing, Dr. Gibbons disputed any suggestion that POTS is more often than not caused by neuroinflammation.

Tr. at 325-26.

34

subgroup is more easily differentiated in autonomic testing. Id. Hyperadrenergic POTS can occur

congruently with autoimmune disease (for example, type I diabetes or limb encephalitis), though

in such cases a patient will experience other severe symptomology consistent with the primary

disease process in question. Id. at 314, 357. This subgroup can also be antibody-mediated or

instigated by the presence of toxic substances. Id. at 325.

Finally, Dr. Gibbons discussed neuropathic/neurogenic POTS – a variant he deemed (based

upon his direct experience) “quite rare.” Tr. at 321-22, 377. Dr. Gibbons described this subgroup

as an immune-mediated form of POTS resulting in “some sort of damage to the autonomic nervous

system” which impairs the typical autonomic functions, resulting in the tachycardia associated

with the illness. Id. at 321, 324-35.47 Neuropathic POTS is typically associated with a particular

antibody (the “ganglionic receptor antibody”) that targets the acetylcholine receptor in the

autonomic ganglia, resulting in autoimmune ganglionopathy. Id. at 358. High amounts of the

ganglionic receptor antibody can cause profound autonomic failure (resulting in a total loss of

control of blood pressure, heartrate bowels, bladder, etc.). Id. Based on his knowledge of the

literature, Dr. Gibbons posited that the ganglionic antibody is the only clinically relevant antibody

associated with neuropathic POTS. Id. at 358. He could not identify any other antibody targeted at

the heart,48 but added that he was aware of ongoing research on the topic, although he deemed it

preliminary. Id. at 358, 375-76, 396.49

In addition to the above, Dr. Gibbons questioned the significance of various pieces of

literature offered by Petitioner’s experts to support the conclusion that all (or most) forms of POTS

are neuropathic in nature. In so doing, Dr. Gibbons emphasized the absence of evidence

establishing that the POTS she experienced was consistent with the immune-mediated form of the

condition. Benarroch, for example, discusses the more common POTS subtypes (hypovolemic and

hyperadrenergic), but allows that POTS can be immune-mediated (as Petitioner proposes). Tr. at

361. Dr. Gibbons, however, posited that Benarroch actually supported his earlier conclusion that

the only known antibody associated with neuropathic version of the condition is the ganglionic

acetylcholine receptor antibody – with no other subtype of the disease demonstrated

“convincingly” to be immune mediated. Id.

Thieben, in his view, followed the same pattern: establishing that neuropathic POTS is a

rare subtype specifically involving antibody-mediated, neuronal damage. Tr. at 364. As Dr.

47

A further subset of neuropathic variant is “cholinergic” POTS. Tr. at 324. The cholinergic variant results from

damage to the “sympathetic cholinergic system” associated with gastrointestinal symptoms (and can be associated

with abnormal sweating and nerve damage). Id. at 324, 370-71.

48

Dr. Gibbons posited, however, that structural damage to the heart directly could cause POTS. Tr. at 396-97.

49

As Dr. Gibbons explained, it is difficult to determine if elevated titers of certain circulating antibodies are clinically

relevant absent (a) evidence that high titers are associated with a disease, and (b) evidence that removing those

antibodies prompts a recovery. Tr. at 376.

35

Gibbons explained, Thieben provided evidence that a small number of POTS patients (6 out of 42

or 14 percent) presented with the above-described ganglionic antibody in low positive values. Id.

at 363. But this percentage appeared high to Dr. Gibbons, as he has seen only one POTS patient

with the same ganglionic antibody in the last ten years of his clinical practice. Id. In addition, those

percentages have never been reproduced in further research. Id. at 364, 442-43. Thieben’s authors

similarly made clear that actual damage to the autonomic nervous system did not explain every

POTS subtype. Id.

Dr. Gibbons next discussed the Blitshteyn paper. Tr. at 364-65. Blitshteyn’s authors tested

POTS patients for certain autoimmune biomarkers (e.g., ANA, TTG, SS-A antibodies, etc.),

concluding (based on their positive readings) that autoimmunity must be common in POTS

generally. Id. at 365. Dr. Gibbons, however, criticized Blitshteyn for the inclusion criteria used in

conducting its analyses. Id. at 366. He noted that the study appeared to have self-selected for

patients who suffer from both POTS and an additional autoimmune disease. Id. at 366-67. It was

thus no surprise that many of the studied patients also tested positive for autoimmune biomarkers.

Id. at 367. More importantly, many biomarkers tested for in Blitshteyn had no known association

(in the causation context) to the patient’s underlying disease process – and therefore their presence

did not establish a causal link. Id. at 367. Thus, Blitshteyn could not, in Dr. Gibbons’s opinion, be

invoked to support a conclusion that POTS is generally autoimmune in nature (as Petitioner’s

causation theories implied). Id. at 368.

Dr. Gibbons also addressed the relationship between neuropathic POTS and vasovagal

syncope of the kind relevant to this case. In his experience, neuropathic POTS actually does not

result in, or even feature, syncope. Tr. at 322. Rather, syncope is typically a product of a properly

functioning autonomic nervous system – thus, patients with autonomic damage would likely not

manifest syncope symptoms. Id. at 323, 394, 421 (describing syncope is a “normal physiologic

response”). Rather, the progressive, neuropathic variant of POTS results in orthostatic hypotension

without the tachycardia typically associated with the non-neuropathic subgroups. Id. at 323-24. In

fact, neuropathic POTS should feature a reduction in syncope (given the resulting damage to the

autonomic system). Id. at 349. All in all, Dr. Gibbons concluded that healthy patients can have

vasovagal syncope with no corresponding autonomic damage. Id. at 434, 436.

Relying on his review of the medical records, Dr. Gibbons characterized Petitioner’s

variant of POTS as most likely hypovolemic rather than neuropathic. Tr. at 326, 394. Dr. Gibbons

could not identify any evidence in the record to suggest or corroborate the propriety of a

neuropathic or hyperadrenergic POTS diagnosis. Id. at 394. He further opined that Ms. McKown’s

onset of POTS was not caused or significantly aggravated by either (or both) of her HPV vaccine

doses. Id. at 326, 394. In his practice, Dr. Gibbons regularly treats POTS patients (some of whom

have received the HPV vaccine and some who have not), and has seen no variances in disease

course. Id. at 429-30. Overall, he felt that some of Petitioner’s overall course could be attributable

36

to deconditioning (in light of her physical fitness routines50) and/or genetics (related to her

height51). Id. at 355-56.

In support, Dr. Gibbons referenced record evidence tending to suggest that Petitioner’s

POTS onset was unrelated to any autoimmune process and did not display what he would expect

to see if her POTS was neuropathic. No clinical test results indicated that she was experiencing

any underlying autoimmune disease process. Tr. at 396. A ganglionic receptor antibody test (which

could support a neuropathic variant of the condition) was never conducted. Id. In addition, as noted

above, Dr. Gibbons posited that symptoms indicative of neuropathic harm would be “striking” in

nature (including symptoms such as: fixed/dilated pupils, invariant heart rate, gastroparesis, and

urinary retention). Id. at 439 (describing an event where “essentially every component of the

autonomic nervous system shuts down”). But there was no record evidence that Petitioner

experienced any such drastic symptoms. And other than Dr. DeMio, none of Petitioner’s treaters

proposed autoimmune disease to explain her POTS. Id. at 356.

Rather, Ms. McKown’s course was more consistent with the hypovolemic variant of the

condition. Tr. at 332-33. In support, Dr. Gibbons referenced records detailing her hospital visit in

April 2013 (following the syncopal incident at the yogurt shop). Id. at 332-33. The orthostatic

vitals taken at the time indicated that Petitioner’s blood pressure was stable during the visit. Id. at

332. Her heart rate did increase significantly upon standing, but her syncopal symptoms resolved

following intake of a liter of fluids. Id. The fact that Petitioner’s symptoms ceased following fluid

intake suggested to Dr. Gibbons that she was suffering from the hypovolemic variant. Id. at 332-

33. In addition, laboratory testing completed during her hospital visit in late April 2013 revealed

an elevated BUN to creatine ratio of 20:1. Id. at 333. He considered such a high ratio as indicative

of dehydration (which would explain the resolution of symptoms following fluid intake). Id.52

In addition, Dr. Gibbons referenced Petitioner’s cardiology appointment with Dr. Dooley

(at which time she was officially diagnosed with POTS). In his view, the description of her

symptoms taken during this visit represented a “classic array” of those seen with POTS/vasovagal

50

Deconditioning did not necessarily mean that a person had been physically inactive. Dr. Gibbons referenced the fact

that astronauts (who are physically fit and trained) can develop POTS after returning to earth. Tr. at 355-56 (“[c]ouch

potato[es]” are not the only ones at risk”).

51

Dr. Gibbons suggested that the literature strongly supports an associations between POTS and having a small stature.

Tr. at 355. This point was not, however, developed at hearing or in the parties’ filings, and I therefore do not give it

substantial weight in Respondent’s favor (or against Petitioner).

52

Apart from the above, Dr. Gibbons acknowledged that the ER record also evidence a complaint of GI discomfort.

Tr. at 331. He thus allowed for the possibility that Petitioner’s GI symptoms could have caused her syncopal episode.

Id.

37

syncope patients that he had treated in the past. Tr. at 335.53 Ms. McKown’s orthostatic vitals again

revealed a table blood pressure reading with an increase in heartrate (from 68 to 100) upon position

change – which he deemed as “not quite meeting [POTS] criteria,” though not ruling it out either

(as it was close enough to the diagnostic measures). Id. at 335. Tilt table testing, however,

confirmed the diagnosis thereafter. Id. at 338-39, 342 (“[s]he fainted with her heart rate dropping,

her blood pressure dropping, and then she recovered”). Based on the above, Dr. Gibbons

eliminated the hyperadrenergic variant as a possible explanation, given that her blood pressure

readings were “pretty much the same or lower” (i.e., they didn’t go up). Id. But this record did not

support the neuropathic variant, because Petitioner had experienced syncope upon position change

– which indicated the absence of autonomic system damage. Id. There was also no evidence of

direct cardiac damage indicated on Petitioner’s EKG. Id. at 432. Thus, Dr. Gibbons concluded that

the hypovolemic variant was the form best supported by record evidence. Id.

Other records generated subsequent to Petitioner’s POTS diagnosis were also in Dr.

Gibbons’s view consistent with what would be experienced by a typical patient with non-

neuropathic POTS. Tr. at 345. For example, Dr. Gibbons referenced a record from January 2014,

in which Ms. McKown complained of “minor near-syncopal episodes” with worsening episodes

now resulting in loss of conscious (for twenty to thirty minutes) and abnormal eye movement. Id.

As Dr. Gibbons explained, recurrent episodes of syncope reflected a typical POTS course. Id. at

346.

Petitioner’s purported prolonged episodes of unconsciousness, however, were in Dr.

Gibbons’s view inconsistent with a POTS diagnosis (regardless of the subtype involved). Tr. at

346, 349. Prolonged unconsciousness, Dr. Gibbons reasoned, is instead associated with inadequate

blood flow to the brain or a brain irregularity (i.e, “both [brain] hemispheres . . . are not working”).

Id. at 346. Dr. Gibbons suggested that these prolonged episodes could possibly be attributable to

an underlying seizure disorder, but Petitioner’s presentation was more consistent with vasovagal

syncope. Id. at 347. Moreover, episodes of unconsciousness extending twenty to thirty minutes

would typically be associated with “significant cerebral deficits” which Petitioner did not

experience. Id. As a result, Dr. Gibbons proposed it most likely that these purported episodes of

prolonged unconsciousness were caused by other mechanisms (such as: hyperventilation, fear,

anxiety, fright, worrying, etc.) in which patients are “just unwilling to return to the situation” that

caused the episodes, and therefore did not conform to any form of POTS, neuropathic or otherwise.

Id. at 348-49.

53

This record also indicated that Ms. McKown (or her caretakers) expressed a concern for “recurrent” syncopal

episodes in years past, but Dr. Gibbons could conclude only that those episodes were at least consistent with her more

recent syncopal symptoms in April 2013. Tr. at 334, 405, 433. Later in his testimony, however, he opined that POTS

patients with a predisposition of fainting (in response to blood being drawn, for example) are more commonly placed

in the hypovolemic or hyperadrenergic categories. Id. at 344.

38

Along those same lines, Dr. Gibbons noted that more recent records from 2014 indicated

that Petitioner had been experiencing one to two episodes of POTS-related syncope per month. Tr.

at 350; see Ex. 7 at 10. The frequency of the syncopal episodes, Dr. Gibbons posited, was also

consistent with non-neuropathic POTS (which, as noted earlier, he would expect to diminish, not

increase, syncopal episodes). Tr. at 350-51. By July 2014, records indicated Petitioner’s POTS

symptoms were improving, but she had now experienced a new onset of joint pain. Id. at 351

(citing Ex. 21 at 1). Dr. Gibbons reported that symptoms of pain are not typically indicative of

POTS, unless the pain was attributable to some other underlying disorder. Id. at 352. POTS, in his

view, is not associated with any form of pain syndrome. Id. He therefore also discounted this

symptom as POTS related in any form.

With respect to timing, Dr. Gibbons opined that Petitioner’s POTS symptoms preceded

receipt of the HPV vaccine. He pointed to the records referencing pre-vaccination syncopal

episodes (for which Petitioner was referred to the cardiologist in the first place – on the very day

she received the first HPV dose). Tr. at 326 (citing Ex. 1 at 44). Records from March 2013

indicated that Ms. McKown reported three syncopal episodes with position change (along with

lightheadedness) before the visit – which Dr. Gibbons classified as “classic” POTS

symptomatology. Id. at 327-28.54 Dr. Gibbons ultimately placed onset around six months prior to

her receipt of the first dose of HPV. Id. at 328, 342-43. He also referenced earlier-in-time

orthostatic measurements taken during her wellness checks at ages eleven through fourteen. Id. at

329. Heart rate measurements taken at this time evidenced resting heart rates ranging from 104

beats per minute to 84 – measures he deemed high for a pediatric patient who was also actively

training for triathlons. Id. In his view, heart rate ranges in the 80-100 range suggests something

was occurring even though it might not be overtly clinical. Id. at 330.

Dr. Gibbons also addressed Dr. Tornatore’s arguments that Petitioner’s pre-vaccination

syncopal episodes were distinguishable because they were merely “situational” – a concept he

deemed to be not a “good medical term.” Tr. at 403. Rather, situational syncope and vasovagal

syncope are in his experience essentially synonymous concepts. Id. (describing “situational”

syncope as “vasovagal syncope related to a situation”). Later on in his testimony, however, he

admitted that certain “situations” could trigger vasovagal syncope (for example, having blood

drawn or receiving a reprimand for bad behavior, as is alleged to have occurred with Petitioner).

Id. Ultimately, he proposed that the earlier instances were most likely associated with, rather than

distinguishable from, Petitioner’s later course. Id. at 326-38, 342-43.

Apart from the above, Dr. Gibbons also questioned the strength of independent evidence

purportedly establishing a connection between the HPV vaccine and POTS. Brinth, for example,

identified young women in Denmark who had recently received the HPV vaccine and were then

54

If the prior episodes of syncope were ignored, Dr. Gibbons maintained that he would place onset of Petitioner’s

POTS in May 2013, given the symptoms reported during the visit described above. Tr. at 410-11, 412-13.

39

referred to a syncope clinic due to reported orthostatic intolerance symptoms. Brinth at 2602-05.

Its authors observed 21 cases of POTS out of 35 studied individuals. Id. at 2605. Significantly,

however, as Dr. Gibbons pointed out, all of the patients tested had suspected their POTS was

caused by the HPV vaccine – and were in fact referred to the trial for that reason. Tr. at 381. In his

view, given the self-selection bias in the inclusion criteria for studied individuals, no firm

relationship could be drawn from Brinth’s results. Id. at 382.

In addition, Dr. Gibbons noted that Brinth’s conclusions (which he admitted caused some

“concern” in the medical community regarding vaccine causation) prompted the European Medical

Agency (“EMA”) to conduct a follow-up study, in which it analyzed over 60,000 reports of onset

of POTS following the receipt of the HPV vaccine. Tr. at 383-85; Assessment Report: Human

Papillomavirus (HPV) Vaccines, EMA (2015), filed as Ex. D, Tab 13 (EC 36-4) (“EMA Report”).

The EMA report found that the incidence rate for the number of patients with post-vaccination

POTS (1 reported per 10,000) proved to be smaller than predicted, resulting in an assessment that

disputed associating the HPV vaccine to POTS. Tr. at 385; EMA Report at 38-39. Dr. Gibbons

admitted on cross examination, however, that the EMA report was based on some post-marketing

surveillance (a passive reporting system informing manufacturers of the incidence rate) which,

Petitioner posited, could have resulted in deflated numbers of reported incidence (as low as one

percent). Tr. at 427-28.

Dr. Gibbons also offered other literature supporting his contention that the HPV vaccine

likely plays no role in the development of POTS. Tr. at 387; J. Skufca, et al., Incidence Rates of

Guillain Barre (GBS), Chronic Fatigue/Systemic Exertion Intolerance Disease (CFS/SEID), and

Postural Orthostatic Tachycardia Syndrome (POTS) Prior to Introduction of Human

Papillomavirus (HPV) Vaccination Among Adolescent Girls in Finland, 3 Papillomavirus

Research 91 (2017), filed as Ex. D, Tab 14 (ECF No. 36-5) (“Skufca”). Skufca is a Finish study

which cataloged onset of various autoimmune disease following receipt of the HPV vaccine

beginning in 2013 (although it admittedly included reports from years prior, from 2002 to 2012,

when the HPV vaccine was not administered). Skufca at 91. Skufca’s authors noted a significant

increase in reported POTS cases the year prior to the vaccine being administered. Tr. at 387.

Around this same time, medical awareness of POTS increased (i.e., outreach campaigns were

conducted to inform physicians of the condition and diagnoses increased). Id. Thus, in Dr.

Gibbons’s view, the increase in reported cases could be attributable merely to greater awareness

of POTS, as opposed to an incidence rate increase attributable to vaccination. Id. at 387-88, 392.55

In addition, Dr. Gibbons offered a wide-in-scope review article on POTS’s purported

association with HPV vaccine. Tr. at 392-93; see B. Butts, et al., Human Papillomavirus Vaccine

55

On cross examination, Dr. Gibbons acknowledged that Finland stopped administering the HPV vaccine around

2012. Tr. at 429.

40

and Postural Orthostatic Tachycardia Syndrome: A Review of the Current Literature, J. Child

Neuro (2017), doi:10.1177/0883073817718731, filed as Ex. J (ECF No. 43-5) (“Butts”). Butts

cataloged various items of literature (including peer-reviewed articles, government statements, and

medical advisory committee notes – some of which were filed in the present matter) in an attempt

to gauge the strength of studies purporting to associate the HPV vaccine with POTS. Butts at 1, 3.

Its authors acknowledged the existence of case reports detailing the onset of POTS post-

vaccination, but ultimately determined that the existing epidemiologic evidence did not support a

causal connection. Id. at 7-10; Tr. at 392-93.

2. Dr. Andrew MacGinnitie

Dr. MacGinnitie served as Respondent’s second expert, offering two written reports in the

matter and testifying at hearing. Expert Report, dated Mar. 28, 2017, filed as Ex. A (ECF No. 23-

1) (“First MacGinnitie Rep.”); Expert Report, dated May 5, 2018, filed as Ex. C (ECF No. 34-1)

(“Second MacGinnitie Rep.”). Based on his review of the record, Dr. MacGinnitie opined that the

HPV and Hep A vaccines Petitioner received did not exacerbate her subsequent eczema flares

thereafter, and from an immunologic standpoint could not cause eczema or POTS. Tr. at 454, 455.

Dr. MacGinnitie is an attending physician and the Clinical Director for the Division of

Immunology at Boston Children's Hospital in Boston, Massachusetts. Curriculum Vitae, filed as

Ex. B (ECF No. 26-1) (“MacGinnitie CV”); Tr. at 444-45. He is also an Associate Professor of

Pediatrics at Harvard Medical School. Tr. at 445. Dr. MacGinnitie received his undergraduate

degree from Yale University, followed by both a medical degree and Ph.D. from the University of

Chicago. Id. at 445. He thereafter completed his residency, followed by a fellowship in allergy and

immunology at Boston Children’s. Id. at 445. He is board certified in pediatrics and allergy and

immunology, and has been in practice as an allergist/immunologist since 2004. Id. Further, he has

seen patients with various immunologic diseases, including reactions to vaccines. Id. Ninety

percent of his patients are children. Id. at 446-47. He estimated that he spends two-thirds of his

time treating patients in a clinical setting. Id. at 450.

In his practice, Dr. MacGinnitie treats many allergic conditions (including eczema/ atopic

dermatitis, food and environmental allergies, and urticaria). Tr. at 447. He diagnoses roughly 150-

160 eczema patients per year. Id. at 447-48. Dr. MacGinnitie also performs research and has

produced roughly thirty-five publications on the topic of food allergies (or associated conditions).

Id. at 452. And he has authored a paper on the effects of vaccination on patients with egg allergies.

Id. at 451. Dr. MacGinnitie serves as a medical reviewer for various journals, including Allergy

41

and Immunology. Id. at 452. As he acknowledged at hearing, however, Dr. MacGinnitie is not a

neurologist (or dermatologist), and he has not treated patients with POTS. Id. at 503-04, 505-07.56

Dr. MacGinnitie began his testimony by defining the various medical terms relevant to Ms.

McKown’s skin condition as described herein, including eczema/atopic dermatitis – which he

deemed interchangeable (Tr. at 508) – as compared to urticaria. Eczema is an erythematous, dry,

flaky rash that can persist from hours to days or months, and can chronically relapse. Tr. at 460-

61. Roughly ten to twenty percent of the population experiences eczema at some point in life,

making it a fairly common occurrence. Id. at 461. Ninety percent of patients are diagnosed as

infants, and some eventually outgrown the condition. Id. Eczema can worsen seasonally or flare

unexpectedly, when skin is dry (or in the midst humid conditions). Id. Hormones can also increase

the likelihood of a flare-up. Id. Due to the above, eczema can be difficult to treat. Id. Eczema is

not a true allergic response, but patients diagnosed with eczema are more susceptible to developing

food allergies and asthma later in life. Id. at 460. As Dr. MacGinnitie explained, symptoms of

inflamed, abraded skin (followed by exposure to various foreign antigens) increase the likelihood

later-onset allergies. Id. Vaccines, in his view, are not considered in the medical community to be

causal of eczema. Id. at 462-63.

Dr. MacGinnitie opined that eczema is not an autoimmune condition. Tr. at 462, 501, 544.

It is also not understood to be a presenting symptom of POTS (as he understands the disease). Id.

at 463. Later on in his testimony, however, Dr. MacGinnitie did acknowledge that the condition is

inflammatory (i.e., mediated by T cells) at least as it relates to the skin – and thus, certain immune-

modifying drugs, like Prednisone, can be used to effectively treat it, as was the case herein. Id. at

509-10. He maintained, however, that eczema can only be associated with distinct “subtypes” of

inflammation. Id. at 523. He also posited that the underlying inflammation associated with the

condition is not systemic in nature. Id. at 462.

On cross examination, Dr. MacGinnitie acknowledged that the innate immune system

likely plays some role in the development of eczema (given the increase in eosinophils associated

with the condition). Tr. at 514. He also agreed that cytokines can “drive[]” an “inflammation axis”

for eczema. Id. at 527. Certain drug therapies for eczema exist that are aimed at specific cytokine

receptors, further underscoring the innate system’s connection. Id. at 514, 524. Dr. MacGinnitie

agreed that cytokines can be involved in the pruritus (i.e. itching) associated with eczema. Tr. at

521. Itching, Dr. MacGinnitie posited, could be caused by cytokines stimulating the relevant nerve

fibers in the skin. Id. at 515-17. Thus, nerves are involved in eczema’s symptoms, given that by

56

On cross-examination, Petitioner’s counsel questioned Dr. MacGinnitie about the various grants he received (from

the government and pharmaceutical companies), which enabled him to complete research. Tr. at 504-05. I do not,

however, find that Dr. MacGinnitie’s receipt of such funding reduced his credibility or suggested bias – any more that

I would find that Dr. Tornatore’s frequent appearances on behalf of petitioners in the Vaccine Program is a per se

basis for finding him not credible as a general matter.

42

definition, pruritus is a “phenomenon mediated in the CNS.” Id. at 522. In so stating, he refuted

the suggestion that histamines cause itching (given that antihistamines do alleviate eczema

symptoms). Id. at 514.57

Urticaria, by contrast, is a term used interchangeably with “hives” or “welts.” Tr. at 449.

As Dr. MacGinnitie described, urticaria refers to raised skin lesions that usually “come and go” in

response to a specific allergen (for example, peanuts). Id. at 449-50. Urticaria can also be chronic

in nature – whereby the accompanying lesions persist for six weeks (or longer), often without any

explanation. Id. at 450. In a typical urticarial response, the body’s mast cells release histamine

(often instigated by exposure to an irritant/allergen), causing hives in response. Id. at 466-67. The

initiating allergen, however, is not itself the direct cause of hives. Id. at 466-67. Based on his

review of the medical literature, Dr. MacGinnitie knew of no studied association between

vaccination and onset of hives. Id. at 467. He allowed for the possibility, however, that hives could

be autoimmune in rare circumstances (i.e., where particular antibodies – antithyroid

autoantibodies, for example – are directed at the mast cells). Id. at 475, 544.58

Dr. MacGinnitie described an allergy as an “inappropriate immune response to a harmless

environmental stimuli” (for example, tree pollen, cat dander, or peanut protein). Tr. at 463. Typical

immune responses include sneezing, watery eyes, or anaphylaxis (a more extreme reaction). Id.

Allergies are typically diagnosed via serum-specific IgE testing or “RAST” – though such testing

can also produce false-positives. Id. at 465. A patient’s prior health history (following exposure to

suspected antigens) can also be helpful in evaluating for allergies. Id. An “intolerance,” however,

is not the same as an allergy. Id. at 464. Allergies, he posited, require systemic involvement (as

evidenced by an overall worsening of the response). Id. For example, a patient who is “lactose-

intolerant” will exhibit milder symptoms than a patient with a true milk allergy. As noted earlier,

allergic responses can result in more extreme symptoms (i.e., anaphylaxis). Id. at 465.

Dr. MacGinnitie proposed that allergies are not associated with a predisposition for

infection, autoimmune disease, or severe autonomic dysfunction. Tr, at 468. Similarly, Dr.

57

On cross examination, Petitioner’s counsel presented Dr. MacGinnitie with two articles, neither of which were filed

prior to hearing nor discussed during examination of Petitioner’s own experts. See G. Yosipovitch & A. Papoiu, What

Causes Itch in Atopic Dermatitis, 8 Curr. Allergy & Asthma Reps. 306 (2008), filed as Ex. 75 (ECF No. 61-4); J.

Hamilton, et al., Dupilumab Improves the Molecular Signature In Skin of Patients With Moderate-to-Severe Atopic

Dermatitis, 134 J. Allergy Clin. Immunol. 1293 (2014), filed as Ex. 76 (ECF No. 61-5). Counsel argued that the papers

established that an “overexpression” of interleukins or neutrophils could cause eczema itch. Tr. at 514, 515-17. Based

on his on-the-spot review of the article, however, Dr. MacGinnitie posited that interleukins or neutrophils might only

be “mediators” of pruritis, rather than causal of it. Id. at 517-20. The Hamilton article, counsel posited, reveals that

eczema can be effectively treated by certain anti-inflammatory drugs (including Dupilumab which targets the Th2-

centered inflammatory axis). Id. at 523-27. Indeed, Dr. MacGinnitie agreed that anti-inflammatories can successfully

treat the condition. Id. at 527. In so agreeing, however, Dr. MacGinnitie maintained that anti-inflammatories like

Dupilumab are commonly associated with eczema and food or environmental allergies. Id.

58

Along those same lines, Dr. MaGinnitie posited that it is uncommon for patients to present with both eczema and

urticaria (given the distinctions described above). Tr. at 509. It is even less common for eczema/urticarial patients to

also have POTS. Id. Dr. MacGinnitie testified that he has never treated a patient with all three conditions. Id.

43

MacGinnitie testified that he knew of no causal link between vaccines and onset of allergies (a

theory, he noted had been considered in the past, but not persuasively established). Id. at 466. As

he explained, he has treated patients who experience an allergic reaction to a vaccine, but none

who experience a worsening of allergy symptoms post-vaccination. Id. Indeed, he recommends

that his allergy patients receive vaccinations (particularly those with asthma), as vaccines can

prevent infections (and subsequent asthma exacerbations). Id.

In light of Petitioner’s claim that her skin symptoms worsened following receipt of the

HPV vaccine (along with some form of immune system dysregulation), Dr. MacGinnitie reviewed

the relevant medical records for any evidence consistent with such a response. Leading up to Ms.

McKown’s syncopal episode at the frozen yogurt shop, Dr. MacGinnitie found no record evidence

she possessed an abnormal immune system (beyond the possibility she had pre-existing

environmental allergies). Tr. at 468. At most, the records established that Petitioner clearly had

eczema (most likely in a mild form) as an infant, along with various preexisting environmental

allergies. Id. at 467, 469. He also observed that a CT scan taken during the April 2013

hospitalization revealed evidence of a sinus infection (which could be a result of her allergy

symptoms). Id. at 488.

Thereafter, Dr. MacGinnitie agreed, the post-vaccination records evidenced a worsening

of eczema (and onset of hives) around May 2013 and into the summer. Tr. at 468. But he described

Ms. McKown’s eczema course as a “classic” case (i.e., it was “within the range of what’s typically

seen” with eczema patients). Id. at 512. Any worsening Petitioner experienced could be attributed

to the “waxing and waning” nature of eczema – which, he posited, is normal for patients with the

condition. Id. at 468-69. Petitioner’s April 2014 skin biopsy was also consistent with eczema,

along with the photographic evidence offered on the day of hearing. Id. at 473 (citing Ex. 1 at 93),

477.

The relevant medical records also establish that Petitioner tested positive for various

environmental allergies around this time (including grass, cat dander, tree pollen, dust mite, and

ragweed). Tr. at 470-71 (citing Ex. 3 at 11; Ex. 1 at 42). Dr. MacGinnitie opined that these allergies

likely pre-dated her receipt of the vaccine doses at issue herein. Id. at 469, 471. By contrast, Dr.

MacGinnitie could not say for certain if Petitioner’s food allergy testing clearly evidenced positive

values. Id. at 470-71. He deemed the majority of her allergy testing (related to strawberry, peach,

oat, and so on) to be false-positives. Id. at 471.

During the Cleveland Clinic visit in August 2014, Petitioner was diagnosed with chronic

urticaria (which was thought to have begun in the summer of 2013). Tr. at 473-74 (citing Ex. 11

at 12-14; Ex. 1 at 33), 532-33. The photographic evidence offered at hearing also revealed evidence

of the condition. Id. at 478. Dr. MacGinnitie acknowledged this diagnosis, and noted that the

treating physician categorized the condition as idiopathic (thus could not identify a cause). Id. at

44

474.59 As noted earlier, Dr. MacGinnitie posited that physicians are rarely able to determine the

cause of chronic urticaria (as it can be a diagnosis of exclusion, unrelated to environmental

triggers). Id. But the testing completed during this visit (including CBC, anti-IgE, anti-IgE receptor

antibodies, tryptase,60 thyroid function, and inflammatory markers) clearly ruled out any

autoimmune basis for the urticaria. Id. at 475-76, 545; see Ex. 22.

Along those same lines, Dr. MacGinnitie could find no clear etiology for the episodes of

joint pain noted in Petitioner’s medical record. Tr. at 478. Indeed, her rheumatologic work-up at

the Cleveland Clinic also did not identify a clear trigger. Id. at 479 (citing Ex. 11 at 24-28). As Dr.

MacGinnitie explained, the Cleveland Clinic treaters seemed to first attribute Ms. McKown’s joint

pain to her skin condition, but then later distinguished the two (or at least determined that the pain

was secondary). Id. at 480. There was also no evidence of actual arthritis (or inflammation in the

joints) versus “arthralgias” (or complaints of joint pain). Id. at 479. Even so, Dr. MacGinnitie

posited that eczema and urticaria usually did not result in secondary joint pain or present with

arthralgias. Id. at 479. Indeed, Dr. MacGinnitie testified that he has never treated a patient with

eczema or urticaria also suffering from related joint pain (along with arthralgias, and myalgias).

Id. at 511.

Before the Cleveland Clinic work-up, Petitioner’s appointment with Dr. Rouster-Stevens

in early July 2014 resulted in a diagnosis of “amplified musculoskeletal pain syndrome.” Tr. at

481 (citing Ex. 21). Notably, however, Dr. Rouster-Stevens determined the condition was not

autoimmune in nature. Id. at 481. According to Dr. MacGinnitie, the only proof of autoimmunity

he could identify at this visit was a low ANA titer – which, he considered an unremarkable finding,

and likely a low positive in any event. Id. Lupus and connective tissue disorder were also ruled

out. Id.

All in all, based on his review of the record in its entirety, Dr. MacGinnitie could not

conclude that Petitioner was experiencing an underlying inflammatory process. Tr. at 482. As he

explained, the best markers for ongoing inflammation are the ESR and CRP (both of which

remained relatively stable throughout Petitioner’s symptoms course). Id. Her February 2014 lab

test results showed only a slighted elevated ESR (which Dr. MacGinnitie deemed “unlikely of

clinical importance” at the time) given that almost forty percent of the population have slightly

elevated ANA (many of which do not have an underlying systemic disease). Id. at 483 (citing Ex.

59

On cross examination, Petitioner offered some suggestion that the urticarial lesions were related to a medication she

had taken in the past (Fludrocortisone). Tr. at 534. Dr. MacGinnitie acknowledged that the records indicated a concern

for a reaction to the medication, but he posited that the chronic nature of symptoms described therein made it unlikely

that Fludrocortisone triggered its onset. Id. at 535-36, 537.

60

Along those same lines, Dr. MacGinnitie noted that Petitioner tested negative for mast cell activation disorder or

mastocytosis (which he defined as an increased in the mast cells resulting in various symptoms including: flushing,

urticaria, POTS, cognitive fog, and anaphylaxis). Tr. at 485, 486 (citing Ex. 11 at 21). Mast cell activation is measured

by analyzing a patients tryptase levels. Id. at 485, 486; see C. Akin, Mast Cell Activation Disorders, 2 J. Allergy Clin.

Immunol. Pract. 252 (2014), filed as Ex. A, Tab 21 (ECF No. 25-1).

45

1 at 77); see M. Satoh, Clinical Interpretation of Antinuclear Antibody Tests in Systemic Rheumatic

Diseases, 19 Mod. Rheumatol. 219 (2009), filed as Ex. A, Tab 9 (ECF No. 23-10). Moreover, lab

results from tests conducted in late summer 2014 were also negative for the traditional

inflammatory markers. Tr. at 484. Dr. MacGinnitie agreed with Dr. Tornatore’s earlier point that

a patient could still have an autoimmune disease even absent positive inflammatory markers, but

he would not opine that this was true for non-CNS illnesses of the kind relevant to this action. Id.

at 482.

Dr. MacGinnitie next turned to the medical theories of causation proffered by Petitioner in

support of her claim. As to Dr. Mikovits’s theory, Dr. MacGinnitie noted that he found her opinion

confusing. Tr. at 455. From what he could understand of it, Dr. Mikovits seemed to allege that

various vaccine components (in combination) can lead to immune dysfunction in both the adaptive

and innate systems. Id. Thus, Dr. Mikovits posited that the aluminum adjuvant component, for

example, is “taken up” by macrophages, which then migrate to the CNS and “differentiate” into

the microglia. Id. Retroviral DNA (another vaccine contaminant) was also mentioned in her theory,

though Dr. MacGinnitie knew of no causative mechanism to support such a theory. Id. Dr.

Mikovits similarly relied on the concept (explained primarily by Dr. Tornatore in reliance on the

Kanduc paper) that molecular mimicry between HPV components and self sequence proteins could

have contributed to the purported autoimmune process resulting in Petitioner’s injuries. Id.

But Dr. MacGinnitie found Dr. Mikovits’s theoretical components wholly unpersuasive

and scientifically unreliable. For example, he maintained that he knew of no evidence supporting

a causal connection between retroviral DNA and the onset of any disease process. Tr. at 455-56.

As he explained, ten to fifteen percent of a person’s own DNA is retroviral, rendering it unclear

how the tiny amounts contained in vaccines would have any adverse effect (given that humans are

routinely exposed to it in larger amounts via skin, gut, and everyday infections). Id. at 455-56.

Dr. Mikovits’s aluminum adjuvant61/mimicry component of her theory, was, in his view,

also scientifically unreliable. Dr. MacGinnitie found no evidence in the literature filed in this case

that immune system macrophages can actually absorb the aluminum component in vaccines

sufficient to cause injury, let alone migrate through the CNS and into the brain microglia, given

the fact that the adjuvant originates in the muscle or subcutaneous tissue after injection. Tr. at 456-

57, 498-99. Moreover, such a theory did not explain how such mechanisms could later result in

POTS or eczema (or any medically acceptable disease process for that matter). Id. at 456-57, 500-

01. And Dr. MacGinnitie greatly doubted the sense behind the theory that aluminum in vaccine

could be pathogenic at all. As he explained, adjuvants have been used in vaccines for over one

hundred years, and the applicable scientific studies have found no evidence that aluminum (or any

other adjuvant) is unsafe. Id. at 497. Vaccines also contain miniscule amounts of aluminum

61

Dr. MacGinnitie explained that adjuvants are included in vaccine ingredients to increase the immune response (or

activate a low level of inflammation, so the immune response is higher). Tr. at 497-98.

46

(around 225 micrograms) in comparison to the amounts ingested/inhaled by humans on a daily

basis. Id. at 498.62

Dr. MacGinnitie allowed that proinflammatory cytokines could both trigger and propagate

a disease process in certain circumstances. Tr. at 540. He took issue, however, with Dr. Mikovits’s

suggestion that cytokines likely played a role in the disease/symptoms course relevant herein. Id.

As he explained, the articles offered by Petitioner in support of such a theory show no evidence of

a pathologic process. Id. In Dr. MacGinnitie’s understanding, propagating (or mediating) a disease

is not the same as triggering it. Id. He also pointed out that a cytokine response is an immediate

product of the innate system’s activation (and therefore not an inherently chronic process). Id. at

540. At most, cytokines can trigger some initial inflammation which would only later lead to a

more “long-term” response in the adaptive system, rather than continuing to multiply in unabated

form. Id. Thus, in Ms. McKown’s case, an innate immune response even involving cytokine

upregulation would not inherently cause the onset of an onset of injury months following activation

(given the rapidity nature of its initial response). Id. at 532-33.

Dr. MacGinnitie similarly critiqued the joint mimicry/T-cell degeneracy theories proffered

by Dr. Tornatore as inconsistent and vague. He began by noting that both could not be

simultaneously explanatory. Tr. at 457. As he understood it, the concept of degeneracy involved

T cells not specific to a presenting antigen nevertheless recognizing multiple antigens, leading to

cross-reactivity63 without molecular mimicry – a process that would be contradictory to a

molecular mimicr

This text is long and has been trimmed here. Open the source document for the complete record.