The opinion
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 15-285V
Originally Filed: March 11, 2022
Refiled in Redacted Form: May 20, 2022
PUBLISHED
Special Master Horner
SHAWN ORGEL-OLSON,
Tetanus/Diphtheria (Td)
Petitioner,
vaccine; Hepatitis A vaccine;
v.
Sweet’s syndrome; Serum
sickness
SECRETARY OF HEALTH AND
HUMAN SERVICES,
Respondent.
Renee J. Gentry, Vaccine Injury Clinic, Georgetown University Law School,
Washington, DC, for petitioner.
Ryan Daniel Pyles, U.S. Department of Justice, Washington, DC, for respondent.
DECISION 1
On March 19, 2015, petitioner, Shawn Orgel-Olson, filed a petition under the
National Childhood Vaccine Injury Act, 42 U.S.C. §300aa-10-34 (2012), 2 alleging that
he suffered “neurological injuries” as a result of his August 3, 2012 Tetanus/Diphtheria
(Td) and Hepatitis A vaccination. 3 In advance of the hearing, petitioner narrowed his
focus, specifically arguing that his correct diagnoses are Sweet’s syndrome and serum
1 When this decision was originally filed the undersigned advised his intent to post it on the United States
Court of Federal Claims' website, in accordance with the E-Government Act of 2002. 44 U.S.C. § 3501
note (2012) (Federal Management and Promotion of Electronic Government Services). In accordance
with Vaccine Rule 18(b), petitioner filed a timely motion to redact certain information. This decision is
being reissued with two redactions within petitioner’s prior medical history marked as “[. . .]” and omitting
disclosure of a certain aspect of two of petitioner’s prior medical encounters that are not germane to the
analysis contained in this decision. Except for those changes and this footnote, no other substantive
changes have been made. This decision will be posted on the court’s website with no further opportunity
to move for redaction.
2All references to “§ 300aa” below refer to the relevant section of the Vaccine Act at 42 U.S.C. § 300aa-
10-34.
3 The petition included an extensive recitation of petitioner’s medical records inclusive of multiple different
diagnoses considered by his treating physicians but was otherwise no more specific in his allegations
than to state that the vaccines at issue caused “neurological injuries.” (ECF No. 1, pp. 1, 32-33.)
1
sickness. (ECF No. 102, p. 11.) For the reasons set forth below, I conclude that
petitioner is not entitled to an award of compensation for this injury.
I. Applicable Statutory Scheme
Under the National Vaccine Injury Compensation Program, compensation
awards are made to individuals who have suffered injuries after receiving vaccines. In
general, to gain an award, a petitioner must make a number of factual demonstrations,
including showing that an individual received a vaccination covered by the statute;
received it in the United States; suffered a serious, long-standing injury; and has
received no previous award or settlement on account of the injury. Finally – and the key
question in most cases under the Program – the petitioner must also establish a causal
link between the vaccination and the injury. In some cases, the petitioner may simply
demonstrate the occurrence of what has been called a “Table Injury.” That is, it may be
shown that the vaccine recipient suffered an injury of the type enumerated in the
“Vaccine Injury Table,” corresponding to the vaccination in question, within an
applicable time period following the vaccination also specified in the Table. If so, the
Table Injury is presumed to have been caused by the vaccination. § 300aa-13(a)(1)(A);
§ 300 aa-11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B).
In many cases, however, the vaccine recipient may have suffered an injury not of
the type covered in the Vaccine Injury Table. In such instances, an alternative means
exists to demonstrate entitlement to a Program award. That is, the petitioner may gain
an award by showing that the recipient’s injury was “caused-in-fact” by the vaccination
in question. § 300aa-13(a)(1)(B); § 300aa-11(c)(1)(C)(ii). In such a situation, of course,
the presumptions available under the Vaccine Injury Table are inoperative. The burden
is on the petitioner to introduce evidence demonstrating that the vaccination actually
caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274,
1278 (Fed. Cir. 2005); Hines v. Sec’y of Health & Human Servs., 940 F.2d 1518, 1525
(Fed. Cir. 1991).
The showing of “causation-in-fact” must satisfy the “preponderance of the
evidence” standard, the same standard ordinarily used in tort litigation. § 300aa-
13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 940 F.2d at 1525. Under that
standard, the petitioner must show that it is “more probable than not” that the
vaccination was the cause of the injury. Althen, 418 F.3d at 1279. The petitioner need
not show that the vaccination was the sole cause of the injury or condition, but must
demonstrate that the vaccination was at least a “substantial factor” in causing the
condition, and was a “but for” cause. Shyface v. Sec’y of Health & Human Servs., 165
F.3d 1344, 1352 (Fed. Cir. 1999). Thus, the petitioner must supply “proof of a logical
sequence of cause and effect showing that the vaccination was the reason for the
injury;” the logical sequence must be supported by “reputable medical or scientific
explanation, i.e., evidence in the form of scientific studies or expert medical testimony.”
Althen, 418 F.3d at 1278; Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144,
1148 (Fed. Cir. 1992). A petitioner may not receive a Vaccine Program award based
2
solely on his or her assertions; rather, the petition must be supported by either medical
records or by the opinion of a competent physician. § 300aa-13(a)(1).
In what has become the predominant framing of this burden of proof, the Althen
court described the “causation-in-fact” standard, as follows:
Concisely stated, Althen’s burden is to show by preponderant evidence that
the vaccination brought about her injury by providing: (1) a medical theory
causally connecting the vaccination and the injury; (2) a logical sequence of
cause and effect showing that the vaccination was the reason for the injury;
and (3) a showing of proximate temporal relationship between vaccination
and injury. If Althen satisfies this burden, she is “entitled to recover unless
the [government] shows, also by a preponderance of the evidence, that the
injury was in fact caused by factors unrelated to the vaccine.”
Althen, 418 F.3d at 1278 (citations omitted). The Althen court noted that a petitioner need
not necessarily supply evidence from medical literature supporting their claim, so long as
the petitioner supplies the medical opinion of an expert. Id. at 1279-80. The court also
indicated that, in finding causation, a Program fact finder may rely upon “circumstantial
evidence,” which the court found to be consistent with the “system created by Congress, in
which close calls regarding causation are resolved in favor of injured claimants.” Id. at 1280.
In this case, petitioner alleges that he suffered Sweet’s syndrome, a serum
sickness like reaction, and/or neurologic injuries, as a result of his Td and Hepatitis A
vaccinations. (ECF No. 102.) Because these injuries are not listed as Table Injuries,
petitioner must satisfy the above-described Althen test for establishing causation in fact.
See 42 C.F.R. § 100.3(a).
II. Procedural History
Mr. Orgel-Olson filed his petition on March 19, 2015. (ECF No. 1.) This case
was initially assigned to Special Master Laura Millman. (ECF No. 4.) On March 24,
2015, petitioner filed his vaccination record, VAERS report, and medical records from a
number of providers. 4 (ECF Nos. 5, 6.) On May 14, 2015, petitioner filed two affidavits
and additional medical records from Stanford Hospitals & Clinics, Paolo Alto Medical
Foundation, Dignity Health Medical Group, University of California-San Francisco
Medical Center, and Dermatology Surgical & Medical Group. (ECF Nos. 11, 12, 13.)
Respondent filed his Rule 4 Report recommending against compensation on July
9, 2015. (ECF No. 17.) The following day, petitioner filed medical records from dentists
Christopher Kurimoto and Jerel Philip, disability records from the California Employment
Development Department, and additional medical records from the University of
4
Specifically, Dignity Health Medical Group, Scripps Memorial Hospital, the University of California-
Berkley, Barton Memorial Hospital, Verdugo Hills Medical Associates, Neurologist Dr. Joydip
Bhattacharya, Allergy & Asthma Associates, UCLA Healthcare, Pacific Center for Integral Health,
Stanford Hospitals & Clinics, Rheumatologist Dr. Lester Miller, Massachusetts General Hospital, Five
Branches Acupuncture Clinic, Licensed Acupuncturist Holly Guzman, and Wellspring Therapy.
3
California-San Francisco Medical Center on July 10, 2015. (ECF No. 18). On March
25, 2016, petitioner filed a letter from his treating physician, Dr. Safwan Jaradeh. (ECF
No. 28.) Dr. Jaradeh, a neurologist at the Stanford neuro-autonomic clinic,
characterized petitioner’s condition as serum sickness leading to autonomic neuropathy.
(Ex. 30, p. 2.) Respondent filed an expert report by neurologist Phillip Low, M.D., and
the accompanying medical literature on June 10, 2016. (ECF No. 31.) Petitioner then
filed updated medical records from Dignity Health on June 29, 2016. (ECF No. 33.)
On March 24, 2017, petitioner’s current counsel of record was substituted as
counsel in this case. (ECF No. 52.) Thereafter, petitioner raised no further argument
based on Dr. Jaradeh’s opinion. (ECF Nos. 100, 102, 104.) Instead, on January 24,
2018, petitioner filed an expert report from neurologist Carlo Tornatore, M.D. (ECF No.
60.) The medical literature accompanying Dr. Tornatore’s report was filed on February
9, 2018. (ECF Nos. 63, 64, 65.) Dr. Tornatore endorsed serum sickness and Sweet’s
syndrome as explanations for petitioner’s condition. (Ex. 32, p. 5.) On June 11, 2018,
respondent filed an expert report and the accompanying medical literature from
dermatologist Michael Girard, M.D. (ECF No. 68.) Respondent also filed a
supplemental report by Dr. Low on June 15, 2018. (ECF No. 70.)
This case was subsequently reassigned to my docket on June 6, 2019. (ECF
No. 74.) Petitioner filed additional medical records from Dominican Medical Group on
October 2, 2019. (ECF No. 82.) Respondent then filed an expert report from
immunologist You-Wen He, M.D., on October 7, 2019. (ECF No. 84.) I initially
scheduled a two-day entitlement hearing for May 19, 2020. (ECF No. 81.) However,
due to the Covid pandemic, the hearing was bifurcated, with the original hearing held as
a one-day video fact hearing to commence on May 19, 2020, and a separate
entitlement hearing to commence the following year when it was anticipated that expert
testimony could be taken in person. (ECF No. 89.)
The video fact hearing was conducted, as scheduled, on May 19, 2020. (See
ECF No. 94 (Transcript of Proceedings (“Tr.”)), 5/19/2020.) Petitioner was the only
witness to testify. During the fact hearing, several additional pieces of evidence were
identified. On May 20, 2020, petitioner filed photographs of the skin condition he
alleged was caused by his vaccine. (ECF No. 91.) On May 26, 2020, petitioner also
filed two videos of fasciculations5 in his arm and leg that he alleges were caused by the
vaccine. (Ex. 53.) On June 21, 2020, petitioner filed a chronology of his symptoms he
had previously created for his doctors. (ECF No. 95.) The parties were permitted an
opportunity to have their experts review the fact hearing testimony and subsequently
produced evidence; however, on August 11, 2020, petitioner filed a joint status report on
behalf of the parties indicating that they did not believe any additional expert reports
were necessary to develop the record. (ECF No. 97.)
5 A Fasciculation is a “small local contraction of muscles, visible through the skin, representing a
spontaneous discharge of a number of fibers innervated by a single motor nerve filament.” Fasciculation,
DORLAND’S MEDICAL DICTIONARY ONLINE, https://www.dorlandsonline.com/dorland/definition?id=18204
(last visited March 2, 2022).
4
Expert testimony was ultimately heard in a two-day entitlement hearing in this
case commencing April 22 and continuing on April 30, 2021. (See ECF No. 110
(Transcript of Proceedings (“Tr.”)), 4/22/2021, and ECF No. 112 (Transcript of
Proceedings (“Tr.”)), 4/30/2021.) 6 Due to the ongoing pandemic, expert testimony was
heard by video rather than in person as originally anticipated. Drs. Tornatore and He
testified on April 22 and Dr. Low testified on April 30. Respondent did not call upon Dr.
Girardi to testify. At the close of the hearing on April 30, both parties confirmed that the
record of this case is closed. (Tr. 243.) Accordingly, this case is now ripe for a
decision.
III. Factual History
a. As Reflected in Petitioner’s Medical Records
Prior to his August 3, 2012 vaccination, petitioner was a relatively healthy, 25-
year-old man. Petitioner previously received polio, tetanus, MMR, and varicella
vaccinations as a child. (Ex. 1, p. 2-6.) Petitioner was seen by University Health
Services at the University of California, Berkeley on November 5, 2009, for flu-like
symptoms including myalgias, headache, and transient rashes on his hands lasting
several weeks. (Ex. 4, pp. 8-10.) Additionally, Dr. Dean Kashino saw petitioner on
December 12, 2011, for a left knee injury and [. . .]. (Ex. 2, p. 279.) The parties agree
that petitioner’s pre-vaccination history is noncontributory to his alleged vaccine-related
injury. (ECF No. 100, p. 2.) In preparation for a trip to Cambodia, petitioner received
the Td and Hepatitis A vaccinations at issue in this case from Dr. Kashino on August 3,
2012. (Ex. 2, p. 266-67.)
Just over two weeks later, on August 20, 2012, petitioner called Dr. Kashino and
reported that he was experiencing dizziness, neck pain, soreness for the past several
days, and that his head had felt swollen for about a week. (Id. at 271.) Petitioner
denied fever, chills, nausea, and abdominal pain. (Id.) Later that day, petitioner
reported to Verdugo Hills Medical Associates emergency department complaining of
head pressure, neck pain, and dizziness for one week. (Ex. 6, p. 2-3.) Petitioner’s
exam was normal apart from mild pharyngeal erythema and congestion of the right
maxillary sinus. (Id. at 2.) Petitioner was prescribed Zithromax (azithromycin) for a
possible sinus infection. 7 (Id. at 2-3.)
6 All three hearing transcripts (ECF Nos. 94, 110, and 112) are continuously paginated and are cited
collectively throughout this decision as “Tr.”
7 The medical records need to be examined closely to answer the question of whether petitioner ever
actually took the prescribed azithromycin. On August 28, 2012, Dr. Kashino documented that petitioner
had not yet had the prescription filled (referencing it as a “Zpack”). (Ex. 2, p. 270.) Later, on August 30,
2012, Dr. Kashino recorded that petitioner declined to take the azithromycin because he doubted the
sinusitis diagnosis. (Id. at 268.) Subsequently, however, petitioner reported to a different physician (Dr.
Bhattacharya) on September 4, 2012. (Ex. 7, pp. 14-15.) At that time, Dr. Bhattacharya elicited a history
in which petitioner reported that he had started taking azithromycin four days prior – this would mean he
started taking the medication on about August 31, one day subsequent to his August 30 encounter with
Dr. Kashino – and subsequently felt “much better.” (Id. at 15.) A later appointment with a third physician
5
On August 28, 2012, petitioner again called Dr. Kashino, this time reporting mild
headaches and sinus congestion for two weeks and questioning whether his symptoms
were vaccine related. (Ex. 2, p. 270.) Petitioner denied that he was experiencing any
fever or rash and Dr. Kashino noted that petitioner’s condition “sounds viral” and that a
“reaction to Hep A vaccine” was “less likely.” (Id.) Petitioner returned to Dr. Kashino on
August 30, 2012. (Id. at 268.) He explained that he experienced soreness in his neck,
pressure in his temples, and lightheadedness about five days after his recent
vaccinations. (Ex. 2, p. 268.) Petitioner noted that his sinus and headache issues were
slow to improve, and that he was experiencing jaw pain and increasing pressure in his
head for a week. (Id.) Petitioner reported pain at the injection site, but was negative for
fever, myalgia, or arthralgia. (Id.) Dr. Kashino felt that petitioner’s symptoms were “very
vague” and believed that petitioner’s jaw pain was the result of TMJ Syndrome and
ordered a general blood workup to check for signs of infection, inflammation, and other
potential explanations of petitioner’s fatigue. (Id. at 269.) Nonetheless, a VAERS report
was completed. (Id. at 263.) It documented fatigue as well as pain in petitioner’s jaw,
temple, and cervical spine. It included no reference to rashes, lesions, or fever. (Id.)
Dr. Kashino later interpreted the lab results as demonstrating “no significant
abnormalities.” (Id. at 126.)
Petitioner was seen by Dr. Joydip Bhattacharya for a neurological consultation on
September 4, 2012. (Ex. 7, p. 14.) He reported onset of head and neck pain and
pressure occurring about one-week post-vaccination and without fever. Petitioner did
not describe any new symptoms and had an unremarkable physical exam; however, he
was feeling much better after starting azithromycin. (Id. at 15-17.) Dr. Bhattacharya
assessed petitioner with “[p]ossible aseptic meningitis VS unusual vaccination reaction,”
but declined to conduct a lumbar puncture because petitioner was “doing [well] and on
the way to recovery.” (Id. at 18.) Dr. Bhattacharya indicated he would do a spinal tap if
petitioner’s recovery stalled. (Id.)
On September 7, 2012, petitioner called Dr. Kashino to explain that his jaw pain
and left-temporal headache had resolved. (Ex. 2, p. 265.) He reported, however, that
he was still fatigued, feeling tenderness in his right temple, and was now suffering
transient rashes and noticing pain in his joints and the fat pads of both hands. (Id. at
54, 261-62, 264.) On September 11, 2012, Dr. Kashino called petitioner to follow up on
his symptoms. (Ex. 2, p. 264.) During this call, petitioner explained that he was also
(Dr. Kaufmann) on September 14, 2012, again confirmed that petitioner had taken the azithromycin (“z
pack”). (Ex. 2, p. 261.) A later record by Dr. Kashino from a visit occurring October 19, 2012, again
indicates that petitioner did not take the prescribed azithromycin; however, it appears that Dr. Kashino
copied over a large portion of the relevant paragraph from his prior August 30 history of present illness
into this later record. (Compare Ex. 2, p. 253, and 268.) At subsequent appointments in December of
2012 petitioner again confirmed to physicians that he started taking the azithromycin on August 31 and
that he felt it helped. (Ex. 2, p. 230; Ex. 13, p. 7.) Thus, notwithstanding petitioner’s testimony that he
only took Flonase and Claritin following his urgent care appointment (Tr. 15), the contemporaneous
medical records preponderantly indicate otherwise. Based on my review of the record as a whole, I
conclude that petitioner did take a course of azithromycin beginning August 31, 2012, and that it did
alleviate at least some of petitioner’s pain symptoms.
6
beginning to experience arthralgias in his legs. (Id.) Petitioner was worried about Lyme
Disease and West Nile Virus because he had gone on a ten-mile hike about two weeks
prior to onset of his illness. (Id.) Dr. Kashino suggested petitioner see an infectious
disease specialist. (Id.)
Petitioner was seen by infectious disease physician Dr. John Kaufmann on
September 14, 2012. (Ex. 2, p. 261.) Dr. Kaufman noted a normal physical exam, and
recorded symptoms of needle-like joint pain that was worse in the hands, rashes on
arms and hands, abdominal pain in the right lower belly, anxiety due to worsening
symptoms, [. . .], fatigue, headache with cervical soreness and bilateral jaw pain, and a
knee sprain. (Id.) Dr. Kaufmann noted that petitioner’s reported arthralgia did not arise
until later, after petitioner had taken the prescribed “z-pack.” (Id.) Dr. Kaufmann felt it
was difficult to find a unifying infectious diagnosis to explain petitioner’s symptoms. (Id.
at 262.) Dr. Kaufmann believed that petitioner’s symptoms would resolve with time and
noted that considering petitioner’s normal initial test results, the next step would involve
invasive testing, such as lumbar punctures or liver and bone marrow biopsies, which Dr.
Kaufmann emphatically recommended against unless petitioner continued to report
severe symptoms. (Id.) Dr. Kaufmann included “adverse effect of vaccines” among his
assessments but specified that it was “per patient perception.” (Id.)
Petitioner returned to Dr. Bhattacharya on September 17, 2012, for a follow-up.
(Ex. 7, p. 7.) Dr. Bhattacharya noted that, in addition to his hands and wrist, petitioner
was also developing joint pain in his leg, feet, and shoulders. (Id. at 8.) He also
observed “some small pruritic reddish lesions” on examination. (Id. at 10.) Dr.
Bhattacharya suggested petitioner had experienced an “[e]pisode of symptoms
suggestive of aseptic meningitis following a tetanus shot and Hepatitis A immunization,
now with polyarticular arthritic symptoms.” (Ex. 7, p.10.) He noted that his symptoms
are suggestive of an inflammatory polyarthropathy, but stressed that lab results had
been negative. Dr. Bhattacharya felt a referral to rheumatology was appropriate, as he
felt suspicion of a primary neurological illness was low, and indicated she would not
pursue any spinal tap unless Dr. Kaufmann (infectious disease) felt it was indicated.
(Id.)
Petitioner then went back to Dr. Kaufmann for a follow up exam on September
21, 2012. (Id. at 259.) He reiterated his concern that he might have been exposed to
something while hiking in southern California. (Id.) Petitioner’s physical exam was
normal, his labs were unremarkable, he was negative for Lyme disease, and his total
protein showed mild elevation. (Id. at 260.) Dr. Kaufmann reiterated that it is “difficult”
to establish a unifying diagnosis for petitioner’s entire illness. (Ex. 2, p. 260.) Dr.
Kaufmann believed that the time course of petitioner’s symptoms ruled out any occult
infection but prescribed Ativan as well as doxycycline as a “desperate last resort” and
based on petitioner’s “strong enthusiasm,” its anti-inflammatory properties, and the
remote possibility that petitioner may have contracted Lyme disease or some other
rickettsial infection. (Id. at 260.)
7
On September 26, 2012, Dr. Kaufmann cleared petitioner to return to work. (Id.
at 256.) However, petitioner called Dr. Kashino on this day to describe new symptoms
of tightening throat muscles that had lasted for several weeks. (Id. at 257.) Dr. Kashino
prescribed ranitidine and suggested an ear, nose, throat specialist if petitioner did not
improve. (Id.) Petitioner was next seen by Dr. Kashino on October 19, 2012. (Id. at
253.) Petitioner’s physical exam was normal, but Dr. Kashino noted that petitioner
continued to suffer from headaches, neck pain, jaw pain, dilated veins, and pressure
over his temporal parietal areas bilaterally. (Id.) Dr. Kashino was still unable to
diagnose petitioner’s condition and indicated that he would seek authorization for a
brain MRI. (Id. at 254.) Petitioner had stopped taking doxycycline after 16 days. (Id. at
253.)
On October 29, 2012, petitioner’s mother called Dr. Kashino indicating an urgent
need to speak with him because it was taking too long to authorize an MRI and she was
afraid petitioner was going to lose his vision. (Id. at 255.) Dr. Kashino returned the call
the same day and spoke to petitioner. He advised that petitioner needed to return to the
neurologist for any MRI order. (Id. at 255.) Petitioner reported headaches of 6 out of
10 on the pain scale, but advised that his joint pain and rashes had resolved. 8 (Id.)
Petitioner returned to Dr. Bhattacharya on October 31, 2012. (Ex. 7, pp. 3-6.)
Dr. Bhattacharya noted that petitioner had originally been seen for aseptic meningitis,
but that he has continued to experience headaches on and off. (Id. at 4.) He assessed
right trigeminal autonomic cephalgia and ordered a brain MRI to evaluate. (Ex. 7, p. 6.)
This MRI was conducted on November 6, 2012, and was largely unremarkable. (Id. at
1-2.)
Petitioner was seen by Dr. Kaufmann for a further follow-up exam on November
2, 2012. (Ex. 2, p. 251.) During this visit, petitioner reported continued pressure in his
head, tingling over his right head and face, a transient rash that would appear in the
mornings, and tightness of the throat muscles. (Id.) Dr. Kaufmann noted that rickettsial
infections were unlikely, but not excluded, and that there was a remote possibility of
typhus despite petitioner’s negative tests. (Id.) Dr. Kaufmann noted that “a unifying
diagnosis remains elusive” and that the symptoms petitioner reported were “most
suggestive of allergic or immunologic issue.” (Id. at 252.) Dr. Kaufmann believed that
an allergy/immunology opinion would be helpful to assist diagnosis “in the challenging
case of this patient.” (Id.)
On November 8, 2012, petitioner reported to UCLA Medical Center Emergency
Services with a chief complaint of dizziness and tingling in his fingers, as well as
“rashes on [bilateral upper extremities] only in the morning.” (Ex. 9, p. 1.) Petitioner
was seen by the Internal Medicine department at UCLA Health on November 21, 2012.
(Id. at 4.) He reported headache, pain in his neck, jaw, hands, feet, knees, wrists, and
elbows, and a morning rash on his biceps and forearms. (Id. at 5.) Petitioner was
8During the hearing I asked petitioner whether there were any symptoms beyond the headache of 6 out
of 10 that he reported by phone to Dr. Kashino that raised a concern for loss of vision. He could not recall
any other symptoms. (Tr. 52.)
8
referred to immunology with a diagnosis of an unclear syndrome and chronic fatigue.
(Id.)
Petitioner was referred to Stanford Hospital and Clinics for further evaluation with
an infectious disease specialist at about this time. (Ex. 2, p. 250.) He had a follow up
appointment with Dr. Kaufmann on December 10, 2012; however, Dr. Kaufmann
remained unable to identify any unifying diagnosis and indicated he would await the
conclusion of petitioner’s evaluation at Stanford. (Id. at 249.) Petitioner also saw Dr.
Kashino on December 10, 2012, and Dr. Kashino similarly deferred further testing
pending petitioner’s infectious disease evaluation from Stanford and an upcoming
rheumatology appointment. (Id. at 247.) Dr. Kashino questioned whether there is a
psychological aspect to petitioner’s condition, but noted that petitioner felt his rashes
prove he has an infectious or immunologic condition. (Id.)
Petitioner was examined by Dr. Julie Parsonnet on December 7, 2012, for an
infectious disease consultation where he underwent several tests and a physical
examination. (Ex. 2, p. 229-245.) He provided Dr. Parsonnet with a list of symptoms
including daily head pressure and headaches, daily joint pain, a speckled rash under his
forearms one to three mornings per week, constant fatigue, right trigeminal nerve
tingling, a tightness of his neck muscles, intense dizziness and imbalance from
November 13 to November 15, heart palpitations one to three days per week, constant
soreness on the back of his neck, daily muscle fasciculations, and sore lymph nodes. 9
(Id. at 234.) Dr. Parsonnet felt that, especially given his extensive workup and lack of
any diagnostically useful test results, fibromyalgia would be the leading possibility
among several conditions given the chronicity and lack of inflammatory markers. (Id. at
236-37.) Dr. Parsonnet also felt a component of TMJ 10 or migraine remained possible,
though those conditions would not explain the myalgia and arthralgia. (Id.) Dr.
Parsonett intended to follow up to discuss therapeutic options after petitioner had seen
rheumatology. (Id.)
Petitioner also saw rheumatologist Dr. Lester Miller on December 11, 2012, for
an evaluation of his joint and muscle pain. (Ex. 13, p. 7; Ex. 2, pp. 221-28.)11 Dr. Miller
noted no abnormalities upon review of petitioner’s physical exam and lab work, with no
9Dr. Kashino also confirmed that he was provided a copy of this list for scanning into his chart. (Ex. 2, p.
246.) Petitioner explained during the hearing that he prepared the list over time as his symptoms were
developing. (Tr. 52-53.) Initially he could not recall whether he continued to update the list after
presenting it to Dr. Parsonnet; however, an updated version of the chronology with entries as late as June
of 2015 was later filed as Exhibit 54.
10Petitioner first raised his trigeminal neuralgia and possible TMJ with his dentist on November 21, 2012.
(Ex. 26, p. 1.) Petitioner’s dentists do not appear to have provided any care or diagnosis relevant to this
case. (Tr. 29-30; Exs. 26-27.)
11Two pages of handwritten notes regarding Dr. Miller’s December 11 encounter are included in Exhibit
13, which is a filing of Dr. Miller’s records; however, Dr. Miller also prepared an extensive letter report to
Drs. Kashino and Kaufmann that is contained in the Dominican Medical Group records at Exhibit 2 and is
also reproduced at Ex. 13, pp. 7-10.
9
evidence of inflammatory polyarthritis on examination and normal inflammatory markers
in bloodwork from August 30 through December 5, 2012. (Ex. 13, pp. 8-9.) Dr. Miller’s
clinical impression was that petitioner had arthralgia, head pressure, periodic rash,
fatigue, sensation of muscle tightening, and other non-specific symptoms, but with no
clear signs of reactive arthropathy, connective tissue disease, or autoimmune process.
(Ex. 13, p. 9.) Dr. Miller noted that “the spectrum of [petitioner’s] symptoms do not fit a
particular infectious process and in my opinion do not fit a particular rheumatic disease .
. . .” (Id.) He doubted that petitioner had fibromyalgia. (Id.) Dr. Miller left open the
possibility of a vaccine-reaction, noting that it is “conceivable” given that Hepatitis A
vaccine has been documented as causing non-specific symptoms such as headache,
malaise, diarrhea, dizziness, nausea, anorexia, fever, skin rash, and vomiting. (Id. at 9-
10.) However, he indicated “[t]here is no way at this point to prove or disprove that
speculation.” 12 (Id. at 10.) He recommended continued observation and NSAIDs for
pain relief, but recommended against any further antibiotics. (Id.)
Petitioner returned to Dr. Parsonnet on December 21, 2012. (Ex. 12, pp. 20-21.)
Dr. Parsonnet recorded an interval history and noted that there is no consensus among
petitioner’s treaters regarding his symptoms. (Id. at 20.) Petitioner stressed that his
symptoms improved while he was on azithromycin and Dr. Parsonnet expressed
willingness to prescribe another course, but otherwise did not recommend any further
testing. She felt consultation with a dentist remained appropriate along with further
follow up with a neurologist. (Id. at 21.)
Petitioner was later seen for an allergy and immunology consultation with Drs.
Tiffany Kim (resident) and Melinda Braskett (attending) at UCLA Medical Center on
January 11, 2013. (Ex. 9, pp. 6-9.) Dr. Kim’s physical exam indicated tension in the
neck and shoulder muscles, but there was no indication of fasciculations and joints were
unremarkable. (Id. at 7.) No rashes or lesions were noted. (Id.) Lab results were
unremarkable. (Id.) In addition to his post-vaccination medical history, petitioner also
related that he had three prior allergic reactions to antibiotics as a child (hives after
penicillin, photosensitivity and neuropathy after cipro, and rash and hives after
erythromycin). (Id. at 6.) Dr. Kim felt that a reaction to vaccination was “possible” and
felt that the prior allergic reactions to antibiotics could suggest “an immunologic
predisposition.” (Id. at 7.) Dr. Kim indicated that the history of migratory arthritis and
rash, especially between the fingers, could suggest a now resolved serum sickness.
(Id.) Petitioner’s main complaints at this visit were throat tightening, muscle
fasciculations, and fatigue. No “clear etiology” was identified, but the assessment
included “[q]uery post vaccine immunologic reaction versus unknown post viral
syndrome” while indicating that persistent muscle fasciculations represented a separate
12 Significant to assessing the contours of Dr. Miller’s openness to “speculation” regarding vaccine
causation of non-specific symptoms, Dr. Miller’s report incorrectly states that petitioner has had arthralgia
and myalgias beginning August 8, 2012. (Ex. 13, p. 7.) This is not consistent either with petitioner’s
contemporaneous medical records or with the written timeline of symptoms petitioner first provided to Dr.
Parsonnet and which Dr. Miller indicated he had reviewed and would not repeat. (Ex. 2, pp. 230-31; Ex.
13, p. 7). Arthralgia and myalgia were not reported at petitioner’s earliest post-vaccination encounters
and Dr. Kashino specifically confirmed the absence of both during his August 28, 2012 encounter. (Ex. 2,
p. 268.)
10
assessment in need of evaluation by a peripheral nerve specialist. (Id.) Further
subspeciality coordination, including with a rheumatologist, was recommended. (Id.)
Upon review, Dr. Braskett noted petitioner’s turbinates were inflamed with visible
postnasal drip and that his lab results were negative for immune complexes and with
normal erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). (Id. at 8.)
Her impression included “[a]dverse reaction to vaccine” and “[l]ikely serum sickness
resolved” and “[p]ersistent fasciculations, unclear etiology – possibly post immunization
or post viral.” (Id.)
Petitioner was then seen by UCLA neuromuscular specialists Drs. Perry Shieh
and Elba Maldonado on January 18, 2013, for evaluation of his muscle fasciculations
and tightness of his throat muscles. (Ex. 9, p. 9.) Petitioner expressed concern that his
progressing fasciculations might be due to a demyelinating condition. (Id.) The
fasciculations were observed at the pectoral and abdominal muscles, but petitioner’s
physical and neurological testing was all normal, and Drs. Shieh and Maldonado
ultimately diagnosed him with likely “benign fasciculation syndrome that the etiology of
which is unknown.” (Id. at 11.) The doctors also expressed the possibility that the
syndrome “could” be “due to post-vaccine immunologic reaction or postviral syndrome.”
(Id.) Thereafter, Dr. Braskett added an addendum to her record to notate that
petitioner’s fasciculations are benign. (Id. at 8.)
Petitioner was seen by immunologist Donna Felsenstein, M.D., at Massachusetts
General Hospital on February 4, 2013. (Ex. 14, p. 17.) Petitioner provided an extensive
history; however, Dr. Felsenstein summarized “fatigue which is somewhat improved as
well as fasciculations” as being primary complaints at this encounter. (Id. at 19.)
Review of systems also noted complaints of tingling in his hands, feet, and chest,
tenderness at certain points on his chest. (Id. at 18.) In addition to extensive lab work,
all of which was negative, Dr. Felsenstein reviewed a photograph of a prior rash on
petitioner’s arm which she described as erythematous maculopapular. (Id. at 18-19.)
Physical exam was normal and Dr. Felsenstein stressed the lack of any weakness on
exam. (Id. at 18-19.) Nonetheless, she felt the fasciculations were concerning and
recommended a third neurology opinion. (Id. at 19.) Dr. Felsenstein concluded that the
etiology of petitioner’s condition remained unclear, but felt it interesting that petitioner’s
girlfriend had experienced a mono-like illness around the time his condition began. (Id.)
Petitioner returned to Dr. Kashino on February 7, 2013. (Ex. 2, pp. 215-17.)
Petitioner reported worsening muscle fasciculations involving his whole body, vibratory
sensations in his hands and feet, tightness around his temples and throat, slightly
improved fatigue, and improved joint pain after removing gluten from his diet. (Id. at
215.) Dr. Kashino noted that “[t]hree physicians have felt that his symptoms were due
to vaccines.” 13 (Id.) Dr. Kashino reviewed petitioner’s symptoms but offered no further
13Dr. Kashino identified the three doctors as Dr. Kaufmann, Dr. Miller, and Dr. Parsonnet. (Ex. 2, p. 215.)
Based on my review of each physician’s encounter records, Dr. Kashino significantly overstates the
degree to which any of the three supported vaccine causation. Dr. Kaufmann indicated that petitioner’s
symptoms could be immunologic, but stressed that a unifying diagnosis remained “elusive” and only
included a vaccine reaction “per patient perception” among his assessments. (Id. at 262.) Dr. Miller felt
that petitioner’s spectrum of symptoms did not fit any identifiable condition. He noted that vaccine-
11
diagnostic assessment and awaited any further developments based outstanding lab
work from the Massachusetts General Hospital evaluation. (Id. at 217.)
On March 4, 2013, petitioner was seen by Dr. Grant de la Motte at the Palo Alto
Medical Foundation, Santa Cruz Division, for a neurology consult. (Ex. 2, pp. 167-71.)
Petitioner recounted his symptoms and explained that he now believed he was
experiencing an “Epstein Barr virus recurrence . . . lyme . . . [or] a vaccine reaction.”
(Id. at 168.) Dr. de la Motte reviewed petitioner’s prior records and noted that
“[l]aboratory work up was extensive and included an impressive list of infectious
diseases and metabolic diseases. The testing was all normal.” (Id. at 171.) Dr. de la
Motte’s physical exam was also normal. (Id. at 170-71.) Dr. de la Motte assessed
subjective muscle twitching, paresthesia, and fatigue. He concluded:
This young man is presenting with multiple somatic symptoms that do not
fit into a neurologic pattern of disease, and therefore, not localizable. His
neurologic exam is normal. I do not see any fasciculations. I doubt his
symptoms will be associated with any defined pathology. I expressed my
concern that an EMG study is low-yield, but he is interested in confirming
the presence of fasciculations. He understands that fasciculations are
nonspecific and can be seen in the normal population, but he would still like
to proceed with the study.
(Id. at 167.)
On April 1, 2013, petitioner received an echocardiogram from Drs. Raj Singh and
Jay Johnson. (Id. at 204.) Petitioner’s echocardiogram was unremarkable outside of
trace mitral regurgitation and trace tricuspid regurgitation. (Id. at 205.) On April 10,
2013, Dr. Kashino saw petitioner and ordered a cognitive metabolic panel, thyroid
studies, and Lyme titers. (Id. at 202.)
During this same period, petitioner was seen by neurologist Dr. Neelam Goyal for
EMG and nerve conduction tests at Stanford Hospital on April 19, 2013. (Ex. 2, p. 163.)
Dr. Goyal concluded that “[t]hese electrodiagnostic studies are normal without evidence
causation was “conceivable,” but considered it unprovable “speculation.” (Ex. 13, pp. 9-10.) Dr.
Parsonett did include Reiters syndrome, a post-infectious syndrome, in her differential diagnosis, but at
the time of her consultation with petitioner felt that his condition was most likely to be fibromyalgia. (Ex. 2,
p. 245.) Dr. Kashino’s summary of petitioner’s prior consultations appears in the “HPI” section of his
record. It is not clear whether it is based on any review of records or petitioner’s own description of his
prior encounters. Dr. Kashino did reference that Dr. Parsonnet had called the CDC with regard to this
case. (Ex. 2, p. 215.) As of April 28, 2013, Dr. Parsonnet recorded: “Discussed with national vaccine
safety group (Clinical Immunization Safety Assessment Network at CDC) who felt symptoms are unlikely
to be related to immunizations. They were concerned about toxic exposure or primary neurologic
process.” (Ex. 12, p. 35.) On July 12, 2013, Dr. Parsonnet discussed with petitioner the fact that she had
contacted the CDC and that the CDC had not ever seen reaction of this duration. (Ex. 12, p. 66; see also
Ex. 14, p. 12 (copy of e-mail by Dr. Parsonnet explaining committee conclusions in greater detail).)
Nothing in the record of petitioner’s July 12, 2013 encounter suggests Dr. Parsonnet had become more
persuaded of a vaccine reaction after conferring with the CDC. She sought to persuade petitioner not to
pursue a spinal MRI, a lumbar puncture, or a course of steroid treatment. (Id.)
12
of a neuropathy, neuromuscular junction pathology, or motor neuron disease.” (Id. at
165.) In a later letter to Dr. Parsonnet dated July 12, 2013, Dr. Goyal wrote that she did
not see any evidence of clear pathology affecting petitioner’s large sensory fibers or
motor system. (Ex. 2, pp. 155-58.) She further noted that there is no evidence of
pathology for petitioner’s fasciculations after reviewing the EMG nerve conduction study
and noted the symptom can be heightened by stress or anxiety. (Id. at 158.) While Dr.
Goyal noted “scant fibrillation potentials” on petitioner’s EMG, she explained that their
significance was unclear but possibly related to mild spondylitic disease of the spine
and unlikely to be related to petitioner’s paresthesias or fasciculations. (Id. at 163-65.)
Dr. Goyal was unable to make a diagnosis and expressed interest in a dedicated lumbar
spine MRI for further evaluation. (Id. at 158.) Dr. Goyal also recommended autonomic
testing given that petitioner’s initial presentation included lightheadedness. (Id.)
By June 13, 2013, Dr. Kashino noted that petitioner was “slowly improving” but
was still unable to make a unifying diagnosis. (Id. at 199.) Dr. Kashino indicated that
Dr. Felsenstein from Massachusetts General Hospital had prescribed doxycycline and
requested a repeat of petitioner’s borrelia test, suggesting further suspicion of Lyme
disease. (Id. at 198.) Yet, on July 17, 2013, Dr. Kashino indicated that “[t]he consensus
is that this is probably a post-vaccine reaction.” (Id. at 196.) The specific basis for this
statement is not indicated; however, in including a probable adverse effect of vaccines
in his assessment, Dr. Kashino reiterated the notation from his February 7, 2013, record
that the conclusion was supported by three physicians. 14 (Id. at 197.) Additionally, Dr.
Kashino observed that petitioner had just completed his course of doxycycline as
prescribed by Massachusetts General Hospital and that Stanford had ordered MRI of
petitioner’s spine. (Id. at 196.) Subsequently, on July 30, 2013, petitioner called Dr.
Kashino’s office to request that he order the Lyme disease tests recommended by
Massachusetts General Hospital. (Id. at 195.) Petitioner also later underwent lumbar
MRI on August 12, 2013. (Ex. 2, p. 148.) Dr. Goyal reviewed petitioner’s MRI and
noted “mild degenerative changes of the lower lumbar spine” and “no significant central
or neuro-foraminal narrowing at any level.” (Id.) Dr. Kashino’s July 17 suggestion of
any consensus is perplexing given his awareness of this ongoing investigation from two
different practice groups. As of September 23, 2013, Dr. Felsenstein noted the cause of
petitioner’s condition remains undefined despite petitioner reporting that other doctors
had concluded it was vaccine related. (Ex. 14, p. 5.)
On September 4, 2013, petitioner expressed to Dr. Kashino that he was feeling
“quite a bit better.” (Ex. 2, p. 192-93.) Dr. Kashino characterized petitioner’s condition
as “probable adverse effect of vaccines” and again noted that “Three physicians support
this, Lester Miller, MD; a southern California allergist/immunologist; and Dr. Julie
14 In that regard, refer back to n. 13, infra. In fact, one of these three physicians, Dr. Parsonett,
specifically recorded in her own records as of December 21, 2012, that there was no consensus among
petitioner’s treating physicians regarding his symptoms. (Ex. 12, p. 20.) By that time, petitioner had
already consulted with Drs. Miller and Kaufmann, the other two physicians contributing to the purported
consensus.
13
[Parsonnet], MD, infectious disease at Stanford.” 15 (Ex. 2, p. 193.) Dr. Kashino
concluded this visit by clearing petitioner to return to work on October 1. 2013. (Id. at
191.) Petitioner had no significant medical treatment for the next six months. However,
he continued to request further tests and treatments. (Ex. 2, p. 190 (10/4/13 request for
thyroid test), p. 189 (10/14/13 request for stress test and additional lab work), p. 188
(10/22/13 request for physical therapy referral for myalgia), p. 186 (12/6/13 request for
redo of prior bloodwork plus prescription for Neurontin).
On March 7, 2014, petitioner presented to neurologist Safwan Jaradeh for the
autonomic testing recommended by Dr. Goyal the prior July. (Ex. 12, p. 110.) Dr.
Jaradeh’s testing revealed “mild to moderate autonomic neuropathy involving the
sympathetic vasomotor and cardiovascular fibers” as well as “parasympathetic
cardiovascular and baroreflex sparing.” (Id. at 111.) Dr. Jaradeh also noted that the tilt
table findings indicated significant orthostatic hypotension and tachycardia. (Id.)
Petitioner left this visit with a post-procedure diagnosis of orthostatic hypotension and
postural orthostatic tachycardia syndrome (POTS). 16 (Id. at 110.)
Petitioner was not seen again until the following September when he presented
to Dr. Kashino on September 11, 2014. In the interim he was reportedly traveling in
Europe for about four months. (Ex. 23, p. 55.) Dr. Kashino appears to have suggested
that petitioner benefited from a period of ignoring his health symptoms. 17 (Id.) At this
visit, petitioner reported new onset of perioral numbness. (Id.) Petitioner expressed a
desire to post a list of his symptoms online so his physicians could more easily
comment. (Id. at 57.)
On September 17, 2014, petitioner presented to dermatologist Molly Shields,
M.D. (Ex. 25, p. 1.) He reported speckled rashes appearing in the morning (for about
one hour) for the past two years. (Id.) He wondered if they were vaccine caused. (Id.)
Dr. Shields indicated that she did not know the cause of petitioner’s cutaneous eruption,
15 In that regard, refer back to n. 13-14, infra. This statement is also repeated in future records, but will
not be further addressed.
16These diagnoses are questionable based on the findings recorded by Dr. Jaradeh. POTS is defined as
a heart rate increase of 30 beats per minute within 10 minutes of standing of head up tilt in the absence of
orthostatic hypotension. Usually, this results in a standing heartrate of 120 beats per minute or higher.
(Eduardo Benarroch, Postural Tachycardia Syndrome: A Heterogeneous and Multifactorial Disorder,
87(12) Mayo Clin. Proc. 1214 (2012) (Ex. A, Tab 1).) In this case, Dr. Jaradeh indicted that petitioner’s tilt
table test indicated tachycardia plus significant orthostatic hypotension. And, in any event, petitioner did
not exceed a 30 beats per minute increase until 15 minutes into the test and his heartrate reached a
maximum of 117 beats per minute after 22 minutes. (Ex. 12, pp. 111-12.) Nor, for that matter, did
petitioner meet the consensus criteria for orthostatic hypotension. The consensus criteria requires at
least a 20 mm drop is systolic blood pressure occurring within three minutes of standing. (Phillip Low and
Wolfgang Singer, Management of neurogenic orthostatic hypotension: an update, 7 LANCET NEUROL. 451
(2008) (Ex. A, Tab 5).) Petitioner ultimately experienced a 36 mm drop in systolic blood pressure, but
blood pressure drop during the first 16 minutes after tilt was described as “minimal.” (Ex. 12, p. 112.)
17The specific notation is somewhat hindered by a typographical error. The record states: “He did well by
ignored his health symptoms.” (Ex. 23, p. 55.) It seems reasonable to interpret this as indicating “[h]e did
well by ignore[ing] his health symptoms.”
14
but suggested it may be vascular and expressed concern regarding a rheumatologic
disorder, though petitioner’s presentation did not fit Still’s disease or juvenile rheumatoid
arthritis. (Id. at 7.) Dr. Shields did not visualize the rashes, but recommended a skin
biopsy when a rash is present. (Id.; see also Ex. 19, p. 18.)
Petitioner also returned to Dr. Goyal the same day. (Id.) He reported “good
energy” and “minimal joint pain,” but indicated he had occasional jaw pain, mild temple
and occipital pain (primarily right), and rashes appearing in the morning. Dr. Goyal
noted fasciculations, chest discomfort, and “odd sensations,” to still be present, and
perhaps worsened. (Id.) A Holter monitor reportedly showed premature ventricular
contractions and petitioner reported sudden onset of perioral tingling and tingling of the
right hand which occurred while he was in Europe. (Id.) Physical exam was noted to be
normal except for subjective pinprick loss over the hand. Dr. Goyal felt the paresthesias
was benign, likely related to headache or anxiety, but agreed to a repeat brain MRI. (Id.
at 19.) Noting the abnormalities previously found on autonomic testing, Dr. Goyal also
noted the possibility of small fiber polyneuropathy and agreed to refer petitioner to an
autonomic clinic for further evaluation. (Id. at 19-20.)
Petitioner was seen again by dermatologist Dr. Shields for a punch biopsy on
October 13, 2014. (Ex. 23, pp. 2-6.) Dr. Shields observed “[p]atches and macular
erythema faint in quality in 2-3 mm macular coalescent to plaques linear quality” and a
sample was taken from the left pretibial region. (Id. at 2.) Petitioner’s punch biopsy was
interpreted by Dr. Laura Pincus. Her dermatopathology report indicated “relatively
sparse perivascular infiltrate with early neutrophilic forms.” (Id. at 5.) The report further
noted that “this could represent Still’s disease, [but] this pattern of infiltration can be
seen in neutrophilic urticarial dermatosis as well.” (Ex. 23, p. 5.) However, the report
also explained that neutrophilic urticarial dermatosis patients “often have an associated
systemic condition, such as Schnitzler’s syndrome, lupus erythematosus, or a
hereditary autoinflammatory fever syndrome. Therefore, the systemic symptoms you
mention might be explained by one of these conditions rather than Still’s disease.” (Id.)
She noted, however, that “[c]onvential urticarial or neutrophilic urticaria are possible
diagnostic considerations for this eruption as well.” (Id.)
Petitioner had a cardiology consultation with Jay A. Johnson, M.D., on October 9,
2014. (Ex. 23, pp. 53-54.) He underwent a stress test and echocardiogram. (Id. at 53.)
The stress test revealed that petitioner had an “outstanding exercise capacity” and the
echocardiogram showed “trivial” mitral and tricuspid valve regurgitation. (Id. at 54.) Dr.
Johnson concluded that petitioner had no evidence of structural or ischemic heart
disease and no evidence of significant arrhythmias or electrical abnormalities. Dr.
Johnson noted the prior finding of premature atrial contraction which may result in
symptoms, but indicated they do not appear pathologic. (Id.) Dr. Johnson felt petitioner
was “extremely sensitive to his body and is fixated on these many multiple mild somatic
complaints . . . I cannot suggest any unifying diagnosis and would be interested in input
from a psychiatric specialist.” (Id.) He indicated that he cannot offer a unifying
diagnosis and recommended input from a psychiatric specialist. (Id.)
15
On October 16, 2014, petitioner had a follow up consultation with Dr. Jaradeh at
the Stanford neuroautonomic clinic. (Ex. 19, pp. 45-46.) Dr Jaradeh suspected that
petitioner “had a form of serum sickness following his immunization. This may have left
him with a transient polyradiculitis and subsequent autonomic dysfunction.” (Id. at 46.)
Dr. Jaradeh also noted, however, that “it is somewhat unusual to continue to have
arthralgias as well as rash.” (Id.) Dr. Jaradeh ordered additional bloodwork, including
adrenal function, and suggested a skin biopsy might be appropriate. (Id.)
Petitioner was seen by dermatologists Tina Bhutani and Timothy Berger on
November 24, 2014 based on a referral from Dr. Shields for a consultation regarding
neutrophilic urticarial dermatosis. (Ex. 23, pp. 1, 4.) The doctors noted that “although
the biopsy may be consistent with Still’s disease or neutrophilic urticaria, we do not feel
that the patient’s clinical presentation is classic for either of these syndromes,” because
petitioner’s ferritin and ESR were normal “which goes against the diagnosis of Still’s
disease.” (Id.) “In addition,” the doctors continued, “neurologic manifestations are
uncommon for both Still’s disease as well as neutrophilic urticaria with systemic
symptoms.” (Id.) The doctors noted that of the variety of conditions that could be
consistent with petitioner’s rashes, each one “may result in very significant stimulation of
the immune system and a persistent cytokine/neutrophil response (Sweet’s syndrome
represents such a syndrome).” (Id.) The doctors noted that petitioner had no
symptoms of inflammatory bowel disease, and that while Bechet’s is possible, he lacked
oral or genital ulcerations and ocular findings—which would be an atypical presentation.
(Ex. 23, p. 2.) Thus, the doctors concluded, the most likely diagnosis given petitioner’s
symptoms is a “recurrent inflammatory condition that may have been triggered by a
significant antigen exposure,” such as Sweet’s. (Id.) The attending note clarifies that
until such time as petitioner’s presentation would develop to be more characteristic of a
defined condition, “we often diagnose these patients as ‘Neutrophilic Dermatosis, NOS’
keeping our minds open as to possible etiopathogenesis.” (Id.)
Following his visit to Drs. Bhutani and Berger, petitioner ceased seeing
specialists and relied primarily on Dr. Kashino for treatment. (Exs. 31, 50.) During
subsequent visits to Dr. Kashino’s office, petitioner continued to report symptoms of
worsening generalized muscle fasciculations involving his whole body, vibratory
sensations in his hands and feet, tightness around his temples and throat, and
improving fatigue and joint pain which he believed were related to his August 3, 2012
vaccinations. (E.g., Ex. 31, p. 19.) On August 8, 2017, petitioner returned to Dr.
Kashino. (Ex. 50, pp. 6-9.) Dr. Kashino noted that he had not seen petitioner since
September 9, 2015, but that petitioner had returned to document that he had not
improved relative to his alleged vaccine reaction. (Id. at 6.)
b. As Reflected in Petitioner’s Affidavit and Testimony
On May 14, 2015, petitioner filed two affidavits in support of his claim. (Exs. 21,
22.) Petitioner explained that prior to his vaccination he was healthy and active,
exercising regularly, and often traveling, hiking, and camping. (Ex. 21, p. 1.) He
affirmed that shortly after he was vaccinated, he began to feel unusually tired with bouts
16
of dizziness, neck soreness, increasing fatigue, and “a strange head pressure running
from temple to temple” around the back of his head. (Id. at p. 2.) He detailed his initial
visit to urgent care where he was diagnosed with a sinus infection and prescribed
Flonase and a Z-Pack. Petitioner indicated that the medications did not help and that
his symptoms became progressively worse. (Id.) Petitioner stated that he attempted to
maintain an active lifestyle despite his symptoms, but that he began to experience joint
pain which required frequent breaks. (Id. at 3.) Petitioner further explained that his
symptoms significantly impaired his job performance, required him to rest during his
workday, and ultimately led him to take medical leave for eight months before finally
quitting. (Id.) At the time of writing his affidavit, petitioner had moved back with his
parents and was still not working. (Id.) Petitioner still experienced “rashes, joint pain,
some fatigue, fasciculations which seem to be increasing in frequency and severity, a
buzzing/vibration sensation across [his] chest, and head pressure around [his] right
temple, among other symptoms,” at the time of writing his affidavit. (Ex. 21, p. 4.) The
second affidavit that petitioner filed affirmed that he has not initiated any civil actions or
collected any awards or settlements in connection to his alleged injury. (Ex. 22, p. 1.).
During the hearing, petitioner testified that he first noticed fatigue, head pressure,
neck pain, and lightheadedness about 4-5 days following his vaccination. (Tr. 12-14.)
He did not recall having any sinus congestion at the time and indicated that neither
Flonase nor Claritin alleviated his symptoms. (Tr. 15-16.) He did not address the
azithromycin discussed above. He indicated pain at the vaccination site lasted for a few
weeks, but the joint pain became severe around Thanksgiving. (Tr. 27-29.) Petitioner
discussed his medical history in some detail and confirmed that Drs. Kaufmann,
Bahttacharya, Braskett, and Kim never offered any definitive diagnosis. (Tr. 19-20, 21.)
He suggested that Dr. Jaradeh attributed his condition to vaccination based on a
perceived temporal relationship. (Tr. 23.) Petitioner has never sought any follow up
treatment for POTS or for dysautonomia. (Tr. 47.) Petitioner explained that Drs.
Bhutani and Berger were the first to suspect Sweet’s syndrome in November of 2014
(Tr. 23-24); however, he also confirmed that he was never subsequently treated on the
basis of having Sweet’s syndrome (Tr. 47).
Petitioner also explained that, by the time of the hearing, he had returned to work
with a more flexible schedule. (Tr. 47-50.) His medical leave ultimately lasted between
six months to a year. (Id.) Petitioner stressed that “[i]t was really distressing to see so
many specialists and people who I thought would have been able to get to the bottom of
what was going on who really didn’t – really didn’t have any way to treat it.” (Tr. 31-32.)
He described it as the most stressful experience of his life. (Tr. 32.)
c. As Reflected by Dr. Jaradeh’s Letter
On March 23, 2016, Dr. Jaradeh drafted a letter to petitioner’s former counsel
supporting this claim. (Ex. 30.) Dr. Jaradeh reiterated petitioner’s prior clinical course
and observed that autonomic testing confirmed “some autonomic nerve impairment
involving particularly the sympathetic fibers,” but noted that clinical examination was
otherwise normal except for the fasciculations. (Ex. 30, pp. 1-2.)
17
Dr. Jaradeh indicated that his initial clinical impression was autonomic
neuropathy. (Id. at 2.) Based on the reported history, he further felt that the problem
was likely related to his vaccination and perhaps with further contribution from his
subsequent treatment. (Id.) He did not specify which treatment(s). Dr. Jaradeh
theorized as follows:
Occasionally, this combination [of vaccines] causes some type of an
immune reaction known as serum sickness where there are circulating
antibodies to the vaccine that somehow provide some type of inflammation
involving the skin, the joints, as well as the nervous system, in this case
autonomic as well as neuromuscular fibers. A less likely alternative would
be that he had a reaction to the infection that he had with the sinus, or the
antibiotic, but this is less plausible given the fact that he has received this
antibiotic in the past and never had a reaction to it.
(Id.) He concludes that “[i]t is my medical opinion that his neurologic situation has
closely followed, and is related to the vaccination.” (Id.)
IV. Expert Reports
a. Petitioner’s Expert
i. Carlo Tornatore, M.D.
Petitioner filed an expert report by neurologist Dr. Carlo Tornatore on January 24,
2018 to support his claim. (Ex. 32.) Dr. Tornatore also testified during the hearing and
was accepted without objection as an expert in neurology. 18 (Tr. 80.) Dr. Tornatore
opined that petitioner suffered from post-vaccinal Sweet’s syndrome and serum
sickness. (Ex. 32, p. 5.)
Dr. Tornatore described Sweet’s syndrome as a condition of the skin that is
distinct from classical auto-immunity because it involves “aberrant control of the innate
immune response, often through interleukin (IL)-1-mediated pathways,” as opposed to
“T-cell-mediated or major histocompatibility complex-related processes.” (Id.) He
18
Dr. Tornatore is a Professor and Chairman of the Department of Neurology at Georgetown University
Medical Center and has been board certified in Neurology since 1991. (Ex. 32, p. 1.) He is also the
Chairman and Neurologist-in-Chief of the Department of Neurology at Medstar Georgetown University
Hospital. (Id.) He is Executive Director of the Georgetown Multiple Sclerosis Patient Centered Specialty
Home as well. (Id.) He completed his residency in Neurology at Georgetown and a post-doctoral
fellowship at the National Institutes of Neurologic Disorders and Stroke at the National Institutes of Health
where he studied the interaction of viruses and immune system. (Id.) Following his fellowship, Dr.
Tornatore joined the faculty at Georgetown where he has been the Director of the Multiple Sclerosis
Center for 21 years. (Id.) Under Dr. Tornatore’s direction, the MS Center currently follows 210 patients
with acute disseminated encephalomyelitis (ADEM), 95 patients with neuromyelitis optica (NMO), 340
patients with transverse myelitis (TM), 45 patients with central nervous system vasculitis, 98 patents with
neurosarcoidosis, and 45 patients with various other inflammatory conditions of the brain and spinal cord
including Bechet’s and Susac’s diseases. (Id.)
18
explained that in auto-inflammatory diseases such as Sweet’s, “autoantibody titers are
absent or low and as opposed to lymphocytes, neutrophils and macrophages are most
often the effector cells.” (Ex. 32, p. 5) (citing Aditi S Murthy & Kieron Leslie,
Autoinflammatory Skin Disease: A Review of Concepts and Applications to General
Dermatology, 232 DERMATOLOGY 534 (2016) (EX. 33).) Dr. Tornatore further explained
that autoinflammatory and autoimmune conditions are not mutually exclusive because
mediators of auto-inflammatory diseases “likely play a role in a variety of conditions
thought of as ‘autoimmune’.” (Id.) Further, according to Dr. Tornatore, because
neutrophilic-mediated processes play a significant role in auto-inflammatory conditions
such as Sweet’s, “it follows that auto-inflammation may play an important role in
dermatoses where neutrophils are predominant.” (Id.)
Dr. Tornatore further illustrated the distinction between auto-inflammatory and
auto-immune responses by noting that it is “innate immunity” which “directly causes
tissue inflammation” in auto-inflammatory diseases while the role that innate immunity
plays in auto-immune diseases is less clear. (Id.) However, Dr. Tornatore noted, it is
possible that innate mechanisms activate the adaptive immune responses that are the
primary mediators of auto-immune diseases. (Id.) Ultimately, Dr. Tornatore suggested
that “[a]uto-inflammation to autoimmunity likely represents a spectrum of disease
processes . . . with many common skin conditions with overlapping features. Prime
examples of dermatoses closer to the auto-inflammatory end . . . are pyoderma
gangrenosum and Sweet’s syndrome both . . . characterized by sterile neutrophilic
infiltrates.” (Id.) (internal citations omitted).
Dr. Tornatore explained that “Classic Sweet’s syndrome [typically] occurs in
middle-aged women after a nonspecific infection of the respiratory or gastrointestinal
tract. Raised erythematous plaques with pseudo-blistering and occasionally pustules
occur on the face, neck, chest, and extremities, accompanied by fever and general
malaise.” (Ex. 32, p. 5) (citing Peter von den Driesch, Sweet’s Syndrome (acute febrile
neutrophilic dermatosis), 31 J. AM. ACAD. DERMATOLOGY 535 (1994) (Ex. 34).) Further,
Dr. Tornatore explained that “involvement of the eyes, joints, and oral mucosa as well
as internal manifestations . . . in the lung, liver, kidneys, and central nervous system
has been described.” (Id.) Dr. Tornatore explained that his review of the literature
found that onset of Sweet’s has been associated with a variety of different vaccinations
including BCG, pneumococcal, and influenza. 19 (Id. at p. 6)
19 Citing Boris Radeff & Monika Harms, Acute Febrile Neutrophilic Dermatosis (Sweet’s Syndrome)
Following BCG Vaccination, 66 ACTA DERMATO-VENEREOLOGICA 357 (1986) (Ex. 35); Paul R. Maddox &
Richard J. Motley, Sweet’s Syndrome: a severe complication of pneumococcal vaccination following
emergency splenectomy, 77 BRIT. J. OF SURGERY 809 (1990) (Ex. 36); Olivier Capentier et al., Sweet’s
Syndrome after BCG Vaccination, 82 ACTA DERMATO-VENEROLOGICA 221 (2002) (EX. 37); Marina
Jovanovic et al., Acute febrile neutrophilic dermatosis (Sweet’s syndrome) after influenza vaccination, 52
J. AM. ACAD. DERMATOLOGY 367 (2005) (Ex. 38); Ronni Wolf et al., Neutrophilic dermatosis of the hands
after influenza vaccination, 48 INT. J. DERMATOLOGY 66 (2009) (EX. 39); Ana Filipa Pedrosa et al., Sweet’s
syndrome triggered by pneumococcal vaccination, 32 CUTANEOUS AND OCULAR TOXICOLOGY 260 (2013)
(EX. 40).
19
Dr. Tornatore explained that in rare circumstances, a neurological form of
Sweet’s can occur. This is referred to as “Neuro-Sweet syndrome.” (Ex. 32, p. 6)
(citing Kinya Hisanaga et al., Neuro-Sweet disease: Clinical manifestations and criteria
for diagnosis, 64 NEUROLOGY 1756 (2005) (EX. 41); Francesco Drago et al., Neuro sweet
syndrome: a systematic review. A rare complication of Sweet syndrome, 117 ACTA
NEUROLOGICA BELGICA 33 (2017) (EX. 42).) Dr. Tornatore suggested that neuro-Sweet
syndrome can affect any part of the nervous system, but most commonly results in
meningitis and encephalitis. (Ex. 32, p. 6.) He noted that petitioner “developed cranial
and neck pain as well as fatigue shortly after receiving the Hepatitis A and Td
vaccinations, symptoms that a treating neurologist felt were consistent with aseptic
meningitis.” (Id.) Dr. Tornatore cited one study that described aseptic meningitis in a
neonate with Sweet’s syndrome, which he contended “supports the biological
plausibility and logical sequence of cause and effect for a vaccination to cause Neuro-
Sweet syndrome, with the neurologic manifestation being aseptic meningitis.” (Id.)
(citing Terris R. Dunn et al., Sweet Syndrome in a Neonate with Aseptic Meningitis, 9
PEDIATRIC DERMATOLOGY 288 (1992) (Ex. 43).) Further, Dr. Tornatore noted that
because petitioner’s symptoms began five days after his vaccination, there appears to
be a temporal relationship as well. (Ex. 32, p. 6.) He concluded his discussion of
Sweet’s syndrome by suggesting that symptoms of Sweet’s syndrome can persist over
several years as petitioner’s have. (Id.)
Dr. Tornatore also explained, however, that he is of the opinion that petitioner’s
polyarthralgia was a result of a vaccine-induced serum sickness. One study cited by Dr.
Tornatore found that 3% or 14 out of 495 Thai health care professionals who received a
flu vaccination developed a serum sickness-like reaction. (Id.) (citing Anucha
Apisarnthanarak et al., Serum Sickness-Like Reaction Associated with Inactivated
Influenza Vaccination among Thai Health Care Personnel: Risk Factors and Outcomes,
49 CLINICAL INFECTIOUS DISEASES 18 (2009) (Ex. 44).) He cited another study defining
serum sickness as “a type III hypersensitivity reaction that occurs after exposure to
foreign antigens . . . Immune complex deposition and activation of the complement
cascade can cause fever, polyarthritis or polyarthralgia, and rash and may result from
exposure to a heterologous protein . . . or to a drug that lacks protein, such as certain
antibiotics.” (Ex. 32 p. 6) (citing Claud Ponvert & Pierre Sheinmann, Vaccine allergy
and pseudo-allergy, 13 EUR. J. OF DERMATOL. 10 (2003) (Ex. 45).) Dr. Tornatore
explained that studies have found that medications and antitoxins made with animal
serum protein, such as diphtheria and tetanus, have been associated with serum
sickness. (Ex. 32, p. 6.) (citing Richard Platt et al., Serum Sickness-Like Reactions to
Amoxicillin, Cefaclor, Cephalexin, and Trimethoprim-Sulfamethoxazole, 158 J. OF
INFECTIOUS DISEASES 474 (1988) (EX. 46); Edgar H. Relyveld et al., Rational approaches
to reduce adverse reactions in man to vaccines containing tetanus and diphtheria
toxoids, 16 VACCINE 1016 (1998) (Ex. 47).) Finally, Dr. Tornatore cited two reports of
serum sickness-like reactions to flu vaccinations, but explained that limited data is
available regarding incidence, associated risk factors, and outcomes. (Ex. 32, p. 6)
(citing James A. Wilde et al., Effectiveness of Influenza Vaccine in Health Care
Professionals: a Randomized Trial, 281 J. AM. MED. ASSOC. 908 (1999) (Ex. 48); Simin
Vessal & Lillian P. Kravis, Immunologic Mechanisms Responsible for Adverse
20
Reactions to Routine Immunizations in Children, 15 CLINICAL PEDIATRICS 688 (1976) (Ex.
49).) Ultimately, Dr. Tornatore concluded that in spite of the limited available data,
these studies and case reports nonetheless support a finding of vaccine causation.
During the hearing, Dr. Tornatore testified largely in accordance with his prior
report. However, especially when challenged on cross-examination, Dr. Torantore’s
testimony also stressed an overarching view that vaccine-induced serum sickness and
Sweet’s syndrome remain a reasonable and likely explanation for petitioner’s condition
regardless of ambiguities or inconsistencies within the details of petitioner’s complex
medical history. He characterized himself as taking the “50,000-foot view” of petitioner’s
presentation and repeatedly urged against “getting into the weed” or “quibbling” over
specific findings. (Tr. 124, 151, 153, 162.) Dr. Tornatore stressed that both serum
sickness and Sweet’s syndrome present with a spectrum of clinical manifestations,
suggesting petitioner does not need to perfectly fit the known symptomology of either
condition. (Tr. 90, 92-93.) He also indicated that neither Sweet’s syndrome nor serum
sickness have any required biomarkers. (Tr. 99-100, 106.) Dr. Tornatore testified: “the
bottom line is everyone keeps saying this is a post-vaccination inflammatory event.
Whether they use the term ‘sweet’s syndrome or ‘serum sickness’ is irrelevant. They’re
all saying the same thing.” (Tr. 144.) Describing petitioner’s “weird symptoms,” he
contended that “you just draw a straight line across and it makes sense.” (Tr. 178.) He
did, however, acknowledge the importance of petitioner’s rash biopsy as a foundation
for the alleged diagnosis of Sweet’s syndrome, explaining that “there was a lot of clinical
judgment that went into it. But clearly it was driven by the skin biopsy.” (Tr. 101-02.)
Dr. Tornatore deferred to Dr. Jaradeh regarding the question of autonomic neuropathy,
but confirmed that his opinion would not change regardless of the presence of
autonomic involvement. (Tr. 161-63.)
b. Respondent’s Experts
i. Phillip Low, M.D.
Respondent relied in part on the opinion of neurologist Dr. Phillip Low to support
his position. (Ex. A.) Dr. Low submitted two reports and also testified during the
hearing. He was accepted at hearing without objection as an expert in neurology. 20 (Tr.
216-17.)
Dr. Low’s first report was in response to Dr. Jaradeh’s above-described letter and
was filed before Dr. Tornatore entered the case. Dr. Low described POTS as “a
condition characterized by a sustained increase in mean heart rate for greater than 30
20
Dr. Low is board certified in neurology and clinical neurophysiology (autonomic) and holds a position as
Professor of Neurology at the Mayo Clinic in Rochester, Minnesota. (Ex. A, p. 1.) He founded and has
headed the Mayo Autonomic Laboratory since 1983. (Id.) He has published over 400 pieces in medical
journals and 4 books on autonomic diseases. (Id.) He developed and validated autonomic function tests
that have become the standard testing for autonomic function disorders. (Id.) He has published
extensively on orthostatic intolerance, postural tachycardia syndrome (POTS), and the autoimmune
autonomic neuropathies. (Id.)
21
beats per minute above resting heart rate within 10 minutes of tilt, associated with
symptoms of orthostatic intolerance when the person stands up, and clears when the
person sits back down.” (Ex. A, p. 2.) He explained that because POTS is a condition
and not a disease with evidence of tissue injury, the diagnostic criterion is an orthostatic
heart rate of greater than 120 bpm. (Id.) According to Dr. Low, adult patients who show
an orthostatic heart rate increase of 30 or more, but less than 120 bpm, are designated
as either mild orthostatic intolerance or mild POTS. (Id.) Dr. Low indicated that
orthostatic intolerance “refers to symptoms of reduced cerebral perfusion and symptoms
of sympathetic activation when a person stands up.” (Id.) POTS is “a classic example
of orthostatic intolerance” where heart rate on standing is excessive due to sympathetic
overactivity. 21 (Id.) Dr. Low described autoimmune autonomic neuropathy as any
number of peripheral neuropathies where the patient’s immune mechanisms target
autonomic fibers or neurons. (Id.) According to Dr. Low, the mechanism of injury is
often an antibody directed against autonomic targets. (Ex. A, p. 3.) Dr. Low explained
that these types of neuropathies are “characterized by severe loss of function in BP
control, control of bladder, bowel, sexual function, or pupils.” (Id.)
Dr. Low noted that there are several components of Dr. Jaradeh’s opinion that
are “fully susceptible to proving or disproving.” (Ex. A, p. 4.) The standard test for the
polyradiculitis diagnosed by Dr. Jaradeh is EMG and nerve conduction study.
Petitioner’s EMG/nerve conduction results showed no abnormalities, suggesting the
diagnosis of polyradiculitis is incorrect. (Id.) Additionally, orthostatic hypotension which
refers to “a fall of at least 20mm within 3 minutes” during a tilt study. (Id.) Petitioner’s
tilt study showed bp of 128, 114, 110, 103, and 110 at supine, 1, 3, 5, and 10 minutes
respectively. (Id.) Dr. Low notes that these results are normal and do not demonstrate
orthostatic hypotension. (Id.) Further, petitioner’s heart rates during the tilt test were
71, 85, 85, 91, and 90 at supine, 1, 3, 5, and 10 minutes respectively which illustrates
heart rate changes “well below the 30 bpm that is a minimum requirement [for a
diagnosis of orthostatic tachycardia].” (Id.) In Dr. Low’s opinion, Dr. Jaradeh based this
diagnosis on a single value from a Finapres22 recording and suggested that “a single
value from the device is highly inaccurate and should be discarded.” (Id.)
Nor, according to Dr. Low, did Dr. Jaradeh’s study reveal any evidence that could
support a diagnosis of autonomic neuropathy. Based on the studies, all indices of
cardiovagal function and adrenergic function were “completely normal.” (Ex. A, p. 4.)
Dr. Low explained that “[t]he best indices of adrenergic function are BP recovery time
and BP overshoot both of which were completely normal.” (Id.) Instead, Dr. Low noted,
the study provides cogent evidence that petitioner had completely normal autonomic
21
Dysautonomia without orthostatic tachycardia is a condition manifesting symptoms similar to POTS, but
without satisfying the diagnostic heartrate criteria. (Ex. A, p. 3.) He explains that it is not known whether
this is a milder form of POTS or something different, but that the condition is known to be dominated by
deconditioning which “refers to a condition where an individual, for whatever reasons, becomes inactive
for a period of time. This lack of exercise in turn results in lightheadedness, fatigue, and an inability to
function.” (Id.) He notes that, as is often the case with POTS, autonomic perturbances are minimal but
psychological factors are often prominent. (Id.)
22 A device used to measure blood pressure continuously. (Ex. A, p. 4.)
22
function and that Dr. Jaradeh’s diagnosis is incorrect. (Id.) Dr. Low explained that
autoimmune autonomic neuropathy manifests through fixed, dilated pupils, decreased
stomach function, bowel and bladder incontinence, and/or orthostatic hypotension. (Id.)
Because petitioner showed none of these signs, Dr. Low concludes that Dr. Jaradeh’s
diagnosis is incorrect. (Id.)
Dr. Low further stressed that all of petitioner’s tests excluded structural disease
and therefore, do not support a finding of any injury in this case. (Ex. A, p. 4.) He noted
that petitioner’s most significant symptoms included head pressure, neck discomfort,
fatigues, and dizziness. (Id. at p. 5.) Dr. Low suggested that these symptoms are “quite
typical of deconditioning” and “by his own description, [] petitioner had changed his
lifestyle from being an active exercising young man to one who shunned physical
activity,” which is behavior that Dr. Low opined commonly leads to deconditioning and
the major symptoms of which petitioner complained. (Id.)
Dr. Low also submitted a supplemental report on June 15, 2018 in response to
Dr. Tornatore. (Ex. E.) Dr. Low explained that neuro-Sweet syndrome is an expansion
of Sweet syndrome and cannot be diagnosed if the petitioner did not suffer from
Sweet’s in the first place. (Id.) Dr. Low explained that the two pillars of diagnosis for
neuro-Sweet syndrome in petitioner’s case would be aseptic meningitis and neuropathy.
(Id.) He explains that peripheral neuropathy is always associated with findings on EMG
and nerve conduction studies. (Id.) Because petitioner’s EMG, brain MRI, and nerve
conduction tests were all normal, Dr. Low concluded that these tests all ruled out
neuropathy and radiculopathy. (Id.)
Dr. Low also explained that aseptic meningitis was considered briefly due to
petitioner’s head pressure and neck discomfort in the absence of fever, however, based
on petitioner’s medical records, “this diagnosis does not seem to have been seriously
considered since the condition was mild and since [the] patient was much improved.”
(Ex. E.) Dr. Low described aseptic meningitis diagnosis as requiring a cerebrospinal
fluid sample which is required to show an increase in white cell count, typically
lymphocytes. (Id.) Because petitioner never received a spinal fluid analysis, the record
lacks any evidence necessary to make a diagnosis of aseptic meningitis. (Id.) Dr. Low
concluded that because petitioner suffered from neither aseptic meningitis nor
peripheral neuropathy, the two pillars of diagnosis for neuro-sweet syndrome have not
been found, and therefore, Dr. Tornatore’s diagnosis is in error. (Id.)
During the hearing, Dr. Low stressed that, given the rarity of Sweet’s syndrome,
the diagnostic criteria is especially important. (Tr. 217.) He opined that petitioner’s
presentation “just doesn’t add up” to Sweet’s syndrome. (Id.) He noted that petitioner’s
rash was evanescent, a contrast to the fixed and painful rash with raised plaques seen
in Sweet’s syndrome. (Tr. 217-18.) He also noted that petitioner’s biopsy showed only
sparse infiltrate whereas dense infiltrate is required for diagnosis. (Tr. 218-19.)
According to Dr. Low, sparse infiltrate is non-specific and comparable to a negative
finding. (Tr. 236.) Dr. Low also stressed the complete absence over time of any
inflammatory markers in petitioner’s blood work as well as suggesting the temporal
23
pattern of petitioner’s symptoms is “all wrong” for neuro-Sweet’s syndrome. (Tr. 221,
224.) He also described the continued evolution of petitioner’s symptoms as
“perplexing.” (Tr. 226.)
ii. Michael Girardi, M.D.
On June 11, 2018, respondent filed an expert report from dermatologist Dr.
Michael Girardi. 23 (Ex. C.) Dr. Girardi did not testify. Dr. Girardi noted that petitioner
made no mention of any rash or skin lesions when he initially complained of an adverse
vaccine reaction on August 30, 2012. (Id. at 3.) Instead, on September 4, 2012,
petitioner noted that he was feeling better following a course of Azithromycin which “is
consistent with the diagnosis made of upper respiratory infection and sinusitis.” (Ex. C,
p. 4.) Additionally, on September 17, 2012, Dr. Bhattacharya noted some small pruritic
reddish lesions, which Dr. Girardi explained are “not consistent with Sweet syndrome,”
but most consistent with hives. (Id.) Dr. Girardi further explained that petitioner’s
transient morning rashes are also inconsistent with Sweet’s, and again most consistent
with hives. (Id.) He noted that petitioner’s December 7, 2012 labs show no
inflammatory markers, let alone any biomarkers that would support a diagnosis of
Sweet’s or serum sickness. (Id.) In particular, he stressed that petitioner showed
normal ESR and CRP levels each time he was tested, and because Sweet’s and serum
sickness both involve inflammatory responses, petitioner’s lack of inflammatory markers
is inconsistent with both conditions. (Id. at 5.) Dr. Girardi believes that Dr. Braskett
incorrectly diagnosed “resolved serum sickness” based on the fact that the lesions
petitioner described as occurring between his fingers are inconsistent with serum
sickness and “most readily seen in common hand dermatitis/eczema”. (Id. at 4.) Dr.
Girardi indicated that petitioner’s “high” tetanus toxoid antibodies is not a significant
finding because “the antibody levels seen on the blood test are what would be expected
after vaccination or booster vaccination.” (Id. at 5.)
Dr. Girardi questioned several conclusions drawn by petitioner’s treating
physicians, opining that the history of petitioner’s rashes is “not at all consistent with
Sweet’s syndrome which typically shows fixed plaques, not a rash that comes and goes
. . . .” (Ex. C, p. 6.) Further, he explained that petitioner reported no annular,
serpiginous, urticarial, multiforme, petechial, or purpuric lesions that may be seen in a
serum sickness or serum sickness-like syndrome which leads him to conclude that
petitioner’s skin lesions “are neither typical of nor consistent with Sweet’s or serum-
sickness.” (Id.)
Dr. Girardi believes that petitioner’s original symptoms were due to sinusitis and
hives. (Id.) This is based on the fact that petitioner’s rashes were transient instead of
permanent, that petitioner had a history of developing hives after certain medications,
23
Dr. Girardi is Professor and Vice Chair of Dermatology for the Yale School of Medicine. (Ex. C, p. 1.)
He has also served as Residency Director for Dermatology at Yale for over 15 years. (Id.) Dr. Girardi
runs a research laboratory focused on inflammatory immune reactions and their interaction with the skin.
(Id.) He is an elected member of the American Society of Clinical Investigation and has published over
150 pieces of medical literature on skin biology. (Id. at 2.)
24
and importantly, that petitioner described rashes on his hands prior to his vaccinations.
(Id.) Dr. Girardi explained that petitioner’s head pressure, sinus congestion, and
pharyngeal erythema are all “very consistent with an upper respiratory infection and
sinusitis.” (Ex. C, p. 6.) Dr. Girardi further supported this conclusion by noting that
petitioner responded well to antibiotics with “substantial alleviation of his sinusitis
symptoms.” (Id. at 7.) He explained that hives is a migratory rash where specific
lesions only last for a matter of hours and that forming hives in response to antibiotics is
not a rare phenomenon. (Id.) Based on the foregoing, Dr. Girardi concluded that
petitioner likely developed hives in response to either the antibiotics he was prescribed,
or his sinusitis. (Id.)
Dr. Girardi also contended that “there is no evidence that [petitioner] has, or ever
had, Sweet syndrome.” (Id.) He cited the von den Driesch report used by petitioner’s
expert to explain the diagnostic criteria for Sweet’s syndrome as presenting on the skin
“multiple, painful, sharply demarcated, raised erythematous plaques on the face, neck,
upper chest, back, and extremities that may show a mamillated appearance with
pseudovesiculation, pseudopustulation and pustules [that are] red to blue-red in color.”
(Ex. C, p. 7 (citing von den Driesch, supra, at Ex. 34).) Dr. Girardi contrasted this
description to the rashes that petitioner experienced which were described as
“intermittent . . . flat, red, speckled . . . faint in quality . . . [and appearing] only in the
morning [lasting] less than an hour.” (Id.) Dr. Girardi explained that petitioner’s medical
records never mention pseudovesiculated or vesiculated, painful, raised red to blue-red
plaques that are characteristic of Sweet’s. (Id.) Nor did petitioner experience any
associated symptoms such as enlarged lymph nodes, erythema nodosum lesions, or
conjunctivitis. (Id.) Based on the diagnostic criterion, as well as petitioner’s lack of
inflammatory markers, Dr. Girardi concluded that petitioner has “never come close to
satisfying the criteria for a diagnosis of Sweet syndrome.” (Id.) Instead, Dr. Girardi
opined that petitioner’s rash is likely the result of chronic urticaria. 24 (Ex. C, p. 9.)
Dr. Girardi also opined that petitioner’s diagnosis of neutrophilic dermatosis is
highly speculative because it is based on a generalized biopsy finding of “sparse
perivascular infiltrate with neutrophils.” (Ex. C, p. 8.) According to Dr. Girardi, this
finding is inconsistent with Sweet’s syndrome, because Sweet’s is accompanied by “an
infiltrate consisting of mononuclear cells and numerous neutrophils with leukocytoclasis,
a marked vasodilation and swelling of the vascular endothelium with moderate
erythrocyte extravasation, and prominent edema of the upper corium frequently leading
to the formation of vesicles or bullae and inflammatory cells that exhibit a bandlike
infiltration throughout the papillary dermis.” (Id.) Because petitioner’s biopsy only
showed “sparse perivascular infiltrate with neutrophils” and none of the more specific
findings listed in the diagnostic criteria for Sweet’s syndrome, Dr. Girardi opined that
24 Dr. Girardi cited a study which specifically notes that Sweet’s syndrome resolves once the inciting
agent is removed from the host. (Ex. C, p. 9 (citing Caroline A. Nelson et al., Neutrophilic dermatoses,
Part I. Pathogenesis, Sweet syndrome, neutrophilic eccrine hidradenitis, and Bechet’s disease, 79 J. AM.
ACAD. OF DERMATOLOGY 987 (2018) (Ex. C. Tab 1).) This study found that reports of Sweet’s syndrome in
association with certain vaccines are rare, and none of the vaccines linked to Sweet’s were of the type
that petitioner received. (Id.)
25
there is no evidence to find that petitioner was in fact suffering from Sweet’s syndrome.
(Id.)
Dr. Girardi’s final discussion focused on petitioner’s diagnosis of serum sickness
induced neuropathy or myopathy. He noted that petitioner has a documented history of
muscle fasciculations and autonomic dysfunction such as his orthostatic hypotension.
(Id.) He indicated, however, that “there is no plausible medical or laboratory evidence
that these [symptoms] are due to inflammation, such as those [that] might be caused by
a serum sickness or neutrophilic syndrome trigged by an adverse vaccination reaction.”
(Id.) He explained that if petitioner did suffer from a systemic serum sickness or serum
sickness-induced myopathy or neuropathy, he would have likely shown increased
muscle enzyme levels, abnormal nerve conduction, brain abnormalities, and/or elevated
inflammatory markers. (Ex. C, p. 8.) Here, however, petitioner showed none of these
things, his muscle enzyme levels were normal, his nerve conductions studies were
normal, his brain MRIs were normal, and his labs revealed no inflammatory markers.
(Id.) Further, because petitioner’s muscle fasciculations were not associated with any
pain or numbness, Dr. Girardi believes that petitioner’s fasciculations were likely the
result of “benign fasciculation syndrome.” (Id.)
Dr. Girardi explained that he is unaware of any credible reports linking Tetanus or
Hepatitis A vaccines to neuro-Sweet’s syndrome, serum sickness, or serum sickness-
like reactions. 25 (Ex. C, p. 9.) He explained that serum sickness and serum sickness-
like reactions “require persistent and high levels of antigen that co-precipitate as
immune complexes with persistent and high levels of antibodies.” (Id.) Thus, high
levels of antibodies alone are not evidence of serum sickness because such a diagnosis
would require an additional finding of persistent and high levels of antigen, which is not
evidenced in petitioner’s medical records. (Id.) Dr. Girardi ultimately concluded that
“there is absolutely no medical history, clinical, dermatologic, histologic, or laboratory
evidence in [petitioner’s medical records] to support the diagnosis of Sweet syndrome,
neuro-Sweet syndrome, serum sickness, or serum sickness-like eruption.” (Id.)
iii. You-Wen He, M.D., Ph.D.
Respondent filed his final expert report by immunologist Dr. You-Wen He on
October 7, 2019. 26 (Ex. F.) Dr. He also testified during the hearing at which he was
accepted without objection as an expert in immunology. (Tr. 185.)
25 In his report Dr. Girardi noted: “I am not aware of any credible reports of the vaccines in question
(DTAP, HepA) leading to any type neuro-Sweet syndrome or serum sickness or serum sickness-like
reactions.” (Ex. C, p. 9.) Dr. Girardi’s reference to the “vaccines in question” suggests his reference to
“DTAP” vaccines was likely a typographical error.
26
Dr. He has been a Professor of Immunology in the Department of Immunology at Duke University
Medical Center since 1986. (Ex. F, p. 1.) His research areas include innate and adaptive viral and
bacterial immunity. (Id.) He has directed research on human immune responses to viral infections
including influenza, HIV, HBV, and HCV. (Id.) He has been the Director of Immunology of Human
Diseases at Duke university for the past five years and is the current co-Principal Investigator for four
clinical trials focusing on cancer immunotherapy. (Id.) He has served as a reviewer for over 20 different
scientific journals and has published extensively immunology. (Ex. G, pp. 9-17.)
26
Dr. He primarily discussed whether petitioner’s condition can be explained by
serum sickness. (Ex. F, p. 3.) He defines serum sickness as a “type III immune
complex-mediated hypersensitivity disease” caused by immunization of heterologous
serum proteins and subsequent illness through the formation of immune complexes.
(Id.) Dr. He explained that once a patient is immunized with a protein antigen, “antibody
IgM and IgG develop beginning 1 week later” and that “persistence of high amount of
antigen in the host” leads to antigen-antibody complex formation. (Id.) These immune
complexes in turn “may deposit in tissues and activate complement system[s].” (Id.)
Further, “complement activation causes the release of complement fragments C3a and
C5a, which causes mast cell degranulation, histamine release, vasodilation, enhanced
vascular permeability, the development of urticarial lesions, and neutrophil recruitment.”
(Id.) Dr. He noted that “studies also suggest complement-independent mechanisms are
involved in serum sickness.” (Ex. F, p. 3.) Serum sickness-like reactions (SSLRs) on
the other hand, “are clinical reactions to a variety of drugs that resemble serum
sickness” and can occur following either infection or vaccination. (Id.)
According to Dr. He, “the most common symptoms of serum sickness are
dermatitis (rash), fever, polyarthralgia, or polyarthritis that usually begin 1-2 weeks after
exposure to the agent.” (Id. at 3-4.) Dr. He noted that almost all serum sickness
patients develop a fever and a pruritic rash lasting between a few days to two weeks.
(Id. at 4.) Further, Dr. He explained, around two-thirds of serum sickness patients
develop arthralgias with pain in their knees, wrists, ankles, shoulders, and jaw. (Id.)
When diagnosing serum sickness, Dr. He explained that lab results usually reveal
systemic changes including neutropenia, development of reactive plasmacytoid
lymphocytes, and elevated levels of ESR and CRP. (Id.) Dr. He also notes that serum
sickness usually resolves within 2 weeks of clearance or removal of the causative agent
but that in “unusual cases, symptoms may persist for 2-3 months if the causative agent
has been administered as a depot or sustained release form.” (Ex. F, p. 4.)
According to Dr. He, Dr. Tornatore’s reliance on the Apisarnthanarak study
finding a 3% incidence rate of serum sickness following a flu vaccination in Thai health
professionals is “quite unusual as there are no other reports that support this level of
incidence from any other countries including the United States.” (Id.) “In fact,” Dr. He
continued, “serum sickness or SSLRs were rarely reported after any vaccination. As
the authors indicated, the one-time observed 3% incidence in Thailand could be due to
the fact that the specific batch of vaccine was manufactured locally.” (Id.) Dr. He
explained that “since 1991, [over 800 million] doses of trivalent inactivated virus vaccine
have been distributed in the United States. As of December 2008, only 45
unconfounded reports . . . of possible serum sickness after receipt of a trivalent
inactivated virus vaccine were submitted to the VAERS.” (Id.) Dr. He further explained
that these 45 case reports fail to establish any link between the flu vaccine and serum
sickness and therefore, even adding these cases to Dr. Tornatore’s limited evidence,
there is still no way to reasonably link petitioner’s vaccinations to serum sickness. (Id.)
27
Dr. He does not believe that petitioner suffered from serum sickness or a SSLR
for four reasons. First, petitioner did not have any fever, and “[v]irtually all serum
sickness patients develop fever that is above 101.3 degrees Fahrenheit as the immune
complex-induced reaction triggers an inflammatory response.” (Ex. F, p. 5.) Second,
petitioner did not develop rash or any skin lesions by his August 30, 2012 exam, which
would take his condition outside the typical timeframe by which such symptoms would
arise following vaccination. Instead, petitioner’s rash developed after taking other
medications. (Id.) Additionally, petitioner’s lab testing consistently showed normal
levels of inflammatory biomarkers. (Id.) Finally, petitioner’s persistent symptoms are
inconsistent with the self-limiting nature of serum sickness and SSLRs. (Id.) In other
words, because serum sickness symptoms resolve once the antigens are cleared from
the host body, petitioner should have not continued to experience symptoms if he was
in fact suffering from serum sickness. (Id.) Importantly, Dr. He explained, a PUBMED
search found no reported cases of serum sickness associated with the Hepatitis A or Td
vaccines. (Id.)
Dr. He also questioned whether petitioner experienced Sweet’s syndrome due to
auto-inflammation as Dr. Tornatore proposes. According to Dr. He, it is unlikely that
petitioner experienced any autoinflammation or autoinflammatory disease regardless of
his diagnosis because such diseases are “characterized by recurrent inflammatory
episodes with heterogenous symptoms that are frequently associated with fever.” (Ex.
F, p. 5.) A second prominent feature of these diseases is an increase in acute-phase
reactants such as CRP. (Id.) Because petitioner “had neither fever nor elevated acute-
phase reactant CRP,” Dr. He concludes that petitioner did not experience any
autoinflammation, and therefore, did not experience an autoinflammatory disease such
as Sweet’s. (Id.) Based on the above, Dr. He concludes that petitioner likely did not
experience serum sickness, nor sweet’s syndrome.
During the hearing, Dr. He testified in accordance with his report and also provided
additional testimony regarding petitioner’s skin biopsy. In contrast to a finding of
“dense” neutrophil infiltrate (which would be “very significant”), “sparse” neutrophil
infiltrate should be interpreted as equivocal and nonspecific. (Tr. 203, 205-06.) He
explained that when taking a tissue sample “it’s actually almost impossible to have zero
hematopoietic cells, immune cell infiltration” and opined that petitioner’s skin biopsy is
not diagnostic of Sweet’s syndrome. (Tr. 191, 203.)
V. Discussion
As the above discussed history shows, petitioner had a prolonged course of
evolving symptoms and underwent a years-long search for a unifying diagnosis to little
avail. His physicians were clearly willing to entertain the possibility that petitioner
suffered some kind of vaccine reaction. However, many diagnoses were proposed,
debated, and ultimately either set aside or never confirmed or pursued. None of the
possible unifying diagnoses proposed by petitioner’s treating physicians enjoyed broad
support among his treatment teams.
28
In the face of that history, petitioner’s expert in this case, Dr. Tornatore, suggests
that two proposed diagnoses from among those considered by the treating physicians
can be substantiated – a neurologic form of Sweet’s syndrome and a serum sickness-
like reaction. He further opines that both of these conditions were caused by the
vaccinations at issue in this case. Additionally, during the hearing, Dr. Tornatore
suggested that there is sufficient suspicion of an inflammatory condition among
petitioner’s treating physicians to support vaccine-causation regardless of diagnosis.
Respondent and his three experts dispute all of these contentions. Additionally,
respondent contends petitioner’s failure to substantiate his correct diagnosis means a
causation-in-fact analysis under the Althen test is not possible. (ECF No. 103, pp. 21-
22.) In order to resolve these differences, two different analyses are required.
Petitioner bears the burden of proving his injury was caused-in-fact pursuant to
the Althen test. However, where diagnosis is in dispute, the Federal Circuit has found it
appropriate for special masters to determine which diagnosis is best supported by the
evidence in the record before applying the Althen test “so that the special master could
subsequently determine causation relative to the injury.” Broekelschen v. Sec'y of
Health & Human Servs., 618 F.3d 1339, 1346 (Fed. Cir. 2010). The Court explained
that because each prong of the Althen test is decided relative to the injury, identifying
the injury is a prerequisite to the analysis. Id. And, in any event, a petitioner must
prove by a preponderance of the evidence the factual circumstances surrounding his
claim. § 300aa–13(a)(1)(A). Importantly, however, “[t]he function of a special master is
not to ‘diagnose’ vaccine-related injuries, but instead to determine ‘based on the record
as a whole and the totality of the case, whether it has been shown by a preponderance
of the evidence that a vaccine caused the [petitioner]’s injury.’” Andreu v. Sec’y of
Health & Human Servs., 569 F.3d 1367, 1382 (Fed. Cir. 2009) (quoting Knudsen v.
Sec’y of Health & Human Servs., 35 F.3d 543, 549 (Fed. Cir. 1994)).
Balancing these considerations, a threshold analysis is required to determine
whether there is preponderant evidence that petitioner suffered either of the two specific
conditions Dr. Tornatore proposes as explanations for petitioner’s clinical history
(Sweet’s syndrome and/or serum sickness). However, even finding that there is not, a
remaining question raised by Dr. Tornatore’s testimony is whether, in the absence of
any reliance on those specific diagnoses, there is nonetheless sufficient basis for the
suspicion of an unspecified inflammatory reaction to preponderantly establish
causation-in-fact pursuant to the Althen test. The analysis below concludes that there is
not.
a. Diagnosis
i. Sweet’s Syndrome or Neuro-Sweet’s Syndrome
Sweet’s syndrome, also known as acute febrile neutrophilic dermatosis, is an
autoimmune/autoinflammatory condition of the skin, usually occurring after a
nonspecific infection of the respiratory or gastrointestinal tract that results in “[r]aised
erythematous plaques with pseudo-blistering and occasionally pustules . . . on the face,
29
neck, chest, and extremities accompanied, by fever and general malaise.” (Ex. 32, p.
5.) It is one of a number of dermatologic conditions known has neutrophilic dermatoses.
Sweet’s syndrome may also involve more vascular bodily systems and involve the eyes,
joints, and oral mucosa, as well as the lungs, liver, kidneys, and rarely in the case of
neuro-Sweet’s syndrome, the central nervous system, most often causing aseptic
meningitis or encephalitis. (Id. at 5-6; see also Tr. at 92-94.)
In this case, of all the many specialists petitioner visited throughout the course of
his years-long search for a diagnosis, including multiple dermatologists, only the team of
Drs. Bhutani and Berger even suggested the possibility of Sweet’s syndrome. This
occurred more than two years after the vaccinations at issue. (Ex. 23, pp. 1-2.) The
suspicion of Sweet’s syndrome expressed by Drs. Bhutani and Berger was based in
significant part on the skin biopsy results interpreted by Dr. Pincus. However, although
Dr. Pincus included neutrophilic dermatosis in a differential diagnosis, she also
indicated that the neutrophil infiltration seen on biopsy was only “sparse” and further
indicated that the eruption biopsied could also be explained by conventional urticaria.
(Ex. 23, p. 16.) Ultimately, despite suggesting Sweet’s syndrome as a possible
diagnosis, Drs. Bhutani and Berger indicated that petitioner’s condition was actually
best characterized as Neutrophilic Dermatosis, NOS (not otherwise specified) and
indicated the need to wait to see if petitioner’s condition develops to be “more
characteristic” of a defined condition from among a wide differential diagnosis while
“keeping our minds open as to possible etiopathogenesis.” (Ex. 23, p. 2.) Petitioner
never had any follow up or treatment based on the suspicion of Sweet’s syndrome,
neuro-Sweet’s syndrome, or neutrophilic dermatosis more generally. (Ex. 23, p. 2; Tr.
47.) Thus, although Sweet’s syndrome garnered some mention by some of petitioner’s
treating physicians, petitioner’s medical records considered as a whole do not, without
more, preponderantly establish that petitioner was diagnosed as suffering Sweet’s
syndrome by any of his treating physicians. Those who considered it did not move
beyond suspicion.
Nonetheless, petitioner suggests there is adequate evidence of record to support
Dr. Tornatore’s additional expert opinion that such a diagnosis can explain petitioner’s
presentation. The most obvious issue with Dr. Tornatore’s opinion is that petitioner’s
own rash is not consistent with the known dermatologic presentation of Sweet’s
syndrome and his biopsy is inadequate to diagnosis neutrophilic dermatosis more
generally. This issue alone is dispositive. Additionally, however, respondent’s experts
also raise several other reasons for doubting that petitioner’s overall presentation is
consistent with either Sweet’s syndrome specifically or with the category of neutrophilic
dermatoses more generally. Finally, petitioner’s initial presentation of headache is not
sufficient to establish the presence of the aseptic meningitis supporting the neuro-
Sweet’s syndrome variant, a point that further contributed to Dr. Tornatore’s overall
diagnostic assessment.
1. Petitioner’s rashes
30
As a dermatosis, Sweet’s syndrome is first and foremost an immune response
that manifests as a dermatologic condition. (E.g., von den Drisech, supra, at Ex. 34, p.
535.) Respondent’s experts are persuasive in explaining that the presence of
characteristic painful skin plaques with dense neutrophil infiltration is critical to
diagnosis. (Tr. 201-02, 217-18, 221-22, 232-33; Ex. C, p. 7; see also Nelson et al.,
supra, at Ex. C, Tab 1, p. 14).) Petitioner’s reliance materials likewise confirm that this
presentation is generally accepted as the major diagnostic criteria for Sweet’s
syndrome. (von den Driesch, supra, at Ex. 34, pp. 535, 544 (Table V).) Without the
characteristic dermatologic presentation, there is no basis to suspect Sweet’s syndrome
as any explanation for petitioner’s broader multi-system presentation.
Throughout the medical records, petitioner’s rashes are variously described as
follows: transient and periodic (Ex. 2, p. 251; Ex. 13, p. 7; Ex. 14, p. 17), patchy and
erythematous (i.e. red) (Ex. 2, p. 225; Ex. 13, p. 7), speckled or splotchy (Ex. 2, p. 234;
Ex. 14, p. 17), pruritic (i.e. itchy) (Ex. 7, p. 10; Ex. 23, p. 13), and maculopapular (Ex.
14, p. 18). With the exception of the one rash that was biopsied, petitioner testified that
his rashes were fleeting, by which he meant they lasted for only minutes to hours. (Tr.
24-26.) There is no indication from either the medical records or petitioner’s testimony
that his rashes were painful. All of this is in contrast to the expected presentation for
Sweet’s syndrome. Whereas the rashes seen in Sweet’s syndrome are fixed, clearly
demarcated, painful, and with skin plaques, petitioner’s rashes had none of these
features in terms of either appearance or pattern of manifestation. Additionally,
petitioner’s rashes were also described as pruritic, which is an added characteristic not
consistent with Sweet’s syndrome. (See, e.g. von den Driesch, supra, at Ex. 34, pp.
537-38 (explaining that multiple sharply demarcated raised erythematous plaques that
are burning and painful, but not pruritic, are considered a “hallmark” of Sweet’s
syndrome).) Moreover, petitioner has provided photographs of his rashes. Comparison
between these photographs and the photographs of Sweet syndrome rashes contained
in the medical literature filed in this case shows, even at a glance, that petitioner’s
rashes are in stark contrast to the rashes depicted among Sweet’s syndrome patients.
Dr. Tornatore agreed. (Tr. 120-22; Compare Ex. 51, and e.g., von den Driesch, supra,
at Ex. 34, p. 538 (fig. 3), Carpentier et al., supra, at Ex. 37, p. 221 (Fig. 1), Jovanovic et
al., supra, at Ex. 38, p. 368 (Fig. 1), Wolf et al., supra, at Ex. 39, p. 1 (Fig. 1), Pendrosa
et al., supra, at Ex. 40, p. 261 (Fig. 1), Hisanaga et al., supra, at Ex. 41, p. 1757 (Fig.
1).)
Nonetheless, Dr. Tornatore stresses that petitioner’s biopsied rash did
demonstrate neutrophil infiltration. (Tr. 83-84, 101-02, 120-26.) Here too, however,
petitioner’s own rash is inconsistent with the diagnostic standard for the condition at
issue. Petitioner’s own biopsy showed only “sparse” neutrophil infiltrate. (Ex. 23, p. 5.)
In contrast, “dense” neutrophil infiltrate on histopathology was a part of the initial
presentation documented by Dr. Douglas Sweet when he coined the term “acute febrile
neutrophilic dermatosis” to describe this condition. (See Nelson et al., supra, at Ex. C,
Tab 1, p. 13.) Dense infiltrate has also been specified as part of the subsequently
developed diagnostic criteria. (See Drago et al., supra, at Ex. 42, p. 34 (Table 1); accord
Maddox & Motley, supra, at Ex. 36, p. 810 (case report indicating that difficult diagnosis
31
of Sweet’s syndrome “hinged” on histopathology showing, inter alia, “intense
neutrophilic infiltrate”); Wolf, supra, at Ex. 39, p. 1 (case report noting dense infiltrate on
histopathology as one of two major criteria offering “clues to the diagnosis”).) When
neutrophil infiltrate is less dense, the differential diagnosis should be widened. (von den
Driesch, supra, at Ex. 34, pp. 539-44.) In fact, Dr. Tornatore concedes that sparse
neutrophil infiltrate is not necessarily diagnostic of Sweet’s syndrome in particular, even
while maintaining that it should be viewed as evidence of inflammation more broadly. 27
(Tr. 121.)
With regard to that broader assertion, however, respondent’s experts also
persuasively contend that the interpretation of the biopsy as including only “sparse”
neutrophil infiltrate should in itself be interpreted with caution as non-specific, if not
rejected as a negative or equivocal finding. (Tr. 191, 203, 205-06, 218-19, 236; Ex. C,
p. 8.) Specifically, Dr. Low testified that the difference between “sparse” and “dense”
neutrophil infiltration is “night and day.” (Tr. 218-19.) He indicated that a finding of
sparse neutrophil infiltrate is a “minor non-specific” abnormality. (Id.) Consistent with
Dr. Pincus’s dermatopathology report, Dr. Low indicated that anyone who scratches a
urticarial rash could have sparse neutrophil infiltrate. 28 (Id.) On further questioning, Dr.
Low even went as far as to suggest the sparse infiltrate could be interpreted as a
negative finding. (Tr. 236.) Dr. He likewise testified that sparse infiltrate is a non-
specific finding. (Tr. 191.) He indicated that whereas “dense” infiltration would be “very
significant,” a finding of “sparse” infiltration is equivocal and may indicate no abnormality
at all. (Tr. 205-06.) He explained that tissue section contamination is always a
possibility and “it’s actually almost impossible to have zero hematopoietic cells, immune
cell infiltration.” (Tr. 203, 205-06.) Respondent’s expert in dermatology, Dr. Girardi,
also indicated in his report that the finding of sparse infiltrate is non-specific. (Ex. C, p.
8.) Further, Dr. Girardi specifically opines that petitioner’s biopsy result is inadequate to
diagnose even a broader neutrophilic dermatosis, calling such a suggestion
“speculative” and instead opining that petitioner suffered hives. (Ex. C, pp. 6-8.) And
again, even if Dr. Pincus was open to the possibility of neutrophilic dermatosis based on
reported clinical history, Dr. Girardi’s opinion that the result should be interpreted as
27Specifically, Dr. Tornatore testified: “But I think the important thing is that here we have a rash, and we
can call it whatever we want. We can call it hives. We can call it atypical Sweet’s. We can call it not
Sweet’s. He – it’s persistent. He did not have it prior to the vaccination. He had a serum sickness-like
reaction, ergo, we can say, well is it related or is it not? Well, of course, that’s that constellation that, you
know, the going from one thing to another. So we may not call it, you know, a classic Sweet’s syndrome,
but it did have neutrophils in it and so it fits in that category of Sweet’s-like syndromes or, you know,
those innate inflammatory dermatologic issues.” (Tr. 121.)
28In her report, Dr. Pincus limited the top-line diagnostic finding to “sparse” perivascular infiltrate with
neutrophils without indicating a diagnosis of neutrophilic dermatosis. Although she discussed the
possibility of an unspecified neutrophilic dermatosis in her further analysis, she also specified both
conventional and neutrophilic urticaria on equal footing as possible considerations. (Ex. 23, p. 16.) Dr.
Pincus’s inclusion of both conventional and neutrophilic urticaria in her report indicates that based on her
own review of the pathology she could not necessarily distinguish petitioner’s biopsy from conventional
hives. This is consistent with respondent’s experts’ shared opinion that the finding is nonspecific and
consistent with ordinary or “conventional” hives. (Ex. 23, p. 16; Tr. 218-19; Ex. C, pp. 7-8.) On the whole,
Dr. Pincus’s report is equivocal with regard to the clinical significance of the underlying pathology.
32
non-specific even as to the broader category of neutrophilic dermatoses is consistent
with the dermatopathology report findings when the report is read as a whole. (Ex. 23,
p. 16; see n. 28, supra.)
Although Dr. Tornatore sought to disregard the distinction between sparse and
dense neutrophil infiltration (Tr. 83-84, 113-15), he is less well qualified to make that
determination. 29 Moreover, Dr. Tornatore presented a far less nuanced view of
petitioner’s skin rashes. His testimony regarding the biopsy result was never more
specific than to assert that the presence of any degree of neutrophil infiltrate indicates
inflammation “period” while also agreeing petitioner’s own rashes were potentially
consistent with hives. 30 (Tr. 83, 114-15, 122-24.) He sought to at least some degree to
defer to the interpretation of the dermatologists. (Tr. 150-51.) However, both
respondent’s dermatology expert and Dr. Pincus indicate that conventional hives are a
possible explanation of petitioner’s biopsy result, inclusive of the finding of some
possible evidence of minimal inflammation.
Based on all of the above, there is not preponderant evidence that petitioner’s
dermatologic presentation fits either the diagnosis of Sweet’s syndrome specifically or
even neutrophilic dermatosis more generally. This finding alone is dispositive as to the
question of whether petitioner had Sweet’s syndrome. Nonetheless, it is not the only
reason for doubting the proposed diagnosis.
2. Overall clinical history
Even setting aside the rashes and skin biopsy, the Sweet’s syndrome diagnosis
still remains an unsatisfying explanation for petitioner’s overall clinical history.
Petitioner’s clinical history stands in significant contrast to Sweet’s syndrome in
29 Dr. Girardi’s qualification as a dermatologist likely leaves him best positioned to interpret skin biopsy
results in terms of overall clinical significance. Additionally, Dr. He’s qualification as an immunologist
qualifies him to speak to the significance of neutrophil counts specifically. Dr. Low and Dr. Tornatore are
both neurologists and therefore comparatively less qualified to speak to the specifics of this biopsy result.
Dr. Low does additionally purport, however, to have added familiarity with skin biopsies due to his specific
work in the area of autonomic dysfunction. Skin biopsies are an important diagnostic tool for
dysautonomia. Nonetheless, it is not clear that this experience would necessarily carry over to
interpreting neutrophil infiltration specifically. Thus, Drs. Girardi’s and He’s opinions are the most
valuable on this point with Drs. Low and Tornatore being closer to being on equal footing with one
another.
30 An important further point confirmed during the hearing is that the medical records and Dr. Pincus’s
dermatopathology report are such that only Dr. Pincus had access to the pathology imaging underlying
her conclusion. (Tr. 123-26.) The experts and other treating physicians must necessarily rely on Dr.
Pincus’s interpretation of the infiltrate as “sparse” with no opportunity to reach any separate assessment.
Thus, Dr. Tornatore’s specific suggestion that it would be “quibbling” to say the infiltrate is not “dense” is
unpersuasive. (Tr. 124.) Dr. Tornatore has no basis for disputing Dr. Pincus’s specific finding that the
infiltrate is “sparse.” This also has a bearing on the weight that can be placed on Drs. Bhutani’s and
Berger’s subsequent invocation of Sweet’s syndrome. There is no basis for concluding that Drs. Bhutani
and Berger based their assessment on any differing interpretation regarding the degree of neutrophil
infiltration shown by the underlying imaging.
33
important ways. Petitioner had no fever at or around the onset of his alleged vaccine
reaction. (Tr. 126) Fever at onset is a hallmark of the condition as it is “acute febrile
neutrophilic dermatosis.” (von den Driesch at Ex. 34, supra, pp. 535, 544 (Table V).)
Moreover, despite having bloodwork completed on numerous occasions throughout his
illness, including on August 30, 2012 (Ex. 2, p. 126), which would have been during or
close in time to the alleged acute phase of his condition, petitioner’s lab results were
consistently within normal limits vis-à-vis markers that would indicate systemic
inflammation. Even by Dr. Tornatore’s own description, Sweet’s syndrome is a
systemic inflammatory condition. (Tr. 82-83, 92.) This suggests that one should expect
elevated inflammatory markers. (Tr. 219-20, 231.) These points, along with petitioner’s
evolving symptomology, contributed to respondent’s experts’ opinion that petitioner did
not have Sweet’s syndrome or any form of neutrophilic dermatosis. (Tr. 217, 226.) In
short, especially when combined with the equivocal skin biopsy, petitioner’s history is
largely lacking for any evidence of a systemic inflammatory immune response.
Dr. Tornatore stresses that in real world practice, all medical conditions present
as a spectrum. Generally, it is not necessary for a patient to have all the signs and
symptoms of a given condition to be properly diagnosed as having that condition. (Tr.
90-93, 169-74.) Moreover, he separately asserts that each of these factors need not be
present in this case. He suggests that fever is not ultimately important to his opinion in
this case. (Tr. 126, 156.) 31 He suggests that elevated inflammatory markers do not
always correlate to symptoms and that there is no pathognomonic marker for Sweet’s
syndrome. (Tr. 99-100, 153-55.) And he disputes that Sweet’s syndrome would be
limited or self-resolving in the absence of treatment. (Tr. 130-31.) (He also opines that
the presence of aseptic meningitis is evidence of inflammation (Tr. 85, 87, 93); however,
this is discussed separately below.)
Dr. Tornatore is correct to the limited extent that these factors relate to minor
rather than major diagnostic criteria for Sweet’s syndrome. (von den Driesch, supra, at
Ex. 34, p. 544 (Table V).) Thus, they are not all necessary for diagnosis. Lacking from
Dr. Tornatore’s opinion, however, is any acknowledgement of the cumulative
significance of these variances. For example, the Sweet’s syndrome diagnostic criteria
included in Dr. Tornatore’s reliance material require the presence of two major criteria
accompanied by two of four minor criteria. The two major criteria are (1) the presence
of characteristic rashes with (2) biopsy results inclusive of predominant neutrophil
infiltration. (Id.) As discussed in the preceding section, neither of these major criteria is
present in this case. The minor criteria include (1) a preceding infection or vaccination
or associated pre-existing condition, (2) periods of malaise and fever, (3) elevated
laboratory values at onset for either ESR, CRP, neutrophils, or leukocytes, and (4)
excellent response to treatment with systemic corticosteroids or potassium iodide. (Id.)
Given his lack of fever, normal bloodwork, lack of treatment, and overall medical history,
31 Dr. Tornatore principally discussed fever in the context of serum sickness and aseptic meningitis rather
than specifically in the context of diagnosing Sweet’s syndrome; however, it is clear from his testimony
that he felt Sweet syndrome was present regardless of his acknowledgement that there was no fever in
this case. (Tr. 126.)
34
literally the only diagnostic criterion that petitioner has demonstrated is that he was
previously vaccinated.
Even if other of petitioner’s symptoms overlap with known sequela of Sweet’s
syndrome, petitioner has none of the diagnostic or characteristic features of Sweet’s
syndrome. In seeking to take the “50,000 foot view” of petitioner’s condition, Dr.
Tornatore has failed to demonstrate that he has adequately grappled with the specific
details of petitioner’s own complicated medical history. In short, he has not shown that
his diagnostic assessment of Sweet’s syndrome was reliably reached in this case. (See,
e.g., Tr. 232 (Dr. Low explaining “there is a spectrum of disorders, but the spectrum is
limited; otherwise you become a very sloppy physician.”)
3. Aseptic meningitis and neuro-Sweet’s syndrome
Dr. Tornatore also based in his opinion in part on his assessment that petitioner’s
initial headache presentation was diagnosed as aseptic meningitis, which he suggested
shows neurologic manifestations of the condition temporally proximate to vaccination.
(Ex. 32, p. 6.) He also relied on this aseptic meningitis diagnosis as contributing to the
Sweet’s syndrome diagnosis by pointing specifically to the neuro-Sweet’s syndrome
variant. (Tr. 93-96, 147.) Without preponderant evidence that petitioner had Sweet’s
syndrome in any form, it is not necessary to examine whether he had the specific neuro-
Sweet’s syndrome variant identified by Dr. Tornatore. However, in the interest of
completeness I briefly note that Dr. Tornatore also is not persuasive on this point.
First, Dr. Bhattacharya’s records better reflect a suspicion of aseptic meningitis
rather than a diagnosis. He initially recorded a “possible” aseptic meningitis. (Ex. 7, p.
18.) He later recorded equivocally during a follow up that petitioner experienced “[a]n
episode of symptoms suggestive of aseptic meningitis . . .” but also indicated suspicion
of a primary neurologic condition was low. (Id. at 10.) During a third visit, after
petitioner complained of continuing headaches “off and on” with head pressure
especially along the right temple, Dr. Bhattacharya assessed right trigeminal cephalgia
and recommended an MRI with attention to the right trigeminal nerve. 32 (Id. at 3-6.)
(Compare Ex. 7, pp. 6, and 18.) In that regard, Dr. Low stressed that petitioner’s
complaints of headache and jaw pain were nonspecific, and his physical exam indicated
no signs of meningismus. (Tr. 223-24.) Moreover, Dr. Bhattacharya never ordered a
spinal tap which both Drs. Tornatore and Low agree is necessary to confirm
meningitis. 33 (Tr. 155-58, 227-28.) Additionally, there was no evidence of meningitis
32 To be clear, the experts disagree as to the meaning of the trigeminal cephalgia assessment. Dr.
Tornatore suggests that it is merely descriptive of the location of petitioner’s symptoms rather than
constituting any separate diagnosis. (Tr. 158-61.) Dr. Low explains, however, that it is a type of migraine.
(Tr. 234.) He opines the assessment of trigeminal cephalgia indicates Dr. Bhattacharya had moved on
from the initial suspicion of meningitis. (Id.)
33 Dr. Tornatore stressed that meningitis is largely a clinical diagnosis confirmed by spinal tap and that
physicians do not use the term lightly. (Tr. 155-58.) Dr. Low, however, stressed that when there is a
suspicion of meningitis, it is very important to get the spinal tap confirmation, because clinical evaluation
alone cannot tell whether the meningitis is aseptic or bacterial, the latter of which is very serious. (Tr. 227-
35
when petitioner had his MRI. 34 (Tr. 226-27.) In fact, petitioner himself testified that Dr.
Bhattacharya provided no definitive diagnosis. (Tr. 19-20.)
In any event, Dr. Tornatore’s opinion is in itself equivocal on this point. Although
he relies on aseptic meningitis as being the most common neurologic presentation for
neuro-Sweet’s syndrome (Tr. 93-94, 147), he also suggested that Dr. Bhattacharya’s
alternative suggestion of a vaccine reaction confirms he felt an inflammatory process
was present regardless of specific diagnosis (Tr. 143-44). Dr. Tornatore’s opinion is
hampered by the fact that in seeking to hedge his opinion he alternatively opines that
petitioner’s headache presentation may be a part of the serum sickness presentation he
opines was also present. (Tr. 136-37.) This underscores the uncertainty regarding the
potential aseptic meningitis diagnosis. Also important, if petitioner did have aseptic
meningitis in advance of other manifestations of Sweet’s syndrome, this would be a very
unusual presentation of the neuro-Sweet’s syndrome. (Tr. 224.) When pressed on this
specific point, Dr. Tornatore returned to contending that the manifestations of
petitioner’s purported Sweet’s syndrome and serum sickness cannot really be teased
apart. (Tr. 145-46.) While Dr. Tornatore’s suggestion of aseptic meningitis is not wholly
without support in the medical records, Dr. Low was more persuasive in opining that “we
have no evidence that this patient ever had anything strongly suggestive of aseptic
meningitis.” (Tr. 225.)
ii. Serum Sickness or Serum Sickness-like Reaction
According to Dr. Tornatore, serum sickness is a short-term hypersensitivity
reaction to foreign antigens causing fever, polyarthritis, polyarthralgia, and/or rash. (Ex.
32, p. 6) (citing Ponvert & Scheinmann, supra, at Ex. 45).) He stressed that serum
sickness is diagnosed by clinical judgment. Though he acknowledged one might expect
an elevated sedimentation rate or low complement levels during the acute phase, he
contended there is no biomarker for serum sickness. (Tr. 105-06.) In petitioner’s case,
he cites headache, dermatologic manifestations, constitutional symptoms, and fatigue,
as evidence of a serum sickness reaction. (Tr. 110-11.)
Respondent’s experts disagree. Although the symptoms Dr. Tornatore identified
are potentially consistent with serum sickness, Dr. He stressed that a serum sickness is
a “strong reaction” in which one would also expect manifestations such as fever,
edema, and swollen lymph nodes. (Tr. 187.) Additionally, Dr. He explained that
inflammatory markers are expected in bloodwork when serum sickness is present. (Tr.
193.) He indicated that if a patient has clinical symptoms, the chances are “pretty slim”
that inflammatory markers would be missed by bloodwork. (Tr. 193.) The expected
markers for inflammation are fever as well as elevated C-reactive protein and
erythrocyte sedimentation rate. (Tr. 192.) Dr. Low testified similarly. (Tr. 220-21, 229.)
28.) Accordingly, he opined that if meningitis was still suspected when petitioner returned with ongoing
symptoms the second time, a spinal tap would have been necessary. (Tr. 227.)
34 The experts also disagree as to whether petitioner’s MRI would have been likely to reveal meningitis if
it were present. (Tr. 158, 225-26.)
36
Here, petitioner experienced headaches and neck pain within five days of
vaccinations, (Ex. 2, p. 54), arthralgias within a week, (Id. at 271), and an evanescent
rash within one month. (Id. at 261-62, 264). However, there was no fever present and
petitioner’s initial August 30, 2012 blood work showed no abnormalities. (Ex. 2, p. 126.)
More extensive testing from samples collected two weeks later on September 10 and
September 14, 2012, further specifically confirmed that C-reactive protein was normal.
(Ex. 2, pp. 112, 124.) At the time, Dr. Kashino felt petitioner’s symptoms were “very
vague” and felt a vaccine reaction was less likely than a viral illness. (Ex. 2, p. 268-70.)
Petitioner also demonstrated sinus congestion and prescribed antibiotics helped
alleviate at least some of his symptoms. (Ex. 6, p. 2; see also n. 7, supra.) None of
petitioner’s physicians at that time suspected a serum sickness-like reaction. It was not
until petitioner saw Drs. Kim and Braskett about five months later that they suggested a
previously-resolved serum sickness based on the prior history. (Ex. 9, pp. 6-9.) On the
whole, it does not appear that petitioner experienced a serum sickness-like reaction.
In any event, even if petitioner did experience a transient serum sickness-like
reaction, there is not preponderant evidence that it explains his broader presentation.
There is no debate in this case that serum sickness itself is a transient condition. (Tr.
91-92, 188.) And, indeed, when Drs. Kim and Braskett first suspected a serum
sickness, they specifically characterized it as previously resolved. (Ex. 9, p. 7.)
Thereafter, none of petitioner’s treating physicians suggested any ongoing serum
sickness.
For his part, Dr. Tornatore did not offer any opinion that petitioner’s alleged
serum sickness caused Sweet’s syndrome. (Tr. 107-09.) In fact, he described the two
conditions as stemming from two different immune processes (hypersensitivity and
complement activation versus autoimmune inflammation) and suggested that he could
not discern which started first. (Tr. 86-91, 136-37.) Rather, he opined that although
petitioner likely only suffered serum sickness for three to four months, residual
symptoms can linger any time an inflammatory event sensitizes a nerve. (Tr. 107-09.)
Importantly, however, respondent’s experts have strongly stressed the lack of evidence
of any systemic inflammatory condition in this case. In fact, the “smoking gun” evidence
cited by Dr. Tornatore to demonstrate vaccine causation are aseptic meningitis and the
neutrophilic infiltrate on the skin biopsy. (Tr. 161-63.) For the reasons discussed
above, these findings are not strong evidence; however, even if they were, they
specifically implicate Sweet’s syndrome rather than serum sickness. In fact, Dr.
Tornatore explicitly testified that the skin biopsy results are not consistent with serum
sickness. (Tr. 109.)
Dr. Jaradeh opined that “I felt at the time that the patient’s neurologic
presentation was that of autonomic neuropathy.” (Ex. 30, p. 2.) He suggested it could
be secondary to a transient polyradiculitis caused by serum sickness. (Ex. 19, p. 46.)
Dr. Low explains, however, that Dr. Jaradeh’s assessment of autonomic neuropathy
lacks evidence and is based solely on an incorrect interpretation of sympathetic
function. (Ex. A, p. 4; see also Phillip Low et al., Effect of Age and Gender on
37
Sudomotor and Cardiovagal function and blood pressure response to tilt in normal
subjects, MUSCLE & NERVE 1561 (1997) (Ex. A, Tab 4) (explaining adrenergic function
tests for autonomic function).) Moreover, if this resulted from polyradiculitis, that
condition should have been detected by the EMG/NCS conducted by Dr. Goyal;
however, it was not. (Ex. A, p. 4; Ex. 2, p. 165.) And, in any event, Dr. Jaradeh did not
explain how serum sickness could lead to autonomic neuropathy. Serum sickness is
understood to be a hypersensitivity reaction whereas autonomic neuropathy is generally
believed to be an autoimmune condition. (Compare, e.g., Mark H Wener, Serum
sickness and serum sickness-like reactions, UPTODATE (2018) (Ex. F, Tab 1), and
Steven Vernino et al., Autoantibodies to ganglionic acetylcholine receptors in
autoimmune autonomic neuropathies, 343(12) NEW ENG. J. MED. 847 (2000) (Ex. A, Tab
9).) The two conditions implicate different immune responses. (Accord Tr. 82-83, 88-89
(Dr. Tornatore explaining hypersensitivity and autoinflammation).)
Thus, if petitioner established only that he experienced a serum sickness, he
would not be entitled to compensation even if that serum sickness was vaccine-caused.
§ 300aa-11(c)(1)(D) (requiring in relevant part that a petitioner “suffered the residual
effects or complications of such illness, disability, injury, or condition for more than 6
months after the administration of the vaccine”); see also Wright v. Sec'y of Health &
Human Servs., 22 F.4th 999, 1005 (Fed. Cir. 2022) (applying traditional tort principles of
causation in the context of the Vaccine Act’s severity requirement).
iii. Sweet’s Syndrome and Serum Sickness Combined
It is also not the case that Dr. Tornatore’s reliance on the concurrent or
overlapping presence of both serum sickness and Sweet’s syndrome provides any
added support for his causal opinion. In fact, Dr. Tornatore’s decision to invoke both
conditions confuses and detracts from the strength of his assessment.
For example, Dr. Tornatore relied on rash as a relevant symptom of both serum
sickness and Sweet’s syndrome. However, when pressed on details, he offered
confusing, if not conflicting, testimony. At the beginning of his testimony, he explained
that he felt petitioner’s skin biopsy result was diagnostic of Sweet’s syndrome and
specifically opined that it was not consistent with serum sickness. (Tr. 83-84, 101-02,
109.) I later questioned him regarding the ten rash photographs submitted into
evidence and he disclaimed the need to assess individual rashes “because we do have
one which clearly showed those phenotype, the pathological features that goes along
with an innate dermatologic autoinflammatory response.” (Tr. 152.) Especially because
the biopsy at issue was taken two years into petitioner’s clinical course, this strongly
implied the view that petitioner’s biopsy result should be viewed as overarching
evidence of most, if not all, of petitioner’s rashes rather than being an equivocal, or non-
specific, outlier as respondent’s experts opined.
When turning his attention to serum sickness, however, Dr. Tornatore suggested
that at least some of petitioner’s rashes should be interpreted as urticaria based on Dr.
Jaradeh’s records. (Tr. 104-05.) Moreover, when pressed he also acknowledged that
38
petitioner’s photographed rashes are not consistent with what is typically seen in
Sweet’s syndrome (Tr. 120-21) and also stated regarding the photographs that “I don’t
have any problem with [respondent’s experts] calling it hives because that is something
you see with serum sickness-like reactions.” (Tr. 114-15). Nonetheless he
simultaneously reiterated the significance of the biopsy result, stating “clearly when this
was biopsied, there was neutrophils in it. Right? And so you can call it what you want,
but it’s still inflammatory, and we still end up in the same place.” (Tr. 115.) However,
this is clearly in contrast to his prior testimony. When I had specifically asked Dr.
Tornatore to distinguish the symptoms of Sweet’s syndrome from the symptoms of
serum sickness, he answered: “I think the skin biopsy shows neutrophil in the skin, that
we – is not consistent with serum sickness. Right? Because that’s an antibody-antigen
complex with complement fixation. So I would say that the skin biopsy, at least for some
of the skin manifestations, would not be consistent with serum sickness.” (Tr. 109.)
Ultimately, during cross examination Dr. Tornatore acknowledged that he does
not know whether petitioner’s initial rashes would have been symptoms of the proposed
serum sickness or the proposed Sweet’s syndrome. (Tr. 145-46.) Moreover, as
described above, Dr. Tornatore’s opinion regarding petitioner’s headache presentation –
possibly aseptic meningitis secondary to Sweet’s but also possibly headache secondary
to serum sickness - presents a similar equivocation. Dr. Tornatore acknowledged that
he cannot distinguish what he suggests is Sweet’s syndrome from what he suggests is
serum sickness and instead opined that he can fall back on the idea that petitioner
suffered an undifferentiated, but inherently suspicious, cascade of events. (Tr. 136-37.)
Overall, there is a significant extent to which Dr. Tornatore uses the possibility of
both conditions – neuro-Sweet syndrome and serum sickness – to act as a catchall and
disguise the fact that neither condition fits well into petitioner’s overall clinical
presentation. This renders Dr. Tornatore’s opinion vague and sometimes inconsistent,
reducing his persuasiveness. When I questioned Dr. Tornatore about the timing of the
two conditions, he indicated that “I can’t give you a clear when did one start and when
did the other begin, because I think it really is a spectrum of overlapping symptoms.”
(Tr. 108.) So, I further asked Dr. Tornatore about specific symptoms. When I asked
whether any of petitioner’s symptoms fit serum sickness but not Sweet’s syndrome, he
revealingly indicated: “No. I think there is – serum sickness, the symptoms that I read off
are so diffuse, including rheumatologic issues, neurologic issues, skin issues, that that’s
too hard. I think you could have so many different things that we can’t say one of them
is not associated with serum sickness. That’s – that would be too difficult.” (Tr. 109.)
b. Althen Test
Because there is not preponderant evidence that petitioner’s overall condition
can be explained by either Sweet’s syndrome, serum sickness, or any combination of
the two, there is no need to complete any Althen analysis relative to either of those
conditions. However, as noted above, even setting aside the specific diagnoses of
Sweet’s syndrome and serum sickness, Dr. Tornatore contends that there is sufficient
evidence of an inflammatory reaction of some kind to substantiate the presence of a
39
vaccine injury. An Althen analysis, especially analysis of Althen prong two,
demonstrates why Dr. Tornatore’s alternative suggestion is inadequate to support
petitioner’s claim.
i. Althen Prong One
Under Althen prong one, a petitioner must provide a “sound and reliable” medical
theory demonstrating that the vaccine received can cause the type of injury alleged.
Boatmon v. Sec’y of Health & Human Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019).
Petitioner’s theory need only be “legally probable, not medically or scientifically certain.”
Knudsen, 35 F.3d at 549. However, the Federal Circuit has clarified that “simply
identifying a ‘plausible’ theory of causation is insufficient for a petitioner to meet her
burden of proof.” LaLonde v. Sec’y of Health & Human Servs., 746 F.3d 1334, 1339
(Fed. Cir. 2014) (citing Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315,
1322 (Fed. Cir. 2010)). Instead, petitioner “must provide a reputable medical or
scientific explanation that pertains specifically to [their] case.” Moberly, 592 F.3d at
1322.
Petitioner stresses that “while they are frequently conflated, theory of causation
and biologic mechanisms are not interchangeable. Petitioner is not required to
demonstrate by a preponderance of the evidence the exact mechanism by which
vaccines directly affect the human body.” (ECF No. 104, p. 2 (emphasis in original).)
While it is true that petitioner need not prove a mechanism of causation, petitioner must
nonetheless present preponderant evidence that the specific vaccine is capable of
causing the specific injury. See Pafford v. Sec’y of Health & Human Servs., No. 01-
0165V, 2004 WL 1717359 at *4 (Fed. Cl. Spec. Mstr. July 16, 2004) (“First, a petitioner
must provide a reputable medical theory causally connecting the vaccination and the
injury. In fine, can [the] vaccine(s) at issue cause the type of injury alleged?”), aff’d 64
Fed. Cl. 19 (2005), aff’d 451 F.3d 1352 (Fed. Cir. 2006). “The assessment of whether a
proffered theory of causation is ‘reputable’ can involve assessment of the relevant
scientific data. Medical literature and epidemiological evidence must be viewed,
however, not through the lens of the laboratorian, but instead from the vantage point of
the Vaccine Act's preponderant evidence standard.” Andreu, 569 F.3d at 1380.
In his initial expert report, Dr. Tornatore focused first and foremost on the specific
conditions of Sweet syndrome and serum sickness. Specifically, he indicated that “I
believe Mr. Orgel-Olsen suffered from post-vaccinal Sweet’s syndrome and serum
sickness, both of which would account for all of his symptoms.” (Ex. 32, p. 5.) Dr.
Tornatore’s discussion of Sweet’s syndrome and serum sickness arguably incorporates
a broader reliance on autoinflammatory disease and hypersensitivity reactions
generally; however, his literature review and reliance materials were limited to evidence
purporting to link vaccination and the specific conditions of Sweet’s syndrome and
serum sickness. 35 (Id. at 6.) Because petitioner has not preponderantly established
35 Dr. Tornatore did file an article by Ponvert and Scheinman that discussed vaccine allergy and pseudo
allergy. (Ponvert and Scheinman, supra, at Ex. 45.) That article discussed reactions to toxoided
vaccines. However, when I asked Dr. Tornatore about the paper during the hearing, he indicated it is
40
that these diagnoses explain his overall condition, these materials and this discussion
are not persuasive in presenting a theory that would otherwise explain how petitioner’s
unknown condition can be caused by his vaccination(s). Apart from these two specific
conditions, Dr. Tornatore’s discussion offers no greater explanation than to suggest
broadly that the immune system can respond aberrantly to some stimuli. His hearing
testimony was similar. (Tr. 83-91.)36 This is inadequate to support petitioner’s claim
under Althen prong one.
ii. Althen Prong Two
Althen prong two requires petitioner to establish by preponderant evidence a
“logical sequence of cause and effect” connecting the vaccination and injury at issue.
See Althen, 418 F.3d at 1278. Althen prong two requires a more specific showing that
the particular vaccinations petitioner received more likely than not did cause the injuries
that he alleges. See, e.g., Doe v. Sec’y of Health & Human Servs., 83 Fed. Cl. 157, 166
(Fed. Cl. 2008); King v. Sec’y of Health & Human Servs., 03-584V, 2010 WL 892296, at
*87 (Fed. Cl. Spec. Mstr. Mar. 12, 2010) (citing Kuperus v. Sec’y of Health & Human
Servs., No. 01–60V, 2003 WL 22912885, at *8 (Fed. Cl. Spec. Mstr. Oct. 23, 2003);
Helms v. Sec’y of Health & Human Servs., No. 96–518V, 2002 WL 31441212, at *18 n.
42 (Fed. Cl. Spec. Mstr. Aug. 8, 2002) (“[I]n many Program opinions issued prior to
Althen involving “causation-in-fact” issues, special masters or judges stated that a
petitioner must demonstrate (1) that the type of vaccine in question can cause the type
of injury in question, and also (2) that the particular vaccination received by the specific
vaccinee actually did cause the vaccinee's own injury.”)).
Althen prong two is often proven on the strength of treating physician opinion.
However, medical records and/or statements of a treating physician do not per se bind
the special master to adopt the conclusions of such an individual, even if they must be
considered and carefully evaluated. See 42 U.S.C. §300aa-13(b)(1) (providing that
“[a]ny such diagnosis, conclusion, judgment, test result, report, or summary shall not be
binding on the special master or court”); Snyder v. Sec'y of Health & Human Servs., 88
Fed. Cl. 706, 746 n.67 (2009) (“there is nothing ... that mandates that the testimony of a
treating physician is sacrosanct—that it must be accepted in its entirety and cannot be
useful only broadly for illustrating the proposition that vaccines trigger innate immune responses. He
disclaimed any reliance on any specific findings from the paper. (Tr. 163-65.)
36 For example, while discussing Sweet’s syndrome and the supporting literature, Dr. Tornatore indicated
that petitioner “had objective evidence of aberrant, innate immunity on his biopsy, period.” (Tr. 83.) He
explained that “[w]e like to kind of pigeonhole disease states, but the reality is the immune system [is] a
spectrum and . . . people don’t necessarily fit very neatly into one category.” (Tr. 84.) He further testified
that “we have an innate immunity that is affecting the skin, which can be triggered by vaccines . . is kind
of at the heart of this case because it’s the objective evidence that we have that there was an
inflammatory disorder at play here” and “[i]f somebody is predisposed to having their immune system on
and that it may irritate the skin, if you were exposed to a foreign antigen via vaccination, for instance, then
the immune system may get turned on.” (Tr. 84.) Dr. Tornatore also referenced adaptive immunity and
molecular mimicry, but only in the context of Sweet’s syndrome in particular. (Tr. 86-88.) With regard to
serum sickness, Dr. Tornatore discussed hypersensitivity and complement binding and activation. (Tr.
88-91.)
41
rebutted”). In many cases treating physicians will consider a host of different conditions
and causal factors while investigation continues; however, the mere consideration of a
possible temporal relationship to vaccination is not the same as reaching a conclusion
as to vaccination. Nor does it necessarily mean the physician thinks a suspected causal
relationship is likely. E.g. Stapleford v. Sec’y of Health and Human Servs., No. 03-
234V, 2009 WL 1456441, at *17 n.24 (Fed. Cl. Spec. Mstr. May 1, 2009) (referencing a
temporal relationship to vaccination “is quite different from an indication that such
physician has reached a conclusion concerning a causal relationship”) (emphasis in
original), aff’d, 89 Fed. Cl. 456 (Fed. Cl. 2009).
Especially important in this case, special masters must consider the medical
records as a whole. § 300aa-13(b)(1) (“In evaluating the weight to be afforded to any
such diagnosis, conclusion, judgment, test result, report, or summary, the special
master or court shall consider the entire record and the course of the injury, disability,
illness, or condition until the date of the judgment of the special master or court.”) The
views of treating physicians should weighed against other, contrary evidence also
present in the record, including the opinions of other treating physicians. Hibbard v.
Sec'y of Health & Human Servs., 100 Fed.Cl. 742, 749 (2011) (not arbitrary or
capricious for special master to weigh competing treating physicians' conclusions
against each other), aff'd, 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec'y of Health &
Human Servs., 100 Fed.Cl. 119, 136 (2011), aff'd, 463 Fed.Appx. 932 (Fed. Cir. 2012);
Veryzer v. Sec'y of Health & Human Servs., No. 06-522V, 2011 WL 1935813, at *17
(Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review den'd, 100 Fed.Cl. 344, 356 (2011),
aff'd without opinion, 475 Fed.Appx. 765 (Fed. Cir. 2012).
In this case, petitioner and Dr. Tornatore are correct that there is a suspicion of
vaccine causation throughout petitioner’s medical records expressed by multiple
treating physicians. There are several reasons, however, why the medical records
considered as a whole do not preponderately satisfy Althen prong two based on
petitioner’s treating physicians’ views. Although the medical records are described in
much greater detail in the fact summary above, given the number of physicians
involved, a brief summary of each treating physician’s view arranged by discipline helps
illustrate:
• Primary care: Dr. Kashino, initially felt petitioner’s symptoms were “vague” and
possibly related to a sinus infection or a viral illness. (Ex. 2, pp. 268, 270.)
Although his office completed a VAERS form on petitioner’s behalf, Dr. Kashino
specified in his own notes that a vaccine reaction was less likely. (Id. at 270.)
However, as petitioner continued seeing many different specialists, Dr. Kashino
later erroneously recorded that these specialists had reached a consensus that a
vaccine reaction occurred. (Ex. 2, p. 196; see also n. 13-15, supra.)
Nonetheless, he never reached any final unifying diagnosis of his own.
• Infectious Disease: Neither Dr. Kaufman nor Dr. Parsonnet identified any
diagnosis within their discipline. Dr. Parsonnet initially suspected fibromyalgia
and recommended a rheumatology referral, but later pursued a consultation with
42
the CDC. She reported the CDC felt vaccine-causation was unlikely without
providing further diagnostic assessment. (Ex. 2, p. 245; Ex. 12, p. 66; Ex. 14, p.
12.) Dr. Kaufmann felt there was no unifying infectious disease diagnosis and
recorded a vaccine reaction “per patient perception.” (Ex. 2, p. 262.)
• Allergy/Immunology: Drs. Kim/Braskett suspected a vaccine reaction,
especially in the form of a previously resolved serum sickness reaction, but noted
petitioner’s condition had no clear etiology. They recommended further
rheumatology consultation. (Ex. 9, pp. 6-9.) Dr. Felsenstein later indicated that
the etiology of petitioner’s condition was unclear but recommended further
neurology consultation over concern regarding the fasciculations. (Ex. 14, p. 19.)
• Neurology/Neuromuscular: Dr. Bhattacharya initially suspected a previously
resolved or resolving aseptic meningitis versus a vaccine reaction but felt the
likelihood of a neurologic condition was low and recommended a rheumatology
consult due to suspicion of inflammatory polyarthropathy. (Ex. 7, pp. 10, 18.) He
later indicated right trigeminal autonomic cephalgia but did not otherwise reach a
final diagnosis. (Id. at 6.) Later, Dr. de la Motte indicated that petitioner was
unlikely to have any neurologic condition and felt the symptoms were somatic
with no associated pathology. (Ex. 2, p. 167.) Drs. Shieh/Maldonado noted the
possibility of a post-vaccine reaction but diagnosed benign fasciculations of
unknown etiology. (Ex. 9, p. 9-11.) Dr. Goyal further confirmed on objective
testing that the fasciculations had no neurologic pathology, provided no
diagnosis, and recommended evaluation by an autonomic specialist. (Ex. 2, pp.
158-63.)
• Autonomic: Dr. Jaradeh felt that petitioner had autonomic neuropathy (refuted
by Dr. Low). (Ex. 30, p. 3.) Based on the circumstances around the time of
onset, he opined that petitioner’s condition may have been caused either by his
vaccinations in combination with his subsequent treatments or by his sinus
infection and/or antibiotics. (Id.) He suggested serum sickness “somehow
provide[d] some type of inflammation” that affected other body systems, including
the autonomic nervous system. (Id.)
• Cardiology: Dr. Johnson felt there was no unifying diagnosis available for
petitioner’s symptoms, felt petitioner was fixated on his somatic complaints, and
recommended a psychiatric consult. (Ex. 23, pp. 53-54.)
• Dermatology: Dr. Shields did not know the cause of petitioner’s skin eruptions
but questioned whether a rheumatologic disorder could be present. (Ex. 25, p.
7.) Dr. Pincus’s interpretation of the skin biopsy was equivocal as discussed
above. (See n. 28, supra.) Drs. Bhutani/Berger subsequently included
neutrophilic dermatosis NOS within a differential diagnosis, but cautioned the
presentation was not yet characteristic of any condition and recommended
keeping an open mind regarding etiopathogenesis. (Ex. 23, pp. 1-2.)
43
• Rheumatology: Dr. Miller opined there was no reactive arthropathy and
indicated petitioner’s condition was not diagnosable as a rheumatologic condition
or infectious disease. He felt a vaccine reaction was “conceivable,” but was
unprovable speculation. (Ex. 13, pp. 7-10.)
Despite the fact that suspicion of vaccine-causation is repeatedly expressed
throughout the medical records, these summaries reveal several important factors that
militate against placing any significant weight on such notations. First, when reviewing
each physician’s individual records, it is clear that, apart from the serum sickness
addressed separately above, no single physician was willing to move beyond suspicion
of vaccine causation as any explanation for petitioner’s overall, prolonged course of
symptoms. Second, there is no consensus diagnosis, leaving no clear etiologic
explanation for the suspicion of vaccine causation and suggesting that the suspicion
was based largely on temporality. Third, and relatedly, most of the suspicion was
expressed after the physician in question had exhausted explanations within their own
discipline. The suspicion was included along with recommendations for other specialist
consultations, suggesting possibilities beyond the opining physician’s own discipline.
However, these suspicions were not borne out by the relevant specialist’s evaluation. 37
And, fourth, many of petitioner’s treating physicians also explicitly expressed doubt as to
the existence any connection to petitioner’s vaccination. Selectively accepting the
opinions of some of petitioner’s treating physicians necessarily means rejecting the
opinions of others; however, given the lack of a unifying diagnosis, the equivocation of
those physicians suspecting vaccine-causation, and the lack of unanimity among
petitioner’s treating physicians as to the possible cause(s) of petitioner’s symptoms,
there is little basis on this record to justify such a preference when considering the
record as a whole. Petitioner himself testified that his physicians were, in effect,
stumped by his presentation. (Tr. 31-32.)
Dr. Tornatore nonetheless testified: “the bottom line is everyone keeps saying
this is a post-vaccination inflammatory event. Whether they use the term ‘sweet’s
syndrome or ‘serum sickness’ is irrelevant. They’re all saying the same thing.” (Tr.
144.) Describing petitioner’s “weird symptoms,” he contended that “you just draw a
straight line across and it makes sense.” (Tr. 178.) In light of the above, and especially
in light of Dr. Tornatore’s own failure to persuasively crystalize petitioner’s clinical
history, this is not persuasive. Dr. Tornatore’s rationale implies that the repeated
suspicion of multiple physicians has a cumulative effect that increases the likelihood
that a vaccine reaction occurred in some form. But this is not true in this case. These
physicians are all simply recording the same initial suspicion of temporality observed by
37 For example, Drs. Parsonnet (infectious disease), Kim/Braskett (allergy/immunology), and Shields
(dermatology), all suggested the answer may be found by rheumatology, but petitioner’s rheumatologist
felt no unifying rheumatology diagnosis is available and that vaccine causation was unprovable
speculation. Similarly, Drs. Kim/Braskett and Dr. Felsenstein (allergy/immunology) recommended a
neurology follow up due to concerns regarding petitioner’s fasciculations, but Drs. Shieh/Maldonado and
Dr. Goyal later determined they were benign and had no neurologic cause.
44
petitioner. 38 It is not consensus, only repetition brought about by the sheer number of
consultations petitioner sought and the inability of any physician to confidently pin-point
the correct diagnosis. There is little to no evidence that the suspicion, no matter how
many times repeated, ever progressed to anything approaching a substantiated
conclusion. Indeed, Dr. Tornatore’s suggestion that an inflammatory injury is supported
by the medical records is predicated in large part by his assumptions that petitioner’s
headache presentation constituted aseptic meningitis and that his skin biopsy proves
his recurrent rashes to be a manifestation of an inflammatory condition. However, for
the reasons discussed above, he is not persuasive on either point. This holds true
regardless of whether these factors contribute to a specific diagnosis. Additionally,
respondent’s experts are persuasive in stressing that petitioner’s blood work throughout
this period remained remarkably free of any indicators of systemic inflammation.
iii. Althen Prong Three
The third Althen prong requires establishing a “proximate temporal relationship”
between the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term
has been equated to the phrase “medically-acceptable temporal relationship.” Id. A
petitioner must offer “preponderant proof that the onset of symptoms occurred within a
timeframe which, given the medical understanding of the disorder's etiology, it is
medically acceptable to infer causation.” de Bazan v. Sec'y of Health & Human Servs.,
539 F.3d 1347, 1352 (Fed. Cir. 2008). Here, it is clear that petitioner experienced
headaches and neck pain within five days of vaccinations, (Ex. 2, p. 54), arthralgias
within a week, (Id. at 271), and an evanescent rash within one month. (Id. at 261-62,
264). Prior program experience suggests that it is plausible that an immunologic
reaction could occur in that timeframe. In this case, it certainly formed the basis for
petitioner’s own subjective belief that his vaccines caused his condition and likely
accounts for the suspicion of vaccine causation entertained by his treating physicians.
Ho
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