Winkler v. Secretary of Health and Human Services

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: December 10, 2021

*************************
DONALD WINKLER, * PUBLISHED
*
Petitioner, * No. 18-203V
*
v. * Special Master Nora Beth Dorsey
*
SECRETARY OF HEALTH * Dismissal Decision; Tetanus-Diphtheria-
AND HUMAN SERVICES, * Acellular Pertussis (“Tdap”) Vaccine;
* Pneumococcal Conjugate (“Prevnar” or
Respondent. * “Prevnar 13”) Vaccine; Guillain-Barré
* Syndrome (“GBS”).
*************************

Michael Patrick Milmoe, Law Offices of Leah V. Durant, PLLC, Washington, DC, for petitioner.
Ryan Daniel Pyles, U.S. Department of Justice, Washington, DC, for respondent.

DECISION 1

I. INTRODUCTION

On February 9, 2018, Donald Winkler (“petitioner”) filed a petition for compensation
under the National Vaccine Injury Compensation Program (“Vaccine Act” or “the Program”), 42
U.S.C. § 300aa-10 et seq. (2012). 2 Petitioner alleges that he suffered Guillain-Barré syndrome
(“GBS”) as the result of a tetanus-diphtheria-acellular pertussis (“Tdap”) vaccination

1
Because this Decision contains a reasoned explanation for the action in this case, the
undersigned is required 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). This means the Decision will
be available to anyone with access to the Internet. In accordance with Vaccine Rule 18(b),
petitioner has 14 days to identify and move to redact medical or other information, the disclosure
of which would constitute an unwarranted invasion of privacy. If, upon review, the undersigned
agrees that the identified material fits within this definition, the undersigned will redact such
material from public access.
2
The National Vaccine Injury Compensation Program is set forth in Part 2 of the National
Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended,
42 U.S.C. §§ 300aa-10 to -34 (2012). All citations in this Decision to individual sections of the
Vaccine Act are to 42 U.S.C. § 300aa.
administered on April 26, 2017. 3 Petition at Preamble (ECF No. 1). Respondent argued against
compensation, stating that “this case is not appropriate for compensation under the terms of the
Act.” Respondent’s Report (“Resp. Rept.”) at 2 (ECF No. 14).

After carefully analyzing and weighing the evidence presented in this case in accordance
with the applicable legal standards, the undersigned finds petitioner is not entitled to
compensation. Accordingly, petitioner’s case must be dismissed.

II. ISSUES TO BE DECIDED

The parties agree petitioner suffered from GBS, although their experts disagree as to the
subtype. 4 Petitioner’s Motion for Ruling on the Record (“Pet. Mot.”), filed Mar. 24, 2021, at 10
(ECF No. 49); Resp. Response to Pet. Mot. (“Resp. Response”), filed June 23, 2021, at 1-2, 11-
12 (ECF No. 52); Pet. Exhibit (“Ex.”) 9 at 2; Resp. Ex. C at 9-10.

The parties dispute causation. Petitioner alleges (1) the Tdap vaccine can cause GBS, (2)
petitioner’s GBS was caused by his Tdap vaccination on April 26, 2017, and (3) there is a
proximate temporal relationship between petitioner’s Tdap vaccination and his development of
GBS. Pet. Mot. at 11-19; Pet. Reply to Resp. Response (“Pet. Reply”), filed July 23, 2021, at 2-
9 (ECF No. 53). Thus, petitioner contends he has satisfied all three Althen prongs and is entitled
to compensation. Pet. Mot. at 20; Pet. Reply at 6, 8-9. On the other hand, respondent asserts that
petitioner is unable to satisfy his burden of proving causation under all three Althen prongs, and
therefore, petitioner’s case should be dismissed. Resp. Response at 1-2, 11-26.

III. BACKGROUND

A. Medical Terminology

1. Guillain-Barré Syndrome

GBS is defined as “an acute monophasic peripheral neuropathy.” 42 C.F.R. §
100.3(c)(15)(i). It is a “rapidly progressive ascending motor neuron paralysis of unknown
etiology, frequently seen after an enteric or respiratory infection.” Guillain-Barré Syndrome,
Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?
id=110689 (last visited Oct. 6, 2021). Typically, GBS first presents “with paresthesias of the
feet, followed by flaccid paralysis of the entire lower limbs, ascending to the trunk, upper limbs,

3
Petitioner received a pneumococcal conjugate (“Prevnar” or “Prevnar 13”) vaccine two days
later on April 28, 2017. Petitioner’s Exhibit (“Pet. Ex.”) 1 at 1. Although the petition does not
allege the Prevnar vaccine played a part in the development of petitioner’s GBS, petitioner’s
expert, Dr. Rinker, and respondent’s expert, Dr. Chaudhry, both discuss the role of the Prevnar
vaccine in this case. See Pet. Ex. 9 at 2, 4; Respondent’s (“Resp.”) Ex. C at 11-12, 15.
Therefore, the undersigned considered all evidence surrounding both vaccines.
4
Because the parties agree petitioner suffered from GBS, the undersigned will not opine as to the
specific subtype.

2
and face; other characteristics include slight fever, bulbar palsy, absent or lessened tendon
reflexes, and increased protein in the cerebrospinal fluid without a corresponding increase in
cells.” Id. Patients suffering from GBS typically reach nadir within four weeks following onset.
Pet. Ex. 11 at 5, 7; 5 see also 42 C.F.R. § 100.3(c)(15)(i).

2. Campylobacter

Campylobacter is “a genus of bacteria of the family Campylobacteraceae, consisting of
gram-negative curved, S-shaped, or spiral rods. . . . [T]hey are found in the oral cavity, intestinal
tract, and reproductive organs. Some species are pathogenic.” Campylobacter, Dorland’s Med.
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=7653 (last visited on
Oct. 12, 2021). According to the Centers for Disease Control and Prevention (“CDC”), 6 a
Campylobacter infection has an incubation period of two to five days. Pet. Ex. 34 at 1.
Campylobacter infection can result in GBS. Id. The CDC “estimates Campylobacter are
responsible for 5-41% of GBS illnesses.” Id.

There are over 20 species of Campylobacter and approximately 90% of human
Campylobacter illnesses are caused by Campylobacter jejuni (“C. jejuni”). Pet. Ex. 34 at 1. C.
jejuni is “a species that is a common cause of enteric campylobacteriosis in humans.”
Campylobacter Jejuni, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/
dorland/definition?id=62516 (last visited on Oct. 12, 2021). Enteric campylobacteriosis or
Campylobacter enteritis (“C. enteritis”) is an “intestinal infection by a species of
Campylobacter; characteristics include diarrhea that may be bloody, abdominal pain with
cramps, and fever. The cause is usually ingestion of contaminated food or water.” Enteric
Campylobacteriosis, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/
dorland/definition?id=62528 (last visited on Oct. 12, 2021); Campylobacter Enteritis, Dorland’s
Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=73277 (last
visited on Oct. 12, 2021). The “CDC estimates that 1.5 million people in the United States
become ill from Campylobacter infection every year.” Pet. Ex. 34 at 1.

B. Procedural History

Petitioner filed his petition on February 9, 2018 and filed medical records on April 9,
2018. Petition; Pet. Exs. 1-8. On February 15, 2019, respondent filed his Rule 4(c) Report, in
which he recommended against compensation. Resp. Rept. at 2.

On August 19, 2019, petitioner filed an expert report from Dr. John R. Rinker. Pet. Ex.
9. This case was reassigned to the undersigned on January 21, 2020. Notice of Reassignment
dated Jan. 21, 2020 (ECF No. 26). On February 7, 2020, respondent filed expert reports from
Drs. J. Lindsay Whitton and Vinay Chaudhry. Resp. Exs. A, C.

5
Christiaan Fokke et al., Diagnosis of Guillain-Barré Syndrome and Validation of Brighton
Criteria, 137 Brain 33 (2014).
6
Campylobacter (Campylobacteriosis), Ctrs. for Disease Control & Prevention,
https://www.cdc.gov/campylobacter/index.html (last reviewed Dec. 23, 2019).

3
 The undersigned held a Rule 5 conference on April 2, 2020. Order dated Apr. 2, 2020
(ECF No. 31). The undersigned preliminarily found that there are three potential causes in this
case, making it difficult to discern which cause was the most likely cause of petitioner’s GBS.
Id. at 1. Thereafter, the parties filed supplemental expert reports from Dr. Rinker and Dr.
Chaudhry. Pet. Ex. 31; Resp. Ex. E.

On March 24, 2021, petitioner filed a motion for a ruling on the record. Pet. Mot.
Respondent filed his response to petitioner’s motion on June 23, 2021 and petitioner filed his
reply on July 23, 2021. Resp. Response; Pet. Reply.

This matter is now ripe for adjudication.

C. Factual History

1. Medical History

Prior to the vaccination at issue, petitioner had a prior medical history including bilateral
carpal tunnel syndrome, hearing loss, bilateral shoulder pain, left knee pain, and shortness of
breath. Pet. Mot. at 2; Resp. Response at 3.

On April 26, 2017, at sixty-six years old, petitioner received a Tdap vaccination at Basin
Medical Clinic (“Basin Clinic”) after stepping on a wire. Pet. Ex. 1 at 1; Pet. Ex. 3 at 9; Pet. Ex.
5 at 7.

On April 28, 2017, two days later, petitioner visited Dr. Michael Olsen, his primary care
physician, at Basin Clinic for a physical examination. Pet. Ex. 5 at 3. He “complain[ed] of
itchy, tingling legs. He denie[d] burning or aching of the legs.” Id. He also reported insomnia,
urinary frequency of 6-7x daily with 1-2x at night, and left knee pain. Id. at 3-4. He denied
diarrhea. Id. at 4. Physical examination was normal. Id. at 5-6. Assessment was daytime
somnolence, fatigue, urinary frequency, hyperlipidemia, varicose veins, and proteinuria. Id. at 6.
Dr. Olsen ordered labs and overnight oximetry. Id. Labs revealed an elevated creatinine level,
high cholesterol, high mean corpuscular volume, high neutrophils, and low lymphocytes. Id. at
9-11. He found petitioner’s “itching of legs most likely [] related to the varicose veins” and
“recommended he see a specialist for evaluation and treatment.” Id. at 6. Petitioner also
received a pneumococcal conjugate (“Prevnar” or “Prevnar 13”) vaccination at this visit. Id.;
Pet. Ex. 1 at 1.

Petitioner returned to Dr. Olsen on May 3, 2017 “complain[ing] of feeling run down,
fatigued, muscle aches, headaches, diarrhea, and urinary frequency x3 days.” Pet. Ex. 5 at 2. He
also reported chills, feeling feverish, sinus congestion, and a bloody nose. Id. Under review of
systems, petitioner reported right upper quadrant abdominal pain, but no dyspepsia, heartburn,
nausea, vomiting, or constipation. Id. He “had diarrhea x3 days up to 6x daily” and there
“[m]ay have been melena or bright red blood per rectum with the diarrhea.” Id. Physical
examination was normal. Id. at 3. Dr. Olsen’s assessment was fatigue, myalgia, urinary

4
frequency, diarrhea, and gastroenteritis. 7 Id. Petitioner was instructed to take Imodium and eat a
bland diet. Id.

On May 11, 2017, petitioner presented to Ashley Regional Medical Center Emergency
Room (“ER”) complaining of diffuse weakness. Pet. Ex. 3 at 7. Petitioner reported difficulty
standing, feeling unstable on his feet, and difficulty using his hands. Id. Petitioner could no
longer pick up a bale of hay and he was having trouble getting off the toilet. Id. “He state[d]
that last Friday he was feeling pretty normal but over the last 5 days he has noticed progressive
weakness. . . . This morning it got so bad that he could not button up his pants.” Id. Petitioner
reported “considerable pain in his left calf intermittently,” limping on his left leg, and his left leg
“feeling much weaker.” Id. He reported his “illness with vomiting and diarrhea as well as
weakness about 2 weeks ago.” 8 Id. Dr. Mitchell Melling noted petitioner “could not stand from
a deep squat and had diffuse weakness” in the ER. Id.

Dr. Melling’s physical examination found “[d]iffuse weakness with strength 2 to 3/5
bilaterally throughout in the proximal muscles. He also ha[d] considerable loss of coordination
in his hands. He ha[d] 3 beats or clonus at the ankle and his deep tendon reflexes [were] a little
brisk throughout.” Pet. Ex. 3 at 8. Plan indicated progressive weakness with GBS as
differential. Id. Petitioner was admitted, and a lumbar puncture and EMG were ordered. Id.

Petitioner was also seen by Dr. Bruce A. Daniel in the ER on May 11, 2017. Pet. Ex. 3 at
26. Under history of present illness, Dr. Daniel documented that petitioner reported “2 weeks of
progressively worsening weakness” that “started after a [Prevnar 13] vaccine and a bout of
diarrhea, which [petitioner] had about the same time 2 weeks ago.” Id. Petitioner reported his
weakness had progressively gotten worse to where “he ha[d] no strength and [could not] even
snap his pants close.” Id. He reported his muscles were achy and his symptoms were “at least
moderate to severe.” Id. Dr. Daniel’s physical examination revealed muscle weakness. Id.
“[Petitioner] [was] able to lift against gravity easily with his extremities” and had no drift or
asymmetry, and Dr. Daniel found petitioner’s hand grip weaker than expected. Id. Petitioner
was almost able to do a squat “but he really ha[d] to work hard to do it.” Id. Additionally, his
reflexes at the knee, patella, and Achilles were “normal to slightly decreased.” Id. at 27. Dr.
Daniel’s differential diagnoses were GBS, fluid-electrolyte abnormality, hypothyroidism, and
other autoimmune or inflammatory disease. Id. He noted petitioner’s C-reactive protein was
negative and his sedimentation rate was elevated at 25 (range 0-20). Id. at 27, 34, 36. Dr. Daniel
opined petitioner had GBS. Id. at 27. He discussed the case with Dr. James D. White and Dr.
Melling, and they agreed to admit petitioner and conduct further workup. Id. Petitioner was
admitted to Dr. Melling’s service. Id.

7
Gastroenteritis is “inflammation of the lining of the stomach and intestines, characterized by
anorexia, nausea, diarrhea, abdominal pain, and weakness.” Gastroenteritis, Dorland’s Med.
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=19818 (last visited
Oct. 6, 2021). Causes of gastroenteritis include food poisoning, viral infections, and
consumption of irritating food or drink. Id.
8
It appears this quote was noted in the history of present illness section every day of petitioner’s
hospital stay. To avoid repetition, this statement will not be repeated.

5
 A physical therapy (“PT”) evaluation was conducted by Justin R. Watkins on May 11,
2017. Pet. Ex. 3 at 43-46. Petitioner reported “slowly getting weak over the past week,” falling
episodes, and having “a very hard time with fine motor tasks that involve his hands[,] and []
getting a lot of cramping in his calves when he walks.” Id. at 43. Petitioner’s grip strength was
-4/5, his shoulder strength was 4/5, and his lower extremity strength was decreased. Id. at 44.
Assessments included increased pain, decreased strength, decreased functional mobility,
impaired activity tolerance, and fine motor deficits. Id. at 46.

On May 12, 2017, Dr. White provided a consultation and conducted electrodiagnostic
studies. 9 Pet. Ex. 3 at 9-11; Pet. Ex. 6 at 48-51. He documented petitioner’s history of present
illness. Pet. Ex. 3 at 9. Dr. White wrote that petitioner reported that “[h]e had a [Tdap] shot and
subsequently developed diarrhea (approximately 2 weeks ago). At around that time, he also had
a [Prevnar 13] vaccine.” Id. Petitioner indicated he was doing better that morning. Id. “He was
able to squat 3 times” and he could pull up his pants, although with substantial difficulty. Id.
Petitioner reported no shortness of breath, frequent urination, and weakness in the arms and legs.
Id.

Dr. White’s physical examination revealed petitioner’s “reflexes [were] l+ at both the
knees and the ankles” and no clonus at the ankle, wrist, or knee. Pet. Ex. 3 at 10. The Babinski
and Hoffmann signs were negative bilaterally. Id. His strength was decreased for the extensor
hallicus longus (“EHL”) and anterior tibialis bilaterally at 4/5. Id. His “strength [was]
symmetric for the gastrocnemius and [Dr. White] [was] unable to overcome gastrocnemius
strength using [his] hands.” Id. Petitioner’s strength was also symmetric within normal range in
his hamstrings, quadriceps, and gluteus medius. Id. For petitioner’s upper extremities, petitioner
had “neurogenic weakness in [abductor pollicis brevis (“APB”)], the hand intrinsics, and the . . .
flexors of all 4 fingers on each side” at 4/5, and well as “4/5 strength for the wrist flexors and
extensors.” Id. “[H]e ha[d] better strength for the biceps and triceps (4+) and for the external
rotators strength [was] near normal.” Id. Sensory examination revealed petitioner’s “[t]hreshold
to vibratory sensation [was] slightly decreased at the ankle.” Id.

Dr. White found petitioner “ha[d] multiple abnormalities on nerve conduction studies . . .
consistent with a diffuse neuropathic process.” Pet. Ex. 3 at 11. Taking the electrodiagnostic
findings, medical history, and physical examination together, Dr. White was “most strongly
suspicious of acute inflammatory demyelinating polyneuropathy (AIDP, also known as [GBS]),”
with a differential diagnosis of early presentation of chronic inflammatory demyelinating
polyneuropathy (“CIDP”) and “diffuse peripheral neuropathy of other etiology.” Id. He
recommended checking petitioner’s “spinal tap looking for elevated protein in the absence of an
elevated white count which would add further evidence to the probability of AIDP.” Id. If
confirmed, he recommended IVIG treatment for five days. Id.

That same day, May 12, 2017, petitioner reported he still could not button his pants or
open a sugar packet. Pet. Ex. 3 at 15. Physical examination by Dr. Melling revealed petitioner’s

9
Dr. White noted petitioner’s extremities were cool prior to the study and he encountered
difficulty maintaining an adequate temperature. Pet. Ex. 3 at 10.

6
clonus and hyperreflexia of his wrists and ankles resolved that morning. Id. Petitioner had
“decreased reflexes in both upper and lower extremities,” and “quite significant weakness
throughout all 4 extremities.” Id. After the EMG confirmed the likelihood of AIDP/GBS,
petitioner received a lumbar puncture that day, which revealed an elevated protein at 49.4 (range
15-45) and confirmed petitioner’s diagnosis. Id. at 15, 39, 42. Dr. Melling assessed petitioner
with GBS (AIDP). Id. at 15. Petitioner was to remain in the hospital “for full treatment course
or until his strength [was] sufficient to go home.” Id. Petitioner started IVIG that afternoon. Id.

On May 13, 2017, petitioner was seen by Dr. Sara Daniel. 10 Pet. Ex. 3 at 16. Petitioner
reported his legs felt much stronger, he could perform more than 10 deep squats, and he could
button up his pants. Id. He also reported his bilateral hands were still weak and Dr. Daniel
found he demonstrated a weak grip that improved as the day progressed. Id. Physical
examination revealed weakness and normal strength. Id. at 17. Petitioner’s bilateral hand
strength was +4/5 “which improved throughout the day [but] continue[d] to remain weak,” and
his lower extremity strength “normalized” at +5/5. Id. Petitioner was to continue his IVIG
treatment, and a PT evaluation 11 was ordered for his proximal muscle weakness. Id.

The following day, on May 14, 2017, petitioner reported “feeling much improved.” Pet.
Ex. 3 at 18. “He [was] now able to walk about without difficulty,” and “[h]is hand strength
[was] improving as well, but remain[ed] weak.” Id. “[W]hile receiving his IVIG [petitioner]
developed . . . hypotension,” but “after slowing the transfusion rate and providing a 1 [liter
normal saline] bolus, [petitioner] improved and was able to complete his treatment.” Id.
Petitioner remained in good, stable condition and comfortable throughout the remainder of the
day. Id. Physical examination by Dr. Daniel revealed bilateral hand strength of +4/5 that
“continue[d] to improve but remain[ed] weaker than baseline,” and lower extremity strength of
+5/5. Id. at 19. Petitioner was to continue with PT and IVIG. Id.

Petitioner reported continued improvement on May 15, 2017. Pet. Ex. 3 at 20. “He
[was] able to care for himself and get dressed, however he continue[d] to worry that his hands
[were] so weak,” specifically his left hand more than his right. Id. Dr. Daniel’s physical
examination revealed +4/5 bilateral hand strength that “continue[ed] to improve but remain[ed]
weaker than baseline,” and +5/5 lower extremity strength. Id. at 21. Dr. Daniel noted petitioner
would likely be discharged after his last IVIG treatment the following day. Id.

Dr. White provided a second consultation on May 15, 2017. Pet. Ex. 3 at 12. Petitioner
was on his fourth day of IVIG and “[was] beginning to experience some increase in strength.”
Id. Petitioner reported “increased facility in performing functional abilities such as snapping of
his pants” and “[h]e [was] now able to open his own orange juice and milk cartons in the
hospital.” Id. Physical examination revealed 1 to 2+ reflexes of knees and ankles, functional but
decreased grip strength, 4 to 4+/5 strength in the hand intrinsics and long flexors of the fingers,
4+ to 5-/5 strength in the triceps, 5- to 5/5 strength in the biceps, 4-/5 decreased strength in EHL,

10
The remaining references to Dr. Daniel are to Dr. Sara Daniel.
11
The only PT record from petitioner’s May 2017 hospitalization was an evaluation from May
11, 2017.

7
4/5 strength in the anterior tibialis, and good strength in the hamstrings and quadriceps. Id. Dr.
White’s impression was AIDP, but CIDP was to be ruled out over time. Id. He ordered
petitioner to follow up with him one week after discharge. Id.

Petitioner was discharged on May 16, 2017. Pet. Ex. 3 at 13. His discharge diagnosis
was GBS and proximal muscle weakness. Id. On discharge, petitioner could do a deep squat.
Id. “His hand grip strength [was] still quite weak but all other muscle groups [] improved
dramatically.” Id.

On May 23, 2017, petitioner saw Dr. White at The Clinic at UBMC (“UBMC”) for a
follow up examination after his hospitalization for GBS/AIDP. Pet. Ex. 6 at 29. In a
handwritten patient questionnaire, petitioner reported shortness of breath, loss of bladder control,
diarrhea, hopelessness, numbness, tingling or burning sensations, and weakness over the past six
months, as well as current aching pain in his calves. Id. at 26, 28. Petitioner reported that he did
not believe he was doing better, but Dr. White noted petitioner “[was] now able to do 13 squats
with no assistance and without difficulty.” Id. at 29. Petitioner was also “able to do 12 toe raises
before beginning to fatigue” and “duck walk normally on the right and with some drop in the
foot on the left.” Id. He had ongoing weakness in the EHL and anterior tibialis with a strength
at 5-/5, and “he ha[d] normal or near normal strength in the hamstrings, gluteus medius[,] and
quadriceps.” Id. Dr. White found petitioner “still ha[d] rather remarkable weakness in the hand
intrinsics,” but “show[ed] improved strength in the APB at 4 to 4+/5, wrist flexion and extension
[at] 4+/5, biceps and triceps [at] 4+ to 5-/5.” Id. Dr. White added that petitioner was able to
button up his pants, put on his shoes without assistance, and go fencing, although petitioner
reported “he gets short of breath easily.” Id. Petitioner believed his symptoms began
approximately May 6, 2017, “or perhaps a little earlier than that.” Id. Dr. White found
petitioner’s symptoms were “strongly suggestive of AIDP,” but CIDP remained a differential
diagnosis. Id. Dr. White ordered petitioner to return in 10 days. Id.

On June 2, 2017, petitioner visited Dr. White complaining of weakness. Pet. Ex. 3 at 2.
Petitioner’s bloodwork revealed a high erythrocyte sedimentation rate at 28 and a high
ceruloplasmin (“CP”) at 17 (range 0-15), and he tested negative for Lyme disease and
antinuclear antibodies. Id. at 3-5; Pet. Ex. 6 at 20-23. Physical examination found weakness in
hand intrinsics and APB. Pet. Ex. 6 at 13. Petitioner’s wrist flexion and extension strength were
4+/5, his biceps and triceps strength was 5-/5, his anterior tibialis strength was 5-/5, and he had
“near normal strength” in his hamstrings, gluteus medius, and quadriceps. Id. Dr. White also
conducted an electrodiagnostic study and needle EMG. Id. at 13-18. Under indication for study,
he noted that “[a]bout 4 weeks ago, [petitioner] developed diarrhea, 3 weeks ago he developed
weakness and was diagnosed with [GBS] (most likely AIDP).” Id. at 13. Dr. White found
petitioner’s medical history “quite classic for [GBS]; he had a bout of diarrhea and one week
later experienced significant weakness with suppressed reflexes.” Id. at 14. Petitioner’s
“electrodiagnostic parameters [] improved for the greater part (with the exception of the left
tibial motor amplitude, which [was] a little lower).” Id. Because the electrodiagnostic
examination that day revealed significant axonopathy in petitioner’s distal muscles, Dr. White

8
inquired whether petitioner had acute motor axonal neuropathy (“AMAN”) 12 or acute motor-
sensory axonal neuropathy (“AMSAN”). 13 Id. He opined that AMAN or AMSAN were “less
likely” because petitioner “had sensory involvement ruling out AMAN. Given his history and
features, [Dr. White] [was] most suspicious of AIDP with axonal involvement,” which petitioner
had “in the more distal muscles of both upper and lower extremities.” Id. at 14-15. Dr. White’s
impression was “[GBS] of the AIDP variety,” with an axonal component. Id. at 15. He noted
that “[t]he possibility of CIDP cannot entirely be ruled out at this point and time will reveal that
if it is present.” Id.

Petitioner next saw Dr. White on June 14, 2017. Pet. Ex. 6 at 11. Physical examination
revealed normal strength in the quadriceps, gluteus medius, hamstrings, and anterior tibialis
bilaterally. Id. Petitioner’s strength in hand intrinsics was 4/5, APB was 4/5, wrist flexors and
extensors were 4+/5, biceps and triceps were 5-/5, and external rotators were 5/5. Id. Dr.
White’s impression was “[GBS] (most likely AIDP) axonopathy noted distally in the upper and
lower extremities on EMG at 3 weeks. [Petitioner] [was] steadily progressing.” Id. Petitioner
was ordered to follow up in two weeks. Id.

On June 26, 2017, petitioner followed up with Dr. White at UBMC for his GBS. Pet. Ex.
6 at 9. Petitioner reported he was able to do 20 squats with no difficulty, but continued to have
ongoing weakness in his hands with symptoms he believed waxed and waned. Id. Physical
examination revealed strength of 5-/5 in his biceps, triceps, wrist flexors, and wrist extensors,
strength of 4+/5 in the long flexors of his fingers, and strength of 4/5 in hand intrinsics and APB.
Id. Dr. White’s impression was “[GBS] (most likely AIDP) with axonopathy noted distally in
the upper and lower extremities . . . . [Petitioner] has had a good response in the lower
extremities but ongoing weakness principally in the hands. Rule out CIDP.” Id. Petitioner was
to return in two weeks. Id.

Petitioner saw Dr. White at UBMC for a follow up examination for his GBS on July 12,
2017. Pet. Ex. 6 at 7. Petitioner reported he was continuing to improve, although “slower than
he would like.” Id. He could open the cap on a water bottle and squat 200 pounds. Id. Dr.
White’s physical examination found “ongoing weakness in the EHL bilaterally,” and normal
strength in the anterior tibialis, hamstrings, gluteus medius, and quadriceps. Id. Petitioner had
ongoing weakness in his hand intrinsics with a grip strength of 4/5, wrist extensors strength of 5-
/5, and wrist flexor strength of 4+/5. Id. Dr. White found petitioner’s bicep and tricep strength
good, but weak at 4+ to 5-/5. Id. Dr. White’s impression remained “[GBS] (most likely AIDP)
with axonopathy noted distally in upper and lower extremities.” Id. Petitioner was ordered to
return in one month. Id.

12
AMAN is “a subtype of [GBS] seen in China, caused by infection with [C. jejuni].” Acute
Motor Axonal Neuropathy, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/
dorland/definition? id=92651 (last visited Oct. 6, 2021).
13
AMSAN is “a rare subtype of [GBS] involving primarily large sensory nerve fibers in the
limbs, with paresthesias and weakness but not paralysis.” Acute Motor-Sensory Axonal
Neuropathy, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=92652 (last visited Oct. 6, 2021).

9
 Petitioner returned to Dr. White on August 9, 2017. Pet. Ex. 6 at 3. Petitioner reported
continued improvement but ongoing weakness with his grip. Id. Physical examination revealed
improving grip strength and hand intrinsic weakness. Id. Petitioner had normal strength in his
wrist flexors, wrist extensors, biceps, triceps, external rotators, anterior tibialis, hamstrings,
gluteus medius, and quadriceps. Id. Dr. White noted “ongoing neurogenic weakness in the right
greater than the left EHL.” Id. He added that “although [petitioner’s] strength is in the normal
range for age, he is probably weak relative to his prior condition.” Id. Dr. White’s impression
remained “[GBS], most likely of the AIDP variety, with axonopathy noted distally in the upper
and lower extremities,” and CIDP was to still be ruled out. Id. Dr. White directed petitioner to
return in one month. Id.

Between August 18 and September 20, 2017, petitioner completed five PT sessions with
Jerry Kulland. Pet. Ex. 2 at 2-9. Initial examination noted tightness, pain, and extreme weakness
in petitioner’s wrists and fingers, sharp pain that increases with activity, and a limitation in
carrying objects. Id. at 9. By his last visit on September 20, 2017, petitioner “report[ed] he
[was] doing good, getting better.” Id. at 4.

On September 11, 2017, petitioner visited UBMC to follow up with Dr. White. Pet. Ex. 6
at 1. Petitioner reported continued improvement. Id. His grip strength was at the low normal
range of 60 pounds (normal is 60-97 pounds for his age), but he had normal strength in his wrist
flexors, wrist extensors, biceps, and triceps. Id. He was weak in the hand intrinsics bilaterally
and “weak in the EHL bilaterally, but show[ed] good strength for the anterior tibialis,
hamstrings[,] [] gluteus medius[,] and quadriceps.” Id. Petitioner reported he was doing PT. Id.
Dr. White’s impression remained GBS, most likely AIDP, and he now included mild situational
depression. Id. Petitioner was instructed to return in one month. Id. at 2. Dr. White noted he
“may repeat electrodiagnostic studies thereafter depending on progress.” Id.

Petitioner next returned to Dr. White on December 13, 2017. Pet. Ex. 6 at 76. Petitioner
reported that his lower extremity strength is good, however his upper extremity strength was not
satisfactory. Id. Physical examination revealed “slightly decreased” strength in hand intrinsics,
APB, wrist flexors and extensors, biceps, and triceps. Id. Dr. White noted that “while
[petitioner’s] strength is within the normal range for a man his age, it is decreased relative to his
prior history.” Id. Dr. White’s impression remained GBS, most likely AIDP. Id.

On January 10, 2018, petitioner presented for follow-up examination and for
electrodiagnostic studies. Pet. Ex. 6 at 59-64. “[Petitioner] ha[d] a history of acute weakness
coming in early May of 2017 and occurring 3 weeks after stepping on a wire, receiving a [Tdap]
shot and developing diarrhea (he also had a [Prevnar 13] vaccine at that time).” Id. at 59. Dr.
White documented that petitioner’s symptoms had not relapsed. Id. Petitioner “complain[ed] of
ongoing weakness primarily in the upper extremities.” Id. Physical examination revealed
“slightly decreased” strength in hand intrinsics, APB, wrist flexors and extensors, biceps, and
triceps. Id. Dr. White found petitioner’s history and electrodiagnostic studies consistent with
GBS. Id. at 60. Also, petitioner’s “electrodiagnostic parameters [were] improving over time, as
[was] his strength. [Petitioner] has not had episodes of relapse and his strength ha[d] been
steadily recovering.” Id. Dr. White opined petitioner’s “persistent weakness [was] secondary to

10
the axonal nature of his condition and the overall trend continue[ed] to be one of improvement.”
Id. Petitioner was directed to return in three weeks. Id.

Petitioner saw Dr. White on January 29, 2018. Pet. Ex. 6 at 54. On a handwritten
document, petitioner indicated his pain was “about the same” since his last visit and he noted
aching pain in his calves. Id. at 53. Petitioner complained of fatigue. Id. at 54. Dr. White
indicated petitioner’s clinical course was “most strongly reminiscent of AMSAN.” Id.

No additional medical records have been filed.

2. Petitioner’s Affidavit

On April 26, 2017, after stepping on a rusty nail, petitioner went to Basin Clinic and
received a Tdap vaccination in his right arm. Pet. Ex. 7 at ¶ 1. At that visit, he made an
appointment for a routine physical examination, which occurred two days later on April 28,
2017. Id. At his April 28, 2017 visit, he received a Prevnar vaccination and completed blood
work. Id. His examination found “elevated cholesterol and itchy legs due to varicose veins.” Id.
He averred that “[he] was in great physical health. [He] routinely enjoyed activities such as
water skiing with one board, riding horses, and cutting [his] own firewood.” Id.

“By early May, [he] began feeling sick with aches and pains.” Pet. Ex. 7 at ¶ 2. He
stated his doctor told him he had the flu. Id. He continued to get worse and had “severe muscle
aches and loss of energy.” Id. By the morning of May 11, 2017, “[he] could no longer take the
pain” and went to the ER. Id. He was admitted to the hospital, and after electrodiagnostic
studies and a lumbar puncture, he was told he had GBS. Id. While in the hospital receiving
IVIG treatments, “[he] experienced sharp pains in [his] arms and legs” and “had aching and
numbness.” Id.

Since discharge, he stated he has had a difficult time at home. Pet. Ex. 7 at ¶ 3. “Just
waking up required an exceptional amount of energy that resulted in severe aches and pains.
[He] had very little strength in [his] arms and hands,” he “had difficulty picking up items,” he
“frequently dropped things,” and he could not zip or snap his pants or open water bottles without
assistance. Id. He became severely depressed. Id. He “was unable to perform [his] usual
activities.” Id. Before his GBS diagnosis, he was active and strong, and “enjoyed activities like
riding horses, fixing [his] fencing, hauling hay, starting [his] lawn mower, cutting firewood,
running power tools, water skiing, dancing, and pulling weeds in [his] garden.” Id. However,
after developing GBS, he “wasn’t even strong enough to pick up [his] eight-month-old
granddaughter.” Id.

As of February 13, 2018, the day in which he executed his affidavit, he was still unable to
do certain activities. Pet. Ex. 7 at ¶ 4. He could not ride a horse and had difficulty getting into a
truck. Id. He continued to suffer from aches and numbness, as well as pain in his muscles and
hands. Id. “The back of [his] legs tire easily.” Id.

11
 D. Expert Reports

1. Petitioner’s Expert, Dr. John R. Rinker

a. Background and Qualifications

Dr. Rinker is a board-certified neurologist with a subspeciality in neuroimmunology. Pet.
Ex. 9 at 1; Pet. Ex. 10 at 2. He received his M.D. from Medical College of Georgia in 2001. Pet.
Ex. 10 at 2. Thereafter, he went to Washington University School of Medicine in St. Louis,
Missouri for his internship, neurology residency, and additional postdoctoral training. Id. Dr.
Rinker currently works as an Associate Professor of Neurology at the University of Alabama,
Birmingham. Id.; Pet. Ex. 9 at 1. His “practice consists primarily of diagnosing and caring for
patients with noninfectious, immune-mediated disorders of the nervous system.” Pet. Ex. 9 at 1.
He has “experience caring for patients with conditions presumed to have been triggered or
aggravated by vaccines, including GBS, Acute Disseminated Encephalomyelitis (ADEM), and
Susac’s syndrome.” Id. Dr. Rinker is a member of various professional societies, councils,
committees, and editorial boards, has given numerous lectures, and has authored or co-authored
over 30 articles. Pet. Ex. 10 at 3-4, 8-9, 13-16.

b. Opinion

i. Althen Prong One

Dr. Rinker opined that vaccines can cause GBS through the mechanism of molecular
mimicry. Pet. Ex. 9 at 4. Dr. Rinker explained that when a person typically encounters a foreign
agent, their adaptive immune system distinguishes foreign antigens from the host; however, in
rare circumstances, “an infection or vaccination may inadvertently provoke the host to mount an
immune response directed against self-antigens which can result in immune-mediated harm to
otherwise healthy tissues.” Id.

Quoting Tishler and Shoenfeld, 14 Dr. Rinker explained that with molecular mimicry,
“antigenic determinants of the microorganisms are recognized by the host’s immune system as
similar to its own antigenic determinants and, because of the structural resemblance, antibodies
and auto-reactive T cells[15] not only destroy the invading pathogen but can react with host
tissues as well.” Pet. Ex. 9 at 4 (quoting Pet. Ex. 37 at 3). Tishler and Shoenfeld further wrote
that “[a]ccording to the mimicry hypothesis, it is possible that any microorganism that expresses

14
Moshe Tishler & Yehuda Shoenfeld, Vaccines and Autoimmunity, in The Autoimmune
Diseases 309 (Noel R. Rose & Ian R. Mackay eds., 4th ed. 2006).
15
T cells, or lymphocytes, are “cells primarily responsible for cell-mediated immunity.” T
Lymphocytes, Dorland’s Online Med. Dictionary, https://www.dorlandsonline.com/dorland/
definition?id=87562 (last visited Oct. 15, 2021). “When activated by antigen, T lymphocytes
proliferate and differentiate into T memory cells and the various types of regulatory and effector
T cells.” Id. Adaptive, not innate, immunity is “mediated by B and T lymphocytes following
exposure to a specific antigen.” Illustrated Dictionary of Immunology 18 (3d ed. 2009).

12
an epitope which could serve as a molecular mimic for an autoantigen could induce autoimmune
disease.” Pet. Ex. 37 at 3.

Dr. Rinker added that vaccination can lead to GBS through molecular mimicry depending
on the presentation of foreign antigens. Pet. Ex. 9 at 4. With GBS, “the immune system mounts
an antigen-specific response against peripheral myelin gangliosides.” Id. at 3. “[A]ntigen
presenting cells ingest and process foreign proteins and molecules and present them in the
context of molecules called Human Leukocyte Antigens (HLA).” Id. at 4-5. These “molecules
are responsible for presenting foreign antigen[s] to immune cells, such as T cells, which in turn
coordinate the immune response against the foreign agent.” Id. at 5.

He cited various articles discussing how molecular mimicry can lead to GBS through
various triggers including vaccination and infection. See, e.g., Pet. Ex. 12 at 4-5, 6 fig.2
(infection); 16 Pet. Ex. 14 at 5 (infection); 17 Pet. Ex. 22 at 4 (vaccination); 18 Pet. Ex. 23 at 21-25
(vaccination). 19 These articles describe molecular mimicry and the pathogenesis of GBS. See
also Pet. Ex. 26 at 2 (“Molecular mimicry . . . [is] involved in the pathogenesis of GBS . . . .”). 20
These articles also note that molecular mimicry is thought to be the same mechanism at play for
GBS post-C. jejuni. See, e.g., Pet. Ex. 12 at 4-5, 6 fig.2; Pet. Ex. 14 at 5; Pet. Ex. 26 at 3 fig.2.

Dr. Rinker acknowledged that two-thirds of GBS cases are preceded by an infection or
illness, most commonly respiratory or diarrheal, within 4 weeks of onset. Pet. Ex. 9 at 3 (citing,
e.g., Pet. Ex. 14 at 1). He agreed that C. jejuni is the most common infectious trigger of GBS,
and noted that according to Jasti et al., 21 “less than 0.1% of C. jejuni infections result in a case of
GBS, suggesting that even though C. jejuni possesses immunological characteristics favorable to
the development of GBS, the syndrome itself develops rarely.” Id. at 5 (citing Pet. Ex. 39 at 10).
Thus, he argued that “the rarity with which GBS occurs even following exposures to known
triggers of the condition, should allow for the possibility that sporadic cases of GBS may occur

16
John A. Goodfellow & Hugh J. Willison, Guillain-Barré Syndrome: A Century of Progress, 12
Nature Revs. Neurology 723 (2016).
17
B.C. Jacobs et al., The Spectrum of Antecedent Infections in Guillain-Barré Syndrome: A
Case Control Study, 51 Neurology 1110 (1998).
18
Nizar Souayah et al., Guillain-Barré Syndrome After Vaccination in United States: Data from
the Centers for Disease Control and Prevention/Food and Drug Administration Vaccine Adverse
Even Reporting System (1990-2005), 11 Neuromuscular Disease 1 (2009).
19
Inst. of Med., Diphtheria and Tetanus Toxoids, in Adverse Events Associated with Childhood
Vaccines: Evidence Bearing on Causality 67 (Kathleen Stratton et al. eds., 1994).
20
Bianca van den Berg et al., Guillain-Barré Syndrome: Pathogenesis, Diagnosis, Treatment and
Prognosis, 10 Nature Revs. Neurology 469 (2014).
21
Anil K. Jasti et al., Guillain-Barré Syndrome: Causes, Immunopathogenic Mechanisms and
Treatment, 12 Expert Rev. Clinical Immunology 1175 (2016).

13
following other immunological stimuli.” Id.; see also Pet. Ex. 39 at 10 (“[W]e are convinced that
GBS, similar to other inflammatory diseases, is the result of a permissive genetic background on
which environmental factors, including infections, vaccination, and the influence of aging, lead
to disease onset and the natural history of disease.”).

Further, Dr. Rinker argued that vaccinations have also been implicated as triggering
GBS. Pet. Ex. 9 at 3, 5; see, e.g., Pet. Ex. 21 at 1. 22 He cited to Schonberger et al. 23 and Salmon
et al. 24 to demonstrate how the flu vaccine has been noted to cause GBS. Pet. Ex. 9 at 3. In
Schonberger et al., the authors looked at 1,098 patients who developed GBS between October 1,
1976 and January 31, 1977 and found 532 of the patients received a A/New Jersey flu
vaccination prior to onset of GBS. Pet. Ex. 42 at 1-2, 5. The data suggested there was “strong
evidence . . . that A/New Jersey flu vaccination incited the onset of GBS in many adult
vaccinees.” Id. at 16. Similarly, Salmon et al. found a small increased risk of GBS after the flu
A (H1N1) 2009 monovalent inactivated vaccine. Pet. Ex. 17 at 6.

Souayah et al. examined reports of GBS following vaccination in the Vaccine Adverse
Event Reporting System (“VAERS”) from 1990 to 2005. Pet. Ex. 22 at 1. Because studies
showed an increased risk of GBS within six weeks after vaccination, the authors considered such
cases suggestive of causal association. Id. at 2. The authors found 1,000 cases of GBS reported
after vaccination, 773 of which were within six weeks of vaccination. Id. Of those 773 cases,
511 cases (the most common) were after flu vaccination, while 28 (the third-most common) were
after tetanus and diphtheria toxoid vaccination and 14 were after a pneumococcal polyvalent
vaccination. Id. at 2-3, 2 tbl.1. Additionally, 103 of the 773 cases were after a combination of
two or more vaccines that were not specified. Id. They found “GBS is more strongly associated
with vaccination for [flu] than for vaccination for other diseases. However, it is also apparent
that [flu] vaccine is not the only one that presents a risk.” Id. at 4. The study suggested that
vaccines other than the flu vaccine can be associated with GBS. Id. at 5. The authors
hypothesized that “GBS observed after vaccination may arise by [] molecular mimicry.” Id. at 4.
They acknowledged that their study had limitations, in part, due to the nature of VAERS. 25 Id. at
5.

22
Valérie Sivadon-Tardy et al., Guillain-Barré Syndrome and Influenza Virus Infection, 48
Clinical Infectious Diseases 48 (2009).
23
Lawrence B. Schonberger et al., Guillain-Barré Syndrome Following Vaccination in the
National Influenza Immunization Program, United States, 1976-1977, 110 Am. J. Epidemiology
105 (1979). This article was also cited by Dr. Chaudhry, respondent’s expert. See Resp. Ex. C,
Tab 19.
24
Daniel A. Salmon et al., Association Between Guillain-Barré Syndrome and Influenza A
(H1N1) 2009 Monovalent Inactivated Vaccines in the USA: A Meta-Analysis, 381 Lancet 1461
(2013).
25
The authors explained that VAERS, a passive surveillance system, “may be subject to
underreporting, differential reporting, ascertainment bias, and variability in report quality and
completeness.” Pet. Ex. 22 at 5.

14
 Using the Souayah et al. article for support, Dr. Rinker opined that the Tdap vaccine can
cause GBS via molecular mimicry. 26 He also cited to a report issued in 1994 by the Institute of
Medicine (“IOM”), now the National Academy of Medicine, who concluded that “[the] evidence
favor[ed] a causal relation between vaccines containing tetanus toxoid (DT and Td) and GBS.”
Pet. Ex. 23 at 24. The IOM relied heavily on a case report by Pollard and Selby 27 of a 42-year-
old patient who suffered three episodes of a demyelinating neuropathy, 21, 14, and 10 days
following tetanus toxoid vaccinations, over a 14 years. Id. at 22-24; see Resp. Ex. A, Tab 17.
Respondent’s experts argued that the 1994 IOM report was outdated and superseded by a report
from 2012. However, Dr. Rinker did not discuss or cite to the 2012 report.

Another article cited by Dr. Rinker was Baxter et al., 28 which evaluated the relationship
between GBS and vaccinations using retrospective data from Kaiser Permanente of Northern
California from 1994 to October 2006. Pet. Ex. 30 at 2. Of the 896 potential cases of GBS, the
authors included 415 in their study. 29 Id. at 3. In the 90 days preceding GBS onset, 277 (66.7%)
cases had a respiratory or gastrointestinal (“GI”) illness, 159 of which (38.3%) were respiratory,
77 (18.6%) were GI, and 41 (9.9%) were both. Id. at 4. Twenty-five of the 415 patients received
a vaccine in the six weeks prior to GBS onset. Id. One received a Tdap vaccine, three 30 received
a tetanus-diphtheria vaccine, and two received a 23-valent pneumococcal polysaccharide
vaccine. 31 Id. at 5 tbl.1. The authors found “no evidence of an increased risk of GBS following
any vaccination, as well as all vaccinations combined;” however, they concluded that they were
“unable to exclude any possible association between vaccines and GBS.” Id. at 5, 7.

For further support, Dr. Rinker cited to various case reports discussing incidents of GBS
following a vaccines containing tetanus. In Newton and Janati, 32 for example, a 47-year-old man
received a pure tetanus toxoid vaccine and developed numbness and weakness in both legs and

26
Although Dr. Rinker noted petitioner’s Prevnar 13 vaccination as a potential trigger of
petitioner’s GBS, he did not opine as to how the Prevnar 13 vaccine specifically can cause GBS.
27
J. D. Pollard & G. Selby, Relapsing Neuropathy Due to Tetanus Toxoid: Report of a Case, 37
J. Neurological Scis. 113 (1978). Petitioner did not file this article.
28
Roger Baxter et al., Lack of Association of Guillain-Barré Syndrome with Vaccinations, 57
Clinical Infectious Diseases 197 (2013). This article was also cited to and discussed by
respondent’s experts. See Resp. Ex. A, Tab 16; Resp. Ex. C, Tab 11.
29
Patients were excluded for various reasons including a lack of or insufficient medical records,
subsequent diagnosis of CIDP, and a diagnosis of the Miller Fisher variant of GBS. Pet. Ex. 30
at 2-3.
30
One of these patients also received a flu vaccine. Pet. Ex. 30 at 5 tbl.1.
31
This is not the pneumococcal vaccine petitioner received.
32
Norris Newton & Abdorassol Janati, Guillain-Barré Syndrome After Vaccination with Purified
Tetanus Toxoid, 80 S. Med. J. 1053 (1987).

15
arms nine days later. Pet. Ex. 40 at 1. There was no prior history of infection, and no adverse
reaction was noted following his prior tetanus vaccination. Id. “Immunologic studies showed a
hypersensitivity to tetanus antigen.” Id. at 1. Instead of molecular mimicry, the authors opined
that the patient’s GBS “appear[ed] to be an example of an autosensitivity disease in which the
mechanisms of delayed T cell hypersensitivity predominate.” Id.

In Ammar, 33 a 40-year-old man received a Tdap vaccine, and within one to two weeks,
he developed weakness and numbness in his legs and was subsequently diagnosed with GBS.
Pet. Ex. 28 at 1-2. Ammar noted the patient did not have diarrhea, fever, cough, or chills in the
weeks preceding his illness, and the Tdap vaccination was the only recognized antecedent event.
Id. at 2.

Bakshi and Graves 34 examined a 22-year old male who received a tetanus-diphtheria
toxoid vaccination and developed bilateral tingling of the fingertips and toes four days later,
which progressed to progressive proximal leg weakness over the following few days. Pet. Ex. 29
at 1. He was admitted to the hospital seven days after vaccination and diagnosed with GBS. Id.
at 1-2. Although C. jejuni testing was not performed, he denied antecedent illness in the six
months prior, and the authors noted no antecedent factors other than vaccination were identified
as potential triggers. Id. Given other cases that reported GBS after tetanus toxoid vaccination,
the authors “suspect[ed] that the tetanus portion of the vaccination produced the GBS,” but
acknowledged they could not provide proof. Id. They were also “unable to exclude that the
GBS was secondary to the diphtheria portion of the vaccination or simply represented a
coincidental occurrence.” Id. The authors concluded “that the benefits of prevention of tetanus
and diphtheria infection far outweigh the risk of GBS.” Id.

Dr. Rinker concluded that the Tdap vaccine can cause GBS “[b]ased on case reports
attesting to the possible causative relationship between tetanus vaccine and GBS, caution from
the IOM about causative association between tetanus vaccines and GBS, and the biological
plausibility of an idiosyncratic, immune-mediated reaction to Tdap causing GBS.” Pet. Ex. 9 at 7.

ii. Althen Prong Two

Dr. Rinker opined that more likely than not, petitioner’s Tdap vaccination caused him to
develop GBS through the mechanism of molecular mimicry. Pet. Ex. 9 at 4, 7. He explained
that petitioner’s April 26, 2017 Tdap vaccine “triggered an idiosyncratic reaction in which his
immune system mounted an autoimmune response directed towards peripheral myelin in his
body.” Id. at 6.

Dr. Rinker explained that petitioner had two potential triggers that preceded the onset of
his GBS: (1) a Tdap vaccination on April 26, 2017 and a Prevnar vaccination on April 28, 2017

33
Hussam Ammar, Guillain-Barré Syndrome After Tetanus Toxoid, Reduced Diphtheria Toxoid
and Acellular Pertussis Vaccine: A Case Report, 5 J. Med. Case Reps. 502 (2011).
34
Rohit Bakshi & Michael C. Graves, Guillain-Barré Syndrome After Combined Tetanus-
Diphtheria Toxoid Vaccination, 147 J. Neurological Scis. 201 (1997).

16
and (2) a diarrheal illness that began on or around May 1, 2017. Pet. Ex. 9 at 2, 4. He opined
that “it is not possible to distinguish whether vaccination or the diarrheal illness alone was
responsible for his GBS, or whether the two immunological stimuli worked in concert to provoke
the immune response.” Id. at 6.

He argued there is insufficient evidence to claim that the diarrheal illness was a more
likely cause of petitioner’s GBS than the Tdap vaccine. Pet. Ex. 9 at 6. In support, Dr. Rinker
noted no microbiological tests were performed to identify a specific organism. Id. In his
supplemental report, he argued that “while [petitioner] may have been affected by C. jejuni in the
days leading up to the onset of his GBS, there [was] no confirmatory laboratory evidence to
support this possibility as the organism was never identified, despite testing.” 35 Pet. Ex. 31 at 1.

Next, he opined “it is possible” the diarrheal illness was not infectious, as “many
transient diarrheal illnesses are caused by toxins produced by bacterial contaminants of food,
rather than the bacteria directly, which are self-limited and resolve without inciting a significant
immune response.” Pet. Ex. 9 at 6.

Lastly, he added that “there are many other potential causes of gastroenteritis that could
have produced [petitioner’s] symptoms” since such illnesses are common, and their causes are
rarely identified. Pet. Ex. 31 at 1. Dr. Rinker stated that according to the CDC, “only 0.2 to 1.7
in every 1,000 diagnosed and undiagnosed Campylobacter illnesses leads to GBS, but [the CDC]
estimates Campylobacter are responsible for 5-41% of GBS illnesses.” Pet. Ex. 34 at 1.
Additionally, the CDC’s Tdap Vaccine Information Statement 36 lists diarrhea as a possible
adverse reaction. Pet. Ex. 33 at 2. However, Dr. Rinker acknowledged that he was unable to
find medical literature to support the time period over which post-vaccination diarrhea may be
expected to occur. Pet. Ex. 31 at 1-2.

Dr. Rinker opined that petitioner’s Tdap vaccine, and not the diarrheal illness, was the
more likely cause of petitioner’s GBS. Pet. Ex. 31 at 1; Pet. Ex. 9 at 6-7. First, as explained in
more detail in the following section, he opined that the latency period between vaccination and
onset (9 to 10 days) and diarrhea and onset (4 to 5 days) “favors the vaccine as the more likely
cause.” Pet. Ex. 9 at 6-7. Next, he noted there was insufficient evidence to support Dr.
Chaudhry’s opinion that petitioner’s diarrheal illness was the immunological trigger when (1) C.
jejuni is an uncommon cause of gastroenteritis and (2) there was nothing in the record linking C.
jejuni to petitioner’s GBS. Pet. Ex. 31 at 2. Dr. Rinker found that “the mere presence of
diarrhea before the onset of GBS, especially when C. jejuni was never identified, provides an
unlikely cause of [petitioner’s] GBS in comparison to the Tdap vaccination.” Id.

35
After a review of the records, it does not appear that testing was done for C. jejuni or any
related organisms. Additionally, in Dr. Rinker’s first expert report, he noted “no microbiological
reports were available.” Pet. Ex. 9 at 6. It is not clear why Dr. Rinker notes testing was done in
his supplemental report.
36
Vaccine Information Statement, Tdap (Tetanus, Diphtheria, Pertussis) Vaccine: What You
Need to Know, Ctrs. for Disease Control & Prevention, https://www.cdc.gov/vaccines/hcp/vis/
vis-statements/tdap.html (last reviewed Apr. 1, 2020).

17
 Dr. Rinker concluded that “[a]lthough documented cases of GBS following tetanus
vaccination are rare, the biological plausibility of GBS following vaccination, and the multiple
published case reports describing GBS following administration of tetanus vaccine, fit the
definition of an idiosyncratic response to tetanus vaccination.” Pet. Ex. 9 at 6. Thus, petitioner
“more likely than not developed GBS as a consequence of his Tdap vaccination.” Id. at 7.

iii. Althen Prong Three

With regard to timing, Dr. Rinker opined an “autoimmune response generated by an
immunization is mediated by the adaptive immune system, which develops over a period of
weeks following antigen exposure.” Pet. Ex. 9 at 6. Such adaptive immune responses increase
between 7 and 14 days following vaccination, “depending on whether the immunization is a
primary or secondary exposure.” Id. at 7. Citing Siegrist, 37 Dr. Rinker opined that “[s]ubsequent
encounters with a foreign antigen typically result in more rapid adaptive immune response than
an initial encounter.” Id. (citing Pet. Ex. 20 at 9 fig.2.3).

Here, Dr. Rinker opined petitioner’s onset was on May 5 or 6, 2017, or 9 to 10 days
following petitioner’s vaccinations, which he found was within the appropriate time frame. Pet.
Ex. 9 at 2, 7. Although petitioner’s diarrheal illness preceded the onset of his GBS by 4 to 5
days, Dr. Rinker opined that “[t]his time course [was] well below the median latency for C.
jejuni infection.” Id. at 6; see also Pet. Ex. 32 at 2 (noting “neurological symptoms of GBS that
follow C. jejuni infection typically occur 1-3 weeks after the onset of diarrheal illness”); 38 Pet.
Ex. 34 at 1 (noting the incubation period of a Campylobacter infection is typically two to five
days). He concluded that “the timing of GBS onset argues more strongly in favor of the vaccine
as the causative immune stimulus rather than the diarrheal illness.” Id. at 7.

He cited various articles that examined the timing between an antecedent immunological
trigger and onset of GBS. First, Dr. Rinker cited Sivadon-Tardy et al., who examined 405
patients with GBS admitted to a French reference center between 1996 and 2004. Pet. Ex. 21 at
1. Of the 405 patients, a causing agent could not be identified in 234 patients (58%) while an
identified cause was found in 171 patients (42%). Id. at 3. They found the median latency
period between flu A and C. jejuni infections and GBS were 15 and 10 days, respectively, while
the median latency period for unidentified causes was 6.5 days. Id. at 8 tbl.2. Of the 14 patients
with evidence of a flu A or B infection prior to onset, one received the flu vaccine 15 days prior
to onset. Id. at 4, 5 tbl.1.

Of the 532 patients in Schonberger et al. who received a flu vaccination prior to onset of
GBS, 71% developed GBS within four weeks after vaccination, with 53% developing GBS in the
second and third weeks after vaccination. Pet. Ex. 42 at 6. They found the largest percentage of
cases (10%) occurred 16 and 17 days post-vaccination. Id. at 6-7, 7 fig.5. Similarly, Souayah et

37
Claire-Anne Siegrist, Vaccine Immunology, in Plotkin’s Vaccines 16 (7th ed. 2017).
38
Ban Mishu Allos, Campylobacter Jejuni Infections: Update on Emerging Issues and Trends,
32 Clinical Infectious Diseases 1201 (2001).

18
al. found an onset peak in the first two weeks after any vaccination, including after tetanus and
diphtheria toxoids and pneumococcal polyvalent vaccine. Pet. Ex. 22 at 3-4.

With regard to tetanus-containing vaccines specifically, Ammar discussed a 40-year-old
man who received a Tdap vaccine, and developed GBS within one to two weeks. Pet. Ex. 28 at
1-2. Bakshi and Graves found a patient with a GBS onset of four days post-tetanus-diphtheria
toxoid vaccination. Pet. Ex. 29 at 1. The patient in Pollard and Selby suffered three episodes of
a demyelinating neuropathy, 21, 14, and 10 days following tetanus toxoid vaccination. Resp. Ex.
A, Tab 17. The patient in Newton and Janati developed GBS nine days after a pure tetanus
toxoid vaccine. Pet. Ex. 40 at 1. Lastly, Baxter et al. found one patient who received a Tdap
vaccine and had an onset of GBS 45 days after vaccination, while three 39 patients received a
tetanus-diphtheria vaccine and their onsets were eight, 12, and 41 days after vaccination. Pet.
Ex. 30 at 5 tbl.1.

Baxter also noted two cases of GBS following a 23-valent pneumococcal polysaccharide
vaccine, 40 with onsets of one day and 14 days. Pet. Ex. 30 at 5 tbl.1. The patient with a 14-day
onset also received a flu vaccine, an inactivated (killed) polio vaccine, and a Japanese
encephalitis vaccine. Id.

2. Respondent’s Expert, Dr. J. Lindsay Whitton

a. Background and Qualifications

Dr. J. Lindsay Whitton received his B.Sc. in molecular biology, his M.B., Ch.B. in
medicine, and his Ph.D. in herpesvirus transcription from the University of Glasgow in Scotland.
Resp. Ex. B at 1. He also completed internships in medicine and surgery, and held various
professor positions since 1986. Resp. Ex. A at 1; Resp. Ex. B at 1. He is currently a Professor in
the Department of Immunology and Microbiology at Scripps Research Institute in California.
Resp. Ex. B at 1. Dr. Whitton is a member of various professional societies and editorial boards.
Id. He has authored or co-authored almost 200 publications. Id. at 2-15.

b. Opinion

i. Althen Prong One

Dr. Whitton opined that the evidence does not support Dr. Rinker’s contention that the
Tdap vaccine 41 can cause GBS through molecular mimicry. Resp. Ex. A at 7. Instead, “it is
well-established that a recent GI infection can incite GBS.” Id. at 12.

39
One of these patients also received a flu vaccine. Pet. Ex. 30 at 5 tbl.1.
40
This is not the pneumococcal vaccine that petitioner received.
41
Because the petition and Dr. Rinker focus solely on the Tdap vaccine, Dr. Whitton does not
discuss the Prevnar vaccine in his expert report. Resp. Ex. A at 1.

19
 He opined that GBS is an autoimmune disease thought to be triggered by molecular
mimicry. Resp. Ex. A at 3; see also Resp. Ex. A, Tab 6 at 1-3 (“Molecular mimicry of pathogen-
borne antigens, leading to generation of crossreactive antibodies that also target gangliosides, is
part of the pathogenesis of GBS.”). 42 He agreed that two-thirds of cases are “preceded by signs
and/or symptoms of an infection, often of the respiratory or GI tracts,” within the four weeks
prior to onset of GBS. Resp. Ex. A at 4; see also Resp. Ex. A, Tab 1 at 2; 43 Resp. Ex. A, Tab 2
at 2; 44 Resp. Ex. A, Tab 5 at 3. 45

Dr. Whitton explained that infectious diseases have an incubation period prior to the
presence of symptoms, while vaccinations do not. Resp. Ex. A at 4. Therefore, an adaptive
immune response can begin a few days after an infection has begun, but before any symptoms of
such infection have appeared. Id. at 5. Because it is the infection and not the illness (symptoms)
that trigger the adaptive immune response, this incubation period “makes it almost impossible to
know exactly when the immune system was first triggered by an infection.” Id. at 5, 10.

Dr. Whitton opined that several studies have failed to support a causal association
between tetanus vaccines and GBS. Resp. Ex. A at 6-7. First, he cited Tuttle et al., 46 a 1997
report on two active surveillance studies examining whether tetanus-toxoid-containing vaccines
can cause GBS. Resp. Ex. A, Tab 11 at 1. Of the 213 adult cases and 93 children cases of GBS,
the authors found only one adult and two children who developed GBS within six weeks of a
tetanus-containing vaccine. Id. at 2-3. They concluded there was “no association of public
health significance [] between tetanus-toxoid-containing vaccine and [GBS].” Id. at 4.

Next, Dr. Whitton cited a letter from Nordin et al. 47 regarding Tdap and GBS. Resp. Ex.
A, Tab 13 at 1. This letter discussed active surveillance results on the safety of the Tdap vaccine
from a prior study 48 of 660,245 doses administered. Id. The authors re-examined the data after

42
Bianca van den Berg et al., Guillain-Barré Syndrome: Pathogenesis, Diagnosis, Treatment and
Prognosis, 10 Nature Revs. Neurology 469 (2014).
43
Pieter A. van Doorn et al., Clinical Features, Pathogenesis, and Treatment of Guillain-Barré
Syndrome, 7 Lancet Neurology 939 (2008).
44
Hugh J. Willison, The Immunobiology of Guillain-Barré Syndromes, 10 J. Peripheral Nervous
Sys. 94 (2005).
45
Richard A. C. Hughes & Jeremy H. Rees, Clinical and Epidemiologic Feature of Guillain-
Barré Syndrome, 176 J. Infectious Diseases S92 (1997).
46
Jessica Tuttle et al., The Risk of Guillain-Barré Syndrome After Tetanus-Toxoid Containing
Vaccines in Adults and Children in the United States, 87 Am. J. Public Health 2045 (1997). This
article was also cited by Dr. Chaudhry. See Resp. Ex. C, Tab 13.
47
James D. Nordin et al., Tdap and GBS Letter, 29 Vaccine 1122 (2011).
48
The original study was not filed.

20
reaching two million doses in the Vaccine Safety Datalink from 2005 to 2009. Id. After looking
at patients who received a Tdap vaccine in the 42 days prior to onset of GBS, they “conclude[d]
that there is no evidence that Tdap is associated with an increased risk of GBS within 6 weeks of
vaccination.” Id.

He also cited to Kuitwaard et al. 49 and Baxter et al., 50 articles that focused on the risk of
GBS recurrence after vaccination, especially flu vaccination. Resp. Ex. A, Tab 12; Resp. Ex. A,
Tab 14. Of the 245 patients with GBS and 76 patients with CIDP in Kuitwaard et al., 51 23 GBS
and eight CIDP patients reported a vaccination in the eight weeks preceding onset. Resp. Ex. A,
Tab 12 at 3. The preceding vaccination in 3% was tetanus, while 7% received multiple
unidentified vaccinations. Id. at 2 fig.1. In both articles, the authors found no cases of recurrent
GBS after vaccination. Id. at 1; Resp. Ex. A, Tab 14 at 1.

However, Dr. Whitton cited literature acknowledging that vaccinations have been
suggested to be associated with GBS. See, e.g., Resp. Ex. A, Tab 1 at 3; Resp. Ex. A, Tab 2 at 4;
Resp. Ex. A, Tab 3 at 7; 52 Resp. Ex. A, Tab 6 at 3-4; Resp. Ex. A, Tab 14 at 1.

With regard to the case reports Dr. Rinker cited to support his theory, Dr. Whitton opined
case reports are unreliable and “cannot be used to imply causality.” Resp. Ex. A at 7. He argued
Dr. Rinker’s reliance on Souayah et al. and VAERS, like case reports, is misplaced because
VAERS reports cannot prove causation. Id. at 9.

Dr. Whitton also criticized Dr. Rinker’s use of outdated reports and recommendations,
including the 1994 IOM report. Resp. Ex. A at 8. Dr. Whitton stated that (1) the vaccine at issue
in the case was not licensed until 2005 and thus, was not considered by the 1994 report, and (2)
the 2012 IOM report 53 superseded the 1994 report. Id. In particular, the 2012 IOM report found
“[t]he evidence [was] inadequate to accept or reject a causal relationship between diphtheria
toxoid-, tetanus toxoid-, or acellular pertussis-containing vaccines and GBS,” as well as CIDP.
Resp. Ex. A, Tab 15 at 35, 37. Additionally, the 2012 report noted the patient in Pollard and

49
Krista Kuitwaard et al., Recurrences, Vaccinations and Long-Term Symptoms in GBS and
CIDP, 14 J. Peripheral Nervous Sys. 310 (2009).
50
Roger Baxter et al., Recurrent Guillain-Barré Syndrome Following Vaccination, 54 Clinical
Infectious Diseases 800 (2012).
51
These patients were all members of the Dutch society of neuromuscular disorders who
received and returned a questionnaire. Resp. Ex. A, Tab 12 at 1.
52
Clarence C. Tam et al., Influenza, Campylobacter and Mycoplasma Infections, and Hospital
Admissions for Guillain-Barré Syndrome, England, 12 Emerging Infectious Diseases 1880
(2006).
53
Inst. of Med., Diphtheria Toxoid-, Tetanus Toxoid-, and Acellular Pertussis-Containing
Vaccines, in Adverse Effects of Vaccines: Evidence and Causality 525 (Kathleen Stratton et al.
eds., 2012).

21
Selby was “subsequently diagnosed with a spontaneously relapsing remitting neuropathy” after
the patient “developed symptoms in association with acute viral infections.” Id. at 36. The IOM
noted “the authors did not rule out other possible causes and did not provide evidence beyond a
temporal relationship with vaccine administration.” Id. at 36-37. Therefore, they found the
patient’s “spontaneous development of peripheral neuropathy [made] it difficult to conclude that
the tetanus toxoid vaccines were the causative agent.” Id. at 37.

ii. Althen Prong Two

Dr. Whitton agreed that there are two proposed causes for petitioner’s GBS: (1) GI
infection and (2) Tdap vaccination. Resp. Ex. A at 11. He found a GI infection is a known
trigger of GBS, while Tdap vaccination is not. Id. He opined that petitioner’s GI infection, not
his diarrheal symptoms or Tdap vaccination, initiated the adaptive immune response that may
have caused petitioner’s GBS, and thus, “the GI infection is the far likelier cause.” Id. at 11-12.

He acknowledged that there is no proof that petitioner had C. jejuni; however, he argued
that it is very common in GBS cases that an organism is not isolated, even those preceded by an
infection. Resp. Ex. A at 6, 10; see, e.g., Resp. Ex. A, Tab 6 at 2 (“In about half of patients with
GBS, a specific type of preceding infection can be identified.”). Hughes and Rees, for example,
noted that “[i]n most cases, the precise infection is not clear from the medical history and has
often resolved by the time neuropathic symptoms develop. Viral or bacterial cultures are usually
negative, and serologic tests may lack sensitivity and specificity.” Resp. Ex. A, Tab 5 at 3.
However, they also acknowledged that “stools from C. jejuni-infected patients may contain
viable organisms for up to 4 weeks.” Id. at 4-5.

iii. Althen Prong Three

Dr. Whitton opined petitioner’s onset of GBS was on or around May 6, 2017, which is 10
days after his Tdap vaccination on April 26, 2017 and 6 days after the onset of his diarrhea on
April 30, 2017. Resp. Ex. A at 6, 10. He found both intervals “fall squarely within the accepted
range when considering the kinetics of the adaptive immune response.” Id. at 10. However, he
argued coincidental cases of GBS within 6 weeks of Tdap vaccination are inevitable and do not
prove, more likely than not, that the Tdap vaccine caused petitioner’s GBS. Id. at 11-12.

Dr. Whitton opined that petitioner’s GI infection “most probably” began before, on, or
near the date of vaccination. Resp. Ex. A at 6. With an infection like Campylobacter, for
example, “onset of disease symptoms usually occurs 2 to 5 days after infection with the bacteria,
but can range from 1 to 10 days.” 54 Resp. Ex. E, Tab 2 at 2; 55 see also Resp. Ex. A at 4-5. If
petitioner’s diarrheal illness was caused by C. jejuni, Dr. Whitton explained “that [the] infection
most probably began 2-5 days prior to the appearance of diarrhea,” which would be around April

54
According to literature filed by Dr. Chaudhry, there is a mean incubation period of three days
(range one to seven days) with a Campylobacter infection. Resp. Ex. C, Tab 7 at 1.
55
Campylobacter, World Health Org. (May 1, 2020), https://www.who.int/news-room/fact-
sheets/detail/campylobacter.

22
25 to April 28, or around the date of petitioner’s Tdap vaccination. Resp. Ex. A at 6. “[S]ince
the incubation period for C. jejuni may be as long as 10 days, petitioner’s GI infection may have
begun as early as [April 20, 2017], 6 days prior to vaccination.” Id. Thus, “[w]hen an
incubation period is incorporated into the timing calculation, it is quite likely that the interval
between stimulation of the adaptive immune system and GBS is longer for GI infection than it is
for the Tdap vaccination.” Id. at 10. However, he acknowledged that “the existence of an
incubation period makes it almost impossible to know exactly when the immune system was first
triggered by an infection.” Id. at 5.

Winer et al. 56 examined the incidence of antecedent events and serological evidence of
preceding infection in 100 patients with GBS. Resp. Ex. A, Tab 10 at 1. They found respiratory
infection symptoms within one month of onset of neuropathic symptoms in 38% of GBS patients
and 12% of controls, and GI infection symptoms in 17% of GBS patients and 3% of controls. Id.
at 1-2. The authors also noted immunizations “were equally common in the patient and control
subjects.” Id. at 1. Serological evidence of a recent infection was identified in 31% of patients,
with C. jejuni (14%) in significantly more patients than controls. Id. at 1, 3-4. Results showed a
peak incidence of symptoms of an infection one to two weeks prior to neuropathic symptom
onset, with the mean latency being shorter for GI infection. Id. at 2, 4. The authors concluded
“the greatest relative risk of developing GBS is seen in the first 2 weeks following infection.”
Id. at 4. Additionally, the authors did not find an association between vaccination and GBS, but
noted “[i]t [was] possible that the number of GBS patients surveyed was not sufficient to detect
vaccine associated cases.” Id. at 5.

Similarly, Hughes and Rees, looking at the association between C. jejuni and GBS, noted
“an average of 10.5 days . . . between the onset of gastroenteritis and the onset of neuropathic
symptoms.” Resp. Ex. A, Tab 5 at 4.

3. Respondent’s Expert, Dr. Vinay Chaudhry

a. Background and Qualifications

Dr. Vinay Chaudhry is board certified in neurology, neuromuscular diseases,
electrodiagnostic medicine, and clinical neurophysiology. Resp. Ex. C at 1; Resp. Ex. D at 35.
He received his M.B. and B.S. in India in 1980 and then completed an internship and various
residencies and fellowships from 1980 to 1989. Resp. Ex. D at 2-3. He is currently a Professor
of Neurology at Johns Hopkins University School of Medicine and the Co-Director of the
Neurology EMG Laboratory at Johns Hopkins Hospital. Id. at 1. Dr. Chaudhry specialized in
the field of neuromuscular diseases. Resp. Ex. C at 1. He has an active clinical practice where
he sees over 2,000 patients per year. Id. He has authored or co-authored over 200 publications.
Resp. Ex. D at 3-20.

56
J. B. Winer et al., A Prospective Study of Acute Idiopathic Neuropathy. II. Antecedent Events,
51 J. Neurology Neurosurgery & Psychiatry 613 (1988).

23
 b. Opinion

i. Althen Prong One

Dr. Chaudhry opined GBS is a post-infectious immune disorder and “molecular mimicry
between an infectious agent and the nerve is the prevailing hypothesis.” Resp. Ex. C at 12; see
also Resp. Ex. C, Tab 2 at 1-2. 57 He agreed with Dr. Whitton that the Tdap vaccine is not an
agent that would trigger GBS through the mechanism of molecular mimicry, and added that
Prevnar is also not a triggering agent. Resp. Ex. C at 11-15.

Consistent with Dr. Rinker’s and Dr. Whitton’s opinions, Dr. Chaudhry cited various
articles that support the finding that “[a]ntecedent infection precedes two-thirds of cases of GBS
with symptoms of upper respiratory tract infection in 60% and of [GI] infection in 30%.” Resp.
Ex. C at 10-11; see also Resp. Ex. C, Tab 1 at 2; 58 Resp. Ex. C, Tab 2 at 2, 4; Resp. Ex. C, Tab 3
at 1; 59 Resp. Ex. C, Tab 9 at 2. 60 He noted that C. jejuni is the most predominant infection that
leads to GBS, as it is found in 25-50% of GBS patients, but other infections are also associated
with GBS. Resp. Ex. C at 11-12; see also Resp. Ex. C, Tab 7 at 4-5 (“C. jejuni infection has
been established as a trigger of GBS . . . . It has been estimated that 30 to 40 percent of GBS
illness is attributable to Campylobacter infection . . . .”). 61

Dr. Chaudhry acknowledged that GBS has been reported shortly after vaccinations like
rabies and influenza A. Resp. Ex. C at 11, 13-14; see Resp. Ex. C, Tab 1 at 2; Resp. Ex. C, Tab
2 at 5-6. However, he argued not all vaccines are the same and there is no evidence of GBS
occurring after Tdap or Prevnar 13 vaccination. Resp. Ex. C at 12-13, 15; Resp. Ex. E at 1. Yet,
medical literature cited by Dr. Chaudhry acknowledged “epidemiological studies [that] have
reported development of GBS following vaccinations,” including those containing tetanus

57
Francine J. Vriesendorp, Guillain-Barré Syndrome: Pathogenesis, UpToDate,
https://www.uptodate.com/contents/guillain-barre-syndrome-pathogenesis/print (last updated
Sept. 25, 2018).
58
Hugh J. Willison et al., Guillain-Barré Syndrome, 388 Lancet 717 (2016).
59
Campylobacter (Campylobacteriosis): Guillain-Barré Syndrome, Ctrs. for Disease Control &
Prevention, https://www.cdc.gov/campylobacter/guillain-barre.html (last reviewed Dec. 20,
2019).
60
Nobuhiro Yuki, Ganglioside Mimicry and Peripheral Nerve Disease, 35 Muscle & Nerve 691
(2007).
61
Ban M. Allos, Clinical Manifestations, Diagnosis, and Treatment of Campylobacter Infection,
UpToDate, https://www.uptodate.com/contents/clinical-manifestations-diagnosis-and-treatment-
of-campylobacter-infection/print (last updated Aug. 9, 2019).

24
toxoid. Resp. Ex. E, Tab 4 at 8-9. 62 Additionally, other literature noted cases of GBS after
Prevnar 13 vaccination. See Resp. Ex. E, Tab 10 at 4. 63

Like Dr. Whitton, Dr. Chaudhry relied on the 2012 IOM report, which found “[t]he
evidence [was] inadequate to accept or reject a causal relationship between diphtheria toxoid-,
tetanus toxoid-, or acellular pertussis-containing vaccines and GBS.” Resp. Ex. C at 12 (quoting
Resp. Ex. A, Tab 15 at 35). Dr. Chaudhry added that the 2012 IOM report reviewed several
publications on the development of GBS after vaccines containing tetanus, diphtheria, and
acellular pertussis antigens alone or in combination, some of which Dr. Rinker relied upon. Id.
at 14 (citing Pet. Ex. 40; Pet. Ex. 29; Resp. Ex. A, Tab 17); see Resp. Ex. A, Tab 15 at 34. The
IOM found these “publications did not provide evidence beyond temporality” and “did not
contribute to the weight of mechanistic evidence.” Resp. Ex. A, Tab 15 at 34-35.

Dr. Chaudhry also cited to Tuttle et al. to opine that the number of cases of GBS
following administration of a tetanus-toxoid-containing vaccine is not greater than the number of
GBS cases expected by chance alone. Resp. Ex. C at 13 (citing Resp. Ex. A, Tab 11). Thus, he
argued “the risk for GBS after administration of tetanus toxoid is extremely low.” Id. at 14.

With regard to pneumococcal vaccines, and Prevnar 13 specifically, Dr. Chaudhry cited
studies finding no or minimal incidences of GBS following such vaccinations. Resp. Ex. C at
12. First, he cited to Haber et al., which found the incidence of GBS after Prevnar 13 vaccine
“far lower” than the background incidence of GBS overall. Id. (citing Resp. Ex. C, Tab 10).
Haber et al. evaluated all adverse events reported to VAERS from June 2012 to December 2015
following Prevnar 13 vaccination in individuals 19 years of age and older. Resp. Ex. C, Tab 10
at 2. Of the 2,976 reports to VAERS during this time period, the authors identified 11 reports of
possible GBS following Prevnar 13 vaccination. Id. at 4. Ten of the 11 reports listed Prevnar 13
as the only vaccine administered, while one report also listed a flu vaccine was administered. Id.
One case had an upper respiratory infection 16 days prior to GBS onset. Id. The authors found
“no disproportionate reporting for GBS.” Id. at 5.

He next cited to safety studies where no cases of GBS were reported. Resp. Ex. C at 12.
In Jackson et al., 64 the authors “conducted a randomized clinical trial to evaluate safety and
immunogenicity of [Prevnar 13] compared to [23-valent pneumococcal polysaccharide vaccine]
in adults aged 70 years and older who had been previously vaccinated with [23-valent
pneumococcal polysaccharide vaccine].” Resp. Ex. C, Tab 15 at 2. The authors note one serious

62
Kishan Kumar Nyati & Roopanshi Nyati, Role of Campylobacter Jejuni Infection in the
Pathogenesis of Guillain-Barré Syndrome: An Update, 2013 BioMed Rsch. Int’l 1.
63
Penina Haber et al., Post-Licensure Surveillance of 13-Valent Pneumococcal Conjugate
Vaccine (PCV13) in Adults Aged ≥ 19 Years Old in the United States, Vaccine Adverse Event
Reporting System (VAERS), June 1, 2012–December 31, 2015, 34 Vaccine 6330 (2016).
64
Lisa A. Jackson et al., Immunogenicity and Safety of a 13-Valent Pneumococcal Conjugate
Vaccine in Adults 70 Years of Age and Older Previously Vaccinated with 23-Valent
Pneumococcal Polysaccharide Vaccine, 31 Vaccine 3585 (2013).

25
adverse event (idiopathic thrombocytopenic purpura) that was considered related to vaccination.
Id. at 5-6. In the follow-up study also authored by Jackson et al., 65 “no vaccine related serious
adverse events [] or deaths were reported.” Resp. Ex. C, Tab 16 at 5.

Lastly, Dr. Chaudry cited to the Prevnar 13 package insert as well as efficacy and safety
of Prevnar 13 from Pfizer. Resp. Ex. C at 12. Neither lists GBS as an adverse event. See Resp.
Ex. C, Tab 14; 66 Resp. Ex. C, Tab 17. 67

Dr. Chaudhry opined that a “Streptococcus pneumonia infection is not one of the
infectious agents reported to precede GBS and hence pneumococcal vaccines against the bacteria
Streptococcus pneumonia is unlikely to cause GBS.” Resp. Ex. C at 12 (emphasis added).

ii. Althen Prong Two

Dr. Chaudhry opined that petitioner’s Tdap and/or Prevnar vaccine did not play a
causative role in the development of his GBS, and instead his GBS was secondary to his
diarrheal illness. Resp. Ex. C at 11, 15; Resp. Ex. E at 1. He found that “[i]n the presence of a
known preceding cause, a rare possible association [with the vaccines] is difficult to envisage.”
Resp. Ex. C at 14.

In support of his opinion that petitioner’s GBS was preceded by a diarrheal illness, Dr.
Chaudhry noted petitioner complained of fatigue, bloody stools, chills, and feeling feverish on
May 3, 2017, and was subsequently diagnosed with gastroenteritis. Resp. Ex. C at 10-11, 15.
Dr. Chaudhry found petitioner’s presentation consistent with the most common symptoms of
Campylobacter infection, which include cramping, abdominal pain, diarrhea, bloody stools,
fever, headache, nausea, and vomiting. Resp. Ex. C at 10-11; Resp. Ex. E at 2-4; see Resp. Ex.
C, Tab 7 at 1-2; Resp. Ex. E, Tab 2 at 2.

Dr. Chaudhry added that Campylobacter infection is the most common cause of diarrhea
and gastroenteritis. Resp. Ex. E at 1-2; Resp. Ex. C at 11; see, e.g., Resp. Ex. C, Tab 6 at 5, 9; 68

65
Lisa A. Jackson et al., Influence of Initial Vaccination with 13-Valent Pneumococcal
Conjugate Vaccine or 23-Valent Pneumococcal Polysaccharide Vaccine on Anti-Pneumococcal
Responses Following Subsequent Pneumococcal Vaccination in Adults 50 Years and Older, 31
Vaccine 3594 (2013).
66
Prevnar 13, Pfizer, https://www.pfizermedicalinformation.com/en-us/prevnar-13 (last visited
Jan. 20, 2020).
67
Proven Efficacy and Safety, Pfizer, https://prevnar13adult.pfizerpro.com/efficacy-and-
safety/proven (last visited Sept. 15, 2019).
68
Ban M. Allos, Microbiology, Pathogenesis, and Epidemiology of Campylobacter Infection,
UpToDate, https://www.uptodate.com/contents/microbiology-pathogenesis-and-epidemiology-
of-campylobacter-infection/print?topicRef=2716&source=see_link (last updated Apr. 18, 2019).

26
Resp. Ex. E, Tab 1 at 1 (“Infection with [C. jejuni] is one of the most common causes of
gastroenteritis worldwide.”); 69 Resp. Ex. E, Tab 2 at 1.

Dr. Chaudhry also cited to statements by Dr. White and Dr. Melling, petitioner’s treating
physicians, where they considered petitioner’s history of diarrhea. Resp. Ex. C at 15. Dr. White,
for example, wrote petitioner’s medical history was “quite classic for [GBS]; he had a bout of
diarrhea and one week later experienced significant weakness with suppressed reflexes.” Pet.
Ex. 6 at 14. Petitioner’s history of diarrhea was also noted by Dr. Melling. See Pet. Ex. 3 at 7.
Dr. Chaudhry argued “the treating physicians considered the history of diarrhea relevant in
making a diagnosis of GBS.” Resp. Ex. C at 15.

Thus, due to petitioner’s presentation on May 3, 2017, treating physician statements, and
because C. enteritis is the leading cause of diarrhea, Dr. Chaudhry found it likely that petitioner
suffered from a C. jejuni infection. Resp. Ex. C at 11.

Although petitioner was not confirmed to have C. jejuni, Dr. Chaudhry contended that (1)
petitioner was never tested for such infection and (2) a majority of C. jejuni infections are likely
undiagnosed. Resp. Ex. E at 2-3; see Resp. Ex. E, Tab 6 at 3. 70 Dr. Chaudhry found petitioner’s
clinical course and “the known [mechanism of] molecular mimicry are highly suggestive if not
indicative of C. jejuni causing [petitioner’s] GBS.” Resp. Ex. E at 3. He concluded that “more
likely than not,” petitioner’s GBS was caused by a C. jejuni-associated diarrhea, “a proven
association,” rather than his Tdap vaccination, “an unproven association.” Id. at 4.

iii. Althen Prong Three

Dr. Chaudhry noted petitioner was admitted to the ER on May 11, 2017 complaining of a
five-day history of diffuse weakness. Resp. Ex. C at 9. Relying on petitioner’s medical records,
he found petitioner’s onset of weakness began on either May 5, 2017 or May 9, 2017. Id.
(compare Pet. Ex. 3 at 7, 9, 13, 15, 20, with Pet. Ex. 6 at 7, 9). However, he then noted that
“[o]ne day prior to the onset (5/4/2017) [petitioner] was able to go fishing and did not have any
weakness.” Id. (citing Pet. Ex. 3 at 9).

He found the onset of petitioner’s diarrheal illness difficult to ascertain. Resp. Ex. C at
15. He cited medical records from petitioner’s May 2017 hospital stay that documented a history
of diarrhea two weeks prior to his admission on May 11, 2017. Id. at 9 (citing Pet. Ex. 3 at 7, 9,
13, 15, 17, 20). However, he also cited to medical records from May 3, 2017 where petitioner
complained of diarrhea for three days and was diagnosed with gastroenteritis. Id. (citing Pet. Ex.
5 at 2-3).

Dr. Chaudhry opined that C. enteritis and diarrhea have been established as a trigger of
GBS between one and two weeks following infection. Resp. Ex. C at 11. The CDC noted there

69
Petitioner also cited this article. See Pet. Ex. 32.
70
Noel McCarthy & Johan Giesecke, Incidence of Guillain-Barré Syndrome Following Infection
with Campylobacter Jejuni, 153 Am. J. Epidemiology 610 (2001).

27
is a mean incubation period of three days (range one to seven days) with a Campylobacter
infection, which “typically occurs between one and two weeks before the onset of neurologic
symptoms.” Resp. Ex. C, Tab 7 at 1, 4-5.

Studies have found onset of C. jejuni-associated GBS “typically occur[s] 1-3 weeks after
the onset of diarrheal illness.” Resp. Ex. E, Tab 1 at 1; see also Resp. Ex. E, Tab 4 at 1 (“Almost
25%-40% of GBS patients worldwide suffer from C. jejuni infection 1-3 weeks prior to the
illness.”). Similarly, Rees et al. 71 found “the median interval between the onset of diarrhea and
neuropathic symptoms was 9 days (range, 2 to 20).” Resp. Ex. C, Tab 8 at 3.

With regard to the vaccinations at issue here, Haber et al. found 11 cases of possible GBS
following Prevnar vaccine with a median onset interval of 9 days (range 2-34 days). Resp. Ex.
C, Tab 10 at 4. Other articles cited by Dr. Chaudhry that note or discuss onset were cited by Dr.
Rinker and/or Dr. Whitton and are discussed above.

IV. DISCUSSION

A. Standards for Adjudication

The Vaccine Act was established to compensate vaccine-related injuries and deaths. §
10(a). “Congress designed the Vaccine Program to supplement the state law civil tort system as
a simple, fair and expeditious means for compensating vaccine-related injured persons. The
Program was established to award ‘vaccine-injured persons quickly, easily, and with certainty
and generosity.’” Rooks v. Sec’y of Health & Hum. Servs., 35 Fed. Cl. 1, 7 (1996) (quoting
H.R. Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).

Petitioner’s burden of proof is by a preponderance of the evidence. § 13(a)(1). The
preponderance standard requires a petitioner to demonstrate that it is more likely than not that the
vaccine at issue caused the injury. Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315,
1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y of Health
& Hum. Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). The petitioner need not make a specific type
of evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of pathological
markers or genetic predisposition, or general acceptance in the scientific or medical communities
to establish a logical sequence of cause and effect.” Capizzano v. Sec’y of Health & Hum.
Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006). Instead, petitioner may satisfy his burden by
presenting circumstantial evidence and reliable medical opinions. Id. at 1325-26.

In particular, petitioner must prove that the vaccine was “not only [the] but-for cause of
the injury but also a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321
(quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999));
see also Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). The
received vaccine, however, need not be the predominant cause of the injury. Shyface, 165 F.3d
at 1351. A petitioner who satisfies this burden is entitled to compensation unless respondent can

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Jeremy H. Rees et al., Campylobacter Jejuni Infection and Guillain-Barré Syndrome, 333 New
Eng. J. Med. 1374 (1995).

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prove, by a preponderance of the evidence, that the vaccinee’s injury is “due to factors unrelated
to the administration of the vaccine.” § 13(a)(1)(B). However, if a petitioner fails to establish a
prima facie case, the burden does not shift. Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d
1570, 1575 (Fed. Cir. 1993).

“Regardless of whether the burden ever shifts to the respondent, the special master may
consider the evidence presented by the respondent in determining whether the petitioner has
established a prima facie case.” Flores v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 157, 162-
63 (2014); see also Stone v. Sec’y of Health & Hum. Servs., 676 F.3d 1373, 1379 (Fed. Cir.
2012) (“[E]vidence of other possible sources of injury can be relevant not only to the ‘factors
unrelated’ defense, but also to whether a prima facie showing has been made that the vaccine
was a substantial factor in causing the injury in question.”); de Bazan v. Sec’y of Health & Hum.
Servs., 539 F.3d 1347, 1353 (Fed. Cir. 2008) (“The government, like any defendant, is permitted
to offer evidence to demonstrate the inadequacy of the petitioner’s evidence on a requisite
element of the petitioner's case-in-chief.”); Pafford, 451 F.3d at 1358-59 (“[T]he presence of
multiple potential causative agents makes it difficult to attribute ‘but for’ causation to the
vaccination. . . . [T]he Special Master properly introduced the presence of the other unrelated
contemporaneous events as just as likely to have been the triggering event as the vaccinations.”).

B. Causation

To receive compensation through the Program, petitioner must prove either (1) that he
suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding to a
vaccine that he received, or (2) that he suffered an injury that was actually caused by a
vaccination. See §§ 11(c)(1), 13(a)(1)(A); Capizzano, 440 F.3d at 1319-20. Because petitioner
does not allege he suffered a Table Injury, he must prove a vaccine he received caused his injury.
To do so, petitioner must establish, by preponderant evidence: “(1) a medical theory causally
connecting the vaccination and the injury; (2) a logical sequence of cause and effect showing that
the vaccination was the reason for the injury; and (3) a showing of a proximate temporal
relationship between vaccination and injury.” Althen v. Sec’y of Health & Hum. Servs., 418
F.3d 1274, 1278 (Fed. Cir. 2005).

The causation theory must relate to the injury alleged. The petitioner must provide a
sound and reliable medical or scientific explanation that pertains specifically to this case,
although the explanation need only be “legally probable, not medically or scientifically certain.”
Knudsen v. Sec’y of Health & Hum. Servs., ; 543, 548-49 (Fed. Cir. 1994). Petitioner cannot
establish entitlement to compensation based solely on his assertions; rather, a vaccine claim must
be supported either by medical records or by the opinion of a medical doctor. § 13(a)(1). In
determining whether petitioner is entitled to compensation, the special master shall consider all
material in the record, including “any . . . conclusion, [or] medical judgment . . . which is
contained in the record regarding . . . causation.” § 13(b)(1)(A). The undersigned must weigh
the submitted evidence and the testimony of the parties’ proffered experts and rule in petitioner’s
favor when the evidence weighs in his favor. See Moberly, 592 F.3d at 1325-26 (“Finders of
fact are entitled—indeed, expected—to make determinations as to the reliability of the evidence
presented to them and, if appropriate, as to the credibility of the persons presenting that

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evidence.”); Althen, 418 F.3d at 1280 (noting that “close calls” are resolved in petitioner’s
favor).

V. CAUSATION ANALYSIS

A. Althen Prong One

Under Althen Prong One, petitioner must set forth a medical theory explaining how the
received vaccine could have caused the sustained injury. Andreu v. Sec’y of Health & Hum.
Servs., 569 F.3d 1367, 1375 (Fed. Cir. 2009); Pafford, 451 F.3d at 1355-56. Petitioner’s theory
of causation need not be medically or scientifically certain, but it must be informed by a “sound
and reliable” medical or scientific explanation. Boatmon v. Sec’y of Health & Hum. Servs., 941
F.3d 1351, 1359 (Fed. Cir. 2019); see also Knudsen, 35 F.3d at 548; Veryzer v. Sec’y of Health
& Hum. Servs., 98 Fed. Cl. 214, 223 (2011) (noting that special masters are bound by both §
13(b)(1) and Vaccine Rule 8(b)(1) to consider only evidence that is both “relevant” and
“reliable”). If petitioner relies upon a medical opinion to support his theory, the basis for the
opinion and the reliability of that basis must be considered in the determination of how much
weight to afford the offered opinion. See Broekelschen v. Sec’y of Health & Hum. Servs., 618
F.3d 1339, 1347 (Fed. Cir. 2010) (“The special master’s decision often times is based on the
credibility of the experts and the relative persuasiveness of their competing theories.”); Perreira
v. Sec’y of Health & Hum. Servs., 33 F.3d 1375, 1377 n.6 (Fed. Cir. 1994) (stating that an
“expert opinion is no better than the soundness of the reasons supporting it” (citing Fehrs v.
United States, 620 F.2d 255, 265 (Ct. Cl. 1980))).

Here, the experts agree that molecular mimicry is not a disputed theory as it relates to
GBS. They also agreed that two-thirds of GBS cases are preceded by a respiratory or GI
infection or illness, with a C. jejuni infection being the most common GI infection. And all of
the experts cited literature discussing how C. jejuni, in particular, can cause GBS via molecular
mimicry. They did not dispute that a GI illness can cause GBS. However, they do dispute
whether the vaccines at issue here can cause GBS.

Due to the facts and circumstances of this case, specifically the fact that petitioner had a
preceding GI illness prior to his GBS, the undersigned’s determination as to causation turns on
an analysis of Althen Prong Two. Assuming that petitioner has proven a sound and reliable
causal mechanism under Althen Prong One, the undersigned finds petitioner did not provide
preponderant evidence of a logical sequence of cause and effect under the facts of this case
where petitioner had a GI illness at the same time as his vaccinations. Thus, the undersigned
turns her focus to Althen Prong Two. See Vaughan ex rel. A.H. v. Sec’y of Health & Hum.
Servs., 107 Fed. Cl. 212, 221-22 (2012) (finding the special master’s failure to rule on Althen
prong one not fatal to his decision because Althen prong two was fatal to petitioner’s case);
Hibbard v. Sec’y of Health & Hum. Servs., 698 F.3d 1355, 1364 (Fed. Cir. 2012) (“discern[ing]
no error in the manner in which the special master chose to address the Althen [prongs]” when
he focused on Althen prong two after “assuming the medical viability of [the] theory of
causation”).

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 B. Althen Prong Two

Under Althen Prong Two, petitioner must prove by a preponderance of the evidence that
there is a “logical sequence of cause and effect showing that the vaccination was the reason for
the injury.” Capizzano, 440 F.3d at 1324 (quoting Althen, 418 F.3d at 1278). “Petitioner must
show that the vaccine was the ‘but for’ cause of the harm . . . or in other words, that the vaccine
was the ‘reason for the injury.’” Pafford, 451 F.3d at 1356 (internal citations omitted).

In evaluating whether this prong is satisfied, the opinions and views of the vaccinee’s
treating physicians are entitled to some weight. Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d
at 1326 (“[M]edical records and medical opinion testimony are favored in vaccine cases, as
treating physicians are likely to be in the best position to determine whether a ‘logical sequence
of cause and effect show[s] that the vaccination was the reason for the injury.’” (quoting Althen,
418 F.3d at 1280)). Medical records are generally viewed as trustworthy evidence, since they are
created contemporaneously with the treatment of the vaccinee. Cucuras v. Sec’y of Health &
Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). The petitioner need not make a specific type
of evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of pathological
markers or genetic predisposition, or general acceptance in the scientific or medical communities
to establish a logical sequence of cause and effect.” Capizzano, 440 F.3d at 1325. Instead,
petitioner may satisfy his burden by presenting circumstantial evidence and reliable medical
opinions. Id. at 1325-26.

To summarize petitioner’s clinical course, petitioner received a Tdap vaccination on
April 26, 2017. Two days later, on April 28, 2017, petitioner received a Prevnar vaccination.
On May 3, 2017, petitioner “complain[ed] of feeling run down, fatigued, muscle aches,
headaches, diarrhea, and urinary frequency x3 days.” Pet. Ex. 5 at 2. He “had diarrhea x3 days
up to 6x daily” and there “[m]ay have been melena or bright red blood per rectum with the
diarrhea.” Id. He was diagnosed with gastroenteritis. On May 11, 2017, petitioner presented to
the ER complaining of diffuse weakness for five days. Petitioner reported vaccination and
diarrhea “about the same time” prior to GBS onset. Pet. Ex. 3 at 26. Subsequent diagnostic
testing, including a lumbar puncture, confirmed petitioner’s GBS diagnosis.

On May 11, 2017, Dr. Melling noted petitioner reported his “illness with vomiting and
diarrhea as well as weakness about 2 weeks ago.” Pet. Ex. 3 at 7. Dr. Melling did not associate
petitioner’s vaccinations with his GBS. That same day, Dr. Bruce Daniel documented that
petitioner reported “2 weeks of progressively worsening weakness” that “started after a [Prevnar
13] vaccine and a bout of diarrhea, which [petitioner] had about the same time 2 weeks ago.” Id.
at 26. On May 12, 2017, Dr. White wrote that petitioner reported that “[h]e had a [Tdap] shot
and subsequently developed diarrhea (approximately 2 weeks ago). At around that time, he also
had a [Prevnar 13] vaccine.” Id. at 9.

After discharge, petitioner continued to see Dr. White. At a visit on June 2, 2017, Dr.
White noted that “[a]bout 4 weeks ago, [petitioner] developed diarrhea, 3 weeks ago he
developed weakness and was diagnosed with [GBS] (most likely AIDP).” Pet. Ex. 6 at 13. Dr.
White found petitioner’s medical history “quite classic for [GBS]; he had a bout of diarrhea and
one week later experienced significant weakness with suppressed reflexes.” Id. at 14. On

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January 10, 2018, Dr. White documented, “[petitioner] ha[d] a history of acute weakness coming
in early May of 2017 and occurring 3 weeks after stepping on a wire, receiving a [Tdap] shot and
developing diarrhea (he also had a [Prevnar 13] vaccine at that time).” Id. at 59.

The experts devoted substantial time to the issue of whether petitioner had a C. jejuni or
other GI infection that led to his development of GBS. From the records provided, it does not
appear that testing was done to confirm whether petitioner had a specific infection, such as C.
jejuni. Dr. Whitton acknowledged that a specific organism was not isolated in petitioner, but he
explained that is common with GBS cases. Dr. Chaudhry agreed. Dr. Chaudhry also found
petitioner’s presentation on May 3, 2017 consistent with the most common symptoms of
Campylobacter infection. He also argued petitioner’s treating physicians considered petitioner’s
history of diarrhea relevant when treating and diagnosing him with GBS. Dr. Chaudhry found
petitioner’s clinical course and “the known [mechanism of] molecular mimicry are highly
suggestive if not indicative of C. jejuni causing [petitioner’s] GBS.” Resp. Ex. E at 3.

Dr. Rinker acknowledged that petitioner’s diarrheal illness was a potential trigger of his
GBS. He opined that “it is not possible to distinguish whether vaccination or the diarrheal illness
alone was responsible for his GBS, or whether the two immunological stimuli worked in concert
to provoke the immune response.” Pet. Ex. 9 at 6. However, Dr. Rinker did not explain how the
vaccines and GI illness could work together in concert to cause GBS. And he did not support
this statement with medical literature or other evidence.

Further, Dr. Rinker argued there was insufficient evidence to claim that the diarrheal
illness was a more likely cause of petitioner’s GBS. However, in his supplemental report, he
found there was sufficient evidence that petitioner’s Tdap vaccination was the more likely cause
for petitioner’s GBS. Dr. Rinker’s opinion that a vaccine was more likely than a GI illness to
cause petitioner’s GBS is not supported by the evidence.

Dr. Rinker attempted to argue that the temporal association between vaccination and
GBS onset favored the vaccines as the more likely cause. However, literature cited by Dr.
Rinker notes there is an incubation period with Campylobacter infections, consistent with Dr.
Whitton’s opinion and literature cited by both Drs. Whitton and Chaudhry. Taking into account
the incubation period between infection and symptom onset would place the date of infection
before or approximately the date of petitioner’s vaccination. Thus, this argument fails.

Dr. Rinker then argues that “the mere presence of diarrhea before the onset of GBS,
especially when C. jejuni was never identified, provides an unlikely cause of [petitioner’s] GBS
in comparison to the Tdap vaccination.” However, as previously stated, no testing was
conducted. This argument does not explain how the Tdap vaccine is the more likely cause of
petitioner’s GBS.

The undersigned is not persuaded by petitioner’s arguments, given petitioner’s clinical
course, treating physician statements, and the experts’ opinions and supporting medical
literature. The undersigned acknowledges that petitioner is not required to eliminate other
potential causes in order to be entitled to compensation. See Walther v. Sec’y of Health & Hum.
Servs., 485 F.3d 1146, 1149-52 (Fed. Cir. 2007) (finding petitioner does not bear the burden of

32
eliminating alternative independent potential causes). However, she finds it reasonable to
consider “evidence of other possible sources of injury”—here, petitioner’s GI illness—in
determining “whether a prima facie showing has been made that the vaccine was a substantial
factor in causing the injury in question.” Stone, 676 F.3d at 1379.

In this case, “the presence of multiple potential causative agents makes it difficult to
attribute ‘but for’ causation to the vaccination.” Pafford, 451 F.3d at 1358-59; see also Walther,
485 F.3d at 1151 n.4 (“Where multiple causes act in concert to cause the injury, proof that a
particular vaccine was a substantial cause may require the petitioner to establish that the other
causes did not overwhelm the causative effect of the vaccine.”). As such, the undersigned finds
petitioner failed to prove that the Tdap and/or Prevnar vaccines were the “but for” cause of
petitioner’s GBS.

For all of the reasons described above, the undersigned finds that petitioner has failed to
provide preponderant evidence of a logical sequence of cause and effect required under Althen
Prong Two.

C. Althen Prong Three

Althen Prong Three requires petitioner to establish a “proximate temporal relationship”
between the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been
defined as a “medically acceptable temporal relationship.” Id. The petitioner must offer
“preponderant proof that the onset of symptoms occurred within a timeframe which, given the
medical understanding of the disease’s etiology, it is medically acceptable to infer causation-in-
fact.” de Bazan, 539 F.3d at 1352. The explanation for what is a medically acceptable time
frame must also coincide with the theory of how the relevant vaccine can cause the injury alleged
(under Althen Prong One). Id.; Koehn v. Sec’y of Health & Hum. Servs., 773 F.3d 1239, 1243
(Fed. Cir. 2014); Shapiro v. Sec’y of Health & Hum. Servs., 101 Fed. Cl. 532, 542 (2011),
recons. den’d after remand, 105 Fed. Cl. 353 (2012), aff’d mem., 503 F. App’x 952 (Fed. Cir.
2013).

Based on the most contemporaneous-in-time medical records, and consistent with the
experts’ opinions, the undersigned finds petitioner’s GBS onset to be on or about May 5 or 6,
2017.

Dr. Rinker opined petitioner’s GBS onset was May 5 or May 6, 2017. Dr. Whitton
agreed that petitioner’s GBS onset was on or around May 6, 2017. Dr. Chaudhry noted the
medical records supported a GBS onset of May 5, 2017.

Even though the experts agree as to GBS onset, they disagree as to whether timing is
appropriate given their proposed triggers at play. Dr. Rinker opined that here, with an adaptive
immune response, the timing for vaccine-caused GBS is appropriate. He cited articles
supporting a timeframe between four days and four weeks after vaccination.

Dr. Whitton agreed that this interval between vaccination and GBS “fall[s] squarely
within the accepted range when considering the kinetics of the adaptive immune response,” but

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argued the interval between infection and GBS is also appropriate. Resp. Ex. A at 10. Because
the onset of disease symptoms with Campylobacter infections occurs one to ten days after
exposure to infection, he found petitioner’s GI illness “most probably” began before, on, or near
the date of vaccination. He acknowledged that “the existence of an incubation period makes it
almost impossible to know exactly when the immune system was first triggered by an infection,”
but maintained that “[w]hen an incubation period is incorporated into the timing calculation, it is
quite likely that the interval between stimulation of the adaptive immune system and GBS is
longer for GI infection than it is for the Tdap vaccination.” Id. at 5, 10.

Dr. Chaudhry agreed with Dr. Whitton that the timing is appropriate for the GI infection
as the cause of petitioner’s GBS. Both Drs. Whitton and Chaudhry cited literature to support an
onset of neurological symptoms one to three weeks following infection.

Petitioner’s GBS onset of May 5 or May 6, 2017 was 9-10 days after petitioner’s Tdap
vaccination, 7-8 days after petitioner’s Prevnar vaccination, and 5-6 days after his diarrheal
illness onset. All of these intervals are appropriate given the undersigned’s knowledge and
experience with the adaptive immune system and molecular mimicry, and respondent’s experts’
opinions. Dr. Rinker does not discuss whether the interval between petitioner’s GI illness and
GBS onset is appropriate. He only argues that the timing is more appropriate for the Tdap
vaccine as the prevailing trigger.

Therefore, the undersigned finds the temporal association is appropriate given the
mechanism of injury and petitioner has satisfied the third Althen prong. However, temporal
association alone is insufficient for petitioner to show vaccine causation for his alleged injury,
and thus, petitioner is not entitled to compensation.

VI. CONCLUSION

For the reasons discussed above, the undersigned finds that petitioner has not established
by preponderant evidence that his vaccinations caused his GBS. Therefore, petitioner is not
entitled to compensation and his petition must be dismissed. In the absence of a timely filed
motion for review pursuant to Vaccine Rule 23, the Clerk of Court SHALL ENTER
JUDGMENT in accordance with this Decision.

IT IS SO ORDERED.

s/Nora Beth Dorsey
Nora Beth Dorsey
Special Master

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