Pierson v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 17-1136V

Filed: January 19, 2022

PUBLISHED

Special Master Horner

CAROLYN PIERSON,

Pneumococcal conjugate

Petitioner, vaccine (Prevnar 13); Guillain-

v. Barre Syndrome (GBS);

Causation-in-fact

SECRETARY OF HEALTH AND

HUMAN SERVICES,

Respondent.

Jeffrey S. Pop, Jeffrey S. Pop & Associates, Beverly Hills, CA, for petitioner.

Austin Joel Egan, U.S. Department of Justice, Washington, DC, for respondent.

RULING ON ENTITLEMENT 1

On August 23, 2017, petitioner filed a petition under the National Childhood

Vaccine Injury Act, 42 U.S.C. § 300aa-10-34 (2012), 2 alleging that the influenza (flu)

vaccine she received on September 30, 2014, caused her to suffer Guillain-Barre

Syndrome (“GBS”). (Pet., p. 1.) Petitioner later amended her petition to allege that she

received the pneumococcal conjugate vaccination (Prevnar 13) on January 6, 2015,

which caused in fact her GBS, instead of the flu vaccine. For the reasons set forth

below, I conclude that petitioner is entitled to compensation.

I. Procedural History

Petitioner filed her petition pro se on August 23, 2017, alleging that she received

a flu vaccination on September 30, 2014 which caused her to develop GBS. (ECF No.

1

Because this decision contains a reasoned explanation for the special master’s action in this case, it will

be posted on the United States Court of Federal Claims’ website in accordance with the E-Government

Act of 2002. See 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 the special master, upon review, agrees that the identified material fits within this definition, it will be

redacted from public access.

2

Within this decision, all citations to § 300aa will be the relevant sections of the Vaccine Act at 42 U.S.C.

§ 300aa-10-34.

1

1.) This case was originally assigned to Special Master Millman who granted

petitioner’s motion to proceed in forma pauperis. (See ECF No. 7.) After an initial

telephonic status conference, petitioner indicated that she was seeking representation.

(ECF No. 8.) On January 16, 2018 a status conference was held and Special Master

Millman ordered petitioner to file her medical records. (ECF No. 9.)

On March 12, 2018, petitioner’s counsel filed a motion to substitute attorney.

(ECF No. 10.) After petitioner secured representation, she filed an amended petition on

April 12, 2018. (ECF No. 12.) Petitioner’s amended petition now alleges that petitioner

received a pneumococcal conjugate vaccination (Prevnar 13) on January 6, 2015 which

caused her to develop GBS. (ECF No. 12.) On April 20, 2018 Petitioner filed her

medical records, her declaration, and a statement of completion. (ECF Nos. 13-15.)

On June 11, 2018, respondent filed a status report requesting petitioner’s pre-

vaccination medical records and Special Master Millman ordered petitioner to file her

medical records dating back three years prior to vaccination. (ECF Nos. 17-18.) On

June 27, 2018, petitioner filed a status report indicating that she had filed all of her

medical records, including primary care, emergency, and diagnostic testing records

dating back to 2012. (ECF No. 19.) On July 30, 2018, respondent filed his Rule 4(c)

report, arguing that the evidence presented did not meet petitioner’s burden and

recommending against compensation. (ECF No. 20.)

On January 23, 2019 petitioner filed an expert report from Dr. Lawrence

Steinman and the accompanying medical literature. (ECF Nos. 22-24.) Petitioner filed

updated medical records from Evergreen Family Medicine Center on February 14,

2019. (ECF No. 26.) Respondent filed a status report on March 18, 2019, indicating

that he intended to file a responsive expert report. (ECF No. 28.) The case was

reassigned to me on June 4, 2019. (ECF No. 30.) On July 1, 2019 respondent filed an

expert report from Dr. Thomas Paul Leist and the accompanying medical literature.

(ECF 32.) After reviewing the Rule 4 report, I ordered respondent to file a supplemental

expert report responding to petitioner’s proffered medical theory concerning molecular

mimicry as well as any missing records from Mercy Medical Center, or a status report

confirming their unavailability. (ECF No. 33.)

I granted petitioner’s motion to issue a subpoena, and thereafter petitioner filed

additional medical records from Mercy Medical Center on August 1, 2019. (ECF Nos.

35, 36.) The parties filed supplemental expert reports from Drs. Steinman and Leist and

the accompanying medical literature on September 3, 2019 and March 20, 2020. (ECF

Nos. 38, 42.) Petitioner filed additional medical literature on March 30, 2020. (ECF No.

44, 45.) On June 30, 2020, respondent filed a second supplemental expert report from

Dr. Leist with additional medical literature. (ECF No. 49.)

On September 14, 2020, I scheduled a two-day entitlement hearing set to

commence on November 17, 2021. (ECF No. 54.) On October 6, 2021, petitioner filed

additional medical literature, a supplemental declaration, as well as declarations from

David Pierson (petitioner’s husband) and Laura Day (petitioner’s co-worker and friend).

2

(ECF No. 59.) On November 3, 2021, petitioner filed a motion for leave to file additional

medical literature out of time. (ECF Nos. 69, 70.) During a prehearing status

conference on November 10, 2021, I granted in part and deferred in part petitioner’s

motion to file the additional medical literature out of time. (ECF 73.) I granted

petitioner’s motion to file Exhibits 64, 66, 68 and 70, while I deferred ruling on

petitioner’s motion with respect to Exhibits 63, 65, 67, 69. (Id.) I indicated that the

relevance of the latter remaining exhibits remained unclear without expert explanation. 3

(Id.)

A two-day entitlement hearing was held remotely on November 17 and 18, 2021,

via Webex. (See ECF Nos. 77-78, Transcript of Proceedings (“Tr”), filed 12/15/2021.)

Thereafter, I ordered respondent to file a status report no later than December 3, 2021,

indicating whether he wished to file a written response to any late-filed exhibits

referenced during the hearing. (See Dkt. Text 11/18/2021.) On November 22, 2021,

respondent filed a status report indicating that respondent did not wish to file a written

response concerning Exhibits 63, 65, 67, and 69. On January 14, 2022, I granted

petitioner’s motion for leave to file out of time only with respect to Exhibit 69. (ECF No.

73 .) This case is now ripe for a decision on entitlement.

II. Factual History

a. As reflected in the medical records

Petitioner’s pre-vaccination medical history is significant for headaches (Ex. 4, p.

11; Ex. 10, p. 13), arthritis (Ex. 3, p. 7), osteopenia (Ex. 4, p. 8), pyelonephritis (Ex. 10,

p. 23), hypertension (Ex. 4, p. 57), and a history of hysterectomy and cholecystectomy

(Ex. 3 at 7). Petitioner received the pneumococcal vaccine (Prevnar 13) on January 6,

2015 at Sav-On Pharmacy in Oregon. (Ex. 2.)

On January 21, 2015 petitioner presented to Eugene/Thurston Urgent Care to

James Daskalos, M.D., with an ongoing unproductive cough since December 17, 2014.

(Ex. 3, p. 1.) Additionally, petitioner complained of sneezing, congestion, wheezing,

shortness of breath, and tingling. (Id.) Dr. Daskalos reported that “initial onset revealed

no significant fever, chills, or myalgias” and noted that her cough was worse at night.

(Id.) A physical exam revealed abnormal breath sounds—wheezing and scatter rhonchi

bilaterally. (Id. at 2) Dr. Daskalos reviewed petitioner’s x-ray which showed a right

lower lobe infiltrate. (Id. at 2-3) He diagnosed petitioner with bronchopneumonia of an

unspecified organism and prescribed doxycycline, Tessalon, and an inhaler. (Id.)

On February 3, 2015 petitioner returned to Eugene/Thurston Urgent Care to see

Dr. Daskalos for an evaluation of her chronic cough. (Ex. 3, p. 11.) Petitioner

complained of headache, tingling, numbness, cough, shortness of breath, and

3

With regard to the exhibits for which I deferred ruling, I permitted petitioner to reference the exhibits

during the hearing, but noted that I would not grant leave to file exhibits that ultimately were not

accompanied by expert discussion by the close of the hearing. Respondent was permitted an opportunity

to f ile a written response by his expert to any of these exhibit referenced during the hearing.

3

wheezing. (Id.) A physical exam revealed bilateral wheezing. (Id. at 12.) Dr. Daskalos

diagnosed petitioner with acute bronchospasm, prescribed prednisone and an inhaler,

and referred her to a pulmonologist. (Id. at 13.) Petitioner later cancelled her

pulmonary appointment because she was “feeling much better.” (Id.)

On February 26, 2015 petitioner returned for another follow-up appointment with

Dr. Daskalos. (Ex. 3, p. 19.) Dr. Daskalos observed that petitioner showed “good

improvement and was asymptomatic last week[,]” though “after completing the steroids

[petitioner] then began having increasing symptoms of shortness of breath and cough-

particularly with exertion” (Id.) Petitioner described no chest pain, though she

experienced some left-sided thoracic posterior pain, but “no swelling of the lower

extremities.” (Id.) “Unrelated to her present complaints[,]” petitioner described

symptoms of “carpal tunnel syndrome[,]” explaining that she is a cake decorator for

Albertson’s. (Id.) A review of systems confirmed chills, fatigue, sweats, shortness of

breath, and wheezing related to her cough. The review of systems continued to indicate

tingling, but also added neurologic weakness for the first time. (Id.) Petitioner’s

physical exam noted wheezing but was otherwise normal. (Ex. 3, pp. 20-21.)

On February 28, 2015 petitioner returned to Eugene/Thurston Urgent Care with a

new symptom of mid-back pain and reported that she was using her husband’s pain

medication. (Id. at 36.) Petitioner reported her pain as an 8/10 and worse with

movement and taking deep breaths. (Id.) Kerry Harrington, PA-C, noted no injury or

trauma. (Id.) Petitioner described numbness and tingling in her hands, with a history of

carpal tunnel syndrome. (Id.) Petitioner reported no leg pain or swelling. (Id.) Her

physical exam revealed general distress due to pain, tenderness of her chest on

palpation, and scattered wheezing. (Ex. 3, p. 27.) Petitioner was diagnosed with

worsening acute bronchospasm, worsening cough, and backache. (Id. at 27-28.)

Petitioner’s d-dimer test was negative. (Id. at 28, 30.) She was prescribed Norco,

Omnicef, and Flexeril; she was advised to alternate heat and ice and perform range of

motion exercises; and cleared to return to work March 9, 2015. 4 (Id. at 28)

On March 1, 2015 petitioner again returned to Eugene/Thurston Urgent Care,

complaining of “constant (but worse at times) numbness/tingling of the left hand and

right hand[,]” since her previous visit. (Ex. 3, p. 36.) She also described “back pain,

now related to numbness and tingling in her hands.” (Id.) Matthew Driver, M.D., noted

that petitioner had been given two courses of prednisone: the first relieved her pain, but

she had breakthrough pain on the second course. (Id.) Petitioner also took Norco with

no relief. (Id.) She was advised to go to the emergency department for a full

evaluation. (Id.) Petitioner’s physical exam indicated that petitioner was ambulatory,

though she “rock[ed] back and forth in apparent pain[.]” (Id. at 37.) No detailed exam

was performed, though Dr. Driver noted that “[petitioner’s] face appears normal.” (Id.)

Petitioner was diagnosed with an unspecified backache. (Id.)

4

As of this visit, Kerry Harrington, PA-C, notes “added an antibx” though her report does not specify any

inf ection. (See Ex. 3, p. 25-28.)

4

Later that day petitioner presented to the emergency department at Mercy

Medical Center with a questionable diagnosis of pneumonia. (Ex. 4, p. 38.) Her “main

complaint [was] pain kind of at the bra line on the right side.” (Id.) She described pain

with twisting, turning, or coughing. (Id.) Petitioner reported no leg pain and Wade Fox,

D.O., noted that “she is not really short of breath, not tachycardic.” (Id.) Dr. Fox

observed, “I think she has basically coughed herself to a musculoskeletal strain in the

back.” (Id.) Petitioner was prescribed more pain medication for her pain and cough.

(Id.) Chest x-rays taken that day revealed no acute cardiopulmonary process. (Ex. 4,

p. 49.) Petitioner was discharged and advised to follow-up with Jennifer Jarasa, M.D.,

as an outpatient. (Id. at 38.)

The next day, March 2, 2015, petitioner returned to Eugene/Thurston Urgent

Care and was seen by PA Harrington. (Ex. 3, p. 42.) She complained of aching lower

back pain, describing the severity as 10/10. (Id.) Petitioner reported that she had

difficulty sleeping due to the pain; and that the Dilaudid did not reduce her pain. (Id.)

She further complained of fatigue, sweats, chest pain/pressure, headache, light

headedness, weakness, blurred vision, ongoing cough, congestion, shortness of breath

and wheezing. (Id.) The physical exam described petitioner’s rocking back and forth

due to pain. (Id. at 43-44.) Petitioner was given a Dilaudid injection and prescribed

Zofran. (Id. at 44.) She was advised to return to the emergency department. (Ex.3, p.

45.)

Later that day, petitioner saw David Rickman, M.D., reporting pain “mostly about

her left upper back” that spread “all over her back” with “some pain in her hands and

legs” that began one to one-and-a-half weeks prior. (Ex. 4, p. 58.) She described

nausea without vomiting, ongoing cough, heaviness in her chest, and shortness of

breath. (Id.) Petitioner denied having leg swelling, leg numbness, tingling, or

weakness. (Id.) Dr. Rickman observed that petitioner “clearly [had] back pain which

[was] somewhat intractable…although [he] [did] not see[] evidence of any more

immediate or acute pathology.” (Id.) Petitioner was given intravenous Zofran and

Dilaudid twice. (Id.) Petitioner was discharged and instructed to follow-up with her

primary care provider, Heidi McNulty, D.O. (Id.)

On March 3, 2015 petitioner saw Dr. McNulty who noted that petitioner

contracted an upper respiratory infection in December and was seen multiple times in

urgent care for her worsening cough, sudden acute pain in the bra line area as well as

“new numbness and pain in the fingers and then in the toes and distal feet.” (Ex. 5, p.

12.) Petitioner was diagnosed with thoracic spine pain, neuropathy, as well as

climacteric arthritis of the hand. (Id. at 17.)

The following day, March 4, 2015, petitioner returned to Eugene/Thurston Urgent

Care complaining of ongoing mid-back pain and requesting pain medication until she

could be seen again by her primary care physician. (Ex. 3, p. 60.) Petitioner received

Dilaudid and Phenergan injections. (Id. at 62.) Her diagnosis remained worsening

backache unspecified, with her cough and bronchospasm improved. (Id.) Later that

same day, petitioner followed up with Dr. McNulty who observed that petitioner had “a

great deal of pain in the mid thoracic region and also in the lumbar area bilaterally” with

5

“burning pain” in her hands. (Ex. 5, p. 9.) Petitioner received an osteopathic

manipulation and was prescribed hydromorphone. (Id. at 11.)

Petitioner was admitted to Mercy Hospital from March 5, 2015 to March 13, 2015.

(Ex. 4, pp. 79-84.) The reason for admission described a one-week history of “upper

and mid back pain, starting from mid chest to all the way down to [petitioner’s] hips on

both sides.” (Id. at 79) Humayun Tufail, M.D., reported that “petitioner does not have

any neurological symptoms” and had “no numbness, tingling in the legs.” (Id.) More

specifically, Dr. Tufail observed that “[h]er pain does not travel or radiate towards her

legs, but is essentially from mid back up to her hip level.” (Id.) Another report from the

day of admission noted that petitioner of lower back pain radiating down to her legs

complained for two weeks with “numbness in her feet and in her hands.” (Id. at 87.) In

her physical exam Tami Marriott, M.D., noted that petitioner “ha[d] a positive straight leg

raise with both legs, just lifting her feet about 8 inches off the bed.” (Id. at 88.) Dr.

Marriott “d[id] not appreciate any numbness or tingling at this time” and concluded

petitioner “ha[d] full strength.” (Id.)

On March 7, 2015, petitioner was scheduled to be discharged when she had two

large bowel movements with dark blood and clots. (Ex. 4, p. 75.) She was seen for

abdominal pain and rectal bleeding by gastroenterologist, Petre Sorin, M.D., who

ordered a colonoscopy. (Id. at 77.) That same day petitioner was seen by Bryan

McVay, M.D., where petitioner reported that “her problems began during the winter

holidays when she had a cough.” (Id. at 72.) Petitioner made “no comment[s] regarding

exacerbation or amelioration” except to say that the oral pain medications were

ineffective, though the IV narcotics relieved her pain. (Id.) Petitioner was transferred to

the intensive care unit for delirium and suspected ischemic colitis. (Id. at 72, 82.)

Petitioner’s colonoscopy revealed colon polyps, internal and external hemorrhoids

(reason for bleeding), and colonic diverticulosis. (Id. at 163.) Petitioner was discharged

from the ICU on March 8, 2015 and underwent a psychiatric evaluation for delirium. (Id.

at 165-66.) Tamara Lee, PMHNP, concluded that the cause of petitioner’s delirium was

multifactorial, though likely attributable to a combination of medications, hospitalization,

and lack of sleep. (Id.)

On March 12, 2015, Matthew Mason, D.O., observed that petitioner “may have

Bell’s palsy.” (Ex. 6, p. 438.) The nursing staff reported that petitioner’s facial droop

appeared “much worse than it previously had,” which prompted Dr. Mason to order

another CT scan. 5 (Id.) The CT scan of petitioner’s head was taken without contrast

and showed no evidence of acute intracranial abnormality. (Ex. 4, p. 145.)

On March 13, 2015, James Guetzkow ordered a transfer to Sacred Heart

Hospital where petitioner could be seen by a neurologist. (Ex. 4, p. 83.) Petitioner’s

5

It is unclear f rom petitioner’s records the exact onset of her f acial droop. This appears to be the first

mention of facial droop. (Ex. 6, p. 438; see also Ex. 4, p. 145 (CT scan taken without contrast on March

12, 2015 notes history of “facial droop”); Ex. 6, p. 386 (hospital transfer on March 13, 2015 noting “RN

stated [s]he is unable to move her legs or L arm, her L side of her face droops, her speech is slurred, CT

scan is clear”).)

6

discharge summary from Mercy Medical Center noted that petitioner “had an onset of

an unusual illness[] during the month before admission.” (Id. at 82.) Petitioner

“developed pain in her thoracic spine with numbness and tingling in [her] hands and

legs” and “had a cough for months with shortness of breath and chest heaviness, but no

fever.” (Id.) Her discharge diagnoses included: subacute flaccid paraparesis, acute

peripheral neuropathy, acute right Bell’s palsy, and thoracic back pain. (Id.) Petitioner

was also diagnosed with gastroenteritis, hemorrhoids, and sigmoid diverticulosis as well

as delirium and hallucinations. (Id.) On examination on the day of discharge, Dr.

Guetzkow found “no strength in [petitioner’s] extremities and no deep tendon reflexes or

Babinski response.” (Id. at 83.) Petitioner also complained of numbness in her hands,

which “predated the onset of the weakness in the legs.” (Id.) Petitioner was transferred

via ambulance to Sacred Heart Hospital. (Ex. 4, p. 83, Ex. 6, pp. 383-387.)

Once petitioner was admitted at Sacred Heart Hospital, she was seen by

neurologist Miguel Estevez, M.D. (Ex. 6, p. 227.) Petitioner’s chief complaint listed

“weakness.” (Id.) Petitioner complained of pain distally in her hands and feet as well as

right side peripheral cranial nerve VII palsy with difficulty closing her right eye and right

upper and lower facial muscle weakness. (Id. at 228.) She further reported difficulty

with swallowing, with weakness on the right lower part of her face “making it difficult to

hold things in her mouth without great care.” (Id.) Dr. Estevez described a “mixture of

pathology” in petitioner’s case—with peripheral nerve involvement and proximal muscle

weakness. (Id. at 229.) Petitioner was ordered to receive IV fluids and undergo labs to

rule out any rheumatologic pathology. (Id.) Dr. Estevez also ordered a lumbar

puncture. (Id. at 229, 234.)

On March 14, 2015, petitioner underwent a brain MRI without contrast, which

revealed no evidence of intracranial mass or abnormal enhancement, and no evidence

of acute ischemia. (Ex. 6, p. 236.) Later that day, petitioner also underwent a cervical

spine MRI which revealed multilevel cervical spondylosis, without evidence of abnormal

epidural or intramedullary spinal cord enhancement; significant disc degeneration at C5-

C6 resulting in moderate central stenosis and foraminal compromise; and asymmetrical

foraminal facet on the left at C4-C5, second to hypertrophic arthropathy. (Ex. 6, p. 235.)

On March 15, petitioner underwent a lumbar puncture which showed normal protein,

elevated glucose, serum total of two nucleated cells, sixty-eight percent lymph, negative

flow cytometry of the CSF, negative herpes simplex viruses, varicella zoster virus, and

syphilis of the CSF. (Ex. 6, p. 226, 234.) Later that day, neurologist Elaine Skalabrin,

M.D., ordered petitioner to receive five days of IVIG treatment. (Id. at 401.)

On March 21, 2015 petitioner saw neurologist Michael Balm, M.D., who

diagnosed her with GBS. (Ex. 6, pp. 226, 391.) Dr. Balm noted that there was an

atypical pattern of weakness, but that he was confident GBS was the correct diagnosis.

(See Ex. 6, p. 391.) Petitioner was scheduled to follow-up with Dr. Balm in six weeks.

(Id. at 390.)

On March 24, 2015 petitioner was discharged from Sacred Heart Hospital. (Ex.

6, pp. 225-227.) Her discharge diagnoses were GBS resulting in bilateral lower

extremity and upper extremity weakness and right peripheral seventh nerve weakness

7

as well as hyponatremia and neuropathic pain secondary to GBS. (Id. at 225.) During

the course of her hospitalization, petitioner’s MS panel revealed negative oligoclonal

bands, but evidence of blood-brain barrier breakdown. (Id. at 226.) Additional serology

showed negative mycoplasma, a low B6 level of unclear significance, negative

paraneoplastic antibodies of the CSF, and negative Rickettsia antibodies of the serum.

(Id.) Dr. Skalabrin explained that “[g]iven petitioner’s progressive lower extremity

greater than upper extremity weakness and essentially areflexic” she was given a

“[preliminary] 6 diagnosis of GBS.” (Id.) In the last several days of her IVIG treatment

petitioner showed significant improvement of her motor function; regained all of her

normal strength in her upper extremities (with the exception of a mild decrease in grip);

and a mild improvement of her facial droop with progressive improvement of her lower

extremity weakness. (Id.) However, petitioner still had significant impairment of the

proximal muscles, left worse than right. (Id.)

Petitioner was admitted for inpatient rehabilitation between March 24, 2015 and

April 29, 2015. (Ex. 4, pp. 178-179; Ex. 6, pp. 1010-1012.) At this time petitioner

presented with “significant neurologic deficits related to Guillain-Barre syndrome.” (Ex.

4, p. 178.) Petitioner was scheduled to receive physical therapy and speech therapy, as

well as rehabilitation nursing for bowel and bladder management. (Id.) Upon her

discharge, petitioner’s diagnoses included: “probable AIDP” (GBS) with predominant

involvement of the lower extremities, neuropathic pain secondary to GBS, hypertension,

hyponatremia (resolved), and osteoarthritis. (Ex. 6, p. 1011.) She was discharged

home and instructed to follow up with outpatient physical therapy and occupational

therapy at Mercy Medical Center and outpatient doctors’ appointments. (Id.)

On July 7, 2015 petitioner saw Dr. Balm for an outpatient neurology appointment.

(Ex. 9, pp. 6-10.) Petitioner described her condition as “95% better,” though she

reported some numbness in her feet and weakness of hip flexors and extensors, as well

as some difficulty getting up from a chair and climbing stairs. (Id. at 6.) She no longer

reported difficulties with speech or swallowing, though she complained of some mild

residual right facial weakness. (Id.) Petitioner reported to Dr. Balm that “she did have

combined Pneumovax and influenza vaccination sometime in late January, and had

onset of significant, severe, deep lumbar aching pain (which she ha[d] never had

before) within a few days after these immunizations.” 7 (Id.) Petitioner underwent an

EMG/NCV study which evidenced mild to moderate chronic axonal

polyradiculoneuropathy, with no evidence of significant demyelination—consistent with

the axonal variant of GBS. (Id. at 8- 9.) Dr. Balm expected petitioner would continue to

have a gradual and slow improvement of her symptoms. (Id.)

6

In f act, the record reads “pulmonary diagnosis of GBS,” which appears to be a typographic error. Based

on the record as a whole, and including to Dr. Balm’s later confirmatory diagnosis, preliminary appears to

best f it the meaning of the passage. (Ex. 6, p. 226.)

7

Petitioner’s vaccination record indicates that she received a Fluzone vaccine on September 30, 2014

and the Prevnar 13 vaccine on January 6, 2015. (Ex. 2.) There is no mention of an influenza vaccine in

January. (See id.)

8

Later that day, petitioner saw Erik Stowell, M.D., for a follow-up appointment.

(Ex. 8, pp. 5-6.) Petitioner described some residual nerve injury, as well as difficulty

walking without assistive devices. (Id. at 5.) She rated her lower extremity strength at a

4 to 5/5, though she still experienced decreased sensation in her hands and feet. (Id.)

Dr. Stowell recommended against petitioner returning to work and instructed her to

“avoid immunization in the future due to the possible relationship between the flu

vaccine and her developing AIDP.” 8 (Id. at 6.)

On October 12, 2015 petitioner returned to Dr. Stowell to discuss her longer-term

disability. (Ex. 8, p. 3.) Dr. Stowell reported petitioner’s history of AIDP “came on after

a flu vaccine with onset of symptoms sometime in January 2015.” (Id.) As of this visit

petitioner was no longer taking pain medications, though she continued to have

weakness and fatigue and felt she could no longer return to her job as a cake decorator.

(Id.) In his physical exam Dr. Stowell observed that petitioner continued to have lower

extremity weakness, requiring the use of a cane, as well as mild incomplete ptosis of

the right eye. (Id.) Dr. Stowell recommended against petitioner returning to work and

recommended a follow-up appointment in six months. (Id. at 3-4.)

In April 2016 petitioner saw Dr. Stowell and Dr. Balm for follow-up appointments.

(Ex. 8, p. 1; Ex. 9, p. 1.) On April 15, 2016, Dr. Stowell questioned whether petitioner

suffered from CIDP. (Ex. 8, p. 1.) Petitioner then reported to Dr. Balm for “evaluation of

CIDP from her rehab provider.” (Ex. 9, p. 1.) Dr. Balm observed that petitioner

“report[ed] no new symptoms, but continuation of chronic symptoms including

numbness and tingling in her toes, fingertips, and perioral area.” (Id.) His impression of

petitioner was that “she is not recovered from [her initial syndrome] (can take a couple

years to get back to complete normal if that happens), and she has been exercising,

has been gaining weight, and has not been sleeping.” (Id. at 4.) Dr. Balm explained

that “[m]any patients report acral paresthesias 9 and perioral tingling,” though he was

unsure whether these symptoms would improve. (Id.)

On November 8, 2017, petitioner went to Centennial Medical Group to establish

care with Shelli Flynn, M.D. (Ex. 33, p. 12.) She complained of pain in the bottom of

her feet and feeling “pins and needles.” (Id. at 14.) Dr. Flynn observed drooping of the

right side of petitioner’s mouth, and mild drooping of her right eyelid. (Id. at 15.) After

several years, Dr. Flynn explained, “it is unlikely she will get much more improvement at

this point.” (Id. at 16.)

By May 7, 2018 petitioner returned to Centennial Medical Group for a follow-up

on her weight and to request a prescription for sleeping pills. (Ex. 33, p. 6.) She

reported that she continued to have “lots of pain in her legs and feet.” (Id. at 8.)

8

Petitioner only received the Prevnar 13-vaccine in January 2015. (Ex. 2; see supra n. 5.)

9

See Acroparethesia, DORLAND’S MEDICAL DICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=724&searchterm=acroparesthesia (last visited Jan.

10, 2022) (“paresthesia of limbs and tips of other extremities due to nerve compression at any of several

levels, or polyneuritis[.]”)

9

Petitioner was continuing to use diclofenac gel, and Dr. Flynn recommended to continue

applying it daily. (Id. at 9.)

On July 16, 2020 petitioner presented to Evergreen Family Medicine for an

annual wellness visit. (Ex. 49, pp. 9-13.) Petitioner indicated that she fell due to her

neuropathy, though she did not report any injuries. (Id. at 12.) Petitioner’s general

appearance was active, alert, and no acute distress. (Id.) A fall risk assessment was

completed with increased fall risk noted. (Id.)

b. Petitioner’s declaration & supplemental declaration

Petitioner filed two declarations and also testified during the two-day entitlement

hearing. (Exs. 1, 54; Tr. 16-98.) In her first declaration, petitioner provided a detailed

account of her hospitalization and treatment. (Ex. 1, pp. 2-4.) During the hearing,

however, petitioner testified that she has difficulty recalling portions of her

hospitalization due to an acute onset of delirium. (Tr. at 44, 52, 83-84; see also Ex. 4,

p. 82 (petitioner transferred to intensive care unit for delirium with hallucinations).)

In her first declaration, petitioner declares that she suffered from the following

preexisting conditions: migraine headaches, arthritis, and high cholesterol. (Ex. 1, p. 1.)

She states that she received a flu vaccine on September 30, 2014, “a few months

before she received the pneumonia shot.” (Id.) Petitioner further states that she does

not recall having a primary care physician prior to her Prevnar 13 shot. (Id.) She was

“generally in good health,” and declares that before January 6, 2015 she did not have

any tingling or numbness in her extremities, and she did not have any difficulty walking.

(Id.)

On January 6, 2015, petitioner states that she received her Prevnar 13 vaccine at

the pharmacy located inside of the Albertsons where she worked. (Ex. 1, p. 2.)

Petitioner declares that on January 21, 2015 she went to the urgent care for a cough

and congestion. (Ex. 1, p. 2.) She further states that she informed the doctor that she

received “a pneumonia shot” a few weeks earlier. (Id.) Petitioner declares that she was

diagnosed with bronchopneumonia, prescribed medication, and given an inhaler. (Id.

(citing Ex. 3, pp. 1-10.)) During her testimony at the hearing, petitioner denied having

pneumonia, congestion, or trouble breathing. (Tr. at 23, 76.) Petitioner testified that

she recalled being prescribed an inhaler, though she didn’t use it. (Tr. at 23-24; 93.)

She further testified that she did not recall undergoing a chest x-ray on January 21,

2015. (Tr. at 24.) Petitioner testified that her husband attends all of her doctors’ visits

with her and typically fills out the paperwork. (Tr. at 67-68.)

Petitioner declares that she returned to Roseburg Urgent Care on February 3,

2015, still experiencing shortness of breath, cough, wheezing, and tingling. (Ex. 1, p.

2.) She was prescribed a prednisone taper and referred to a pulmonologist. (Id. (citing

Ex. 3, pp. 11-18.)) Petitioner states that “around this time” she started developing

“really horrible back pain.” (Id.) She states that she “had never felt this kind of pain

before,” but put off going to the doctor because she thought her symptoms would

10

improve. (Id.) Petitioner declares that the tingling in her hands and legs increased to

the point where she could no longer work. (Id.) Petitioner explains that she returned to

urgent care on February 26, 2015 and was prescribed a second prednisone taper for

her tingling and weakness. (Id.) During this visit, petitioner’s records indicate, in part,

that “[u]nrelated to her present complaints, [petitioner] [had] symptoms of carpal tunnel

syndrome.” (Tr. at 33; Ex. 3, p. 19.) Petitioner testified that she was never diagnosed

with carpal tunnel syndrome. (Tr. at 33-34, 37.) When asked why her medical records

indicated a history of carpal tunnel syndrome, petitioner testified “I don’t know if it was

put down that way or not, but I have no problem with my wrists.” (Tr. at 71.)

Petitioner states that her back pain, weakness and tingling continued to intensify;

and “[her] back pain spread to include [her] legs and hands.” (Ex. 1, p. 2.) Over the

course of the next week, petitioner states that she was seen “almost daily at the urgent

care because of [her] pain despite being on pain medication and getting injections for

the pain.” (Id.) She states that she was sent to the ER twice for different tests but

never diagnosed. (Id.) Petitioner’s medical records indicate that she underwent a

second chest x-ray on March 2, 2015. (Tr. at 38; Ex. 3, p. 35.) When asked about the

x-ray petitioner testified during the hearing that she could not remember much from this

period of time. (Tr. at 38; 41.) Petitioner declares that she established care with a

family doctor, Dr. McNulty, for an evaluation and labs. (Ex. 1, p. 2.)

Petitioner declares that she went to the Mercy Medical Center emergency room

on March 5, 2015 for possible hospital admission. (Ex. 1, p. 2 (citing Ex. 3, pp. 25-69;

Ex. 4, pp. 38-39, 58-59; and Ex. 5, pp. 5-17.)) Petitioner states she was hospitalized

between March 5, 2015 and March 13, 2015. 10 (Id.) During the hearing, petitioner

testified that “[s]ome of this I can’t remember…my mind was not working real good at

that point.” (Tr. at 44; see also Ex. 4, p. 82 (petitioner transferred to intensive care unit

for delirium with hallucinations).) Petitioner testified that she could not recall suffering

from rectal bleeding during her hospitalization, though she remembered undergoing a

colonoscopy. (Tr. at 82-83.) Subsequently, she was transferred to Sacred Heart

Hospital. (Ex. 1, pp. 2-3.) Petitioner testified that multiple doctors and nurses

discussed the possibility that a vaccine caused her GBS. (Tr. 50-51.) Though she

could not recall which doctor or nurse, she testified that her treating physicians inquired

about her vaccinations while she was at Eugene at Riverbend (Sacred Heart Hospital).

(Id.) Petitioner declares that she saw neurologist Dr. Estevez who observed her muscle

weakness and ordered labs as well as a lumbar puncture. (Ex. 1, p. 3 (citing Ex 6, pp.

227-230).) On March 15, 2015, she began a five-day course of IVIG infusions. (Ex. 1,

p.3; Tr. at 43.) Petitioner was ultimately diagnosed with GBS. (Tr. at 43; Ex. 1, p. 3.)

Petitioner declares that she was discharged from Sacred Heart Hospital on March 24,

2015 and transferred to Oregon Rehabilitation Center. (Id.) Petitioner remained in

rehabilitation for approximately six weeks. (Tr. at 44.)

10

Petitioner further testified that she was paralyzed while at Mercy Medical Center before being

transf erred. (Tr. at 46.) Petitioner described an incident where she “tried to stand up, and [she] just

completely went down.” (Tr. at 46.)

11

Petitioner declares that she received inpatient care at Oregon Rehabilitation

Center between March 24, 2015 and April 29, 2015, including daily physical therapy,

speech therapy, and occupational therapy. (Ex. 1, p. 3.) At the time she was

discharged, petitioner declares that she was able to walk 160 feet with a wheeled

walker, and “able to make transfer alone.” (Id.; Tr. at 44-45.) When she returned home,

petitioner states that her husband built a ramp leading to their house for her wheelchair.

(Ex. 1, p. 3.) For approximately one month, petitioner states that she slept on the first

floor of her house and struggled climbing the stairs. (Id.) She also traveled to her

mother’s assisted living facility to use the handicap shower. (Id.; Tr. at 45.)

Petitioner declares that she established care with a family medicine doctor, Dr.

Herbert, on May 1, 2015. (Ex. 1, p. 3.) At the time petitioner states that she used a

wheeled walker to walk. (Id.) According to petitioner, Dr. Herbert told her to continue

her pain management medications for her ongoing pain. (Id. (citing Ex. 7, pp. 10-14).)

Then, between May 7, 2015 and June 12, 2015, petitioner states that she completed

outpatient physical therapy sessions, and was discharged with a home exercise

program. (Id.) Petitioner declares that she was unable to use a treadmill due to

weakness and poor balance, though she was able to use a stationary bike for exercise.

(Id.; Tr. at 45.) At a follow-up appointment with her pain management doctor on May

26, 2015, Dr. Stowell encouraged petitioner to continue physical therapy. (Id. at 4

(citing Ex. 9, pp. 7-9).)

On July 7, 2015, petitioner had an outpatient neurology appointment with Dr.

Balm. (Ex. 1, p. 4.) Petitioner declares that she still had “numbness and weakness in

[her] legs and feet and fatigued easily.” (Id.) Petitioner describes “difficulty walking and

going up and down stairs.” (Id.) Petitioner states that she underwent a nerve

conduction study; and that Dr. Balm informed her that the results were consistent with

GBS. (Id. (citing Ex. 9, pp. 6-14.) That same day, petitioner had a follow-up

appointment with Dr. Stowell, “who [told] her to continue my home exercise program

and to avoid future vaccinations.” (Id. (citing Ex. 8, pp. 3-4.))

By October 2015, petitioner states that she required a cane to walk, she could

not walk far without tiring, and she “needed constant breaks” while grocery shopping.

(Ex. 1, p. 4.) According to petitioner, Dr. Stowell confirmed that she was unable to

return to work as a cake decorator. (Id. (citing Ex. 8, pp. 1-2; Ex. 9, pp. 1-5).

In April 2016 petitioner states that she returned to see Dr. Stowell and Dr. Balm.

(Ex. 1, p. 4.) She declares that she continued to easily fatigue “but made improvements

in [her] strength and no longer needed a cane to walk.” (Id.) Petitioner states that Dr.

Stowell “thought there was a possibility [she] could have CIDP but Dr. Balm’s assistant

confirmed [she] did not have CIDP.” (Id. (citing Ex. 8, pp. 1-2; Ex. 9, pp. 1-5.))

Petitioner declares that she still suffered from numbness and tingling in her hands and

feet. (Id.)

On February 24, 2017 petitioner established care with another family medicine

doctor, Dr. Grady. (Ex. 1, p. 4.) She declares that she suffered from numbness in her

12

hands, feet, and tongue, and that it “felt like [she] had a film on my feet when [she] tried

to walk.” (Id.) According to petitioner, “Dr. Grad reaffirmed that all of these symptoms

were caused by my GBS.” (Id. (citing Ex. 10, pp. 6-11.)) In June 2017 Dr. Grady

prescribed Voltaren gel for petitioner to apply to her feet and legs. (Id.)

Petitioner states that she still suffers the residual effects of GBS. (Ex. 1, p. 4; Tr.

at 46.) Petitioner testified that she still has “slight tingling in [her] fingers and in [her]

feet.” (Tr. at 46.) She further testified that she takes a sleeping pill at night “because

the tingling in my feet, [] wake me up, because I’ll still get a little jolt every once in a

while.” (Id.) She also described residual “numbness in my tongue[.]” (Id.) Lastly,

petitioner testified that she requires assistive devices for walking to the Coast or for

distance. (Id.)

In her supplemental declaration, petitioner states that she began noticing some

pain and tingling in her hands and feet in mid to late January 2015. (Ex. 54, p. 1.) She

furthers states that within a week or two of noticing the tingling, petitioner noticed

numbness in her hands and feet. (Id.) Petitioner describes the tingling sensations like

“jolts of lightning.” (Id.) These symptoms gradually worsened over the course of a

month, when petitioner declares that she had to stop working. (Id.) Petitioner states

that she complained regularly to her coworkers about the tingling and pain in her

fingers. (Id.) The pain in her fingers “was different from previous stiffness in [her]

hands that [she] would get from cake decorating.” (Id. at 2.)

Petitioner further states that she went to urgent care several times to be

evaluated, and told the doctor about the tingling and pain, “but the doctor was more

focused on the cough that [she] had at the end of December.” (Ex. 54, p. 2.) According

to petitioner, if the doctor had not asked about a cough or illness, she would not have

brought it up because she “did not feel like the cough was a big deal.” (Id.)

Lastly, petitioner declares that the final stub she received from Albertsons

covered the week of February 22, 2015 to February 28, 2015. (Ex. 54, p. 2.) She

states that she had to stop working at this time because she “had a very intense and

deep pain in [her] back in addition to the pain in [her] hands and feet.” (Id.) Petitioner

testified that based upon her final pay stub, she estimates that she quit working on

February 25, 2015. (Tr. at 30-31.)

c. Declaration of David Pierson

Mr. Pierson, petitioner’s husband, states that he and petitioner received

“pneumonia shots” on January 6, 2015. (Ex. 55, p. 1.) He describes petitioner’s cough

as lasting as long as a “mild cold would last.” (Id.) He states that petitioner’s cough

was gone before the start of the New Year. (Id.)

Mr. Pierson declares that when he would wake up during the night, he started

noticing petitioner “sitting on the edge of the bed and rocking back and forth like she

13

was on a rocking chair.” 11 (Ex. 55, p. 1.) He describes petitioner sitting “with her hands

about a foot away from her face in a prayer-like position” and “[i]t looked like she was

examining her hands.” (Id. at 2.) When her husband asked what was wrong, petitioner

“would tell [him] that her feet were aching but that she would be fine.” (Id.) He states

that “[t]his started happening more frequently when I would get up to go to the

bathroom.” (Id.) Subsequently, petitioner’s husband states that petitioner started

openly complaining about tingling in her hands and feet; and he observed her

“downstairs sitting and rocking.” (Id.)

Mr. Pierson further states that “around this time” petitioner developed pain along

with the tingling in her hands and feet. (Ex. 55, p. 2.) As he describes it, “[a]ll these

symptoms sort of developed together.” (Id.) He declares that petitioner’s tingling and

pain had been “occurring for around a month by the time that it got so bad that she had

to quit” her job. (Id.) According to her husband, petitioner’s symptoms never went

away, though now she is “steady on her feet but needs to concentrate closely when she

walks” and “also needs to use handrails when she goes up and down the stairs.” (Id.)

Mr. Pierson also testified at the hearing. (Tr. at 98-124.) His testimony was

primarily the same as the statements contained in his declarations. (See Ex. 55.) As

petitioner indicated in her testimony, her husband attends her doctors’ visits with her

and fills out the paperwork. (Tr. at 64, 67.) In his testimony, Mr. Pierson indicated that

some of the handwriting on the written forms was likely his handwriting, though all of the

signatures were that of petitioner. (Tr. at 119.) He testified that he visited petitioner

every day while she was at Mercy Medical Center, arriving around 10:00 A.M. and

leaving at approximately 7:00 P.M. (Tr. at 106.) He denied that petitioner had any

difficulty walking at the time she was admitted to Mercy Medical Center. (Tr. at 105.)

While at Mercy Hospital, he described an incident where petitioner fell trying to get out

of bed unassisted. 12 (Tr. at 107-108.) By the time petitioner was transferred Sacred

Heart Medical Center petitioner’s husband testified that petitioner had no feeling below

her waist. (Tr. at 107.) Regarding petitioner’s carpal tunnel diagnosis, Mr. Pierson

testified that she never indicated that she had carpal tunnel, and in fact “[s]he used her

hands all the time, and she never ever complained about anything wrong with her

hands.” (Tr. at 111.)

d. Declaration of Laura Day

In her declaration, Laura Day describes working side-by-side with petitioner

decorating cakes in the bakery. (Ex. 56, p. 1.) She states that petitioner was a “hard

worker who never complained.” (Id.) She further states that that petitioner started

complaining of pain and tingling in her hands and feet, though “since she was not a big

11

Mr. Pierson does not provide a date or timeline for the onset of these symptoms. (See Ex. 55, p. 1-2.)

During the hearing, Mr. Pierson testified that petitioner began rocking on the bed “[p]robably in January.”

(Tr. at 120.)

12

Mr. Pierson did not provide the date of this fall. (See Tr. at 107-108.)

14

complainer she would keep working through her shift.” (Id.) After several weeks of

petitioner’s complaints of pain, Ms. Day suggested she go home to rest. (Id.)

Ms. Day states that petitioner began having trouble writing on the cakes because

of the pain and tingling in her hands, such that “[she] would write on the cakes to help

her out.” (Ex. 56, p. 2.) According to Ms. Day, the day petitioner stopped working, 13

she and petitioner started their shift around 7:00 or 8:00 A.M. but “[b]y midday,

[petitioner] walked up and told [her] she could not do this anymore.” (Id.) She states

that petitioner left in the middle of the shift. (Id.) At this time, petitioner had been

complaining to Ms. Day for about a month. (Id.) She states that “[h]er complaints were

infrequent in the beginning but started to increase over the month.” (Id.) Ms. Day

declares that by the time petitioner stopped working, “she had tremendous pain and

weakness in her hands and feet.” (Id.)

Ms. Day’s testimony during the hearing substantially reflected the statements in

her declaration. (See Ex. 56.) Ms. Day testified that she did not know that petitioner

had experienced carpal tunnel syndrome (as reflected in petitioner’s medical records).

(Tr. at 14.) Furthermore, Ms. Day testified that she did not notice petitioner coughing

while at work. (Id.)

III. Expert Opinions

a. Petitioner’s expert Lawrence Steinman, M.D., initial report, Exhibit 12

Dr. Steinman received his medical degree from Harvard in 1973. (Ex. 13.) He is

currently a professor of the department of neurology at Stanford University. (Ex. 12, p.

1.) Dr. Steinman has treated patients, both adults and children, who suffered from

various forms of autoimmune disease of the nervous system, including optic neuritis,

acute disseminated encephalomyelitis (ADEM), inflammatory neuropathy, transverse

myelitis, neuromyelitis optica (NMO), and multiple sclerosis (MS). (Id.) Dr. Steinman’s

research focuses on how the immune system attacks the nervous system and he has

published on the subject of molecular mimicry. (Id. at 1-4; Ex. 13.) He holds over 50

American and European patents, including several U.S. patents relating to vaccines.

(Id. at 4.)

Dr. Steinman opines that petitioner’s Prevnar 13 vaccine triggered her GBS. (Ex.

12, p. 1.) Upon his review of petitioner’s medical records, Dr. Steinman notes that

petitioner’s onset of neuroinflammation began January 21, 2015, with tingling, reported

along with sneezing, congestion, cough, shortness of breath, and wheezing. (Id. at p. 4

(citing Ex. 3, p. 1.) On February 26, 2015 petitioner reported chills, fatigue, sweats,

tingling, weakness, cough, shortness of breath, and wheezing. (Id. at p. 4 (citing Ex. 3,

p. 19.) According to Dr. Steinman, tingling and weakness “are more likely than not

indications of GBS.” (Ex. 12, p. 4.) Later, in March 2015, Dr. Steinman observes that

13

Ms. Day does not provide the exact date other than to say, “the day that [petitioner] stopped working.”

(See Ex. 56, p. 1-2.)

15

petitioner was diagnosed with subacute onset flaccid paraparesis, acute peripheral

neuropathy, and Bell’s palsy – all indicative of GBS. (Ex. 12, p. 5) Dr. Steinman opines

that the onset of petitioner’s inflammatory neuropathy began fifteen days after she

received the Prevnar 13 immunization on January 6, 2015 – though he notes that

petitioner’s diagnosis of GBS occurred nine weeks later. 14 (Id.) Dr. Steinman bases his

theory of how the Prevnar 13 vaccine can cause GBS through the concept of molecular

mimicry. (Id. at 8-9.) He explains that molecular mimicry describes how shared

structures on a virus or bacteria, or in a vaccine, can trigger a cross-reactive response

to self. (Id. at 9.)

First Dr. Steinman notes that the Prevnar 13 vaccine contains a sterile

suspension of saccharides of the capsular antigens of Streptococcus pneumoniae

serotypes 1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F and 23F, individually linked to

non-toxic diphtheria CRM197 protein. 15 (Id. at 9 (citing Prevnar-13 Prescribing

Information 1-43 (last revised July 2016) (Ex. 23).) Dr. Steinman suggests that

antibodies to phospholipids are present in GBS patients. (Id. at 10 (citing B. Gilburd et

al., Autoantibodies to Phospholipids and Brain Extract in patients with the Guillain-Barre

Syndrome: Cross-Reactive or Pathogenic?, 16 AUTOIMMUNITY 23 (1993) (Ex. 24)).) Dr.

Steinman’s own research indicates that phospholipids are components of the myelin

sheath in humans, and that they are targeted by antibodies in neuroinflammation in the

central nervous system as well. (Id. (citing Jennifer Kanter et al., Lipid microarrays

identify key mediators of autoimmune brain inflammation, 12 NATURE M EDICINE 138

(2006) (Ex. 25)).) In Ho et al., Dr. Steinman and his fellow researchers found that

autoantibodies in MS target a phosphate group in phosphatidyl serine and oxidized

phosphatidyl choline derivatives. (Id. (citing Peggy P. Ho et al., Identification of

Naturally Occurring Fatty Acids of the Myelin Sheath That Resolve Neuroinflammation,

4 Sci. Translational Med. 137ra73 (2012) (Ex. 26)).) Notably, two of the six GBS

patients tested in the Gilburd et al. study showed reactivity to phosphatidyl serine or

phosphatidyl choline. (Id. (citing Gilburd et al, supra, at Ex. 24, p. 27.)) Based on these

studies Dr. Steinman concludes that “in inflammation of the central nervous system, in

humans with multiple sclerosis and in pre-clinical models of experimental autoimmune

14

Dr. Steinman explains that chronic inflammatory Demyelinating Polyneuropathy (CIDP) is “closely

related to GBS and it is considered the chronic counterpart of that acute disease.” (Ex. 12, p. 8 (citing

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) Information Page, NINDS,

http://www.ninds.nih.gov/disorders/cidp/cidp.htm (last updated Mar. 27, 2019, 16:20) (Ex. 21)).) He

opines, however, that petitioner suffered from GBS and not CIDP. (Ex. 12, p. 8.) Dr. Steinman states

that once petitioner was initially diagnosed and treated for her GBS with IVIg “she made a strong

recovery.” (Id.) Despite petitioner’s ongoing, chronic symptoms of tingling and numbness in her toes,

f ingertips and perioral area, he explains that petitioner “never regressed to the point where she was at

when she was f irst diagnosed with GBS.” (Id.) Rather, her symptoms plateaued. (Id.) Dr. Steinman

f urther adds that petitioner has only ever been diagnosed with GBS, and not CIDP. (Id.) Dr. Steinman

notes, however, if petitioner did have CIDP “the same medical theory would apply to show that the

Prevnar 13 immunization could similarly trigger CIDP.” (Id.)

15

“CRM197 is a nontoxic variant of diphtheria toxin isolated from cultures of Corynebacterium diphtheriae

strain Cy (β197) grown in a casamino acids and yeast extract-based medium. CRM197 is purified through

ultraf iltration, ammonium sulfate precipitation, and ion-exchange chromatography.” (Ex. 12, p. 9 (citing

Prevnar-13 Prescribing Information, supra, at Ex. 23).)

16

encephalomyelitis, as well as in inflammation of the peripheral nervous system there is

evidence of an antibody response to phosphatidyl-choline structures.” (Id. at 10-11

(citing Gilburd et al, supra, at Ex. 24; Kanter et al, supra, at Ex. 25; Ho et al., supra, at

Ex. 26).)

In his initial report, Dr. Steinman concludes that these phospholipids are present

in the Prevnar 13 vaccine. (Ex. 12, p. 11.) Looking at the Prevnar 13 package insert,

Dr. Steinman observes that the phospholipid phosphorylcholine is expressed in the 19A

component of Prevnar 13. 16 (Id. (citing Prevnar-13 Prescribing Information, supra, at

Ex. 23; Yi-Ping Chuang et al., Impact of the glpQ2 Gene on Virulence in a

Streptococcus pneumoniae Serotype 19A Sequence Type 320 Strain, 83 INFECTION AND

IMMUNITY 682 (2015) (Ex. 27)).) Beginning with his first supplemental report, however,

Dr. Steinman clarified that his theory pertains specifically to the phosphoglycerol

component of the vaccine and acknowledges that the vaccine does not include

phospholipids. (Ex. 35.)

In a perfect world, Dr. Steinman suggests that his theory would reach a higher

level of certainty if petitioner’s physicians had measured anti-phospholipid antibodies at

the time of her injury—before immune therapy with IVIg was administered. (Ex. 12, p.

18.) Yet, Dr. Steinman opines that components of the Prevnar 13 vaccine administered

to petitioner are immunologically cross-reactive with both myelin and axonal

components. (Id.) Ultimately, the antibodies created to combat the vaccine’s

components mistakenly interact with myelin and axonal mimics – triggering GBS. (Id.)

Even though petitioner’s diagnosis of inflammatory neuropathy was construed as

“chronic axonal polyradiculoneuropathy,” Dr. Steinman maintains that petitioner’s theory

about “the potential immune targeting of phosphatidyl choline is robust.” (Id. (citing Ex.

9, pp. 8-9.)) He explains that axons, like myelin, have the major membrane

phospholipid phosphatidyl choline. (Id. (citing David J. Read et al., Neuropathy Target

Esterase Is Required for Adult Vertebrate Axon Maintenance, 29 J. OF NEUROSCIENCE

11594 (2009) (Ex. 30.)).)

Finally, Dr. Steinman opines that the timing in petitioner’s case is consistent with

what has been reported for the onset of GBS. (Ex. 12, pp. 18-20.) He first notes that

petitioner’s inflammatory neuropathy began 15 days after receipt of the Prevnar 13

16

Dr. Steinman opines that immunity to this phospholipid is involved in neuroinflammation in both the

central and peripheral nervous systems. (Ex. 12, p. 11.) The enzyme for metabolizing lipids and

producing phosphorylcholine is present in strains 3, 6B, 19A, and 19F. (Id. (citing Jonathan D. Kornspan

and Shlomo Rottem, The Phospholipid Profile of Mycoplasmas, 2012 J. OF LIPIDS 1 (2012) (Ex. 28)).)

Strains 3, 19A, and 19F are present in Prevnar 13. (Ex. 12, p. 11 (citing Prevnar-13 Prescribing

Information, supra, at Ex. 23.)) Dr. Steinman also notes that he sought further clarification on the

chemistry of the Prevnar vaccine from the CDC, who could not provide proprietary manufacturing

inf ormation from the manufacturer. (Id. at 14-17.) Dr. Steinman also notes the well-known molecular

mimicry between Campylobacter and components of the peripheral nerve axon, triggering the axonal

variant of GBS. (Ex. 12, p. 17-18 (citing Guillain-Barre Syndrome Fact Sheet, NINDS,

http://www.ninds.nih.gov/disorders/gbs/details_gbs.htm (last updated Mar. 16, 2020, 13:03) (Ex. 20)).)

Dr. Steinman acknowledges that in petitioner’s case the trigger is the phospholipids in Prevnar 13, “but

the concept is congruent with the Campylobacter molecular mimic[.]” (Id. at 18.)

17

vaccine. (Ex. 12, p. 18.) Though petitioner’s actual diagnosis and approved treatment

for GBS was not made until approximately 9 weeks after the Prevnar 13 vaccination.

(Id.) First, Dr. Steinman notes an increased incidence of peripheral neuroinflammation

in GBS in this time frame in cases post-H1N1-vaccination in 1976. (Id. (citing Lawrence

B. Schonberger et al., Guillain Barre Syndrome following vaccination in the National

Influenza Immunization Program, United States, 1976-1977, 110 AM. J. OF

EPIDEMIOLOGY 105 (1979) (Ex. 31)).) While Schonberger et al. does not cover Prevnar

13, Dr. Steinman suggests that it serves as a “surrogate in this case.” (Id. at 20.)

Second, Dr. Steinman cites the study from Haber et al., which showed that for a person

of petitioner’s age, GBS was the third most frequently reported adverse reaction

following the Prevnar 13 immunization. 17 (Id. (citing 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 (2015) (Ex. 32)).) Taken together,

Dr. Steinman opines that the timing in petitioner’s case is consistent with the onset of

GBS.

b. Respondent’s expert Thomas P. Leist, M.D., Ph.D., initial report,

Exhibit A

Dr. Leist received his undergraduate degree from the University of Zurich in

Switzerland in 1982. (Ex. B.) He received his Ph.D. in biochemistry from the University

of Zurich in 1985. (Id.) Dr. Leist received his medical degree from the University of

Miami in 1993. (Id.) He completed his residency in Neurology at the Cornell medical

Center / Sloan Kettering Memorial Cancer Center in New York. (Id.) From 1997 to

2000 Dr. Leist was a clinical senior staff associate at NINDS at the NIH in Bethesda,

Maryland. (Id.) He is board certified in Psychiatry and Neurology, Adult Neurology.

(Id.) Dr. Leist is currently a professor of Neurology at Thomas Jefferson University and

the Chief / Division of Clinical Neuroimmunology Director of the Comprehensive Multiple

Sclerosis Center. (Ex. B.) He has participated as a researcher in multiple clinical trials

and authored or co-authored over fifty medical articles peer-reviewed journals. (Id. at 6-

11.)

Dr. Leist opines that no association has been established between the

pneumococcal conjugate vaccines (Prevnar-13 and Pneumovax 23) and GBS; and the

onset of petitioner’s acute neurological symptoms occurred outside the typical onset of

42 days, considered plausible based on Langmuir et al.’s reanalysis of GBS cases

following the 1976-1977 H1N1 flu vaccine. (Ex. A, p. 4 (citing Alexander D. Langmuir et

al., An Epidemiological and Clinical Evaluation of Guillain-Barre Syndrome Reported in

Association with the Administration of Swine Influenza Vaccines, 119 AM. J. OF

EPIDEMIOLOGY 841(1984) (Ex. A, Tab. 2.)).)

17

Table 2b in the Haber et al. study indicates that GBS was the third most frequently reported adverse

reaction following the Prevnar 13 vaccination among person aged 65 years and older between 2013 and

2015. (Haber et al., supra, at Ex. 32, p. 4.) More specifically, Table 2b reports 10 individuals out of 138

total who reported an onset of GBS post-vaccination. (Id.)

18

Turning first to the association between the pneumococcal conjugate vaccines

and GBS, Dr. Leist relies on two studies: Baxter et al. and Tseng et al. (Ex. A, pp. 4-5.)

He stresses that both of these studies failed to find an association between Prevnar-13

and GBS. (Id. (citing Roger Baxter et al., Lack of Association of Guillain-Barre

Syndrome with Vaccinations, 57 CLINICAL INFECTIOUS DISEASES 197 (2013) (Ex. A, Tab.

1); Hung Fu Tseng et al., Pneumococcal Conjugate Vaccine Safety in Elderly Adults, 2

OPEN FORUM INFECTIOUS DISEASES 100 (2018) (Ex. A, Tab. 3)).) Dr. Leist criticizes Dr.

Steinman’s theory, which he asserts does not offer evidence specifically linking the

Prevnar 13 vaccine and GBS. (Id.) Dr. Steinman references an article by Haber et al.,

which Dr. Leist stresses found that there was no disproportionate reporting of GBS

following Prevnar 13-vaccination. (Id.) In fact, Dr. Leist suggests that the authors of

Haber et al. did not opine on the causality of the cases of GBS that were reported to

VAERS based on temporal association. (Id.) Without more, Dr. Leist opines that there

is no demonstrated causal link between the 13-valent conjugate pneumococcal vaccine

and GBS. (Id.)

Regarding the onset of petitioner’s symptoms, Dr. Leist opines that petitioner

developed acute facial and lower extremity weakness on or about March 11 or 12, 2015

– or approximately sixty days after the administration of petitioner’s Prevnar 13 vaccine.

(Ex. A, p. 5.) Dr. Leist notes that petitioner was admitted for observation for her altered

mental state due to narcotic pain medication (for severe low back pain) on March 5,

2012, but no neurological deficits were appreciated at the time. (Id. (citing Ex. 4, p.

87.)) She was scheduled to be discharged March 7, 2015 when she had two bowel

movements with dark blood and clots, which prompted further evaluation. (Id. (citing

Ex. 4, pp. 72-75.)) Dr. Leist next observes that petitioner had a brain CT on March 12,

2015, after developing right facial weakness. (Id. (citing Ex. 4.2, p. 83; Ex. 4.3, pp. 144-

45.)) Reports from March 14, 2015 indicate that petitioner suffered “sudden onset [of]

r[ight] side lower facial weakness approx[imately] 3 days ago after the colonoscopy

[performed on March 8, 2015,] then developed upper r[ight] side facial/eye weakness

subsequently.” (Id. (citing Ex. 6.1, p. 192.)) Dr. Leist concludes, based on these

records, that petitioner developed symptoms of GBS approximately sixty days post-

vaccination. (Id.)

Dr. Steinman opined that the onset of petitioner’s GBS began fifteen days post-

vaccination, approximately January 21, 2015. (Ex. 12, p. 4.) Dr. Leist, however,

stresses that petitioner’s records from January 21, 2015 and February 2, 2015 note only

the presence of “tingling.” (Ex. A, p. 5-6.) Specifically, Dr. Leist emphasizes that

petitioner’s medical records do not elaborate on the term tingling, the records do not

mention when the tingling started, whether it was continuous or intermittent, or whether

there were aggravating factors (e.g., petitioner’s work in decorating cakes). (Ex. A, p.

6.) Dr. Leist suggests that petitioner’s history of carpal tunnel syndrome (Ex. 3, p. 19) or

her reported hyperventilation, associated with shortness of breath, may have caused

the tingling. (Ex. A, p. 6.) Moreover, Dr. Leist points to a two-to-three-week period

where petitioner reportedly felt much better, which prompted her to cancel her

appointment with a pulmonologist. (Id. (citing Ex. 3, pp. 13, 19.)) Dr. Leist

19

characterizes petitioner’s records as “separate time periods of different symptoms rather

than the crescendo of a single, extended episode of worsening sensory and motor

complaints as would be expected were the dose of pneumococcal conjugate vaccine

given on January 6, 2015 the inciting agent for the process.” (Ex. A, p. 6.)

According to Dr. Leist, another alternative cause for petitioner’s development of

acute neurologic symptoms is the suspected infection she suffered on February 26,

2015. (Ex. A, p. 6.) Petitioner complained of chills, sweats, fatigue and left thoracic

pain on February 26, 2015, which progressed to 8/10 mid back pain made worse with

movement and breathing by February 28, 2015, resulting in 10/10 back pain with

worsening numbness in the hands on March 1, 2015. (Id. (citing Ex 4, pp. 56, 61; Ex. 6,

p. 38.)) According to Dr. Leist, “[c]hills and sweats suggest [the] presence of an

infectious process and [petitioner] was started on cefdinir on February.” 18 (Ex. A, p. 6.)

Dr. Leist also proposes that the accepted time interval for GBS following flu

vaccination is informative. (Ex. A, p. 6.) According to Dr. Leist, that time interval is no

less than three days and no longer than forty-two days. (Id. (citing references Langmuir

et al., supra, at Ex. A, Tab. 2).) Dr. Leist opines that petitioner developed acute facial

and lower extremity weakness on or about March 11 or 12, 2015 – or approximately

sixty days after the administration of petitioner’s Prevnar 13 vaccine. (Ex. A, p. 5.) He

concludes that petitioner’s onset falls outside the forty-two day time interval. (Ex. A, p.

6-7.)

c. Dr. Steinman’s first supplemental report, Exhibit 35

In his first supplemental report, Dr. Steinman stresses that Baxter et al., a study

relied upon by Dr. Leist, only studied Pneumovax 23 not Prevnar 13. (Ex. 35, p. 3

(citing Baxter et al., supra, at Ex. A, Tab. 1.) He adds that Tseng et al., the second

study relied upon by Dr. Leist, reported a confidence interval 19 unadjusted at 1.22. (Ex.

35, p. 3 (citing Tseng et al., supra, at Ex. A, Tab. 3, p. 6.)).) Dr. Steinman explains that

a confidence interval above 1 “is not an indication that [the Prevnar 13] vaccine in the

elderly is ‘totally safe.’” (Ex. 35, p. 3.) Based on the epidemiological studies available,

Dr. Steinman states that while he may tell a patient that it is “highly unlikely” that the

Prevnar 13 vaccine would cause a complication like GBS, he cannot tell that patient that

it could not cause GBS. (Id.) Dr. Steinman also supplements his theory of molecular

mimicry. (Ex. 35, pp. 4-11.) Dr. Steinman now proposes that there are two molecular

18

Cef dinir is a “semisynthetic, third-generation cephalosporin effective against a wide range of bacteria,

used in the treatment of otitis media, bronchitis, pharyngitis, tonsilitis, sinusitis, bacterial pneumonia, and

skin and soft tissue infections; administered orally.” Cefdinir, D ORLAND’S MEDICAL D ICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=13359 (last visited Oct. 21, 2021.) From my review

of the record, it appears that petitioner was prescribed cefdinir on March 3, 2015. (Ex. 5, p. 2, 6.)

19

A conf idence interval is “a type of statistical interval estimated for an unknown parameter: a range of

values believed to contain the parameter, with a predetermined degree of confidence. Its endpoints are

the confidence limits, and it has a stated probability (the confidence coefficient) of containing the

parameter.” Confidence interval, D ORLAND’S MEDICAL D ICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=13359 (last visited Oct. 21, 2021.)

20

mimics that are relevant to GBS in the composition of Prevnar 13: one from the

phosphoglycerol in the composition of the pneumococcal polysaccharide antigen, and a

second from the CRM protein conjugate. (Id. at 4.)

Dr. Steinman identifies the phosphoglycerol component of the vaccine and

explains that the phosphoglycerol is essential for the Prevnar 13 vaccine to be effective.

(Ex. 35, pp. 4-11.) He notes that the polysaccharides in pneumococcus that are

contained in the Prevnar vaccine are complex and allow for the chemical attachment of

capsular polysaccharides via the glycerol moieties known as phosphoglycerol and

phosphocholine (or phosphatidylcholine). (Ex. 35, p. 6.) In support, Dr. Steinman

highlights diagrams and sections of the patent for Prevnar 13, showing the

phosphoglycerol molecules. (Id. (citing United States Patent 9,492, 559 B2 (Ex. 36)).)

The patent application provides, “[a]n important consideration during conjugation is the

development of conditions that permit the retention of potentially sensitive non-

saccharide substituent functional groups of the individual components, such as 0-Acetyl,

phosphate or glycerol phosphate side chains that may form part of the saccharide

epitope.” (Id. (citing United States Patent 9,492, 559 B2, supra, Ex. 36, p. 34)).) Dr.

Steinman stresses that the glycerophosphate and phosphorylcholine play a critical role

in the immunogenicity of Prevnar 13. (Id. at 9 (citing Janoi Chang et al., Relevance of

O-acetyl and phosphoglycerol groups for the antigenicity of Streptococcus pneumoniae

serotype 18C capsular polysaccharide, 30 VACCINE 709007096 (2012) (Ex. 37);

Czeslaw Lugowski and Harold J. Jennings, Structural determination of the capsular

polysaccharide of Streptococcus pneumoniae Type 18C, 131 CARBOHYDRATE RES. 119

(1984) (Ex. 38); Junichiro Ohori et al., Phosphorylcholine intranasal immunization with a

13-valent pneumococcal conjugate vaccine can boost immune response against

Streptococcus pneumoniae, 38 VACCINE 699 (2020) (Ex. 39)).) Dr. Steinman quotes the

Chang et al. study to show that the glycerophosphate side chain must be preserved in

the manufacturing process to conserve an adequate immune response to the 18C

component. (Ex. 35, p. 8.) Lastly, Dr. Steinman cites a study, from Nakos et al., where

phospholipid antibodies were found in patients with GBS. (Ex. 35, p. 10 (citing George

Nakos et al., Anti-phospholipid antibodies in serum from patients with Guillain-Barre

syndrome, 31 INTENSIVE CARE M ED. 1401 (2005) (Ex. 40)).) The authors found that

phosphatidylinositol, cardiolipin, phosphatidic acid, and phosphatidylcholine were the

main antigens. (Id.)

The second area of molecular mimicry concerns a protein component, called

CRM197. (Ex. 35, p. 11 (citing Prevnar-13 Prescribing Information, supra, at Ex. 23).)

This protein component is used to conjugate the pneumococcal polysaccharides in the

Prevnar 13 vaccine to an immunogenic protein carrier. (Id.) Dr. Steinman explains that

Contactin-1 is “targeted in some cases of GBS.” (Id. (citing Janev Fehmi et al., Nodes,

paranodes and neuropathies, 89 J. OF NEUROLOGY, NEUROSURGERY, AND PSYCHIATRY 61

(2018) (Ex. 41); Constance Manso et al., Contactin-I IgG4 antibodies cause paranode

dismantling and conduction defects, 139 BRAIN 1700 (2016) (Ex. 42); Yumako Miura et

al., Contactin I IgG4 associates to chronic inflammatory demyelinating polyneuropathy

with sensory ataxia, 138 BRAIN 1484 (2015) (Ex. 43)).) In order to test the components

21

of the Prevnar 13 vaccine, Dr. Steinman conducted BLAST searches 20 to align

contactin-1 with the components of CRM197 in the Prevnar vaccine. (Ex. 35, p. 11) Dr.

Steinman classifies his criteria for a molecular mimic as a run of 5 or more of 12 amino

acids that are identical. (Id.) Based on his own published research, Dr. Steinman

opines that the identity of 5 of 12 amino acids were sufficient to “trigger clinically

relevant neuroinflammation with paralysis.” (Id. at 13 (citing Anand Gautam et al., A

polyalanine peptide containing only five native myeline basic protein residues induces

autoimmune encephalomyelitis, 127 J. OF EXPERIMENTAL M EDICINE 605 (1992) (Ex. 46);

Anand Gautam et al., Minimum structural requirements for peptide presentation by

major histocompability complex class II molecules: Implications in induction of

autoimmunity, 91 PROCEEDINGS OF THE NAT’L. ACAD. OF SCENCES OF THE U.S. OF AM. 767

(1994) (Ex. 47); Anand Gautam et al., A viral peptide with limited homology to a self-

peptide can induce clinical sign of experimental autoimmune encephalomyelitis, 161 J.

OF IMMUNOLOGY, 60 (1998) (Ex. 48)).) He also adds that the 5/12 amino acids that are

identical need not be consecutive. (Ex. 35, p. 12.)

Dr. Steinman submitted his BLAST results in the Immune Epitope Database

(IEDB) 21 to determine whether other researchers have identified the epitope(s). (Ex. 35,

p. 16.) Dr. Steinman first tested the sequence WEQAKALSVE and determined that this

sequence is found on human immune cells and it is also “an epitope in diphtheria toxin,

which provide the basis for CRM197.” (Id.) Dr. Steinman tested a second sequence,

EYMAQACAGNRVRR, which also has “known cross-reactivity with epitopes described

in humans and on the c. diphtheria microbe that is the basis for CRM197.” (Id. at 17.)

These results, Dr. Steinman explains, demonstrate a compelling theory that molecular

mimics in the Prevnar 13 vaccine, received by petitioner, trigger inflammatory

neuropathy culminating in GBS. (Id.)

d. Dr. Leist’s supplemental reports, Exhibits C & D

In his first supplemental report, Dr. Leist opines that Dr. Steinman’s theory

regarding how an immune response against phospholipids causes GBS is not

applicable to the Prevnar 13 vaccine because phospholipids are not a listed component

of the vaccine. (Ex. C, pp. 1-2.) Dr. Leist explains that the polysaccharide preparations

used in pneumococcal conjugate vaccines “are purified and the identity of the individual

polysaccharides is ascertained by testing modalities including NMR, residual protein,

antigenicity, and molecular weight (ADDC pamphlet).” (Id. (citing Prevnar Prescribing

Information, 1-43 (last updated Aug. 2017) (Ex. C, Tab. 2); Prevenar 13 suspension for

20

According to its own website, the Basic Local Alignment Search Tool (BLAST) “can be used to infer

f unctional and evolutionary relationships between sequences as well as help identify members of gene

f amilies.” See https://blast.ncbi.nlm.nih.gov/Blast.cgi (last visited Oct. 22, 2021).

21

The IEDB “catalogs experimental data on antibody and T cell epitopes studied in humans, non-human

primates, and other animal species in the context of infectious disease, allergy, autoimmunity, and

transplantation. The IEDB also hosts tools to assist in the prediction and analysis of epitopes.” See

https://www.iedb.org/home_v3.php (last visited Sept. 1, 2021).

22

injection, EMC, https://www.medicines.org.uk/emc/product/453/smpc/ (last updated

Mar. 2021) (Ex. C, Tab. 3)).) Additionally, Dr. Leist notes that the CRM197 carrier

protein used in the Prevnar 13 vaccine is extensively purified. (Id.) Based on the

filtration steps involving ultrafiltration, precipitation, chromatography, and centrifugation,

Dr. Leist maintains that these components are not likely present in the vaccine beyond

trace amounts. (Id.)

In his second supplemental report, Dr. Leist reiterates that alternative causes

more than likely explain the onset of petitioner’s tingling symptoms and her GBS

generally. (Ex. D, p. 2.) Dr. Leist maintains that the tingling that petitioner reported in

her January 21 and February 6, 2015 visits was likely related to carpal tunnel. (Id.) Dr.

Leist highlights a note from petitioner’s February 26, 2015 visit which reads: “[u]nrelated

to [her] present complaints-patient having symptoms of carpal tunnel syndrome-[she]

[sic] is a cake decorator for Albertson’s-she does plan to retire in less than one year.”

(Id. (citing Ex. 3, p. 19.)) Moreover, Dr. Leist notes records from an emergency room

visit on March 2, 2015 indicating that “[petitioner] has no leg numbness, tingling, or

weakness” (Ex. 4, p. 58); records from March 5, 2015 where Dr. Marriott indicated

petitioner’s 10-point review of systems was negative and observed no numbness or

tingling (Ex. 4, pp. 87-88) 22; and records on March 7, 2015 where Dr. McVay recorded

no focal deficits. (Ex. 4, p. 74.) Instead, Dr. Leist maintains that petitioner’s new

neurological symptoms appeared on or about March 11, and 12, 2015. (Ex. D, p. 2

(citing Ex. 4, p. 58.)) Dr. Leist highlights that

GBS usually begins abruptly with distal, relatively symmetrical onset of

paresthesias. Sensory disturbances are accompanied by or quickly

followed by progressive weakness. Patients are able to identify a definite

date of onset of sensory and motor disturbance. Progression is rapid, with

about 50% of patients reaching clinical nadir by two weeks and more than

90% by 4 weeks.

(Ex. D, p. 2 (quoting Ted M. Burns, Guillain-Barre Syndrome, 28 SEMINARS IN

NEUROLOGY 152 (2008) (Ex. D, Tab. 1)).) Not only does Dr. Leist stress that petitioner

here did not experience symptom onset within the 42-day time interval, but he also

maintains that an infectious condition is likely the proximate cause of her acute

progression of symptoms. (Ex. D, p. 2.)

Dr. Leist also disagrees with Dr. Steinman’s assertion that phospholipids are

present in Prevnar-13. (Ex. D, p. 3.) While Dr. Steinman explains that

phosphorylcholine is present in the 19A component of the vaccine, Dr. Leist stresses

that the Chuang et al. article actually reports on the effect of the glgQ2 gene on

virulence of streptococcus pneumoniae serotype 19A. (Id. (citing Chuang et al., supra,

at Ex. 27.)) He emphasizes that “[t]he article does not provide information of the

22

In the history of present illness, Dr. Marriott recorded that petitioner “states she does have numbness in

both feet and hands” though upon Dr. Marriott’s physical examination Dr. Marriott reports “I do not

appreciate any numbness or tingling at this time. She has full strength.” (Ex. 4, p. 87)

23

constituents of the Prevnar-13 vaccine.” (Ex. D, p. 3.) In fact, Dr. Leist asserts that the

Prevnar vaccine is a conjugate polysaccharide vaccine, and it does not contain

streptococcus pneumoniae components other than polysaccharides. (Id. (citing United

States Patent 7955605 Section 14 (Ex. D, Tab. 2.))

Regarding Dr. Steinman’s theory regarding phosphoglycerol, Dr. Leist

summarizes Dr. Steinman’s theory as follows: “since select patients with Guillain-Barre

syndrome have antibodies against phospholipids and since phosphoglycerol residues

are a building block[] of phospholipids[,] substances containing phosphoglycerol

residues such as select polysaccharides would…be expected to be able to induce

antiphospholipid antibodies.” (Ex. D, p. 5.) This theory, Dr. Leist explains, is based on

“the inaccurate assumption that Prevnar-13 contains phospholipids and that

phosphoglycerols and phospholipids can be considered as essentially the same.” (Id. at

4.)

Finally, in response to Dr. Steinman’s theory regarding the CRM197 carrier

protein, Dr. Leist likewise agrees that antibodies to contactin-1 have been described in

patients with GBS and CIDP. (Ex. D, p. 4.) However, Dr. Leist stresses that Dr.

Steinman takes too great an analytical leap. Dr. Leist maintains that Dr. Steinman’s

BLAST search results do not provide any causal link to show that CRM197

protein-containing polysaccharides vaccines actually induce antibodies against

contactin-1. (Id.) Nor does Dr. Steinman discuss why this theoretical mechanism is

more likely to cause injury than the infection that Dr. Leist identified in petitioner’s record

in late February / beginning of March 2015. (Id. (citing Ex. 3, p. 43.))

e. Dr. Steinman’s second supplemental report, Exhibit 50

Dr. Leist opines that petitioner showed a “[l]ack of progression of neurologic

symptoms for well over a month” which he argues is inconsistent with the expected

course of GBS. (Ex. D, p. 2.) In response, Dr. Steinman argues that petitioner’s

records show a progression of numbness and tingling more likely than not related to

GBS. (Ex. 50, p. 1-2.) Dr. Steinman notes petitioner’s symptoms of tingling and

weakness appearing on February 26, 2015. (Id. at 1-2 (citing Ex. 3, p. 19).) At a follow-

up on March 1, 2015, petitioner reported numbness and tingling in both hands since

February 28, 2015. (Ex. 50 p. 2 (citing Ex. 3, pp. 36-41).) According to Dr. Steinman,

these records show that “there was a progression of the numbness and tingling to

involve symmetrically both hands.” (Ex. 50, p. 2.) Dr. Steinman notes that petitioner

presented to the ER at Mercy Hospital on March 2, 2015 reporting pain in her left upper

back, which also spread to her hands and legs, though no leg numbness, tingling, or

weakness was reported. (Ex. 50, p. 3 (citing Ex. 4, pp. 58-59).) According to Dr.

Steinman, petitioner’s discharge summary on March 13, 2015 reveals “further

manifestations of inflammatory neuropathy.” (Ex. 50 p. 3.) Quoting the discharge

summary, Dr. Steinman notes that petitioner “had an onset of an unusual illness the

24

month before admission;” 23 she developed subacute flaccid paraparesis, acute

peripheral neuropathy, Bell’s palsy, and thoracic back pain. (Ex. 50. p. 3 (citing Ex. 4,

pp. 82-84) (emphasis in original).) Taken together, Dr. Steinman seems to suggest that

these records evidence a progression that is consistent with GBS. (See id.)

Dr. Steinman further disagrees with Dr. Leist’s reliance on the Burns article. (Id.)

Dr. Steinman proposes that the clinical course and onset described by Burns represents

the typical onset, while petitioner’s case was clearly “not of the ‘usual’ variety that Dr.

Burns writes about.” (Id.) Regarding Dr. Leist’s opinion regarding alternative causes for

petitioner’s GBS, Dr. Steinman stresses that no infectious condition was ever

diagnosed. (Ex. 50, p. 4.) Dr. Steinman states that the most commonly associated

agent with GBS is Campylobacter jejuni. (Id. (citing Hans-Peter Hartung, Infections and

the Guillain-Barre syndrome, 66 J. OF NEUROLOGY, NEUROSURGERY, AND PSYCHIATRY 277

(1999) (Ex. 51)).) Yet, Dr. Steinman explains that it is difficult to “invoke an infectious

cause for a condition without evidence of the infection.” (Ex. 50 p. 4.)

Finally, Dr. Steinman offers additional support in favor of his molecular mimicry

theory relative to CRM197. (Ex. 50, p. 5.) He proposes an added step which he

explains will further validate petitioner’s causal theory. (Id.) Dr. Steinman reiterates that

two regions of mimicry have been studied between contactin-1 and CRM in Prevnar 13

vaccine. (Id.) Citing a study by Raju et al., Dr. Steinman observes that humans have

been shown to mount T cell responses to these regions of the diphtheria molecule:

WEQAKLSVE and EYMAQACAGNRVRR. (Id. (citing Raghavanpillai Raju et al.,

Epitopes for human CD4+ cells on diphtheria toxin: structural features of sequence

segments forming epitopes recognized by most subjects, 25 EUR. J. OF IMMUNOLOGY

3207 (1995) (Ex. 52)).) Dr. Steinman highlights the results of this study, which differ in

only one amino acid from CRM, which he stresses provides “actual detailed data for

molecular mimics in the CRM in the Prevnar 13 vaccine received by petitioner.” (Id. at

6.)

f. Dr. Steinman’s testimony

Dr. Steinman’s testimony during the entitlement hearing was substantially similar

to his expert reports. (Exs. 12, 25, 50; Tr. at 125-225; 319-331.) Consistent with his

reports, Dr. Steinman explained that the “majority of cases of Guillain Barre that are

associated with a microbe, they’re known microbes.” (Tr. at 132-33.) Among those

cases, forty-five to sixty percent of cases are associated with Campylobacter, ten to

fifteen percent of cases are associated with CMV, cytomegalovirus, and five to ten

percent of cases are associated with Epstein Barr virus (EBV) infection. (Tr. at 133.)

Regarding onset in these cases, I asked Dr. Steinman whether onset of infection

occurred before the onset of GBS, or at some later point during the course of the

disease. (Tr. 134-45.) Dr. Steinman testified that the infection “could have been at its

tail end four weeks or one week before, or it could have been newly diagnosed at that

23

Based on my review of the records, petitioner was admitted to the hospital on March 5, 2015. (Ex. 4, p.

79-80.) By Dr. Steinman’s estimation above this would place petitioner’s “onset of unusual illness the

month before admission” at or around February 5, 2015.

25

point” but acknowledged that the exact timing of onset of infection remains unclear. (Tr.

at 135.) At best, Dr. Steinman testified that “there was some evidence of a predated

infection.” (Id.)

In petitioner’s case, Dr. Steinman testified that the onset and duration of

petitioner’s cough, and whether her cough evidences an infection, is difficult to interpret

without a microbial diagnosis. (Tr. at 135-36.) Dr. Steinman testified that petitioner

tested negative for several possible infectious causes of GBS (Tr. 137-40):

Campylobacter (Ex. 6, p 211-12), c. difficile (Id.), Rickettsia and Leptospirosis (Id. at

213), and Borrelia (Id. at 215). Results for syphilis, herpes simplex virus, and the zoster

virus were also all negative. (Ex. 6, pp. 215-16.) Petitioner was not tested for Epstein

Barr virus (“EBV”). (Tr. at 140; see Ex. 6, pp. 211-223.) Dr. Steinman observed,

however, that “[EBV is] one of the most common persistent viruses that we all pick up,

usually somewhere in adolescence.” (Tr. at 140.) Dr. Steinman further testified that

petitioner’s chest x-rays were normal and did not support a diagnosis of

bronchopneumonia. (Tr. at 141.) Petitioner’s cough, according to Dr. Steinman, was a

nagging cough, one that was “unsolved and didn’t amount to a pneumonia.” (Tr. at

142.)

Concerning the typical course and onset of GBS, Dr. Steinman testified that he

places the outermost medically appropriate onset date for vaccine-caused GBS at eight

weeks, or 56 days, post-vaccination. (Tr. at 146, 200.) Dr. Steinman draws support for

this time frame from the Schonberger article. (Tr. at 144 (citing Schonberger et al.,

supra, Ex. 31.)) Dr. Steinman testified that Figure 6 in Schonberger shows the

expected incidence rate “remain[s] high, above that cross-hatched area, at eight weeks,

and then they diminish a little more at nine and ten weeks, and then they finally blip

down to the baseline at eleven weeks.” (Tr. at 144 (citing Schonberger et al., supra, Ex.

31, p. 9.)) This, Dr. Steinman concludes, leads him to place “a cutoff somewhere

around the end of week eight.” (Tr. at 144-45.) Dr. Steinman’s testimony regarding

petitioner’s symptoms reflected the same theory presented in his expert reports, placing

onset of petitioner’s GBS on approximately January 21, 2015. (Tr. at 147-152.) He

testified that the nadir of petitioner’s GBS occurred “somewhere in the first, second

week of March, when [petitioner] was put on IVIG.” (Tr. 152-53.)

Dr. Steinman’s testimony concerning his theories of molecular mimicry were

substantially the same as those expressed in his expert reports. (Exs. 12, 35, 50; Tr. at

154-188.) During his testimony, Dr. Steinman referenced a three-dimensional model

from the Bryson exhibit (Exs. 58, 59) to identify the 23F carbohydrate, a component of

the Prevnar 13 vaccine, as well as the Lys 100 (or Lysine), an antibody in humans that

binds to the phosphate. (Tr. at 164.) Examining the same model, in the Lysine, Dr.

Steinman identified the side chain as the phosphate head group. (Id.) Dr. Steinman

also referenced Figure 2B and 2D in the Ho et al. article, where he identified on the

diagram the phosphate head group in seven out of eight examples. (Tr. at 174-77; Ho

et al., supra, Ex. 26, Fig. 2B, Fig. 2D, p. 4.) In addition to the presence of these

antibodies, I asked Dr. Steinman about the significance of these specific antibodies

demonstrating a cross reaction. (Tr. at 178.) Pointing to Table 2 in Gilburd et al., Dr.

26

Steinman testified that among six patients, two showed antibodies to

phosphatidylethanolamine, one showed antibodies to phosphatidylserine, and one

showed antibodies to phosphatidylcholine, while the remaining two patients showed

antibodies to cardiolipin. (Tr. at 178-79 (citing Gilburd et al, supra, Ex. 24, Tab. 2, p.

26.)

Regarding the course of petitioner’s GBS, Dr. Steinman testified that “the

crescendo was very low, and it began to intensify about 30 days before the 5th day of

March, and then it became deafeningly loud at the end of February and the first few

days of March.” (Tr. at 326.) Concerning petitioner’s diagnosis of subacute flaccid

paraparesis, I asked Dr. Steinman how he interpreted the characterization of

“subacute.” (Tr. at 326-37.) Dr. Steinman testified that while “subacute is not chronic,”

subacute can be “a few weeks,” though he admitted that “I don’t think it has a formal

definition.” (Tr. at 327.)

g. Dr. Leist’s testimony

The testimony provided by Dr. Leist also closely resembled the opinions offered

in his expert reports. (Exs. A, C, D; Tr. at 229-318.) Dr. Leist estimates that petitioner’s

onset of GBS occurred in or about early March 2015—based on petitioner’s records

indicating that she developed rapid lower extremity weakness on or about March 12,

2015. (Tr. at 236.) He testified that “[t]he rapid onset of flaccid paralysis is one of the

cardinal features of Guillain-Barre syndrome.” 24 (Tr. at 237.) Dr. Leist opines that

petitioner’s lower extremity weakness developed on or about March 12, 2015 based on

a record from March 9, 2015. (Id. (citing Ex. 4, p. 165.) He testified that on March 9

petitioner “was moving all four extremities[,] [s]he wanted to get out of bed,” and “she

wanted to go to the chair.” (Tr. at 238.) Dr. Leist interprets this record to mean that

petitioner “was moving her extremities on that date, meaning that the later documented

weakness in the lower extremities was not present on March 9, 2015.” 25 (Id.) Taken

together, Dr. Leist testified the fact that petitioner was “moving around March 9,” she

developed new neurologic symptoms around March 12 (lower extremity weakness), she

was referred to a higher level of care, and the results of her lumbar puncture on March

15, all indicate that petitioner’s onset of GBS “occurred around that period of time.” (Tr.

at 243.) I asked Dr. Leist, given the expected course of GBS and given that petitioner

experienced her severest weakness in mid-March, whether it was reasonable to place

her nascent symptoms of weakness as occurring as early as mid-February. (Tr. at

245.) Dr. Leist did not discount this possibility. (See id.) Dr. Leist opined that onset of

GBS resembles a clear crescendo, as opposed to a variable course. (See Tr. at 246.)

24

A rapid onset of flaccid paralysis, Dr. Leist testified, can be characterized as paralysis occurring over

two weeks in 50 percent of cases and within four weeks in 90 percent of cases. (Tr. at 243 (citing Burns,

supra, at Ex. D, Tab. 1, p. 153).)

25

Dr. Leist acknowledged that GBS presents as ascending weakness and that it is not necessary for a

person to be unable to move all four extremities in order to be diagnosed with an onset of GBS. (Tr. at

268.)

27

Dr. Leist further testified that petitioner’s significant bowel event or the

“recrudescence of respiratory complaints” at the end of February could have been a

likely cause of petitioner’s GBS. (Tr. at 246.) Though the stool culture was negative,

Dr. Leist explained that stool cultures are invariable, due to the time difference between

when the infection would occur and the actual onset of GBS. (Tr. at 247.) The stool

culture, in his opinion, could not definitively rule out the presence of C. jejuni. (Id.) Dr.

Leist further proposed that the antibiotics that petitioner was prescribed could have

interfered with the detection of, or eliminated, the C. jejuni pathogen. (Tr. at 249.)

Dr. Leist testified that he disagrees with Dr. Steinman’s molecular mimicry theory

because it is based on “the inaccurate assumption that Prevnar-13 contains

phospholipids 26 and that phosphoglycerol and phospholipids can be considered as

essentially the same.” (Tr. at 257.) Dr. Leist testified he “do[es not] think that lipids are

a named constituent of the Prevnar 13” vaccine. (Id.) Therefore, Dr. Leist stresses that

the applicability of the Ho et al. article is “at most tangential.” (Id.) Dr. Leist also

criticizes Dr. Steinman’s reliance on Nakos, noting that the authors could not determine

whether the antibodies at issue are “a sign of injury, or whether it was actually

pathophysiologically important[.]” (Tr. at 260-61.) Overall, Dr. Leist testified that he

agrees the individual steps in Dr. Steinman’s theory are logical, though he opines that

they don’t connect. 27 (Tr. at 264-65.)

Looking at petitioner’s discharge summary, Dr. Leist testified that petitioner was

diagnosed with subacute flaccid paraparesis. (Tr. at 302.) Dr. Leist further testified that

“subacute can be a day or two or so.” (Tr. at 306.) While in contrast, he testified that

acute would mean “less than a 24-hour period.” (Tr. at 307.) Petitioner’s discharge

26

In his initial report, Dr. Steinman opined that the “trigger is the phospholipids in Prevnar 13[.]” (Ex. 12,

p. 18.) However, Dr. Steinman explained that after reviewing the Prevnar 13 vaccine patent he

determined that the mimic is phosphoglycerol. (Tr. at 329.) This ref inement in Dr. Steinman’s opinion is

also addressed in greater detail in the Koller decision. Koller v. Sec’y of Health & Human Servs., No.16-

439V, 2021 WL 5027947, *16-17 (Fed. Cl. Spec. Mstr. Oct. 8, 2021).

27

Specifically, he testified

So f rom that point of view, obviously there is a sequence homology. You also see some

individuals who have these response, at least the individuals that were used for Exhibit 52

[Raju et al.], can have such a response without having illness. So in a certain way, it

reminds me a little bit of the – it reminds me that there are individual arguments, but that

the consequential steps in between so actually injury occurs as a consequence of this

sequence homology or as a consequence of this – of an immune response that is present

against a certain sequence, like in these healthy individuals that we just talked about, these

steps are not there. So in a certain way, the way almost would have to be the opposite way

around. Take patients that have – if they exist, which I would think would be difficult to do

– that have alleged injury secondary to the Prevnar, and then show that they developed –

that they developed immune response on the other side. I mean, Dr. Steinman proposes

individual steps, that individually look logical, but they don’t connect…I view them as

speculative, so from that point of view, they don’t connect in what I would consider a reliable

theory.

(Tr. at 264-65.)

28

summary was authored on March 13, 2015. (Tr. at 306; Ex. 4, p. 83.) Therefore, Dr.

Leist estimates that petitioner’s onset was likely on or about March 12, 2015—according

to his definition of subacute. (Tr. at 306-307.) According to Dr. Leist, his interpretation

is also supported by the record as showing that “on [March 9], [petitioner] was not

flaccid” because she was able to move all four extremities. (Tr. at 306.)

IV. Applicable Statutory Scheme

Under the National Vaccine Injury Compensation Program, compensation

awards are made to individuals who have suffered injuries after receiving vaccines. In

general, to gain an award, a petitioner must make a number of factual demonstrations,

including showing that an individual received a vaccination covered by the statute;

received it in the United States; suffered a serious, long-standing injury; and has

received no previous award or settlement on account of the injury. Finally – and the key

question in most cases under the Program – the petitioner must also establish a causal

link between the vaccination and the injury. In some cases, the petitioner may simply

demonstrate the occurrence of what has been called a “Table Injury.” That is, it may be

shown that the vaccine recipient suffered an injury of the type enumerated in the

“Vaccine Injury Table,” corresponding to the vaccination in question, within an

applicable time period following the vaccination also specified in the Table. If so, the

Table Injury is presumed to have been caused by the vaccination, and the petitioner is

automatically entitled to compensation, unless it is affirmatively shown that the injury

was caused by some factor other than the vaccination. § 300aa-13(a)(1)(A); § 300 aa-

11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B).

In many cases, however, the vaccine recipient may have suffered an injury not of

the type covered in the Vaccine Injury Table. In such instances, an alternative means

exists to demonstrate entitlement to a Program award. That is, the petitioner may gain

an award by showing that the recipient’s injury was “caused-in-fact” by the vaccination

in question. § 300aa-13(a)(1)(B); § 300aa-11(c)(1)(C)(ii). In such a situation, of course,

the presumptions available under the Vaccine Injury Table are inoperative. The burden

is on the petitioner to introduce evidence demonstrating that the vaccination actually

caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d

1274, 1278 (Fed. Cir. 2005); Hines v. Sec’y of Health & Human Servs., 940 F.2d 1518,

1525 (Fed. Cir. 1991). In this case, petitioner alleges that she suffered GBS, which is

not listed on the Vaccine Injury Table relative to Prevnar 13. Accordingly, petitioner

must satisfy this burden of proof for a cause-in-fact claim.

The showing of “causation-in-fact” must satisfy the “preponderance of the

evidence” standard, the same standard ordinarily used in tort litigation. § 300aa-

13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 940 F.2d at 1525. Under that

standard, the petitioner must show that it is “more probable than not” that the

vaccination was the cause of the injury. Althen, 418 F.3d at 1279. The petitioner need

not show that the vaccination was the sole cause of the injury or condition, but must

demonstrate that the vaccination was at least a “substantial factor” in causing the

condition, and was a “but for” cause. Shyface v. Sec’y of Health & Human Servs., 165

29

F.3d 1344, 1352 (Fed. Cir. 1999). Thus, the petitioner must supply “proof of a logical

sequence of cause and effect showing that the vaccination was the reason for the

injury;” the logical sequence must be supported by “reputable medical or scientific

explanation, i.e., evidence in the form of scientific studies or expert medical testimony.”

Althen, 418 F.3d at 1278; Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144,

1148 (Fed. Cir. 1992). A petitioner may not receive a Vaccine Program award based

solely on his or her assertions; rather, the petition must be supported by either medical

records or by the opinion of a competent physician. § 300aa-13(a)(1).

In what has become the predominant framing of this burden of proof, the Althen

court described the “causation-in-fact” standard, as follows:

Concisely stated, Althen’s burden is to show by preponderant evidence

that the vaccination brought about her injury by providing: (1) a medical

theory causally connecting the vaccination and the injury; (2) a logical

sequence of cause and effect showing that the vaccination was the reason

for the injury; and (3) a showing of proximate temporal relationship

between vaccination and injury. If Althen satisfies this burden, she is

entitled to recover unless the [government] shows, also by a

preponderance of the evidence, that the injury was in fact caused by

factors unrelated to the vaccine.

Althen, 418 F.3d at 1278 (citations omitted). The Althen court noted that a petitioner

need not necessarily supply evidence from medical literature supporting petitioner’s

causation contention, so long as the petitioner supplies the medical opinion of an

expert. Id. at 1279-80. That expert’s opinion must be “sound and reliable.” Boatmon v.

Sec’y of Health & Human Servs., 941 F.3d 1351, 1359-60 (Fed. Cir. 2019) (citing

Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548-49 (Fed. Cir. 1994)).

The Althen court also indicated, however, that a Program fact-finder may rely upon

“circumstantial evidence,” which the court found to be consistent with the “system

created by Congress, in which close calls regarding causation are resolved in favor of

injured claimants.” 418 F.3d at 1280.

V. Additional Background and Program Case Law

Guillain-Barre syndrome is an acute-onset, monophasic, polyneuropathy.

(Burns, supra, Ex. D, Tab. 1, p. 1); (Baxter et al., supra, Ex. A, Tab. 1, p. 1.) GBS is

generally considered an autoimmune condition and is associated with a number of

triggers, including infections and vaccination. (Baxter et al., supra, Ex. A, Tab. 1, p. 1.)

Among published case series, approximately two-thirds of all cases are preceded by a

gastrointestinal or respiratory infection within three months prior. (Id.; Hartung, supra,

Ex. 51, p. 277.) Campylobacter jejuni, cytomegalovirus (CMV), Epstein-Barr virus, and

Mycoplasma pneumoniae are known precipitants of GBS, with other infections occurring

no more often in GBS than in controls. (Hartung, supra, Ex. 51, p. 1.) The infection

most commonly associated with GBS is Campylobacter jejuni. (Id.)

30

A small but significant increase in the number of GBS cases post-vaccination

was observed with the 1976 swine influenza vaccine. (Baxter et al., supra, Ex. A, Tab.

1, p. 1.) Several studies assessing the risk of GBS post seasonal influenza vaccines

since 1976 have shown either no risk, or a small attributable risk, approximately 1 case

per million doses. (Id. at 1-2.) Studies assessing the risk of GBS following the 2009

H1N1 monovalent influenza vaccines in the United States found an attributable risk

ranging from 1 to 5 per million doses. (Id. at 2.)

It is generally accepted that GBS results from molecular mimicry. This is most

clearly demonstrated in the case of Campylobacter jejuni. (Tr. at 170; Nakos et al.,

supra, Ex. 40, p. 1; Burns, supra, Ex. D, Tab. 1, p. 4.) The theory of molecular mimicry

describes how shared structures on a virus or bacteria, or components of a vaccine, can

trigger a cross-reactive response self. (Ex. 12, p. 9.) “Such mimicry works by showing

the immune system stretches of amino acids that look like self.” (Lawrence Steinman,

Autoimmune Disease, SCI. AM. 107 (1993) (Ex. 22, p. 3).) Anti-ganglioside 28

autoantibodies are most commonly suspected as the vehicle for molecular mimicry in

cases of GBS; however, this has not been definitively established and other

autoimmune targets have also been proposed. (Nakos et al., supra, Ex. 40, p. 2;

Gilburd et al., supra, Ex. 24, p. 1.)

Molecular mimicry is a well-established theory in the Vaccine Program and has

been persuasively linked to several autoimmune conditions. See e.g., W.C. v. Sec'y of

Health & Human Servs., No. 07-456V, 2011 WL 4537877, at *11-12 (Fed. Cl. Spec.

Mstr. Feb. 22, 2011), (finding that molecular mimicry is a well-regarded theory in some

contexts but finding against molecular mimicry in the context of flu vaccine causing or

worsening MS), mot. for rev. denied, 100 Fed. Cl. 440 (2011), aff'd, 704 F.3d 1352 (Fed.

Cir. 2013); Swaiss v. Sec’y of Health & Human Servs., 15-286V, 2019 WL 6520791

(Fed. Cl. Spec. Mstr. Nov. 4, 2019) (finding that Petitioner’s small fiber neuropathy

variant of GBS was more likely than not caused by molecular mimicry following the

Tdap vaccine); H.J. v. Sec'y of Health & Human Servs, No. 11-301V, 2015 WL 6848357

(Fed. Cl. Spec. Mstr. Nov. 6, 2015) (finding Tdap vaccine caused Petitioner to develop

rheumatoid arthritis via molecular mimicry); Salmins v. Sec'y of Health & Human Servs.,

No. 11–140V, 2014 WL 1569478 (Fed. Cl. Spec. Mstr. Mar. 31, 2014) (finding that HPV

vaccine caused Petitioner to develop GBS via molecular mimicry); Roberts v. Sec'y of

Health & Human Servs., No. 09-427V, 2013 WL 5314698 (Fed. Cl. Spec. Mstr. Aug. 29,

2013) (finding that Tdap vaccine led Petitioner to develop transverse myelitis via

molecular mimicry); Hayes v. Sec’y of Health & Human Servs., No. 06-738V, 2010 WL

2985632 (Fed. Cl. Spec. Mstr. July 12, 2010) (finding that, by the process of molecular

mimicry, the flu vaccine was a substantial cause of Petitioner's transverse myelitis,

ADEM, bilateral optic neuritis, and developmental delay). In particular, the association

between the flu vaccine and GBS has been well-established in the Program. 42 C.F.R.

28

“[A]ny of a group of glycosphingolipids in which the polar head group on ceramide is a sialic acid–

containing oligosaccharide linked via a glucose residue; they occur predominantly in tissues of the central

nervous system.” Ganglioside, DORLAND’S MEDICAL DICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=19729&searchterm=ganglioside (last visited Jan. 4,

2022.)

31

§ 100.3(a); see also Chinea v. Sec’y of Health & Human Servs., No. 15-095V, 2019 WL

1873322 at *29 (Fed. Cl. Spec. Mstr. Mar. 15, 2019); Strong v. Sec’y of Health &

Human Servs., No. 15-1108V, 2018 WL 1125666 (Fed. Cl. Spec. Mstr. Jan. 12, 2018);

Stitt v. Sec’y of Health & Human Servs., No. 09-653V, 2013 WL 3356791 (Fed. Cl.

Spec. Mstr. May 31, 2013); Stewart v. Sec'y of Health & Human Servs., No. 06-777V,

2011 WL 3241585, at *16 (Fed. Cl. Spec. Mstr. July 8, 2011); see also Barone v. Sec'y

of Health & Human Servs., No. 11-707V, 2014 WL 6834557 (Fed. Cl. Spec. Mstr. Nov.

12, 2014).

Flu vaccine-GBS cases often rely upon the theory of molecular mimicry,

specifically proposing that antibodies produced by B cells in response to the vaccine’s

viral antigen components cross-attack the myelin sheath (where the target antigen and

gangliosides of the myelin sheath share structural homology), causing demyelination of

peripheral nerves. See Chinea, 2019 WL 1873322, at *15. Nonetheless, this does not

explain all cases of GBS and other known triggers of GBS do not have established

homologies. (Nakos et al., supra, Ex. 40, p. 2; Gilburd et al., supra, Ex. 24, p. 23.) GBS

was added as a Table Claim in 2017 for the flu vaccine, though it is not recognized for

the pneumococcal vaccine at issue in this case. 42 C.F.R. § 100.3(a).

While molecular mimicry “is a generally accepted scientific principle, mere

invocation of the scientific term does not carry a petitioner’s burden in a Program case.”

Deshler v. Sec'y of Health & Human Servs., No. 16-1070V, 2020 WL 4593162, at *20

(Fed. Cl. Spec. Mstr. July 1, 2020) (citing Forrest v. Sec’y of Health & Human Servs.,

No. 14-1046V, 2019 WL 925495, at *3 (Fed. Cl. Spec. Mstr. Jan. 18, 2019)). This is

because “the finding of sequence homology does not necessarily mean the similarity

has significance to the immune system.” Tullio v. Sec'y of Health & Human Servs., No.

15-51V, 2019 WL 7580149, at *15 (Fed. Cl. Spec. Mstr. Dec. 19, 2019), aff’d, 149 Fed.

Cl. 448 (2020); see also Caredio v. Sec'y of Health & Human Servs., No. 17-0079V,

2021 WL 4100294, at *31 (Fed. Cl. Spec. Mstr. July 30, 2021) (“demonstration of

homology alone is not enough to establish a preponderant causation theory”) (emphasis

in original) (citing Schultz v. Sec'y of Health & Human Servs., No. 16-539V, 2020 WL

1039161, at *22 n.24 (Fed. Cl. Spec. Mstr. Jan. 24, 2020) (“[m]ere demonstration of

theoretical homology alone, based on computer-driven searches involving databases of

amino acid sequences, does not carry the day”)), mot. for rev. denied, 2021 WL

6058835 (Fed. Cl. Dec. 3, 2021).

In a decision often cited in cases of molecular mimicry, W.C. v. Secretary of

Health & Human Services, the Federal Circuit outlined the reasons why that petitioner's

theory of molecular mimicry was insufficient to prove petitioner's flu vaccine caused

multiple sclerosis, finding, “[p]etitioner provided no evidence that the portions of the

influenza virus shown by Wucherpfennig to mimic myelin basic protein were present in

the influenza vaccine Petitioner received,” and “[p]etitioner also did not provide evidence

that any peptide from the influenza vaccine he received was cross-reactive with myelin

basic protein-specific T-cells.” 704 F.3d at 1360-61 (citing decision below). The Federal

Circuit further found that the epidemiologic studies cited by the Special Master, which

showed that MS was not exacerbated by the influenza vaccination, were more

32

persuasive than petitioner's expert's theory and affirmed the denial of compensation by

the Special Master. See id. at 1361.

Similarly, Judge Horn affirmed the Special Master’s decision in Tullio v. Secretary

of Health & Human Services, finding that although petitioner’s theory of molecular

mimicry provided some evidence, petitioner failed to provide evidence that any peptide

from the influenza vaccine he received was cross-reactive with the specific T cells. 149

Fed.Cl. 448, 468 (citing W.C. v. Sec’y of Health & Human Servs., 704 F.3d at 1360-61;

Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1351 (Fed. Cir.

2010)). Finding that the four studies petitioner presented on tetramers lacked

persuasive value, petitioner was left supporting his claim with epidemiologic studies and

his expert’s BLAST searches. See Tullio, 149 Fed.Cl. at 469-70. Regarding the BLAST

searches, Judge Horn outlined the reasons why these searches were insufficient,

quoting the Special Master’s decision, explaining that because all proteins “‘are built

from the same 20 amino acids, it is inevitable that some sequences of amino acids will

repeat.’” Id. at 471 (citing decision below). Thus, “‘the finding of sequence homology

does not necessarily mean the similarity has significance to the immune system.’” Id.

(citing decision below). Though not dispositive, the Special Master found the

epidemiologic studies did not support petitioner’s hypothesis. Id. at 473-75. Taken

together, the Special Master’s decision was not arbitrary or capricious. Id. at 478.

As the above caselaw illustrates, a petitioner must offer more than superficial

invocation of molecular mimicry as the causal mechanism. “It also cannot be enough

that a medical expert can simply identify homologous peptides from a generic BLAST

search that are not, in any way, linked to the biological process that is dysfunctional or

has suffered injury.” Brayboy v. Sec'y of Health & Human Servs., No. 15-183V, 2021

WL 4453146, at *19 (Fed. Cl. Spec. Mstr. Aug. 30, 2021). 29 Ultimately, “[t]he line must

be drawn somewhere between speculation and certainty.” Id. Preponderant evidence

under Althen prong one exists where a petitioner can identify “a cross-reaction between

components of the vaccine and proteins in the body that are directly responsible for the

health and productivity of the organ at issue.” Id. On the other hand, while direct,

29

See also Forrest v. Sec'y of Health & Human Servs., No. 14-1046V, 2019 WL 925495 at *4 (Fed. Cl.

Spec. Mstr. Jan. 28, 2019) (f inding that Dr. Steinman's theory that a flu vaccine caused TM via molecular

mimicry was not sufficiently developed to meet Petitioner's burden under Althen prong one because Dr.

Steinman had “not investigated his hypothesis[,]” other than through computerized homologies revealing

“some overlap in sequences of amino acids[.]”). In that case, the special master discredited Dr.

Steinman's theory, in part, because he “appear[ed] to have made errors in proclaiming the degree of

similarity [in the homologies] that he f ound[.]” Id. There have also been instances where Dr. Steinman’s

use of BLAST searches has been found to help support a f inding of vaccine causation. See E.M. v. Sec’y

of Health & Human Servs., No. 14-753V, 2021 WL 3477837, at *36-39 (Fed. Cl. Spec. Mstr. July 9, 2021)

(f inding persuasive Dr. Steinman’s evidence of “numerous examples of sequences in the 2011 Fluarix

vaccine and between earlier seasonal flu vaccines, that share similar homologies with the [protein] alpha3

nicotinic AChR, which is associated with small fiber neuropathy”); White v. Sec’y of Health & Human

Servs., No. 15-1521, 2019 WL 7563239, at *24 (Fed. Cl. Spec. Mstr. Dec. 19, 2019) (crediting Dr.

Steinman's molecular mimicry theory and BLAST searches where there were “sufficient homologies

between the basic myelin protein and two of the strains of the HPV L1 strains…and between MOG and all

f our HPV antigens in the vaccine[,]” which could cause TM).

33

testable evidence of pathology may be the strongest scientific evidence, this level of

certainty goes beyond petitioner’s preponderant burden in this Program. 30 In the

Vaccine Program, it is well understood that petitioners are not obligated to prove the

precise mechanism of injury as a component of their causation theory. Kottenstette v.

Sec'y of Health & Human Servs., 861 F. App'x 433, 441 (Fed. Cir. 2021); Knudsen v.

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

Although the flu vaccine stands alone as being presumed to cause GBS within

this Program, cases concerning GBS have also concluded that vaccines other than the

flu vaccine can cause GBS. See Salmins v. Sec'y of Health & Human Servs., No. 11-

140V, 2014 WL 1569478 at *14 (Fed. Cl. Spec. Mstr. March 31, 2014) (accepting Dr.

Souayah's opinion that the HPV vaccine (Gardasil) “can cause” GBS although there

was no published medical literature demonstrating homology); Peugh v. Sec'y of Health

and Human Servs., No. 99–638V, 2007 WL 1531666 (Fed. Cl. Spec. Mstr. May 8, 2007)

(hepatitis B vaccine caused GBS) 31; Whitener v. Sec'y of Health & Human Servs., No.

06-0477V, 2009 WL 3007380 (Fed. Cl. Spec. Mstr. Sept. 2, 2009) (meningococcal

vaccine found causal of GBS); but see Isaac v. Sec'y of Health & Human Servs., 108

Fed. Cl. 743 (2013) (denying review where petitioner alleged that the tetanus vaccine

caused GBS), aff'd without opinion, 540 Fed. App’x. 999 (Fed. Cir. 2013).

Recently, two decisions regarding GBS alleged to have been caused-in-fact by

the Prevnar 13 vaccine have reached opposing conclusions. In Deshler v. Secretary of

Health & Human Services, petitioner alleged that she suffered from GBS as a result of

receiving the Prevnar 13 vaccine in 2015. 2020 WL 4593162, at *1. Petitioner in that

case presented two similar theories, the first regarding a molecular mimic involving the

polysaccharides of S. pneumoniae, a known infectious cause of GBS, and a second

30

In Tullio v. Secretary of Health and Human Services, Judge Horn observed that, to the extent that the

Special Master required experts to “conduct[] experiments about molecular mimicry” the Special Master’s

“Testability” portion of the decision was inconsistent with the Program’s role which is “not to be seen as a

vehicle f or ascertaining precisely how and why…vaccines sometimes destroy the health and lives of

certain children while safely immunizing most others.” 149 Fed.Cl. at 477-78 (quoting Knudsen v. Sec’y

of Health & Human Servs., 35 F.3d 543, 549 (Fed. Cir. 1994)). But compare Terran v. Sec’y of Health &

Human Servs., 41 Fed. Cl. 330, 336 (1998) aff’d, 195 F.3d 1302 (Fed. Cir. 1999) (indicating that special

masters may consider whether an expert’s opinion is and has been “tested”) with, Andreu v. Sec’y of

Health & Human Servs., 569 F.3d 1367, 1380 (Fed. Cir. 2009) (quoting Bunting v. Sec’y of Health &

Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991) (observing that petitioners do not have to prove their

cases with scientific certainty).

31

On October 13-14, 2004, former Special Master Sweeney held a hearing—which became known as the

“Hepatitis B – Neurological Demyelinating Omnibus Proceeding”—to determine whether a causal

association exists between the Hepatitis B vaccine and several demyelinating illnesses (multiple

sclerosis, TM, chronic inflammatory demyelinating polyneuropathy, and GBS) alleged in four paradigm

cases. Stevens v. Sec’y of Health & Human Servs., No. 99-594V, 2006 WL 659525 (Fed. Cl. Spec. Mstr.

Feb. 24, 2006); Werderitsh v. Sec'y of Dept. of Health & Human Servs., No. 99-310V, 2006 WL 1672884

(Fed. Cl. Spec. Mstr. May 26, 2006); Peugh, 2007 WL 1531666; Gilbert v. Sec'y of Dept. of Health &

Human Servs., No. 04-455V, 2006 WL 1006612 (Fed. Cl. Spec. Mstr. Mar. 30, 2006). These cases were

then reassigned to former Special Master Laura Millman, who found that in all four cases, the Hepatitis B

vaccine was causal. Peugh, 2007 WL 1006612, at *1, *17–18.

34

theory suggesting that the diphtheria conjugate component (CRM197) was a key factor

in triggering GBS. Id. at *20. Petitioner in that case failed to meet her burden under

Althen prong one because petitioner’s experts could not present evidence of a shared

structural homology between the polysaccharides contained in the pneumococcal

vaccine and self-structures of the peripheral nervous system. Id. at *20-21. Both of

petitioner’s experts in that case drew comparisons to the C. jejuni bacterium, and GBS’

autoimmune etiology generally—which fell short where Dr. Levy acknowledged that the

underlying pneumococcal bacterial strains in the Prevnar-13 vaccine “were not

themselves…associated with GBS (unlike, for example, C. jejuni).” Id. at *5. The Chief

Special Master was further persuaded by respondent’s expert’s testimony in that case,

where Dr. Whitton opined that the pathogenic nature of CRM197 “could not be conflated

with what was known about the diphtheria toxoid used as a conjugate in other

vaccines.” Id. at *20 (internal citation omitted.) Thus, petitioner’s Althen prong one

theory was left relying on epidemiologic studies and a temporal relationship to the

vaccine. Id. at *19-21. The Chief Special Master found that the epidemiologic studies

cited by Dr. Souayah in that case, Baxter, Haber, and Cordonnier, failed to

preponderantly show that the Prevnar-13 vaccine can cause GBS. Deshler v. Sec’y of

Health & Human Servs., No. 16-1070V, 2020 WL 4593162 at *21 (Fed. Cl. Spec. Mstr.

July 1, 2020).

In Koller v. Secretary of Health & Human Services, petitioner also alleged that

the Prevnar 13 vaccine he received in 2015 caused his GBS. No. 16-439, 2021 WL

5027947 at *1 (Fed. Cl. Spec. Mstr. Oct. 8, 2021). Petitioner’s expert in that case, Dr.

Steinman, theorized that a molecular mimic existed between a component of the

Prevnar 13 vaccine and the myelin sheath of the peripheral nervous system, causing

petitioner’s GBS. Id. at *8. Unlike in Deshler, Dr. Steinman proposed a mimic involving

phosphoglycerol, a key component of phospholipids which make up seventy percent of

the myelin. Id. According to his theory, the immune reaction to the phosphoglycerol in

the vaccine induces an attack on the phosphoglycerol attached to the phospholipids in

the myelin. Id. Respondent’s expert, Dr. Leist, criticized Dr. Steinman’s theory for

failing to identify a single amino acid, or side chain, sufficient for molecular mimicry. Id.

at *16. Dr. Leist further stressed that the presence of a naturally occurring amino acid in

a protein was insufficient to invoke molecular mimicry. Id. at *16. Support for Dr.

Steinman’s theory in that case was grounded in three key pieces of medical literature:

Chang et al., Ho et al., and Gilburd et al., as well as the Prevnar 13 vaccine patent

application. Id. at *16-18, 20. In particular, Dr. Steinman offered the Ho et al. article to

demonstrate that the phosphate group in phospholipids in myelin was targeted by

autoantibodies in MS patients, thus triggering demyelination. Id. at *20. Dr. Steinman

proposed that the Prevnar 13 vaccine triggers the same cross-reactive mechanism,

which can cause similar demyelination in the peripheral nerves, causing GBS. Id.

Under Althen prong one, the Special Master concluded that requiring “definitive proof or

epidemiology would impermissibly raise the petitioner’s burden of proof.” Id.

Prior decisions, including those discussed above, do not control the outcome of

this case. Boatmon v. Sec’y of Health & Human Servs., 941 F.3d 1351, 1358-59 (Fed.

Cir. 2019); Hanlon v. Sec’y of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998).

35

Federal Circuit holdings regarding legal issues are binding on special masters. Guillory

v. Sec’y of Health & Human Servs., 59 Fed. Cl. 121, 124 (2003), aff’d 104 F. App’x. 712

(Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Human Servs., No. 13-159V,

2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014). However, decisions

by other special masters or by the Court of Federal Claims are not binding. Hanlon, 40.

Fed. Cl. at 630. Nor, for that matter, are special masters obligated to distinguish

decisions reaching a different result. Boatmon, 941 F.3d at 1358. The discussion

above is provided only to provide context given that both GBS and molecular mimicry

are commonly encountered within this Program while this specific combination of

vaccination and injury is rare by comparison. See, e.g. Doe v. Sec’y of Health & Human

Servs., 76 Fed. Cl. 328, 338-39 (2007) (“[o]ne reason that proceedings are more

expeditious in the hands of special masters is that the special masters have the

expertise and experience to know the type of information that is most probative of a

claim”).

VI. Discussion

As explained above, petitioner’s burden is to demonstrate by preponderant

evidence each of the three Althen prongs for determining causation-in-fact (i.e. a

medical theory, a logical sequence of cause and effect, and a proximate temporal

relationship). Althen, 418 F.3d at 1278. Provided petitioner can affirmatively meet this

burden, she bears no burden of eliminating alternative causes. Walther v. Sec’y of

Health & Human Servs., 485 F.3d 1146, 1150 (Fed. Cir. 2007); de Bazan v. Sec’y of

Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). Importantly, however,

respondent may present evidence relating to an alternative cause to demonstrate the

inadequacy of petitioner’s evidence supporting her case in chief. de Bazan, 539 F.3d at

1353.

a. Althen prong one

Under Althen prong one, petitioner must provide a “reputable medical theory,”

demonstrating that the vaccine received can cause the type of injury alleged. Pafford v.

Sec’y of Health & Human Servs., 451 F.3d 1352, 1355–56 (Fed. Cir. 2006) (citations

omitted). Such a theory must only be “legally probable, not medically or scientifically

certain.” Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548-49 (Fed. Cir.

1994). Petitioner may satisfy the first Althen prong without resort to medical literature,

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

accepted medical theory. Andreu v. Sec'y of Health & Human Servs., 569 F.3d 1367,

1378–79 (Fed. Cir. 2009) (citing Capizzano v. Sec’y of Health & Human Servs., 440

F.3d 1317, 1325–26 (Fed. Cir. 2006)). However, “[a] petitioner must provide a

‘reputable medical or scientific explanation’ for [her] theory. While it does not require

medical or scientific certainty, it must still be ‘sound and reliable.’” Boatmon v. Sec’y of

Health & Human Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019) (quoting Knudsen, 35

F.3d at 548-49).

36

Here, consistent with much of the above discussion regarding GBS, Dr.

Steinman proposes that the Prevnar-13 vaccine can cause GBS via molecular mimicry.

He opines that there are two molecular mimics that are relevant to GBS in the

composition of Prevnar 13: one from the phosphoglycerol in the composition of the

pneumococcal polysaccharide antigen, and a second from the CRM protein conjugate.

(Ex. 35, p. 4.)

1. Phosphoglycerol

Although antiganglioside antibodies have primarily been suspected as causal in

GBS, Dr. Steinman observes that two prior studies have shown GBS patients to have

autoantibodies to phospholipids. First, Gilburd et al. (1993) sought to investigate

autoantibodies in GBS by testing the reactivity of GBS sera with various

phospholipids—those that are known constituents of myelin that also serve as

autoantigens in other autoimmune conditions. (Gilburd et al., supra, Ex. 24, p. 1.) Their

results indicated that six out of sixteen GBS sera studied had antibodies to one of more

of the phospholipid antigens. (Id. at 5.) At the time, the authors theorized that these

results “may be produced by a cross reaction of autoantibodies to [a] yet unidentified

myelin constituent.” (Id. at 5-6.) However, Gilburd et al. did not find a significant

association between the presence of any specific antiphospholipid antibodies or anti-

DNA antibodies in GBS when compared to controls. (Id. at 6.) The authors ultimately

concluded that the autoantibody production was “more likely the result of myelin

damage and the liberation of various myelin antigens into circulation.” (Id.) Dr.

Steinman testified that this study shows that many of the antibodies in GBS target

phospholipids. (See Tr. at 169.) While the authors “didn’t have enough insight at the

time or they never asked what part of the phospholipid is being targeted[,]’” Dr.

Steinman testified that some of the same phospholipids were demonstrated by a later

study, Ho et al (discussed further below), as being targeted in the context of multiple

sclerosis. (Id.) Thus, while the authors’ data was not conclusive, Dr. Steinman

explained that the later discoveries published in Ho et al. allowed him to reevaluate the

Gilburd et al. data.

Second, the results from Nakos et al. (2005) also reveal that phospholipid

antibodies were found in patients with GBS. (Nakos et al, supra, Ex. 40, p. 1405.) The

authors observe that many earlier studies attempted to evaluate the clinical relevance of

anti-phospholipid antibodies, but with conflicting results. (Id. at 5.) In their study, Nakos

et al. obtained four blood samples before and after treatment for GBS, testing the

samples for IgM, IgA, and IgG antibodies to phosphatidylcholine, phosphatidylinositol,

cardiolipin, phosphatidic acid, phosphatidylserine, phosphatidylglycerol,

phosphatidylethanolamine, sphingomyelin, and gangliosides. (Id. at 1.) Anti-

phospholipid antibodies of the IgM, IgA and IgG families were detected in all of the GBS

patients, and none of the controls. (Id. at 5.) The authors found that

phosphatidylinositol, cardiolipin, phosphatidic acid, and phosphatidylcholine were the

main antigens. (Id. at 1.) Soon after the administration of ƴ-globulin IgG antibodies to

37

phosphatidylcholine, phosphatidylinositol, phosphatidic acid, and cardiolipin were

significantly increased—Nakos et al. posit that this increase could be related to the

antiphospholipid activity in the infused ƴ-globulin (in which significant levels of IgG anti-

phospholipid antibodies were detected). (Id. at 6.) According to Nakos et al., their

results demonstrate that there is a more extensive immune reaction occurring in GBS

beyond the well-known anti-ganglioside production, though “it is not well understood

whether these anti-phospholipid antibodies play a role in the pathogenesis of the

polyneuropathy or represent a part of a more extensive immunoreaction that takes

place in the GBS.” (Id. at 6-7.) These results, Dr. Steinman testified, show that in GBS

patients “a lot of the anti-phospholipid antibodies are being made, and they include,

again, some of the phospholipids that [Ho et al.] studied in the MS patients, the

[phosphatidylcholine,] the [phosphatidylserine,] the phosphatidylethanolamine[.]” (Tr. at

170.)

Although these studies are insufficient on their own to establish these

autoantibodies as injurious, Dr. Steinman additionally cites his own prior study, Ho et

al., which shows in a different context – multiple sclerosis – that phospholipids within

myelin can be the target of autoimmune attack. Ho et al. (2012) describes how the

autoantibodies against phospholipids contribute to demyelination in multiple sclerosis,

and how the autoantibodies target a phosphate group attached to the lipids. (Ho et al.,

supra, Ex. 26, p. 3.) In cases of MS, the immune system attacks the phosphate

headgroup—a component of the phospholipids in the myelin. (Id. at 9.) The authors

explain that “[w]hereas the polar head groups are the lipid components targeted by the

antibodies, the fatty acid side chains are the components that mediate the lipids’ anti-

inflammatory effects.” (Id.)

Dr. Steinman persuasively explains that Ho et al. demonstrates how the immune

system could likewise attack the phosphate headgroup on the phospholipids in the

myelin in the context of GBS. (Tr. at 166-70.) In that regard, Dr. Steinman also points

to Gilburd to suggest that that paper demonstrates not merely the presence of relevant

autoantibodies among the GBS patients, but also provides at least some reason to

suspect that these autoantibodies cross react. (Tr. at 178.) During the hearing Dr.

Steinman referenced six patients in the study, two of which had antibodies to

phosphatidylethanolamine. (Id.) One patient also showed antibodies to

phosphatidylcholine, which Dr. Steinman explained “which we also saw in the paper by

Ho.” (Id.) Though it was a small study, he explained that Gilburd et al. looked at many

of the same molecules, each of which contained phosphoglycerol (cardiolipin,

phosphatidylethanolamine, phosphatidylcholine, and phosphatidylserine). (Tr. at 178-

79.)

This leaves the critical remaining question of whether this proposed cross-

reaction can be linked to the Prevnar 13 vaccine. Dr. Steinman has identified a

phosphoglycerol component present in the vaccine that is essential for the Prevnar 13

vaccine to be effective. (Ex. 35, pp. 4-11.) Specifically, the polysaccharides in

38

pneumococcus that are contained in the Prevnar vaccine “allow for the chemical

attachment of capsular polysaccharides via the glycerol moieties” known as

phosphoglycerol and phosphocholine (or phosphatidylcholine). (Ex. 35, p. 6.) The

glycerophosphate and phosphorylcholine play a critical role in the immunogenicity of

Prevnar 13. (Id. at 9 (citing Chang et al., supra, at Ex. 37; Lugowski and Jennings,

supra, at Ex. 38; Ohori et al., supra, at Ex. 39.) 32 Dr. Steinman explained that the

homology to the phosphoglycerol in the vaccine exists at the polar head group for this

specific phospholipid, as well as phosphatidylserine. (Tr. at 173-74.) This is significant

because the Ho et al. study demonstrates that phospholipids cross-react at the polar

headgroup. (Ho et al., supra, at Ex. 26, pp. 3, 9.) Moreover, Dr. Steinman points out

that Ho et al. shows that among the phospholipid polar headgroups within the myelin

tissue that cross-react are those that contain a phosphoglycerol chain. (Tr. at 166-67.)

Dr. Leist disagrees with Dr. Steinman’s theory because it is based on “the

inaccurate assumption that Prevnar-13 contains phospholipids 33 and that

phosphoglycerol and phospholipids can be considered as essentially the same.” (Ex. D,

p. 4; see also Tr. at 257 (“[I] was of the impressions that Dr. Steinman was inferring that

Prevnar 13 included phospholipids . . . .”).) Dr. Leist testified he “do[es not] think that

lipids are a named constituent of the Prevnar 13” vaccine. (Tr. at 257.) Therefore, Dr.

Leist stresses that the applicability of the Ho et al. article is “at most tangential.” (Id.)

However, Dr. Steinman has persuasively explained that his theory does not merely rely

on phospholipids broadly, but involves molecular mimicry between phosphoglycerol,

attached to the phospholipids, and the same phosphate group contained within the

polar head of the phospholipids in myelin. (See Tr. at 167-68 (Dr. Steinman’s

description of the phosphate headgroup in the Ho et al. article (supra, Ex. 26, at Fig. 2,

p. 4.)) Dr. Leist also criticizes Dr. Steinman’s reliance on Nakos, noting that authors

could not determine whether the antibodies examined were pathophysiologically

important or merely a sign of injury. (Tr. at 260-61.) Dr. Steinman acknowledged this

conclusion by Nakos et al., though he countered that in light of the findings in Ho et al.,

the data in Nakos et al. can now be reexamined and reconsidered. (Tr. at 176-78; 212-

13.)

Overall, Dr. Leist testified that he agrees the individual steps in Dr. Steinman’s

theory are logical, though he opines that they don’t connect. (Tr. at 264-65.) Yet, this

is consistent with petitioner’s burden of proof under Althen insofar as a petitioner can

establish causation through expert opinion and rely on circumstantial evidence so long

32

The question of how Dr. Steinman established the presence of phosphoglycerol is explained in greater

detail in the Special Master’s decision in Koller. See Koller, 2021 WL 5027947 at *8-10. Dr. Steinman

has presented the same theory in both cases.

33

In his initial report, Dr. Steinman opined that the “trigger is the phospholipids in Prevnar 13[.]” (Ex. 12,

p. 18.) However, Dr. Steinman explained that after reviewing the Prevnar 13 vaccine patent he

determined that the mimic is phosphoglycerol. (Tr. at 329.) This ref inement in Dr. Steinman’s opinion is

also addressed in greater detail in the Koller decision. Koller, 2021 WL 5027947 at *16-17.

39

as the opinion is based on sound and reliable scientific explanation. Boatmon, 941 F.3d

at 1359-60; Althen, 418 F.3d at 1280. “The assessment of whether a proffered theory

of causation is ‘reputable’ can involve assessment of the relevant scientific data.

Medical literature and epidemiological evidence must be viewed, however, not through

the lens of the laboratorian, but instead from the vantage point of the Vaccine Act's

preponderant evidence standard.” Andreu, 569 F.3d at 1380. That is, the fact that

petitioner’s medical theory is novel does not preclude a finding that it is nonetheless

preponderantly established based on sound and reliable scientific explanation. Accord

Kottenstette v. Sec'y of Health & Human Servs., 861 F. App'x 433, 441 (Fed. Cir. 2021);

Knudsen, 35 F.3d at 548-59. Accord Althen, 418 F.3d at 1280 (The Federal Circuit

explaining that “[w]hile this case involves the possible link between [tetanus toxoid]

vaccination and central nervous system injury, a sequence hitherto unproven in

medicine, the purpose of the Vaccine Act’s preponderance standard is to allow the

finding of causation in a field bereft of complete and direct proof of how vaccines affect

the human body.”)

Although epidemiologic evidence has not detected a statistically significant

association between GBS and the Prevnar 13 vaccine, researchers and clinicians

remain interested in the possibility of a causal relationship and have reported this in the

medical literature through case reports. (Nidhi Ravishankar, Guillain-Barre Syndrome

Following PCV Vaccine, 4 J. OF NEUROLOGY AND. NEUROSURGERY 134 (2017) (Ex. 66);

Chad Conner et al., 13-Valent Pneumococcal Conjugate Vaccine-Induced Guillain-

Barre Syndrome, 158 ALLERGY AND AIRWAY A59 (Ex. 64).) 34 “[C]ase reports ‘do not

purport to establish causation definitively, and this deficiency does indeed reduce their

evidentiary value’…. [but] ‘the fact that case reports can by their nature only present

indicia of causation does not deprive them of all evidentiary weight.’” See Paluck v.

Sec'y of Health & Human Servs., 104 Fed. Cl. 457, 475 (2012) (quoting Campbell v.

Sec'y of Health & Human Servs., 97 Fed. Cl. 650, 668 (2011), aff’d 786 F.3d 1373 (Fed.

Cir. 2015)). Standing alone these case reports would be far too weak to support

petitioner’s claim. In the present case, however, they provide some limited support for

the idea that Dr. Steinman, though presenting a novel theory, is not isolated in the

relevant medical community in believing there can be a connection between this

particular vaccine and injury. Contra Boatmon, 941 F.3d at 1360-61 (rejecting

petitioner’s Althen prong one showing in part because “[i]t would be an extension of the

Triple Risk Model to include vaccination-induced cytokine activity in the list of

34

Dr. Steinman acknowledged that “there’s a paucity of case reports. There’s a couple that have been

cited to, [] I would say, [they’re] weak evidence…[f]or the bacterium itself” S. pneumoniae. (Tr. at 217.)

Ravishankar is a case report highlighting a woman who developed severe respiratory failure from GBS

af ter receiving a PCV13 vaccine in January 2015 and a second dose of PPSV23 in August 2015.

(Ravishankar, supra, at Ex. 66, p. 1.) Dr. Steinman testified further that Ravishankar has a “tarnished

history” because the author published the article in two different places, which he explained affects its

“academic purity, but I don’t think it breaks any laws.” (Tr. at 217-18.) Dr. Steinman also acknowledged

that the case report from Conner et al. was not a paper, but instead a medical student presentation. (Tr.

at 218-19.)

40

exogenous stressors as Dr. Miller proposes. Dr. Miller himself concedes that, outside of

Vaccine Act litigation, vaccinations have not been identified as an exogenous stressor

for SIDS.”)

In contrast, respondent cites Baxter et al. (2013), a large retrospective study

assessing the risk of GBS following the Pneumovax 23 vaccine – notably, a different

vaccine. 35 (Baxter, supra, at Ex. A, Tab. 1, pp. 1-2.) The authors did not find any

association between Pneumovax and the development of GBS within six weeks

following vaccination. (Id. at 7.) Haber et al. (2016) assessed adverse events following

Prevnar-13 vaccination, as recorded in the Vaccine Adverse Event Reporting System

(“VAERS”). (Haber et al., supra, at Ex. 32, pp. 1-2.) That study verified 11 GBS

reports, with a reporting rate of 0.7 cases per million doses of the vaccine among adults

(above the age of 19). (Id. at 5.) The authors did not identify any new safety signals

when reviewing the VAERS reports. (Id.) (Petitioner acknowledges the overall Haber

findings, but stresses the 11 verified cases of post-Prevnar GBS as, in effect, case

reports. (Tr. at 216).)

Petitioners in the Vaccine Program are not required to present epidemiological

evidence to establish their causation burden under Althen. Moberly v. Sec'y of Health &

Human Servs., 592 F.3d 1315, 1325 (Fed. Cir. 2010). 36 On balance, neither Baxter et

al. nor Haber et al. significantly undermines petitioner’s theory. Baxter et al. found no

increased risk of GBS following vaccination, though the study involved a different,

unconjugated version of the vaccine. (Baxter et al., supra, at Ex. A, Tab. 1.) Although

the vaccines may be related, Dr. Steinman has supported his theory with specific

investigation into the immunogenicity of components of the Prevnar-13 vaccine

specifically. Haber et al. found “no disproportionate reporting for GBS,” though as other

special masters have observed, articles relying on VAERS data are subject to

significant limitations. 37 Specifically, the authors of the Haber et al. study caution that

35

The pneumococcal conjugate vaccine (PCV13 or Prevnar13) “includes purified capsular polysaccharide

of 13 serotypes of Streptococcus pneumoniae (1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 19A, 19F, 18C, and 23F)

conjugated to a nontoxic variant of diphtheria toxin known as CRM197.” While the pneumococcal

polysaccharide vaccine (PPSV23 or Pneumovax23) “includes purified preparations of pneumococcal

capsular polysaccharide. PPSV23 contains polysaccharide antigen from 23 types of pneumococcal

bacteria.” Types and Composition of Pneumococcal Vaccines, CDC,

https://www.cdc.gov/vaccines/vpd/pneumo/hcp/about-vaccine.html (last visited Jan. 11, 2022).

36

However, “[n]othing in Althen or Capizzano requires the Special Master to ignore probative

epidemiological evidence that undermines petitioner’s theory.” D'Tiole v. Sec’y of Health & Human

Servs., 726 F. App’x 809, 811 (citing Andreu, 569 F.3d at 1379 (“Although Althen and Capizzano make

clear that a claimant need not produce medical literature or epidemiological evidence to establish

causation under the Vaccine Act, where such evidence is submitted, the Special Master can consider it in

reaching an inf ormed judgment as to whether a particular vaccination likely caused a particular injury.”

(emphasis added)); Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148-49 (Fed. Cir. 1992)

(considering negative epidemiological studies).

37

See Bender v. Sec’y of Health & Human Servs., No. 11-693V, 2018 WL 3679637, at *31 (Fed. Cl.

Spec. Mstr. July 2, 2018) (“[b]ecause it is a passive reporting system, VAERS database findings …

cannot be reasonably interpreted to suggest causation. For this reason, special masters do not typically

41

“[i]t is important to the note the limitations of VAERS, which may include underreporting,

varying quality of reports (for example reports may lack details, contain errors or be

missing information), and the lack of an unvaccinated comparison group.” (Haber et al.,

supra, Ex. 32, p. 5.)

Furthermore, petitioner’s Althen prong one theory is generally consistent with this

Program’s overall understanding of GBS and its causes. That is, as explained above, it

is well established that GBS represents an autoimmune condition, likely resulting from

molecular mimicry, but with multiple suspected triggers many of which do not have

definitively identified homologies. Moreover, while molecular mimicry is most often

discussed in the context of proteins and amino acids, the common example of

molecular mimicry in GBS is with c. jejuni, which is a molecular mimic to ganglioside

sugar structures within myelin. See, e.g., Chinea v. Sec’y of Health & Human Servs.,

No. 15-095V, 2019 WL 1873322 (Fed. Cl. Spec. Mstr. Mar. 15, 2019); Stitt v. Sec’y of

Health & Human Servs., No. 09-653V, 2013 WL 3356791 (Fed. Cl. Spec. Mstr. May 31,

2013). And, in any event, prior cases have found that GBS can be causally linked to

vaccines other than the flu vaccine via molecular mimicry even in the absence of direct

proof of homology and cross-reaction. See, e.g., Salmins v. Secretary of Health &

Human Servs., 11-140V, 2014 WL 1569478 at *14 (Fed. Cl. Spec. Mstr. Mar. 31, 2014).

Here, Dr. Steinman does purport to demonstrate a homology between the

phosphoglycerol within the Prevnar vaccine and the phosphate head group attached to

the phospholipids in myelin. Moreover, in relying on Ho, et al, he further purports to

demonstrate cross-reaction to myelin in the context of a different, though also

demyelinating, condition. His extrapolation occurs in relying on Gilburd et al., Ho et al.,

and Nakos et al, to circumstantially demonstrate how this proposed homology and

cross-reaction can be pathophysiologically relevant in the specific context of post-

Prevnar GBS, relying primarily on the fact that relevant autoantibodies have been

detected among those suffering GBS. Especially given the overall understanding of

GBS and its causes, this extrapolation is sound and reliable, as well as consistent with

petitioner’s preponderant burden of proof.

2. CRM197

Dr. Steinman’s second proposed molecular mimic concerns a protein component

of the vaccine called CRM197, which is used to conjugate the pneumococcal

polysaccharides in the Prevnar 13 vaccine to an immunogenic protein carrier, and

Contactin-1, an axonal adhesion molecule that is targeted in some cases of GBS. 38

af f ord great weight to VAERS data in determining causation”) (citing Analla v. Sec'y of Health & Human

Servs., 70 Fed. Cl. 552, 558 (2006) (“the Court [of Federal Claims] uniformly has upheld the Chief Special

Master's concerns about the reliability of VAERS data”)).

38

Dr. Leist likewise agrees that antibodies to contactin-1 have been described in patients with GBS and

CIDP. (Ex. D, p. 4.) Citing a study by Raju et al., Dr. Steinman observes that humans have been shown

to mount T cell responses to regions of the diphtheria molecule: WEQAKLSVE and

EYMAQACAGNRVRR. (Ex. 50, p. 5 (citing Raju et al., supra, at Ex. 52.).) According to Dr. Steinman,

42

(Ex. 35, p. 11 (citing Fehmi et al, supra, at Ex. 41; Manso et al., supra, at Ex. 42; Miura

et al., supra, at Ex. 43.) On this record, Dr. Steinman’s CRM197 theory of molecular

mimicry is much less developed than his theory pertaining to phosphoglycerol.

Because I have concluded that petitioner has satisfied Althen prong one based on the

phosphoglycerol theory, I do not reach the question of whether the theory that CRM197

can cross react with Contactin-1 to cause GBS could potentially be preponderantly

established.

b. Althen prongs two and three

Having shown that the Prevnar-13 vaccine can cause GBS, petitioner must also

establish that it did cause GBS in this specific case. Pafford v. Sec'y of Health &

Human Servs., 451 F.3d 1352, 1356 (Fed. Cir. 2006). This latter aspect of petitioner’s

prima facie showing is generally broken down into two further questions pursuant to

Althen prongs two and three. The second Althen prong requires proof of a logical

sequence of cause and effect usually supported by facts derived from a petitioner's

medical records. Althen, 418 F.3d at 1278; Andreu, 569 F.3d at 1375–77; Capizzano,

440 F.3d at 1326; Grant v. Sec'y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed.

Cir. 1992). The third Althen prong requires establishing a “proximate temporal

relationship” between the vaccination and the injury alleged. Althen, 418 F.3d at 1281.

That term has been equated to the phrase “medically-acceptable temporal relationship.”

Id. A petitioner must offer “preponderant proof that the onset of symptoms occurred

within a timeframe which, given the medical understanding of the disorder's etiology, it

is medically acceptable to infer causation.” de Bazan v. Sec'y of Health & Human

Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008).

In this case, petitioner’s ultimate diagnosis is undisputed. Petitioner’s treating

physicians and both experts agree that petitioner suffered from GBS. (Ex. 6, p. 225; Ex.

12, p. 5; Ex. A, p. 5.) However, determining the onset of petitioner’s GBS is complicated

by the fact that during the relevant period she appears to have been suffering several

complaints or conditions that may have obscured the onset of what was ultimately

diagnosed as GBS, including: a prolonged cough, suspected carpal tunnel syndrome,

severe back pain, and delirium during her hospitalization. Given petitioner’s complex

presentation, the parties disagree as to the initial onset of petitioner’s GBS as well as

the results of this study differ in only one amino acid from CRM, which provides “actual detailed data for

molecular mimics in the CRM in the Prevnar 13 vaccine received by petitioner.” (Id.) However, Dr. Leist

criticizes Dr. Steinman’s reliance on Raju et al. Dr. Leist testified that the T cell clones that were utilized

in the study were derived from seven healthy humans of different histocompatibility complex haplotypes.

(Tr. at 261-62.) According to Dr. Leist, the fact that these healthy individuals developed T cell responses

goes to show that simply identifying sequence homologies doesn’t necessarily indicate that the

homologies are pathophysiologically important for susceptibility to the disease. (Tr. at 262.) Dr. Leist

points out that CRM is a protein commonly used in other vaccines as well. (Tr. at 263-64.) “[I]f CRM

would be a major source of cross-reactive immune response of this pathophysiological importance that

leads to GBS,” Dr. Leist suggests that “the conglomeration of CRM-containing vaccines would have stood

out as causing th[is] injury.” (Tr. at 264.)

43

her time-course to the nadir of her condition. Both of these issues affect whether

petitioner’s GBS can fairly be considered to be post-vaccinal relative to her Prevnar

vaccination. Accordingly, Althen prongs two and three intersect in that the medical

understanding of the evolution of petitioner’s condition pre-diagnosis informs the timing

of onset, which then informs both the logical sequence of cause and effect and the

temporal relationship to vaccination.

With respect to the appropriate timing for a post-vaccinal GBS, the parties have

filed two seminal papers by Schonberger and Langmuir respectively addressing the

timing of onset of GBS following the 1976 swine flu vaccine. (Ex. 12 pp. 18-20; Ex. A, p.

6; Tr. at 147; 284.) Both experts utilize these papers as a reasonable, albeit imperfect,

proxy for assessing the appropriate timing for GBS to be attributable to the

pneumococcal vaccine at issue in this case. (Id.) Schonberger is an epidemiologic

study evaluating over 1,000 individuals who were diagnosed with GBS in the 1976-77

timeframe. (Schonberger, supra, at Ex. 31.) Schonberger observed that the expected

peak onset occurred 16 to 17 days post-vaccination (among the population of cases

considered), though the majority of all GBS cases considered in the chart began within

four weeks. (Schonberger, supra, Ex. 31, pp. 6-7.) However, Schonberger observed a

statistically significant increase in reported cases as far out as nine to ten weeks post-

vaccination. 39 (Schonberger, supra, at Ex. 31, pp. 1, 9.) While Schonberger et al. does

not cover Prevnar 13, Dr. Steinman suggests that it serves as a “surrogate in this case.”

(Ex. 12, p. 20.) Dr. Leist explained, however, that the Schonberger article was re-

examined by Langmuir et al. (Tr. at 259.) Dr. Leist testified that Langmuir et al.

indicates that an association between the then-marketed vaccines and GBS could be

observed “between – up to 42 days later.” (Tr. at 284; Langmuir et al., supra, Ex. A,

Tab. 2, at p. 865.) While Dr. Leist is correct that Langmuir expressed preference for the

42-day onset period, the authors of Langmuir et al. reported that their results support an

association “for at least six [weeks] and may have continued at a low level of increased

risk as long as eight [weeks], but not longer.” (Langmuir et al., supra, Ex. A, Tab. 2, at

p. 25.) Dr. Steinman is therefore persuasive in placing the outermost medically

appropriate onset date for vaccine-caused GBS at eight weeks, or 56 days, post-

vaccination. (Tr. at 146.)

Here, petitioner received her Prevnar 13 vaccine on January 6, 2015. (Ex. 2.)

Thus, the 56-day timeline proposed by Dr. Steinman would require onset of petitioner’s

GBS to occur no later than about March 3, 2015, in order for it to be considered

causally-related to her prior Prevnar-13 vaccination. 40 During that period, petitioner

39

Dr. Steinman testified that Figure 6 in Schonberger shows the expected incidence “remain[s] high,

above that cross-hatched area, at eight weeks, and then they diminish a little more at nine and ten weeks,

and then they f inally blip down to the baseline at eleven weeks.” (Tr. at 144;citing Schonberger et al.,

supra, Ex. 31, p. 9.) This, Dr. Steinman concludes, leads him to place “a cutoff somewhere around the

end of week eight.” (Tr. at 144-45.)

40

Note, however, that the Federal Circuit holding in Paluck v. Secretary of Health & Human Services,

cautions against setting “hard and fast deadline[s]” for onset. See, 786 F.3d 1373, 1383-84 (Fed. Cir.

2015) (stating that “[t]he special master further erred in setting a hard and fast deadline” for onset and

noting that the medical literature filed in the case “do not purport to establish any definitive timeframe for

44

sought care on multiple occasions, primarily at urgent care, beginning on January 21,

2015. She was later hospitalized beginning on March 5, 2015. Flaccid paralysis was

confirmed by no later than March 13, 2015, and she was ultimately diagnosed with GBS

on March 21, 2015. (Ex. 6, pp. 391, 226)

Dr. Steinman proposes that petitioner’s onset of neuroinflammation began

January 21, 2015, when petitioner reported tingling along with her symptoms of

sneezing, congestion, cough, shortness of breath, and wheezing. (Ex. 12, p. 4 (citing

Ex. 3, p. 1.)) Then on February 26, 2015 petitioner additionally reported weakness

along with her ongoing tingling and constitutional symptoms of chills, fatigue, sweats,

cough, shortness of breath, and wheezing. (Id. at p. 4 (citing Ex. 3, p. 19.) According to

Dr. Steinman, the tingling and weakness “are more likely than not indications of GBS.”

(Ex. 12, p. 4.) Dr. Steinman observes that later, in March 2015, petitioner was

diagnosed with subacute onset flaccid paraparesis, acute peripheral neuropathy, and

Bell’s palsy – all indicative of GBS. (Ex. 12, p. 5.) Thus, Dr. Steinman opines that the

onset of petitioner’s inflammatory neuropathy began with tingling on or about January

21, 2015, or fifteen days after she received the Prevnar 13 immunization on January 6,

2015 – though he notes that petitioner’s diagnosis of GBS occurred nine weeks later.

(Id.)

While petitioner’s earliest reports of tingling are potentially consistent with GBS,

they do not in themselves provide preponderant evidence supporting Dr. Steinman’s

opinion that the onset of petitioner’s neuroinflammation began January 21, 2015.

Petitioner’s medical records do not elaborate on the nature of the reported tingling,

including when the tingling started or whether it was continuous or intermittent, but do

suggest there were other aggravating factors (e.g., petitioner’s work in decorating

cakes). (See Ex. A, p. 6.) Specifically, a record from February 26, 2015 by Dr.

Daskalos at Eugene/Thurston Urgent Care states: “[u]nrelated to her present

complaints-patient having symptoms of carpal tunnel syndrome-she[] is a cake

decorator for Albertson’s-she does plan to retire in less than one year.” (Ex. 3, p. 19.)

Two days later, February 28, 2015, PA Kerry Harrington at Eugene Thurston Urgent

Care also observed that petitioner “ha[s] history of carpal tunnel syndrome.” 41 (Ex. 3, p.

25.) Petitioner also appears to have suffered from arthritis prior to her Prevnar 13

vaccination (Ex. 6, p. 14), which Dr. Leist testified could be another explanation for

intermittent numbness and tingling in the hands. (Tr. at 69-70 (“I have like swollen

knuckles…[j]ust working in a bakery, you know, using my hands and stuff, I had swollen

knuckles”); see also Ex. 3, p. 7; Ex. 5, p. 2 (petitioner diagnosed with climacteric arthritis

onset of clinical symptoms.”). Notwithstanding Langmuir’s disagreement, there is some limited, albeit not

preponderant, evidence from Schonberger to suggest onset could potentially exceed eight weeks.

41

Relevant to this specific notation, petitioner denied ever having been diagnosed with carpal tunnel

syndrome. (Tr. at 33.) Upon my review of the record, petitioner’s medical records do not contain any

diagnosis of carpal tunnel syndrome. However, a careful reading of Dr. Daskalos’ record suggests that

he recorded an impression of petitioner’s reported symptoms both as being consistent with carpal tunnel

syndrome and as being unrelated to her other complaints. This impression stands on its own terms

irrespective of any previously established carpal tunnel syndrome diagnosis.

45

of the hand 42).) Moreover, if petitioner experienced her first symptoms of GBS by

January 21, 2015, and did not reach the nadir of her condition until Mid-March, that

would be an unusually prolonged period from first manifestation to nadir of GBS.

(Burns, supra, at Ex. D, Tab. 1. p. 2.)

However, in contrast to these earlier records, on March 1, 2015, petitioner was

noted to have tingling that was reportedly “constant” and “severe” that began on

February 28, 2015. (Ex. 3, p. 36.) Additionally, when petitioner was ultimately

diagnosed with GBS by Sacred Heart Medical Center, ongoing neuropathic hand and

foot pain was identified as a symptom relevant to her GBS diagnosis. (Ex. 6, p. 225-

27.) The first report of hand and leg pain occurred at petitioner’s March 2, 2015

emergency department encounter, shortly after she first reported onset of severe and

constant tingling. (Ex. 4, p. 58.) Thus, although petitioner’s initial reports of tingling are

themselves inconclusive, if neuropathic pain was the first symptom of petitioner’s GBS,

it was likely evidenced in the medical records by no later than March 2, 2015, which falls

within 56-days of her vaccination.

In contrast, Dr. Leist opines that the onset of petitioner’s GBS occurred more

than sixty days post-vaccination based on the onset of her lower extremity weakness.

(Ex. A, p. 5.) Dr. Leist notes that petitioner was admitted for observation for her altered

mental state due to narcotic pain medication (for severe low back pain) on March 5,

2012, but no neurological deficits were appreciated at the time. (Id. at 5 (citing Ex. 4, p.

87.)) She was scheduled to be discharged March 7, 2015 when she had two bowel

movements with dark blood and clots, which prompted further evaluation. (Id. (citing

Ex. 4, pp. 72-75.)) Dr. Leist observes that petitioner had a brain CT scan on March 12,

2015, after developing right facial weakness. (Id. (citing Ex. 4, p. 83; Ex. 4, pp. 144-

45.)) Reports fro

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