Datte v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 18-2V

Filed: May 9, 2025

Special Master Horner

MARILYN DATTE,

Petitioner,

v.

SECRETARY OF HEALTH AND

HUMAN SERVICES,

Respondent.

Robert Krakow, Law Office of Robert J. Krakow, P.C., New York, New York, for

petitioner.

Jennifer Leigh Reynaud, U.S. Department of Justice, Washington, DC, for respondent.

RULING ON ENTITLEMENT1

On January 2, 2018, petitioner, Marilyn Datte, filed a petition under the National

Childhood Vaccine Injury Act, 42 U.S.C. § 300aa-10, et seq. (2012),2 alleging that she

suffered Guillain-Barré Syndrome (“GBS”) caused-in-fact by a pneumococcal conjugate

(Prevnar 13) vaccination she received on January 15, 2015. (ECF No. 1.) For the

reasons set forth below, I conclude that petitioner is entitled to an award of

compensation.

I. Applicable Statutory Scheme

Under the National Vaccine Injury Compensation Program, compensation

awards are made to individuals who have suffered injuries after receiving vaccines. In

general, to gain an award, a petitioner must make a number of factual demonstrations,

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

§ 300aa-10-34.

1

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 unless it is affirmatively shown that the injury was caused by some

factor other than the vaccination. § 300aa-13(a)(1)(A); § 300aa-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 that context, 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 ex rel.

Sevier v. Sec’y of Health & Human Servs., 940 F.2d 1518, 1525 (Fed. Cir. 1991).

GBS is a Table injury if onset occurs 3-42 days following receipt of a flu vaccine.

42 C.F.R. § 100.3(a)(XIV)(D). However, GBS is not a Table Injury relative to the

Prevnar 13 vaccine at issue in this case. 42 C.F.R. § 100.3(a)(XII). To succeed on a

claim that petitioner’s Prevnar 13 vaccine caused GBS, petitioner must satisfy the

burden of proof for “causation-in-fact.”

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 but must demonstrate that the

vaccination was at least a “substantial factor” in causing the condition, and was a “but

for” cause. Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344, 1352 (Fed. Cir.

1999). Thus, the petitioner must supply “proof of a logical sequence of cause and effect

showing that the vaccination was the reason for the injury[,]” with the logical sequence

being supported by “reputable medical or scientific explanation.” Althen, 418 F.3d at

1278; Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992).

Ultimately, petitioner must satisfy what has come to be known as the Althen test, which

requires: (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

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the injury; and (3) a showing of proximate temporal relationship between vaccination

and injury. Id.

A petitioner may not receive a Vaccine Program award based solely on his or her

assertions, but may support the petition with either medical records or by the opinion of

a competent physician. § 300aa-13(a)(1). Medical records are generally viewed as

particularly trustworthy evidence, because they are created contemporaneously with the

treatment of the patient. Cucuras v. Sec’y of Health & Human Servs., 993 F.2d 1525,

1528 (Fed. Cir. 1993). However, medical records and/or statements of a treating

physician’s views do not per se bind the special master to adopt the conclusions of such

an individual, even if they must be considered and carefully evaluated.

§ 300aa-13(b)(1). A petitioner may rely upon circumstantial evidence. Althen, 418 F.3d

at 1280. In that regard, 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. While

scientific certainty is not required, that expert’s opinion must be based on “sound and

reliable” medical or scientific explanation. Boatmon v. Sec’y of Health & Human Servs.,

941 F.3d 1351, 1359 (Fed. Cir. 2019).

Cases in the Vaccine Program are assigned to special masters who are

responsible for “conducting all proceedings, including taking such evidence as may be

appropriate, making the requisite findings of fact and conclusions of law, preparing a

decision, and determining the amount of compensation, if any, to be awarded.” Vaccine

Rule 3. Special masters must ensure each party has had a “full and fair opportunity” to

develop the record but are empowered to determine the format for taking evidence

based on the circumstances of each case. Vaccine Rule 3(b)(2); Vaccine Rule 8(a);

Vaccine Rule 8(d). Special masters are not bound by common law or statutory rules of

evidence but must consider all relevant and reliable evidence in keeping with

fundamental fairness to both parties. Vaccine Rule 8(b)(1). The special master is

required to consider “all [] relevant medical and scientific evidence contained in the

record,” including “any diagnosis, conclusion, medical judgment, or autopsy or coroner’s

report which is contained in the record regarding the nature, causation, and aggravation

of the petitioner’s illness, disability, injury, condition, or death,” as well as the “results of

any diagnostic or evaluative test which are contained in the record and the summaries

and conclusions.” § 300aa-13(b)(1)(A). The special master is required to consider the

entirety of record, draw plausible inferences, and articulate a rational basis for the

decision. Winkler v. Sec’y of Health & Human Servs., 88 F.4th 958, 963 (Fed. Cir.

2023) (citing Hines, 940 F.2d at 1528).

II. Procedural History

This case was originally assigned to another special master. (ECF No. 4.)

Petitioner filed medical records, medical literature, a declaration, and an affidavit

regarding damages (ECF Nos. 5-10, 15, 18; Exs. 1-20) and then filed her statement of

completion in February of 2018. (ECF No. 19.) In November of 2018, respondent filed

his Rule 4(c) Report, recommending against compensation. (ECF No. 30.) Petitioner

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filed an expert report by neuroimmunologist, Lawrence Steinman, M.D., the following

April. (ECF Nos. 36-38; Exs. 22-47.) This case was subsequently reassigned to

undersigned in August of 2019. (ECF Nos. 42-43.)

In October of 2019, respondent filed expert reports from neurologist, Vinay

Chaudhry, M.D., and immunologist, Robert Fujinami, Ph.D. (ECF Nos. 45-46; Ex. A-D.)

Petitioner filed additional medical records in January and March of 2020. (ECF Nos. 49,

53; Ex. 48-49.) From September of 2020 to April of 2021, the parties engaged in two

additional rounds of expert reports. (ECF Nos. 63-65, 68-69, 72, 78; Exs. 50-77, E-G.)

Thereafter, a two-day entitlement hearing was scheduled to commence on February 7,

2023. (ECF No. 83.) Petitioner subsequently filed updated medical records. (ECF Nos.

86, 89, 91, 94, 96; Exs. 78-95.)

In September of 2022, respondent filed a joint status report on behalf of the

parties, agreeing that this case was ripe for the previously scheduled entitlement

hearing. (ECF No. 100.) However, two months later, petitioner filed a motion for leave

to file additional exhibits. (ECF No. 102; Exs. 96-104.) Petitioner was permitted to file

the exhibits (ECF No. 103), but the entitlement hearing was rescheduled to commence

on April 4, 2023. (ECF No. 106.) Respondent then filed a supplemental report from Dr.

Fujinami on March 1, 2023. (ECF No. 113; Ex. H.) Following the prehearing status

conference on March 29, 2023, the parties each filed further additional medical

literature. (ECF Nos. 125, 127; Exs. 108; I.)

A two-day entitlement hearing was held remotely via Zoom on April 4th and 5th,

2023. (See Transcript of Proceedings (“Tr”), at ECF Nos. 129-30.) During the hearing,

petitioner presented testimony from Dr. Steinman and respondent presented testimony

from Dr. Fujinami. (See id.) Following the hearing, I ordered the parties to file post-

hearing briefs, and the parties completed their filings on December 7, 2023. (ECF Nos.

132, 135, 138.) This case is now ripe for a decision on entitlement.

III. Factual History

a. As reflected in the medical records

On January 15, 2015, petitioner received the subject Prevnar 13 vaccine. (Ex.

16.) She was 65 years old at the time of vaccination, and her past medical history was

significant for type II diabetes, fatty liver disease, hypertension, glaucoma,

hypothyroidism, anxiety, and obstructive sleep apnea. (Ex. 10, pp. 25-27, 31-33, 37-44,

47-52.) No new significant health issues were noted during the January 15, 2015

encounter. (Id. at 18-22.)

Ten days later, on January 25, 2015, petitioner presented to the emergency

department with complaints of tingling in both her hands and feet. (Ex. 9, p. 181.) She

was diagnosed with “new onset peripheral neuropathy/diabetes” and discharged with

instructions to follow up with her primary care physician. (Id. at 173-74, 181.) The next

day, petitioner returned to the emergency department with the same complaints of

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tingling in her hands and feet. (Id. at 213.) She further complained of progressive

numbness in her hands and feet and weakness, reporting that she was experiencing

difficulties raising either arm in the air. (Id. at 213, 227.) Additionally, she presented

with a “[p]etechiae like rash” on her face and redness in both sclera. (Id. at 227.) A

CT scan of her brain and MRI of the brain and cervical spine were unrevealing. (Id. at

255, 264-66.) Petitioner was again discharged, but this time with a neurology referral.

(Id. at 218-21.)

However, petitioner’s condition continued to progress. After returning home

following her discharge from the emergency room, petitioner reported experiencing pain

in her neck, head, and sinuses as well as an unsteady gait. (Ex. 10, p. 88.) As the day

progressed, she lost her sense of taste, started to experience tingling in her tongue, and

began to have no strength in her arms and legs. (Id.) The following morning, on

January 27, 2015, petitioner reported waking up around 5 a.m. with a headache,

vomiting, and difficulty swallowing. (Id. at 89.) She was so weak that she could not

stand or move her arms or legs. (Id.) At this point, petitioner decided she needed to

return to the emergency room. (Id.) However, due to her extreme weakness, petitioner

called EMS and was transported by ambulance to MidMichigan Medical Center -

Midland. (Id.; Ex. 9, p. 407, 411.) Upon arrival, petitioner was extremely weak in her

upper and lower limbs and had dysphagia, shortness of breath, and accelerated

hypertension. (Ex. 9, p. 407, 411; Ex. 10, p. 89; Ex. 12, p. 45.) She was immediately

transferred to the intensive care unit for further treatment. (Ex. 10, p. 89.) Her treating

providers noted a high clinical suspicion for GBS. (Id. at 80, 90; Ex. 12, p. 47.)

Petitioner’s treating neurologist, Gregory Dardas, M.D., indicated that she “recently had

a pneumonia vaccine but otherwise has been in her usual state of health.” (Ex. 10, pp.

79-80.) By January 28, 2015, petitioner’s working diagnosis was acute inflammatory

demyelinating polyradicular neuropathy. (Ex. 9, p. 352; Ex. 12, p. 43.) Dr. Dardas

noted that petitioner was “quadriparetic but not quadriplegic.” (Ex. 12, pp. 43-44.) A

nerve conduction study performed on January 29, 2015, confirmed diffuse axonal and

demyelinating polyneuropathy consistent with GBS. (Ex. 9, p. 937.) Petitioner’s

treating pulmonologist concurred in diagnosis, assessing petitioner with acute

respiratory failure due to ascending paralysis consistent with the acute inflammatory

demyelinating polyneuropathy (“AIDP”) form of GBS. (Ex. 12, pp. 21-22.) The

pulmonologist also noted that petitioner’s presentation of hypertension with “wide

fluctuations” was consistent with GBS induced autonomic dysfunction. (Id. at 22.)

During her hospitalization, she underwent a lumbar puncture, which was

negative, and a five-day course of IVIG treatment. (Ex., 10, pp. 79-80, 90; Ex. 9, pp.

335, 348; Ex. 12, pp. 33-34, 47.) She also completed various therapies to regain

functionality. (Ex. 9, pp. 1044-52.) Despite these treatments, petitioner’s condition

continued to deteriorate. (Ex. 12, p. 34.) Petitioner experienced acute respiratory

failure that was attributed to “acute inflammatory demyelinating polyneuropathy status

post IVIG.” (Ex. 9, p. 340.) As a result, she was intubated and placed on a mechanical

ventilator. (Id. at 348; Ex. 12, pp. 36-38.) Due to an inability to wean off the ventilator,

petitioner required a tracheostomy and a percutaneous endoscopic gastrostomy, as well

as a bronchoscopy for mucus plugging and atelectasis of the left lower lung. (Ex. 9, pp.

5

327-29, 337-38, 1034; Ex. 12, pp. 34, 37.) On February 8, 2015, physicians observed

that petitioner could shrug her shoulders and noted a “flicker of movement” in both

hands and feet. (Ex. 9, p. 338.) The next day, on February 9, 2015, her neurologist

documented that while petitioner had shown some signs of modest improvement, “she

certainly has quite a ways to go.” (Ex. 12, pp. 39-40.) He noted that she was able to

move her hands and feet on command and could “move with gravity,” but she could not

lift her head or limbs off the bed. (Id. at 39; Ex. 9, p. 336.) Facial weakness and lack of

sensation to pinprick were also noted. (Ex. 12, p. 39.)

On February 10, 2015, petitioner was discharged from MidMichigan Medical

Center and transported to Select Specialty Hospital for long-term acute care. (Ex. 2, pp.

39-40; Ex. 12, pp. 33-38.) On discharge, petitioner was still bedridden, struggling with

weakness, and required ventilation; however, she was noted to be making some

progress and able to move all extremities. (Ex. 12, pp. 34, 37.) Subsequent chest x-

rays showed additional density and pulmonary congestion in her right lung, which was

attributed to pneumonia. (Ex. 2, pp. 997, 1000; Ex. 4, pp. 80, 82, 84.) Then, on

February 13, 2015, petitioner was admitted to the intensive care unit at Covenant

Hospital after she experienced severe respiratory distress and became unresponsive

due to hypotension. (Ex. 2, pp. 30, 32; Ex. 18, pp. 10, 16, 64-67.) She was treated for

septic shock, SIRS, pneumonia, urinary tract infection (“UTI”) with methicillin-resistant

Staphylococcus epidermidis (“MRSE”), an infection at her tracheostomy site, as well as

acute pancreatitis. (Ex. 18, pp.16-17.) On February 19, 2015, petitioner returned to

Select Specialty Hospital. (Id. at 16-18; Ex. 2, pp. 30, 32.) During her stay, she saw

speech-language pathologists to work on swallowing and tongue strength. (Ex. 2, pp.

793-96.) She also had her tracheostomy removed. (Ex. 20, p. 406.) Physician notes

indicate that her extremity weakness was improving, although she continued to struggle

with blood pressure fluctuation, pneumonia, bowel issues, and UTI. (Ex. 4, pp. 4-52.)

By March 17, 2015, petitioner was cleared for discharge and transferred to Huron

Woods Nursing Center for occupational and physical therapy. (Ex. 2, pp. 27-28; Ex. 4,

pp. 3-5; Ex. 20, pp. 406-08.) A physical examination showed that petitioner was unable

to move her lower extremities or to turnover/sit up on her own. (Ex. 20, p. 408.) She

also complained of muscle pain and weakness. (Id. at 407-08.) She worked on

functional activities, such as hygiene and toileting, mobility, balancing, and

strengthening. (Id. at 185.) Petitioner made substantial progress in regaining strength

and functional activities during rehabilitation. (Id. at 129.) During this rehabilitation, on

April 2, 2015, petitioner was diagnosed with deep vein thrombosis in her right leg and

was transferred to Covenant Hospital again for treatment for two days. (Ex. 18, pp.

543-45, 552.) Then, on April 19, 2015, petitioner was sent to McLaren Medical Center

due to a repeat episode of supraventricular tachycardia. (Ex. 20, p. 79.) She was

discharged the same day and returned to Huron Woods. (Id.)

Petitioner was discharged home from Huron Woods on May 29, 2015. (Ex. 20,

pp. 358, 367.) She was discharged home with a walker and wheelchair. (Id. at 367.)

Petitioner’s discharge summary noted that she was ambulatory with a walker and

minimal to moderate assistance. (Id. at 368.) Additionally, the discharge summary

6

indicated that petitioner could complete most of her activities of daily living with minimal

to moderate assistance. (Id.) Petitioner continued with in-home physical and

occupational therapy. (Ex. 10, pp. 13-14; Ex. 5, p. 46; Ex. 13, p. 52.)

On June 1, 2015, petitioner followed up with her primary care provider. (Ex. 10,

p. 13.) At this visit, her primary care provider reported that petitioner was navigating

short distances with a walker. (Id.) However, her primary care provider documented

that petitioner was unable to walk with her walker independently, noting that she

required a one person assist. (Id.) She had ceased taking her Neurontin medication for

paresthesia due to nausea and diarrhea. (Id.) While she was still experiencing

weakness, most of her weakness was now in her feet. (Id. at 13, 15.) Notably, the

history of present illness indicates that petitioner’s GBS “started 10 days after getting

the prevnar 13” vaccine. (Id. at 13.) Petitioner’s physician assessed her with “Guillain-

Barre syndrome following vaccination.” (Id. at 15.)

From July 14 through August 25, 2015, petitioner participated in physical therapy

at Auburn Physical Therapy. (Ex. 5, p. 2.) She worked on strength, endurance,

stability, transfers, bed mobility, gait training, balance, and postural training. (Id. at 7.)

Upon discharge, petitioner reported “85-90% improvement.” (Id. at 2.) She reported

being able to ambulate independently at home and walk for about one hour with a cane,

although she was limited in her ability to ambulate on uneven surfaces or play with her

grandchildren. (Id. at 2.)

At a follow up exam on October 15, 2015, petitioner indicated that she was doing

well and ambulating with a cane. (Ex. 10, p. 1.) Petitioner’s primary care provider

indicated that she continued to show slow improvement, although her balance was a

little off and she still had “prickling in hands and feet.” (Id.) On March 8, 2016,

petitioner’s neurologist indicated that her GBS was “more or less completely resolved.”

(Ex. 12, pp. 12-15.)

As of March 16, 2017, “Guillain-Barre syndrome following vaccination was still

listed as one petitioner’s active problems. (Ex. 13, p. 28.) Petitioner was noted to be

experiencing continued numbness in both feet at this time; however, it was unclear

whether this symptom was due to GBS or petitioner’s preexisting diabetes myelitis. (Id.)

On September 26, 2017, petitioner presented to her neurologist, reporting issues with

her feet, including plantar fascia pain, that worsened when she was standing or walking.

(Ex. 12, pp. 6-7.) Petitioner’s presentation suggested that her symptoms were the result

of “something other than diabetic neuropathic pain.” (Id. at 6.) The EMG and nerve

conduction study were “notable for diffuse axonal and to a lesser extent demyelinating

polyneuropathy.” (Id. at 7.) Petitioner’s neurologist noted the difficulty in ascertaining

the chronicity of her presentation and opined that the clinical findings were likely related

to her history of GBS and diabetes. (Id.)

Petitioner’s primary care provider continued to document her GBS as an active

problem in 2020 and 2021. (Ex. 78, pp. 8, 14, 19, 23, 28; Ex. 48, p. 1.) At an encounter

on March 31, 2021, her primary care provider noted that petitioner still experiences

neuropathy in both feet from her GBS. (Ex. 78, p. 27.)

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b. Petitioner’s declaration

Petitioner declares that, prior to the subject vaccination, she was generally

healthy, her diabetes was under control, though she was monitored for hypertension

and several other conditions. (Ex. 17, ¶ 5.) Petitioner was administered a Prevnar 13

vaccine on January 15, 2015, during an appointment for her annual physical. (Id. ¶¶ 4,

6-8.)

According to petitioner, she noticed tingling in her fingers and toes while walking

on the treadmill in the late afternoon of January 25, 2015. (Ex. 17, ¶ 9.) Petitioner’s

husband transported her to the emergency department at Mid-Michigan Medical Center

in Midland. (Id. ¶ 10.) She was diagnosed with diabetic neuropathy and sent home with

a prescription. (Id. ¶ 11.) Petitioner declares the next day, January 26, 2015, she

awoke with tingling extending to her feet and hands. (Id. ¶ 12.) She also describes

difficulty walking, prompting her husband to take her back to the emergency department

a second time. (Id.) Petitioner declares she was sent home with no prescribed

medications. (Id. ¶ 14.) An appointment was scheduled with neurologist Dr. Gregory

Dardas. (Id. ¶ 13.)

On January 27, 2015, petitioner describes difficulty standing and walking,

requiring assistance to bathroom. (Ex. 17, ¶ 15.) Petitioner declares her husband

called an ambulance and she was transported to the Mid-Michigan emergency

department for the third time where she was subsequently admitted to the ICU. (Id.

¶¶ 15-16.) Petitioner recalls “I was unable to move most of my body. I was unable to

walk or stand. I felt numb all over and had trouble breathing and swallowing.” (Id. ¶ 16.)

Petitioner was started on IVIG treatment for GBS. (Id. ¶ 17.) On January 29, 2015,

petitioner was put on a ventilator. (Id. ¶ 18.) On January 31, 2015, petitioner

underwent her last IVIG treatment. (Id. ¶ 19.) She recalls, “I was semi-conscious at

times.” (Id.) On February 5, 2015, petitioner underwent surgery to place a feeding tube

and tracheostomy. (Id. ¶ 20.)

Petitioner recalls that she started to experience signs of slow improvement while

at Select Specialty Hospital. (Ex. 17, ¶ 25.) Once petitioner was discharged to Huron

Woods, she started physical and occupational therapy. (Id. ¶ 26.) She remembers that

she was first able to attempt to stand in April of 2015. (Id.) By the end of May of 2015,

petitioner recalls that she experienced progress with walking. (Id.) After being

discharged from Huron Woods, petitioner continued her rehabilitation with in-home

physical and occupational therapy. (Id. ¶ 27.) By the end of June of 2015, petitioner

avers being able to walk short distances with the assistance of a cane. (Id.) In July of

2015, petitioner’s in-home physical and occupational therapy concluded, and she

started to work with outpatient physical therapy through the end of August of 2015. (Id.

¶¶ 27-28.) At the time of filing her declaration in January of 2018, petitioner continued

to experience pain and discomfort in her feet and fingertips. (Id. ¶ 29.) She avers that

her continuing symptoms worsen when she is on her feet but that the pain and

discomfort subside when she is sitting or lying down. (Id.)

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IV. Summary of Expert Opinions

a. Petitioner’s Expert, Lawrence Steinman, M.D.3

Petitioner filed three expert reports and a letter from Dr. Steinman. (Exs. 22, 50,

75, 96.) Dr. Steinman also testified at the hearing. (Tr. 5.) He opined that petitioner’s

GBS was caused by her January 15, 2015, Prevnar 13 vaccination. (Id. at 36-37; Ex.

22, pp. 1, 22.) Dr. Steinman identified two molecular mimics relevant to GBS in the

composition of the Prevnar 13 vaccine, one relating to phosphoglycerol within the

pneumococcal polysaccharide antigen, and a second from the CRM protein conjugate.4

(Ex. 22, p. 12; Tr. 43.)

Initially, Dr. Steinman sought to determine if the Prevnar 13 vaccine contained

phospholipids, which he could not confirm. (Ex. 22, p. 14; Tr. 63-64 (citing Prescribing

Information, Prevnar 13 (Pneumococcal 13-Valent Conjugate Vaccine [Diphtheria

CRM197 Protein]): Suspension for Intramuscular Injection [hereinafter Prevnar 13

Package Insert] (Ex. 15; see also Ex. 31)); Ex. 75, p. 5.) However, he explained that

the patent for the vaccine confirms that the Prevnar 13 vaccine contains

phosphoglycerol linkages, which he opined are supportive of his causal theory. (Ex. 75,

pp. 5-8 (citing U.S. Patent No. 9,492,559 B2 (issued Nov. 15, 2016) [hereinafter Prevnar

13 Patent] (Ex. 51)); Tr. 65-67.) That is, Dr. Steinman clarified during the hearing that

the vaccine contains phosphoglycerol, which he indicated is a component of

phospholipids, not phospholipids.5 (Tr. 43, 90, 161.) Upon his review of Chuang et al.,

Dr. Steinman determined that the 19A strain of S. pneumoniae contains an expression

of phosphorylcholine, which plays a key role in the pathophysiology of pneumonia

infection. (Ex. 22, p. 14 (citing Yi-Ping Chuang et al., Impact of the glpQ2 Gene of

Virulence in a Streptococcus Pneumoniae Serotype 19A Sequence Type 320 Strain, 83

INFECTION & IMMUNITY 682 (2015) (Ex. 36)).) The authors explain that surface

phosphorylcholine expression in S. pneumoniae 19AST320 during the exponential

phase “contributes to the severity of pneumonia by promoting adherence and host cell

cytotoxicity.” (Id. (quoting Chuang et al., supra, at Ex. 36, p. 1).) Dr. Steinman thus

3

Dr. Steinman received his medical degree from Harvard in 1973. (Ex. 23.) He completed an internship

and residency at Stanford University Hospital in 1973 and 1947, respectively, before going on to complete

a neuroimmunology fellowship at the Weizmann Institute of Science in 1977. (Id. at 1; Tr. 10.) He

returned to Stanford university to complete an additional neurology residency in 1980. (Ex. 23, p. 1; Tr.

10.) Since then, Dr. Steinman has worked as a professor in the neurology department at Stanford

University. (Ex. 22, p. 1; Tr. 5, 10.) In his clinical capacity, Dr. Steinman has treated both adult and

pediatric patients who suffered from various forms of autoimmune disease of the nervous system, and he

has diagnosed hundreds of GBS patients. (Ex. 22, p. 1; Tr. 6-9.) In his research capacity, Dr. Steinman’s

has focused on how the immune system attacks the nervous system, and he has published on the

subject of molecular mimicry. (Ex. 22, pp. 1-4; Ex. 23, pp. 5-45; Tr. 11-12, 14-15.) Dr. Steinman is board

certified in neurology. (Ex. 23, p. 2; Tr. 17.) At the hearing, Dr. Steinman was proffered as an expert in

neurology and neuroimmunology without objection. (Tr. 26, 30-31.)

4

Because this ruling resolves entitlement in petitioner’s favor based on the phosphoglycerol theory, the

CRM protein theory is not discussed as it is not necessary to reach that theory.

5

Respondent asserts that this change in Dr. Steinman’s approach should be viewed as discrediting.

(ECF No. 135, pp. 23-25.)

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concluded the Prevnar 13 vaccine could immunize against this component of

pneumococcus. (Id. at 15 (citing Jennifer L. Kanter et al., Lipid Microarrays Identify Key

Mediators of Autoimmune Brain Inflammation, 12 NATURE MED. 138 (2006) (Ex. 33);

Peggy P. Ho et al., Identification of Naturally Occurring Fatty Acids of the Myelin Sheath

that Resolve Neuroinflammation, 4 SCI. TRANSLATIONAL MED. 1 (2012) (Ex. 34); Denong

Wang et al., Uncovering Cryptic Glycan Markers in Multiple Sclerosis (MS) and

Experimental Autoimmune Encephalitis (EAE), 75 DRUG DEV. RSCH. 172 (2014) (Ex.

35).) He explained that the enzyme for metabolizing lipids and producing

phosphorylcholine is present in strains 3, 6B, 19A and 19F. (Id. (citing Chuang et al.,

supra, at Ex. 36).) Moreover, strains 3, 19A, and 19F are present in Prevnar 13. (Id.

(citing Prevnar 13 Package Insert, supra, at Ex. 15); Ex. 50, pp. 7, 18 (citing Prevnar 13

Patent, supra, at Ex. 51).) Dr. Steinman further noted that the vaccine contains 18C

and 23F, both of which contain phosphoglycerol. (Ex. 50, pp. 7, 18; Tr. 71-72, 78, 311.)

Citing his own research, Dr. Steinman explained that phospholipids (and

therefore phosphoglycerol) are components of myelin sheath, and they are targeted by

antibodies in neuroinflammation. (Ex. 22, p. 13 (citing Kanter et al., supra, at Ex. 33; Ho

et al., supra, at Ex. 34; Wang et al., supra, at Ex. 35); Tr. 43, 97, 298-99.) In Ho et al.,

Dr. Steinman and his colleagues demonstrated that “[l]ipids constitute 70% of the myelin

sheath, and autoantibodies against lipids may contribute to the demyelination that

characterizes multiple sclerosis.” (Ex. 22, p. 13 (quoting Ho et al., supra, at Ex. 34).)

The authors explained that they used lipid antigen microarrays and lipid mass

spectrometry to identify lipid targets of the autoimmune response in an MS brain and in

an animal model of MS. (Id.) Ho et al. found that autoantibodies in MS target a

phosphate group in phosphatidylserine and oxidized phosphatidylcholine derivatives.

(Id.; Tr. 97-98, 303-04.) The main target of the human immune response to the myelin

lipids was the phosphoglycerol component – common to phosphatidyl-ethanolamine,

phosphatidylcholine, phosphatidylserine. (Ex. 50, p. 4 (citing Ex. 22).)

Dr. Steinman also observed that antibodies to phospholipids are seen in GBS.

(Ex. 22, p. 13 (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. 32)).) Prior to the Ho et al. study, Gilburd et al. published

results demonstrating that the sera of 6 out of 16 GBS patients had autoantibodies to

one or more of the antigens studied (phosphatidyl-ethanolamine, phosphatidylcholine,

and phosphatidylserine). (Id. (citing Gilburd et al., supra, at Ex. 32).) Dr. Steinman

stressed that two of the six patients tested had reactivity to phosphatidylserine or

phosphatidylcholine. (Id.) Dr. Steinman explained that the structure of

phosphatidylcholine and phosphatidylserine have in common a polar head group

targeted by antibodies. (Id. at 14 (citing Ho et al., supra, at Ex. 34; Tr. 82-83).) He

stressed that the phospholipids discussed in the Gilburd et al. paper all share a

common phosphoglycerol group. (Ex. 50, pp. 4, 17.) This is the component of the

phospholipids that is attacked by the immune system in MS – as shown in the later

paper by Ho et al. (Id. at 4.) He acknowledged that petitioner’s theory of causation

relies on a scientific analogy to the documented MS immune response. (Id.) Dr.

Steinman opined, however, that the findings in the Gilburd et al. paper are clarified by

10

application of the later findings by Ho et al., allowing a reinterpretation of the Gilburd et

al. study’s conclusion, which “can all be explained by the same immune response in

each disease to a common structure.” (Id.) In particular, in light of the Ho et al. paper,

Dr. Steinman stressed the authors of the 1993 Gilburd et al. paper would have been

“able to reinterpret and correct their assertion that these immune responses were the

‘effect’ and not the ‘cause.’” (Id.)

Additionally, Dr. Steinman observed that in Nakos et al., phospholipid antibodies

were found in patients with GBS, similar to the Gilburd et al. study’s findings. (Ex. 50,

pp. 11-12 (citing G. Nakos et al., Anti-Phospholipid Antibodies in Serum from Patients

with Guillain-Barré Syndrome, 31 INTENSIVE CARE MED. 1401 (2005) (Ex. 55)).) In fact,

four blood samples were obtained before and after treatment and tested for antibodies

to phosphatidylcholine, phosphatidyl-inositol, cardiolipin, phosphatidic acid,

phosphatidylserine, phosphatidylglycerol, phosphatidylethanolamine, sphingomyelin,

and gangliosides. (Id. (citing Nakos et al., supra, at Ex. 55); Tr. 86-88, 315-20.)

Antiphospholipid antibodies of the IgM, IgA, and IgG families were detected in all GBS

patients but in none of the controls. (Ex. 50, p. 12 (citing Nakos et al., supra, at Ex.

55).) Phosphatidylinositol, cardiolipin, phosphatidylcholine, and phosphatidic acid were

the main antigens, with cardiolipins presenting within one day of infusion. (Id.; Tr. 87-

88, 316-18.) Accordingly, Dr. Steinman opined that Prevnar 13 could immunize against

this phosphoglycerol component of pneumococcus common to the linkage for the

polysaccharides in the vaccine. (Ex. 50, p. 12.)

Dr. Steinman opined that the common structure is phosphoglycerol. (Ex. 50, p.

4.) The Ho et al. paper indicates that the polar head group in phosphoglycerol and

phosphocholine are the main targets of immune attack in MS patients. (Id. at 8 (citing

Ho et al., supra, at Ex. 34).) Ho et al. observed that the saturated, nonpolar side chains

mediate the protective effects of the therapeutic lipids; and the palmitic acid

(representative of such fatty acid side chains present within the lipids) was able to

reproduce the therapeutic effects of the lipids in vitro and in vivo. (Id. at 21 (quoting Ho

et al., supra, at Ex. 34, p. 9); Tr. 84.) Yet, while the fatty acid side chains are the

protective moiety, Dr. Steinman maintains that the phosphoglycerol is the target of the

antibody. (Ex. 50, p. 21; Tr. 86 (discussing Nakos et al., supra, at Ex. 55), 90 (citing Ho

et al., supra, at Ex. 34).) Dr. Steinman cited Barbar et al., which showed that

“antibodies can have exquisite specificity for the polar head group, although they may

bind with different affinities (strengths) depending on the bigger carrier molecule

connected to the phosphate head group.” (Ex. 96, p. 5 (citing Elisar Barbar et al.,

Binding of Phenylphosphocholine–Carrier Conjugates to the Combining Site of

Antibodies Maintains a Conformation of the Hapten, 35 BIOCHEMISTRY 2958 (1996) (Ex.

102)).) He further cites Bryson et al., which found that immunization with a

pneumococcal vaccine containing 23F makes an antibody that recognizes the polar

head group on phosphoglycerol. (Tr. 96, 311 (citing Steve Bryson et al., Structures of

Preferred Human IgV Genes – Based Protective Antibodies Identify How Conserved

Residues Contact Diverse Antigens and Assign Source of Specificity to CDR3 Loop

Variation, 196 J. IMMUNOLOGY 4723 (2016) (Ex. 103)).)

11

Dr. Steinman drew further support from the Chang et al. paper demonstrating

that a phospholipid linkage is “quite necessary” for immunogenicity of the capsular

polysaccharides. (Ex. 50, p. 10 (citing Janoi Chang et al., Relevance of O-acetyl and

Phosphoglycerol Groups for Antigenicity of Streptococcus Pneumoniae Serotype 18C

Capsular Polysaccharide, 30 VACCINE 7090 (2012) (Ex. 52)); Tr. 72-74, 76-77.) The

authors explain that serotype 18C contains a repeating unit that has a complex structure

– “a branched pentasaccharide with two apparently labile substituents: glycerol-

phosphate and O-acetyl group.” (Ex. 50, p. 10 (quoting Chang et al., supra, at Ex. 52);

Tr. 72-73.) The “loss of these groups may potentially reduce the ability of the 18C

polysaccharide to induce the desired immune response,” thus the authors conclude the

glycerol-phosphate “must be preserved for conserving adequate antigenicity of the 18C

capsular polysaccharide.” (Ex. 50, p. 10 (quoting Chang et al., supra, at Ex. 52); Tr. 72-

74.) Lugowski et al. further suggests the Glycerol-1-P-OH is critical for the linkage to

the 18C polysaccharide. (Ex. 50, pp. 10-11 (citing Czeslaw Lugowski & Harold

Jennings, Structural Determination of the Capsular Polysaccharide of Streptococcus

Pneumoniae Type 18C (56), 131 CARBOHYDRATE RSCH. 119 (1984) (Ex. 53)).)

Dr. Steinman additionally proposed that alum adjuvant in the Prevnar 13 vaccine

can lead to an increase in pro-inflammatory cytokines, such as IL-1 and IL-18, and

contribute to the pathogenesis of GBS. (Ex. 50, pp. 23-25.) He maintains IL-1 and IL-

18 are strongly upregulated during active GBS and its animal models but reduce as

GBS resolves. (Id. at 23 (citing Rosetta Pedotti et al., Severe Anaphylactic Reactions to

Glutamic Acid Decarboxylase (GAD) Self Peptides in NOD Mice that Spontaneously

Develop Autoimmune Type I Diabetes Mellitus, 4 BMC IMMUNOLOGY 1 (2003) (Ex. 59);

Stefanie Kuerten & Paul V. Lehmann, The Immune Pathogenesis of Experimental

Autoimmune Encephalomyelitis: Lessons Learned for Multiple Sclerosis, 31 J.

INTERFERON & CYTOKINE RSCH. 907 (2011) (Ex. 60); Ludwig Kappos et al., Induction of a

Non-Encephalitogenic Type 2 T Helper-Cell Autoimmune Response in Multiples

Sclerosis After Administration of an Altered Peptide Ligand in a Placebo-Controlled,

Randomized Phase II Trial, 6 NATURE MED. 1176 (2000) (Ex. 61); Stephanie Eisenbarth

et al., Crucial Role for the Nalp3 Inflammasome in the Immunostimulatory Properties of

Aluminum Adjuvants, 453 NATURE 1122 (2008) (Ex. 62); Anna Sokolovska et al.,

Activation of Dendritic Cells and Induction of CD4+ T Cell Differentiation by Aluminum-

Containing Adjuvants, 25 VACCINE 4575 (2007) (Ex. 63); J.W. Mannhalter et al.,

Modulation of the Human Immune Response by the Non-Toxic and Non-Pyrogenic

Adjuvant Aluminum Hydroxide: Effect on Antigen Uptake and Antigen Presentation, 61

CLINICAL & EXPERIMENTAL IMMUNOLOGY 143 (1985) (Ex. 64)).) Jander and Guido

reported that IL-18 serum levels were significantly higher in GBS patients than in

noninflammatory neurologic disease controls – thus “implicating the Th1-inducing

cytokine IL-18 in the pathogenesis of acute immune-mediated PNS demyelination.” (Id.

at 23-24 (quoting Sebastian Jander & Guido Stoll, Interleukin-18 is Induced in Acute

Inflammatory Demyelinating Polyneuropathy, 114 J. NEUROIMMUNOLogy 253 (2001) (Ex.

67)).) On the whole, Dr. Steinman opined these papers constitute strong evidence for

how the pneumococcal vaccine containing alum as an adjuvant would lead to

inflammatory polyneuropathy. (Id. at 24.) However, Dr. Steinman stated during the

12

hearing that his opinion regarding any pro-inflammatory role played by the alum

adjuvant is not an essential component of his causal theory. (Tr. 115-16, 118.)

Dr. Steinman cited two reports of GBS following pneumococcal vaccination. (Ex.

75, p. 10 (citing Nidhi Ravishankar, Guillain-Barre Syndrome Following PCV Vaccine, 2

CLINICS IN SURGERY 1 (2017) (Ex. 76); Hassan El Khatib et al., Case Report: Guillain-

Barre Syndrome with Pneumococcus – A New Association in Pediatrics, 11 IDCASES 36

(2018) (Ex. 77)).) The first case report describes a 66-year-old female with a past

medical history of hypertension, hyperlipidemia, and GERD, who developed GBS after

receiving Prevnar 13 and the 23-valent pneumococcal conjugate (“Pneumovax 23”)

vaccinations. (Ravishankar, supra, at Ex. 76.) The second case report describes a 13-

year-old male who presented with hypoactivity, slurred speech, and lower extremity

weakness and developed septic shock due to pneumococcus with acute respiratory

distress syndrome. (El Khatib et al., supra, at Ex. 77.) That patient was also found to

have neurological findings of GBS. (Id.)

Dr. Steinman acknowledged two epidemiologic studies showing that

pneumococcal vaccines do not pose an increased risk of GBS. (Ex. 22, p. 21 (citing

Hung Fu Tseng et al., Pneumococcal Conjugate Vaccine Safety in Elderly Adults, OPEN

F. INFECTIOUS DISEASES, May 2018, at 1 (Ex. 45); Roger Baxter et al., Lack of

Association of Guillain-Barré Syndrome with Vaccinations, 57 CLINICAL INFECTIOUS

DISEASES 197 (2013) (Ex. 46; see also Ex. A, Tab 6).) However, he stressed that the

study by Baxter et al., investigated results following administration of Pneumovax 23,

not Prevnar 13. (Id. (citing Baxter et al., supra, at Ex. 46.) And while these

epidemiologic studies are reassuring, Dr. Steinman contends they do not rule out

Prevnar 13 as a cause of GBS. (Id.)

Regarding this particular case, Dr. Steinman observed that petitioner received

the Prevnar 13 vaccine on January 15, 2015. (Ex. 22, p. 21 (citing Ex. 1, p. 1).) Twelve

days later, she presented with a chief complaint of “ascending weakness,” which he

opined was the onset of GBS. (Id. (citing Ex. 10, pp. 80-81); Tr. 33-34.) Though there

are no epidemiologic studies on point, he opined an interval of 12 days between

immunization and GBS “certainly fits with the time course” reported by Schonberger et

al. for GBS following swine flu immunization. (Ex. 22, p. 21 (citing Lawrence

Schonberger et al., Guillain-Barre Syndrome Following Vaccination in the National

Influenza Immunization Program, United States, 1976-1977, 100 AM. J. EPIDEMIOLOGY

105 (1979) (Ex. 47)); Tr. 41-42, 156-57.) Lastly, Dr. Steinman opined alternate causes,

such as petitioner’s type II diabetes, are highly unlikely to have caused her GBS. (Ex.

22, p. 22.)

13

b. Respondent’s Experts

i. Vinay Chaudhry, M.D.6

Respondent filed two expert reports drafted by Dr. Chaudhry. (Exs. A, E.) Dr.

Chaudhry opined that petitioner suffered from GBS that began with tingling on or about

January 24, 2015 (nine days post-vaccination), peaked with quadriparesis on or about

January 29, 2015, and improved to normal strength by March 8, 2016. (Ex. A, p. 5.) He

further opined that petitioner suffered from the AIDP variant of GBS. (Id.) Dr. Chaudhry

acknowledged that acute motor axonal neuropathy (“AMAN”), a variant of GBS, is

known to be caused by the mechanism of molecular mimicry but disagreed that this can

be extended to the AIDP form of GBS that petitioner suffered. (Id. at 7.) Dr. Chaudhry

stressed, in particular, that “[i]t is well established that ganglioside antibodies arising as

a result of molecular mimicry between the lipooligosaccharides of infective organisms

and the surface molecules on the motor axons, induce axon injury by complement

fixation, attracting macrophages and depositing membrane attack complexes in AMAN

form of GBS.” (Ex. E, p. 2 (citing Nobuhiro Yuki, Ganglioside Mimicry and Peripheral

Nerve Disease, 35 MUSCLE & NERVE 691 (2007) (Ex. A, Tab 9); Peter D. Donofrio,

Guillain-Barré Syndrome, 23 CONTINUUM (MINNEAPOLIS MINN.) 1295 (2017) (Ex. E, Tab

2); Francine J. Vriesendorp, Guillain-Barré Syndrome: Pathogenesis, UPTODATE,

https://www.uptodate.com/contents/guillain-barre-syndrome-pathogenesis (last visited

Nov. 18, 2020) (Ex. E, Tab 3)).) He stressed that gangliosides “have a completely

different composition than phosphoglycerol moiety proposed by Dr. Steinman.” (Id.)

Unlike in AMAN, the specific antibody in AIDP has not been identified and its

pathogenesis is not known, but Dr. Chaudhry suggested that it may be the result of a

mechanism other than ganglioside mimicry. (Id.; Ex. A, p. 7 (citing Yuki, supra, at Ex. A,

Tab 9).)

Dr. Chaudhry further observed that the authors of the Gilburd et al. paper

concluded the autoantibodies produced by GBS patients to various phospholipids and

nuclear antigens are likely “produced as a result of the myelin damage rather than

cause the demyelination.” (Ex. A, p. 8 (quoting Gilburd et al., supra, at Ex. 32).) He

criticized Dr. Steinman’s reinterpretation of the data from this paper and maintained “the

authors did not find an association between the antibodies and GBS when compared to

controls.” (Ex. E, p. 2 (citing Gilburd et al., supra, at Ex. 32).) Dr. Chaudhry also

contended the papers from Kanter et al., Ho et al., and Wang et al. discuss lipid arrays

6

Dr. Chaudhry currently serves as a professor of neurology at Johns Hopkins University School of

Medicine and co-director of the EMG Laboratory at Johns Hopkins Hospital. (Ex. A, p. 1.) He received

his medical degree from the All India Institute of Medical Sciences, New Delhi, India. (Ex. B, p. 2.) He

completed his clinical and research fellowships in neuromuscular diseases at Johns Hopkins University

School of Medicine. (Id. at 3.) Dr. Chaudhry is board certified in Neurology, Neuromuscular diseases,

Electrodiagnostic Medicine (Nerve Conduction and EMG), and Clinical Neurophysiology. (Ex. A, p. 1.)

He holds an active clinical practice and sees close to 2000 patients a year (for over 25 years) mostly

related to peripheral nerve disease. (Id.) He is involved in clinical research and has over 120

publications, including peer reviewed articles, reviews and book chapters. (Id.) Dr. Chaudhry has directly

mentored over 50 fellows and 100s of medical students and neurology residents. (Id.) He routinely

reviews articles for over 25 different journals and has previously served on the editorial board of three

journals. (Id.)

14

in multiple sclerosis, which is a disease of the central nervous system in which

oligodendrocytes, not Schwann cells, produce myelin. (Ex. A, p. 8 (citing Kanter et al.,

supra, at Ex. 33; Ho et al., supra, at Ex. 34; Wang et al., supra, at Ex. 35).) He stressed

GBS and MS are two distinct diseases that do not share the same pathogenesis. (Id.)

He further stressed that neither the subject vaccine nor the subject condition are

discussed in these papers. (Id.) Importantly, the Nakos et al. manuscript also

concludes “[i]t 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.” (Ex. E, p. 2 (quoting Nakos et al., supra,

at Ex. 55, p. 6).)

To demonstrate the safety of the Prevnar 13 vaccine, Dr. Chaudhry cited several

studies monitoring post-vaccination adverse effects. (Ex. A, pp. 5-7.) Haber et al.

evaluated the safety of Prevnar 13 by analyzing data from the Vaccine Adverse Event

Reporting System (“VAERS”) from June 2012 to December 2015. (Id. at 6 (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

(2016) (Ex. A Tab 5; see also Ex. 58)).) Dr. Chaudhry also cited Baxter et al., which

included 13 years and 30 million person-years of data for a case-controlled analysis,

finding no evidence of an increased risk of GBS following any vaccination or

vaccinations combined. (Id. (citing Baxter et al., supra, at Ex. 46).) Although Prevnar

13 was not available for use during this study period, Dr. Chaudhry noted the 23-valent

polysaccharide pneumococcal vaccine was included in the study. (Id.) Additionally, an

article by Tseng et al., compared the safety of Prevnar 13 and Pneumovax 23 and

found no evidence of increased risk of adverse events with Prevnar 13 among 313,136

doses of Prevnar 13. (Id. at 7 (discussing Tseng et al., supra, at Ex. 45).)7 Jackson et

al. studied the safety of Prevnar 13 among adults ≥ 70 years of age who were

previously immunized with the Pneumovax 23 vaccine – finding no reported cases of

GBS among the 936 vaccinated subjects. (Id. (citing Lisa Jackson et al.,

Immunogenicity and Safety of a 13-Valent Pneumococcal Conjugate Vaccine in Adults

70 Years of Age and Older Previously Vaccinated with 23-Valent Pneumococcal

Polysaccharide Vaccine, 31 VACCINE 3585 (2013) (Ex. A Tab 7)).) Lastly, Dr. Chaudhry

noted that seven clinical studies conducted in the U.S. and Europe assessed the safety

of Prevnar 13 and included 91,593 adults (48,806 of which received Prevnar 13)

ranging in age from 18 through 101 years. (Id. (citing Pfizer Medical Information:

Prevnar 13, PFIZER, https://www.pfizermedicalinformation.com/en-us/prevnar-13 (last

visited Oct. 19, 2019) (Ex. A, Tab 8, pp. 8-12)).) Dr. Chaudhry observed that serious

adverse events were reported within one month of vaccination in 0.2%-1.4% of 5,057

subjects vaccinated with Prevnar 13, but GBS was not among the reported events. (Id.)

Dr. Chaudhry contended that, despite Dr. Steinman’s great lengths to identify

phosphoglycerol in Prevnar 13, he “could never conclusively ascertain if

phosphoglycerol is present in Prevnar 13,” and asserted the conformational structure

7

In his report, Dr. Chaudhry miscited this study as “Vaccine 2013,” which would seem to refer to Jackson

et al., infra.

15

between an exogenous agent and self-antigen alone are not sufficient to prove that

molecular mimicry is the pathogenic mechanism for a disease. (Ex. E, pp. 2-3.) Rather,

Dr. Chaudhry offered four criteria he opines must be satisfied to conclude that a disease

such as GBS is triggered by molecular mimicry: (1) an epidemiological association

between the infectious agent and the immune-mediated disease, (2) identification of T

cells or antibodies directed against the patient’s target antigens, (3) identification of

microbial mimics of the target antigen, and (4) reproduction of the disease in an animal

model. (Id. at 3 (citing Yuki, supra, at Ex. A, Tab 9).) According to Dr. Chaudhry, none

of these criteria have been met for Prevnar 13. (Id.)

Lastly, Dr. Chaudhry disputed petitioner’s reliance on the time frame for GBS

following swine flu vaccination, stressing that temporal association in one case does not

support causation and that none of the Prevnar 13 studies reported GBS in pre-

licensure and post-licensure cases up to 42 days post-vaccination. (Ex. A, p. 9.)

ii. Robert S. Fujinami, Ph.D.8

Dr. Fujinami filed four expert reports on behalf of respondent. (Exs. C, F-H.) He

also provided testimony at the entitlement hearing. (Tr. 168.) Dr. Fujinami opined that,

if Dr. Steinman’s theory were correct, then the Prevnar 13 vaccine “would induce

pathogenic antibodies against phosphatidylcholine, which is contained in all myelin.”

(Ex. C, p. 3.) Because myelin is present in both the peripheral nervous system and the

central nervous system, Dr. Fujinami explained that the phospholipids that are central to

Dr. Steinman’s theory are thus contained in both the peripheral nervous system and the

central nervous system; however, GBS is an immune mediated disease of the

peripheral nervous system, not the central nervous system. (Id.) He questioned, then,

why the neuroinflammation putatively caused by antibodies to phosphatidylcholine only

induces damage in the peripheral nervous system and not the central nervous system.

(Id.) To that end, in this case, petitioner did not experience central nervous system

involvement. (Id.) Petitioner’s CT and MRI of her head, as well as blood work, were all

normal. (Id. (citing Ex. 22, p. 5).) If there was central nervous system involvement with

inflammation in the myelin, Dr. Fujinami stressed it would be noted in the medical

records. (Id.)

8

Dr. Fujinami currently serves as a professor in the Department of Pathology, Division of Microbiology

and Immunology, and an Adjunct Professor in the Department of Neurology at the University of Utah

School of Medicine. (Ex. D, p. 1; Tr. 168.) He received his undergraduate degree in microbiology from

the University of Utah and doctorate from Northwestern University. (Ex. D, p. 1; Tr. 169.) Dr. Fujinami

completed his postdoctoral training at The Scripps Research Institute and advanced to Assistant

Professor investigating how viruses/infections could induce autoimmune disease. (Ex. D, p. 1; Tr. 169-

70.) While at Scripps, Dr. Fujinami and Dr. Michael Oldstone first introduced molecular mimicry as a

theoretical concept in the early 1980's, with respect to viruses and their putative role in the propagation of

autoimmunity. (Ex. C, p. 1.) He is accordingly one of the scientific “fathers” of the concept, though he is

not a medical doctor. Dr. Fujinami has published hundreds of articles about microbial infection, vaccines,

and autoimmune disease. (Ex. D, pp. 20-37.) He has also served on various panels for the National

Institute of Health, Institute of Medicine, National Academy of Sciences, National Science Foundation,

and National Multiple Sclerosis Society. (Ex. C, p. 2.) At the hearing, Dr. Fujinami was proffered as an

expert in immunology, neuroimmunology, and neurobiology without objection. (Tr. 183.)

16

Like Dr. Chaudhry, Dr. Fujinami is critical of Dr. Steinman’s reliance on the

Gilburd et al. study. (Ex. C, p. 3.) He too stressed that Gilburd et al. concluded the

autoantibodies to various phospholipid antigens were probably produced as a result of

myelin damage, rather than the cause of demyelination. (Id.; Tr. 186-87.) However, he

recognized that the authors did not specifically look at whether the phospholipid

antigens caused demyelination. (Tr. 259-63.)

Dr. Fujinami also took issue with Dr. Steinman’s reinterpretation of the Ho et al.

paper. (Ex. G, pp. 1-2 (citing Ho et al., supra, at Ex. 34); Tr. 208-09.) Dr. Fujinami

stressed that Ho et al. did not address “what initiated the antibody response or the

extensive inflammation” in the central nervous system of MS patients. (Ex. G, p. 2

(citing Ho et al. supra, at Ex. 34).) He also disagreed with Dr. Steinman’s emphasis on

the polar head group containing a phosphate molecule as demonstrated in the Ho et al.

article. (Tr. 209-10.) He explained his understanding of Dr. Steinman’s opinion

regarding the affinity of the antibody binding to the glycolipid as depending on the length

of the carbon chains that are hooked to the phosphate group; however, Dr. Fujinami

pointed out that these phosphate head groups appear in both the non-reactive, as well

as the reactive, entities. (Id. at 209-10, 229-30.) He thus interpreted the Ho et al. article

as demonstrating that “not all molecules that have that phosphate group react with the

antibodies.” (Id. at 230.) In fact, with regard to all of the examples provided by Dr.

Steinman (Exs. 32, 34, 55), Dr. Fujinami opined the authors are investigating the nature

of the autoantibodies, and “not the induction of the autoantibodies. They do not speak

to phospholipids inducing neuroinflammatory disease.” (Ex. G, p. 2 (citing Gilburd et al.,

supra, at Ex. 32; Ho et al., supra, at Ex. 34; Nakos et al., supra, at Ex. 55); Tr. 224, 226-

27, 280-83.)

Contrary to Dr. Steinman’s analysis, Dr. Fujinami opined that if

phosphatidylcholine, or derivatives of this structure, are present in the Prevnar 13

vaccine (19A component), then based on the findings by Ho et al., the structure should

protect against, rather than enhance or cause, neuroinflammation. (Ex. C, p. 3 (citing

Ho et al., supra, at Ex. 34); Tr. 208-09.) Dr. Steinman and his colleagues in Ho et al.

treated mice immunized with a peptide derived from myelin (in powerful adjuvants) with

a derivative of oxidized phosphatidylcholine (PGPC) using different treatment regimens.

(Ex. C, p. 4 (citing Ho et al., supra, at Ex. 34).) Yet, Dr Fujinami observed in all of the

different treatments the disease was markedly reduced. (Id.) Specifically, the authors

observed that “PGPC unexpectedly reduced the severity of EAE throughout the disease

course.” (Id. (quoting Ho et al., supra, at Ex. 34, p. 3).)9 The authors found that PGPC

suppressed autoreactive T cell activation. (Id.) The authors even go so far as to

conclude “[t]he identification of lipids targeted by autoantibodies affords the opportunity

to mine small lipid-soluble molecules as potential new drugs for autoimmune disease.”

(Id. (quoting Ho et al., supra, at Ex. 34, p. 10).) According to Dr. Fujinami, Dr. Steinman

is opining that phosphatidylcholine in the vaccine causes GBS, while in the Ho et al.

paper (which he is a co-author of), he concludes the lipids like phosphatidylcholine

could prevent or treat autoimmune disease. (Id.)

9

“PGPC” is 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine. (Ho et al., supra, at Ex. 34, p. 2.)

17

Dr. Fujinami noted, as Dr. Steinman does, that the Prevnar 13 vaccine contains

aluminum phosphate adjuvant (alum). (Ex. C, p. 4.) In response to petitioner’s theory,

Dr. Fujinami presented work from two groups independently published in peer-reviewed

journals showing that genetically susceptible animals immunized with whole myelin, or

myelin derived proteins, adsorbed to alum did not develop autoimmune

neuroinflammatory disease (i.e., EAE, a preclinical model for MS). (Id. (citing Maryline

Sicotte et al., Immunization with Myelin or Recombinant Nogo-66/MAG in Alum

Promotes Axon Regeneration and Sprouting After Corticospinal Tract Lesions in the

Spinal Cord, 23 MOLECULAR & CELLULAR NEUROSCIENCE 251 (2003) (Ex. C, Tab 2); Maja

Wållberg et al., Vaccination with Myelin Oligodendrocyte Glycoprotein Adsorbed to

Alum Effectively Protects DBA/1 Mice from Experimental Autoimmune

Encephalomyelitis, 33 EUR. J. IMMUNOLOGY 1539 (2003) (Ex. C, Tab 3)); Tr. 241-43.)

Wållberg et al. also demonstrated that “genetically susceptible mice ‘vaccinated’ with

myelin oligodendrocyte glycoprotein adsorbed to alum were actually protected from the

autoimmune neuroinflammatory disease.” (Ex. C, p. 4 (citing Wållberg et al., supra, at

Ex. C, Tab 3); Tr. 242-43.) Further, Dr. Fujinami explained that Sicotte et al. observed

that myelin/alum immunized animals were found to have better axon repair when the

spinal cord was subsequently damaged. (Ex. C, p. 4 (citing Sicotte et al., supra, at Ex.

C, Tab 2); Tr. 241-42.) Thus, Dr. Fujinami contended that myelin adsorbed to alum (like

the glycoconjugates in the formulation of the Prevnar 13 vaccine) injected into

experimental animals does not induce EAE and that this immunization can protect

against subsequent attempts to induce EAE. (Ex. C, p. 4 (citing Prevnar 13 Package

Insert, supra, at Ex. 31, p. 25); Tr. 243-45.) While Dr. Steinman opined that various

cytokines, including IL-18, are found in GBS patients, Dr. Fujinami indicated “there is no

link showing that an alum-based vaccine is able to persist and drive a chronic IL-18

response in autoimmune disease.” (Ex. F, p. 2.)

Dr. Fujinami further suggested that Dr. Steinman erroneously discounted the

Tseng et al. and Baxter et al. studies because they focus on Pneumovax 23 and not

Prevnar 13. (Ex. C, p. 5.) Dr. Fujinami explained that the polysaccharide vaccine

contains the same 19A component of pneumococcus as the conjugate vaccine. (Id.

(citing Usama Assaad et al., Pneumonia Immunization in Older Adults: Review of

Vaccine Effectiveness and Strategies, 7 CLINICAL INTERVENTIONS AGING 453 (2012) (Ex.

C, Tab 1)).) Thus, if the 19A component is of importance to petitioner’s theory, Dr.

Fujinami stressed it is contained in both pneumococcal vaccines. (Id.) Dr. Fujinami

also responded to Dr. Steinman’s opinion that putative pathogenic phospholipids are

contained in the Streptococcus pneumoniae (“S. pneumoniae”) strains used in the

formulation of the vaccine. (Ex. F, p. 1.) Petitioner theorizes that polysaccharides and

phospholipids, present in the strains of S. pneumonia, generate the putative pathogenic

antibodies involved with GBS. (Id.) Following this logic, Dr. Fujinami suggested that if

the same elements (polysaccharides and phospholipids) are present in the bacteria,

individuals infected with S. pneumoniae should also develop GBS. (Id.; Tr. 217-19.)

However, he stressed this is not the case. (Ex. F, p. 1; Tr. 217-19.) He acknowledged

that two case reports apparently link S. pneumoniae and GBS, though he opined these

reports provide little to no support for Dr. Steinman’s theory. (Ex. F, pp. 1-2; Tr. 218.)

18

V. Discussion

a. Althen prong one

Under Althen prong one, petitioner must provide a “reputable medical theory,”

showing that the subject vaccine can cause the type of injury alleged. Pafford v. Sec’y

of Health & Human Servs., 451 F.3d 1352, 1355-56 (Fed. Cir. 2006) (quoting Pafford v.

Sec’y of Health & Human Servs., No. 01-0165V, 2004 WL 1717359, at *4 (Fed. Cl.

Spec. Mstr. July 16, 2004)). Such a theory need 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. See 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 [the proposed causal] theory. While it

does not require medical or scientific certainty, it must still be ‘sound and reliable.’”

Boatmon, 941 F.3d at 1359 (first quoting Moberly v. Sec’y of Health & Human Servs.,

592 F.3d 1315, 1322 (Fed. Cir. 2010); then quoting Knudsen, 35 F.3d at 548-49).

As with many cases in the Program, petitioner’s theory involves molecular

mimicry. (Ex. 22, p. 10.) Molecular mimicry is a concept with several constituent parts

whereby a susceptible host encounters a foreign antigen that has sufficient similarity

(“homology”) with components of host tissue such that the immune system “cross-

reacts,” producing antibodies that attack the host tissue instead of the foreign antigen to

ultimately cause disease or injury. (Tr. 44-45; INST. OF MED., ADVERSE EFFECTS OF

VACCINES: EVIDENCE AND CAUSALITY (Kathleen Stratton et al. eds., 2012) [hereinafter

IOM Report] (Ex. 71, p. 99).) Molecular mimicry “is a generally accepted scientific

principle, [but] 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. 28,

2019)). “[T]he 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 ex rel. D.C. v. Sec’y of Health & Human Servs., No.

17-0079V, 2021 WL 4100294, at *31 (Fed. Cl. Spec. Mstr. July 30, 2021)

(“[D]emonstration of homology alone is not enough to establish a preponderant

causation theory.” (emphasis omitted) (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))), mot. for rev. denied, No. 17-79V, 2021 WL 6058835 (Fed. Cl. Dec. 3, 2021).

In that regard, Dr. Chaudhry asserts on respondent’s behalf that four criteria – (1)

supportive epidemiology, (2) identification of T cells or antibodies directly against human

antigens, (3) identification of the mimics of the target antigen, and (4) reproduction in an

19

animal model – must be demonstrated in order to conclude that GBS can be triggered

by molecular mimicry following Prevnar 13 vaccination. (Ex. E, p. 3 (citing Yuki, supra,

at Ex. A, Tab 9).) As noted above, however, petitioners in this Program are not required

to establish scientific certainty. See, e.g., Gross v. Sec’y of Health & Human Servs.,

No. 17-1075V, 2022 WL 9669651, at *36 (Fed. Cl. Spec. Mstr. Sept. 22, 2022) (finding

that criteria such as proposed by Dr. Chaudhry is tantamount to “require[ing] scientific

certainty, which is a bar too high”). With regard to the application of molecular mimicry,

prior cases have expressed that “[t]he line must be drawn somewhere between

speculation and certainty.” Brayboy v. Sec’y of Health & Human Servs., No. 15-183V,

2021 WL 4453146, at *19 (Fed. Cl. Spec. Mstr. Aug. 30, 2021). Thus, for example, in

Brayboy, an omnibus proceeding addressing autoimmune premature ovarian

insufficiency, the special master found it sufficient that the petitioners “identified 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” and further expressed

that requiring additional steps, or insisting on direct, testable evidence, would

impermissibly heighten petitioners’ burden of proof. Id.

GBS is an acute inflammatory polyneuropathy affecting the peripheral nerves

and, in the case of AIDP, most notably affecting myelin tissue. (Hugh J. Willison et al.,

Guillain-Barré Syndrome, 388 LANCET 717 (2016) (Ex. A, Tab 1, pp. 1, 3).) While the

condition is believed to be of an autoimmune etiology, the pathogenesis of GBS is

incompletely understood. (Nakos et al., supra, at Ex. 55; Gilburd et al., supra, at Ex. 32,

p. 2; Willison et al., supra, at Ex. A, Tab 1; Tr. 76.) Although there is no established

association between S. pneumoniae infection and GBS (Ex. A, p. 6; Tr. 217), it is

generally accepted that a number of different infectious antigens can cause GBS,

including unspecified upper respiratory infections (Guillain-Barré Syndrome Information

Page, NAT’L INST. NEUROLOGICAL DISORDERS & STROKE,

https://www.ninds.nih.gov/Disorders/All-Disorders/Guillain-Barré-Syndrome-Information-

Page (last visited Jul. 25, 2017) (Ex. 29); Baxter et al., supra, at Ex. 46, pp. 1, 4;

Willison et al., supra, at Ex. A, Tab 1, pp. 2, 4). This includes both viral and bacterial

infections. (Willison et al., supra, at Ex. A, Tab 1, p. 4; Baxter et al., supra, at Ex. 46, p.

1.) Additionally, for at least one of these antigens, C. jejuni, there is sufficient proof to

conclude that molecular mimicry is the mechanism of causation leading to GBS, albeit

resulting primarily in the axonal subtype of GBS and involving a molecular mimic not at

issue here. (Ex. A, p. 5; Ex. E, pp. 1,3; Tr. 76, 161; Yuki, supra, at Ex. A, Tab 9, p. 2;

IOM Report, supra, at Ex. 71, pp. 100-01.) Evidence also supports homology between

various other antigens and myelin tissue. (See IOM Report, supra, at Ex. 71, p. 100

(hepatitis B virus); Willison et al., supra, at Ex. A, Tab 1, p. 2 (noting cases of GBS

shortly after rabies vaccination).) Thus, there is little question that multiple antigens are

implicated as causes of GBS. Additionally, Dr. Chaudhry agrees on respondent’s behalf

that at least some formulations of the flu vaccine have been identified as a cause of

GBS, suggesting that antigenic triggers for GBS are not limited to active infections. (Ex.

A, p. 6.) Petitioner’s expert opines that this understanding of GBS provides some basic

support for his opinion that the Prevnar 13 vaccine can cause GBS. (See Tr. 76; Ex.

75, p. 13.)

20

In some prior cases, this background information has partly informed the special

masters’ analysis of a petitioner’s theory of causation with respect to GBS. See, e.g.,

J.G. v. Sec’y of Health & Human Servs., No. 20-664V, 2023 WL 2752634, at *30 (Fed.

Cl. Spec. Mstr. Feb. 13, 2023) (observing that “[t]he experts do not dispute the theory of

molecular mimicry, or that it is a sound and reliable theory generally as it relates to

GBS” and that “[m]olecular mimicry has been accepted as a sound and reliable theory

in many Vaccine Program cases dealing with demyelinating conditions, including GBS”);

Osso v. Sec’y of Health & Human Servs., No. 18-575V, 2023 WL 5016473, at *21 (Fed.

Cl. Spec. Mstr. July 13, 2023) (molecular mimicry accepted as a “sound and reliable

theory”); Harris v. Sec’y of Health & Human Servs., No. 18-944V, 2023 WL 2583393, at

*22 (Fed. Cl. Spec. Mstr. Feb. 21, 2023) (finding that “the fact that GBS is well accepted

as an autoimmune condition with a wide variety of suspected antigenic triggers,

inclusive of antigens from both infection and vaccination, provides meaningful evidence

supporting petitioner’s burden of proof with respect to Althen prong one”). But see

Trollinger v. Sec’y of Health & Human Servs., No. 16-473V, 2023 WL 2521912, at *30

(Fed. Cl. Spec. Mstr. Feb. 17, 2023) (finding that “Dr. Steinman’s theory had a one-size-

fits-all quality, in which he strained to shoehorn the science behind the flu-GBS

association into the context of the pneumococcal vaccine” and further noting that, “[i]f

this were sufficient to establish that this particular vaccine ‘can cause’ GBS, it is hard to

imagine the theory not also applying to each and every one of the sixteen Program-

covered vaccines/vaccine antigenic components”), mot. for rev. denied, 167 Fed. Cl.

127 (2023). Although only the flu vaccine is presumed to be a cause of GBS in this

Program (42 C.F.R. § 100.3(a)), petitioners have been found entitled to compensation in

at least isolated instances for GBS caused by many other vaccines. This includes

vaccines that target both viruses and bacteria. See, e.g., Salmins v. Sec’y of Health &

Human Servs., No. 11-140V, 2014 WL 1569478, at *14 (Fed. Cl. Spec. Mstr. Mar. 31,

2014) (finding that HPV vaccine “can cause” GBS); Peugh v. Sec’y of Health & Human

Servs., No. 99-638V, 2007 WL 1531666, at *17 (Fed. Cl. Spec. Mstr. May 8, 2007)

(finding as part of an omnibus proceeding that hepatitis B vaccine can GBS); Whitener

v. Sec’y of Health & Human Servs., No. 06-0477V, 2009 WL 3007380, at *20 (Fed. Cl.

Spec. Mstr. Sept. 2, 2009) (finding that meningococcal vaccine can cause GBS); Koller

v. Sec’y of Health & Human Servs., No. 16-439V, 2021 WL 5027947, at *7-20 (Fed. Cl.

Spec. Mstr. Oct. 8, 2021) (finding that pneumococcal conjugate vaccine, Prevnar 13,

can cause GBS); Mohamad v. Sec’y of Health & Human Servs., No. 16-1075V, 2022

WL 711604, at *9-18 (Fed. Cl. Spec. Mstr. Jan. 27, 2022) (finding that Tdap vaccine can

cause GBS); J.G., 2023 WL 2752634, at *29-32 (finding that hepatitis A vaccine can

cause GBS). In fact, given the nature of the condition, molecular mimicry has been

accepted as a theory of causation for GBS even in the absence of any demonstration of

homology and cross-reaction. Salmins, 2014 WL 1569478, at *14.

Within that context, Dr. Steinman opines that the Prevnar 13 vaccine can be

considered among the causes of GBS, presenting several pieces of medical literature to

demonstrate that (1) the Prevnar 13 vaccine contains phosphoglycerol groups that are

necessary to the vaccine’s immunogenicity (Ex. 50, pp. 18-19 (citing Chang et al.,

supra, at Ex. 52; Prevnar 13 Patent, supra, at Ex. 51); Tr. 96 (citing Bryson et al., supra,

at Ex. 103)); (2) the phosphate portion of the phospholipid molecule has immune

21

reactivity in myelin tissue, albeit demonstrated in the context of a different demyelinating

condition (multiple sclerosis) (Ex. 22, p. 13 (quoting Ho et al., supra, at Ex. 34); Ex. 50,

pp. 8, 12 (citing Ho et al., supra, at Ex. 34); Tr. 94-95); (3) GBS patients develop anti-

phospholipid antibodies (Ex. 22, pp. 13-14 (citing Gilburd et al., supra, at Ex. 32); Ex.

50, pp. 11-12 (citing Nakos et al., supra, at Ex. 55)), and (4) these antibodies are cross-

reactive with phospholipids present in myelin tissue (Ex. 50, p. 4 (citing Gilburd et al.,

supra, at Ex. 32; Ho et al., supra, at Ex. 34); Tr. 94-95).

Dr. Steinman’s theory does not involve the anti-ganglioside antibodies that are

most commonly associated with GBS. However, literature filed in this case indicates

that fewer than half of GBS patients have anti-ganglioside antibodies. (Donofrio, supra,

at Ex. E, Tab 2, pp. 1-2.) Thus, we do not actually know the full scope of the antibodies

that may be implicated in the pathology of GBS, leaving little reason to doubt Dr.

Steinman’s theory on that basis. (See, e.g., id. at 11 (“Since a wide range of viruses

and bacterial agents can incite an antibody in AIDP, it has been difficult to find a

common antigenic stimulus for the illness. Equally difficult has been the identification of

specific antibody biomarkers in myelin.”); Willison et al., supra, at Ex. A, Tab 1, p. 1

(noting that “there are many clinical and investigative components to consider” when

diagnosing GBS, “especially in atypical cases,” and that “diagnostic biomarkers are not

available for most variants of the syndrome” as “[i]dentification of biomarkers and

establishment of their pathophysiological roles, if any, in experimental models has been

a major research challenge”); accord Gross, 2022 WL 9669651, at *36 (indicating that

“the literature filed by the parties does not support the notion that gangliosides are the

only player in the game of molecular mimicry”).) To this point, I have previously

emphasized that the “S” in GBS stands for “syndrome” and that “GBS variants are

generally believed to have a multitude of both clinical presentations and causes,” McGill

v. Sec’y of Health & Human Servs., No. 15-1485V, 2023 WL 3813524, at *27 n.16 (Fed.

Cl. Spec. Mstr. May 11, 2023), raising the question of whether a single causal theory

can explain every instance of GBS, post-vaccination or otherwise.

I have previously concluded that Dr. Steinman’s phosphoglycerol theory is sound

and reliable, and preponderantly supports a legally probable, though not scientifically

certain, theory of causation sufficient to satisfy petitioner’s burden of proof under Althen

prong one, based on the same medical literature cited in this case. Pierson v. Sec’y of

Health & Human Servs., No. 17-1136V, 2022 WL 322836, at *27-31 (Fed. Cl. Spec.

Mstr. Jan. 19, 2022); Bartoszek v. Sec’y of Health & Human Servs., No. 17-1254V,

2024 WL 4263604, at *17-22 (Fed. Cl. Spec. Mstr. Aug. 27, 2024); see also Cooper v.

Sec’y of Health & Human Servs., No. 18-1885V, 2024 WL 1522331, at *13-18 (Fed. Cl.

Spec. Mstr. Mar. 12, 2024). I again reach the same conclusion based on the evidence

of record in this case. Additionally, other special masters have reached similar

conclusions based on substantially similar underlying evidence. Koller, 2021 WL

5027947, at *16-20 (Gowen); Maloney v. Sec’y of Health & Human Servs., No. 19-

1713V, 2022 WL 1074087, at *30-31 (Fed. Cl. Spec. Mstr. Mar. 17, 2022) (Dorsey);

Gross, 2022 WL 9669651, at *35-36 (Dorsey); Sprenger v. Sec’y of Health & Human

Servs., No. 18-279V, 2023 WL 8543435, at *18-19 (Fed. Cl. Spec. Mstr. Nov. 14, 2023)

(Dorsey); Parker v. Sec’y of Health & Human Servs., No. 20-411V, 2023 WL 9261248,

22

at *20-22 (Fed. Cl. Spec. Mstr. Dec. 20, 2023) (Dorsey); Anderson v. Sec’y of Health &

Human Servs., No. 18-484V, 2024 WL 557052, at *30-31 (Fed. Cl. Spec. Mstr. Jan. 17,

2024) (Dorsey); Simeneta v. Sec’y of Health & Human Servs., No. 18-859V, 2024 WL

4881411, at *30-33 (Fed. Cl. Spec. Mstr. Oct. 31, 2024) (Dorsey); see also Tracy ex rel.

R.S. v. Sec’y of Health & Human Servs., No. 16-213V, 2022 WL 1125281, at *29-32

(Fed. Cl. Spec. Mstr. Mar. 30, 2022) (Special Master Sanders accepting a similar theory

in the context of transverse myelitis).10

However, acceptance of this theory has not been unanimous among special

masters. Bielak v. Sec’y of Health & Human Servs., No. 18-761V, 2023 WL 35509, at

*33-37 (Fed. Cl. Spec. Mstr. Jan. 3, 2023) (Corcoran); Trollinger, 2023 WL 2521912, at

*26-30 (Corcoran); Gamboa-Avila v. Sec’y of Health & Human Servs., No. 18-925V,

2023 WL 6536207, at *25-29 (Fed. Cl. Spec. Mstr. Sept. 11, 2023) (Corcoran), mot. for

rev. denied, 170 Fed. Cl. 441 (2024), appeal filed, No. 24-1765 (Fed. Cir. May 1, 2024);

Jaye v. Sec’y of Health & Human Servs., No. 20-672V, 2024 WL 3691413, at *14-17

(Fed. Cl. Spec. Mstr. July 18, 2024) (Corcoran); Morrison v. Sec’y of Health & Human

Servs., No. 18-386V, 2024 WL 3738934, at *19-21 (Fed. Cl. Spec. Mstr. July 18, 2024)

(Oler).11 These contrary decisions are not binding on me. Boatmon, 941 F.3d at 1358-

59; Hanlon v. Sec’y of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998).

Nonetheless, I have considered the points raised by these decisions. I simply reach a

different conclusion based on my overall weighing of the evidence on this record.

Notably, even when reaching a different result, there has still been agreement that

record evidence comparable to what has been presented in this case at a minimum

does offer reliable support for the conclusion that phosphoglycerol is found

in the pneumococcal vaccine; that the immune system produces antibodies

in reaction to the relevant antigens containing the phosphoglycerol; and that

individuals with neuropathies (although some suffer from the

distinguishable disease MS) have been shown in small sample studies to

possess antibodies specific to myelin-containing phospholipids.

Trollinger, 2023 WL 2521912, at *28.

10

Other special masters have also found that petitioners have preponderantly established that the

Prevnar 13 vaccine case cause GBS based on the other causal theory Dr. Steinman presented. Byrd v.

Sec’y of Health & Human Servs., No. 20-1476V, slip op. (Fed. Cl. Spec. Mstr. July 8, 2024) (Gowen)

(accepting petitioner’s causal theory based on molecular mimicry between CRM197 and contactin-1);

Anderson, 2024 WL 557052, at *31-32 (Dorsey) (same); Sprenger, 2023 WL 8543435, at *19-20 (Dorsey)

(same); Gross, 2022 WL 9669651, at *36-37 (Dorsey) (same); Maloney, 2022 WL 1074087, at *32

(Dorsey) (same).

11

Some additional cases were resolved against petitioners based on different theories of causation.

McConnell v. Sec’y of Health & Human Servs., No. 18-1051V, 2022 WL 4008238, at *7-9 (Fed. Cl. Spec.

Mstr. Aug. 19, 2022); Deshler, 2020 WL 4593162, at *19-21.

23

I have considered the issues raised by respondent’s experts in this case, but do

not find that they cast sufficient doubt on Dr. Steinman’s theory such that they would

prevent petitioner from meeting her burden of proof under Althen prong one.12

As a threshold matter, respondent’s experts stress that the S. pneumoniae has

carbohydrates in common with the vaccine and contend that the fact that there has

been no recognized causal association between the pneumococcal infection and GBS

undercuts any causal role for phosphoglycerol in the Prevnar 13 vaccine. (Tr. 218-19;

Ex. F, pp. 1-2; Ex. E, p. 1.) However, Dr. Fujinami explained during the hearing that he

cannot say with certainty whether the specific phosphoglycerol component of the

vaccine that Dr. Steinman relies upon is present in the natural bacterium. (Tr. 291.) In

any event, petitioner need not “demonstrate that a vaccine’s infectious counterpart is a

known-disease trigger.” Morrison, 2024 WL 3738934, at *18.

Additionally, respondent stresses three epidemiologic studies that he contends

should weigh against any theory that the Prevnar 13 vaccine can cause GBS. (ECF No.

135, pp. 17-18.) The Federal Circuit has previously stressed that a petitioner is not

obligated to prove a case with epidemiology. Capizzano, 440 F.3d at 1325. Yet,

“[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 (Fed. Cir. 2018). Baxter et al. is a 2013

study that examined 415 incident cases of GBS from the Kaiser Permanente Northern

California (“KPNC”) patient population to compare “the odds of vaccination in the 6 and

10 weeks prior to onset of GBS to the odds of vaccination during the same time

intervals in all vaccinated individuals in the entire KPNC population.” (Baxter et al.,

supra, at Ex. A, Tab 6, p. 1.) The study included two instances of GBS occurring within

6 weeks of administration of the polysaccharide pneumococcal (as opposed to

conjugate) vaccine. (Id. at 6 tbl.2.) The study did not detect any increased risk of GBS

following any vaccination, even flu vaccination. (Id. at 5-6.) However, despite the large

size of the study, the authors concluded that “we are unable to exclude any possible

association between vaccines and GBS,” explaining that “we had limited power to fully

assess the risk of GBS following vaccination due to the rarity of the outcome.” (Id. at 7.)

Haber et al. is a 2016 study that used Vaccine Adverse Events Reports System

(“VAERS”) data to examine the safety profile of the Prevnar 13 vaccine. (Haber et al.,

12

There have also been some significant differences in the record evidence of the various decisions

weighing the theory Dr. Steinman presents in this case. For instance, while some prior cases denying

compensation for GBS based on this theory found significance in the distinction between B- and T-cell

responses, respondent’s expert in Cooper specifically disclaimed a hardline distinction between such

responses, testifying instead that “nothing is pure B cell/Tcell”. Compare Cooper, 2024 WL 1522331, at

*17, with Deshler, 2020 WL4593162, at *19-20, and Bielak, 2023 WL 35509, at *29-37. The Morrison

decision turned in part on acceptance of the pathological role of anti-ganglioside antibodies in GBS as

suggested by Dr. Whitton. 2024 WL 3738934, at 19-21. Yet, respondent’s expert in Bartoszek, Dr. Kedl,

asserted to the contrary that this is “tenuous, speculative and clinically unproven,” and that “the vast

majority of literature stands in sharp contrast to the assertion that there is any causal relationship

between ganglioside-specific antibodies and GBS.” 2024 WL 4263604, at *19-20, n.16. Thus, despite

the accumulating number of decision and rulings by special masters, it is still important to look closely at

respondent’s expert presentation in each case. (ECF No. 135, p. 24, n.17 (respondent urging a different

result from the undersigned’s prior Pierson case based on the rebuttal evidence filed in this case).)

24

supra, at Ex. A, Tab 5.) Eleven cases of GBS were reported within 42 days of a

Prevnar 13 vaccination, which would constitute 0.7 cases per million doses of the

vaccine as distributed. (Id. at 5.) However, the authors cautioned that VAERS is a

passive surveillance system, meaning that the data is susceptible to underreporting,

specific reports are of varying quality, and no control group is available. (Id.) Finally, in

2018, Tseng et al. compared adverse events among the elderly following the

polysaccharide pneumococcal vaccine against adverse events following the conjugate

pneumococcal vaccine. (Tseng et al., supra, at Ex. 45.) Four instances of GBS were

observed following the conjugate vaccine as compared to eight instances of GBS

following the polysaccharide. (Id. at 6 tbl.3.) Therefore, the authors concluded that the

risk of GBS following the conjugate vaccine was no greater than any risk following the

polysaccharide vaccine. (Id. at 7.) However, the study did not assess the observed

rate of GBS following the polysaccharide against any control, though the authors

alluded to the polysaccharide vaccine as having a “well-established” safety profile. (Id.)

I have considered all the epidemiology submitted in this case, and although I give some

weight to these studies highlighted by respondent, I do not find that they cast significant

doubt on the viability of Dr. Steinman’s theory.

Regarding the details of Dr. Steinman’s theory, respondent’s experts also

contend that, although there is evidence in the medical literature that phospholipid

antibodies may enhance disease after disease onset, there is no evidence to support a

causal role for these antibodies. (Tr. 187-90, 194-95, 232; Ex. A, p. 8; Ex. E, p. 2.)

They specifically note that Gilburd et al. suggested that the autoantibodies found in GBS

patients were “a result of myelin damage, rather than cause the inflammatory

demyelination.” (Ex. A, p. 8 (quoting Gilburd et al., supra, at Ex. 32); Tr. 187-90, 262-

63.) Dr. Fujinami further hypothesized that the antibodies are better explained by

epitope spreading. (Tr. 219-32.) However, Dr. Steinman observed that there is no

evidence in the literature to support the assertion that these antibodies are merely an

after effect of demyelination, noting that they “come up very early” in GBS patients that

were tested. (Id. at 292, 295-96.) He further noted that Nakos et al. examined “real

disease” and found that seven out of nine GBS patients had relevant antibodies within

days. (Id. at 312, 315-17.) According to Dr. Steinman, the timeframe within which the

Nakos et al. study detected the antibodies leaves epitope spreading “the least likely”

explanation for the data. (Id. at 322; accord Greenslade v. Sec’y of Health & Human

Servs., No. 14-1140V, 2024 WL 3527665, at *38 (Fed. Cl. Spec. Mstr. June 28, 2024)

(crediting expert testimony that epitope spreading takes “a few weeks” and develops

after significant tissue damage has already occurred).)

Dr. Fujinami also asserted that Dr. Steinman placed too much emphasis on the

Ho et al. study and, more specifically, on any causal role for the phosphate head group.

(Tr. 209, 230 (citing Ho et al., supra, at Ex. 34).) He noted that both the reactive and

non-reactive molecules identified by Ho et al. contain a phosphate head group and have

a similar structure. (Id. at 209-10, 229-30.) He thus opined the literature demonstrates

that “not all molecules that have that phosphate [head] group react with the antibodies.”

(Id. at 230.) Dr. Steinman agreed with Dr. Fujinami’s assessment of the Ho et al. study

as demonstrating that not all antibodies will bind to phosphoglycerol but explained that

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this is due to the fact that the antibodies that recognize phosphoglycerol also recognize

what is attached. (Id. at 304-08.) He noted that there was also evidence in the Ho et al.

study that the lipid side chains, which include the phosphoglycerol head group, actually

facilitate antibody binding. (Id. at 306.) However, he explained that Barbar et al.

showed that “no matter what’s attached to those phosphate groups, those antibodies

are still going to be recognizing the phosphate head group.” (Id. at 128-30, 136; Ex. 96,

p. 5 (citing Barbar et al., supra, at Ex. 102).) Thus, he explained that while there are

“exceptions to the set of observation we made” in the Ho et al. study, there is “a

confluence of evidence from this paper [Ho et al.], from Bryson, from Nakos, even from

Gilburd that shows that in GBS, antibodies are made to phospholipids and the

phospholipids also contain that phosphoglycerol,” with “some of the strongest binding”

being to phosphatidylserine, phosphatidylcholine, and phosphatidylethanolamine, which

“are all major targets of the immune response” in GBS. (Tr. 308-09, 311.) Although Dr.

Fujinami opined that it is impossible to know whether the suggested immune response

is to the phosphoglycerol component in particular (Id. at 192, 195 (discussing Nakos et

al., supra, at Ex. 55)), petitioner need not prove scientific certainty to establish

entitlement to compensation in this Program. Knudsen, 35 F.3d at 548-49.

Accordingly, petitioner has preponderantly shown that the Prevnar 13 vaccine

can cause the AIDP form of GBS. Because I have concluded that Dr. Steinman’s

theory of molecular mimicry based on phosphoglycerol is sound and reliable, I do not

reach the additional question of whether Dr. Steinman’s separate theory based on

CRM197 is likewise sound and reliable.

b. Althen prong three

Under the third Althen prong, a petitioner must demonstrate a “proximate

temporal relationship” between the subject vaccination and the alleged injury. Althen,

418 F.3d at 1278. To do this, petitioner must provide “preponderant proof that the onset

of symptoms occurred within a timeframe for which, given the medical understanding of

the disorder’s etiology, it is medically acceptable to infer causation-in-fact.” de Bazan v.

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

omitted).

The parties do not dispute that onset of petitioner’s GBS occurred within 9-12

days of her Prevnar 13 vaccination. (ECF No. 121, pp. 24-25; ECF No. 123, pp. 25

n.12, 56-57; ECF No. 132, pp. 5 n.7, 72-73; ECF No. 135, pp. 2, 31-32.) However,

respondent disputes Dr. Steinman’s reliance on a study by Schonberger et al., to

establish petitioner’s onset of her GBS as falling within a timeframe consistent with his

theory of causation. (ECF No. 121, p. 25 (discussing Schonberger et al., supra, at Ex.

47).) Respondent contends that Dr. Steinman’s reliance on the Schonberger et al.

study “has two glaring defects.” (Id.) First, the study looked at a completely different

vaccine – the 1976 swine flu vaccine. (Id.) Second, and relatedly, the studied vaccine

did not contain the alum adjuvant contained in the Prevnar 13 vaccine. (Id.)

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Regarding the first point, respondent is correct in noting that the study involved a

different vaccine than the one at issue in this case; however, the findings of this study

have been utilized in assessing risk periods in subsequent studies that have looked at

other potential causes of GBS. (Baxter et al., supra, at Ex. 46, pp. 6-7 (referencing the

1976 swine flu vaccine study as helpful for selecting an appropriate time interval); see

also Haber et al., supra, at Ex. 58, p. 5 (noting that the study results “verified 11 GBS

reports with symptoms onset within 42 days of [Prevnar 13] vaccination” and

referencing the Schonberger study in the bibliography).) Other special masters have

also referenced Schonberger et al. in evaluating whether petitioners, who have alleged

that they suffered GBS following Prevnar 13 vaccinations, have met their burden of

proof under the third Althen prong. See, e.g., Godfrey v. Sec’y of Health & Human

Servs., No. 17-1419V, 2025 WL 896840, at *28 (Fed. Cl. Spec. Mstr. Feb. 26, 2025)

(Dorsey); Koller, 2021 WL 5027947, at *22-23 (Gowen).

Regarding the second point, Dr. Steinman testified that his opinion regarding the

role of the alum adjuvant contained in the Prevnar 13 vaccine is not an essential

component of his causal theory. (Tr. 115-16, 118.) But in any event, respondent’s

argument is limited to merely noting the existence of this distinction. (ECF No. 135, p.

32.) He has not pointed to any medical evidence suggesting that the presence of an

alum adjuvant is a meaningful distinction vis-à-vis the expected timing of onset. (See

id.) On respondent’s behalf, Dr. Fujinami explains that he cannot predict timing based

on Dr. Steinman’s proposed causal theories. (Tr. 248.)

However, Dr. Fujinami acknowledged on respondent’s behalf that the presence

of antiphospholipid antibodies within 3-4 days after induction of disease is consistent

with the expected time frame for an adaptive immune response, though he does not

agree they are causally relevant. (Tr. 200; see also Tr. 284-87 (discussing Kanter et al.,

supra, at Ex. 33).) The IOM report notes that, “[f]or may antigens the latency (lag

phase) between primary exposure and development of the primary antibody response is

7 to 10 days,” and while this time frame “is not specific to any particular antigen, it can

be used as a reference point for the latency between antigen exposure and the initiation

of some of the immune-mediated mechanisms described.” (IOM Report, supra, at Ex.

71, p. 87.) Dr. Fujinami further acknowledged that the studies by Ho et al. and Kanter et

al. support an experimental change in disease course 10 days following injection. (Tr.

207.) This understanding is consistent with Schonberger et al., in which the authors

found increased risk of onset of GBS primarily within five weeks of vaccination with the

1976 swine flu vaccine. (Schonberger et al., supra, at Ex. 47.)

Accordingly, petitioner has preponderantly shown that onset of her GBS occurred

within a medically acceptable time frame from which to infer vaccine causation under

the third Althen prong.

c. Althen prong two

The second Althen prong requires preponderant proof of a logical sequence of

cause and effect, which is usually supported by facts derived from petitioner’s medical

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records. Althen, 418 F.3d 1278; Andreu, 569 F.3d at 1375-77; Capizzano, 440 F.3d at

1326; Grant, 956 F.2d at 1148. Medical records are generally viewed as trustworthy

evidence. Cucuras, 993 F.2d at 1528. These records are generally contemporaneous

to the medical events and “contain information supplied to or by health professionals to

facilitate diagnosis and treatment of medical conditions. With proper treatment hanging

in the balance, accuracy has an extra premium.” Id. However, medical records and/or

statements of a treating physician’s views do not per se bind the special master.

§ 300aa-13(b)(1) (providing that “[a]ny such diagnosis, conclusion, judgment, test result,

report, or summary shall not be binding on the special master or court”); Snyder v. Sec’y

of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (reasoning that “nothing

. . . mandates that the testimony of a treating physician is sacrosanct—that is must be

accepted in its entirety and cannot be rebutted”). A petitioner may support a cause-in-

fact claim through presentation of either medical records or an expert medical opinion.

See § 300aa-13(a). The special master is required to consider all relevant evidence of

record, draw plausible inferences, and articulate a rational basis for the decision.

Winkler, 88 F.4th at 963 (citing Hines, 940 F.2d at 1528).

In his post-hearing brief, respondent stresses that petitioner must do more to

meet her burden of proof under Althen prong two than simply rely on the other Althen

elements, quoting the Federal Circuit as rejecting the notion that “proof that an injury

could be caused by a vaccine and that the injury occurred within an appropriate period

of time following the vaccination is sufficient to require an award of compensation.”

(ECF No. 135, pp. 28-29 (quoting Hibbard v. Sec’y of Health & Human Servs., 698 F.3d

1355, 1366 (Fed. Cir. 2012)).) Indeed, the Althen court held that “neither a mere

showing of a proximate temporal relationship between vaccination and injury, nor a

simplistic elimination of other potential causes of the injury suffices, without more, to

meet the burden of showing actual causation.” 418 F.3d at 1278. However, the Federal

Circuit has also explained that “a petitioner is certainly permitted to use evidence

eliminating other potential causes to help carry the burden on causation and may find it

necessary to do so when the other evidence on causation is insufficient to make out a

prima facie case.” Walther v. Sec’y of Health & Human Servs., 485 F.3d 1146, 1151

(Fed. Cir. 2007). And, while respondent stresses that part of the Federal Circuit’s

Capizzano precedent that explains that the second Althen prong “is not without

meaning,” he omits the Circuit’s further explanation that:

[I]n our view, the chief special master erred in not considering the opinions

of the treating physicians who concluded that the vaccine was the cause of

Ms. Capizzano’s injury. The fact that these physicians’ diagnoses may have

relied in part on the temporal proximity of Ms. Capizzano’s injuries to the

administration of the vaccine is not disqualifying. We see no reason why

evidence used to satisfy one of the Althen [] prongs cannot overlap to satisfy

another prong. In other words, if close temporal proximity, combined with

the finding that hepatitis B vaccine can cause RA, demonstrates that it is

logical to conclude that the vaccine was the cause of the RA (the effect),

then medical opinions to this effect are quite probative.

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440 F.3d at 1326 (internal citations omitted).

Here, there is no question that petitioner suffered from GBS following her

January 15, 2015 Prevnar 13 vaccination. (Tr. 161; Ex. A, p. 5.) When she was first

diagnosed by her treating neurologist as having GBS on January 27, 2015, the

neurologist noted in the relevant history that “[s]he had recently had a pneumonia

vaccine but otherwise has been in her usual state of health.” (Ex. 10, pp. 79-80.)

Thereafter, her primary care provider assessed “Guillain-Barre syndrome following

vaccination” in the context of her post-inpatient follow up care. (Id. at 13-15.) “[M]edical

records and medical opinion testimony are favored in vaccine cases, as treating

physicians are likely to be in the best position to determine whether ‘a logical sequence

of cause and effect show[s] that the vaccination was the reason for the injury.’”

Capizzano, 440 F.3d at 1326 (quoting Althen, 418 F.3d at 1280). And, while these

notations are not detailed, “[o]rdinary medical care offers little beyond clinical history

that would confirm the cause of GBS.” Bartoszek, 2024 WL 4263604, at *23. The

treater notations are also further buttressed by Dr. Steinman’s opinion. See § 300aa-

13(a)(1) (suggesting that petitioners may substantiate their vaccine claims with

reference to medical records or the support of expert medical opinion). Based on a

review of the medical records, Dr. Steinman likewise opined on petitioner’s behalf that

her Prevnar 13 vaccine caused her GBS. (Tr. 34, 36-37.) In addition to presenting a

theory of causation, Dr. Steinman further explained that there is no evidence of any

preceding infection or other potential alternative cause that could explain petitioner’s

condition. (Id. at 36-37, 155-56.) Dr. Chaudhry likewise opined on respondent’s behalf

that petitioner “belonged to one third of GBS cases where no antecedent infection is

established.” (Ex. A, p. 9.) And this, of course, is some evidence supporting petitioner’s

case. Walther, 485 F.3d at 1151.

Respondent maintains that the treater notations contained within petitioner’s

medical records are inadequate to support petitioner’s burden of proof because they

were not accompanied by a medical theory. (ECF No. 30, p. 7; ECF No. 135, p. 30.)

However, “[a]ny expectation that treating physicians will record the precise biological

theories behind their belief that a patient’s condition was caused by a particular trigger

is discordant with the reality of medical treatment.” Campbell v. Sec’y of Health &

Human Servs., 97 Fed. Cl. 650, 667 (2011). Moreover, as indicated in Capizzano, it is

not disqualifying if a treater’s opinion is informed in part by temporality. 440 F.3d at

1326. Respondent’s interpretation of the relevant notations is also clouded by his

position as to Althen prong one. (ECF No. 30, p. 7 (arguing that, “[a]bsent a persuasive

medical or scientific theory establishing that Prevnar vaccine can cause GBS as alleged

by petitioner, any suggestion that the Prevnar vaccine did cause petitioner’s GBS is

mere speculation”); ECF No. 135, p. 30 (contending that “the Prevnar-13 vaccine does

not have any known association with GBS”).) However, for the reasons discussed

above, there is a viable theory of causation. See Capizzano, 440 F.3d at 1326

(explaining evidence pertaining to the Althen prongs can overlap).

Respondent further stresses that, even if treating physician statements do

constitute supportive medical opinions, they are not sacrosanct and can be rebutted.

29

(ECF No. 135, p. 30 (citing Snyder, 88 Fed. Cl. at 746 n.67).) Significantly, however,

respondent does not raise any other treating physician opinion or any fact from

petitioner’s own clinical history that would rebut the assessment that petitioner suffered

GBS related to her preceding vaccination. Instead, respondent raises only two broader

arguments, neither of which is persuasive. First, citing Dr. Fujinami’s report, respondent

argues that “if Dr. Steinman’s hypothesis were correct, many other tissues in the body

would be targeted by the immune response to the Prevnar-13 vaccine, not just the

myelin in the peripheral nervous system.” (ECF No. 135, p. 30 (citing Ex. H, pp. 1-2).)

Second, citing Dr. Chaudhry’s report, respondent argues that only the AMAN variant of

GBS has been shown to result from molecular mimicry, whereas petitioner suffered

AIDP. (Id. at 30-31 (citing Ex. A, p. 5).) Respondent indicates that “Dr. Chaudhry

observes that it is ‘well established that ganglioside antibodies arising as a result of

molecular mimicry’ can cause the AMAN form of GBS.” (Id. at 31 (quoting Ex. E, p. 2).)

Dr. Steinman explained, however, that gangliosides are present in both the

central and peripheral nervous system. (Tr. 7, 76.) Yet, AMAN, which both Dr.

Steinman and Dr. Chaudhry agree results from molecular mimicry-related ganglioside

antibodies, is likewise a peripheral nerve disorder. (Id.; Ex. E, p. 2.) Thus, Dr.

Chaudhry’s emphasis on molecular mimicry in AMAN undercuts Dr. Fujinami’s criticism.

However, medical literature accompanying Dr. Chaudhry’s report also explains that “a

wider range of immune stimulants cause acute inflammatory demyelinating

polyneuropathy compared with acute motor axonal neuropathy,” and that “a wider range

of anti-nerve autoantibodies directed at both proteins and glycolipids could be

responsible for acute inflammatory demyelinating polyneuropathy immunopathology

than is the case for acute motor axonal neuropathy.” (Willison et al., supra, at Ex. A,

Tab 1, p. 4.) Therefore, Dr. Chaudhry’s suggestion that molecular mimicry is relevant

only to the AMAN variant of GBS is also not persuasive.

The Capizzano court explained that a petitioner who satisfies Althen prongs one

and three may nonetheless fail to satisfy Althen prong two where “medical records and

medical opinions do not suggest that the vaccine caused the injury, or where the

probability of coincidence or another cause prevents the claimant from proving that the

vaccine caused the injury by preponderant evidence.” 440 F.3d at 1327. These are not

the circumstances of this case, even if the evidence specific to Althen prong two is

relatively thin. Petitioner has preponderantly demonstrated a logical sequence of cause

and effect establishing that the Prevnar 13 vaccine did cause GBS in this case.

d. Factor unrelated

Once petitioner has satisfied his own burden of proof, the burden shifts to

respondent to demonstrate by a preponderance of the evidence that the injury was

caused by factors unrelated to vaccination. § 300aa-13(a)(1)(B); Deribeaux v. Sec’y of

Health & Human Servs., 717 F.3d 1363, 1367-69 (Fed. Cir. 2013). In this case,

respondent has not offered any other factor as a potential cause of petitioner’s GBS.

(ECF No. 121, pp. 25-26; ECF No. 135, p. 32.)

30

VI. Conclusion

After weighing the evidence of record within the context of this Program, I find by

preponderant evidence that petitioner suffered GBS caused-in-fact by the Prevnar 13

vaccination she received on January 15, 2015. A separate damages order will be

issued.

IT IS SO ORDERED.

s/Daniel T. Horner

Daniel T. Horner

Special Master

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