# Tracy v. Secretary of Health and Human Services

> United States Court of Federal Claims · April 15, 2022

URL: https://www.frixlaw.com/law-library/cases/6332197

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** April 15, 2022
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Herbrina Sanders
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

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- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/6332197

## How later opinions describe it (automated extraction)

- explaining that the respondent’s burden is to show that the “factor unrelated” was the “sole substantial factor” in causing the injury

## Opinion text

Sn the Guited States Court of Federal Claims

OFFICE OF SPECIAL MASTERS
Filed: March 30, 2022

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NICOLE TRACY and DANNY * No. 16-213V
STOTLER, on behalf of R.S., their minor *
child, **
*
Petitioners, * Special Master Sanders
*
Vv. **
** Ruling on Entitlement; Pneumococcal
SECRETARY OF HEALTH ** Conjugate (“Prevnar 13” or “PCV 13”)
AND HUMAN SERVICES, * Vaccine; Transverse Myelitis (“TM”);
* Molecular Mimicry
Respondent. *

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Mari Bush, Mari C. Bush, L.L.C., Boulder, CO, for Petitioner.
Althea Davis, United States Department of Justice, Washington, DC, for Respondent.

RULING ON ENTITLEMENT?

On February 11, 2016, Nicole Tracy and Danny Stotler (“Petitioners”) filed a petition for
compensation on behalf of their minor child R.S. pursuant to the National Vaccine Injury
Compensation Program.” Pet. at 1, ECF No. 1; 42 U.S.C. §§ 300aa-1 to -34 (2012). Petitioners
allege that the pneumococcal conjugate (“PCV 13” or “Prevnar 13”) vaccine R.S. received on
March 18, 2013, caused her to suffer from transverse myelitis (“TM”).? Pet. at 1.

After carefully analyzing and weighing all the evidence and testimony presented in this
case in accordance with the applicable legal standards,‘ I find that Petitioners have provided

' This Ruling shall be posted on the United States Court of Federal Claims’ website, in accordance with the
E-Government Act of 2002, 44 U.S.C. § 3501 note (2012) (Federal Management and Promotion of
Electronic Government Services). In accordance with Vaccine Rule 18(b), a party has 14 days to identify
and move to delete medical or other information that satisfies the criteria in § 300aa-12(d)(4)(B). Further,
consistent with the rule requirement, a motion for redaction must include a proposed redacted Ruling. If,
upon review, I agree that the identified material fits within the requirements of that provision, such material
will be deleted from public access.

? National Childhood Vaccine Injury Act of 1986, Pub L. No. 99-660, 100 Stat. 3755. Hereinafter, for ease
of citation, all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. § 300aa
(2012).

> Transverse myelitis (“TM”) is “myelitis in which the functional effect of the lesions spans the width of
the entire cord at a given level.” Dorland’s Illustrated Medical Dictionary 1, 1218 (32nd ed. 2012)
[hereinafter “Dorland’s”|. Myelitis is “inflammation of the spinal cord|[.]” Dorland’s at 1218.

‘While I have reviewed all of the information filed in this case, only those filings and records that are most
relevant to the decision will be discussed. Moriarty v. Sec'y of Health & Hum. Servs., 844 F.3d 1322, 1328
preponderant evidence that the Prevnar 13 vaccine R.S. received on March 18, 2013, was the
cause-in-fact of her TM. Accordingly, Petitioners are entitled to compensation and this case shall
proceed to the damages phase.

L Procedural History

Petitioners filed their petition for compensation on February 11, 2016. Pet. at 1. The same
day, Petitioners filed R.S.’s immunization record, affidavits, and medical records. Pet’r’s Exs. 1-
15, ECF Nos. 1-3-1-17. Petitioners filed a statement of completion on March 17, 2016. ECF No.
9. On May 5, 2016, Petitioners submitted an updated medical record and an amended statement of
completion. Pet’r’s Ex. 16, ECF Nos. 12-13.

Respondent filed his Rule 4(c) report on June 16, 2016, recommending that compensation
be denied. Resp’t’s Report at 1, ECF No. 14. A status conference was held on June 23, 2016, to
discuss Respondent’s “concern[s] about both whether the Prevnar [13] vaccine could cause
[R.S.’s] injuries and whether an alternative cause was actually responsible for [R.S.’s] injuries.”
Sched. Order, ECF No. 15; see also Min. Entry, docketed June 23, 2016. Following the conference,
the presiding special master ordered Petitioners to file an expert report. Sched. Order at 1. Prior to
filing an expert report, Petitioners submitted updated medical records and an amended statement
of completion on December 16, 2016. Pet’r’s Exs. 17-21, ECF Nos. 20-21. This case was
transferred to me on January 12, 2017. ECF Nos. 22-23.

On February 23, 2017, Petitioner filed an expert report from Lawrence Steinman, M_D.,
and supporting medical literature. Pet’r’s Exs. 22-45, ECF Nos. 25-1—25-5. Respondent filed his
responsive expert report from Stephen McGeady, M.D., on June 30, 2017, along with supporting
medical literature. Resp’t’s Exs. A-J, ECF Nos. 29-1—29-10.

Petitioners submitted a supplemental expert report and medical literature on August 28,
2017. Pet’r’s Exs. 46-53, ECF Nos. 30-1—30-8. Three days later, Petitioners filed additional
medical records and documentation regarding R.S.’s disability status. Pet’r’s Exs. 54-58, ECF
Nos. 31-1—31-5. Respondent filed a supplemental expert report and medical literature on October
31, 2017. Resp’t’s Exs. K-S, ECF Nos. 32-1—32-9. Petitioner filed an updated medical record on
March 15, 2018. Pet’r’s Ex. 59, ECF No. 38-1.

I held a status conference with the parties on May 8, 2018. See Min. Entry, docketed May
8, 2018. During the status conference, I discussed the expert reports and noted “areas where the
expert reports may benefit from additional clarification[.]” See Sched. Order at 1-2, ECF No. 40.
Following the conference, I ordered the parties to discuss the case and to file a joint status report
indicating how they wish to proceed. /d. at 2. On July 18, 2018, Petitioners filed a status report on
behalf of both parties and noted that they would like to proceed with additional expert reports.
ECF No. 44. The same day, Petitioners filed a supplemental expert report and supporting medical

(Fed. Cir. 2016) (“[w]e generally presume that a special master considered the relevant record evidence
even though he does not explicitly reference such evidence in his decision.”’) (citation omitted); see also
Paterek v. Sec'y of Health & Hum. Servs., 527 F. App'x 875, 884 (Fed. Cir. 2013) (‘[f]inding certain
information not relevant does not lead to—and likely undermines—the conclusion that it was not
considered.”).
literature. Pet’r’s Exs. 60-68, ECF Nos. 45-1-45-10, 46-49. Respondent filed a responsive
supplemental report on September 4, 2018, along with supporting medical literature on October
22, 2018. Resp’t’s Exs. T-Z, ECF Nos. 50-1, 52-1—52-6. On October 29, 2018, Petitioners filed a
status report requesting that this case proceed to an entitlement hearing. ECF No. 53.

I scheduled this matter for an entitlement hearing to take place on January 15—16, 2020.
Hearing Order, ECF No. 55. Petitioners filed their pre-hearing brief on October 25, 2019. Pet’r’s
Br., ECF No. 59. The same day, Petitioners filed a status report indicating that they wished to
provide an expert report from R.S.’s treating neurologist Teri Schreiner, M.D., and to present her
testimony during the hearing. ECF No. 60. [held a status conference with the parties on November
6, 2019, to discuss Petitioners’ request. See Min. Entry, docketed Nov. 6, 2019. Following the
conference, I suspended Respondent’s deadline for filing his responsive pre-hearing brief and
ordered Petitioners to file their treating physician’s report by December 2, 2019. Sched. Order at
2, ECF No. 63. On November 27, 2019, Petitioners filed a status report noting Dr. Schreiner’s
limited availability on the scheduled dates of the entitlement hearing and requesting it be
rescheduled. ECF No. 64. Petitioners filed a written letter from Dr. Schreiner on December 3,
2019. Pet’r’s Ex. 71, ECF No. 66-1.

On December 3, 2019, I held a status conference with the parties to discuss Petitioners’
request. See Min. Entry, docketed Dec. 3, 2019. Following the conference, I ordered Respondent
to determine if, after a review of her report, further examination of Dr. Schreiner was necessary.
Sched. Order, ECF No. 67. I further ordered Petitioners to file a formal motion requesting a
postponement of the entitlement hearing and reinstated Respondent’s deadline for filing his
responsive pre-hearing brief. /d. Petitioners filed their motion to reschedule the entitlement hearing
on December 17, 2019. ECF No. 68. The next day, Respondent indicated via e-mail that his
responsive brief would not contain new causation theories or counter positions. Informal Comm.,
docketed Dec. 17, 2019. On December 18, 2019, I denied Petitioners’ motion to postpone the
entitlement hearing. ECF No. 69.

Petitioners filed an updated medical record on December 19, 2019. Pet’r’s Ex. 72, ECF
No. 71-1. The next day, Respondent submitted his responsive pre-hearing brief. Resp’t’s Resp.,
ECF No. 72. Respondent refiled highlighted medical literature on December 23, 2019. Resp’t’s
Exs. U-GG, ECF Nos. 76-1—76-13. On December 29, 2019, Petitioner filed a YouTube video link
exhibit. Pet’r’s Ex. 73, ECF No. 78. Petitioner refiled highlighted medical literature exhibits on
January 2, 3, and 6, 2020. Pet’r’s Exs. 74-95, ECF Nos. 80-1—81-12, 84-1-84-3. The entitlement
hearing was held as scheduled on January 15, 2020, in Denver, CO. See Min. Entry, docketed Jan.
21, 2020. However, it was not held in its entirety as a result of the presentation of a new theory of
causation from Petitioners’ expert, Dr. Steinman. See Tr. 72-78. I continued the hearing to take
the remaining direct testimony of Dr. Steinman. Tr. 80-85. I noted that Dr. Steinman’s testimony
would serve as a supplemental expert report regarding his new theory of causation, to which
Respondent could then respond following the conclusion of the hearing. Tr. 84:22—25, 85:1-23.

Following the entitlement hearing, Petitioners filed the U.S. patent for the Prevnar 13
vaccine on January 17, 2020. Pet’r’s Ex. 96, ECF No. 87-1. On January 22, 2020, Respondent filed
a status report requesting time to evaluate Petitioners’ expert’s new theory of causation that was
presented during the hearing. ECF No. 88. I held a status conference with the parties on January
23, 2020, to discuss Respondent’s request. See Min. Entry, docketed Jan. 23, 2020. Following the
conference, I ordered Respondent to file a responsive supplemental expert report responding to
Petitioners’ new theory of causation by March 6, 2020. Non-PDF Order, docketed Feb. 18, 2020.
On February 12, 2020, I scheduled the entitlement hearing to resume on April 6—7, 2020. Hearing
Order, ECF No. 91.

Respondent submitted medical literature on March 6, 2020. Resp’t’s Exs. HH—II, ECF Nos.
92-1—92-2. I held a status conference with the parties on March 26, 2020, to discuss the
implications of the COVID-19 pandemic. See Min. Entry, docketed Mar. 27, 2020. The same day,
I cancelled the entitlement hearing and ordered Respondent to submit his supplemental expert
report. Non-PDF Order, docketed Mar. 27, 2020.

On April 27, 2020, Respondent filed his supplemental expert report addressing Petitioners’
new theory of causation, along with supporting medical literature. Resp’t’s Exs. JJI-LL, ECF Nos.
93-1—93-3. Petitioners filed a supplemental report and medical literature on May 28, 2020. Pet’r’s
Exs. 97-100, ECF Nos. 95-1—95-5. On July 15, 2020, Respondent filed an additional supplemental
report. Resp’t’s Ex. MM, ECF No. 96-1. Petitioners submitted a final supplemental report on
August 7, 2020. Pet’r’s Exs. 101-102, ECF Nos. 98-1—98-2. I scheduled this matter to continue
the entitlement hearing on January 14, 2021. Hearing Order, ECF No. 99. The entitlement hearing
resumed as scheduled on January 14, 2021. See Min. Entry, docketed Jan. 14, 2021.

Following the entitlement hearing, Petitioners filed an opening post-hearing brief on
February 26, 2021. Pet’r’s Br., ECF No. 102. On March 29, 2021, Respondent filed his post-
hearing response brief. Resp’t’s Resp., ECF No. 103. Petitioners filed their post-hearing reply brief
on April 30, 2021. Pet’r’s Reply, ECF No. 105. On February 4, 2022, Petitioners filed a notice of
additional authority citing recent decisions of special masters as support for their claim. ECF No.
108. This matter is now ripe for consideration.

IL. Factual Background
A. Medical Records

R.S. was born full-term on June 13, 2012, and was healthy at birth. Pet’r’s Ex. 5 at 6, ECF
No. 1-7. R.S. visited James Wigington, M.D., at Salida Family Medicine for her infant
examinations. See Pet’r’s Ex. 5. Dr. Wigington noted a “normal assessment” at R.S.’s one and
two-month infant well-child visits. Jd. at 13, 17. R.S. received her first dose of the Prevnar 13
vaccine during her two-month well-child visit on August 16, 2012. /d. at 20-21.
On September 22, 2012, R.S. returned to Dr. Wigington for a cough. /d. at 23. He assessed
her with acute bronchitis’ and prescribed Azithromycin® and an Albuterol’ inhaler. /d. at 25. R.S.
returned two days later and noted that her bronchitis was improving. /d. at 26-28. On October 8,
2012, R.S. returned to Dr. Wigington with complaints of “wheezing and cough[ing]” that were
“Just not getting any better.” /d. at 29. Her wheezing was reported as worse in the morning. /d.
Petitioners noted R.S. had a runny nose that was “mucousy.” /d. Dr. Wigington assessed R.S. with
bronchitis and prescribed prednisolone.* /d. at 31. R.S. underwent a chest X-ray on October 9,
2012, which showed “mild thickening in the central peribranchial soft tissue.” /d. at 32. The
impression was “[m]ild [reactive] airway disease.’ No infiltrates.” Jd. R.S. returned for a four-
month well-visit on October 24, 2012, and her assessment was normal. /d. at 33-35. She received
the second dose of the Prevnar 13 vaccine during this visit. /d. at 36.

R.S. returned to Dr. Wigington on November 9, 2012, with complaints of post-nasal drip,
nasal blockage, cough, wheezing, and “acting fussy.” /d. at 37. Dr. Wigington assessed her with
“bronchiolitis infectious”'® and prescribed Azithromycin and continued nebulizers. /d. at 39.

On December 11, 2012, R.S. presented for her six-month well-child visit. Jd. at 40. Dr.
Wigington’s assessment of R.S. was normal except for nasal congestion. /d. at 42. He prescribed
Claritin.'! Jd. at 43. Two days later, on December 13, 2012, R.S. returned to Dr. Wigington with
complaints of a cough that was described as “consistent again.” /d. at 44. Petitioners noted that
R.S. had a runny nose and that R.S. “continue[d] to wheeze and . . . up [to] 3-4 times NOC and
seem|[ed] to ‘gasp’ for air.” /d. Dr. Wigington assessed R.S. with “[r]eactive airway disease and
probably [upper respiratory infection (““URI’)].” /d. at 46. Dr. Wigington also noted that R.S.
“[p]ossibly had [respiratory syncytial virus (‘“RSV”)!] during the summer,” and “since then has

> Bronchitis is “inflammation of a bronchus or bronchi; there are both acute and chronic varieties.
Symptoms usually include fever, coughing, and expectoration.” Dorland’s at 252.

° Azithromycin is “an antibiotic, derived from erythromycin, that inhibits bacterial protein synthesis,
effective against a wide range of gram-positive, gram-negative, and anaerobic bacteria; used in the
treatment of mild to moderate infections caused by susceptible organisms, administered orally and
intravenously.” Dorland’s at 187.

7 Albuterol is “a B-adrenergic agonist . . . ; administered by inhalation as a bronchodilator for the treatment
and prophylaxis of bronchospasm associated with . .. chronic obstructive airway disease, the treatment of
asthma-associated bronchospasm, and the prophylaxis of exercise-induced bronchospasm.” Dorland’s at
45,

* Prednisolone is “a synthetic glucocorticoid derived from cortisol, administered orally in replacement
therapy for adrenocortical insufficiency and as an anti-inflammatory and immunosuppressant in a wide
variety of conditions.” Dorland’s at 1508.

* Reactive airway disease is “any of several conditions characterized by wheezing and allergic reactions:
the most commons ones are asthma, bronchiolitis, and chronic obstructive lung disease.” Dorland’s at 542.
!° Bronchiolitis infectious refers to bronchitis. See supra, note 5.

"! Claritin is the “trademark preparation of loratadine.” Dorland’s at 368. Loratadine is “a nonsedating
antihistamine . . . with no significant antimuscarinic effects; used for the treatment of allergic rhinitis and
chronic idiopathic urticaria and as a treatment adjunct in asthma, administered orally.” /d. at 1074.

” Respiratory syncytial virus (“RSV”) refers to “any of a group of viruses belonging to the genus
Pneumovirus, isolated originally from chimpanzees . . . . In humans, they cause respiratory disease that is
particularly severe in infants, in whom it causes bronchiolitis [] and sometimes pneumonia.” Dorland’s at
2064.
had recurrent URIs with coughing and wheezing.” /d. Dr. Wigington prescribed R.S. liquid
Albuterol instead of nebulizers. /d.

On January 28, 2013, R.S. returned to Dr. Wigington for evaluation of her cough. /d. at 49.
Petitioners noted that R.S. was “feeling congested in the chest,” had a “cough [that was] hacking”
in nature and “sound[ed] loose.” /d. Dr. Wigington assessed R.S. with acute bronchitis and noted
her history of recurrent and protracted URIs. /d. at 49-51. He prescribed prednisolone, a vaporizer,
and Albuterol nebulizer. /d. at 51.

Due to her recurrent respiratory issues, R.S. presented to pulmonary specialist Deborah
Liptzin, M.D., on March 8, 2013. /d. at 52. Dr. Liptzin noted that R.S. had a history relevant for
“recurrent cough/wheeze with respiratory illnesses[.]” /d. at 53. She noted a “high suspicion for
asthma[]”!? but that “[A]lbuterol and steroids [were] not helping her wheeze/cough as well as
inspiratory wheeze would go against that.” /d. Dr. Liptzin recommended a treatment course
consistent with asthma, including Flovent4 and Albuterol nebulizers. /d. at 54.

RS. returned to Dr. Wigington for her nine-month well-child visit on March 18, 2013. Jd.
at 56. He noted that R.S.’s physical examination and development were normal. /d. R.S. received
her third dose of the Prevnar 13 vaccine during this visit. /d. at 59.

On April 1, 2013, R.S. presented to the emergency room for complaints of a sudden onset
of decreased movement of her lower extremities, lethargy, and weakness. Pet’r’s Ex. 8 at 2, ECF
No. 1-10. Petitioners noted that R.S. had URI symptoms for more than one week, including a
cough and runny nose. /d. at 2-3. The attending physician Richard Ruiter, M.D., ordered lab work,
a chest X-ray, and head CT, which yielded normal results. /d. at 4. Dr. Ruiter’s final impression
of R.S. was a URI and lethargy, and he discharged R.S. home. /d. at 3.

The following day, on April 2, 2013, R.S. presented to a different emergency room. Pet’r’s
Ex. 9 at 2, ECF No. 1-11. Petitioners’ chief complaint was that “[t]here is something not right”
with R.S. /d. They stated that they picked R.S. up from daycare after the facility called and told
them that R.S. was “lethargic.” /d. Petitioners noted that R.S. was “alert,” but that “any time they
tr[ied] to move [R.S.] or change her diaper, she seem[ed] to cry out in pain.” /d. They reported
that, at a different ER the previous day, “a CT of [her] head, chest X-ray, CBC, renal electrolytes,
and urinalysis . .. were reported . . . as normal.” /d. Petitioners reported that R.S. “ha[d] not been
wanting to eat or drink very much since yesterday.” /d. On examination, R.S. did “not move her
upper or lower extremities[,]” although “[s]he seem[ed] to have good tone in both upper and lower
extremities.” /d. at 3. The attending ER physician Gregory Collins, M.D., noted that R.S.
“seem[ed] to whimper and cry with any movement” and “prefer[ed] to lie in a supine position.”

'S Asthma is “recurrent attacks of paroxysmal dyspnea, with airway inflammation and wheezing due to
spasmodic contraction of the bronchi. Some cases are allergic manifestations in sensitized persons; others
are provoked by factors such as vigorous exercise, irritant particles, psychological stresses, and others.”
Dorland’s at 168.

| Flovent is the “trademark preparation of fluticasone propionate.” Dorland’s at 719. Fluticasone
propionate is “a synthetic corticosteroid used topically as an anti-inflammatory and antipruritic in treatment
of corticosteroid-responsive dermatoses, intranasally in treatment of allergic rhinitis, other inflammatory
nasal conditions, and nasal polyps, and by inhalation in maintenance treatment of asthma.” /d. at 722.

6
Id. R.S. underwent a lumbar puncture (“LP”), which showed a mildly low glucose level at 39, a
protein level of 48, and red blood cells. /d. She also underwent a cervical spine MRI, which showed
a “[d]iffuse abnormal signal and mild expansion of the cervical and upper thoracic spinal cord,
from C2 d[own] to about T4 level.” /d. at 13. Dr. Collins noted that “[t]his favor[ed] an acute
inflammatory process of the cervical spine, involving predominantly the central gray matter
structures and posterior columns. Idiopathic [TM] c[ould] be considered, as well as additional
acute inflammatory encephalomyelitis/myelitis.”'° Jd. He admitted R.S. for further evaluation.
Pet’r’s Ex. 10 at 44, ECF No. 1-12. At the time, the on-call pediatric attending, Elizabeth Martin,
M_D., noted that R.S. “has had [two] normal [white blood counts], one low-grade fever at home[,]
but no other documented fever and no focal sign of infection.” /d.

The next day, R.S. underwent a neurological evaluation with Brian Grabert, M.D. /d. at 47.
Dr. Grabert’s examination revealed “no movement in [R.S.’s] upper or lower extremities except
to touch and then she had withdrawal.” /d. at 48. Dr. Grabert also noted “flaccid muscle tone in
[R.S.’s] upper extremities and markedly decreased tone in [her] lower extremities.” /d. Dr. Grabert
wrote that R.S. “seemed to have some synesthesia, meaning with touching her upper extremities,
she started to whimper, less so in the lower extremities.” /d. Dr. Grabert wrote that R.S.’s MRI
was “consistent with [TM] with multiple segment involvement from C1 down to T4.” /d. at 48,
858. R.S.’s infectious disease work-up was negative. /d. at 858-59. He assessed R.S. with TM and
treated her with high dose Solumedrol '° and one IVIG treatment. /d. After receiving this course of
treatment, Dr. Grabert noted that R.S. was “regaining some strength” and had “daily improvements
in her strength, tone, and abilities.” /d. at 859. R.S. was discharged on April 9, 2013, with a
recommendation for physical therapy (“PT”) and prescriptions for a sixteen-day Orapred"’ taper,
Prevacid Solutab,'* and gabapentin.'? /d. at 857-59.

On April 10, 2013, R.S. followed up with Dr. Wigington. Pet’r’s Ex. 5 at 63. Petitioners
reported that upon discharge the day before, R.S. had “good head movement and [was] able to
move [her] arms a little bit[,] but [she] still [had] no movement from her legs.” /d. Dr. Wigington’s
assessment of R.S. was TM, and he noted R.S.’s plans to begin PT. /d. at 65.

R.S. returned to the ER for admission on April 17, 2013, for the purpose of placement of a
central venous catheter and treatment with plasmapheresis.”° Pet’r’s Ex. 11 at 1, ECF No. 1-13.
The attending physicians noted that R.S.’s TM was “most-likely post-infectious[.]” /d. at 3. A

'° Encephalomyelitis is “inflammation involving both the brain and the spinal cord.” Dorland’s at 613.

‘© Solumedrol is the “trademark preparation of methylprednisolone sodium succinate.” Dorland’s at 1731.
Methylprednisolone sodium succinate is “the 21-succinate sodium salt of methylprednisolone, having
actions and uses similar to those of the base; it is highly soluble in water and is chiefly used for the rapid
achievement of high blood levels of methylprednisolone in short-term emergency treatment; administered
by intramuscular or intravenous injection.” Jd. at 1154.

'’ Orapred is a brand name for prednisolone. Dorland’s at 1508: see also supra, note 8.

'8 A Prevacid Solutab is a water-soluble form of Prevacid. Prevacid is the “trademark preparation of
lansoprazole.” Dorland’s at 1513. Lansoprazole “acts as a proton pump inhibitor; used to imhibit the
secretion of gastric acid for the symptomatic treatment of duodenal and gastric ulcers... .” Jd. at 1004.

'? Gabapentin is “an anticonvulsant that is . . . used as adjunctive therapy in the treatment of partial seizures
and the management of postherpetic neuralgia; administered orally.” Dorland’s at 753.

°° Plasmapheresis is “the removal of plasma from withdrawn blood, with re-transfusion of the formed
elements into the donor[.|” Dorland’s at 1456.
repeat MRI conducted on April 23, 2013, showed “[i]nterval improvement in edema throughout
the cervical spinal cord with only residual signal abnormality involving the dorsal columns of the
spinal cord from C2—C3 through C6—C7[, with no] abnormalities following contrast... .” Pet’r’s
Ex. 5 at 85. Her diagnoses included TM, neurogenic bowel and bladder,”! quadriparesis,?” and
neuropathic pain. /d. at 90. During treatment, R.S. “had significant return of motor function... .”
Pet’r’s Ex. 11 at 6. R.S. completed her course of treatment on April 24, 2013, and she was
transferred to inpatient rehabilitation. /d.

After several weeks of inpatient rehabilitation, R.S. “showed improvements with all
mobility tasks[,] as she was able to roll from supine [position] to her side with minimal assistance.”
Id. at 269. The attending physician noted that R.S. also “showed improved trunk stability while in
supported standing [position] by pushing up with her arms and maintaining the position well.” Jd.
R.S. “demonstrated improved ability to reach outside her base of support and reach over [her] head
to get toys while in [a] sitting [position].” /d. R.S. was discharged from inpatient rehabilitation on
May 17, 2013. Id.

On June 21, 2013, R.S. presented to Dr. Wigington for her twelve-month well-visit. Pet’r’s
Ex. 5 at 126. He noted that R.S. was “making very good progress,” although she was “still hav[ing]
lower extremity .. . and some upper extremity deficits.” /d. Petitioners reported that R.S. “[could]
move [her] legs .. . [and] roll over[,]” but she was unable to “crawl[] or stand[.]” /d. at 126, 129.
Dr. Wigington’s assessment of R.S. was normal. /d. at 129. He indicated that “[n]o immunizations
were given [to R.S.] at this [visit]” because Petitioners were “concerned that immunizations had
[a] part in [her TM].” Jd.

R.S. followed up with rehabilitation specialist Elizabeth Knight, M.D., on June 28, 2013.
Id. at 141. Petitioners noted that R.S. was receiving two PT and occupational therapy (“OT”) visits
each week and “doing exercises athome ... .” /d. They reported that R.S. was “still on Neurontin,”
but only taking it twice per day.” /d. Petitioners continued that R.S. was “[a]ble to bear weight
through her legs.” /d. R.S.’s father reported that her “[a]rms [were] almost 100%.” /d. Petitioners
indicated that R.S. was “starting to commando crawl, and if placed in a hands/knees position, [she
would] hold that position and even rock back and forth.” /d. She could also “sit unassisted, and
[could] even play with a toy in both hands.” /d. Dr. Knight’s assessment of R.S. was “[twelve]-
month-old girl with history of [TM], who is making nice functional gains.” /d. at 143. She advised
R.S. to continue with her therapy regimen and to follow up in three months. /d. at 144. RS.
followed up with neurologist Dr. Schreiner following her inpatient admission on July 12, 2013. /d.
at 151. Dr. Schreiner did not opine as to the cause of R.S.’s TM during this visit. Jd. at 151-57.

On October 11, 2013, R.S. had a follow-up with rehabilitation specialist Michael Dichiaro,
M_D. /d. at 164. Dr. Dichiaro wrote that R.S. was “[p]rogressing towards crawling — [she could]
bring [her] knees to [her] elbows to crawling position. [She was] army crawling, [and had]
increased movements in [her] legs.” /d. He also noted improving tone in R.S.’s bilateral lower

*! Neurogenic bowel and bladder refers to “any condition of dysfunction of the urinary bladder [or bowel]
caused by a lesion of the central or peripheral nervous system.” Dorland’s at 222.

2 Quadriparesis is “muscular weakness affecting all four limbs[.]” Dorland’s at 1565.

*3 Neurontin is the “trademark for preparations of gabapentin.” Dorland’s at 1268: see also supra, note 19.

8
extremities. /d. at 167. Dr. Dichiaro indicated that R.S. was “making nice gains” with her TM. /d.
He recommended continued PT and OT, and to follow up in three months. /d.

The same day, R.S. presented for a neurological follow-up with Dr. Schreiner. /d. at 168.
Petitioners stated that they “d[id] not think that [R.S. was] feel[ing] pain in her legs, but they
[thought] that she [was] feel[ing] pressure.” /d. at 169. They also noted that R.S. was “stiff? when
she [woke up in the morning], but not during the day.” /d. Dr. Schreiner wrote that R.S.’s TM was
“likely idiopathic.” /d. at 172. She indicated that R.S. “continue[d] to have impressive recovery of
function[,]” and that, while “[t]here [was] some question of sensory disturbance, . . . it [did] not
appear to be limiting [R.S.’s] progress.” /d. She also noted “no evidence of bowel/bladder
dysfunction,” but that R.S. “will be seen again by urology ... .” /d. Dr. Schreiner recommended
vaccinating R.S., but also noted that R.S. should “avoid live virus vaccines.” /d.

RS. returned to Dr. Schreiner on April 21, 2014. /d. at 212. Petitioners told Dr. Schreiner
that R.S. was “making good progress[,]” and “no longer [gave] the indication of pain in her legs.”
Id. at 213. They continued that R.S. was talking and had normal bowel function. /d. They also
reported that they would “begin to wean [R.S. off] the .. . Neurontin[]” that night. Jd On
examination, R.S. had decreased upper extremity reflexes, but exhibited normal tone and strength.
Id. at 216. She also exhibited increased lower extremity reflexes with up-going toes, along with
“Ts]ome weakness and spasticity when standing[.|” /d. Dr. Schreiner’s impression was that R.S.
“continue[d] to have impressive recovery of function . . . [and her sJensory disturbance [had]
improved.” /d. Dr. Schreiner “agree[d] with weaning [the] . . . Neurontin,” and recommended a
dose of Lipoic acid” at 300mg. Jd.

On August 26, 2014, R.S. followed up with rehabilitation specialist Dr. Dichiaro. /d. at
238. Petitioners stated that R.S. was “continuing to improve,” and that she had “no recent illnesses
or hospitalizations.” /d. They reported that R.S. was “[s]tarting to walk short distances with a push
toy or without [supra-malleolar orthosis (‘SMO”)].”° [She was t]alking in sentences. [Her] arms
[were] close to normal in strength and coordination.” /d. Dr. Dichiaro noted that R.S. had “some
[muscle] tone in [her] lower extremities, and [was] variable, improving. [R.S. was] tight in the
morning, but work[ed] through it quickly, [within five] minutes.” /d. at 239. Petitioners noted that
R.S. was still taking “Neurontin .5ml at night,” but that they “[had] missed a few doses without
any difference.” /d.

On October 25, 2014, R.S. returned to Dr. Wigington with complaints of a deep cough,
wheezing, and loss of appetite for one day. /d. at 252. His examination of R.S. revealed no nasal
discharge or sinus tenderness, but he heard wheezing upon listening to her lungs. /d. at 254. Dr.

4 Lipoic acid is “a necessary cofactor of the pyruvate dehydrogenase, branched-chain a-keto acid
dehydrogenase, and a-ketoglutarate dehydrogenase complexes; it contains a reactive disulfide group that
can bind and transfer reaction intermediates .. . It is used as a dietary supplement for its antioxidant
properties.” Dorland’s at 1062.

5 “SMO” stands for “supra-malleolar orthosis,” which “supports the leg just above the anklebones or
malleoli.” Scheck & Siress, SMO (Supra-Malleolar Orthosis), PROSTHETICS, ORTHOTICS, PEDORTHICS
https:/Awww.scheckandsiress.com/wp-content/uploads/2016/08/SMO-JM.pdf (last visited Feb. 18, 2022).
It is “often worn by children” and “is designed to maintain a vertical, or neutral heel while also supporting
the three arches of the foot. This can help improve standing, balance and walking.” Jd. at 1.

9
Wigington assessed R.S. with bronchiolitis infectious, and noted that, “[w]ith [R.S.’s] history of
[TM, he would] treat aggressively.” /d. at 255. He prescribed a course of Azithromycin. Jd.

From October 29 to October 31, 2014, R.S. was admitted at the hospital for “increased
cough and hypoxia”® at home[.]” /d. at 269. A chest CT conducted in the ER revealed mild
pulmonary edema?’ and severe central airway disease. /d. at 256-57. R.S. also tested positive for
RSV. /d. at 261, 269. She was admitted for IV fluids, oxygen, and nebulizer treatments. /d. at 269.
During her treatment course, R.S. “stabilized, but continued to have significant rhonchi”®
bilaterally and some left-sided rows.” /d. R.S. was “started on IV Solumedrol and on the morning
of discharge[,| her breath sounds were definitely improved with decreased rhonchi and no audible
rales.” Id. She was discharged home on Prelone syrup”? and Albuterol nebulizers. /d. R.S.’s
discharge diagnoses included RSV bronchiolitis, reactive airway disease, and “ongoing lower
extremity weakness secondary to prior [TM].” Jd.

R.S. presented to pulmonologist Paul Stillwell, M.D., on December 2, 2014. Jd. at 286.
Petitioners noted that R.S. got “sick every [three] weeks, with recovery in between. She [got] a
runny nose with or without fever that lead [sic] to cough and wheeze and dyspnea.” /d. Petitioners
expressed “concern[] that [R.S. was] too sick too often.” /d. Dr. Stillwell’s impression included
asthma, restrictive lung disease, and TM, which was noted to be “improving.” /d. at 287-88. He
recommended increased asthma medications and Albuterol treatments. /d.

On January 26, 2015, R.S. returned to Dr. Dichiaro for a follow-up. Pet’r’s Ex. 12 at 74,
ECF No. 1-14. Dr. Dichiaro noted that R.S. was “doing very well . . . [with no] major illnesses,
[and Petitioners] .. . noted that [R.S. was] continuing to get stronger.” /d. On examination, Dr.
Dichiaro wrote that R.S. had poor truncal tone, right ankle clonus,*? and she was dragging her toes
bilaterally. /d. at 76. He recommended a gait analysis and continued PT/OT. /d. at 77.

R.S. presented to Dr. Schreiner for a neurological follow-up on May 11, 2015. /d. at 94.
Dr. Schreiner wrote that R.S. was “weaker on [her] right” side and was walking with a walker in
addition to her orthotics. /d. On examination, she noted that R.S. had increased tone on her right
greater than left side, and there was no evidence of sensory disturbance. /d. at 97. She indicated
that R.S. was scheduled to receive a Botox"! injection the following week. /d. at 94. Dr. Schreiner’s

26 Hypoxia is the “reduction of oxygen supply to tissue below physiologic levels despite adequate perfusion
of the tissue by blood.” Dorland’s at 908.

°7 Edema is “the presence of abnormally large amounts of fluid in the intercellular tissue spaces of the body,
usually referring to subcutaneous tissues. It may be localized (as from venous obstruction, lymphatic
obstruction, or increased vascular permeability) or systemic (as from heart failure or renal disease).”
Dorland’s at 593.

?8 Rhonchus is a “sound . . . consisting of a dry, low-pitched, snore-like noise, produced in the throat or
bronchial tube due to a partial obstruction such as by secretions.” Dorland’s at 1642.

°° Prelone syrup is a “trademark preparation of prednisolone.” Dorland’s at 1508; see also supra, note 8.
°° Clonus is the “alternate muscular contraction and relaxation in rapid succession. 2. a continuous rhythmic
reflex tremor initiated by the spinal cord below an area of spinal cord injury, set in motion by reflex testing.”
Dorland’s at 373.

3! Botox is “the trademark for preparations of onabotulinumtoxin A.” Dorland’s at 241. Onabotulinumtoxin
A is “a preparation of botulinum toxin type A, purified from the neurotoxin type A complex produced by
Clostridium botulinum type A and consisting of the neurotoxin and several accessory proteins. It is

10
impression was that R.S. was “progressing nicely, but ha[d] morbidity of lower extremity
spasticity, [and] weakness.” /d. at 97. She documented Petitioners’ plan for R.S. to attend
“Ti |ntensive rehab[ilitation] at Kennedy Krieger in June [of 2015].” /d. at 98.

RS. presented for an intensive rehabilitation evaluation with Devika Bhushan, M.D., at the
Kennedy Krieger Institute on June 1, 2015. Pet’r’s Ex. 13 at 1, ECF No. 1-15. Dr. Bhushan noted
that R.S. “experienced a viral respiratory illness and got [the] Prevnar [13 vaccination] in the
period leading up to her [symptom] presentation.” /d. at 65. She wrote that R.S. had “great gross
and fine motor control over her trunk and bilateral arms. She [was] working on walking using a
walker.” /d. at 1. Dr. Bhushan indicated that “[R.S.] underwent Botox treatment of her hip flexors,
adductors, and hamstrings, which were previously spastic, but now have normal [range of motion
(“ROM”)].” /d. Dr. Bhushan noted that the main goal of R.S.’s rehabilitation was increasing R.S.’s
walking ability. Jd. During her admission, R.S. “received comprehensive care by nursing, social
work, pediatrics, child life, education, neuropsych[ology], behavioral psych[ology], OT, PT,
speech, and nutrition.” /d. at 66. By the time of her discharge on June 13, 2015, R.S.’s upper
extremities and trunk muscle tone, bulk, and strength were all within normal limits. /d. at 65-66.
She had slightly diminished lower extremity muscle tone. /d. at 66. R.S. was “able to ambulate
with [the] help of [a] walker, but sometimes by dragging [her] toes and/or crossing one leg in front
of [the] other... .” Jd.

On June 9, 2015, R.S. presented to neuro-immunologist Carlos Pardo, M.D. for an
evaluation. Pet’r’s Ex. 14 at 1, ECF No. 1-16. Dr. Pardo reviewed R.S.’s history and conducted a
neurological examination. /d. at 1-3. Dr. Pardo wrote that “the major limitation now is the presence
of spastic paraparesis.” >? /d. at 3. He noted that “it is very clear that [R.S.] experienced myelopathic
syndrome that left her with a spastic paraparesis.” /d. He recommended aggressive PT and
rehabilitation. Jd.

R.S. returned to Dr. Wigington for her three-year well-child visit on September 10, 2015.
Pet’r’s Ex. 5 at 306. In regard to R.S.’s TM, Petitioners stated that they “thought [it] to be vaccine
induced.” /d. They reported that R.S. had been seen by a rehabilitation specialist, and it was
believed that she would be able to walk eventually. /d. R.S. received additional Botox injections
on December 9, 2015. Pet’r’s Ex. 18 at 4, ECF No. 20-2.

The next day, R.S. followed up with Dr. Stillwell for her asthma and restrictive lung
disease. Jd. at 15, 18. He noted that he was “happy [with] how well [R.S.] ha[d] done since [her]
last visit.” /d. at 18. Dr. Stillwell wrote that R.S. had an “ongoing recovery of function” related to
her weakness from TM. /d. at 15-16.

On March 17-19, 2016, R.S. was hospitalized for a “potential altered mental status” and
viral symptoms, such as fever, vomiting, and ear and throat pain. /d. at 32, 39, 42. The attending
physician noted that R.S. had an “extensive workup . . . which was unrevealing of [an] etiology
for [her] altered mental status.” /d. Her examination was normal absent a “barky” cough. /d. at 37.
The attending physician wrote that she “[d]oubt[ed it was] meningitis or encephalitis . . . [or]

administered intramuscularly to prevent chronic migraine; to treat cervical dystonia, upper limb spasticity,
strabismus, and blepharospasm; and to temporarily improve the appearance of glabellar lines. It is
administered subcutaneously to treat severe primary axillary hyperhidrosis.” /d. at 242.

>? Paraparesis is “partial paralysis of the lower limbs.” Dorland’s at 1379.

ll
recurrence of [TM] at this time based on [R.S.’s] exam.” /d. at 32, 35. She wrote that a viral illness
was a “likely etiology, as [R.S. was] improving, now afebrile .. . and [her white blood count]
would suggest viral suppression.” /d. at 32-33. R.S. was diagnosed with an upper respiratory
“symptom,” potential for altered mental status, and acute otitis media*’ and was prescribed
antibiotics. /d. at 34.

R.S. received Botox injections on March 29, 2016. /d. at 89. Dr. Dichiaro noted that R.S.’s
“It]one [had] increased to [both] hamstrings and hip adductors.” /d. at 89-90. She continued to
receive Botox injections throughout 2016. Pet’r’s Ex. 21 at 28-29, ECF No. 20-5.

R.S. followed up with Dr. Schreiner on May 16, 2016. Pet’r’s Ex. 55 at 10, ECF No. 31-2.
Dr. Schreiner described R.S.’s hospitalization in March of 2016 and wrote that R.S. “became very
ill and had recurrence of weakness. As she recovered from her illness, her weakness improved.”
Id.; see also Pet’r’s Ex. 59 at 114, ECF No. 38-1. On examination, R.S. exhibited weakness in her
lower extremities, greater on the right than left side, but “[nJo clubbing, ** cyanosis,** or edema.”
Pet’r’s Ex. 55 at 12. Dr. Schreiner also noted “increased tone [greater on the right than left] with
tight adductors .. . normal tone in upper extremities[ and s]ome weakness and spasticity when
standing[.]” /d. at 13. Included in Dr. Schreiner’s impression was “residual [bilateral lower
extremity] spasticity and weakness.” /d. Dr. Schreiner advised R.S. to follow up in one year. /d.

RS. returned to the Kennedy Krieger Institute for inpatient rehabilitation from June 20 —
July 2, 2016. Pet’r’s Ex. 19 at 1, 34, ECF No. 20-3. R.S.’s goal for rehabilitation was “to improve
functioning status post spinal cord injury secondary to [TM].” /d. at 1. Occupational therapist
Samantha Hughes, D.O., indicated that R.S. continued to use a rolling walker, bilateral forearm
crutches, and leg braces. /d. at 2; see also Pet’r’s Ex. 54 at 2, ECF No. 31-1. She wrote that R.S.
was “able to stand with single or bilateral upper extremity support and supervision[.]” Pet’r’s Ex.
19 at 4. R.S.’s upper extremity strength and ROM were within normal limits. /d. R.S.’s lower
extremity tone was noted as “slightly low[.]” /d at 10. She could dress herself with “at best
minimal assistance.” /d. at 6-7. R.S. continued to receive PT treatment for her weakness and “gross
motor development” throughout 2016 and 2017.*° See, e.g., Pet’r’s Ex. 56, ECF No. 31-3.

R.S. followed up with Dr. Dichiaro on February 10, 2017. Pet’r’s Ex. 55 at 81. He noted
that her TM was “making nice gains[.]” /d. Dr. Dichiaro noted that R.S. was no longer using a
walker, had increased bilateral lower extremity tone, and was “working on walking with one

33 Otitis media is “inflammation of the middle ear: subtypes are distinguished by length of time from onset
(acute versus chronic) and by type of discharge (serous versus suppurative).” Dorland’s at 1351.

4 Clubbing is “a digital deformity produced by proliferation of the soft tissues about the terminal phalanges
of the fingers or toes, with no constant osseous changes; seen in various types of chronic disease of the
thoracic organs.” Dorland’s at 375.

35 Cyanosis is “a bluish discoloration, especially of the skin and mucous membranes due to excessive
concentration of deoxyhemoglobin in the blood.” Dorland’s at 452.

3° While I have reviewed all of the records filed in this case, I have addressed only the medical records I
have deemed relevant to this Decision. Moriarty v. Sec'y of Health & Hum. Servs., 844 F.3d 1322, 1328
(Fed. Cir. 2016) (“We generally presume that a special master considered the relevant record evidence even
though he does not explicitly reference such evidence in his decision.”) (citation omitted); see also Paterek
v. Sec'y of Health & Hum. Servs., 527 F. App'x 875, 884 (Fed. Cir. 2013) (‘Finding certain information not
relevant does not lead to—and likely undermines—the conclusion that it was not considered.”).

12
crutch.” /d. Regarding R.S.’s gait, he noted that she walked “primarily on [her] toes, dragging [her]
toes bilaterally[.]” /d. at 83. Dr. Dichiaro’s assessment included lower extremity weakness. /d.
R.S. received Botox injections during this visit. /d. at 84; see also Pet’r’s Ex. 59.

On August 10, 2017, R.S. returned to Dr. Schreiner for a follow-up. Pet’r’s Ex. 59 at 112.
Dr. Schreiner noted that R.S. continued to “make gains, but has residual [bilateral lower extremity ]
spasticity and weakness.” /d. She wrote that R.S. was able to walk with the use of bilateral walking
sticks. /d. at 117. She also noted that R.S. had a wide-based gait “with pelvic tilt[ing] and flinging
motion of [her] legs.” Jd.

R.S. sought treatment for her TM throughout 2018.°” As of August 14, 2019, R.S. was still
in the care of Dr. Schreiner. Pet’r’s Ex. 72 at 27, ECF No. 71-1. Dr. Schreiner described R.S.’s
TM as “idiopathic [TM] at [ten] months of age.” /d. She indicated that she would be writing a
letter on R.S.’s behalf for the Program. /d. Dr. Schreiner noted that R.S. still had residual bilateral
lower extremity weakness and was receiving Botox injections. /d. at 6, 27. Dr. Schreiner wrote
that R.S. had a “stunningly good” physical therapist, who she saw two times per week, along with
receiving PT at school. /d. at 28. Petitioner has not filed any additional medical records.

B. Petitioners’ Affidavits & Fact Testimony

Petitioners submitted two affidavits in support of their petition and Ms. Nicole (“Niki”)
Tracy testified at the entitlement hearing.** See Pet’r’s Exs. 1, 2, ECF Nos. 1-3, 1-4; see also Tr.
12-45. The first of Petitioners’ affidavits was authored by Ms. Tracy, R.S.’s mother. Pet’r’s Ex. 1
4 1. Ms. Tracy described R.S.’s health both pre and post vaccination consistent with R.S.’s medical
records. /d. J] 12-51. Ms. Tracy averred that she and her husband “had no concerns about [R.S.’s]
health or development during [R.S.’s] early months.” /d. 9 15. She testified that R.S. was “able to
use her arms and legs well[]” and she did not have “[a]ny problems . . . with her bladder or
bowel[.]” Tr. 16:23—25, 17:1-4. She noted R.S.’s history of pulmonary issues and recurrent
bronchitis. Pet’r’s Ex. 1 JJ 18, 19, 22, 23, 25, 26. Ms. Tracy testified that based on her interactions
with R.S.’s treaters, R.S.’s asthma and respiratory illnesses were considered “separate and apart
from the [TM.]” Tr. 17:11-15.

Ms. Tracy wrote that “[a]s of March 18, 2013 [the day of R.S.’s Prevnar 13 vaccination], .
.. RS. was beginning to crawl, could hold her own weight while standing[,] hold[] onto a table or
object, was sitting unassisted, and was able to feed herself with her fingers.” Pet’r’s Ex. 1 { 28.
She testified that in the two weeks following R.S.’s vaccination, “[s]he was great. Nothing was out
of the norm.” Tr. 20:8—14. Ms. Tracy described the date of onset and wrote that “April 1, 2013[,]
began as other days in [Petitioners’] household. R.S. woke up, had breakfast[,] and went to
daycare[.]” Pet’r’s Ex. 1 § 31. She continued that “[a]t 4:45, [her] day care [sic] provider called
[her] and told [her that the provider] was worried about R.S.” /d. Specifically, the provider told
Ms. Tracy that R.S.’s “eyes were glassy, she cried whenever she was touched[,] and she was unable
to bear any weight on her legs.” Jd. Ms. Tracy wrote that when she arrived at the daycare, R.S.
was “limp... [and s]he screamed in pain as [Ms. Tracy] tried to buckle her into her car seat.” /d.

37 :

See id.
38 At the time of the entitlement hearing on January 15, 2020, Ms. Tracy testified as “Nicole Stotler.”
However, her affidavit was drafted as “Nicole Tracy” so I will refer to her as such throughout this section.

13
4 32. Ms. Tracy testified that R.S.’s condition was “very different” than anything she had
experienced with R.S.’s illnesses. Tr. 22:23—24. She described R.S.’s initial ER evaluation at a
local hospital that night and noted that “[w]hen the evaluation was done. . . R.S. was extremely
lethargic but would call out every time she was moved.” Pet’r’s Ex. 1 4.34. Ms. Tracy continued
that R.S.’s “cries were becoming softer[]” and she was “hardly vocal.” /d. She also noted that R.S.
was “weak and no longer moving her arms.” /d. Ms. Tracy testified that the ER physician told her
that R.S. “just d[id not] feel good. She’s tired, so that’s why she[ is] not moving.” Tr. 24:19—20.
Ms. Tracy wrote that she slept next to R.S.’s crib that night, because at that point, “R.S. was not
moving.” Pet’r’s Ex. 1 ¥ 34.

She averred that “[a]t about 4 am the following morning, R.S. woke up[,] tried to nurse,
but could not hold up her head to do so. Her eyes were open[,] but she seemed non[-]responsive.”
Id. 435. Ms. Tracy noted that she and her husband then took R.S. to a different hospital in Colorado
Springs, where R.S. underwent cervical spine and brain MRIs and a lumbar puncture “to rule out
central nervous system pathology.” /d. J{] 35-38. During her testimony, Ms. Tracy clarified that
R.S. was admitted and this testing occurred on April 2, 2013; R.S.’s TM diagnosis was made the
same day. Tr. 26:10—25. By April 4, 2013, R.S. could not hold herself up or move her arms and
legs. Tr. 28:15—25, 29:1-2. She wrote that R.S. received “five days of high dose intravenous
steroids and received one IVIG treatment[]” for clinical indications of weakness and TM. Pet’r’s
Ex. 1 J] 38-39. Ms. Tracy indicated that R.S. has received treatment for her TM throughout 2013
and thereafter, including the placement of a CVC line, plasmapheresis (“PLEX”) treatments,
inpatient rehabilitation, and outpatient PT and OT. Jd. J] 40, 42-46, 49. She also noted that R.S.’s
treating neurologist is Dr. Teri Schreiner. /d. § 47. Ms. Tracy documented R.S.’s pre and post
vaccination condition with photographs, which she also discussed during her testimony. /d. J 29;
see also Tr. 18-30.

Ms. Tracy described R.S.’s condition as of January of 2016 and noted that R.S.’s “condition
has improved, but she remains disabled. Her primary issues relate to mobility and other medical
consequences... .” /d. | 50. She wrote that R.S. receives three outpatient PT sessions per week
and two outpatient OT sessions per month. /d. 4 51. Ms. Tracy averred that R.S. “is able to walk
with the assistance of a walker and has recently begun working on transitioning to forearm
crutches.” /d. She wrote that R.S. “suffers from spasticity and tone in her legs and receives regular
Botox injections every [ninety] days to help relieve that tightness.” /d. Ms. Tracy noted that these
difficulties “with getting [R.S.’s] legs completely straight[ make p]otty training [] an issue[.]” /d.
She indicated that R.S. sees a urologist and pediatric pelvic floor specialist to assist with her
ongoing bladder issues. /d.; see also Tr. 35:20—21. She further wrote that R.S. attends school and
“tries her best to keep up with kids her age[] but is forced to rely on the help of her teachers and
aides for outdoor activities.” Pet’r’s Ex. 1 951. Ms. Tracy testified that they keep a wheelchair at
school, “for fire drills and things like that.” Tr. 35:14-19.

Ms. Tracy noted that Dr. Schreiner told her not to vaccinate R.S. with any live vaccines.
Tr. 43:17-19; Pet’r’s Ex. 1 44. On cross-examination, Ms. Tracy testified that she did not recall
R.S.’s treaters telling her that the cause of R.S.’s TM was idiopathic or post-infectious. Tr. 41-42.
Under my questioning, Ms. Tracy explained that R.S.’s pulmonary and respiratory issues, such as
her asthma and tendency for bronchitis resolved when R.S. was five years old. Tr. 42:19—25, 43:1-
9. On re-direct, Ms. Tracy stated that immediately after R.S. developed TM, her respiratory issues

14
became more difficult to deal with because she had decreased diaphragm strength from the TM.
Tr. 44:21—25, 45:12-14.

Petitioners’ second affidavit was authored by Mr. Danny Stotler, R.S.’s father. Pet’r’s Ex.
2 94 1-2. Mr. Stotler’s affidavit is essentially identical to Ms. Tracy’s affidavit and a recitation of
its contents is unnecessary. See id. J] 3-33; see also Pet’r’s Ex. 1.

Il. Experts
A. Expert Review
1. Petitioners’ Expert, Teri Schreiner, M.D.

Dr. Schreiner received her medical degree from the University of Rochester in 2006.
Pet’r’s Ex. 69 at 1, ECF No. 61-1. She completed a residency in pediatrics at the University of
Colorado in 2008. /d. She also completed residencies in neurology and child neurology at the same
institution in 2009 and 2011, respectively. /d. Dr. Schreiner held academic appointments in neuro-
immunology at the University of Colorado from 2011 to 2017. /d. She currently serves as an
Associate Professor of Neurology at the University of Colorado. /d. She is board-certified in
psychiatry and neurology with special qualifications in child neurology. /d. at 2. Dr. Schreiner’s
qualifications as a pediatric neuro-immunologist include, in part, her clinical experience treating
children with immune-mediated demyelinating conditions such as TM, presenting on the biology
of such conditions, and publishing extensively on disorders of the spinal cord, as well as neurologic
complications of vaccinations, specifically. See id. at 2-12; see also Pet’r’s Ex. 71 at 1-2. She is
also “one of a small group of pediatric neuroimmunologists in the country that specialize in
pediatric demyelinating disorders.” Pet’r’s Ex. 71 at 1. Much of Dr. Schreiner’s research and
publications specifically involves disorders of the spinal cord. /d.

2. Petitioners’ Expert, Lawrence Steinman, M.D.

Dr. Steinman received his medical degree from Harvard University in 1973. Pet’r’s Ex. 23
at 1. He completed his post-graduate training at Stanford University, where he completed an
internship in surgery in 1973, a residency in pediatrics in 1974, and a residency in pediatric and
adult neurology from 1977 to 1980. /d. He became board-certified in neurology in 1984. /d. at
2. He served as the Chairman of the Immunology Program at Stanford for approximately ten years
from 2002 to 2011. /d. at 1. He currently serves as a Professor of Neurology, Pediatrics, and
Genetics at Stanford University’s Department of Neurology and Neurological Sciences. /d. Dr.
Steinman’s curriculum vitae includes over five-hundred and forty published articles of which he
is a listed author. See id. at 5-45.

During the hearing, he noted he “did residency training in pediatrics and neurology.” Tr.
47:16-17. He explained that the focus of his medical research is on “how the immune system
attacks the nervous system in diseases like multiple sclerosis, like [TM], and like some of the
inflammatory neuropathies.” Tr. 48:11—14. Dr. Steinman testified that his current clinical practice
involves “treat[ing] patients with [TM,]” including children and infants. Tr. 48:15—19. He stated
that he has testified many times in the Vaccine Program. Tr. 119-120.

15
Dr. Steinman submitted three expert reports and testified during the first part of the
entitlement hearing. See Pet’r’s Exs. 22, 46, 60; Tr. 46-107. Following the break in proceedings,
Dr. Steinman submitted two additional expert reports and subsequently testified during the second
part of the entitlement hearing. Pet’r’s Exs. 97, 101; Tr. 118-128, 187-194. Petitioners did not
offer Dr. Steinman as an expert during either part of the hearing. I believe this was an oversight.
However, he has been recognized as an expert in neurology in numerous Program cases before
me, as well as other special masters. Therefore, I will sua sponte recognize him as such.

3. Respondent’s Expert, Stephen McGeady, M.D.

Dr. McGeady received his medical degree from Creighton University in Omaha, Nebraska
in 1967. Resp’t’s Ex. B at 1. From there, Dr. McGeady was in the 1“ Infantry of the U.S. Army in
Vietnam from 1968-1969 and was then employed at the Fitzsimons Army Hospital in Denver, CO
from 1969-1970. Id. Dr. McGeady completed a residency in pediatrics at St. Christopher’s
Hospital in Philadelphia, PA in 1972. /d. He also completed a fellowship in psychiatry and allergy
at Duke University in Durham, NC in 1974. Jd. Dr. McGeady has been the Emeritus Chief of the
Allergy, Asthma, and Immunology Division at duPont Hospital for Children in Wilmington, DE
since 2007. /d. He has also served as a Professor of Pediatrics at Jefferson Medical College in
Philadelphia since 2005. /d. Dr. McGeady is board-certified in pediatrics and allergy and
immunology. /d. He has received numerous honors, and he holds memberships in several
professional and scientific societies. /d. at 2. His curriculum vitae lists over two-hundred and sixty
publications, including articles, abstracts, book chapters, and editorials of which he is a listed
author. See id. at 2-14.

During the hearing, Dr. McGeady explained that as part of his clinical practice, he
supervises fellows in allergy and immunology. Tr. 130:23—25. He also interacts with medical
students “as part of their pediatrics rotation.” Tr. 131:13-—16. Dr. McGeady noted that he has “had
exposure to” patients with TM, but he personally has not been “involved in direct care of those
patients.” Tr. 132:23—25, 133:1-—5. Instead, he noted that he has “supervised people who cared for
them directly.” Tr. 133:5—6. Dr. McGeady testified that since he is not a neurologist, it “would not
be expected” for him to provide treatment to patients with TM. Tr. 133:11—17. He explained that
his testimony is instead limited to “the immunology of Petitioner[s’] theory of causation[.]” Tr.
133:18-20. Dr. McGeady noted that he has testified approximately thirty times in the Vaccine
Program. Tr. 134:1-3.

Dr. McGeady submitted three expert reports prior to the first entitlement hearing, and he
did not testify during the first part of the hearing as a result of Petitioners’ new theory of causation.
See Resp’t’s Exs. A, K, T. Following the break in proceedings, Dr. McGeady submitted two
additional reports, and subsequently testified during the second part of the hearing. Resp’t’s Exs.
JJ, MM; Tr. 129-185. Respondent offered Dr. McGeady as an expert in pediatric immunology,
pediatric clinical allergy/immunology, and pediatrics without objection, and I recognized him as
such. Tr. 134:20—25, 135:1-7.

B. Expert Reports and Testimony

1. Petitioners’ Expert, Dr. Schreiner

16
Dr. Teri Schreiner, R.S.’s treating neurologist, submitted a letter in support of Petitioners’
claim, and she did not testify at the entitlement hearing. Pet’r’s Ex. 71. She wrote that she has been
R.S.’s primary treating neurologist and “has been involved in her care since her presentation in
April[ of] 2013.” Jd. at 1. Dr. Schreiner thoroughly described her extensive qualifications in
pediatric demyelinating diseases and opined that “it is more likely than not that the immunizations
that [R.S.] received on March 18, 2013[,] were responsible for the immune response causing the
inflammation in her spinal cord.” /d. at 1-2. She wrote that “there is sufficient biologic evidence
(to be further detailed by Dr. Steinman) and circumstantial evidence to support this link.” /d. at 3.

She wrote that since 2013, she has seen R.S. “regularly to monitor her progress.” /d. at 2.
Dr. Schreiner indicated that she saw R.S. most recently on August 14, 2019. Jd. She described
R.S.’s condition consistent with the medical records from this visit, noting that R.S. “was able to
walk with bilateral walking aids. She had a wide-based [gait] with a pelvic tilt and [exhibited a]
flinging motion of her legs .. . toe-dragging . . . [and] impaired sensation to vibration bilaterally.”
Id. She continued that as a result, R.S. has difficulty ambulating, is at risk for falls, and will
“continue to require equipment (ankle braces, walking aides, etc.)[,] procedures (orthopedic
surgeries and [B]otox for spasticity)[,]” and PT. /d.

Regarding causation, Dr. Schreiner opined as to the mechanism by which a vaccine causes
TM. /d. She noted that “[o]ne of the most plausible explanations is molecular mimicry.” /d. Dr.
Schreiner explained that molecular mimicry “describes a process whereby a person 1s vaccinated
against a disease. The person[’s] immune system is ‘trained’ to fight that disease. However, the
immune system confuses the signatures and fights a similar-appearing se/f-protein.” Jd. (emphasis
in original). She continued that “[i]n the case of [TM], this is a protein in the spinal cord. The
inflammatory attack on the spinal cord damages the axons that transmit signals from the brain to
the body and sensations from the body to the brain.” Jd.

Dr. Schreiner discussed the time between R.S.’s vaccination and the onset of her TM. /d.
She wrote that “the timing of [TM two] weeks after vaccination would be consistent with an
immune-mediated attack as a result of vaccination.” /d. Dr. Schreiner also addressed potential
alternative causes for R.S.’s TM, such as infections and autoimmune diseases, and noted that the
testing for alternative causes of TM were negative. /d. She elaborated that R.S. did not have any
“known illnesses prior to the onset of [TM] to suggest an infectious trigger[]” and “[o]ver the [five]
years that [she] has cared for [R.S.], she has not developed any systemic signs of lupus or other
autoimmune disorder to implicate this as the cause of [R.S.’s TM].” Jd.

2. Petitioners’ Expert, Dr. Steinman

Dr. Steinman submitted five expert reports and testified during the hearing. See Pet’r’s Exs.
22, 46, 60, 97, 101; Tr. 46-107, 118-128, 187-194. In his first expert report, Dr. Steinman
concluded that R.S.’s “Prevnar 13 vaccine, by a preponderance of evidence, triggered [TM] in
[R.S.].” Pet’r’s Ex. 22 at 12. Dr. Steinman explained that this is possible because of the concept of
molecular mimicry. /d. at 5. He relied on a diagram,*” which “describes how shared structures on
a virus or bacteria or in a vaccine can trigger a cross-reactive response to [it]self]:]”

°° L,. Steinman, Autoimmune Disease, 269 SCIENTIFIC AMERICAN 106-14 (1993).

17
FOREIGN SELF-
HLA ANTIGENIC ANTIGENIC
\ PEPTIDE PEPTIDE

ae e

I Ce Lf

=, v4 WY =
J

rei @ presented by the HT.

HLA types, a fore
lar mimicry provokes the T cells

Id. (citing Pet’r’s Ex. 34, ECF No. 25-4). The diagram depicts how “T cells recognize foreign
antigens when they are presented by the HLA molecules of the immune system.” Pet’r’s Ex. 34 at
4. Dr. Steinman noted that “[i]Jn some people, especially those who have certain HLA types, a
foreign antigen may resemble antigen[s] produced by the body.” /d. He concluded that “[s]uch
molecular mimicry provokes the T cells to attack body tissues that contain the self-antigens.” /d.
Dr. Steinman continued that “[i]n autoimmune diseases, the immune system . . . mistakenly attacks
the body’s own tissue, causing inflammation and, in some cases, damage to myelin within the
spinal cord.” Pet’r’s Ex. 22 at 7. Based on this, he noted that “some scientists suggest that [TM]
may also be an autoimmune disorder.” /d. Dr. Steinman testified that ‘autoimmune’ and ‘immune-
mediated’ mean the same thing. Tr. 52:15—20.

He vehemently dismissed Dr. McGeady’s criticisms of his molecular mimicry theory,
noting that he “shall not debate whether molecular mimicry is a viable theory.” Pet’r’s Ex. 46 at
1. He wrote that he has “written about this [theory] in numerous peer reviewed publications . . .
testified about [it] in over twenty cases before this [C]ourt . . . [and i]n many cases[,].. .
prevailed[.]” /d.

Dr. Steinman described molecular mimicry in the context of an inflammatory condition of
peripheral nerves, Guillain-Barré syndrome (“GBS”).”° Pet’r’s Ex. 22 at 7. He wrote that
“phospholipids are seen in [GBS].” /d. He explained that “phospholipids are components of the
myelin sheath in humans, and that they are targeted by antibodies in neuroinflammation in the
central nervous system[.]” /d. (citing Pet’r’s Exs. 37, 38, ECF No. 25-5).*! He relied on an article
by Gilburd et al.,*? in which the authors found that ‘sixteen [GBS] sera were studied for the
presence of antibodies to... phosphatidyl-ethnolamine, phosphatidyl-choline, phosphatidylserine

*° Guillain-Barré Syndrome (“GBS”) is “rapidly progressive ascending motor neuron paralysis of unknown
etiology, frequently seen after an enteric or respiratory infection. An autoimmune mechanism following
viral infection has been postulated. It begins with paresthesias of the feet, followed by flaccid paralysis of
the entire lower limbs, ascending to the trunk, upper limbs, and face; other characteristics include slight
fever, bulbar palsy, absent or lessened tendon reflexes, and increased protein in the cerebrospinal fluid
without a corresponding increase in cells. Variant forms include acute autonomic neuropathy, Miller-Fisher
syndrome, acute motor axonal neuropathy, and acute motor-sensory axonal neuropathy.” Dorland’s at
1832.

“' J. Kanter, et al., Lipid Microarrays Identify Key Mediators of Autoimmune Brain Inflammation, 12:1
NATURE MEDICINE 138-43 (2006); P. Ho, et. al., Identification of Naturally Occurring Fatty Acids of the
Myelin Sheath that Resolve Neuroinflammation, 4 SCIENCE TRANSLATION MEDICINE 137-52 (2012).

” B. Gilburd, et al., Autoantibodies to Phospholipids and Brain Extract in Patients with the Guillain-Barré
Syndrome: Cross-Reactive or Pathogenic’, 16:1 AUTOIMMUNITY 23-27 (1993).

18
.. . [S]ix of the [sixteen] GBS sera had autoantibodies to one or more of the antigens studied.”’
Pet’r’s Ex. 22 at 7 (citing Pet’r’s Ex. 39, ECF No. 25-5). He further relied on an article by Ho et
al. to note that “[I]ipids constitute 70% of the myelin sheath, and autoantibodies against lipids
may contribute to the demyelination that characterizes multiple sclerosis (“MS”).” Pet’r’s Ex. 22
at 7 (citing Pet’r’s Ex. 38 at 1). The authors of the Ho et al.* article, including Dr. Steinman,
described an animal model of MS they used to “explore the role of identified lipids in autoimmune
demyelination.” See id. Dr. Steinman wrote that the authors “found that autoantibodies in MS
target a phosphate group in phosphatidylserine and oxidized phosphatidylcholine derivatives.”
Pet’r’s Ex. 22 at 7; see also Pet’r’s Ex. 38 at 1. He cited a diagram used in the Ho et al.* article,
which shows the “structure of phosphatidyl choline, phosphatidylserine[,] and the common
location of the polar head groups targeted by antibodies[:]”

B Polar head group
Nonpolar

side chains PC +

—?> *
—> ~

Ha"

Pet’r’s Ex. 22 at 8 (citing Pet’r’s Ex. 38 at 4). Based on the articles by Ho et al. and Gilburd et al.,
Dr. Steinman concluded that in diseases involving inflammation of the central nervous system
(“CNS”), as well as in inflammation of the peripheral nervous system, “there is evidence of an
antibody response to phosphotidyl [sic] choline structures.” Pet’r’s Ex. 22 at 8. Dr. Steinman then
opined that phospholipids are contained in the Prevnar 13 vaccine. /d. Based on this, he concluded
that it would “[t]hus [] be logical [] that a vaccine like Prevnar 13 would immunize the recipient
against this [phosphorylcholine] component of pneumococcus. And immunity to this phospholipid
[] is involved in neuroinflammation in both the central and peripheral nervous system.” Pet’r’s Ex.
22 at 8.

He discussed in detail his focus on the phospholipids contained in the PCV 13 vaccine, as
well as Dr. McGeady’s criticism that the vaccine does not contain phospholipids. Pet’r’s Ex. 22 at
8; Pet’r’s Ex. 46; Pet’r’s Ex. 60. At the entitlement hearing held in January of 2020, Dr. Steinman
conceded this point, and agreed that Dr. McGeady was correct in his assertion that the PCV 13
vaccine does not contain phospholipids. Tr. 61:6—9. Dr. Steinman altered his theory so that he no
longer relied on the presence of phospholipids in the Prevnar 13 vaccine. See Tr. 57:11—58:10. Dr.
Steinman clarified that he made a mistake in referring to phospholipids within his written reports.
Tr. 57:14-18 (citing Pet’r’s Exs. 22, 46, 60). He explained that he altered his theory on the stand
because he wanted to “help the Court get it right.” Tr. 79:15. This mistake in nomenclature
prompted Dr. Steinman to alter his theory and focus on the sugars (polysaccharides) in the vaccine,
rather than the fatty acids (phospholipids). Tr. 57:11-25, 58:1-3, 63:11-16. He testified that
instead of phospholipids, he “should have used the term ‘phosphoglycerol’ and called them

“SP. Ho, et. al., Identification of Naturally Occurring Fatty Acids of the Myelin Sheath that Resolve
Neuroinflammation, 4 SCIENCE TRANSLATION MEDICINE 137-52 (2012).

“4 See Ho, et. al., supra note 43.

See id.

19
‘phospho polysaccharides.’” Tr. 57:15—18. Dr. Steinman emphasized that the phosphoglycerol is
the target, not the phospholipid. Tr. 61:3—6. He maintained that the attack is still on the phospho
element of the molecule and Petitioners’ theory of causation does not change depending on
whether or not the molecule is a sugar or a fatty acid. Tr. 67:1—13, 69:21—25, 70:1—3. While this
case ultimately involves saccharides, Dr. Steinman incorporated many of his same arguments that
he originally posited regarding lipids. Dr. Steinman explained that his theory is therefore that “the
immune response to the phosphoglycerol or phosphocholine molecule in the Prevnar 13 vaccine
cross-reacts with the phosphoglycerate or phosphocholine head — polar head group in the
components of the myelin sheath[.]” Tr. 95:5—10.

Dr. Steinman relied on the similarities between cases of MS and TM and opined that the
phosphoglycerols attached to polysaccharides in the PCV 13 vaccine, cross-react with the
phosphoglycerols attached to the phospholipids in the spinal cord to cause TM. Tr. 60:16—-61:14.
To support his position, Dr. Steinman focused on the article by Ho et al.,*° wherein the authors
isolated the components and asked, “are there any structural features that allow us to see what the
[more] specific point of attack of the immune system was.” Tr. 56:22—25. He testified that they
found that the “point of attack” was a “phosphate group in a chemical structure that links these
complex molecules together . . . called glycerol.” Tr. 57:1-4. Specifically, the authors found that
the antibodies were “directly targeting the . . . phosphate glycerol polar group” in six out of seven
cases:

The arrows
represent the point
of attack on the
phosphate polar
head group of
phosphoglycerol,

as seen in six out aan re
of seven cases.

I
hs
12-DeropionssGhceros Prosprocmire F
; 7
“~" MG

1 Polenitcyt-2-Olnoyt ser-Gtycoro-3-Ethyipboaptwochctine &

a

Tr. 60:1—-19. Dr. Steinman broke it down even more and stated that “[i]t[ is] the phosphate on the
glycerol, so it’s targeting the phospho of the phosphoglycerol|[]” in patients with MS. Pet’r’s Ex.
97 at 6; Tr. 60:19-20. Dr. Steimman’s theory therefore focused on the phosphoglycerols in the
Prevnar 13 vaccine, independent of whether they are attached to a lipid, as seen in the case of MS,
or a saccharide carrier, like in the Prevnar 13 vaccine. See Tr. 67:1—13, 69:21—25, 70:1—3. Dr.
Steinman wrote that he “did specifv which epitope is shared by the CNS and the phosphoglycerol
molecule.” Pet’r’s Ex. 97 at 2 (emphasis in original). He elaborated on this and noted that the
immune system is making an antibody to either the saccharide attached to the Prevnar 13 vaccine
or the lipid in MS patients; the attack is still on the phosphate group. Pet’r’s Ex. 97 at 2-3 (citing
Tr. 89:4-15, 90:17).

46 See Ho, et. al., supra note 43.

20
Dr. Steinman explained why he compared MS with TM. Tr. 103:3—23. He stated that they
are both neuroinflammatory conditions of the CNS and “both can involve the spinal cord.” Tr.
103:12-13. He explained that “[t]he difference is that MS is a chronic life-long disease that
relapses and remits.” Tr. 103:15—16. Whereas TM “‘is most often . . . a one-time only disease.” Tr.
103:16-18. Dr. Steinman indicated that “one very important distinguishing criteria [sic]” for
diagnosis is the longevity of the disease. Tr. 103:19-23. He continued that MS is often
misdiagnosed as TM because “[w]hen it recurs, a person can say, ‘oh, the first attack of [TM] was
just the beginning of [] MS.”’ Tr. 103:24—25, 104:1—3. Dr. Steinman noted that “[y]ou really
can[not]” diagnose TM as distinct from MS prior to a relapse of TM. Tr. 104:23—25.

Dr. Steinman acknowledged on cross-examination that the Ho et al.*” article does not
discuss TM, but rather MS. Tr. 122:10—20. However, on rebuttal, Dr. Steinman noted that while
the authors discussed MS, they also discuss phosphoglycerol, which is listed in the U.S. patent for
the Prevnar 13 vaccine.** Tr. 190:4—11 (citing Pet’r’s Exs. 38, 96). Dr. Steinman disagreed with
Dr. McGeady’s contention that “phosphoglycerol is too small[]” to be immunogenic and that it
changes formation “depending on what[ is] attached to the phosphoglycerol.” Tr. 190:17—21. Dr.
Steinman stated that he has not “seen any data to support that,” but he noted that the Ho et al.*”
article “refutes that.” Tr. 190:21—23 (citing Pet’r’s Ex. 38). He explained that “it does[ not] matter
what the phosphoglycerol is attached to if they’re lipids. They could have long-chain fatty acids,
short-chain fatty acids. The immune system still, like a laser, hits the phosphoglycerol.” Tr.
190:24—25, 191:1-3.

He further relied on the U.S. patent for the Prevnar 13 vaccine”? and noted that it “refers to
the glycerol phosphate more than a dozen times|.|” Tr. 94:1—3 (citing Pet’r’s Ex. 96). Dr. Steimman
opined that it is “the lipids [] in the myelin sheath[ that are] attacked through th[e] same phosphate
head group on phosphoglycerol or on phosphocholine.” Tr. 96:1—7. He based his opinion on the
“shared structure and what[ is] known about how the immune system attacks the components of
the Prevnar [13] vaccine, and how [the immune system attacks the components of the myelin
sheath] in a human disease somewhat related to [TM] known as [MS.]” Tr. 96:1—7. Dr. Steinman
explained that this is possible because the glycerol phosphate in the polysaccharide of the Prevnar
13 vaccine is “identical” to the glycerol phosphate “that was the focus of the immune attack in MS
when [the] glycerol phosphate was holding it on to the lipid.” Tr. 90:25, 91:1—2; see also Pet’r’s
Ex. 60 at 2-3. Dr. Steinman provided diagrams of the molecular structures of phosphoglycerol and
glycerophospholipids:

Phosphoglycerol Glycerophospholipid
pP ono-b- R’
HO _- > 9 | 2
\ R-C-O-CH 06
© bu-o-heoz
HO a |
oN
Polar head group Polar head group

‘7 See Ho, et. al., supra note 43.

48 U.S. Patent No. 9.492.559 B2 (filed Nov. 15, 2016).
* See Ho, et. al., supra note 43.

°° See U.S. Patent, supra note 48.

21
Pet’r’s Ex. 60 at 2-3.

Regarding the Prevnar 13 vaccine specifically, Dr. Steinman explained that in the vaccine,
“it[ is] the sugars of the pneumococcus coupled to this phosphoglycerol.” Tr. 62:15—17. Dr.
Steinman relied on the package insert?! for the Prevnar 13 vaccine that noted that “[t]he
pneumococcal 13-valent conjugate vaccine 1s a sterile suspension of the capsular polysaccharide
antigens of Streptococcus pneumoniae [“s. pneumoniae” serotypes 1, 3, 4, 5, 6A, 6B, 7F, 9V, 14,
18C, 19A, 19F, and 23F individually conjugated by reductive amination to the non-toxic diphtheria
CRM197 protein.” Pet’r’s Ex. 35 at 1, ECF No. 25-4. Based on this, Dr. Stemman maintained that
“it is unmistakably clear that the Prevnar 13 [vaccine] contains ‘capsular polysaccharide antigens
of Streptococcus pneumonia.’” Pet’r’s Ex. 46 at 2 (citing Pet’r’s 35 at 1).

He also relied on the Lugowski et al.** article to note that “there is explicitly . . . a
phosphoglycerol attached to a galactoside in the 18C pneumococcal sugar.” Tr. 62:19-23 (citing
Pet’r’s Ex. 53, ECF No. 30-8). The Lugowski et al. article contains a description and diagram of
the molecular structure of the streptococcus pneumoniae serotype 18C “written in words.” Pet’r’s
Ex. 53 at 1; Tr. 90:14—16. It indicates that there is a phosphorous containing molecule in the
streptococcus pneumoniae polysaccharide capsule of serotype 18C, which is contained in the
current pneumococcal vaccine:

The specific capsular polysaccharide of Streptococcus pneumoniae type 18C
(56) contains D-glucose, D-galactose, L-rhamnose, and glycerol residues, and phos-
phate and O-acety! groups in the molar ratios of 3:1:1:1:1:1. Accumulated data
from methylation analyses of the native and the specifically degraded, native
polysaccharide indicated that it is composed of the repeating unit shown; it also
contains O-acetyl groups, of undetermined location, in the molar ratio to L-rham-

nose of 1:1.
a-D-Glep
1
{
2
Phosphoglycerol —>-4)B-D-Giqp(1-+4)B-D-Galp(1+4)a-D-Giep(13)a-L-Rhap(1>
polar head group ;
Oo
|
Glycerol-1-P-OH
ll
oO

Pet’r’s Ex. 53 at 2. Dr. Steinman further relied on the diagram contained in the Chang et al.”
article, which, without words, shows “the [same] capsular polysaccharide in streptococcus
pneumonia serotype 18C[:]”

*! Preynar-13 Package Insert, FOOD & DRUG ADMINISTRATION (https://www.fda.gov/vaccines-blood-
biologics/vaccines/prevnar-13).

» C. Lugowski & H. Jennings, Structural Determination of the Capsular Polysaccharide of Streptococcus
Pneumoniae Type 18C, 131 CARBOHYDRATE RES. 119-29 (1984).

3 J. Chang, et al., Relevance of O-acetyl and Phosphoglycerol Groups for the Antigenicity of Streptococcus
pneumoniae Serotype 18C Capsular Polysaccharide, 30 VACCINE 7090-96 (2012).

22

Phosphoglycerol hea
polar head group Ta
py

Tr. 88:9-18 (citing Pet’r’s Ex. 52 at 2). He used the diagram to point out the phosphate group,
which serves as “part of the anchor to the [] phosphoglycerol component.” Tr. 88:17—22. He stated
that without that, “18C would have no immunogenicity.” Tr. 88:24—25. The authors of the Chang
et al. article found that “[t]he loss of these [phospho polar head] groups may potentially reduce the
ability of the 18C polysaccharide to induce the desired immune response.” Pet’r’s Ex. 52 at 1. The
authors concluded that “[t]he linkage is a central component of the 18C polysaccharide structure”
and the “glycerol phosphate [group] must be preserved for conserving adequate antigenicity of the
18C capsular polysaccharide[]” contained in the PCV 13 vaccine. Jd. Dr. Steinman opined that
“ijt is doubtful that the preparatory procedures for purifying 18C capsular polysaccharide[s]
would destroy covalent linkages.” Pet’r’s Ex. 46 at 4. As support, he noted that “removal of the
covalent chemical linkage of the phosphate group would be unlikely because it would reduce the
immunogenicity of the vaccine itself.” Jd. at 5 (citing Pet’r’s Ex. 52).

Dr. Steinman then relied on the Chuang et al.** article, which “describe[s] a phosphate
choline in the polar group in the serotype 19A of the streptococcus pneumonia bacteria.” Tr. 93:2—
5 (citing Pet’r’s Ex. 40 at 1, ECF No. 25-5). Dr. Steinman testified that the importance of the
phosphocholine molecule to streptococcus pneumonia serotype 19A is that its presence “increases
the severity of the pneumonia that pneumococcus can cause.” Tr. 93:16—22. The authors of the
Chuang et al. article found that the phosphorylcholine polar head group in serotype 19A of s.
pneumoniae is critical to the success of the infection in serotype 19A. Pet’r’s Ex. 40 at 1. Dr.
Steinman explained that this means an effective vaccine against serotype 19A must also generate
an immune response to that head group. Tr. 93:19-24. He concluded, using these articles as
support, that if there is “no phosphoglycerol, [there would be] no good immune response, even to
the polysaccharides[]” because the attack is on that phospho polar head group. Tr. 191:5—9. He
explained that if “[y]ou take [the phosphoglycerol] away, you lose the immunogenicity.” Tr.
58:13—14. He maintained based on the medical literature that the phosphoglycerol “is the vital
connection to keep in the vaccines. If it[ is] taken away . . . it loses immunogenicity[,]” and “of
course, you want a vaccine to be immunogenic.” Tr. 58:6—13, 61:10—14, 63:6—7 (citing Pet’r’s
Exs. 40, 52, 53).*°

* Y. Chuang, et al., Impact of the glpQ2 Gene on Virulence in a Streptococcus pneumoniae Serotype 19A
Sequence Type 320 Strain, 83 INFECTION & IMMUNITY 682-92 (2015).

> Y. Chuang, et al., Impact of the glpQ2 Gene on Virulence in a Streptococcus pneumoniae Serotype 19A
Sequence Type 320 Strain, 83 INFECTION & IMMUNITY 682-92 (2015); J. Chang, et al., Relevance of O-
acetyl and Phosphoglycerol Groups for the Antigenicity of Streptococcus pneumoniae Serotype 18C
Capsular Polysaccharide, 30 VACCINE 7090-96 (2012): C. Lugowski & H. Jennings, Structural

23
Dr. Steinman noted that “the antibody arm of the immune system precisely recognizes
small structures[]” such as “the ‘small’ phosphate polar head group that is present in the CNS.”
Pet’r’s Ex. 101 at 4. Since the same phosphate polar head group is also present in Prevnar 13, this
fact “strongly suggests that it could trigger a cross-reactive immune response to the CNS[.]” /d.
He maintained that “[t]his theory therefore describes how components of Prevnar 13 can elicit
cross-immunity to components of the myelin sheath that are known to be targeted in inflammation
in the central nervous system resulting in [TM].” Pet’r’s Ex. 22 at 9.

Dr. Steinman further addressed the points raised in Dr. McGeady’s report and noted that
Dr. McGeady presumed the wrong polysaccharide in the Prevnar 13 vaccine. Pet’r’s Ex. 97 at 3.
Dr. Steinman wrote that the large carrier molecule in the Prevnar 13 vaccine is not the
polysaccharide capsule of one or two pneumococcal serotypes, it is the diphtheria CRM protein.
Id. He relied on the package insert*® for Prevnar 13 to support this conclusion. /d. (citing Pet’r’s
Ex. 35 at 25). Dr. Steinman also relied on the e-mail response he received from the Center for
Disease Control (“CDC”), which “clearly state[d] that the [d]iphtheria CRM protein is the
carrier[]” protein. Pet’r’s Ex. 97 at 4—5; see also Pet’r’s Ex. 60 at 4.

He then responded to Dr. McGeady’s assertion that “the immune system produc[ing]
antibod[ies] promiscuously to molecules such as phosphoglycerol regardless of their molecular
position[] ignore[d] the complexity of antibody production ....” Pet’r’s Ex. 101 at 1. He continued
that “[t]he precision of antibodies is exquisite and the phosphate polar head group on the glycerol
was targeted regardless of what its attachments were.” /d. at 2 (citing Pet’r’s Ex. 38). Dr. Steinman
noted that his opinion relied on “actual experimental evidence presented in an outstanding peer
reviewed journal, not on generalities about the ‘promiscuity’ of antibody antigen interaction.” See
id. Dr. Steinman opined that Dr. McGeady “engage[d] in generalities about the immune system
and its specificities[.]” Pet’r’s Ex. 101 at 1. He relied on an article by Pinto et al.,°’ to demonstrate
the specificity of antibodies to even small sugars. Pet’r’s Ex. 97 at 8 (citing Pet’r’s Ex. 100, ECF
No. 95-5). The authors analyzed the neutralizing antibody to the spike protein in SARS CoV-2 and
noted that it “actually binds a sugar, called fucose, on the spike protein.” Pet’r’s Ex. 97 at 6 (citing
Pet’r’s Ex. 100 at 7). They found that the antibody binding regions, called complementarity
determining regions (“CDRs”), “sandwich the SARS-CoV-2 glycan . . . through contacts with the
core fucose moiety[.]” Pet’r’s Ex. 100 at 3. Dr. Steinman explained that “[s]mall molecules are
targeted by the immune system when they are conjugated to a carrier. In MS, the carriers [] are the
myelin proteins.” Pet’r’s Ex. 97 at 6 (citing Pet’r’s Ex. 38); Tr. 57:9-10, 60:7—20. He continued
that “[i]t is known that the surface area of [an antibody] has only a small portion of the antibody
surface that contacts a small portion of the antigen.” Pet’r’s Ex. 97 at 6. Based on this, Dr. Steinman
wrote that “the capacity of an antibody to bind a small sugar or a small molecule like
phosphoglycerol is not unusual.” Jd.

Dr. Steinman discussed Dr. McGeady’s assertion that TM is more suggestive of a cell-
mediated damage than it is of an antibody-mediated injury. Pet’r’s Ex. 60 at 6. He wrote that “Dr.

Determination of the Capsular Polysaccharide of Streptococcus Pneumoniae Type 18C, 131
CARBOHYDRATE RES. 119-29 (1984).

°° See Prevnar-13 Package Insert, supra note 51.

°7 —D. Pinto, et al., Cross-neutralization of SARS-CoV-2 by a Human Monoclonal SARS-CoV Antibody,
NATURE https://doi.org/10.1038/s41586-020-2349-y (2020).

24
McGeady is incorrect on this.” /d. He testified that “[TM] is never just cell-mediated, nor 1s it ever
just antibody-mediated.” Tr. 188:2—4. Dr. Steinman explained that an “[a]ntibody mediated injury
is a cornerstone of our understanding of [TM].” Pet’r’s Ex. 60 at 6. He relied on an article by
Kaneko et al.,>* to highlight that TM “is driven by antibodies to either [aquaporin 4 (“AQP4”)] or
to myelin oligodendrocyte glycoprotein [(“MOG’”)].” /d. (citing Pet’r’s Ex. 65 at 1, ECF No. 45-
7). The authors noted that “[w]hether MOG-IgG is pathogenic and directly involved in the
pathogenesis is not fully understood, but some recent studies support MOG-IgG’s pathogenicity.”
See id. They continued, “[flor example, MOG-IgG can induce alteration of oligodendrocyte
cytoskeleton organization in vitro . . . biopsied cases showed there were depositions of IgG and
complements associated with demyelination in the lesions of cases with MOG-IgG+ disease[.]”
Pet’r’s Ex. 65. Dr. Steinman wrote that this “is consistent with the MS pattern IT pathology and
suggests a pathogenic role for humoral immunity in the lesion formation.” Pet’r’s Ex. 60 at 6.

Dr. Steinman applied his theory to the facts of R.S.’s case. Pet’r’s Ex. 22 at 6. He again
cited the package insert’ for the Prevnar 13 vaccine and reiterated its contents, including
saccharides of capsular antigens of s. pneumoniae serotypes 18C and 19A. /d. (citing Pet’r’s Ex.
35 at 1). He noted that to manufacture the vaccine, “[t]he individual polysaccharides are purified
through centrifugation, precipitation, ultrafiltration, and column chromatography. The
polysaccharides are chemically activated to make saccharides, which are directly conjugated by
reductive amination to the protein carrier CRM197, to form the glycoconjugate.” See id. The
package insert explains that “[t]he individual glycoconjugates are compounded to formulate
Prevnar 13.” See Pet’r’s Ex. 35. It continues that “[p]otency of the formulated vaccine is
determined by quantification of each of the saccharide antigens and by the saccharide to protein
ratios in the individual glycoconjugates.” Jd.

He relied on the TM fact sheet from the National Institute of Neurological Disorders and
Stroke (“NINDS”), which notes that TM “may be an autoimmune disease and may be triggered
by vaccines.” Pet’r’s Ex. 22 at 6 (citing Pet’r’s Ex. 36 at 1, ECF No. 25-5). The fact sheet notes
that “[r]esearchers are uncertain of the exact causes of [TM]. The inflammation that causes such
extensive damage to nerve fibers of the spinal cord may result from viral infections or abnormal
immune reactions.” See id. It continues that “[i]nfectious agents suspected of causing [TM] include

8K. Kaneko et al., CSF Cytokine Profile in MOG-IgC+ Neurological Disease is Similar to AQP4-IgC+
NMOSD but Distinct from MS: a cross-sectional study and potential therapeutic implications, 0:0 J.
NEUROL. NEUROSURG. PSYSCHIATRY 1-10 (2018).

»° See Prevnar-13 Package Insert, supra note 51.

°° Transverse Myelitis Fact Sheet, NAT'L INST. OF NEURO. DISORDERS & STROKE

(http://www .ninds .nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Transverse-Myelitis-Fact-
Sheet).

25
varicella zoster®! .. . herpes simplex,°” cytomegalovirus, °’ Epstein-Barr, influenza, echovirus,°
[HIV], hepatitis A, [] rubella[,°’ bJacterial skin infections, middle ear infections (otitis media),
and [bacterial pneumonia.]” Pet’r’s Ex. 36 at 1. It also notes that “[TM] may also occur as a
complication of . . . vaccinations, including those for chickenpox and rabies.” /d. Dr. Steinman
noted additional support for TM being an autoimmune condition. Pet’r’s Ex. 22 at 7. He wrote that
some individuals with TM also have other autoimmune diseases such as “systemic lupus
erythematosus,°* Sjégren’s syndrome,” and sarcoidosis[.]”’° /d.

Dr. Steinman noted evidence supporting his conclusion that R.S. experienced an
autoimmune reaction to the Prevnar 13 vaccine resulting in TM. Pet’r’s Ex. 60 at 1. He testified
that R.S.’s TM was “[m]Jost certainly” an inflammatory TM. Tr. 51:12—14. He relied on R.S.’s
abnormal spinal fluid results (“slightly elevated” at 48) from April 2, 2013. Pet’r’s Ex. 60 at 1
(citing Pet’r’s Ex. 10 at 47; Pet’r’s Ex. 9 at 3); see also Tr. 98:7-10. Dr. Steinman cited a study by

*! Varicella zoster is “a virus of the genus ‘varicellovirus’ that is the etiologic agent of chickenpox and
herpes zoster.” Dorland’s at 2065.

° Herpes simplex virus is “a group of acute infections caused by human herpesviruses | and 2, characterized
by small fluid-filled vesicles on the skin or a mucous membrane with a raised erythematous base; it may be
a primary infection or recurrent because of reactivation of a latent infection . . . Precipitating factors include
fever, exposure to cold temperature or ultraviolet rays, sunburn, cutaneous or mucosal abrasions, emotional
stress, and nerve injury.” Dorland’s at 2062.

° Cytomegalovirus “infect[s] humans and nonhuman primates, with the production of unique large cells
bearing intranuclear inclusions. It includes the species human herpesvirus 5[.|” Dorland’s at 466.

* Epstein-Barr is also referred to as human herpesvirus 4. Dorland’s at 2061. Human herpesvirus 4 is “a
virus of the genus lymphocryptovirus that causes infectious mononucleosis[.|” Jd. at 852-53.

°° Echovirus is “any of numerous species and strains of the family Picornaviridae, some of which cause
aseptic meningitis or a febrile rash[.]” Dorland’s at 590.

°° Hepatitis A is “a usually self-limited viral disease of worldwide distribution caused by the hepatitis A
virus, more prevalent in areas of poor hygiene and low socioeconomic standards. It is transmitted almost
exclusively by the fecal-oral route, although parenteral transmission is possible; there is no carrier state.
The incubation period is about 30 days, with a range of 15 to 50 days. Most cases are clinically inapparent
or have mild flulike symptoms; jaundice, if present, is usually mild.” Dorland’s at 844.

°7 Rubella is “an acute, usually benign, infectious disease caused by viruses of genus Rubivirus, . . . affecting
most often children and nonimmune young adults. The virus enters the respiratory tract via droplet nuclei
and spreads to the lymphatic system. The first symptoms are a slight cold, sore throat, and fever, followed
by enlargement of the postauricular, suboccipital, and cervical lymph nodes, and later appearance of a fine
pink rash that begins on the head and spreads to become generalized.” Dorland’s at 1657.

8 Lupus erythematosus is the “name formerly given to numerous types of localized destruction or
degeneration of the skin caused by cutaneous diseases|.]” Dorland’s at 1079.

°° Sjogren’s syndrome is “a symptom complex of unknown etiology, usually occurring in middle-aged or
older women, marked by the triad of keratoconjunctivitis sicca with or without lacrimal gland enlargement,
xerostomia with or without salivary gland enlargement, and the presence of a connective tissue disease,
usually rheumatoid arthritis but sometimes systemic lupus erythematosus, scleroderma, or polymyositis.
An abnormal immune response has been implicated.” Dorland’s at 1848.

” Sarcoidosis is “a chronic, progressive, systemic granulomatous reticulosis of unknown etiology,
characterized by hard tubercles . . . It can affect almost any organ or tissue, including the skin, lungs, lymph
nodes, liver, spleen, eyes, and small bones of the hands and feet.” Dorland’s at 1668. Reticulosis is “an
abnormal increase in cells[.|” Jd. at 1632.

26
Al Deeb et al.,”! which provided a study on TM, including a “review of CSF [levels] in [thirty-
two] patients, [two] were normal, and the remainder were abnormal.” Pet’r’s Ex. 60 at 1 (citing
Pet’r’s Ex. 62 at 1, ECF No. 45-4). The authors found that “[c]ells were raised in [twenty-six
patients]... they were predominantly lymphocytes in all patients, and protein was high in [twenty-
eight patients.]” Pet’r’s Ex. 62 at 3. Dr. Steinman compared this study to R.S. and noted that her
“protein was high and [her] cells were normal[.]” Pet’r’s Ex. 60 at 2; see also Tr. 49:1—7. He
opined that “these findings indicate an abnormal CSF and what is seen when there is
neuroinflammation.” Pet’r’s Ex. 60 at 2.

He also relied on R.S.’s April 2, 2013 MRI findings which “definitively showed [T.]”
Id. (citing Pet’r’s Ex. 10 at 47). Dr. Steinman wrote that “[b]y history, CSF findings and imaging[, ]
there is evidence of an inflammatory response in the central nervous system known as [TM].”
Pet’r’s Ex. 60 at 2. As further support, he also noted that R.S. received three treatments that are
“aimed at treating inflammatory disease[s] of the spinal cord[,]” including IV steroids, IVIG, and
plasmapheresis. Tr. 49:7—21. Dr. Steinman also noted that “infectious etiologies were ruled out by
testing,” including R.S.’s CSF and comprehensive metabolic panel. Pet’r’s Ex. 60 at 2 (citing
Pet’r’s Ex. 9 at 7, 9, 13-14). Dr. Steinman therefore concluded that R.S.’s diagnosis is an
inflammatory autoimmune TM. Pet’r’s Ex. 60 at 2.

Dr. Steinman also wrote that “[t]he extensive [TM] from C2 to T4 [in R.S.] was likely the
result of the strong recall response to the third dose of Prevnar 13 on March 18, 2013.” Pet’r’s Ex.
22 at 9. He noted the dates of R.S.’s earlier doses of Prevnar 13 and explained that antibodies to
such phosphoglycerols in the vaccine could indeed interact with myelin components in the spinal
cord, triggering TM. Tr. 52:23-25, 53:1-3; see also Pet’r’s Ex. 6 at 1. He testified that the cause
of R.S.’s TM was “a component in the Prevnar 13 vaccine that is critical for its immunogenicity .
.. and the immune system attack[ed] one of the components of the vaccine.” Tr. 52:23—25, 53:1-
3. Dr. Steinman explained that he based this opinion on “three different levels of research.” Tr.
53:4—5. He relied on investigations in his lab that have been published in peer-reviewed journals,
the composition of the Prevnar 13 vaccine as described on the package insert, and a comparison
between the immune response in MS and TM. Tr. 53:4—20.

From there, Dr. Steinman indicated that R.S. received the Prevnar 13 vaccine on March 18,
2013, and experienced the onset of TM “within two weeks[.]” Pet’r’s Ex. 22 at 9. Specifically, he
testified that R.S. developed the first symptoms of TM “around April 1°[.]” Tr. 50:2-4. Dr.
Steinman stated that “thirteen days between [R.S.’s] immunization . . . would be right in the
bullseye of when neuroinflammatory conditions are likely to [] manifest.” Tr. 99:9-13. He wrote
that this timeframe is “entirely consistent with what is seen following immunization and the onset
of central nervous inflammation in acute disseminated encephalomyelitis [““ADEM”)”].” Pet’r’s

7! $M. Al Deeb et al., Acute Transverse Myelitis — A Localized Form of Postinfectious Encephalomyelitis,
120 BRAIN 1115-997 (1997).

” Acute disseminated encephalomyelitis (“ADEM”) is “an acute or subacute encephalomyelitis or myelitis
characterized by perivascular lymphocyte and mononuclear cell infiltration and demyelination; it occurs
most often after an acute viral infection, especially measles, but may occur without a recognizable
antecedent. It is believed to be a manifestation of an autoimmune attack on the myelin of the central nervous
system. Symptoms include fever, headache, and vomiting; sometimes tremor, seizures, and paralysis; and

27
Ex. 22 at 10 (citing Pet’r’s Ex. 44, ECF No. 25-5). Dr. Steinman relied on the article by Bennetto
and Scolding, which noted that the timing of the first symptoms of ADEM post vaccination “varies
slightly with the precipitant: [] 1-14 days after non-neural vaccines, .. . and 1-3 weeks (or more)
after rabies inoculation.” Pet’r’s Ex. 44 at 3. Dr. Steinman also relied on the study by Schonberger
et al," which describes the onset time for GBS following the 1976 HINI flu vaccination. Pet’r’s
Ex. 22 at 10 (citing Pet’r’s Ex. 45, ECF No. 25-5). The authors found that there was an increased
risk for developing GBS up to six weeks and “even in weeks two and three” post vaccination.
Pet’r’s Ex. 22 at 11. They wrote that “[71%] of the vaccinated cases... became ill within the first
four weeks after vaccination and 52[%] in the second and third weeks after vaccination.” Pet’r’s
Ex. 45 at 6. They explained that “[b]y two-day intervals between vaccination and onset, the largest
percentage of cases (10%) occurred on the 16" and 17" days after vaccination[.]’ Jd. at 6-7. Dr.
Steinman admitted that neither cited example covers the Prevnar 13 vaccine or TM, specifically.
Pet’r’s Ex. 22 at 12. He wrote that he “think[s] these are weak surrogates for [TM] and Prevnar
13, but it is the best we can use at this point in this context.” Jd.

Dr. Steinman admitted that infections “sometimes trigger [TM.]” Tr. 99:24—-25, 100:1. He
described post-infectious cases of TM. Pet’r’s Ex. 22 at 7. He wrote that in post-infectious cases,
“immune system mechanisms, rather than active viral or bacterial infections, appear to play an
important role in causing damage to spinal nerves.” /d. He explained that “stimulation of the
immune system in response to infection indicates that an autoimmune reaction may be
responsible[]” for post-infectious TM. /d. He nonetheless awarded the Prevnar 13 vaccine “a
higher probability” of triggering TM in R.S. compared to “an unknown, [R.S.’s] recurrent
respiratory infection[.]” Pet’r’s Ex. 46 at 5.

On cross-examination, Dr. Steinman admitted that he has never diagnosed a patient with
TM attributed to the Prevnar 13 vaccine or published on the same. Tr. 118:13-17. Dr. Steinman
acknowledged that his submitted medical literature does not discuss molecular mimicry with
respect to the Prevnar 13 vaccine and TM. Tr. 123:24—25, 124:1-2. However, he stated that while
such literature does not “directly” discuss this concept, “the nuanced answer is” that it “lead[s] you
right up to the gate.” Tr. 124:3-7 (citing Pet’r’s Exs. 38, 52). He further conceded that his provided
medical literature does not contain case reports regarding a patient developing TM after the
Prevnar 13 vaccine. Tr. 122:21—25, 123:1—17. Dr. Steinman was also confronted with the Chang
et al.”° article, which Respondent argued did not indicate that without phosphoglycerol, the vaccine
would lose immunogenicity. Tr. 127:8—13 (citing Pet’r’s Ex. 52). To support his conclusion, Dr.
Steinman read verbatim from the Chang et al. abstract, stating that ““the loss of these groups. . .
[glycerol phosphate and the O-acetyl group] may potentially reduce the ability of the 18C
polysaccharide . . . to induce the desired immune response.”’ Tr. 127:18—23 (citing Pet’r’s Ex. 52
at 1). He read that the “glycerol phosphate must be preserved for conserving adequate antigenicity
of the 18C capsular polysaccharide.”’ Tr. 127:25, 128:1-2 (citing Pet’r’s Ex. 52 at 1).

lethargy progressing to coma that can be fatal. Many survivors have residual neurologic deficits.” Dorland’s
at 613.

® LL. Bennetto & N. Scolding, Inflammatory/Post-Infectious Encephalomyelitis, 75 J. NEUROL.
NEUROSURG. PSYCH. 22-28 (2004).

™ L. Schonberger, et al., Guillain-Barré Syndrome Following Vaccination in the National Influenza
Immunization Program, United States, 1976-1977, 110:2 AM. J. EPIDEMIOL. 105-24 (1979).

™® See Chang, et. al., supra note 53.

28
On rebuttal, Dr. Steinman noted that the focus of his research for the last forty years has
been on “how the immune system attacks the brain... and spinal cord in [TM.]” Tr. 187:7-14.
Dr. Steinman stated that the major difference between the way he views this case as compared to
Dr. McGeady, is that he “based Petitioners’ theory on actual data.” Tr. 189:6-7. He admitted,
however, that “the data are imperfect.” Tr. 189:7.

3. Respondent’s Expert, Dr. McGeady

Dr. McGeady submitted five expert reports and testified at the entitlement hearing. See
Resp’t’s Exs. A, K, T, JJ, MM; Tr. 129-185. In his first report, Dr. McGeady concluded with a
reasonable degree of medical certainty that the Prevnar 13 [vaccine] received by [R.S.] on [March
18, 2013,] did not cause her to develop TM on [April 1, 2013].” Resp’t’s Ex. A at 9; Resp’t’s Ex.
K at 5. He noted his issues with Dr. Steinman’s theory of molecular mimicry. Resp’t’s Ex. A at 4.
Dr. McGeady wrote that Dr. Steinman “has embraced the phenomenon of molecular mimicry as a
cause of disease for many years.” /d. He noted, however, that “[h]is enthusiasm is not shared by
all investigators[.|” /d. He testified that Dr. Steinman’s theory of molecular mimicry causing TM
has not been “convincingly proven.” Tr. 166:1—3. He continued that “it is inaccurate to imply, as
Dr. Steinman seems to do, that molecular mimicry is a common and well-established mechanism
of autoimmune disease, or that it has ever been demonstrated to be a cause of TM.” Resp’t’s Ex.
K at 2. Dr. McGeady cited three articles to support his opinion that “[i]n the absence of more
compelling evidence, authorities in the field of autoimmunity are quite circumspect about
accepting molecular mimicry as a pathophysiologic mechanism[.]” Resp’t’s Ex. A at 4 (citing
Resp’t’s Exs. C, D, E, ECF Nos. 29-3-29-5).”°

Dr. McGeady noted his concerns with Dr. Steinman’s first proposed theory prior to the
entitlement hearing in January of 2020. He wrote that Dr. Steinman’s “assertion appears to say
that the Prevnar 13 vaccine[] contains phospholipid antigens which elicit [an] antibody that is
capable of cross reacting with phospholipids in the CNS[,] resulting in TM.” Resp’t’s Ex. A at 6.
He continued that the problem with Dr. Steinman’s theory is that it “infers that the Prevnar 13
[vaccine] actually contains phospholipids or pneumococcal organisms capable of producing
phospholipids.” /d. Dr. McGeady cited Dr. Steinman’s reliance on the Prevnar 13 package insert
which describes the process of manufacturing the Prevnar 13 vaccine. /d. (citing Pet’r’s Ex. 22 at
6; Pet’r’s Ex. 35). He noted that the package insert indicates that “[t]he individual polysaccharides
are purified through centrifugation precipitation, ultrafiltration[,] and column chromatography.”
Resp’t’s Ex. A at 6 (citing Pet’r’s Ex. 35). Dr. McGeady wrote that while he does “not dispute the
fact that some pneumococci synthesize phospholipids in their biologic cycle .. . [he] could not
find any statement that the phospholipids are actually present in the Prevnar 13 vaccine.” Resp’t’s
Ex. A at 6. As support, he noted that as the “Prevnar 13 [vaccine] contains a suspension of
saccharides of capsular antigens that have been extensively purified by biochemical techniques,
and does not contain intact organisms, it would seem probable that there are no phospholipids in
the vaccine.” /d. Based on this, Dr. McGeady opined that “[t]heir absence would reject Dr.
Steinman’s hypothesis of molecular mimicry.” Jd.

7°L, Albert, et al., Molecular Mimicry and Autoimmunity, 341 N. ENGL. J. MED. 2068-74 (1999); M.B.A.
Oldstone, Molecular Mimicry, Microbial Infection, and Autoimmune Disease: Evolution of the Concept,
296 CTMI 1-17 (2005); N. R. Rose, Learning from Myocarditis: Mimicry, Chaos and Black Holes, 6 F1000
PRIME REP. 25-25 (2014).

29
Dr. McGeady criticized Dr. Steinman’s reliance on the Chang et al.”’ article to support his
conclusion. Resp’t’s Ex. K at 3 (citing Pet’r’s Ex. 52). He noted that the Chang et al. article showed
“that the phosphoglycerol group in the S. pneumoniae 18[C] organism is essential to maximal
immunogenicity.” See id. He explained that the “phosphoglycerol group found in the [S].
pneumonia 18[C] polysaccharide does not constitute a phospholipid.” Resp’t’s Ex. K at 3. Instead,
Dr. McGeady noted that “[a] phospholipid is a complex molecule which consists of a
phosphoglycerol group (i.e.[,] a molecule of glycerol to which a molecule of phosphoric acid has
become attached), and usually two chains of long chain fatty acids[.]” Resp’t’s Ex. T at 2. Dr.
McGeady continued that the structures described in Dr. Steinman’s report “demonstrate a
phosphoglycerol group, but this is not the same as a phospholipid.” Resp’t’s Ex. K at 4 (citing
Pet’r’s Exs. 46, 52). He continued that the “phosphoglycerol group in the pneumococcal 18[C]
polysaccharide does not include the fatty acid and therefore does not constitute a phospholipid.”
Resp’t’s Ex. T at 2. He maintained that Dr. Steinman’s theory “does not demonstrate the presence
of phospholipids in the polysaccharide.” /d. at 3. Dr. McGeady also criticized Dr. Steinman’s
reliance on the Chang et al. article because the “polysaccharides in that study [were] conjugated
to tetanus toxoid[,] while Prevnar [13] 1s a diphtheria toxoid conjugate.” Resp’t’s Ex. K at 4 (citing
Pet’r’s Ex. 52). He opined that the “differences in the resulting vaccines could lend different
relevance to the putative immunogenicity of the phosphoglycerol group.” Resp’t’s Ex. K at 4.

Then, Dr. McGeady responded to Dr. Steinman’s direct testimony whereby he altered his
theory to focus on “the phosphoglycerol moiety of the Prevnar 13 vaccine” being necessary for
maximum vaccine antigenicity instead of phospholipids. Resp’t’s Ex. JJ at 1. He addressed Dr.
Steinman’s contention “that phosphoglycerol constitutes a shared epitope with structures in the
human [CNS].” /d. Dr. McGeady noted that Dr. Steinman “d[id] not, and indeed cannot, specify
which epitope he speculates is shared with the CNS.” /d. Dr. McGeady opined that “an epitope
shared between the CNS and the vaccine Prevnar 13 cannot be specified, because it would have to
consist of a phosphoglycerol group in conjunction with a polysaccharide found within the CNS to
match that in the vaccine.” Resp’t’s Ex. MM at 2. He wrote that “[s]uch a structure is not known.”
Id.

Dr. McGeady maintained that the issue with Petitioners’ theory is that “the
phosphoglycerol or phosphocholine is connected to a lipid in the human CNS and a saccharide in
the Prevnar vaccine[.]” Tr. 141:10—14. He opined that “those two [molecules] would be perceived
differently by the immune system.” Tr. 141:14-15. He also maintained that this is because the
antibody is “very discriminating in what it recognizes[]” and “the production and function of the
antibody” is not only dependent on recognizing the phospho head, but also what it is attached to.
Tr. 161:24—25, 162:1-5. Dr. McGeady noted that in Dr. Steinman’s hypothesis, “the large carrier
molecule in Prevnar 13 would presumably be the polysaccharide capsule of one or two
pneumococcal serotypes with the phosphoglycerol component[.]”’ Resp’t’s Ex. JJ at 2. Dr.
McGeady compared this to the antibody generated in patients with MS, as mentioned by Dr.
Steinman, which recognizes phosphocholine attached to “some component of the human CNS[.]”
Id. He wrote that the antibody in patients with MS “would certainly be different from [the]
pneumococcal polysaccharide[]” found in the Prevnar 13 vaccine. /d. He noted that “when you
look at phosphocholine or phosphoglycerol as it appears in the polysaccharide vaccine, it’s one
way, and an antibody made to that is... . going to recognize that configuration.” Tr. 141:24—25,

77 See Chang, et. al., supra note 53.

30
142:1-3. Dr. McGeady continued that “[w]hen you look at that same configuration . . . in the
[CNS], where it[ is] attached to long-chain fatty acids, .. . the immune system is not going to see
that in the same way.” Tr. 142:4-10. Dr. McGeady testified that the phosphoglycerol or
phosphocholine molecule in the polysaccharide vaccine is not in the same configuration as it is in
the CNS. Tr. 143:16-21. Dr. McGeady opined that where the phospho polar head of the
phosphoglycerol or phosphocholine combines to saccharides vs. lipids is “definitely different[.]”
Tr. 140:1-3. He therefore indicated that the “antibody produced which recognizes
phosphocholine[,] would be that generated by two dissimilar large molecules, having in common
only phosphocholine attached as a [small molecule], or [] share phosphocholine as an epitope.”
Resp’t’s Ex. JJ at 2. Based on this, Dr. McGeady opined that “[iJt is unlikely that two such
dissimilar molecules would generate [an] antibody with closely related binding capabilities given
the exquisite selectivity of antibody binding.” /d.

Dr. McGeady opined that “to suggest that the immune system produces antibod[ies]
promiscuously to molecules such as phosphoglycerol regardless of their molecular position, is to
ignore the complexity of antibody production[.]” Resp’t’s Ex. MM at 2. He explained that
antibodies “combine with the molecular structure that caused them to be generated, in a ‘lock and
key’ relationship.” Resp’t’s Ex. JJ at 2. Therefore, the antibody “will bind to only the molecular
structure that caused it to be produced or to very closely related structures.” /d. Dr. McGeady
concluded that given this specificity, “it is most unlikely that a phosphoglycerol group in Prevnar
13 caused production of an antibody that recognizes both phosphoglycerol in the conjugated
polysaccharide vaccine and in the tissues of the spinal cord.” Resp’t’s Ex. MM at 2. He wrote that
this is because the “phosphocholine in [the] pneumococcal polysaccharide is antigenically
different from [the] phosphocholine in tissues such as myelin protein of the human CNS.” /d.
Specifically, he wrote that the “unlikeliness of this phenomenon . . . is compounded by the fact
that for it to occur[,] the phosphocholine . . . would have to be in nearly identical configuration in
both Prevnar 13 and the unidentified carrier of MS patients in order to give rise to these similar
antibodies.” Resp’t’s Ex. JJ at 2; see also Resp’t’s Ex. KK at 3, ECF No. 93-2.”* Dr. McGeady
testified that the configuration must be “very, very similar” between the CNS and the Prevnar 13
vaccine “in order for [] cross-reaction to occur[]” and he “just do[es not] think we have that here.”
Tr. 142:11-24. Dr. McGeady stated that the polar head group of phosphoglycerol or the
phosphocholine between the CNS and the Prevnar vaccine is not “enough to create the type of
cross-reaction” that Dr. Steinman proposed. Tr. 143:1-5.

He continued that the “immune system[,]. . . requires antigens to be of a certain size before
an immune response is generated . . . [and s]mall molecules with a weight of less than 10,000
daltons are not able to elicit an immune response as stand-alone immunogens.” Resp’t’s Ex. JJ at
2 (citing Resp’t’s Ex. KK at 2); see also Tr. 140:15-17. Dr. McGeady noted that size becomes
important based on whether it is “immunogenic by itself or whether it requires the presence of a
larger molecule.” Tr. 140:23-25. Dr. McGeady wrote that the molecular weight of
phosphoglycerol is 200 daltons, “indicating that it is not immunogenic by itself.” Resp’t’s Ex. JJ
at 2; Tr. 137:8—-9. He explained, however, that “antibodies can be produced to small molecules
[haptens] if they are attached to large molecules [carriers].” Resp’t’s Ex. JJ at 2.

78 T.G. PARSLOW, Immunogens, Antigens, & Vaccines in MEDICAL IMMUNOLOGY 73 (D.P. Stites et al.
eds., 10th ed. 2001).

31
Dr. McGeady attacked Dr. Steinman’s reliance on the Ho et al.” article. Tr. 146:5-25. He
opined that this article did not support Petitioners’ theory because the authors ‘“used mini array[s]
comprising 17 lipids to profile autoantibody responses and cerebrospinal fluid from
remitting/relapsing MS ... .”’ Tr. 146:15—18 (citing Pet’r’s Ex. 38). He continued that ““[t]he
analysis revealed antibody reactivity to three of the seven[]’”’ lipids. Tr. 146:19—20. Dr. McGeady
testified that to him, “that kind of supports what [his] contention is, [] that this antibody is
extremely discriminating[ and i]f it just reacted with the phosphate polar head, it would have
reacted with all seven of those.” Tr. 146:21—25. Dr. McGeady emphasized that the Ho et al. authors
looked at phosphate polar heads connected to lipids, only. Tr. 147:8—-13. He noted that the authors
did not “explore whether or not there would be a reaction when that polar head was configured on
a different carrier, such as a saccharide, as opposed to [the] same with lipid[s.]” Tr. 185:6—14.
When asked, Dr. McGeady repeated his distinction between MS and TM to opine that the Ho et
al. article is not applicable to R.S.’s case. Tr. 180:15—23. He stated that he was not making a
distinction between MS and TM for the purposes of molecular mimicry. Tr. 180:24—25. He simply
maintained that they are separate diseases “[a]nd the pathology of them is distinct.” Tr. 181:6—11.

Dr. McGeady further questioned Dr. Steinman’s reliance on the Chang et al.*° article,
“showing that the phosphocholine is necessary for the immunogenicity of specific pneumococcal
serotypes in a polysaccharide vaccine[.]” Resp’t’s Ex. JJ at 3. Dr. McGeady highlighted that this
is “dissimilar to [the] Prevnar [13 vaccine, ] in that it is conjugated to tetanus rather than diphtheria
toxoid.” /d. (citing Pet’r’s Ex. 52). He noted that “[w]hat is not known from that research” is
whether antibodies directed to phosphocholine are “actually produced by this vaccine... .”
Resp’t’s Ex. JJ at 3. Based on this, Dr. McGeady opined that “[i]t is possible, perhaps likely, that
the need for phosphocholine in [the polysaccharide vaccine] is in the role of a structural or bridging
component, rendering the polysaccharide maximally immunogenic rather than providing any
direct antigenic function by itself.” /d. Dr. McGeady testified that the Chang et al. article showed
that “when you immunized animals... they made antibod[ies] when you gave them the saccharide,
but they made [the] antibody 1,000 times more when you gave them the saccharide attached to
tetanus toxoid.” Tr. 158:7—-15. Dr. McGeady noted that “the vaccine [the Chang et al. authors]
were looking at [] is actually different from the Prevnar in the sense that the Prevnar is attached to
diphtheria toxoid; this was tetanus toxoid.” Tr. 158:15—19. He stated that the Chang et al. article
“showed that it needed the carrier protein in order to have maximal antigenicity.” Tr. 158:24—25.
Dr. McGeady acknowledged that it also showed that “the phosphocholine is necessary for []
antigenicity.” Tr. 159:10-12.

He wrote that an additional flaw in Dr. Steinman’s theory is that “the assertion that cross-
immunity to myelin sheath components of the CNS elicits antibodies that result in TM is not
consistent with the reported immunopathology of TM.” Resp’t’s Ex. A at 7. Dr. McGeady
alternatively proposed that “the known immunopathology of TM is considerably more suggestive
of cell[-]mediated immune damage than it is of [an] antibody[-]mediated injury.” Resp’t’s Ex. K
at 4. He explained the difference between cell-mediated immune damage and antibody-mediated
damage. Tr. 149:23-25. Cell-mediated immunity is “carried out by . . . T cells.” Tr. 150:1-3. One
such type of T cell is the “cytotoxic T cell that does what the name would suggest, it kills cells that
are seen as something that should[ not] be there[]” and “attracts other inflammatory cells, such as

” See Ho, et. al., supra note 43.
80 See Chang, et. al., supra note 53.

32
monocytes and macrophages, to the site.” Tr. 150:4—-9. Dr. McGeady explained that antibodies
“come[] as a result of these T cells activating the other cells called B cells that [] produce the
antibody.” Tr. 150:11—13. He continued that once the antibody is produced, “it recognizes this
‘nonself? and binds to it[.]” Tr. 150:13—15. Once that happens, the antibody “interfer[es] with the
cell.” Tr. 151:6~7. He relied on an article by Awad et al.,*! to explain that “biopsies taken during
the acute phase of TM[] found infiltration of CD4+ and CD8+ T cells together with [the]
perivascular spread of monocytes and evidence of astroglial and microglial activation.” Resp’t’s
Ex. A at 7 (citing Resp’t’s Ex. F, ECF No. 29-6). Dr. McGeady wrote that “this pathological
description does not rule out a role for autoantibod[ies] in acute TM[.]” Resp’t’s Ex. A at 7. He
maintained that “it suggests that other immune mechanisms are primarily operative[] in producing
tissue injury.” /d. The authors of the Awad et al. article noted, however, that such “infiltrates of
CD4+ and CD8+ T-lymphocytes were found to be prominent[,] suggesting [an] immune-mediated
disease process.” Resp’t’s Ex. F at 3.

As support for this conclusion that cellular processes predominate the pathology of TM,
Dr. McGeady described three mechanisms by which “[a]ntibody mediated tissue injury ordinarily
occurs[.]” Resp’t’s Ex. T at 5. He noted that one mechanism is opsonization, “a process by which
[an] antibody coats a target cell or tissue, [a] complement is activated|,] and phagocytic cells such
as neutrophils and monocytes/macrophages ingest or attempt to ingest the target cell or tissue[.]”
Id. (citing Resp’t’s Ex. GG at 1, ECF No. 76-13).°* A second mechanism is by “causing
inflammation such as when [an] antibody binds to a cell or tissue complement[,] is activated[,] and
chemotactic molecules are generated causing the same phagocytic cells to accumulate and release
potent tissue degrading enzymes.” Resp’t’s Ex. T at 5 (citing Resp’t’s Ex. GG at 1). Dr. McGeady
noted that such events “lead to [an] injury to the antibody coated cells or tissue[s] and to nearby
structures[.]” Resp’t’s Ex. T at 5. This leads to the third mechanism, “interference with normal
cellular function whereby [an] antibody binds to a critical structure of a cell causing [a] gain or
loss of function, but not creating an inflammatory cell infiltrate.” /d. (citing Resp’t’s Ex. GG at 1).
Dr. McGeady wrote that in each of the mechanisms for an antibody mediated injury, the “cells
signifying this type of immunopathology in its acute phase are neutrophils, but these are not
reported to be present in biopsies .. . of TM[.]” Resp’t’s Ex. T at 5—6 (citing Resp’t’s Ex. F at 3).®
Instead, he maintained that “CD4+ and CD8+ T cells and monocytes which are characteristic of
cellular immune pathology[,|” are found instead. Resp’t’s Ex. T at 6 (citing Resp’t’s Ex. F at 3).

He indicated that further evidence in support of the immunopathology “not being antibody
mediated is the recent description of the elevated levels of the pro-inflammatory cytokine IL-6 in
the cerebrospinal fluid” of both adult and pediatric cases of TM. Resp’t’s Ex. K at 4 (citing Resp’t’s
Exs. F, GG). Dr. McGeady defined IL-6 as “a proinflammatory chemical that[ is] generated in the
course of an inflammatory reaction.” Tr. 151:8-10. He testified that a finding of elevated IL-6 is
relevant in a case of pediatric TM because it is “known to be generated by T cells and by
macrophages[]” but not by B cells, “the antibody producers.” Tr. 151:14—-19. “So[,] finding [IL-6]
would make you think that [] one arm of the immune system is activated and the other is

8! A. Awad, et al., Idiopathic Transverse Myelitis and Neuromyelitis Optics: Clinical Profiles and
Therapeutic Choices, 9 CURRENT NEUROPHARMACOLOGY 417-28 (2011).

® A. ABBAS ET AL., Cytokines in CELLULAR & MOLECULAR IMMUNOLOGY 519 (Elsevier eds., 9th ed.
2018).

8 See Awad, et. al., supra note 81.

33
quiescent.” Tr. 151:19—21. Dr. McGeady explained that “IL-6 is produced by cells of the innate
immune system, such as microglial cells, by endothelial cells[,] and by T cells. IL-6 is not known
to be produced by B cells or generated in large quantities during antibody related reactions.”
Resp’t’s Ex. K at 4. He continued that “the finding of elevated IL-6 in TM is indicative of a cellular
immune process or innate immune activation rather than an autoantibody driven process [] as Dr.
Steinman hypothesizes.” /d at 4-5. Dr. McGeady therefore opined

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/6332197. Public record. Not legal advice.