# Pasco v. Secretary of Health and Human Services

> United States Court of Federal Claims · October 11, 2022

URL: https://www.frixlaw.com/law-library/cases/8213138

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** October 11, 2022
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Herbrina Sanders
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/8213138

## How later opinions describe it (automated extraction)

- explaining that an idiopathic diagnosis cannot be a “factor unrelated,” as it is idiopathic
- explaining that the respondent’s burden is to show that the “factor unrelated” was the “sole substantial factor” in causing the injury

## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: September 23, 2022

* * * * * * * * * * * * * * *
MISTY PASCO, parent and next friend * No. 16-500V
of M.P., a minor, *
*
*
Petitioner, * Special Master Sanders
*
v. *
* Ruling on Entitlement; Measles-
SECRETARY OF HEALTH * Mumps-Rubella Vaccine; Varicella
AND HUMAN SERVICES, * Vaccine; Acute Disseminated
* Encephalomyelitis (“ADEM”); Transverse
Respondent. * Myelitis (“TM”); Substantial Factor
* * * * * * * * * * * * * * *
Richard Gage, Richard Gage, P.C., Cheyenne, WY, for Petitioner.
Tyler King, United States Department of Justice, Washington, DC, for Respondent.

RULING ON ENTITLEMENT 1

On April 22, 2016, Misty Pasco (“Petitioner”) filed a petition for compensation on behalf
of her minor child M.P. pursuant to the National Vaccine Injury Compensation Program. 2 Pet. at
1, ECF No. 1; 42 U.S.C. §§ 300aa-1 to -34 (2012). Petitioner alleges that the measles-mumps-
rubella (“MMR”) and varicella vaccines M.P. received on May 14, 2015, caused her to suffer from
transverse myelitis (“TM”). 3 Pet. at 1–2. Petitioner filed an amended petition on January 30, 2018,
alleging that M.P.’s May 14, 2015 vaccinations were the cause-in-fact of her TM and acute

1
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.
2
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).
3
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.
disseminated encephalomyelitis (“ADEM”). 4 Am. Pet. at 2, ECF No. 52. Petitioner further alleges
that M.P.’s vaccinations caused the Table injury of encephalitis. 5 Id.

After carefully analyzing and weighing all the evidence and testimony presented in this
case in accordance with the applicable legal standards, 6 I find that Petitioner has provided
preponderant evidence that the MMR and varicella vaccines M.P. received on May 14, 2015, were
the cause-in-fact of her TM and ADEM. However, in light of M.P.’s ADEM diagnosis, Petitioner
has failed to satisfy her burden for her Table claim of encephalitis. Accordingly, Petitioner is
entitled to compensation and this case shall proceed to the damages phase.

I. Procedural History

Petitioner filed her petition for compensation on April 22, 2016. Pet. at 1. On May 6, 2016,
Petitioner filed M.P.’s medical records and a statement of completion. Pet’r’s Exs. 1–14, ECF Nos.
9-1–11-6, 12. 7 Petitioner filed additional medical records on July 6 and 18, 2016. Pet’r’s Exs. 15–
16, ECF Nos. 17–18.

Respondent filed his Rule 4(c) report on August 5, 2016, recommending that compensation
be denied. Resp’t’s Report at 1, ECF No. 19. Petitioner filed an additional medical record on
August 8, 2016. Pet’r’s Ex. 17, ECF No. 20-1. The presiding special master held a status
conference pursuant to Vaccine Rule 5 on August 9, 2016. See Min. Entry, docketed Aug. 10,
2016. Following the status conference, the presiding special master ordered Petitioner to file an
expert report on causation that “address[ed] the lingering concerns about potential alternative
causes of [M.P.’s] alleged condition.” Sched. Order at 1, ECF No. 21. Prior to filing an expert
report, Petitioner submitted M.P.’s vaccination record on August 30, 2016. Pet’r’s Ex. 18, ECF
No. 22-1.

On January 4, 2017, Petitioner filed an expert report from Lawrence Steinman, M.D.
Pet’r’s Exs. 19–20, ECF Nos. 30-1–30-2. This case was reassigned to me on January 9, 2017. ECF
Nos. 31–32. Respondent filed a responsive expert report from Hayley Gans, M.D., along with
supporting medical literature, on May 2, 2017. Resp’t’s Exs. A–B, A Tabs 1–18, ECF Nos. 35-1–

4
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
lethargy progressing to coma that can be fatal. Many survivors have residual neurologic deficits.” Dorland’s
at 613.
5
Encephalitis is generally “inflammation of the brain.” Dorland’s at 612.
6
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
(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.”).
7
Petitioner’s original exhibit number 8 was stricken from the record and a corrected version was re-filed
on December 13, 2016. See Pet’r’s Ex. 8, ECF No. 27-1; see also ECF Nos. 25–26.

2
35-2, 36–37. The following day, Respondent filed an additional expert report from Michael Kruer,
M.D. Resp’t’s Exs. C–D, ECF Nos. 38-1–38-2. Respondent filed supporting medical literature on
June 16, 2017. Resp’t’s Exs. C Tabs 1–14, ECF Nos. 40-1–41-10.

I held a status conference with the parties on July 11, 2017. See Min. Entry, docketed July
11, 2017. Following the status conference, I ordered Petitioner to file a responsive supplemental
expert report specifically “addressing th[e] alternative cause[]” in this case. Sched. Order at 1, ECF
No. 44. Petitioner submitted a supplemental expert report and supporting medical literature on
November 2, 2017. Pet’r’s Exs. 21–25, ECF Nos. 46-1–46-5. The same day, I ordered Respondent
to file his responsive supplemental expert reports. Non-PDF Order, docketed Nov. 2, 2017.
Following one extension of time, Respondent filed a motion to stay the filing of his responsive
supplemental expert reports on the basis that the Department of Health and Human Services was
awaiting an appropriation from Congress. ECF Nos. 47–48. Appropriations were restored the same
day that Respondent’s motion was filed, and I therefore denied Respondent’s motion on January
23, 2018. ECF No. 49. The same day, Respondent filed his responsive supplemental expert reports.
Resp’t’s Exs. E, E Tab 1, F, ECF Nos. 50-1–50-3.

On January 29, 2018, I held a status conference with the parties. See Min. Entry, docketed
Jan. 29, 2018. During the status conference, the parties discussed the legal burden applicable to
claims, such as Petitioner’s, in which there is a dispute concerning competing causes. Sched. Order
at 1, ECF No. 51. Petitioner noted she planned to file an amended petition alleging that M.P. suffers
from ADEM, “which is a form of encephalitis.” Id. The parties agreed that M.P.’s ADEM and
human metapneumovirus (“HMPV”) infection 8 diagnoses were not in dispute. Id. Petitioner
explained that at the time the original petition was filed, the Program “regularly treated ADEM as
a [T]able injury when pled as encephalitis.” Id. at 2. Petitioner “acknowledged that ADEM is now
among the exclusionary criteria for encephalitis in the [Table].” Id. Petitioner filed an amended
petition on January 30, 2018, alleging that M.P. suffers from TM, ADEM, and Table encephalitis.
Am. Pet., ECF No. 52.

In response to Petitioner’s amended petition, Respondent filed a status report stating his
position on March 5, 2018. ECF No. 53. Specifically, Respondent argued that Petitioner failed to
establish a Table claim for encephalopathy or an ADEM/TM causation-in-fact claim, and
Respondent requested that this matter be scheduled for an entitlement hearing. Id. Petitioner filed
a response on April 7, 2018, arguing that the evidence supports her claim. See ECF Nos. 54–55.
Two days later, Petitioner filed additional medical literature. Pet’r’s Exs. 26–32, ECF Nos. 56-1–
56-7. Petitioner filed an affidavit on April 16, 2018. Pet’r’s Ex. 33, ECF No. 57-1.

The following day, on April 17, 2018, I held a status conference with the parties. See Min.
Entry, docketed Apr. 17, 2018. During the conference, I indicated that “the medical records do not
seem to support an encephalitis/encephalopathy [T]able injury.” Sched. Order at 1, ECF No. 58.
Petitioner indicated that she wished to proceed on her causation-in-fact claim. Id. The parties

8
A human metapneumovirus (“HMPV”) infection is “a species that causes respiratory infection in humans
that is clinically similar to, but less severe than, that caused by respiratory syncytial virus.” Dorland’s at
1144. 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.” Id. at 2064.

3
reiterated that they do not dispute M.P.’s ADEM or HMPV infection diagnosis, or the timing of
her symptoms. Id. They also maintained that the main issue in this case is “a legal question
concerning the burdens relating to whether the viral infection or the vaccinations caused [M.P.’s]
injuries.” Id. Following the status conference, I ordered the parties to file briefs articulating their
positions on the legal burdens applicable to this case. Id. at 2. The parties filed simultaneous
memoranda regarding their legal burdens on August 13, 2018. Pet’r’s Mem., ECF No. 61; Resp’t’s
Mem., ECF No. 62.

While awaiting an entitlement hearing, Petitioner filed an updated medical record on
December 27, 2019. Pet’r’s Ex. 34, ECF No. 64-1. On August 19, 2020, Petitioner filed a notice
of additional authority regarding her legal burden. ECF No. 65. I scheduled this matter for an
entitlement hearing to take place on June 2–3, 2021. Hearing Order, ECF No. 69. The parties relied
on their previously filed memoranda in place of pre-hearing briefings. Pre-Hearing Order, ECF
No. 70. The entitlement hearing was held remotely as scheduled on June 2, 2021. See Min. Entry,
docketed June 2, 2021. Following the entitlement hearing, Petitioner filed a status report indicating
that she did not wish to file post-hearing briefings and requesting I issue a Decision based on the
existing record. ECF No. 80. This matter is now ripe for consideration.

II. Factual Background

A. Medical Records

M.P. was born full-term on May 8, 2014, and was healthy at birth. Pet’r’s Ex. 3 at 1, ECF
No. 9-3. M.P. had normal newborn examinations Id. at 6. During M.P.’s well-child visits during
her first year, Petitioner requested that M.P. receive her vaccinations on a modified schedule of
two per visit. See Pet’r’s Ex. 4, ECF No. 9-4. M.P. did not experience adverse reactions to her
scheduled vaccinations in the first twelve months of her life. See id.

On May 5, 2015, M.P. presented to Phoenix Indian Medical Center (“PIMC”), her primary
care provider, for persistent ear pain. Id. at 43. Petitioner reported that M.P. had gone to urgent
care on April 15, 2015, and was diagnosed with otitis media (“OM”) 9 and prescribed amoxicillin. 10
Id. M.P. presented to PIMC for her twelve-month well-child visit on May 14, 2015. Id. at 49.
Petitioner noted “no concerns” regarding M.P. Id. M.P.’s examination was normal, and she
received the MMR and varicella vaccinations during this visit. Id. at 51–53.

One week later, on May 21, 2015, M.P. returned to Dr. Bernadette Freeland-Hyde at PIMC
with symptoms of fever, cough, and congestion that began three days prior (four days post

9
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.
10
Amoxicillin is “a semisynthetic derivative of ampicillin effective against a broad spectrum of gram-
positive and gram-negative bacteria; used especially in the treatment of infections due to susceptible strains
of Haemophilus influenzae, Escherichia coli, Proteus mirabilis, Neisseria gonorrhoeae, streptococci
(including Streptococcus faecalis and S. pneumoniae), and non-penicillinase-producing staphylococci.”
Dorland’s at 65.

4
vaccination). Id. at 55. Her examination showed bilateral bulging tympanic membranes, 11 teary
discharge, and a low-grade fever of 99 degrees Fahrenheit. Id. at 55–56. M.P.’s pediatrician
diagnosed her with bilateral OM and prescribed antibiotics. Id. On May 25, 2015, Petitioner took
M.P. to the emergency room (“ER”) with complaints of continued fevers. Id. at 57. Her
temperature was 102.6 degrees Fahrenheit. Id. Petitioner reported that M.P.’s fever had resolved
the day after being diagnosed with OM but then had returned later that same day, along with
vomiting and “loose stools.” Id. Regarding M.P.’s “loose stool[,]” her pediatrician noted that M.P.
was taking antibiotics for her OM. Id. The examination of M.P.’s ears, nose, and throat revealed
normal bilateral tympanic membranes and no rhinorrhea or nasal drainage. Id. at 65. Her
neurological examination was normal. Id. The attending physician diagnosed M.P. with a fever,
vomiting, bilateral OM, and an insect bite on her right thigh. Id. at 66. The physician prescribed
acetaminophen (Tylenol) and Azithromycin, 12 and M.P. received an injection of Ceftriaxone. 13 Id.

The next day, on May 26, 2015, M.P. returned to her pediatrician’s office. Id. at 76.
Petitioner reported that M.P.’s fever, diarrhea, and vomiting had resolved, but Petitioner expressed
concerns over M.P.’s poor oral intake. Id. M.P.’s pediatrician recommended fluids and to follow
up in one day. Id. at 77.

On May 27, 2015, M.P. followed up with her pediatrician “for prolonged weakness.” Id. at
80. Petitioner reported that M.P. still had poor oral intake, was very weak, and was “refusing to
walk[.]” Id. Her pediatrician noted a “6.5[%] weight loss since [May 21, 2015.]” Id. An
examination of M.P. revealed that she was alert and responsive but exhibited hypotonia 14 and
lethargy. Id. at 81. M.P.’s pediatrician referred her to the ER. Id. M.P.’s ER examination showed
that she was alert but had diminished strength. Pet’r’s Ex. 5 at 6, ECF No. 10-1. The attending
physician admitted M.P. for dehydration. Id. at 8. Petitioner reported that “around the 25th or 26th
[of May,]” M.P. had not been using her upper extremities and “she seemed tired and weak overall.”
Id. at 18. A respiratory panel was positive for HMPV and M.P.’s urinalysis was concerning for a
UTI. Id.

M.P. underwent a neurological examination on May 29, 2015, which showed that she was
irritable, crying, had poor neck control, and exhibited little movement in her lower extremities. Id.
at 33. An MRI of the brain and spinal cord on May 30, 2015, revealed “longitudinal myelitis.” Id.

11
Tympanic membranes are also called “membrana tympanica” or “eardrums.” They are “the obliquely
placed, thin membranous partition between the external acoustic meatus and the tympanic cavity. The
greater portion, the pars tensa, is attached by a fibrocartilaginous ring to the tympanic plate of the temporal
bone; the much smaller, triangular portion, the pars flaccida, is situated anterosuperiorly between the two
malleolar folds.” Dorland’s at 1128.
12
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.
13
Ceftriaxone sodium is “a semisynthetic, β-lactamase–resistant, broad-spectrum, third-generation
cephalosporin effective against a wide range of gram-positive and gram-negative bacteria; administered
intravenously or intramuscularly.” Dorland’s at 312.
14
Hypotonia is “a condition of diminished tone of the skeletal muscles, so that they have diminished
resistance to passive stretching and are flaccid; this usually means the nerve supply is compromised.”
Dorland’s at 907.

5
at 18. The impression of M.P.’s MRI was a “symmetric, central increased T2 signal of the cord
extending from the cranio-cervical junction to T10.” Id. at 162. The MRI also showed “[l]ong
segment cord signal abnormality . . . with vague cord enhancement.” Id. Such findings were “most
consistent with [ADEM].” Id. A lumbar puncture performed to collect cerebrospinal fluid (“CSF”)
revealed elevated white blood cells, but normal red blood cells, protein, and glucose. Id. at 41, 163.
M.P. was assessed with “longitudinally extensive transverse myelitis[.]” Id. at 41. M.P. received
IV steroids and IVIG for four days with a plan to continue oral steroids for three to four weeks
“and then slowly taper over another [four] weeks” following discharge. Id. at 35, 41. A note from
the attending neurologist dated June 2, 2015, indicated that M.P. “had a history of recent
vaccination and [a] possible viral infection.” Id. at 33. M.P. was discharged on June 6, 2015, with
a full range of motion (“ROM”) of her upper extremities and right lower extremity. Id. at 24. She
still had fine motor deficits and was unable to crawl. Id.

On June 8, 2015, M.P. returned to her pediatrician for a follow-up. Pet’r’s Ex. 10 at 23,
ECF No. 11-2. Petitioner reported that M.P. was irritable the day before. Id. Upon examination,
M.P. was alert but still had motor deficits. Id. Her pediatrician noted that the “etiology is unclear
as [M.P.] tested positive for [an HMPV infection] and also received the MMR/varicella vaccines
about [one and a half] weeks prior to the onset of [her] symptoms.” Id. The pediatrician’s
assessment of M.P. included a “fussy baby from post hospitalization from transverse myelitis –
unclear if [M.P.] is in pain from [the] high dose of prednisolone or from myelitis.” Id. at 24.

M.P. followed up with neurologist Vinodh Narayanan, M.D., on June 12, 2015. Pet’r’s Ex.
15 at 1, ECF No. 17-1. Dr. Narayanan noted that M.P. had TM and “perhaps subtle features of
ADEM.” Id. Upon examination, M.P. was unable to sit by herself, and her left ankle was tight. Id.
Dr. Narayanan noted that M.P. was otherwise alert, smiling, and interactive. Id. His plan was to
continue tapering her prednisolone. Id. M.P. had another follow up with Dr. Narayanan on June
17, 2015. Id. at 6. He noted that M.P. was improving with physical therapy (“PT”). Id. An
examination revealed tight heels. Id.

From June 24 to December 23, 2015, M.P. received treatment with PT. Pet’r’s Ex. 11 at 1,
ECF No. 11-3. The note from her initial appointment on June 24, 2015, indicates that M.P.’s TM
and ADEM diagnosis “ha[d] possibly been linked to [the] MMR [vaccine she] received [eleven]
days prior to her hospitalization.” Id. The physical therapist noted that M.P. was “regaining the
ability to prop sit but [wa]s dependent for mobility.” Id.

M.P. returned to Dr. Narayanan for a follow-up on August 25, 2015. Pet’r’s Ex. 15 at 2.
He noted that M.P. was “now completely done with her steroid taper.” Id. He also noted that
Petitioner started M.P. in hyperbaric oxygen15 and acupuncture therapies. Id. Upon examination,
Dr. Narayanan indicated that M.P. was “able to stand and walk on a broad[-]based gait[, s]he
circumducts [sic] the left leg, and has some genu recurvatum 16 on the left.” Id. He further noted
that M.P. exhibited diminished tone in her legs and “w[ould] lose her balance and fall

15
Hyperbaric oxygen treatment is “exposure of a patient to oxygen under pressure greater than normal
atmospheric pressure, done for individuals who need more oxygen than they can take in by breathing in the
normal atmosphere or with an oxygen mask.” Dorland’s at 1356.
16
Genu recurvatum refers to the “hyperextension of the knee; called also back knee.” Dorland’s at 771.

6
periodically.” Id. His impression of M.P. was “resolving symptoms of myelitis” and he
recommended continued PT. Id.

On December 8, 2015, M.P. returned to Dr. Narayanan for a follow-up. Id. at 3. Dr.
Narayanan noted that M.P. was “making steady progress in her motor skills[]” but that “[h]er
speech development ha[d] been a bit slow.” Id. He wrote that M.P. was also being treated by a
naturopathic physician, “who ordered [a] hair analysis for heavy metals.” Id. Dr. Narayanan noted
that M.P.’s hair analysis showed elevated iodine and uranium. Id. He indicated that he was “not
sure how to interpret this test result and [] referred [Petitioner] back to [the] naturopathic
physician.” Id.

M.P. underwent a speech evaluation on December 16, 2015. Pet’r’s Ex. 11 at 28. The
evaluation revealed that both M.P.’s receptive and expressive language scores fell below average
for her age. Id. However, the evaluator noted that M.P. appeared to have improved language skills
each week and did not qualify for speech services. Id. By the end of M.P.’s PT treatment on
December 23, 2015, the physical therapist noted that M.P. still had significant motor skill delay
due to her acute TM diagnosis. Id. at 36.

M.P. attended additional PT throughout 2016. Pet’r’s Ex. 34 at 35, ECF No. 64-1. On
November 8, 2016, M.P.’s physical therapist told Petitioner that M.P. could benefit from orthotic
braces 17 to correct the pronation18 in her legs. Id. M.P. presented to podiatrist Ana Burns, D.P.M.,
for orthotics on November 23, 2016. Id. at 33. During this visit, Petitioner reported that M.P.
experienced pain in her lower extremities at nighttime after running and jumping during the day.
Id.

On February 8, 2017, M.P. returned to Dr. Burns for a follow-up. Id. at 28. Dr. Burns noted
that M.P. exhibited “[bilateral lower extremity] weakness[,] gait abnormality[, and] pronation”
with a slight foot drag on her right side. Id. at 28, 30. She wrote that “[M.P.] has [a history] of
[TM] from vaccination which resulted in [bilateral lower extremity] weakness.” Id. at 29. Dr.
Burns noted that such conditions improved with arch supports. Id. at 30. She also ordered M.P. to
continue her strengthening exercises. Id. Dr. Burns noted that M.P. wears athletic shoes with her
issued orthotics. Id. at 29. Petitioner reiterated that M.P. would cry after running all day and
described the pain as a 7/10. Id. Dr. Burns recommended ibuprofen (Advil) for the pain. Id.

Over a year later, on June 12, 2018, M.P. presented for a neurology follow-up. Id. at 27.
The physician noted that M.P. exhibited “paresthesias of the skin [especially] in the legs.” Id. Upon
examination, M.P. did not show any “features of a peripheral neuropathy.” Id. The physician noted
her opinion that “it was unlikely that [M.P.’s] new sensory symptoms [were] connected with the

17
Orthotic braces are also called “supra-malleolar orthosis,” which “support[] the leg just above the
anklebones or malleoli.” Scheck & Siress, SMO (Supra-Malleolar Orthosis), PROSTHETICS, ORTHOTICS,
PEDORTHICS https://www.scheckandsiress.com/wp-content/uploads/2016/08/SMO-JM.pdf (last visited
July 7, 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.” Id.
18
Pronation is “the act of assuming the prone position, or the state of being prone. Applied to the hand, the
act of turning the palm posteriorly (or inferiorly when the forearm is flexed), performed by medial rotation
of the forearm. Eversion of the foot is sometimes referred to as pronation of the foot.” Dorland’s at 1526.

7
episode of myelopathy in 2015.” Id. She recommended further testing and potentially a repeat MRI
of M.P.’s spine. Id.

M.P. presented for her five-year well-child visit on May 14, 2019. Id. at 20–21. Petitioner
reported that she still had concerns regarding M.P.’s speech. Id. at 20. She noted that “[s]ometimes
[M.P.’s] words come out backwards in a sentence when speaking[ and she f]orgets what some
words are.” Id. Petitioner indicated that M.P. was receiving a speech evaluation through her school.
Id. M.P.’s examination was normal. Id. at 22–24. M.P.’s pediatrician recommended a follow-up in
one year. Id. at 24. Petitioner has not filed any additional medical records.

B. Petitioner’s Affidavit & Fact Testimony

Petitioner submitted one affidavit in support of her petition and testified at the entitlement
hearing. See Pet’r’s Ex. 33, ECF No. 57-1; Tr. 12–22. Petitioner’s description of the onset of M.P.’s
symptoms post vaccination was consistent with M.P.’s medical records. Pet’r’s Ex. 33 ¶ 5.
Petitioner testified that “prior to [M.P.] getting sick or being injured, she was like a normal one-
year-old.” Tr. 13:12–13. Petitioner wrote that M.P. “began to show signs of being sick on May 18,
2015, with a cough, fever, and congestion.” Pet’r’s Ex. 33 ¶ 5. On May 25, 2015, M.P.’s “fever
was 102.6 [degrees Fahrenheit] and she suffered from vomiting and diarrhea.” Id. ¶ 6. M.P. “was
also crying and apparently in pain.” Id. Petitioner attested that “M.P.’s condition kept deteriorating.
She became very, very lethargic.” Id. ¶ 7. She noted that M.P. “was sleeping much more than
usual. When she awoke, she did not want to eat or drink[,] and she did not interact with [Petitioner]
like she normally did.” Id. Petitioner continued that M.P. “had a loss of balance and would fall
backwards if not supported.” Id. “She was[ not] using her arms like she normally did and then she
was unable to walk.” Id. Petitioner testified that when M.P. lost the ability to walk, she also “could[
not] roll over . . . [or] sit up.” Tr. 13:16–18.

From there, Petitioner described M.P.’s initial hospitalization on May 27, 2015. Pet’r’s Ex.
33 ¶ 8. She noted that M.P. “could[ not] use her hands to hold her bottle.” Tr. 13:19–20. Petitioner
wrote that M.P. “spent [thirteen] days in the hospital and among [sic] numerous test[s] and
procedures, [including] a lumbar puncture and an MRI[, . . . she] was diagnosed with [TM] and
[ADEM].” Pet’r’s Ex. 33 ¶¶ 8–9. Petitioner noted that M.P. needed PT to regain her ability to
walk. Id. ¶¶ 10–11.

Petitioner explained the level of care M.P. received. Tr. 15:17–24. Petitioner explained that
M.P.’s PT began while she was still in the hospital and continued in their home with a physical
therapist for about two years. Tr. 14:3–18, 16:1–3. Petitioner stated that M.P. continues to receive
PT at home with Petitioner by “walk[ing] around the block . . . walk[ing] on uneven surfaces, [and]
walking backwards.” Tr. 16:4–8. She noted that M.P. tells Petitioner that her legs or feet hurt
following their walks or after a lot of activity. Tr. 17:5–8. Petitioner testified that she “would have
to massage [M.P.’s] legs and her feet quite often.” Tr. 17:8–9. She also described doing “little baby
leg lifts” to “help strengthen [M.P.’s] abdominal muscles.” Tr. 16:8–11. She noted that M.P. started
off wearing AFOs for about a year “to help support her feet and walking.” Tr. 15:20–23. “Later
on, she was also fitted for orthotics for her shoes,” which she wore for another year. Tr. 15:21–24.

Petitioner testified that at age three to four, M.P. was doing “okay.” Tr. 16:24–25. She
stated that M.P. attended pre-school but “would come home very tired, very fatigued.” Tr. 17:1–

8
2. M.P. would also tell Petitioner that her legs hurt after “playground time on the slides and stuff[.]”
Tr. 17:2–4. Petitioner testified that M.P. is in age-appropriate first grade and “has[ not] had any
issues of testing for a lower grade[.]” Tr. 19:1–3. However, “strenuous activity does [still] cause
her pain afterwards.” Tr. 17:11–14. A lot of strenuous activity, such as playing in the pool,
Petitioner explained, causes M.P. to be “pretty tired[]” and to need naps. Tr. 17:14–19. Petitioner
also noted that as a result of her speech delays, M.P. “still does tend to put words in the wrong
order[]” and struggles “finding the right word to say.” Tr. 18:5–24.

On cross-examination, Petitioner was asked about her eldest daughter’s illness prior to the
onset of M.P.’s symptoms. Tr. 19:17–25, 20:1–3. Petitioner testified that she did not recall her
eldest daughter being sick with pneumonia around May 18, 2015, but Petitioner stated that if the
medical records reflect that, she did not have a reason to doubt their accuracy. Tr. 20:4–15, 21:8–
20. She also stated that she and her husband were both sick following M.P.’s hospitalization with
“a cold[,]” but that they did not seek medical treatment. Tr. 20:16–23.

III. Experts
A. Expert Review
1. Petitioner’s Expert, Lawrence Steinman, M.D.

Dr. Steinman received his medical degree from Harvard University in 1973. Pet’r’s Ex. 20
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. Id. He became board certified in neurology in 1984. Id. at
2. He served as the Chairman of the Immunology Program at Stanford for approximately ten years
from 2002 to 2011. Id. at 1. He currently serves as a professor of neurology, pediatrics, and genetics
in Stanford University’s Department of Neurology and Neurological Sciences. Id. 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 that he also “did a fellowship in chemical immunology[,
which is] the chemistry applied to immunology.” Tr. 23:19–20. Dr. Steinman testified that he is
currently a “general neurology attending, [and] also get[s] called in consultation . . . on cases where
having some immunology background could assist the team.” Tr. 24:6–9. He further noted that he
runs a research laboratory, and his research is based in “trying to understand how the nervous
system is attacked by the immune system[]” in diseases such as multiple sclerosis (“MS”). Tr.
24:11–15.

Dr. Steinman submitted two expert reports and testified during the entitlement hearing. See
Pet’r’s Exs. 19, 21; Tr. 22–101, 174–188. Petitioner “presented” Dr. Steinman “as an expert in
neurology and immunology[]” without objection. Tr. 26:2–21.

2. Respondent’s Expert, Hayley Gans, M.D.

Dr. Gans received her medical degree from the State University of New York Health
Science Center at Syracuse in Syracuse, New York in 1991. Resp’t’s Ex. B at 1. Dr. Gans
completed an internship and residency in pediatrics at Stanford University School of Medicine in

9
1992 and 1994, respectively. Id. She also completed a fellowship in pediatric infectious diseases
from the same institution in 1998. Id. Dr. Gans served as an assistant professor of pediatrics at
Stanford from 2006–2015. Id. She has been a clinical associate professor at the same institution
since 2015. Id. Dr. Gans is board certified in pediatrics and pediatric infectious diseases. Id. She
has received several honors and awards, has served on numerous committees, and holds
memberships in several professional and scientific societies. Id. at 2–3. Her curriculum vitae lists
nearly one hundred publications, including articles, abstracts, book chapters, and presentations of
which she is a listed author. See id. at 4–7. The “bulk of [her] work has been on the immune
response to vaccines.” Tr. 142:8–9.

Discussing her clinical practice, Dr. Gans testified during the hearing that she “initially []
practiced in both pediatric infectious disease clinical service as well as serving in the immunology
clinics at Stanford University in the pediatrics hospital.” Tr. 138:17–20. She currently “codirect[s]
the pediatric infectious disease committee for immunocompromised hosts.” Tr. 138:25, 139:1. Dr.
Gans also “serv[es] in the general pediatric infectious disease service at Stanford.” Tr. 139:4–5.
She testified that she treats patients and has “direct patient care responsibilities[]” but is a
“consultant[] on the service.” Tr. 139:6–11. Dr. Gans explained that she is “brought in” to care for
individuals who have “any form of demyelination [including] . . . ADEM, [TM], other encephalitis,
encephalopathy or other neurologic conditions.” Tr. 139:15–20. She noted that part of the reason
she is brought in is because “infections are a large part of the cause of these outcomes.” Tr. 139:22–
23. As part of her research, Dr. Gans “focuses on the host pathogen interface, so sort of the immune
response to a[n] infection or pathogen, . . . using immunizations in children to actually look at their
immune response.” Tr. 140:1–7. Dr. Gans stated that she has testified twice in the Vaccine
Program. Tr. 142:22–25, 143:1–4.

Dr. Gans submitted two expert reports and testified during the entitlement hearing. Resp’t’s
Exs. A, E; Tr. 137–174. Respondent offered Dr. Gans as an expert in pediatrics, pediatric infectious
diseases, and pediatric immunology specifically related to vaccinations without objection, and I
recognized her as such. Tr. 143:15–25, 144:1–24.

3. Respondent’s Expert, Michael Kruer, M.D.

Dr. Kruer received his medical degree from the University of Arizona College of Medicine
in 2004. Resp’t’s Ex. D at 2. He completed a residency in pediatrics in 2007 at Phoenix Children’s
Hospital. Id. at 1–2. He also completed fellowships in molecular neurogenetics and
neurodevelopmental disabilities at Oregon Health & Science University in 2011. Id. He is board
certified in pediatrics, neurology, and neurodevelopmental disabilities. Id. at 1. Dr. Kruer
previously served as an assistant professor of pediatrics and neurosciences at the University of
South Dakota College of Medicine. Id. He also served as an attending neurologist and associate
scientist at Sanford Children’s Hospital in Sioux Falls, South Dakota. Id. He currently serves as
an associate professor in the departments of Child Health, Cellular & Molecular Medicine and
Neurology at the University of Arizona College of Medicine in Phoenix. Id. He is also the Director
of the Pediatric Movement Disorders Program at Phoenix Children’s Hospital. Id. Dr. Kruer serves
on several boards and committees and has received numerous honors and awards. Id. at 2–5. His
curriculum vitae includes approximately eighty publications of which he is a listed author. See id.
at 5–25.

10
During the hearing, he noted he “did a fellowship in neuroimmunology.” Tr. 103:13–14.
Dr. Kruer explained that his specialization is in neurogenetics and neuroimmunology. Tr. 104:11–
12. He stated that about forty percent of his time is spent seeing patients and the remaining time is
“[s]pent conducting patient-oriented research and performing administrative and teaching duties.”
Tr. 104:13–17. Dr. Kruer testified that he treats patients with demyelinating conditions “quite
often[.]” Tr. 104:18–23. He noted he has testified “over a dozen” times in the Program. Tr. 106:12.

Dr. Kruer submitted two expert reports and testified during the entitlement hearing. See
Resp’t’s Exs. C, F; Tr. 102–136. Respondent offered Dr. Kruer as an expert in pediatric neurology
and neuroimmunology. Tr. 106:13–15. Petitioner did not object to offering Dr. Kruer as an expert
in pediatric neurology but noted an objection to his admission as an expert in immunology. Tr.
106:22–25, 107:1–16. Dr. Kruer then testified under voir dire that he is “a fellowship-trained
clinical neuroimmunologist.” Tr. 108:9–10. He has “published a number of papers in the field,
[and he is] one of the attending physicians within the division of pediatric neuroimmunology at
Phoenix Children’s Hospital’s Barrow Neurologic Institute.” Tr. 108:11–15. Petitioner rescinded
her objection and Dr. Kruer was admitted as an expert in pediatric neurology and immunology. Tr.
108:16–21.

B. Expert Reports and Testimony

1. Petitioner’s Expert, Dr. Steinman

Dr. Steinman submitted two expert reports and testified during the hearing. See Pet’r’s Exs.
19, 21; Tr. 22–101, 174–188. Dr. Steinman “100 percent” agreed with M.P.’s diagnoses of TM
and ADEM. Pet’r’s Ex. 19 at 4; Tr. 35:5–7. He defined ADEM as “the example of when the
immune system attacks something in the brain.” Tr. 38:20–21. He noted that “it extends both in
experimental animal[ models] and in humans often down into the spinal cord, so you get this
involvement in both the brain and the spinal cord.” Tr. 39:8–11. Dr. Steinman testified that there
are many different manifestations of ADEM, including encephalopathy, alterations in the level of
consciousness, motor and sensory problems, and issues with the autonomic nervous system. Tr.
39:12–18. Dr. Steinman defined TM as “a similar phenomenon where the immune system impacts
structures in the spinal cord, leading to paralysis, sensory loss, [and] autonomic disorders.” Tr.
39:24–25, 40:1. Dr. Steinman concluded that “[i]f not for the vaccines [M.P. received] on May 14,
2015, and the contemporaneous infection with the human metapneumovirus, she would not likely
have developed neuroinflammation with acute [TM] and ADEM.” Pet’r’s Ex. 19 at 2.

Dr. Steinman wrote this occurrence was possible because of the concept of molecular
mimicry. Id. at 6. He relied on an article he wrote containing 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[,]” to demonstrate the concept. Id. (citing Pet’r’s Ex. 55 at 4, ECF No. 75-1). 19 He noted in
the article that “a foreign antigen may resemble antigen[s] produced by the body. Such molecular
mimicry provokes the T cells to attack body tissues that contain the self-antigens.” See id.

19
L. Steinman, Autoimmune Disease, 269 SCIENTIFIC AMERICAN 106–14 (1993).

11
Dr. Steinman further explained the concept of molecular mimicry and supported his theory
with studies on experimental autoimmune encephalomyelitis (“EAE”), 20 “to [help] understand
how the components of the MMR and varicella vaccines and the human metapneumovirus might
trigger neuroinflammation in the brain and the spinal cord of M.P.” Id. at 5–6 (citing Pet’r’s Exs.
50–53, ECF Nos. 74-6–74-9). 21 He noted that he relied on EAE as a comparison because “[t]he
experimental model of ADEM involves transverse myelitis . . . and is known as [EAE].” Id. at 5.
Dr. Steinman wrote that “the latest version of this EAE, acute optic neuritis[,] . . . provides a test
system for investigating one of the most common clinical presentations of an adverse reaction to
routine vaccination.” Id. at 6 (citing Pet’r’s Ex. 51). 22, 23 Dr. Steinman authored a commentary on
EAE and explained that Dr. Thomas Rivers and his colleagues “established [the first model of
EAE] to try to understand what caused neurological reactions to certain viral infections like
smallpox and in some circumstances to vaccinations like rabies[.]” See id. Dr. Rivers found that
following diseases such as smallpox, vaccinia and measles, and during or post rabies vaccination,
“an occasional patient develops symptoms and signs referable to the central nervous system.” See
Pet’r’s Ex. 51 at 1. Dr. Steinman indicated that “studies on the EAE model” bring together
“seemingly opposite poles of immunity[,]” allergy and autoimmunity, because such studies show
that “components of the allergic response are critical in the modulation of Th1 autoimmunity[]” to
produce neuroinflammation. Id. Dr. Steinman also addressed the Absoud et al. 24 article filed by
Respondent and noted that the authors determined that “molecular mimicry, . . . [is] one of the two
proposed mechanisms” for spinal cord inflammation and the development of TM. Tr. 68:17–23
(citing Resp’t’s Ex. A, Tab 17 at 4, ECF No. 37-7).

Dr. Steinman then discussed the target of the molecular mimic in his theory. Pet’r’s Ex. 19
at 5. He wrote that the body produces “adaptive immune responses to two key myelin antigens,
myelin basic protein (“MBP”) and myelin oligodendroglial glycoprotein (“MOG”)[, which] are

20
Experimental autoimmune encephalomyelitis or experimental allergic encephalomyelitis (“EAE”) is “an
animal model for acute disseminated encephalomyelitis [ADEM,] in which the characteristic
pathophysiology and clinical signs of this disease are produced by immunization of an animal with extracts
of brain tissue or with myelin basic protein together with Freund adjuvant[.]” Dorland’s at 614. EAE is an
umbrella term for inflammatory demyelinating diseases, including optic neuritis and neuromyelitis optica.
Dr. Steinman noted that since EAE’s “first description . . . the model has served as a starting point for our
understanding of autoimmunity[.]” Pet’r’s Ex. 51 at 1. Dr. Steinman did not otherwise describe what he
meant by the word “experimental.”
21
S. Sagan, et al., Tolerance Checkpoint Bypass Permits Emergence of Pathogenic T cells to Neuromyelitis
Optica Autoantigen Aquaporin-4, 113(51) PROC. NAT’L ACAD. SCI. 14781–86 (2016); L. Steinman, Optic
Neuritis, A New Variant of Experimental Encephalomyelitis, A Durable Model for All Seasons, Now in its
Seventieth Year, 197:9 J. EXP. MED. 1065–72 (2003); A. Gautam, et al., A Polyalanine Peptide with only
Five Native Myelin Basic Protein Residues Induces Autoimmune Encephalomyelitis, 176 J. EXP. MED. 605–
09 (1992); A. Gautam, et al., Minimum Structural Requirements for Peptide Presentation by Major
Histocompatibility Complex Class II Molecules: Implications in Induction of Autoimmunity, 91 PROC.
NAT’L ACAD. SCI. 767–71 (1994).
22
L. Steinman, Optic Neuritis, A New Variant of Experimental Encephalomyelitis, A Durable Model for
All Seasons, Now in Its Seventieth Year, 197:9 J. EXP. MED. 1065–72 (2003).
23
Dr. Steinman cites to reference number 18 in his report as support for this argument, which corresponds
to an article by Sagan et al. However, his discussion appears to actually quote reference number 19, an
article authored by Dr. Steinman himself. I believe this error was inadvertent.
24
M. Absoud, et al., Pediatric Transverse Myelitis, 87 NEUROL. 47–52 (2012).

12
detectable and likely critical in the pathogenesis of [TM] and ADEM.” Id. Dr. Steinman relied on
medical literature to support his opinion. He cited an article by Abramsky et al., 25 which noted that
MBP, “one of the major proteins of the myelin sheath, is one of the targets of the immune system”
in TM. Tr. 54:20–25 (citing Pet’r’s Ex. 45 at 3, ECF No. 74-1). Similarly, O’Connor et al. 26 found
that another antigen targeted in ADEM is MOG. Tr. 55:2–6 (citing Pet’r’s Ex. 46 at 2, ECF No.
74-2). The article by van Haren et al.27 indicated that “autoantibodies to defend components of
myelin in ADEM, . . . included MOG antibodies and [MBP] antibodies.” Tr. 56:18–25 (citing
Pet’r’s Ex. 47, ECF No. 74-3). The authors of the Zamvil et al. 28 article noted that “one of the
known antigenic targets of [TM] is MOG.” Tr. 57:11–16 (citing Pet’r’s Ex. 48 at 1, ECF No. 74-
4). Dr. Steinman further relied on a case study by Rostasy et al. 29 showing a patient with
neuromyelitis optica (“NMO”), a subset of acute demyelinating diseases, who tested negative for
aquaporin-4 (the antigen relevant to NMO) but was positive for MOG antibodies. Tr. 57:22–25,
58:1–8 (citing Pet’r’s Ex. 49 at 1–2, ECF No. 74-5). Dr. Steinman stated that this study described
“findings that are somewhat similar to what was seen in M.P.” Tr. 58:5–6. Dr. Steinman noted that
M.P. was also negative for aquaporin-4 and was not tested for MOG antibodies. Tr. 58:2–3. He
argued that this body of literature therefore supports his position that “MOG is high up on the list
of what might be in the vaccine that is known to be associated with [ADEM and TM].” Tr. 58:6–
8. He did not elaborate on this point but further used these articles to argue that “the mimics that
[he] found . . . are relevant to the disease that[ is] in question.” Tr. 57:3–6.

Dr. Steinman addressed the fact that “immunity to nervous system antigens like myelin is
rather widespread in” healthy individuals. Pet’r’s Ex. 21 at 4, 6. He wrote that “[o]ne of the reasons
that most normal individuals are free of autoimmune demyelinating disease is that immunity to
myelin is necessary but not sufficient to get actual disease.” Id. at 6. To get actual disease and a
self-reactive immune response to peripheral nerves triggering ADEM and TM, “[o]ther genetic
and environmental factors are necessary[.]” Id. He cited an article by Ota et al., 30 which showed
that “there are T cells reactive to [MBP]” in healthy individuals. Id. at 4 (citing Pet’r’s Ex. 58 at
2, ECF No. 75-4). He also cited an article by Pette et al., 31 demonstrating that “in healthy
individuals[,] T cells reactive to [MBP] were as readily detectable as in [multiple sclerosis]
patients[.]” Id. at 5 (citing Pet’r’s Ex. 59 at 1, 3, ECF No. 75-5). Dr. Steinman relied on the Ota et
al. and Pette et al. studies to demonstrate that “you can detect immune responses in healthy people
without multiple sclerosis [in] the [MBP,]” which is also “one of the antigens . . . target[ed] in

25
O. Abramsky & D. Teitelbaum, The Autoimmune Features of Acute Transverse Myelopathy, 2 ANN.
NEUROL. 36–40 (1977).
26
K. O’Connor, et al., Self-antigen tetramers discriminate between myelin autoantibodies to native or
denatured protein, 13(2) NAT. MED. 211–17 (2007).
27
K. van Haren, et al., Serum autoantibodies to myelin peptides distinguish acute disseminated
encephalomyelitis from relapsing-remitting multiple sclerosis, 19 MULT. SCLER. 1–10 (2013).
28
S. Zamvil & A. Slavin, Does MOG Ig-positive AQP4-seronegative opticospinal inflammatory disease
justify a diagnosis of NMO spectrum disorder?, 2:62 NEUROL. NEUROIMMUNOL. NEUROINFLAMM. 1–7
(2015).
29
K. Rostasy, et al., Persisting myelin oligodendrocyte glycoprotein antibodies in aquaporin-4 antibody
negative pediatric neuromyelitis optica, 19(8) MULT. SCLER. 1052–59 (2012).
30
K. Ota, et al., T-Cell Recognition of an Immuno-Dominant Myelin Basic Protein Epitope in Multiple
Sclerosis, 346 NATURE 183–88 (1990).
31
M. Pette, et al., Myelin Basic Protein-Specific T Lymphocyte Lines from MS Patients and Healthy
Individuals, 40 NEUROL. 1770–78 (1990).

13
[TM].” Tr. 64:8–14, 65:7–11 (citing Pet’r’s Exs. 58–59). Dr. Steinman stated that the authors of
these studies found that “even though it[ is] necessary to have these types of responses, it[ is] not
sufficient, because you can have that response, and there are certain features in those individuals
which make them continue to be healthy despite easily being able to detect such responses.” Tr.
64:18–23. He referred to this as the concept of a “host response.” Tr. 65:4–6. Dr. Steinman
maintained that “molecular mimicry is a key mechanism in understanding how tolerance to ‘self’
structures like myelin proteins is broken.” Pet’r’s Ex. 21 at 6.

As further support for his theory, Dr. Steinman ran numerous “BLAST” searches using the
protein database compiled by the National Library of Medicine to identify homologies between
the components of the MMR and varicella vaccines and the human metapneumovirus “to see if
there were any homologies with either [MBP] or with [MOG]” as they are the two proteins known
to be “under scrutiny” in ADEM and TM. Pet’r’s Ex. 19 at 7; Tr. 55:10–19. Dr. Steinman
“explicit[ly ]” noted that he “found [homology] in each component of the two vaccines [M.P.
received], but [] also found it in the metapneumovirus.” Tr. 55:23–25, 60:25–61:1. Based on these
findings, Dr. Steinman maintained that all three factors worked in concert to cause M.P.’s TM and
ADEM. Tr. 56:1–9. Dr. Steinman opined that the combination of the MMR and varicella
vaccinations with M.P.’s human metapneumovirus “created a ‘perfect storm’ whereby the three
components . . . all contain molecular mimics with key myelin proteins, known to be targeted in
acute [TM] and ADEM[,]” which caused her injuries. Pet’r’s Ex. 19 at 1–2. He noted that in all
cases where he finds homology of a relevant protein or enzyme to the disease, he could make an
argument that there could be causation. Tr. 98:16–21. But in cases where he finds homology but
is unable to find it to a relevant enzyme, “he would[ not] participate in the case.” Tr. 100:22–101:5.
Overall, “homology is not enough for [him].” Tr. 101:8–9. He requires the homology to “be in one
of the proteins or enzymes that[ is] implicated in the disease.” Tr. 101:9–11.

Prior to discussing his specific findings of the BLAST searches, Dr. Steinman relied on
medical literature to support his “criterion for a ‘meaningful molecular mimic[.]”’ Pet’r’s Ex. 19
at 7 (citing Pet’r’s Exs. 51–54);32 see also Tr. 58:15–20. Dr. Steinman 33 asserted that these articles
showed that the “identity of 5 of 12 amino acids, not even consecutive amino acids, was sufficient
to trigger experimental encephalomyelitis[]” in animal models. See id. He argued that an article by
Gautam et al. 34 showed that 5 of 11 amino acids were identical between a herpesvirus and MBP,
with only 3 consecutive proteins but the authors “were [still] able to induce encephalomyelitis” in
mice. Pet’r’s Ex. 19 at 8 (citing Pet’r’s Ex. 54 at 1, 5). Dr. Steinman further argued that a second
32
L. Steinman, Optic Neuritis, A New Variant of Experimental Encephalomyelitis, A Durable Model for All
Seasons, Now in its Seventieth Year, 197:9 J. EXP. MED. 1065–72 (2003); A. Gautam, et al., A Polyalanine
Peptide with only Five Native Myelin Basic Protein Residues Induces Autoimmune Encephalomyelitis, 176
J. EXP. MED. 605–09 (1992); A. Gautam, et al., Minimum Structural Requirements for Peptide Presentation
by Major Histocompatibility Complex Class II Molecules: Implications in Induction of Autoimmunity, 91
PROC. NAT’L ACAD. SCI. 767–71 (1994); A. Gautam, et al., A Viral Peptide with Limited Homology to a
Self Peptide Can Induce Clinical Signs of Experimental Autoimmune Encephalomyelitis, 161 J. IMMUNOL.
60–64 (1998).
33
It appears that Dr. Steinman cited incorrect reference numbers within his expert report and that such cites
to references 19–22 are off by one number. See Pet’r’s Ex. 19. I believe this error was inadvertent, and I
will cite to each reference based on the correct article.
34
A. Gautam, et al., A Viral Peptide with Limited Homology to a Self Peptide Can Induce Clinical Signs of
Experimental Autoimmune Encephalomyelitis, 161 J. IMMUNOL. 60–64 (1998).

14
article by Gautam et al.35 showed that “identity at 5 amino acids” in a chain of 6 peptides was
sufficient to trigger neuroinflammation in mice. Id. at 8–9 (citing Pet’r’s Ex. 53 at 1, 4). He cited
a third article by Gautam et al.36 to show that “a peptide with 4 of 11 amino acids induced
neuroinflammation[]” in mice. Id. at 9–10 (citing Pet’r’s Ex. 52 at 2–3). Dr. Steinman summarized
overall that the “criterion [sic] [described in the medical literature] was sufficient to provide
experimental evidence for eliciting experimental ADEM when such mimics were injected into
mice.” Pet’r’s Ex. 21 at 2. Dr. Steinman acknowledged that having 12 out of 12 identical amino
acids would have “a higher incidence and a stronger disease[,]” but he maintained that 5 out of 12
was a minimum sequence. Tr. 58:20–21, 60:9–17 (citing Pet’r’s Exs. 52–54). He noted that he
“put the line in the sand at [a sequence of] 5 out of 12[]” amino acids. Tr. 60:20–24.

Dr. Steinman then discussed the results from his eleven “BLAST” searches targeted at
MOG or MBP versus the components of the MMR and varicella vaccines and the HMPV infection.
See Pet’r’s Ex. 19 at 6–28; see also Pet’r’s Exs. 42–43, ECF Nos. 73-8–73-9. 37 Dr. Steinman did
not discuss findings associated with the human metapneumovirus versus MBP. See Pet’r’s Ex. 19
at 28. Of his eleven BLAST searches, seven revealed homologies of at least 5 out of 12 identical
amino acids for a statistically significant match susceptible to molecular mimicry consistent with
the literature. Id. at 6–28; Pet’r’s Exs. 52–54. 38 Dr. Steinman argued that all matches from his
eleven BLAST searches reached the threshold for inducing neuroinflammation sufficient to cause
experimental ADEM described in the medical literature. See id. He testified that his theory of
molecular mimicry does not change depending on whether the vaccine contained a live virus or
not. Tr. 75:8–18.

Dr. Steinman addressed Dr. Kruer’s discussion that one of the Gautam et al. 39 articles
showed mimics with many plant viruses, including shallot and cabbage leaf curl viruses, and MBP.
Pet’r’s Ex. 21 at 3 (citing Pet’r’s Ex. 54 at 3). Dr. Steinman opined that “finding such homologies
is not unexpected.” Id. Paying close attention to green beans, Dr. Steinman found a study
discussing such a finding. Id. at 4. He relied on the Daroca et al. 40 article wherein three patients
developed asthma and rhinitis “caused by exposure to raw, but not to cooked, green beans[]” via
molecular mimicry. Id. (citing Pet’r’s Ex. 57 at 1, ECF No. 75-3). All patients “tolerated [the]

35
A. Gautam, et al., Minimum Structural Requirements for Peptide Presentation by Major
Histocompatibility Complex Class II Molecules: Implications in Induction of Autoimmunity, 91 PROC.
NATL. ACAD. SCI. 767–71 (1994).
36
A. Gautam, et al., A Polyalanine Peptide with only Five Native Myelin Basic Protein Residues Induces
Autoimmune Encephalomyelitis, 176 J. EXP. MED. 605–09 (1992).
37
MMR II (Measles-Mumps-Rubella Virus Vaccine Live) – Package Insert, FOOD & DRUG
ADMINISTRATION (https://www.fda.gov/vaccines/MMRII); Varivax Varicella Virus Vaccine Live –
Package Insert, FOOD & DRUG ADMINISTRATION (https://www.fda.gov/vaccines/varivax).
38
A. Gautam, et al., A Polyalanine Peptide with only Five Native Myelin Basic Protein Residues Induces
Autoimmune Encephalomyelitis, 176 J. EXP. MED. 605–09 (1992); A. Gautam, et al., Minimum Structural
Requirements for Peptide Presentation by Major Histocompatibility Complex Class II Molecules:
Implications in Induction of Autoimmunity, 91 PROC. NAT’L ACAD. SCI. 767–71 (1994); A. Gautam, et al.,
A Viral Peptide with Limited Homology to a Self Peptide Can Induce Clinical Signs of Experimental
Autoimmune Encephalomyelitis, 161 J. IMMUNOL. 60–64 (1998).
39
A. Gautam, et al., supra note 34.
40
P. Daroca, et al., Asthma and Rhinitis Induced by Exposure to Raw Green Beans and Chards, 85 ANN.
ALLERGY ASTHMA IMMUNOL. 215–18 (2000).

15
ingestion of green beans.” Id. He noted that the authors found that “the route of administration and
the route of exposure is exceptionally important.” Tr. 92:19–25 (citing Pet’r’s Ex. 57). The patients
in the study who experienced a reaction to raw green beans did not have a reaction when they
ingested the same. See Pet’r’s Ex. 57. Dr. Steinman summarized that oral challenges in the Daroca
et al. study were negative, “but exposure to other routes was allergenic.” Pet’r’s Ex. 21 at 4. Dr.
Steinman opined that the “route of introduction of a molecular mimic is quite critical to whether
or not it would be capable of inducing ADEM or TM.” Id. Dr. Steinman alluded to the fact that
vaccines are injected and posited, “[i]f we injected green beans [into oneself], [he] wonder[s] what
would happen.” Id.; Tr. 93:1–3.

Dr. Steinman relied on additional medical literature to support his theory that the MMR
and varicella vaccines can trigger ADEM and TM and did so in M.P.’s case. An article by Bennetto
and Scolding41 noted that the MMR vaccine is associated with ADEM. Pet’r’s Ex. 19 at 4 (citing
Pet’r’s Ex. 41 at 2–3, ECF No. 73-7); Tr. 43:17–25, 44:1–3. The authors found that “the non-neural
measles, mumps, and rubella vaccinations are most commonly associated with post-vaccination
encephalomyelitis.” See Pet’r’s Ex. 41. He also relied on the article by Young et al., 42 which
indicated that “[n]umerous infections, mostly viral, and other immunologic triggers such as
vaccinations have been associated with ADEM[.]” Tr. 40:20–22 (citing Pet’r’s Ex. 28 at 3, ECF
No. 56-3). The information published by Boston Children’s Hospital 43 noted that “ADEM may []
follow a vaccination, although this is rare.” Tr. 41:20–24 (citing Pet’r’s Ex. 31 at 2, ECF No. 56-
6). He further relied on the National Institute of Health’s ADEM information page, which noted
that “ADEM often follows viral or bacterial infections, or less often, vaccination for measles,
mumps, or rubella.” Tr. 40:25, 41:1–9 (citing Pet’r’s Ex. 29, ECF No. 56-4).44 Dr. Steinman argued
this description is “highly pertinent” to M.P.’s case because she had a metapneumovirus and a
vaccination with MMR. Tr. 41:9–11. Dr. Steinman cited an abstract by Stuve et al. 45 showing that
ADEM’s “clinical symptoms follow an infection or vaccination.” Tr. 45:22–25, 46:11–19 (citing
Pet’r’s Ex. 27, ECF No. 56-2). He testified that the authors of the Klein et al. 46 article filed by
Respondent found that there were “seven outcomes based on being known adverse outcomes, . . .
theoretical/biologically plausible outcomes following MMR and/or varicella vaccines, ADEM,
ataxia, arthritis, encephalitis, meningitis, encephalopathy, and [] Kawasaki” disease. Tr. 70:10–15
(citing Resp’t’s Ex. C, Tab 6 at 3, ECF No. 41-6). However, on cross-examination, Dr. Steinman
admitted that the study did not contain data showing increased incidents of disease or “signal”
after vaccinations. Tr. 83:2–5 (citing Resp’t’s Ex. C, Tab 6).

41
L. Bennetto & N. Scolding, Inflammatory/Post-Infectious Encephalomyelitis, 75 J. NEUROL.
NEUROSURG. PSYCH. 22–28 (2004).
42
N.P. Young, et al., Acute Disseminated Encephalomyelitis: Current Understanding and Controversies,
28:1 SEMIN. NEUROL. 84–94 (2008).
43
Acute Disseminated Encephalomyelitis (ADEM) – Symptoms & Causes, BOSTON CHILDREN’S
HOSPITAL (http://www.childrenshospital.org/conditions-and-treatements/conditions/a/acute-disseminated-
encephalomyelitis-adem/symptoms-and-causes).
44
Acute Disseminated Encephalomyelitis Information Page, NAT’L INST. OF NEUROL. DISORDERS &
STROKE (https://www.ninds.nih.gov/Disorders/All-Disorders/Acute-Disseminated-Encephalomyelitis-
Information-Page).
45
Abstract of O. Stuve, et al., Acute disseminated encephalomyelitis. Pathogenesis, diagnosis, treatment,
and prognosis, 76(6) NERVENARZT 701–07 (2005).
46
N. Klein, et al., Safety of Measles-Containing Vaccines in 1-Year-Old Children, 135:2 PEDIATR. 322–31
(2015).

16
On cross-examination, Dr. Steinman addressed the Baxter et al. 47 article, which found that
there was no statistically significant increased risk of immunization in either the 5 to 28-day or the
2 to 42-day risk interval prior to the onset of TM. Tr. 83:12–14 (citing Resp’t’s Ex. E, Tab 1, ECF
No. 50-2). The authors also found that the Tdap vaccine was associated with a statistically
significant increase in the risk in the 5 to 28-day exposure interval, but not the 2 to 42-day interval,
for the onset of ADEM. Resp’t’s Ex. E, Tab 1. Dr. Steinman opined that the Baxter et al. study
did not show data of increased incidents of disease or “signal” after vaccinations. Tr. 83:12–14.
Dr. Steinman argued, however, that “the methodology [used in that study] would not allow a case
like [M.P.’s] to even be addressed, because it dealt with only one vaccine at a time . . . so [the
authors] would[ not] have counted [M.P.’s] case.” Tr. 83:15–17, 84:1.

On rebuttal, after much discussion regarding the wording used in the Baxter et al. study
(“combination vaccines” versus “combinations of vaccines”), Dr. Steinman maintained that the
authors purported not to “analyze combinations of vaccines[,]” so M.P.’s case would not have been
captured by this study. Tr. 175:5–14 (citing Resp’t’s Ex. E, Tab 1). Despite the authors’ inclusion
of the sentence “we evaluated all administered vaccines, both individually and combined[,]” Dr.
Steinman maintained that the authors analyzed vaccines with multiple viruses contained in the
same syringe, such as the DTaP or MMR vaccines, rather than those requiring “two jabs[.]” Tr.
184:8–25, 185:1–10. Under my questioning, he read verbatim from the article which indicated the
authors “did not analyze combinations of vaccines.” Tr. 188:15–16 (citing Resp’t’s Ex. E, Tab 1).

Dr. Steinman also discussed literature showing an association with HMPV and ADEM. Dr.
Steinman cited an article by Athauda et al., 48 which found that the human metapneumovirus has
been associated with ADEM “in a case where there was also an H1N1 influenza infection.” Pet’r’s
Ex. 19 at 5 (citing Pet’r’s Ex. 44 at 1, ECF No. 73-10). Dr. Steinman stated that the case report
shows an instance of “multiphasic ADEM associated with both human metapneumovirus and
influenza type A and H1N1.” Tr. 44:15–25, 45:1 (citing Pet’r’s Ex. 44). The patient in the study
had not received any recent immunizations. Pet’r’s Ex. 44 at 1. Dr. Steinman opined that this
example “does[ not] fit [M.P.’s case] perfectly, but it[ is] certainly an example of the
metapneumovirus [] caus[ing] ADEM.” Tr. 45:10–13.

He then discussed the package inserts for the vaccines at issue. The MMR vaccine package
insert notes an association with ADEM and TM. Pet’r’s Ex. 19 at 4 (citing Pet’r’s Ex. 42 at 7).49
The package insert indicates that “[e]ncephalitis and encephalopathy have been reported
approximately once for every 3 million doses of [the] MMR II or [MMR]-containing vaccine
administered since licensure of these vaccines.” See id. He testified that the package insert also
“list[s] encephalitis, . . . encephalopathies, measles inclusion body encephalitis, . . . [ADEM],
[TM], and so on[]” as “known adverse reaction[s] to [the] MMR vaccine.” Tr. 42:10–24 (citing
Pet’r’s Ex. 42 at 7). He further relied on the package insert for the varicella vaccine to note that it

47
R. Baxter, et al., Acute Demyelinating Events Following Vaccines: A Case-Centered Analysis, 63:11
CLIN. INFECT. DIS. 1456–62 (2016).
48
D. Athauda, et al., Multiphasic Acute Disseminated Encephalomyelitis (ADEM) Following Influenza Type
A (Swine Specific H1N1), 259 J. NEUROL. 775–78 (2012).
49
See supra note 37.

17
has been associated with encephalitis and TM. Pet’r’s Ex. 19 at 4 (citing Pet’r’s Ex. 43 at 5)50; Tr.
43:2–15.

Dr. Steinman argued that based on all the mimics found in his BLAST searches, and
because ADEM and TM can be attributed to the MMR and varicella vaccines and to the human
metapneumovirus infection, the “vaccinations and the infection constitute a ‘perfect storm’ for
ADEM and TM” in M.P. Pet’r’s Ex. 19 at 28. Dr. Steinman testified that the term “perfect storm”
is “a metaphor . . . for many factors [that] caused the boat to go down[.]” Tr. 80:2–4. Specifically,
he argued that the vaccines M.P. received on May 14, 2015, were a substantial factor in causing
her injuries. Tr. 38:4–8, 74:18–21. As support for his theory that M.P.’s vaccines triggered mimics
resulting in neuroinflammation and subsequent ADEM and TM, he reiterated that the mimics are
present “in all potential factors[]” for M.P.’s condition. Tr. 76:12–14. Dr. Steinman explained that
while “the presence of mimicry is necessary to explain how a vaccine or virus might cause [M.P.’s]
diseases,” the act of “simply having the [molecular] mimic would not be sufficient to get an
autoimmune disease.” Tr. 61:17–18. He opined that “[t]he host, in this case M.P., had to have some
other things in her either genetics or from an environmental impact on her immune system that
contributed to why she got sick.” Tr. 61:18–21. Dr. Steinman argued that the other factor was her
metapneumovirus. Tr. 45:16–17.

He relied on M.P.’s May 30, 2015 brain and spinal cord MRI findings, which showed
evidence “consistent with [ADEM]” to show neuroinflammation. Tr. 31:23–25, 32:5–12, 33:5–7
(citing Pet’r’s Ex. 5 at 162–64). He reiterated that the MRI showed “a long segment of the spinal
cord with abnormalities, all the way from where the spinal cord becomes the brain stem to thoracic
level 10, . . . and vague cord enhancement.” Tr. 32:6–10. He further noted that there was “bilateral
symmetrical periventricular T2 hyperintensities, and a subtle area of the so-called T2
hyperintensity[,] and T1 hypointensity in a brain structure called the corpus collosum.” Tr. 33:2–
5. Dr. Steinman testified that the MRI impression was consistent with neuroinflammation in the
form of ADEM. Tr. 32:5–6. Dr. Steinman also noted that the MRI showed spinal cord
abnormalities “that are a manifestation of extensive [TM].” Tr. 33:8–10. M.P.’s “neurologic exam
was concerning for [] longitudinally extensive [TM].” Tr. 32:11–12. He further relied on M.P.’s
abnormal CSF results and noted they were consistent with a manifestation of extensive TM. Tr.
33:8–11 (citing Pet’r’s Ex. 5 at 163). Dr. Steinman explained that M.P.’s treaters “did a panel for
multiple sclerosis, looking for IgG.” Tr. 33:10–12 (citing Pet’r’s Ex. 5 at 163). He testified that
this is “not really a panel for multiple sclerosis. It [is] a panel for neuroinflammation, but that[ is]
the way [her treaters] reported it.” Tr. 33:12–14. Dr. Steinman opined that M.P.’s treaters “were
comprehensive.” Tr. 33:15.

Dr. Steinman responded to Drs. Gans’ and Kruer’s expert reports, in which they opined
that M.P.’s injuries could be explained by her human metapneumovirus alone. Pet’r’s Ex. 21 at 1.
Dr. Steinman pointed out that he “clearly stated” in his previous report that M.P. had an HMPV
infection. Id. He acknowledged that HMPV alone can cause ADEM and TM. Tr. 81:2–4. He wrote
that given the timeline of M.P.’s cold symptoms, including a runny nose beginning three days after
her May 14, 2015 vaccinations, this was “most likely[] the onset of her HMPV symptoms.” Pet’r’s
Ex. 21 at 1. Dr. Steinman opined that M.P.’s vomiting and loss of mobility reported on May 25
and 26, 2015, were the first symptoms of her ADEM with TM. Id. He posited that “[b]y that time,
50
See id.

18
[M.P. was] at the time when the MMR and [v]aricella vaccines are most likely to cause the ADEM
with TM.” Id. He continued that based on his nearly 40 years of research and experience, “[t]here
is no way for medical science, as it presently exists, to assign a percentage of cause from the three
known potential choices[]” of M.P.’s injury. Id.; Tr. 62:16–18. He testified that there is not a
known medical way to “parse out whether [M.P.’s] neurologic injury was caused by the varicella
vaccine versus the metapneumovirus or the MMR or any of the components of the MMR
vaccine[.]” Tr. 76:2–8. Dr. Steinman acknowledged that Dr. Gans did not attempt to assign a
statistical percentage for the causes of M.P.’s ADEM and TM, rather she “state[d] that the HMPV
is the ‘more likely’ cause.” Pet’r’s Ex. 21 at 1. Dr. Steinman opined that “[t]he term ‘more likely’
. . . assigns a percentage of greater than 50%, which is of course statistical and quantitative.” Id. at
1–2.

He further highlighted that Dr. Gans did not provide any proof that “HMPV has been shown
to be a more common identifiable cause of ADEM than MMR or [v]aricella vaccines.” Id. at 2.
Dr. Steinman stated that Dr. Gans merely opined that “viruses are a more common cause than
vaccines.” Id. Dr. Steinman argued that “Respondent cannot escape th[e] reality[]” that “we have
three potential causes including the contents of the vaccines [M.P.] received.” Id. He continued
that M.P. did not experience her ADEM and TM until she was exposed to all three potential causes.
Id. Under my questioning, Dr. Steinman testified that he would not have expected the course of
M.P.’s illness to be different depending on whether it was caused by an infection versus
vaccination. Tr. 96:8–12.

Dr. Steinman attacked Dr. Gans’ position that M.P.’s family members showed signs of
illness with HMPV around the same time as M.P. and therefore her vaccinations were not
responsible for her injuries. Pet’r’s Ex. 21 at 2; Tr. 36:4–10. Dr. Steinman interpreted M.P.’s older
sister’s May 21, 2015 pneumonia diagnosis and her parents’ upper respiratory symptoms to mean
that “everyone was infected with the same microbe[.]” Tr. 36:15–18. He opined that given M.P.’s
positive testing for the metapneumovirus on May 28, 2015, “everyone had a pneumovirus
infection.” Tr. 35:9–19, 36:18–20 (citing Pet’r’s Ex. 5 at 199). Dr. Steinman argued he “turn[ed]
Dr. Gans’ argument on its head,” and highlighted that “none of [M.P.’s family members] got
ADEM and TM, because they did not also have the MMR and [v]aricella vaccines.” Pet’r’s Ex.
21 at 2. Dr. Steinman stated that “[o]nly one person got vaccinated, and that person[, M.P.,] got
[TM] and [ADEM].” Tr. 36:21–23, 56:11–15. Dr. Steinman maintained that this “fact reinforces
Petitioner’s case and emphasizes [his] line of reasoning[.]” Id. On cross-examination, to account
for the different outcomes of the HMPV infection experienced by M.P. compared to her parents,
Dr. Steinman agreed that there are differences in the immune system of someone M.P.’s age and
someone her parents’ ages. Tr. 85:16–17. He stated it is possible that an adult “could have had an
infection in the past and built up a resistance or antibodies to an infection that a child may not
have[.]” Tr. 85:18–22.

On rebuttal, Dr. Steinman responded to Dr. Gans’ assertions that M.P. suffered a primary
exposure to HMPV, versus her family members who experienced a secondary exposure, which is
why M.P. developed ADEM and TM. Tr. 176:5–8. He opined it was speculation to assume “who
had how many exposures to this virus and when they had them.” Tr. 176:11–14. Furthermore, Dr.
Steinman maintained that a “stronger argument” exists for the fact that “immunological reactions
are much stronger in a secondary response[] because your immune system[ is] all fired up[]”

19
because “[y]our antibodies [have a] much higher affinity. Your T-cells have memory.” Tr. 176:18–
22, 181:14–15. Dr. Steinman agreed that he and Dr. Gans are in a fundamental disagreement about
the effect of multiple exposures to the same pathogen on the immune system. Tr. 180:20–25,
181:1–15. He maintained that based on this discussion, he was not “adding a component of
rechallenge” to his theory of causation because he did not want to speculate about M.P.’s “first
exposure or second exposure.” Tr. 182:5–19.

Regarding timing, Dr. Steinman identified the onset of M.P.’s symptoms as occurring
approximately eleven days post vaccination. Tr. 38:1. As support for this conclusion, he noted that
the first sign of a neurological complaint occurred on May 27, 2015, when M.P. “was very weak
and refusing to walk.” Tr. 31:17–21. He further noted M.P. exhibited floppiness and was lethargic.
Tr. 31:21. While Dr. Steinman noted that vomiting could be a sign of some neurological illnesses,
including TM, he maintained that M.P.’s treaters did not note signs of neurological deficits until
May 27, 2015. Tr. 28:19–25, 29:6–9 (citing Pet’r’s Ex. 4 at 80–82). Dr. Steinman supported this
position by noting that the visit note from May 25, 2015, indicates that M.P.’s neurologic
examination showed she had a normal level of consciousness, normal motor and sensation, and
“grossly normal” cranial nerves. Tr. 30:19–24 (citing Pet’r’s Ex. 4 at 65). He testified, consistent
with M.P.’s medical record, that her fever, vomiting, and diarrhea ceased around May 26, 2015,
prior to the start of her neurologic symptoms. Tr. 31:3–12 (citing Pet’r’s Ex. 4 at 77).

Dr. Steinman opined that the timing of the onset of M.P.’s symptoms after receipt of the
vaccines was “appropriate to implicate the vaccine as causative[.]” Tr. 37:21–25, 73:2–5. Dr.
Steinman argued that M.P.’s hospitalization and ADEM diagnosis within two weeks of her
vaccinations “fits with [the] Bennetto and Scolding[]” article. Pet’r’s Ex. 19 at 28 (citing Pet’r’s
Ex. 41).51 The authors found the “[t]he timing of the first symptoms varies slightly with the
precipitant: typically 1–14 days after non-neural vaccines, a week or less after the appearance of a
rash in exanthematous [sic] illnesses, and 1–3 weeks (or more) after rabies inoculation.” See id.
He relied on the ADEM information page published by the Cleveland Clinic which noted that
although rare, “on occasion ADEM occurs after a vaccination” but that “[m]ost cases of ADEM
begin about seven to 14 days after the infection.” Tr. 71:21–23, 72:2–6 (citing Pet’r’s Ex. 30, ECF
No. 56-5). 52 An article by Sapuan et al. 53 indicated that ADEM “occurs a few days to several
weeks after infections or vaccinations.” Tr. 72:19–20 (citing Pet’r’s Ex. 32 at 1, ECF No. 56-7).
He maintained that the onset of M.P.’s neurologic symptoms fits “[v]ery comfortably[]” within
the appropriate onset timeframe described in the medical literature. Tr. 72:10–13.

2. Respondent’s Expert, Dr. Gans

Dr. Gans submitted two expert reports and testified at the entitlement hearing. See Resp’t’s
Exs. A, E; Tr. 137–174. She agreed that M.P. suffered from ADEM and TM. Tr. 145:23–25. Dr.
Gans opined that the cause of M.P.’s ADEM and TM was her HMPV infection. Resp’t’s Ex. A at
7.

51
See L. Bennetto & N. Scolding, supra note 41.
52
Acute Disseminated Encephalomyelitis (ADEM), CLEVELAND CLIN.
(https://my.clevelandclinic.org/health/diseases/14266-acute-disseminated-encephalomyelitis-adem).
53
S. Sapuan & H. Basri, Acute Disseminated Encephalomyelitis (ADEM) Presenting with Bilateral Optic
Neuritis, 14(1) MALAYS. J. MED. SCI. 71–74 (2007).

20
Dr. Gans discussed M.P.’s medical records and noted that M.P.’s platelet count during her
May 27, 2015 hospitalization was elevated, “suggesting inflammation[.]” Id. at 3 (citing Pet’r’s
Ex. 5 at 9). She noted that M.P.’s fever, rash, URI, otitis media, and anorexia are “all consistent
with what has been described in young children who [] acquire their primary [] infection with
HMPV[.]” Id. at 5. Dr. Gans opined that M.P.’s history “is entirely consistent with an infection
caused by HMPV from the 10 days of intermittent fever and rash, URI symptoms, OM, AGE,
refusal to eat, followed by progressive neurologic symptoms consistent with a spectrum of
demyelinating disease.” Id. at 6. She testified that HMPV can cause neurologic diseases and that
she does not “believe that there[ is] evidence to suggest [the MMR and varicella] vaccines caused
[ADEM or TM] in this case[.]” Tr. 148:6–8, 149:1–6, 150:4–9 (citing Pet’r’s Ex. 44).54 Dr. Gans
stated that M.P. “very clearly [] had an infection . . . [and w]e know very clearly that [] infection
in itself solely as [a] cause of illness” with a “neurologic outcome, particularly ADEM and any
form of that.” Tr. 150:11–17. She therefore concluded that M.P.’s “clinical disease, work-up[,]
and physicians’ assessments of [her] condition support the presence of an acute illness with
HMPV[,] which then progressed to demyelination.” Resp’t’s Ex. A at 5.

As support for her assertion that HMPV was the “acute process” for M.P.’s injuries, Dr.
Gans relied on M.P.’s family’s illness around the same time as M.P. and her vaccinations. Id. at
5–6. Dr. Gans opined that M.P.’s family’s illness was “most likely also HMPV,” which circulates
during the spring. Id. at 5. She noted that the neurologic outcomes of HMPV “are almost
exclusively seen in children <3 years of age . . . [as] age is the major risk factor for severe disease
secondary to HMPV.” Resp’t’s Ex. E at 2 (citing Resp’t’s Exs. A, Tabs 1–5, ECF Nos. 36-1–36-
5). 55 Dr. Gans addressed Dr. Steinman’s claim that while M.P.’s family members experienced
illness around the same time as M.P., they did not develop neurologic symptoms because they did
not also receive the vaccinations at issue. Id.; Tr. 158:3–5. Dr. Gans wrote that this assertion “is
wrong.” Resp’t’s Ex. E at 2. She explained that she does not “think that what you saw for M.P.
was related to something in her immune system trigger[ing] her that then made her respond to the
human metapneumovirus differently than the rest of her family.” Tr. 169:16–19. She explained
that “[r]ather, the reason why is because children are naïve to infections and upon first exposure
experience more severe disease and more disseminated forms of the disease.” Resp’t’s Ex. E at 2.
Dr. Gans opined that M.P.’s May 2015 HMPV infection was her primary infection “given her age
and the severity of her response.” Tr. 158:15–16, 168:7–10, 172:3–6, 173:13–15. Dr. Gans stated
that there is “variability” in the way people react to any pathogen. Tr. 158:7–8. She testified that
“likely this was not the family’s first interaction with this virus, and therefore, they[ were] going
to have a different immune response.” Tr. 158:20–23. Dr. Gans testified that she thinks “the rest
of her family had the advantage of having experienced this at a time when . . . their immune system
was just going to allow them to handle it.” Tr. 169:19–22. She therefore maintained that “age, not

54
See D. Athauda, et al., supra note 48.
55
B. van den Hoogen, et al., A Newly Discovered Human Pneumovirus Isolated from Young Children with
Respiratory Tract Disease, 7:6 NATURE MED. 719–26 (2001); J. Kahn, Epidemiology of Human
Metapneumovirus, 19:3 CLIN. MICROBIOL. REV. 546–57 (2006); V. Schildgen, et al., Human
Metapneumovirus: Lessons Learned over the First Decade, 24:4 CLIN. MICROBIOL. REV. 734–54 (2011);
J. Williams, et al., Population-Based Incidence of Human Metapneumovirus Infection Among Hospitalized
Children, 201:12 J. INFECT. DIS. 1890–98 (2010); K. Edwards, et al., Burden of Human Metapneumovirus
Infection in Young Children, 368:7 N. ENGL. J. MED. 633–44 (2013).

21
vaccine receipt, was the reason M.P. had [a] more severe disease than other family members with
the same infection.” Resp’t’s Ex. E at 2.

However, after much discussion, Dr. Gans stated that M.P. could still have developed
ADEM after her secondary exposure to HMPV and that she is likely to have a severe reaction to
HMPV anytime she is exposed. Tr. 172:10–22. Dr. Gans explained that the “immune response is
going to be triggered in the same direction typically, no matter how many times [the patient] is
exposed.” Tr. 171:2–4. But because of cellular memory, the immune system “learn[s], and it[ is]
less severe the next time.” Tr. 171:4–5.

She admitted that much of the pathophysiology about HMPV is unknown, but “appears
highly associated with CNS manifestations that include demyelinating disease.” Resp’t’s Ex. A at
6. As support, Dr. Gans relied on medical literature showing that an antecedent acute viral illness
has been shown to be the cause of demyelinating processes more frequently than vaccines. Id. at
7. She cited several articles showing that the HMPV infection has been found to be the “second
leading cause of bronchiolitis and pneumonia in children <5 years of age, with outbreaks peaking
mostly during spring.” Id. at 5 (citing Resp’t’s Exs. A, Tabs 1–5). 56

Dr. Gans wrote that “[s]tudies have associated HMPV with acute encephalopathies ranging
from subcortical encephalitis to multifocal demyelinating encephalitis.” Id. at 6. She cited a study
by Arnold et al., 57 which showed that in a pediatric group with encephalitis, “5% of children
showed neurologic symptoms who were infected with HMPV.” Id. (citing Resp’t’s Ex. A, Tab 6,
ECF No. 36-6). The authors noted that there have been reports “suggesting that HMPV may also
cause disease of the [CNS] but its true role in encephalitis is not established.” Resp’t’s Ex. A, Tab
6 at 1. They discussed nine patients “with evidence of HMPV infection and a spectrum of CNS
abnormalities ranging from uncomplicated seizures to fatal encephalitis.” Id. Dr. Gans also cited
a retrospective study of patients with encephalitis by Glaser et al., 58 which found that HMPV was
the third most common respiratory pathogen causing neurologic disease in a study of 204 patients
with a “possible etiologic agent[.]” Resp’t’s Ex. A at 6 (citing Resp’t’s Ex. A, Tab 11 at 6, ECF
No. 37-1). Dr. Gans relied on the Arnold et al. and Glaser et al. articles to note that “the [CNS]
profile is normal in the majority” of cases of HMPV infected children with neurologic diseases.
Id. (citing Resp’t’s Exs. A, Tabs 6, 11); see also Resp’t’s Exs. A, Tabs 7–10, ECF Nos. 36-7–36-
10.

She then discussed a case report by Schildgen et al., 59 which described a case where a child
died of encephalitis. Resp’t’s Ex. A at 6 (citing Resp’t’s Ex. A, Tab 7). The authors noted that this
case “might be correlated with primary [HMPV].” Resp’t’s Ex. A, Tab 7 at 1. They also noted that
“[a]lthough neurologic symptoms have been described for infections caused by other
paramyxoviruses, such as . . . mumps and measles, no such symptoms have been associated with

56
See id.
57
J. Arnold, et al., Human Metapneumovirus Associated with Central Nervous System Infection in Children,
28 PEDIATR. INFECT. DIS. 1057–60 (2009).
58
C.A. Glaser, et al., Beyond Viruses: Clinical Profiles and Etiologies Associated with Encephalitis, 43
CLIN. INFECT. DIS. 1565–77 (2006).
59
O. Schildgen, et al., Human Metapneumovirus RNA in Encephalitis Patient, 11:3 EMERGING INFECT.
DIS. 467–71 (2005).

22
HMPV infection.” Id. Nonetheless, they opined that the child in the study died from edema caused
by encephalitis “probably induced or triggered by HMPV.” Id. The child’s lab results showed an
elevated CSF and no other suggestions of inflammation. Id. No other bacterial or viral pathogens
were detected, except for HMPV. Id. at 2. The authors determined that “while testing of the CSF
was not positive for viral RNA, . . . the brain tissue tested at autopsy was positive[,] despite the
child having a normal CSF profile and negative CSF [polymerase chain reaction (“PCR”),] for
HMPV.” See id. The authors also found inflammation in the lung at autopsy. Id. at 3. Based on
this, the authors maintained they demonstrated the “first fatal encephalitis that might be associated
with HMPV infection.” Id. at 4.

Dr. Gans relied on a similar case report by Fernandez et al., 60 wherein “both the respiratory
and CSF were positive for HMPV[]” in a ten-year-old girl who developed acute encephalitis.
Resp’t’s Ex. A at 6 (citing Resp’t’s Ex. A, Tab 8). The authors concluded that “[t]he detection of
[HMPV] in [the CSF] strongly suggests its causative role in acute encephalitis.” Resp’t’s Ex. A,
Tab 8 at 1. They maintained this is because “it has been isolated from the respiratory tract during
the acute phase of several cases of encephalitis and in postmortem lung and brain tissue of a patient
with a fatal encephalitis.” Id. Using the reports from Schildgen et al. and Fernandez et al., Dr. Gans
argued that “[t]his suggests that the neurologic disease caused by HMPV may result from direct
viral invasion and that the virus is not very inflammatory in the CNS[.]” Resp’t’s Ex. A at 6 (citing
Resp’t’s Exs. A, Tabs 7–8). She opined “that the virus is tissue bound and not free in fluids (similar
to other neuropathic viruses such as [herpes simplex virus]).” Id.

She also cited articles by Leake et al. and Hughes et al. to note that “CNS manifestations
of neurologic disease may result from a post-infectious phenomenon[.]” Id. (citing Resp’t’s Exs.
A, Tabs 12–13, ECF Nos. 37-2–37-3). 61 The authors of the Leake et al. 62 article noted that “[t]he
lack of evidence for ongoing infection or vaccination in most cases and the usual time lapse of a
few weeks between infectious symptoms or signs and ADEM onset have promoted the view that
ADEM is a postinfectious immune disease.” Resp’t’s Ex. A, Tab 12 at 2. However, the authors
also noted that “ADEM has been observed after vaccination with animal brain-derived rabies
vaccines and, rarely, after administration of other vaccines.” Id. In post-infectious cases of ADEM,
the authors noted that molecular mimicry between MOG and MBP has been proposed as an
explanation for the autoreactive immune responses to the CNS. Id. Further, the authors of the
Hughes et al. 63 article found that two thirds of the patients with Guillain-Barré syndrome (“GBS”)
in their “two large series” studies had an infection within the previous six weeks. Resp’t’s Ex. A,
Tab 13 at 2.

60
I. Sanchez Fernandez, et al., Human Metapneumovirus in the Cerebrospinal Fluid of a Patient with Acute
Encephalitis, 69:5 ARCH. NEUROL. 649–53 (2012).
61
J. Leake, et al., Acute Disseminated Encephalomyelitis in Childhood: Epidemiologic, Clinical and
Laboratory Features, 23 PEDIATR. INFECT. DIS. 756–64 (2004); R. Hughes, et al., Guillain-Barré
syndrome, 366 LANCET 1653–66 (2005).
62
J. Leake, et al., Acute Disseminated Encephalomyelitis in Childhood: Epidemiologic, Clinical and
Laboratory Features, 23 PEDIATR. INFECT. DIS. 756–64 (2004).
63
R. Hughes, et al., Guillain-Barré syndrome, 366 LANCET 1653–66 (2005).

23
The authors of the Pidcock et al. 64 article found “47% of children with acute [TM] had an
antecedent infectious process with onset on average 11 days prior to onset of neurologic
symptoms.” Resp’t’s Ex. A at 6 (citing Resp’t’s Ex. A, Tab 15, ECF No. 37-5). The authors
determined that “[o]f the 13 children in the study with an antecedent immunization, 8 had signs of
an antecedent illness.” See id. They concluded that “the young age of children in their study with
acute [TM] predicts that most children will have an antecedent immunization prior to symptom
onset given the vaccine schedules[.]” Resp’t’s Ex. A, Tab 15. They continued that “together with
the lack of any consistent vaccine association,” this “undermine[s] a potential causal link between
immunization and acute [TM].” See id. Dr. Gans further relied on the article by Absoud et al., 65
which showed 66% of cases of pediatric TM were associated with an acute illness. Resp’t’s Ex. A
at 7 (citing Resp’t’s Ex. A, Tab 17). Finally, she cited an article by Wolf et al., 66 documenting an
antecedent illness in 50–100% of the time prior to the onset of TM. Resp’t’s Ex. A at 7 (citing
Resp’t’s Ex. A, Tab 16 at 2, ECF No. 37-6). The authors noted that “[o]ther less common
provoking factors [of TM] include vaccines[.]” Resp’t’s Ex. A, Tab 16 at 2. They indicated that
molecular mimicry is one proposed theory for the immunopathogenesis of infiltrations of the spinal
cord, including TM. Id.

Based on the medical literature, Dr. Gans argued that “it is well supported that children
who are infected with HMPV and are not vaccinated suffer from neurologic complications and
thus HMPV alone is sufficient as a cause for the ADEM/TM that M.P. experienced.” Resp’t’s Ex.
E at 1. Dr. Gans wrote that there is “substantial epidemiologic and pathophysiologic data providing
a causal relationship of HMPV to ADEM/TM and no data supporting a causal relationship with
vaccines, solely a temporal association.” Id. Dr. Gans maintained that the reports of vaccines
preceding the onset of ADEM or TM “are temporal only with no specimens showing an actual link
to disease and only speculation of how vaccines may cause demyelination.” Id.

On the other hand, there is “support for HMPV to cause [ADEM], and that it does so alone.”
Tr. 152:14–21 (citing Resp’t’s Ex. E, Tab 1). 67 Dr. Gans opined “this clearly makes HMPV a more
likely agent as a cause of ADEM/TM . . . .” Resp’t’s Ex. E at 1. As additional support, Dr. Gans
relied on the studies performed through the Vaccine Safety Datalink. Id. She noted that such
studies provide a “systematic review of vaccine outcomes in a full population.” Id. In the study by
Baxter et al., 68 the authors looked at the relationship between receipt of a vaccine and the
development of ADEM/TM. Id. at 2 (citing Resp’t’s Ex. E, Tab 1 at 1). The authors used a “a case-
centered design, which compare[d] vaccination patterns during an exposure interval prior to the
outcome in cases [versus] the entire study population, matched by age, sex, and site.” See id. The
study included 64 million vaccine doses. Id. Overall, the authors found that “[f]or TM, there was
no statistically significant increased risk of immunization[]” in either the 5 to 28-day or the 2 to
42-day risk interval prior to onset. Resp’t’s Ex. E, Tab 1 at 1, 5. “For ADEM, the Tdap [] vaccine
was associated with a statistically significant increase in risk in the 5 to 28-day exposure interval

64
F.S. Pidcock, et al., Acute Transverse Myelitis in Childhood: Center-Based Analysis of 47 Cases, 68:18
NEUROL. 1474–80 (2007).
65
See M. Absoud, et al., supra note 24.
66
V. Wolf, et al., Pediatric Acute Transverse Myelitis Overview and Differential Diagnosis, 27:11 J. CHILD
NEUROL. 1426–36 (2012).
67
See R. Baxter, et al., supra note 47.
68
See id.

24
. . . but not the longer 2 to 42-day interval.” Id. The authors determined this shorter interval
indicated a “possible association of ADEM with [the] Tdap vaccine[.]” Id. at 1.

Dr. Gans addressed the methodology used in the Baxter et al. study and noted that the
authors “did[ not] exclude people who had been given more than one vaccine, but they actually
did[ not] do their analysis to look at what happens when somebody receives measles and varicella
and everything else[.]” Tr. 154:15–18. She explained “their analysis looked at [vaccines] one at a
time[.]” Tr. 154:21–22. She stated her understanding is that their “analysis was not done to
understand any impacts or additive effects of having more than one vaccine[.]” Tr. 155:3–9. Under
my questioning, Dr. Gans agreed that “whether or not you have one vaccine or a multitude of
vaccines does not increase the immunologic response that could trigger cross-reaction that would
be pathogenic.” Tr. 165:16–20.

Regarding the time of onset of M.P.’s neurologic symptoms, Dr. Gans opined that the
temporal association of MMR and varicella vaccines “are neither necessary nor contributors to the
[TM] which can be explained solely by [M.P.’s] acute viral illness.” Resp’t’s Ex. A at 7.

On cross-examination, Dr. Gans maintained that there is “no association in large studies of
live viral vaccines with [neurologic] outcomes.” Tr. 163:1–2. Even when confronted with medical
literature that showed “at least a potential association between the MMR vaccination and
ADEM[,]” Dr. Gans testified that she does not think there is an association described in large
studies. Tr. 163:7–11. She noted that she has “seen [the association] with case reports or VAERS
reporting.” Tr. 163:11–12. Dr. Gans explained “there[ is] biologic plausibility” for the MMR
vaccine to cause ADEM in the literature “because we know that the actual viruses within those
[vaccines] cause ADEM.” Tr. 163:16–19. Dr. Gans stated that it is her belief that there is no
evidence that the MMR and varicella vaccines can cause ADEM or TM. Tr. 164:23–25. She
testified she would never expect to see it happen. Tr. 165:8–10.

3. Respondent’s Expert, Dr. Kruer

Dr. Kruer submitted two expert reports and testified during the entitlement hearing. See
Resp’t’s Exs. C, F; Tr. 102–136. He opined that “M.P.’s ADEM/TM is far-more likely to be caused
by infection than by [her] vaccination[s.]” Resp’t’s Ex. C at 2. Dr. Kruer considered M.P.’s human
metapneumovirus to be the alternate cause that is a “much more likely” explanation for her injuries.
Tr. 116:15–17, 124:16–18.

He opined that “Dr. Steinman’s contention that MMR and varicella immunizations
somehow caused M.P.’s ADEM is purely speculative.” Resp’t’s Ex. C at 2. He argued that “[j]ust
because something can happen does[ not] mean that it did happen.” Tr. 111:1–2. He wrote that
there is no evidence to indicate that the administration of M.P.’s vaccinations led to her ADEM.
Resp’t’s Ex. C at 2. He testified he “just do[es not] think that there[ is] evidence that[ is] nearly as
compelling supporting the vaccines in question and the pathogenesis of ADEM as compared to
alternate explanations that are also under consideration[]” in M.P.’s case. Tr. 116:8–12. Instead,
Dr. Kruer opined that M.P. suffered from at least one, but possibly two, intercurrent infections
around the time of her MMR and varicella vaccinations, and then developed ADEM. Resp’t’s Ex.
C at 2. As support, Dr. Kruer attributed M.P.’s runny nose, cough, and fever to her HMPV infection

25
rather than to her ADEM. Id. He further noted that M.P. experienced diarrhea contemporaneously
with the other symptoms. Id. Dr. Kruer attributed M.P.’s diarrhea to a possible second infection or
her antibiotic use, and noted that ADEM neither causes this symptom nor runny nose, cough, and
fever. Id.

Dr. Kruer addressed Dr. Steinman’s claim that M.P.’s vaccinations must have been the
cause of her injuries because, although her family members were sick, M.P. was the only person
in her family to receive a vaccination and to develop TM and ADEM. Tr. 118:2–5. Dr. Kruer
opined that “just arguing that because [M.P.’s onset of injuries] happened at that point in time, that
that necessarily construed an association [with the vaccine], it just d[oes not] hold up.” Tr. 118:10–
12. He stated that his “most significant concern” about this contention was that “it was[ not] clear
to [him] that no other members of the family had received the vaccines.” Tr. 118:8–10. Dr. Kruer
then testified that MMR and varicella vaccinations typically provide lifelong immunity and do not
require boosters. Tr. 125:5–25, 126:1–8. Under my questioning, Dr. Kruer clarified that when he
indicated he did not know if M.P.’s family members had been vaccinated around the time of her
HMPV infection, he was “talking about the primary series[]” of such vaccinations, not boosters.
Tr. 126:9–15.

Dr. Kruer further opined that it is not necessary to invoke the vaccine as a cause of M.P.’s
injuries when her infection is also a known cause of TM and ADEM. Tr. 117:2–9. As support for
his opinion, Dr. Kruer relied on medical literature showing that ADEM is rarely associated with
vaccination, and associations between MMR and varicella vaccinations, specifically, and ADEM
is even more rare. Resp’t’s Ex. C at 2 (citing Resp’t’s Ex. C, Tab 6). 69 On cross-examination, he
discussed literature showing an association between vaccinations and ADEM. He addressed the
Klein et al. 70 study, which noted that ADEM is a known outcome of the MMR and/or varicella
vaccines. Tr. 115:8–9 (citing Resp’t’s Ex. C, Tab 6 at 3). In Dr. Kruer’s opinion, this article did
not “show a clear signal associating the vaccines in question with ADEM.” Tr. 115:19–21.

Instead, Dr. Kruer cited literature showing an association between ADEM and infections.
Dr. Kruer relied on an article by Pohl,71 which noted that ADEM is “typically preceded by an
infection, and this association has been included in the definition of ADEM as a typically post-
infectious entity.” Resp’t’s Ex. C at 2 (citing Resp’t’s Ex. C, Tab 2, ECF No. 41-2). Dr. Kruer
indicated that a study by Hynson et al. 72 showed that a precipitating infection is identified in
approximately 75% of ADEM cases. Id. (citing Resp’t’s Ex. C, Tab 3 at 2, ECF No. 41-3). The
authors found that of the 31 children in their study, 22 patients, or 71%, had prodromal illnesses
prior to the development of ADEM, “with the majority of these being upper respiratory tract
infections or nonspecific febrile illnesses.” Resp’t’s Ex. C, Tab 3 at 2. They also noted that 2
patients, or 6%, had received the Hepatitis B vaccine three to six weeks before developing ADEM.

69
See N. Klein, et al., supra note 46.
70
See id.
71
D. Pohl, Epidemiology, Immunopathogenesis and Management of Pediatric Central Nervous System
Inflammatory Demyelinating Conditions, 21 CURR. OP. NEUROL. 366–72 (2008).
72
J.L. Hynson, et al., Clinical and Neuroradiologic Features of Acute Disseminated Encephalomyelitis in
Children, 56 NEUROL. 1308–12 (2001).

26
Id. Dr. Kruer also cited a study by Menge et al., 73 which demonstrated no association between
ADEM and immunization but a strong association between antecedent infection and ADEM.
Resp’t’s Ex. C at 2 (citing Resp’t’s Ex. C, Tab 7, ECF No. 41-7). The authors nonetheless
concluded that “the pathogenic events that trigger the initial clinical attack [of ADEM] . . . remain
unknown.” Resp’t’s Ex. C, Tab 7 at 2.

On cross-examination, Dr. Kruer further relied on the Baxter et al.74 article to argue that
there is a more compelling association between infection and ADEM and TM compared to
immunization, which has a “very weak [association with ADEM and TM] at best.” Tr. 124:1–9
(citing Resp’t’s Ex. E, Tab 1). Dr. Kruer argued that “the preponderance of evidence[, based on
the papers discussed during the hearing,] indicate[s] that ADEM is simply more commonly, more
typically associated with a preceding infection, and that, in fact, if there is a signal for ADEM after
vaccination, it[ is] actually a rare occurrence.” Tr. 120:1–5.

Dr. Kruer addressed Dr. Steinman’s theory pursuant to Althen prong one. Dr. Kruer wrote
that while he “agree[s] with most of Dr. Steinman’s statements[,]” he “believe[s] there are fallacies
in [Dr. Steinman’s] reasoning and thus his contentions are not logically supported.” Resp’t’s Ex.
F at 1. Dr. Kruer argued that the BLAST results “do not establish molecular mimicry.” Resp’t’s
Ex. C at 2. He described molecular mimicry as “something that does require a degree of sequence
homology but that also requires evidence of an autoreactive response that was directly related to
that homology.” Tr. 109:13–16. Dr. Kruer explained that “[t]riggering an autoimmune response
not only requires sequence homology, it [also] requires that the responsible protein be taken up
and processed by antigen-presenting cells[.]” Resp’t’s Ex. C at 3. The protein must then be
“cleaved to generate the theorized peptides, . . . outcompete the thousands of other peptide
combinations produced to [] stimulate the generation of autoreactive T and/or B-cell clones,”
which then “help direct the immune response.” Id. (citing Resp’t’s Ex. C, Tab 10, ECF No. 41-
10).75

He further argued that Dr. Steinman’s “arbitrary criteria” to define a meaningful molecular
mimic as “a run of 5 or more of 12 amino acids that are identical” is “not widely accepted in the
scientific community.” Id. at 2 (citing Pet’r’s Ex. 19 at 7). He argued that the “degree of sequence
homology that Dr. Steinman shows is inconsequential[.]” Id. at 3. Dr. Kruer opined that the
“criterion does not stand up to further scrutiny.” Id. He continued “[g]iven that there are only 20
possible characters in the amino acid ‘alphabet,’ and that most proteins are several hundred amino
acids long, when one applies a moving window analysis, possibilities abound for matching peptide
sequences.” Id. He relied on an article by O’Brien et al.76 to note that “the optimal epitope length
needed to maximally activate T-cells via MHC receptors is 18–20 amino acids long[], 12–15
residues for CD4+ T cell recognition of MHC Class II, and shorter peptides of 7–9 residues for
MHC I and CD8+ T-cells.” Id. at 2–3 (citing Resp’t’s Ex. C, Tab 9, ECF No. 41-9).

73
T. Menge, et al., Acute Disseminated Encephalomyelitis: An Acute Hit Against the Brain, 20 CURR. OP.
NEUROL. 247–54 (2007).
74
See R. Baxter, et al., supra note 47.
75
J. Fourneau, et al., The Elusive Case for a Role of Mimicry in Autoimmune Diseases, 40 MOLECULAR
IMMUNOL. 1095–102 (2004).
76
C. O’Brien, et al., Peptide Length Significantly Influences in vitro Affinity for MHC Class II Molecules,
4:6 IMMUNOME RES. 1–7 (2008).

27
As additional support, Dr. Kruer cited an article by Kanduc et al., 77 which “analyzed viral
proteins and compared them to the [approximately] 30,000 known human proteins[.]” Id. at 3
(citing Resp’t’s Ex. C, Tab 14, ECF No. 40-4). The authors found a total of 2,907,096 matches of
5 amino acid residues. See id. Based on this article, Dr. Kruer opined “it is not surprising that Dr.
Steinman was able to find a handful of matches in his own BLAST searches.” Resp’t’s Ex. C at 3.
Dr. Kruer further noted that when humans become ill with viral infections, on average multiple
times per year, it is reflected by ≥5 amino acids in a stretch of homology. Id. He opined that “[i]f
all that was required to induce autoimmunity was such sequence overlap, 100% of the population
should be afflicted with an autoimmune disease. Yet this is clearly not the case.” Id. Similarly, Dr.
Kruer testified, consistent with his written report, that “there are 3,713,010 matches of human
proteins with themselves.” Tr. 111:12–17 (citing Resp’t’s Ex. C at 3). He opined that “[a]gain, if
all that was required for autoimmunity was sequence homology, infection should not even be
needed to trigger autoimmunity; one’s own body should provide ample opportunity for
autoimmunity to develop.” Resp’t’s Ex. C at 3. He therefore argued that “just because Dr.
Steinman was able to show there[ is] a degree of homology between two things, this [statistic] is
an example that there are literally more than 3 million other peptides that show such homology.”
Tr. 111:23–25, 112:1.

Dr. Kruer addressed Dr. Steinman’s conclusion regarding the immunity to nervous system
proteins including myelin in healthy individuals despite the fact that most healthy people do not
suffer from autoimmune diseases. Resp’t’s Ex. F at 1. Dr. Kruer wrote that he “completely agree[s]
. . . [and] that is exactly [his] point.” Id. Dr. Kruer explained that “[i]f peptide homology were the
only factor that was necessary to trigger autoimmunity, then even innocuous exposures like green
beans, could wantonly elicit a state of autoimmunity in otherwise healthy people.” Id. He used this
analogy to “drive home the point that more than molecular mimicry is necessary for autoimmune
disease (like [TM] and/or ADEM) to actually occur.” Id. He noted that Dr. Steinman agrees with
him on this point and “thus undermines [Dr. Steinman’s] own argument[.]” Id.

Then, Dr. Kruer attacked Dr. Steinman’s BLAST searches and their relevance to M.P.’s
case. Resp’t’s Ex. C at 3. Dr. Kruer posited that “[c]omputer-based simulations are simply not able
to predict whether any of these peptides stimulated autoimmunity in M.P.’s case.” Id. Dr. Kruer
opined that Dr. Steinman’s method “only goes so far[]” and his “subsequent conclusions went
beyond what was able to be demonstrated solely by a BLAST search.” Tr. 110:16–20. Dr. Kruer
posited that while Dr. Steinman’s BLAST searches “indicate limited sequence homology[,]” they
“do nothing to show that these theoretical peptides w[ould] actually be produced, let alone incite
an autoimmune response.” Resp’t’s Ex. C at 2.

Dr. Kruer continued that “even if one overlooks the oversimplified criteria for molecular
mimicry that [Dr. Steinman] presents, and assumes that molecular mimicry were . . . triggered by
vaccine exposure[,]” in M.P.’s case, “the most that this sequence of events would lead to is a
situation where M.P. would have autoreactive B- and/or T-cells circulating in her body.” Resp’t’s
Ex. F at 1. He maintained that Dr. Steinman agreed that “this has been shown to be necessary but
not sufficient T [cell involvement] for autoimmune disease to result.” Id.

77
D. Kanduc, et al., Massive Peptide Sharing Between Viral and Human Proteomes, 29 PEPTIDES 1755–
66 (2008).

28
Dr. Kruer opined that to prove the relationship between the vaccines at issue and M.P.’s
injuries, he would “require homology and an autoreactive response, and the homology and
autoreactive response need to be from the inciting peptide to the insuming [sic] target of
reactivity.” Tr. 120:19–25, 121:1–3. The target of reactivity is “against a specific relevant . . . brain
protein.” Tr. 121:3–4. He indicated that “it is true that anti-[MBP] and anti-[MOG] autoantibodies
are present in a fraction of ADEM cases.” Resp’t’s Ex. C at 3 (citing Resp’t’s Exs. C, Tabs 11–12,
ECF Nos. 40-1–40-2).78 Dr. Kruer relied on an article by Ramanathan et al. 79 to argue that “[i]t is
not clear that these autoantibodies cause disease in and of themselves, even when present.” Id.
(citing Resp’t’s Ex. C, Tab 13, ECF No. 40-3). Dr. Kruer testified that “anti-MOG antibodies are
not invariably present. There are some cases that have them; there are some that do[ not].” Tr.
121:20–22. He noted that M.P. “was never shown to have autoantibodies to any of the proteins Dr.
Steinman BLAST[ed],” therefore, the BLAST searches do not “conclusively show sequence
homology to proteins known to be relevant to this case.” Resp’t’s Ex. C at 3. Dr. Kruer testified
that additional supporting evidence of this reaction in M.P. would have been to do a blood or spinal
fluid test for anti-MOG antibodies at the time of an active response. Tr. 121:16–20, 122:11–17.
He noted that this testing was not performed in M.P.’s case. Tr. 122:20–23.

To substantiate his argument that establishing sequence homology does not show evidence
of a cross-reaction, Dr. Kruer ran his own BLAST search. Resp’t’s Ex. C at 3; Tr. 113:14. He
posited that by the age that M.P.’s ADEM occurred, “[m]ost children in the U.S. have been eating
baby foods for several months” and “are thus exposed to a host of new proteins that occur as natural
components of these new foods.” Resp’t’s Ex. C at 3. Dr. Kruer then BLASTed a green bean
protein versus MBP. Id. He explained that he BLASTed the protein portion of the green bean to
show that limited sequence homology, is “hardly a remarkable thing.” Tr. 113:15–16. He opined,
“[i]t[ is] actually very, very common when comparing two proteins or portions of a protein[.]” Tr.
113:16–18. He found sequence homologies in three places “of 5, 6, and 7 amino acids in a 12
residue stretch between green bean protein and [MBP].” Resp’t’s Ex. C at 4. Based on these results,
Dr. Kruer argued that by Dr. Steinman’s standards, “it is just as likely that green beans caused
M.P.’s ADEM as it is that her MMR and varicella vaccines were to blame.” Id. at 4–5. Dr. Kruer
stated that the green bean example “was meant to illustrate that there are many, many proteins that
could show a similar degree of sequence homology.” Tr. 114:16–19. He concluded it showed that
just because Dr. Steinman could prove a sequence homology, it does not mean molecular mimicry
occurred in this case. Tr. 114:22–25.

On cross-examination, Dr. Kruer stated it is “possible” for the MMR and varicella vaccines
to trigger ADEM and TM. Tr. 120:9–18. However, he maintained that it is not likely that the
vaccines are related to M.P.’s injuries. Tr. 123:21–23.

78
K. van Haren, et al., Serum Autoantibodies to Myelin Peptides Distinguish Acute Disseminated
Encephalomyelitis from Relapsing-Remitting Multiple Sclerosis, 19:13 MULTIPLE SCLEROSIS J. 1726–33
(2013); M. Baumann, et al., Clinical and Neuroradiological Differences of Paediatric Acute Disseminating
Encephalomyelitis with and without Antibodies to the Myelin Oligodendrocyte Glycoprotein, 86 J. NEUROL.
NEUROSURG. PSYCH. 265–72 (2015).
79
S. Ramanathan, et al., Anti-MOG Antibody: The History, Clinical Phenotype, and Pathogenicity of a
Serum Biomarker for Demyelination, 15 AUTOIMMUN. REV. 307–24 (2016).

29
IV. Applicable Legal Standards

To receive compensation under the Vaccine Act, a petitioner must demonstrate either that:
(1) the petitioner suffered a “Table injury” by receiving a covered vaccine and subsequently
developing a listed injury within the time frame prescribed by the Vaccine Injury Table set forth
at 42 U.S.C. § 300aa-14, as amended by 42 C.F.R. § 100.3; or (2) that petitioner suffered an “off-
Table injury,” one not listed on the Table, as a result of his receiving a covered vaccine. See 42
U.S.C. §§ 300aa-11(c)(1)(C); Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321
(Fed. Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1319–20 (Fed. Cir.
2006). Petitioner alleges that M.P. suffered from encephalitis, which is a Table injury for the MMR
vaccination. 80 Thus, Petitioner must prove that M.P.’s encephalitis meets the Table criteria for that
injury.

Petitioner also alleges that M.P.’s ADEM and TM were caused-in-fact by the vaccines at
issue. To establish causation-in-fact, a petitioner must demonstrate by a preponderance of the
evidence that the vaccine was the cause of the injury. 42 U.S.C. § 300aa-13(a)(1)(A). A petitioner
is required to prove that the vaccine was “not only a but-for cause of the injury but also a substantial
factor in bringing about the injury.” Moberly, 592 F.3d at 1321–22 (quoting Shyface v. Sec’y of
Health & Hum. Servs., 165 F.3d 1344, 1352–53 (Fed. Cir. 1999)).

In the seminal case of Althen v. Sec’y of the Dept. of Health & Hum. Servs., the Federal
Circuit set forth a three-pronged test used to determine whether a petitioner has established a causal
link between a vaccine and the claimed injury. See 418 F.3d 1274, 1278–79 (Fed. Cir. 2005). The
Althen test requires petitioners to set forth: “(1) a medical theory causally connecting the
vaccination and the injury; (2) a logical sequence of cause and effect showing that the vaccination
was the reason for the injury; and (3) a showing of a proximate temporal relationship between
vaccination and injury.” Id. at 1278. To establish entitlement to compensation under the Program,
a petitioner is required to establish each of the three prongs of Althen by a preponderance of the
evidence. Id. “[T]hese prongs must cumulatively show that the vaccination was a ‘but-for’ cause
of the harm, rather than just an insubstantial contributor in, or one among several possible causes
of, the harm.” Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1358 (Fed. Cir. 2006).
“[C]lose calls regarding causation are resolved in favor of injured claimants.” Althen, 418 F.3d at
1280. Further, evidence used to satisfy one prong of the test may overlap to satisfy another prong.
Capizzano, 440 F.3d at 1326.

A petitioner who satisfies all three prongs of the Althen test has established a prima facie
showing of causation. Hammitt v. Sec’y of Health & Hum. Servs., 98 Fed. Cl. 719, 726 (2011). A
petitioner who demonstrates by a preponderance of the evidence that he suffered an injury caused
by vaccination is entitled to compensation unless the respondent can demonstrate by a
preponderance of the evidence that the injury was caused by factors unrelated to the vaccination.
See Althen, 418 F.3d at 1278; Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 547 (Fed.
Cir. 1994). In such a case, the government must not merely prove the existence of an alternative
cause, but that such an alternative actually caused the injury. Knudsen, 35 F.3d at 549.
Consequently, when and if a petitioner establishes a prima facie case, the burden then shifts to the

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Petitioner does not allege, nor does the evidence support, a Table claim for injuries sustained as a result
of M.P.’s varicella vaccination. See Am. Pet. at 2.

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government to prove that an alternative cause, unrelated to the administration of the vaccine, was
the “sole substantial factor” in causing the alleged injury. de Bazan v. Sec’y of Health & Hum.
Servs., 539 F.3d 1347, 1354 (Fed. Cir. 2008); see also Hammitt, 98 Fed. Cl. at 726 (explaining
that the respondent’s burden is to show that the “factor unrelated” was the “sole substantial factor”
in causing the injury). Additionally, a factor unrelated “may not include ‘any idiopathic,
unexplained, unknown, hypothetical, or undocumentable cause, factor, injury, illness or
condition.’” 42 U.S.C. § 300aa-13(a)(2); see also Doe v. Sec’y of Health & Hum. Servs., 601 F.3d
1349 (Fed. Cir. 2010) (explaining that an idiopathic diagnosis cannot be a “factor unrelated,” as it
is idiopathic).

In considering the reliability of a petitioner’s evidence of a prima facie case, the special
master may consider alternative causes for a petitioner’s condition that are reasonably raised in the
record, even if the respondent does not pursue a formal alternative cause argument. Doe, 601 F.3d
at 1358. This is especially true where there are multiple factors acting in concert, and the “causative
effect” of the vaccine may be “overwhelmed” by competing alternative causes. Walther v. Sec’y
of Health & Hum. Servs., 485 F.3d 1146, 1151 (Fed. Cir. 2007) (“Where multiple causes act in
concert to cause the injury, proof that the particular vaccine was a substantial cause may require
the petitioner to establish that the other causes did not overwhelm the causative effect of the
vaccine”); see also Shyface, 165 F.3d at 1352. Thus, in weighing a petitioner’s case-in-chief, a
special master may consider evidence that the petitioner’s alleged injury could have been caused
by alternative causes. Walther, 485 F.3d at 1151. Proof of a “logical sequence of cause and effect”
will eliminate potential likely alternatives. Id.

V. Discussion

A. Experts

Although special masters have the discretion to be informed by past rulings and
experiences, case-specific filings and testimony are the most helpful types of evidence, given the
fact-specific nature of each decision. See Doe v. Sec’y of Health & Hum. Servs., 76 Fed. Cl. 328,
338–39 (2007). To that end, experts are an essential piece of a petitioner’s claim and Respondent’s
defense. Where both sides offer expert testimony, a special master’s decision may be “based on
the credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe v. Sec’y of Health & Hum. Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000)). This case
ultimately turns, not only on M.P.’s medical history, but also the persuasiveness of the written
reports, supporting documentation, and expert testimony. I therefore must assess each expert’s
opinion and assign weight accordingly. This assessment will inform my analysis pursuant to each
prong of Althen.

Indeed, all three experts have extensive experience and impressive credentials in
neurology, immunology, and demyelinating diseases, such as TM and ADEM. See, e.g., Pet’r’s
Ex. 20; Resp’t’s Exs. B, D. However, Dr. Steinman delivered his testimony with fewer
equivocations than both of Respondent’s experts. While Drs. Gans and Kruer have provided useful
testimony and persuasive explanations in previous cases before me, as well as other special masters
in the Program, presently, Drs. Kruer and Gans presented their opinions riddled with assumptions,
reversals, and concessions when compared to Dr. Steinman’s analysis. See Broekelschen, 618 F.3d

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at 1347 (citing Lampe, 219 F.3d at 1362) (finding that where both sides offer expert testimony, a
special master’s decision may be “based on the credibility of the experts and the relative
persuasiveness of their competing theories”). For instance, Dr. Kruer strongly disagreed with Dr.
Steinman’s assumption that no other members of M.P.’s family received MMR or varicella
vaccines around the time M.P. and her family became ill. Dr. Kruer then acknowledged that MMR
and varicella vaccinations typically have lifelong immunity and do not require boosters. Despite
this acknowledgment, he maintained that he does not know for sure that M.P.’s family members
did not receive the primary series of such immunizations at the same time as M.P.’s vaccinations.
Tr. 125:5–25, 126:1–15. It is generally well-accepted that the primary series of MMR and varicella
vaccinations are administered during early childhood (ranging from 12 to 15 months of age). 81
Therefore, I find it is not more likely that M.P.’s older family members received the primary series
of MMR or varicella vaccinations at the same time as M.P. Dr. Kruer’s argument that M.P.’s
vaccinations played no role in causing her condition is undercut by his reliance on the unsupported
assumption that her family was also vaccinated without adverse effect.

Likewise, Dr. Gans repeatedly demonstrated a reluctance to acknowledge any probative
value of certain evidence. When confronted with the body of medical literature submitted by
Petitioner that shows a potential association between the MMR vaccination and ADEM, she
testified that “[t]here[ has] been no association in large studies of live viral vaccine with these
outcomes.” Tr. 163:1–2. She later acknowledged that she has “seen it with case reports or VAERS
reporting.” Tr. 163:11–12. However, she opined that these individual instances are only evidence
of “biologic plausibility” for the MMR vaccine to cause ADEM in the literature. Tr. 163:12–15.
Dr. Gans then hedged in her discussion of the impact of a primary versus secondary exposure to
the HMPV infection on M.P.’s immune system. Dr. Gans testified that “the most important thing
that you[ are] seeing here is not that M.P. had vaccines[; i]t[ is] that M.P. never saw human
metapneumovirus before.” Tr. 168:7–10. During that same line of questioning, Dr. Gans later
stated “because of the way that people respond to things, whether first, second, third, I think that
if M.P. was going to have a more severe reaction to this virus, she would have a more severe
reaction anytime[.]” Tr. 172:17–21. While Dr. Gans has specific and relevant knowledge regarding
a child’s immune response to vaccines, the main focus of her testimony was a discussion of the
medical literature that was largely unhelpful. When considering the parties’ arguments in relation
to the biological mechanism and immunologic response involved in M.P.’s demyelinating
conditions, Dr. Steinman’s delivery contributed significantly more to the value of his testimony
than Drs. Kruer and Gans.

B. Petitioner’s Table Claim

Pursuant to the Table (in January of 2018, at the time the amended petition was filed),
encephalitis is a compensable injury if the first symptoms thereof occurred within 5 to 15 days
after the administration of the MMR vaccine. 42 U.S.C. § 300aa-14(a). In general, to succeed on
such a claim, a petitioner would need to establish that the injured party experienced an acute
encephalitis as defined by the Qualifications and Aids to Interpretation (“QAIs”). 42 C.F.R. §
100.3(c)(3) (2018). The QAIs indicate that a petitioner must show evidence of an acute encephalitis
within the applicable time period that results in chronic encephalopathy. See id. Acute encephalitis

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See Child and Adolescent Immunization Schedule, CENTER FOR DISEASE CONTROL & PREVENTION,
https://www.cdc.gov/vaccines/schedules/hcp/imz/child-adolescent.html (last visited July 29, 2022).

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is demonstrated by evidence of neurologic dysfunction plus evidence of an inflammatory process
in the brain. § 100.3(c)(3)(i). Evidence of neurologic dysfunction consists of either: one neurologic
finding referable to the CNS, including “[f]ocal cortical signs ([] aphasia, alexia agraphia, cortical
blindness), cranial nerve abnormalities, visual field defects, abnormal presence of primitive
reflexes . . . or cerebellar dysfunction ([] ataxia, dysmetria, or nystagmus);” or an acute
encephalopathy. See §§ 100.3(c)(3)(i)(A)(1)–(2). An acute encephalopathy for children less than
18 months old who did not suffer a seizure “is indicated by a significantly decreased level of
consciousness that lasts at least 24 hours.” § 100.3(c)(2)(i)(1). Evidence of an inflammatory
process in the brain must include “[CSF] pleocytosis (>5 [WBC]/mm3 in children >2 months of
age and adults; >15 WBC/mm3 in children <2 months of age)” or at least two of

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/8213138. Public record. Not legal advice.