McGrail v. Secretary of Health and Human Services

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 17-926V
(to be published)
*************************
MARTIN MCGRAIL as father and natural *
guardian of minor S.M., and AMY * Chief Special Master Corcoran
MCGRAIL as mother and natural guardian *
of minor S.M., *
* Filed: March 23, 2021
Petitioners, *
* Ruling on Entitlement; Transverse
v. * Myelitis; Hepatitis B Vaccine;
* Molecular Mimicry; Althen Prong
SECRETARY OF HEALTH AND * One; Althen Prong Three; Treater
HUMAN SERVICES, * Support
*
Respondent. *
*
*************************
Jeffrey S. Pop, Esq., Jeffrey S. Pop & Assoc., Beverly Hills, CA, for Petitioners.
Christine Becer, U.S. Department of Justice, Washington, DC, for Respondent.
RULING ON ENTITLEMENT 1
On July 10, 2017, Martin and Amy McGrail, as parents and natural guardians of S.M., a
minor, filed this action seeking compensation under the National Vaccine Injury Compensation
Program (the “Program”). ECF No. 1. The Petitioners allege that a Hepatitis B vaccine
administered to S.M. on July 14, 2014, caused her to incur transverse myelitis (“TM”). Although
an initial hearing in the matter was held in late-January 2020, the parties have since jointly agreed
1
This Ruling will 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 (2012). This means the Decision will be available to anyone with access
to the internet. As provided by 42 U.S.C. § 300aa-12(d)(4)(B), however, the parties may object to the published
Ruling’s inclusion of certain kinds of confidential information. Specifically, under Vaccine Rule 18(b), each party has
fourteen (14) days within which to request redaction “of any information furnished by that party: (1) that is a trade
secret or commercial or financial in substance and is privileged or confidential; or (2) that includes medical files or
similar files, the disclosure of which would constitute a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b).
Otherwise, the entire Ruling will be available to the public in its current form. Id.
that the matter could be resolved via ruling on the record, rather than by holding a follow-up
hearing for testimony from the remaining experts and other additional fact witnesses.
Having reviewed the record, all expert reports and associated literature, and listened to
those witnesses and experts who testified at the 2020 hearing, I hereby find that Petitioners are
entitled to a damages award. Petitioners have preponderantly established that S.M. likely
experienced TM post-vaccination, rather than acute flaccid myelitis (“AFM”) as Respondent
maintains. Petitioners have also met their burden under Althen v. Sec’y of Health & Hum. Servs.,
418 F.3d 1274, 1278 (Fed. Cir. 2005)—although resolution of this case presents a very close call,
since Petitioner’s overall showing on the first and third Althen prongs was not notably robust when
evaluated closely.
I. Fact History
S.M. was born on October 1, 2013, via spontaneous vaginal delivery without complication.
Ex. 18 (filed on compact disk) at 65; Affidavit of Amy McGrail, filed as Ex. 1 (on compact disk)
at 1 (“Affidavit”). Prior to her receipt of the vaccine at issue, S.M. was a healthy child without any
significant medical conditions. S.M. did suffer from seasonal allergies for which she received
nebulizer treatments with Xopenex and Pulmicort as needed. Ex. 7 (filed on compact disc) at 105.
S.M.’s family history does not include any serious medical conditions relevant to the claim. Ex. 7
at 94–95; Affidavit at 1.
On June 20, 2014 (a few weeks before receiving the vaccine at issue), S.M. was seen by
Dr. Mary Yee, one of S.M.’s pediatricians, for a three-day history of congestion, cough, and yellow
nasal discharge. Ex. 7 at 104. S.M. was deemed afebrile, however, with a rectal temperature of 99
degrees. Id.; Tr. at 89. She was prescribed antibiotic treatment with amoxicillin, and her symptoms
dissipated by July 8, 2014. Tr. at 137, 158.
The following month, on July 14, 2014, Ms. McGrail took S.M. to Pediatric Associates in
Neptune, New Jersey for a routine well-child visit and to receive the third dose of the Hepatitis B
vaccine. Ex. 7 at 94. No medical concerns were raised during the visit, and Dr. Yee noted that S.M.
did not experience any immediate reaction to the vaccination. Id.Three days later, at approximately 3:30 p.m. on July 17, 2014, Ms. McGrail received a
phone call from S.M.’s daycare informing her that S.M. was sleepy, irritable, and had developed
a fever and therefore needed to be picked up. Affidavit at 2; Ex. 5 (filed on compact disk) at 23–
31. After retrieving S.M., Ms. McGrail took her to Dr. Yee to be evaluated for a newly developed
fever, limpness, and difficulty breathing. Affidavit at 2. Dr. Yee noted that S.M. had a fever of
100.6 degrees, was lethargic, and was constantly crying in pain. Ex. 7 at 102. Dr. Yee
recommended S.M. be taken to the emergency department for further evaluation. Id.; see also Ex.
9 (filed on compact disk) at 29–30.
2
Upon arriving at Jersey Shore University Medical Center, S.M. was evaluated in the
emergency department at approximately 5:20 p.m. by Dr. Richard Sultan, D.O. Ex. 5 at 19–21, 24.
A physical examination conducted by Dr. Sultan revealed that S.M. had a fever and was in acute
neurological distress. Id. at 20–21. He noted that S.M. had good motor control of her head but had
no control of her trunk, was having difficulty breathing, and was exhibiting spontaneous movement
of her extremities. Id. Based upon these observations, Dr. Sultan’s differential diagnoses included
acute disseminated encephalomyelitis, TM, botulism, Guillain-Barré syndrome (“GBS”), tick
paralysis, and myasthenia gravis. Id. at 21. To further refine his diagnosis, Dr. Sultan ordered
several diagnostic tests, including an MRI and cerebral spinal fluid (“CSF”) test. Id. S.M. was
admitted to the pediatric intensive care unit at 5:28 p.m. and broad-spectrum antibiotics were
administered. Id. at 31, 38; Ex. 105 filed Oct. 15, 2019 (ECF No. 35-9) at 412.
At around 6:30 p.m. on July 17th, S.M. underwent a lumbar puncture to collect a CSF
specimen. Ex. 4 (filed on compact disk) at 64. Analysis of the sample revealed elevated protein
levels. Id. A few hours later, at 11:58 p.m., S.M. underwent a spinal MRI. Ex. 5 at 85. The results
of that MRI showed “[d]iffuse increased signal intensity within the cervical cord and upper
thoracic cord…with expansion of the cord particularly within the cervical spine without evidence
of enhancement following the administration of contrast.” Id. These findings were consistent with
Dr. Sultan’s initial TM diagnosis, and he thereafter began a five-day course of treatment with
Solumedrol. 2 Id.; Ex. 105 at 413. Within two days of this treatment, S.M. experienced improved
mobility of her lower extremities, though her upper extremities remained flaccid. Ex. 5 at 108. A
repeat MRI conducted on July 23, 2014 showed “significant improvement of edema within the
cervical cord” with the lesion now extending only between C3 and T4 where it had previously
extended from C2 to T6. Id. at 88.
In the course of S.M.’s initial treatment, consideration was given to whether an infectious
cause could be identified for her neurologic presentation. Thus, on July 19, 2014, S.M. was
evaluated by Dr. Aswine Bal, an infectious disease specialist. Ex. 5 at 17–18. His physical
examination of S.M. revealed hypotonia in her upper extremities and decreased tone in her lower
extremities. Id. at 17. Though Dr. Bal observed some movement and brisk reflexes in S.M.’s lower
extremities, he noted that she was still unable to move her arms or sit unassisted. Id. Regarding the
proposed diagnosis of TM, Dr. Bal agreed that the MRI results of July 17th supported the diagnosis,
and explained that TM is usually preceded by a viral infection or vaccination. Id. at 18. An
extensive infectious disease work-up was positive for a rhinovirus infection, so broad-spectrum
antibiotic treatments were discontinued. Ex. 100, filed Oct. 15, 2019 (ECF No. 35-3) at 65; Ex.
105 at 419, 484.
S.M. was discharged from Jersey Shore University Medical Center on July 31, 2014, with
a diagnosis of TM. Ex. 5 at 103. She was transferred to the Children’s Hospital of Philadelphia
2
Solumedrol is an anti-inflammatory synthetic glucocorticoid. Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=89219 (last visited Mar. 3, 2021).
3
(“CHOP”) for additional treatment. Id. Upon her admission to CHOP, S.M. was noted to have
persistent hypotonia and absent reflexes in her upper extremities, but she was able to spontaneously
move and had brisk reflexes in her lower extremities. Ex. 100 at 67. S.M. continued to exhibit
breathing difficulty leading treaters to intubate her. Id. at 71–72. Because S.M. continued to
experience intermittent fevers, additional laboratory studies were ordered. Id. at 71.
On August 1, 2014, S.M.’s cultures again revealed the presence of a rhinovirus infection,
with no other infections detected. Ex. 7 at 430–31. Based on these results, in addition to the MRI
and CSF studies that were conducted at Jersey Shore University Medical Center, treaters at CHOP
initially suspected that S.M. was “suffering from a monophasic demyelinating event rather than
the first presentation of a chronic demyelinating disorder.” Ex. 100 at 81. Thus, an eight-day course
of Plasmapheresis 3 (“PLEX”) treatment was initiated. Id. at 81–82, 184. On August 12, 2014, S.M.
underwent a repeat MRI which showed residual non-enhancing abnormalities from C3 to T2 with
“subtle signal abnormality in the cord at the T10 level.” Id. at 174–75.
S.M. received her final PLEX treatment on August 13, 2014, and was evaluated for
discharge to a rehabilitation facility on August 14, 2014. Ex. 100 at 183. During her physical
evaluation, S.M. was noted to have “4/5 strength” and normal responses to touch in both legs, but
0/5 strength in her upper extremities—though she was now exhibiting some spontaneous
movement in her right wrist and left fingers. Id. at 184. She also appeared to have regained some
muscle tone in both her upper and lower extremities. Id. S.M. was thereafter discharged to
Children’s Specialized Hospital for inpatient rehabilitation with Dr. Michele Fantasia. Id. at 186;
see generally Ex. 6 (filed on compact disk). After completing intensive physical and occupational
therapy, S.M. showed continued improvement in her physical condition, but she did not return to
her pre-vaccination baseline. Ex. 6 at 93–99. She was discharged from Children’s Specialized
Hospital on September 14, 2014.
Since September 2014, S.M. has continued to pursue outpatient physical and occupational
therapy with noted improvement. Ex. 6 at 93–99, 876–78, 892–94, 904–06, 918–20, 954–56; Ex.
14 (filed on compact disk) at 1–7. On January 5, 2017, S.M. was re-evaluated by CHOP
neurologist, Dr. Amy Waldman. Ex. 14 at 1–7. During her evaluation, Dr. Waldman noted that
S.M. had not experienced any worsening or new episodes of neurologic dysfunction since the
initial onset of her symptoms in July 2014. Id. at 1. Regarding S.M.’s diagnosis, Dr. Waldman
acknowledged the original TM diagnosis S.M. had received during her initial hospital admission,
but she also considered the possibility that S.M. had suffered from AFM—a condition that became
prevalent in the fall of 2014 and is thought to be associated with Enterovirus D68 infections. Id. at
5.
3
Plasmapheresis is a procedure in which plasma is removed from the blood and is then transfused back into the body
with added donor components such as frozen plasma or albumin. Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=39455&searchterm=plasmapheresis (last visited Mar. 3,
2021).
4
To date, S.M. “remains profoundly quadriplegic” with moderate to severe spasticity. Tr. at
123. Her quadriplegia makes her more susceptible to other conditions including orthopedic
problems, scoliosis, bladder complications, urinary tract infections, kidney disease, bowel
dysfunction, megacolon and perforation, and skin breakdown. Id. at 124, 164. S.M.’s condition is
not expected to improve. Id. at 124, 140.
II. Experts and Testifying Witnesses
A. Petitioners’ Fact Witnesses and Treaters
1. Mr. Martin McGrail
Mr. McGrail, S.M.’s father, offered testimony at the entitlement hearing. 4 See generally
Tr. at 132–47. He began by discussing S.M.’s health prior to receiving the third dose of the
Hepatitis B vaccine, noting that she was an overall healthy child who only occasionally required
allergy medications (Pulmicort and Xopenex). Id. at 134–35, 137. Mr. McGrail did not recall S.M.
experiencing any unusual health problems close in time to her vaccination. Id. at 137. He did note
that approximately three or four weeks before her vaccination, S.M. experienced some congestion
and was diagnosed with an upper respiratory infection, but it was treated with antibiotics and had
completely resolved by the time she received the vaccine. Id. at 142–43.
According to Mr. McGrail, Ms. McGrail took S.M. to her doctor’s appointment on the
morning of July 14, 2014. Tr. at 137–38. Three days later, on July 17, 2014, Mr. McGrail recalls
that S.M. appeared healthy and was not exhibiting any signs of illness (fever, cough, runny nose,
etc.). Id. at 138. He did, however, recall that S.M. was given a nebulizer treatment with Pulmicort
for a cough and shortness of breath—symptoms the McGrails attributed to S.M.’s allergies. Id. at
143–44; Ex. 5 at 32. S.M. was also given Tylenol for teething discomfort at that time. Tr. at 143–
44; Ex. 5 at 32. That afternoon, he received a phone call from Ms. McGrail informing him that she
had to pick S.M. up from daycare to take her to the pediatrician. Tr. at 139. Mr. McGrail later
learned that S.M. was taken to the emergency room, and he arrived at the hospital that evening. Id.
at 139. At the hospital, Dr. Sultan informed Mr. McGrail of S.M.’s TM diagnosis and that her
condition could be associated with a viral illness or vaccination. Id. at 139, 146–47.
2. Ms. Amy McGrail
Ms. McGrail offered both a written affidavit and testimony during the entitlement hearing.
Tr. at 149–69. She described S.M. as an overall healthy baby prior to receiving the third dose of
4
As noted above, an initial hearing was held in January 2020, at which time a number of fact witnesses and experts
testified. But not all experts were heard at this time; in particular, Respondent’s experts did not testify.
5
the Hepatitis B vaccine. Id. at 152–54. While S.M. did suffer from a milk protein allergy in addition
to seasonal allergies, those conditions were well managed with special formula and allergy
medications. Id.
Ms. McGrail recalled taking S.M. to her pediatrician, Dr. Yee, on the morning of July 14,
2014 for a routine visit and vaccination. Tr. at 153, 159. According to her, S.M. was in good health
on the day of her appointment. Id. at 159–60. When S.M. awoke on the morning of July 17, 2014,
Ms. McGrail did not observe any unusual signs or symptoms of illness before taking S.M. to
daycare. Id. at 160–61. Though she did not recall administering Xopenex and Pulmicort to S.M.
that morning, she indicated that giving S.M. these medications was not unusual given the
frequency of S.M.’s allergy symptoms. Id. at 161–62, 166–67.
At approximately 3:00 p.m. that day, Ms. McGrail received a phone call from S.M.’s
daycare informing her that S.M. had developed a fever and needed to be picked up earlier than
usual. Tr. at 162. On the way to pick up S.M., Ms. McGrail scheduled an emergency appointment
with Dr. Yee to have S.M. evaluated for her fever. Id. Following an examination of S.M., Dr. Yee
urged Ms. McGrail to take S.M. to the emergency room for further evaluation. Id. at 163. A few
hours after S.M.’s admission to the Jersey Shore University Medical Center, Ms. McGrail was told
that S.M. was suffering from TM and required steroid treatment. Id. She did not recall ever being
told that S.M. had a viral infection while at Jersey Shore University Medical Center. Id. at 164.
According to Ms. McGrail, S.M. was eventually transferred to CHOP for PLEX treatments, and it
is at that time when she first became aware that S.M. was concurrently experiencing a rhinovirus
infection. Tr. at 164.
3. Dr. Mary Yee
Dr. Yee, S.M.’s pediatrician of approximately six years, provided testimony at the
entitlement hearing on Petitioners’ behalf. Tr. at 62–109. Dr. Yee completed her medical education
at SCB Medical College in India before completing her residency training in Cleveland, Ohio. Id.
at 63. She is a board-certified pediatrician and has been working as a primary care physician for
approximately twenty-eight years. Id.
As Dr. Yee recalled, S.M. was in overall good health and was developing normally prior
to receiving the third dose of the Hepatitis B vaccine. Tr. at 68–94. Any health concerns for which
S.M. was seen for, including an E. coli infection, bronchitis, bronchiolitis, colic, and allergies, are
common among children, and S.M. responded well to the treatments she received for these various
issues. Id. at 70–71, 76–79, 82–87, 89–91. On the morning of July 14, 2014, Dr. Yee recalled that
S.M. appeared healthy and developmentally normal. Id. at 91–93. She administered the third dose
of the Hepatitis B vaccine and did not note any immediate adverse reactions. Id.
6
When S.M. returned to Dr. Yee in the afternoon of July 17, 2014, S.M. seemed very
irritable and lacked muscle tone. Tr. at 95. Dr. Yee performed an extensive physical evaluation,
but her examination did not reveal any signs of illness. Id. at 96. Based upon her observations, Dr.
Yee recommended S.M. be taken to the emergency department to be evaluated by a neurologist.
Id. at 95.
Since S.M. first received her TM diagnosis, Dr. Yee has continued to see S.M. for primary
care visits. Tr. at 97; Ex. 140 at 21–109. Dr. Yee described S.M.’s present condition as “not
good”—she is paraplegic and continues to exhibit poor muscle tone and spasticity. Tr. at 99. She
is unable to urinate on her own and thus requires catheterization. Id. at 97. According to Dr. Yee,
S.M. continues to need extensive physical and occupational therapy for her condition. Id. at 99.
4. Dr. Michele Fantasia, M.D.
Dr. Fantasia provided a single report and testimony at the entitlement hearing on behalf of
Petitioners. See Dr. Fantasia Report, filed as Ex. 83 on June 17, 2019 (ECF No. 33-2) (“Fantasia
Rep.”); Tr. at 110–31.
Dr. Fantasia is a board-certified pediatric physiatrist specializing in physical medicine and
rehabilitation. Tr. at 110. She received her bachelor’s degree (biology) from Fairleigh Dickinson
University, followed by her medical degree from the New Jersey Medical School. Dr. Fantasia
Curriculum Vitae, filed as Ex. 84 on June 17, 2019 (ECF No. 33-3) (“Fantasia CV”); Tr. at 111.
She then completed her internship and residency in pediatrics, physical medicine, and
rehabilitation at the University of Medicine and Dentistry of New Jersey before obtaining board
certification in these subjects. Fantasia CV at 1; Tr. at 111–12. Currently, Dr. Fantasia serves as
the Director of the Spinal Cord Injury and General Rehabilitation programs at Children’s
Specialized Hospital in New Brunswick, New Jersey. Fantasia CV at 1; Tr. at 112. Dr. Fantasia
first became familiar with S.M.’s case in August 2014, when S.M. was admitted to Children’s
Specialized Hospital for inpatient rehabilitation. Tr. at 113. She served as S.M.’s treating
physiatrist during S.M.’s admission, and she has continued to follow-up with S.M. since that time.
Id.
In her testimony, Dr. Fantasia discussed the defining characteristics of both TM and AFM.
Tr. at 113–16. She described TM as an “autoimmune disease of the spinal cord with still debated
unclear etiologies” that results in spastic paralysis. Id. at 113. She also emphasized that TM is a
disease that targets both gray and white matter of the spinal cord. Id. at 115. This characteristic,
according to Dr. Fantasia, is what primarily distinguishes TM from AFM—a disease that is
generally limited to gray matter of the anterior horn cells of the spinal cord. Id. at 114–15.
7
Another distinguishing feature highlighted by Dr. Fantasia between TM and AFM was the
spastic nature of TM-induced paralysis, as compared to the flaccid paralysis caused by AFM. Tr.
at 113–14, 116, 118–19, 127. CSF studies can also help differentiate between a TM and AFM
diagnosis, because protein levels are typically higher in cases of TM. Id. at 115, 131. Dr. Fantasia
did acknowledge, however, that distinguishing between TM and AFM can be difficult during the
acute phase because the initial “findings can be very similar.” Id. at 115, 127. Over the course of
her twenty-year-long career, Dr. Fantasia has seen approximately sixty patients suffering from
TM, but only about three or four patients with AFM. Id. at 114–15. She attributed this disparity to
the fact that AFM—which is a subtype of acute flaccid paralysis—was not defined until 2014, and
was therefore not a diagnosis that physicians would have considered. Id. at 115, 128.
Based upon the medical records made available to her, plus her direct experience treating
S.M., Dr. Fantasia opined that S.M. more likely than not suffered from TM. Tr. at 114, 117, 130.
Though she largely deferred to the opinions of the neuroradiologist who interpreted S.M.’s MRI
studies, Dr. Fantasia offered additional evidence based on her own observations of S.M.’s
condition to support her conclusion. Id. at 114, 118–20. She began by noting that S.M. exhibits
spastic paralysis, hypertonia 5, increased reflexes, and clonus 6. Id. at 119. These symptoms are
caused by damage to both motor and sensory neurons, and are typical of TM. Id. By contrast, if
S.M. had experienced AFM, her muscle tone would have remained flaccid or “floppy.” Id. at 119,
127. She also noted that S.M. suffers from severe sensory deficits, leaving her more prone to tissue
damage. Id. at 122. While some sensory deficits may be observed in AFM cases, they tend to be
less profound than those seen in TM. Id. The severity and extent of S.M.’s sensory and motor
deficits led Dr. Fantasia to conclude that the TM diagnosis she had received was likely accurate.
Id. at 114, 130.
5. Dr. Aswine Bal, M.D., MPH
Though Dr. Bal, an infectious disease specialist, did not testify at the entitlement hearing,
he offered a report in support of Petitioners’ claim. See Report, filed as Ex. 108 on Jan. 16, 2020
(ECF No. 44-1) (“Bal Rep.”). In it, Dr. Bal outlined his involvement in the treatment of S.M.,
including the clinical findings he considered in rendering his TM diagnosis. Id.
Dr. Bal completed his undergraduate education at Ravenshaw University in Cuttak, India.
Bal Curriculum Vitae, filed as Ex. 109 on Jan. 16, 2020 (ECF No. 44-2). He then obtained his
Bachelor of Medicine and Bachelor of Surgery from S.C.B. Medical College in Cuttak, India
5
Hypertonia describes excessive tone of the skeletal muscles, so that they have increased resistance to passive
stretching and reflexes are often exaggerated; this usually indicates upper motor neuron injury. Dorland’s Illustrated
Medical Dictionary 886 (33rd ed. 2020) (hereinafter “Dorland’s”).
6
Clonus describes a continuous rhythmic reflex tremor initiated by the spinal cord below an area of spinal cord injury,
set in motion by reflex testing. Dorland’s at 368.
8
before completing a rotating internship at S.C.B. Medical College Hospital. Id. at 1. Dr. Bal went
on to receive a master’s degree in public health from Yale University while simultaneously
completing a residency in preventative medicine at the Yale University School of Medicine. Id.
He then completed a residency in pediatrics at Newark Beth Israel Medical Center in Newark,
New Jersey before returning to Yale University to complete a fellowship in pediatric infectious
disease. Id. Currently, Dr. Bal serves as a professor of pediatrics at Rutgers Robert Wood Johnson
Medical School, in addition to his clinical practice as an attending physician in pediatric infectious
disease at Jersey Shore University Medical Center. Id. at 2.
Dr. Bal’s report notes that he first became involved in S.M.’s treatment on July 19, 2014—
hence contemporaneous with her vaccination and immediate hospitalization days thereafter. Bal
Rep. at 1. At that time, S.M. had already undergone an MRI and CSF studies, and her treating
neurologist, Dr. Sultan, had already proposed a working diagnosis of TM. Id. at 1–2. During his
initial infectious disease consultation with S.M., Dr. Bal recommended she undergo viral studies,
including a viral respiratory panel. Id. at 2. He was, however, unable to find the reported laboratory
results for those tests despite diligent efforts to locate them. 7 Id. Dr. Bal was thus unable to explain
the report of a positive rhinovirus test in the July 30, 2014 transfer note, but nonetheless concluded
that even if S.M. was at the time suffering from a rhinovirus infection, it was unlikely to have
contributed to her developing TM. Id. He did not, however, provide an explanation or references
in support of this opinion.
After eliminating infectious etiologies for S.M.’s condition, Dr. Bal considered the
possibility that the Hepatitis B vaccination S.M. had received just a few days prior to the onset of
her symptoms may have played a causal role. Bal Rep. at 2–3. He found several case reports
describing instances of TM and other demyelinating conditions post-vaccination, though he also
acknowledged that case reports are insufficient to establish a causal association. Id. at 3. Thus, Dr.
Bal concluded that S.M.’s Hepatitis B vaccine could at least not be ruled out as the cause of S.M.’s
condition. Id.
B. Petitioners’ Experts
1. Dr. Jeffrey Silverman, M.D.
Dr. Silverman, a radiologist, provided one expert report and testified at the entitlement
hearing on Petitioners’ behalf. See Silverman Report, filed as Ex. 72 June 17, 2019 (ECF No. 32-
1) (“Silverman Rep.”); Tr. at 4–55.
Dr. Silverman obtained his bachelor’s degree in cellular biology and biochemistry from
Revelle College at the University of California, San Diego before obtaining his medical degree
7
S.M.’s positive Rhinovirus result is reported in the medical record, albeit briefly. Ex. 105 at 484.
9
from the University of California, San Diego School of Medicine. Silverman Curriculum Vitae,
filed as Ex. 73 on June 17, 2019 (ECF No. 32-2) (“Silverman CV”). He completed an internal
medicine internship before completing his residency in radiology, followed by several visiting
fellowships in various subspecialties of radiology. Id. at 1–2. Dr. Silverman is board certified in
radiology, but he does not hold certification in neuroradiology. Id. at 3; Tr. at 14, 44. Presently,
Dr. Silverman serves as a clinical associate professor at the University of Southern California Keck
School of Medicine. Silverman CV at 3. Over the course of his career, Dr. Silverman estimates
that he has reviewed approximately 10,000 brain and spine images—though he admittedly reviews
fewer pediatric studies now than in previously held positions. Tr. at 11, 15–16.
In preparing his opinions, Dr. Silverman reviewed MRI and CT 8 images obtained between
July 2014 and May 2016, as well as the written reports for those images contained in the medical
record. Tr. at 17. He concluded that S.M.’s radiological studies were all compatible with a TM
diagnosis. Id. at 17–21; Silverman Rep. at 3.
Dr. Silverman explained how radiological evidence can help distinguish between TM and
AFM diagnoses. Tr. at 23–24, 48. TM is characterized by “lesions extending for three or four
spinal segments” and the area of signal intensity “generally involves more than two-thirds of the
cross-sectional area of the spinal cord.” Id. It is also common for TM to involve both gray and
white matter. Id. at 24. This is in direct contrast to AFM, which is largely restricted to gray matter 9
of the anterior horn cells 10—a feature that will appear as a “white butterfly” on T2-weighted
MRIs—and extends only one or two levels. Id. at 24, 36, 41–42; see also B. Erlt-Wagner et al.,
Acute Flaccid Myelitis in a 10-Year-Old Girl, 290 Radiology 31, 31 (2019), filed as Ex. 78 on
June 17, 2019 (ECF No. 32-7) (referring to Centers for Disease Control (“CDC”) diagnostic
criteria for AFM, including “MRI showing a spinal cord lesion largely restricted to gray matter
and spanning one or more spinal segments.”) (“Erlt-Wagner”); E. Gordon-Lipkin et al.,
Comparative Quantitative Clinical, Neuroimaging, and Functional Profiles in Children with Acute
Flaccid Myelitis at Acute and Convalescent Stages of Disease, 61 Developmental Medicine and
Child Neurology 366, 371 (2019), filed as Ex. 124 on Jan. 16, 2020 (ECF No. 45-7) (concluding
that the white matter of the spinal cord is largely spared abnormalities during both the acute and
convalescent stages of AFM). Dr. Silverman also noted that AFM is quite rare, and thus physicians
8
A computed tomography (CT) scan employs an emergent x-ray beam measured by a scintillation counter, with the
results recorded and processed by a computer for reconstruction display. CT scans are useful when a disease of the
central nervous system is implicated and degenerative abnormalities can be identified. Mosby’s Manual of Diagnostic
and Laboratory Tests 1026 (5th ed. 2014).
9
On cross examination, Dr. Silverman clarified that AFM can also involve some white matter, but maintained that
gray matter involvement tends to be far more extensive. Tr. at 51–52.
10
Dr. Silverman acknowledge that during the acute stage of AFM, T2-weighted MRIs can show “ill-defined,
abnormal, hyperintense signal…throughout the spinal cord gray matter,” but will become better defined in the anterior
horns of the gray matter as time progresses. Tr. at 51.
10
are much more likely to see cases of TM, even though the two can overlap somewhat in
presentation. Tr. at 47.
By comparing S.M.’s radiological studies against these characteristics, Dr. Silverman
concluded that S.M.’s presentation more closely aligned with that of TM. Tr. at 30. Notably, S.M.
exhibited signal intensity spanning more than two-thirds of the cross-sectional area of her spinal
cord, in addition to severe swelling and involvement of both gray and white matter. Id. (citing Ex.
132).
To further support his conclusion, Dr. Silverman compared S.M.’s imaging studies to those
of known TM and AFM patients. Tr. at 34–35. Such a comparison revealed that S.M. shared
several characteristics consistent with TM, including increased signal intensity through more than
two-thirds of the cross-sectional area of the cord, gray and white matter involvement, and cord
edema. Id. at 34 (comparing Illustrative Adult TM MRI, filed as Ex. 133 on Jan. 16, 2020 (ECF
No. 46-6), with Ex. 132). When Dr. Silverman compared S.M.’s imaging results with those of a
known AFM case, however, the hallmark “white butterfly” of AFM is notably absent from S.M.’s
images. Tr. at 37 (comparing Illustrative Child AFM MRI, filed as Ex. 134 on Jan. 16, 2020 (ECF
No. 46-7), with Ex. 132 at 4). Based upon these comparisons, Dr. Silverman concluded that S.M.’s
radiological imaging studies were most consistent with a TM diagnosis. Tr. at 43.
2. Dr. Elizabeth Egan, M.D., Ph.D.
Dr. Egan, a pediatric infectious disease physician, provided three expert reports on
Petitioners’ behalf. Dr. Egan Report, filed as Ex. 23 on Apr. 13, 2018 (ECF No. 13-1) (“First Egan
Rep.”); Supplemental Report, filed as Ex. 46 on Nov. 30, 2018 (ECF No. 19-1) (“Second Egan
Rep.”); Second Supplemental Report, filed as Ex. 141 on July 29, 2020 (ECF No. 67-1) (“Third
Egan Rep.”). Based on her review of the medical records and hearing testimony, Dr. Egan
concluded that S.M.’s TM was more likely than not caused by the third Hepatitis B vaccine dose
that she received. See Third Egan Rep. at 7–8.
Dr. Egan received her bachelor’s degree (biology) from Barnard College at Columbia
University before obtaining both a medical degree and a Ph.D. in genetics from Tufts University.
Elizabeth Egan Curriculum Vitae, filed as Ex. 24 on Apr. 13, 2018 (ECF No. 13-2). She completed
an internship and residency in pediatrics at Boston Children’s Hospital before completing
fellowships in pediatric infectious disease and molecular parasitology at Boston Children’s
Hospital and the Harvard School of Public Health respectively. Id. at 1. Since 2015, Dr. Egan has
served as an assistant professor at Stanford University School of Medicine where she teaches
pediatrics, microbiology, and immunology. Id. She also works as an attending physician in
pediatric infectious disease at Lucille Packard Children’s Hospital in Stanford, California. Id. at 1.
11
Dr. Egan is board certified in pediatrics and pediatric infectious disease, and her research on
subjects related to these fields has been published in several peer-reviewed journals. Id. at 2, 4–6.
Dr. Egan spent some time in her reports distinguishing AFM from TM. AFM, she
explained, is characterized by hyporeflexia, intact sensation, pain in the affected limb, pleocytosis,
and spinal cord lesions with primarily anterior horn involvement. Second Egan Rep. at 2 (citing J.
Sejvar et al., Acute Flaccid Myelitis in the United States, August – December 2014: Results of
Nationwide Surveillance, 63 Clinical Infectious Diseases 737, 737–45 (2016), filed as Ex. E on
Aug. 21, 2018 (ECF No. 18-3); K. Messacar et al., Enterovirus D68 and Acute Flaccid Myelitis –
Evaluating the Evidence for Causality, 18 Lancet e239, e239–47 (2018), filed as Ex. F on Aug.
21, 2018 (ECF No. 18-4) (“Messacar”)). TM is a rare demyelinating condition that affects
approximately 1-8 per million people in the United States, with twenty percent of cases occurring
in children. First Egan Rep. at 6 (citing T.F. Scott et al., Evidence Based Guideline: Clinical
Evaluation and Treatment of Transverse Myelitis, 77 Neurology 2128, 2128 (2011), filed as Ex.
26 on Apr. 13, 2018 (ECF No. 13-4)). TM is characterized by the “acute onset of motor, sensory,
and/or autonomic dysfunction” due to a demyelinating lesion in the spinal cord. Third Egan Rep.
at 2. Patients with TM may experience weakness, spasticity, pain, decreased sensation, and spinal
cord edema involvement of both gray and white matter. Id.
Based on her review of the medical record and the entitlement hearing testimony of Drs.
Silverman, Fantasia, and Yee, Dr. Egan noted that S.M. exhibited diffuse edema throughout her
spinal cord, and there is no evidence to suggest that the spinal cord involvement was limited to the
anterior horn cells as would be expected in AFM. Second Egan Rep. at 3. Additionally, S.M. did
not experience hyporeflexia, nor did laboratory testing reveal evidence of an Enterovirus infection.
Id. at 3–4; Third Egan Rep. at 3–7. Thus, Dr. Egan concluded that the evidence best supported
S.M.’s initial diagnosis of TM. Second Egan Rep. at 4; Third Egan Rep. at 2–7.
Dr. Egan next evaluated the evidence supporting a causal relationship between TM and
vaccines. While infections often precede its onset, there was literature support for vaccines also
playing a causal role. One article found that twenty-eight percent of the studied TM patient subjects
(13/47) had experienced symptoms onset within thirty days of receiving an immunization—with
two of thirteen having received the Hepatitis B vaccine. First Egan Rep. at 6 (citing F.S. Pidcock
et al., Acute Transverse Myelitis in Childhood: Center-based Analysis of 47 Cases, 68 Neurology
1474, 1476 (2007), filed as Ex. 27 on Apr. 13, 2018 (ECF No. 13-5) (“Pidcock”), at 1476).
Additional literature offered by Dr. Egan also considered a possible association between
vaccination and the development of TM, though none conclusively established a causal link. B.
Banwell et al., Incidence of Acquired Demyelination of the CNS in Canadian Children, 72
Neurology 232, 232–38 (2009), filed as Ex. 28 on Apr. 13, 2018 (ECF No. 13-6); V. Wolf et al.,
Pediatric Acute Transverse Myelitis Overview and Differential Diagnosis, 27 J. Child Neurology
1426, 1426–36 (2012), filed as Ex. 29 on Apr. 13, 2018 (ECF No. 13-7).
12
Dr. Egan proposed molecular mimicry as the probable mechanism by which the Hepatitis
B vaccine could cause TM. First Egan Rep. at 6–9. Her theory relied on homology between the
Hepatitis B surface antigen, SHBsAg, and myelin basic protein (“MBP”). Id. at 7 (citing D.
Bogdanos et al., A Study of Molecular Mimicry and Immunological Cross-Reactivity Between
Hepatitis B Surface Antigen and Myelin Mimics, 12 Clinical & Developmental Immunology 217,
222 (2005), filed as Ex. 33 on Apr. 13, 2018 (ECF No. 14-1) (“Bogdanos”)). Dr. Egan also
identified myelin oligodendrocyte glycoprotein (“MOG”) as a source of potential cross-reactivity.
Id. at 7–8; Bogdanos at 222. Though Bogdanos did not find evidence of cross-reactivity between
SHBsAg and MBP, reactivity to at least one MOG epitope was observed in sixty percent of study
participants post-vaccination. Bogdanos at 220. This observation was deemed statistically
significant, and according to Dr. Egan provided experimental evidence that antibodies produced
in response to the Hepatitis B vaccine can cross-react with neural tissue resulting in demyelination.
First Egan Rep. at 8.
Dr. Egan also identified several case reports describing instances of TM following receipt
of the Hepatitis B vaccine. First Egan Rep. at 8 (citing L. Herroelen et al., Central-Nervous-System
Demyelination after Immunisation with Recombinant Hepatitis B Vaccine, 338 Lancet 1174,
1174–75 (1991), filed as Ex. 37 on Apr. 13, 2018 (ECF No. 14-5) (reporting two cases of central
nervous system (“CNS”) demyelinating disease in patients within six weeks of receiving the
recombinant Hepatitis B vaccine); E. Sindern et al., Inflammatory Polyradiculoneuropathy with
Spinal Cord Involvement and Lethal Outcome after Hepatitis B Vaccination, 186 J. Neurological
Sci. 81, 81–85 (2001), filed as Ex. 38 on Apr. 13, 2018 (ECF No. 14-6) (reporting a fatal case of
inflammatory polyradiculoneuropathy in a thirty-six-year-old man nine days after he received the
Hepatitis B vaccine); C. Vital et al., Postvaccinal Inflammatory Neuropathy: Peripheral Nerve
Biopsy in 3 Cases, 7 J. Peripheral Nervous System: JPNS 163, 163–67 (2002), filed as Ex. 39 on
Apr. 13, 2018 (ECF No. 14-7) (reporting two cases of inflammatory polyneuropathy within
twenty-one days of receiving the Hepatitis B vaccine, and one case of an inflammatory
polyneuropathy developing within fifteen days of receiving the yellow fever vaccine)).
Dr. Egan acknowledged that large epidemiological studies have not yet found an
association between the Hepatitis B vaccine and demyelinating conditions. First Egan Rep. at 9
(citing A. Ascherio et al., Hepatitis B Vaccination and the Risk of Multiple Sclerosis, 344 New
Eng. J. Med. 327, 327–32 (2001), filed as Ex. 40 on Apr. 13, 2018 (ECF No. 14-8); J. Mouchet et
al., Hepatitis B Vaccination and the Putative Risk of Central Demyelinating Diseases – A
Systematic Review and Meta-Analysis, 36 Vaccine 1548, 1548–55 (2018), filed as Ex. 41 on Apr.
13, 2018 (ECF No. 14-9); R. Baxter et al., Acute Demyelinating Events Following Vaccines: A
Case-Centered Analysis, 63 Clinical Infectious Diseases 1456, 1456–62 (2016), filed as Ex. 42 on
Apr. 13, 2018 (ECF No. 14-10) (“Baxter”)). But she deemed such studies to have limited value
13
due to the overall rarity of demyelinating conditions, while emphasizing case reports and the
absence of other identifiable causes for S.M.’s condition. First Egan Rep. at 9–10.
3. Dr. Lawrence Steinman, M.D.
Dr. Steinman, a neurologist and immunologist, filed three expert reports. Report, dated
Nov. 30, 2018, filed as Ex. 47 (ECF No. 19-2) (“First Steinman Rep.”); Supplemental Report,
dated Oct. 10, 2019, filed as Ex. 90 (ECF No. 34-1) (“Second Steinman Rep.”); Supplemental
Report, dated July 29, 2020, filed as Ex. 142 (ECF No. 67-2) (“Third Steinman Rep.”). He
opined—consistent with Dr. Egan—that the Hepatitis B vaccine S.M. received caused her to
develop TM, although his focus was less on direct causation and more on other prongs of the test
for entitlement.
Dr. Steinman currently serves as a professor in the departments of neurology, pediatrics,
and genetics at Stanford University. Steinman Curriculum Vitae, filed as Ex. 97 (ECF No. 34-8)
(“Steinman CV”) at 1. He obtained his bachelor’s degree from Dartmouth College before earning
his medical degree from Harvard University. Id. He then completed his internship and residency
in surgery, pediatrics, and pediatric and adult neurology at Stanford University. Id. He also
completed several fellowships in the area of immunology. Id. He is board certified in neurology,
though much of his work in the field also involves immunological concepts and theories. Id. at 2.
He estimates that he has treated hundreds of patients with TM and other, similar neurological
conditions, including multiple sclerosis and neuromyelitis optica throughout his career. Steinman
Rep. at 1.
Regarding the competing diagnoses, Dr. Steinman opined (consistent with S.M.’s treaters
plus Dr. Egan) that the evidence presented most strongly supported a diagnosis of TM. Third
Steinman Rep. at 6–10. Relying on Dr. Silverman’s hearing testimony, Dr. Steinman noted that
the AFM diagnostic criteria set forth by the CDC requires a spinal cord lesion “largely restricted
to gray matter,” but that S.M.’s MRI demonstrated extensive involvement of both gray and white
matter. Id. at 6–7 (citing Tr. at 41; Erlt-Wagner at 31). Dr. Steinman similarly deferred to Dr.
Fantasia’s opinions and her conclusion that S.M.’s clinical presentation was most consistent with
TM. Third Steinman Rep. at 7 (citing Tr. at 114, 118–20). Though S.M.’s lumbar puncture did not
reveal pleocytosis, 11 Dr. Steinman emphasized that negative CSF studies are not unusual and do
not preclude a TM diagnosis. Third Steinman Rep. at 8–9. Yet because pleocytosis is more
prevalent in AFM cases, its absence from S.M.’s CSF studies was actually further evidence of the
unlikelihood of the proposed AFM diagnosis. Id. at 9.
11
Pleocytosis describes the presence of greater than normal number of cells in cerebrospinal fluid. Dorland’s at 1438.
14
According to Dr. Steinman, S.M. more likely than not developed TM as a result of the third
Hepatitis B vaccine dose she received on July 14, 2014. Third Steinman Rep. at 12–13. To support
his contention, Dr. Steinman highlighted several case reports and literature reviews describing
instances in which patients developed TM or other demyelinating conditions following receipt of
the Hepatitis B vaccine. See, e.g., First Steinman Rep. at 4 (citing L. Fonesca et al., Early-Onset
Acute Transverse Myelitis Following Hepatitis B Vaccination and Respiratory Infection, 61 Arq
Neuropsiquiatr 265, 265–68 (2003), filed as Ex. 59 on Nov. 30, 2018 (ECF No. 20-4) (three-year-
old boy experienced TM following an upper respiratory infection and vaccination with the
Hepatitis B vaccine); Third Steinman Rep. at 3–4 (citing N. Agmon-Levin et al., Transverse
Myelitis and Vaccines: A Multi-Analysis, 18 Lupus 1198, 1198–1204 (2009), filed as Ex. 111 on
Jan. 16, 2020 (ECF No. 44-4) (“Agmon-Levin”) (documenting thirteen cases of TM following
receipt of the Hepatitis B vaccine between 1970 and 2009); J. Stübgen, Immune-Mediated Myelitis
Following Hepatitis B Vaccination, 12 Autoimmunity Rev. 144, 144–49 (2012), filed as Ex. 113
on Jan. 16, 2020 (ECF No. 44-6) (identifying three more cases of TM following receipt of the
Hepatitis B vaccine in addition to those described in Agmon-Levin, and noting that “HBV
[Hepatitis B] vaccines were the most common immunization associated with acute myelitis.”)).
Dr. Steinman also cited the packaging insert for the Recombivax HB Hepatitis B vaccine, which
lists TM as a reported adverse reaction. Third Steinman Rep. at 4 (citing Merk & Co., Inc.,
Recombivax HB Package Insert, 1, 5 (2018), filed as Ex. 112 on Jan. 16, 2020 (ECF No. 44-5)).
Dr. Steinman also addressed the science he felt supported the association of TM after
receipt of the Hepatitis B vaccine. Like Dr. Egan, Dr. Steinman proposed that the mechanism by
which S.M.’s TM could come have come about was molecular mimicry—cross-reactivity between
antibodies produced in response to the Hepatitis B vaccine and the MBP found in the spinal cord,
due to antigenic similarities between the amino acid sequences making up the MBP and vaccine
components. Second Steinman Rep. at 4–6. As evidence of the potentiality of such mimicry, Dr.
Steinman turned to the National Institutes of Health Immune Epitope Database, which he
maintained revealed a shared epitope 12 between the Hepatitis B virus surface antigen (SHBsAg)
and MBP. Id.Dr. Steinman further bulwarked his theory with reference to an animal-model study in
which researchers found that this shared homology had elicited a pro-inflammatory response and
cytotoxicity. Second Steinman Rep. at 5 (citing S. Ellmerich et al., High Incidence of Spontaneous
Disease in an HLA-DR15 and TCR Transgenic Multiple Sclerosis Model, 174 J. Immunology
1938, 1938, 1944–45 (2005), filed as Ex. 94 on Oct. 10, 2019 (ECF No. 34-5)). In addition, pro-
inflammatory cytokines—specifically gamma interferon—stimulated during the innate response
to vaccination can increase permeability of the blood-brain barrier, thereby allowing cytotoxic T-
cells access to the CNS. Second Steinman Rep. at 5–6 (citing L. Steinman, A Brief History of TH17,
the First Major Revision in the TH1/TH2 Hypothesis of T-Cell Mediated Tissue Damage, 13 Nature
12
An epitope is an antigenic determinant. Dorland’s at 630.
15
Medicine 139, 143 (2007), filed as Ex. 95 on Oct. 10, 2019 (ECF No. 34-6)). This made it more
likely that the secondary, pathologic adaptive response that was key to Dr. Steinman’s theory could
come about.
The larger focus of Dr. Steinman’s reports, however, was his contention that the timeframe
in which S.M.’s TM manifested post-vaccination was medically reasonable. S.M. experienced
onset of her TM approximately seventy-seven hours (three days and five hours) after receiving her
third dose of the Hepatitis B vaccine. Third Steinman Rep. at 13. As a general rule, the expected
lag phase post-vaccination (when B and T cells are activated and differentiate into effector and
memory cells) would be between one to three days, with the logarithmic phase—the period during
which serum antibody levels increase—then occurring in the following three to five days. First
Steinman Rep. at 4 (citing K. Stratton et al., Adverse Effects of Vaccines: Evidence and Causality,
Institute of Medicine 58 (2012), filed as Ex. 56 on Nov. 30, 2018 (ECF No. 20-1) (“IOM Rep.”)).
However, since S.M. had been exposed to the Hepatitis B vaccine twice before, she would likely
mount an adaptive response to the third dose of the same vaccine in an even shorter amount of
time. First Steinman Rep. at 4. Thus, the onset of S.M’s symptoms approximately three days post-
vaccination was medically acceptable in his view.
C. Respondent’s Experts
1. Dr. Margaret Fisher, M.D.
Dr. Fisher, a pediatric infectious disease physician, offered four reports in support of
Respondent’s position. Expert Report, filed as Ex. A on July 30, 2018 (ECF No. 17-1) (“First
Fisher Rep.”); Supplemental Expert Report, filed as Ex. G on Mar. 8, 2019 (ECF No. 29-1)
(“Second Fisher Rep.”); Second Supplemental Expert Report, filed as Ex. Z on Dec. 16, 2019
(ECF No. 40-7) (“Third Fisher Rep.”); Third Supplemental Expert Report, filed as Ex. EE on Sept.
14, 2020 (ECF No. 68-1) (“Fourth Fisher Rep.”). Based upon her review of the medical record,
scientific literature, expert reports, and entitlement hearing testimony, Dr. Fisher concluded that
S.M. more likely than not suffered from AFM, and she attributed the AFM to a preceding infection
rather than vaccination. First Fisher Rep. at 5.
Dr. Fisher obtained her bachelor’s degree (chemistry) from the Susquehanna University in
Pennsylvania before obtaining her medical degree from the University of California, Los Angeles.
Dr. Fisher Curriculum Vitae, filed as Ex. B on July 30, 2018 (ECF No. 17-2). She then completed
her residency in pediatrics and a fellowship in pediatric infectious disease at St. Christopher’s
Hospital for Children in Philadelphia, Pennsylvania. Id. at 2. Dr. Fisher is a professor of pediatrics
at both Drexel University College of Medicine and St. George’s University School of Medicine.
Id. In addition to her teaching duties, Dr. Fisher serves as an attending pediatric physician and
medical director at Unterberg Children’s Hospital at Monmouth Medical Center. Id. at 4. She is
16
board certified in both pediatrics and pediatric infectious disease, and she has published journal
articles and lectured on these topics extensively. Id. at 12–47.
In her first report, Dr. Fisher described the AFM outbreak that occurred in the Summer of
2014—the exact period relevant to this case. First Fisher Rep. at 3–4. Citing to CDC advisories
and reports, Dr. Fisher described sixty-four cases of “acute onset of limb weakness in a person less
than or equal to 21 years of age with onset on or after 01 August, 2014, and with spinal MRI
lesions largely restricted to the spinal grey matter.” Id. at 3 (citing Centers for Disease Control and
Prevention, Acute Neurological Illness with Focal Limb Weakness of Unknown Etiology in
Children, CDC Health Alert Network (Sept. 26, 2014), filed as Ex. C on Aug. 21, 2018 (ECF No.
18-1); Centers for Disease Control and Prevention, Acute Flaccid Myelitis: Interim Considerations
for Clinical Management (Nov. 7, 2014), filed as Ex. D on Aug. 21, 2018 (ECF No. 18-2) (“CDC
Clinical Management”)). She also emphasized that the majority of patients presenting with AFM
were experiencing severe respiratory illness, and in some cases required ventilation for respiratory
failure. First Fisher Rep. at 3. While corticosteroid treatment was recommended for cases in which
spinal cord edema was likely to result in additional damage, neither it nor PLEX were
recommended for treatment of AFM. Id. (citing CDC Clinical Management at 6, 8). It was later
determined that a causal association existed between enterovirus infections—specifically EV-D68
infections—and the development of AFM. First Fisher Rep. at 4 (citing Messacar at e245).
Though acknowledging that differentiating between a diagnosis of AFM and TM is
difficult, Dr. Fisher ultimately concluded that the medical record suggested that S.M. more likely
than not suffered from AFM. First Fisher Rep. at 5; Second Fisher Rep. at 2–3. First, Dr. Fisher
observed symptoms and treatment evidence from the medical record that she maintained were
more consistent with AFM. First Fisher Rep. at 3. She noted that S.M. experienced symptoms of
an upper respiratory infection approximately three weeks prior to the onset of her condition—a
timeframe consistent with the pathogenesis of AFM following an enterovirus infection. Id.; Third
Fisher Rep. at 1. She also emphasized S.M.’s limited improvement despite corticosteroid
treatment. First Fisher Rep. at 2–3. Similarly, S.M.’s condition did not show significant
improvement with PLEX treatment. Id.Second, Dr. Fisher noted that the circumstances of S.M.’s symptoms manifestation were
inconsistent with TM—but consistent with AFM. According to Dr. Fisher, the time between
S.M.’s receipt of the Hepatitis B vaccine and the onset of her condition was too brief for molecular
mimicry to have occurred. First Fisher Rep. at 5. By contrast, about half of AFM cases occurred
after “an infectious illness at an average of 11 ± 10 days prior to the onset of neurologic
symptoms.” Id. at 4 (citing Pidcock at 1476). The onset of S.M.’s symptoms three weeks after she
was seen by her pediatrician for an upper respiratory illness would thus be consistent with a post-
infectious AFM diagnosis. First Fisher Rep. at 4–5.
17
Dr. Fisher also identified a preceding enterovirus infection as the most likely etiology for
S.M.’s condition. First Fisher Rep. at 4–5. To support her position, she again referenced the
pediatrician visit on June 20, 2014, three weeks prior to the onset of S.M.’s neurologic symptoms.
First Fisher Rep. at 4. During the visit, S.M. was evaluated for congestion, yellow nasal discharge,
and a fever for which she was prescribed oral antibiotics (amoxicillin). See Ex. 7 at 104. And S.M.
appeared to show respiratory difficulties the evening before and morning of her first hospital
admission. First Fisher Rep. at 4. While Petitioners attributed these symptoms to S.M.’s allergies,
Dr. Fisher opined that they were also consistent with an enterovirus infection. Id.Dr. Fisher also pointed out the positive rhinovirus finding on S.M.’s respiratory panel
workup as consistent with an enterovirus infection, because rhinovirus and enterovirus are cross-
reactive. First Fisher Rep. at 2. And even if S.M.’s respiratory panel accurately reflected a
rhinovirus rather than an enterovirus infection, it was still possible that her AFM stemmed from
an infectious etiology because most AFM cases “have not had a specific viral pathogen identified.”
Second Fisher Rep. at 3 (citing M. Elrick et al., Clinical Subpopulations in a Sample of North
American Children Diagnosed with Acute Flaccid Myelitis, 2012-2016, 173 JAMA Pediatrics 134,
137 (2019), filed as Ex. H on Mar. 8, 2019 (ECF No. 29-2)); see also Third Fisher Rep. at 2–3.
2. Dr. Ross Kedl, Ph.D.
Dr. Kedl, a professor of immunology at the University of Colorado, offered three expert
reports on Respondent’s behalf. Expert Report, filed as Ex. K on Mar. 8, 2019 (ECF No. 29-5)
(“First Kedl Rep.”); Supplemental Report, filed as Ex. T on Dec. 16, 2019 (ECF No. 40-1)
(“Second Kedl Rep.”); Supplemental Report, filed as Ex. FF on Sept. 14, 2020 (ECF No. 68-2)
(“Third Kedl Rep.”). Based upon his review of the medical record, scientific literature, expert
reports, and entitlement hearing testimony, Dr. Kedl concluded that S.M.’s illness, however
characterized—though he largely deferred to Dr. Fisher on this point and agreed with her opinion
that S.M. more likely than not suffered from AFM—was not caused by the Hepatitis B vaccine.
First Kedl Rep. at 8–9.
Dr. Kedl received both his bachelor’s degree in biology and Ph.D. in pathobiology from
the University of Minnesota. Ross Kedl Curriculum Vitae, filed as Ex. L on Mar. 8, 2019 (ECF
No. 29-6). He then completed a post-doctoral fellowship at the Howard Hughes Medical Institute
in Denver, Colorado. Id. at 1. Since 2004, Dr. Kedl has served as a professor of immunology at
the University of Colorado Department of Immunology and Microbiology. Id. at 3. He is a co-
author of several patents relating to vaccine development and immunological modifiers. Id. at 4–
5. Much of Dr. Kedl’s research has been focused on vaccine development and the role of vaccine
adjuvants in stimulating immunologic responses, and he is extensively published on these and
related subjects. Id. at 11–19; see also First Kedl Rep. at 2. Dr. Kedl does not, however, possess a
18
medical degree, nor does he have medical experience in treating or diagnosing patients with
infectious or neurological disease.
Deferring to Dr. Fisher’s opinions regarding S.M.’s diagnosis, 13 Dr. Kedl’s first report
largely focused on possible alternative etiologies for S.M.’s condition. He began by explaining
how the two arms of the immune system—humeral and cellular immunity—operate during an
adaptive immune response. First Kedl Rep. at 4–5. According to Dr. Kedl, cellular immunity is
driven by T cell activity, while humeral immunity (implicated in a causal theory like molecular
mimicry) relies on B cell antibody production. Id. at 4. During an initial exposure to an antigen,
both CD4+/helper T cells and CD8+/cytotoxic T cells migrate from lymphoid tissue to the
infection site. During the same initial exposure, B cells increase antibody production while
remaining localized in lymphoid tissue and bone marrow. Id. Once the infection is cleared, some
T cells will remain present in the formerly-infected tissue, and are thereafter referred to as resident
memory T cells. Id. Other T cells will recirculate throughout the body, serving as monitors for
future infections. Id. These T cells are referred to as central memory T cells. Id. It is these memory
T cells which allow for a faster immunologic response to subsequent infections. Id. While the
response of B cells to subsequent infection will also be accelerated, it remains delayed relative to
the T cell response. Id. (citing IOM Rep. at 57–58).
Based on the foregoing, Dr. Kedl concluded that:
activation of adaptive immunity in less than 3 days requires the existence of
immune memory, [ ] immune-mediated tissue disruption within this
timeframe requires memory T cell residence within, or entrance into, the
tissue site of interest, and [ ] antibody-mediated tissue damage would be
expected to take longer than 3 days and would still require the previous
generation of memory T cells.
First Kedl Rep. at 5.
During his review of the medical record—specifically S.M.’s pathology and laboratory
studies—Dr. Kedl highlighted certain results he deemed antithetical to the conclusions of
Petitioners’ causation experts. First Kedl Rep. at 5. First, he noted that the results of S.M.’s CSF
study on July 14, 2014 revealed elevated albumin, IgG, and red blood cells, but did not show white
blood cell infiltrate. Id. (citing Ex. 4 at 64–65). This finding, according to Dr. Kedl, is “consistent
with damage to the blood-CSF barrier, but not with T cell infiltration or associated tissue damage.”
First Kedl Rep. at 5. Because the formation of memory B cells is a T cell-dependent event, the
absence of T cell expansion across the blood-brain barrier similarly precludes B cell—and later,
13
From an immunologic perspective, Dr. Kedl noted that S.M.’s rhinovirus infection and the lack of cellular infiltrates
in her CSF studies were most consistent with Dr. Fisher’s proposed AFM diagnosis. First Kedl Rep. at 4.
19
antibody—access to CNS tissue. Id. Dr. Kedl thus rejected Dr. Steinman’s contention that the third
dose of a Hepatitis B vaccine could have elicited a secondary T and B cell response sufficient to
cause CNS tissue damage in the timeframe at issue—but remain undetectable in CSF studies.
Second Kedl Rep. at 2–3; Third Kedl Rep. at 4–5.
Dr. Kedl next addressed other specific aspects of the molecular mimicry theory proposed
by Dr. Steinman. First Kedl Rep. at 5–6; Second Kedl Rep. at 4–6. He emphasized that sequential
homology is quite common, and is thus (in his view) insufficient to establish the likelihood of
cross-reactivity. Second Kedl Rep. at 4–5 (citing A. Silvanovich et al., The Value of Short Amino
Acid Sequence Matches for Prediction of Protein Allergenicity, 90 Toxicological Sciences 252,
252 (2006), filed as Ex. X on Dec. 16, 2019 (ECF No. 40-5) (“Silvanovich”)). Significantly, Dr.
Kedl highlighted that PADPGSRP—the amino acid sequence Dr. Steinman identified as the source
of homology between MBP and SHBsAg—is not actually found in SHBsAg. Second Kedl Rep. at
4. Even after Dr. Steinman revised his opinion—identifying PADPGSRPHLIRLF as the amino
acid sequence giving rise to cross-reactivity—Dr. Kedl opined that the fifty-seven percent
similarity between this sequence and SHBsAg sequences remained insufficient to establish a
causal association between the Hepatitis B vaccine and TM. Third Kedl Rep. at 5–7 (citing
Bogdanos at 219; Silvanovich at 252).
Dr. Kedl further criticized reliance on case reports to establish a causal relationship
between the Hepatitis B vaccine and TM, especially given the existence of several reliable
epidemiological studies which reached the opposite conclusion. First Rep. at 6–7 (citing Baxter
(also filed by Respondent as Ex. M); see also M. Hocine et al., Hepatitis B Vaccination and First
Central Nervous System Demyelinating Events: Reanalysis of a Case-Control Study Using the
Self-Controlled Case Series Method, 25 Vaccine 5938, 5938–43 (2007), filed as Ex. P on Mar. 8,
2019 (ECF No. 29-10) (“Hocine”); A. Schattner, Consequence or Coincidence? The Occurrence,
Pathogenesis and Significance of Autoimmune Manifestations after Viral Vaccines, 23 Vaccine
3876, 3876–86 (2005), filed as Ex. S on Mar. 8, 2019 (ECF No. 29-13) (“Schattner”)).
III. Procedural History
After the case’s commencement in 2017, Petitioners filed medical records in support of
their claim. Respondent thereafter filed a Rule 4(c) Report on January 19, 2018, asserting that
compensation was not appropriate in this case. Respondent’s Report, filed Jan. 19, 2018 (ECF No.
10). Petitioners subsequently filed expert reports from Drs. Egan, Steinman, and Silverman along
with supporting literature and reports from treaters, including Drs. Fantasia and Bal, between the
spring of 2018 and winter 2020. Respondent filed responsive reports from Drs. Fisher and Kedl,
along with literature in opposition to Petitioners’ position. A two-day entitlement hearing was
scheduled to take place on January 28-29, 2020. See Scheduling Order, dated Dec. 6, 2019.
20
On January 22, 2020, it was brough to my attention that Respondent’s counsel was ill and
would require special accommodation for the upcoming entitlement hearing. See Scheduling
Order, dated Jan. 22, 2020. The parties therefore agreed that only Drs. Silverman, Yee, and
Fantasia, along with both Mr. and Mrs. McGrail, would testify at the time originally set for the
hearing. See Scheduling Order, dated Jan. 22, 2020. All other witnesses were to testify during two
additional days of hearing on June 10-11, 2020. See Scheduling Order, dated Jan. 31, 2020 (ECF
No. 56). On May 1, 2020, however, the parties indicated that they no longer wished to proceed
with the additional days of entitlement hearing testimony, and were instead amenable to the case
being resolved on the existing record. Joint Status Report, filed May 1, 2020 (ECF No. 65).
Thereafter, the parties submitted briefs in support of their respective positions, concluding the
process on November 13, 2020. The matter is now ripe for resolution.
IV. Parties’ Respective Arguments
A. Petitioner’s Motion
Petitioners argue that S.M. developed TM after receiving the third dose of the Hepatitis B
vaccine on July 14, 2014. Motion for Ruling on the Record, filed on Nov. 13, 2020 (ECF No. 70)
(“Mot.”) at 8. Relying on the reports of Drs. Steinman, Egan, and Silverman, in addition to the
medical literature and testimony of treating physicians, Petitioners posit that sequential
homologies in amino acid sequences of Hepatitis B vaccine components and MBP allowed for
cross-reactivity, leading to demyelination of the spinal cord and resulting in an acute onset of TM.
Id. at 40–43.
Petitioners specifically contend that the onset of S.M.’s condition occurred on July 17,
2014—approximately seventy-seven hours after receiving her third dose of the Hepatitis B
vaccine. Mot. at 56–69. That morning, S.M.’s parents noted that she was exhibiting allergy
symptoms (shortness of breath and coughing), for which they administered a Pulmicort nebulizer
treatment. Tr. at 143–44; Ex. 5 at 32. S.M.’s parents described S.M. as otherwise healthy and
behaving normally prior to her being taken to daycare. Mot. at 19–20. It wasn’t until approximately
3:00 in the afternoon that Ms. McGrail was informed by S.M’s daycare that she had developed a
fever and needed to be picked up. Id. at 20; Tr. at 162. At the recommendation of S.M.’s
pediatrician, Dr. Yee, S.M. was taken to the local emergency department for further evaluation of
her symptoms. Mot. at 11.
Upon admission to Jersey Shore University Medical Center, S.M. underwent a spinal MRI
which produced results deemed most consistent with TM. Mot. at 12 (citing Ex. 4 at 28–29). CSF
studies performed that same evening were negative for pleocytosis, but did reveal elevated IgG.
Mot. at 52, 62 (citing Ex. 4 at 64–65). Based on S.M.’s clinical presentation and the results of both
her MRI and CSF studies, her treating neurologist, Dr. Sultan, diagnosed her with TM. Mot. at 23–
24 (citing Ex. 105 at 479–80).
21
Between July 17 and August 14, 2014, S.M. received steroid and PLEX treatments before
being transferred to Children’s Specialized Hospital for intensive inpatient physical therapy. Mot.
at 13–14. After a month of inpatient rehabilitation, S.M. was discharged from Children’s
Specialized Hospital and was instructed to follow-up with her treating physiatrist, Dr. Fantasia. Id.
at 15. S.M. continued with outpatient physical, occupational, and speech therapies, but she still
experiences residual sequelae, including severe spasticity, neuromuscular derangements, bladder
dysfunction, bowel dysfunction, extremities contracture, orthopedic complications, and other
issues related to quadriplegia. Id. at 1.
It was not until S.M. was evaluated by Dr. Waldman on January 7, 2017—more than two
years after the onset of her condition—that AFM was raised as a possible diagnosis. Mot. at 33.
But even as she acknowledged that the onset and clinical course of S.M.’s condition appeared
consistent with AFM, Dr. Waldman’s visit notes document an encounter diagnosis of TM. Ex. 14
at 5.
B. Respondent’s Opposition
Respondent first disputes Petitioners’ proposed TM diagnosis, arguing instead that S.M.
suffers from post-infectious AFM. Respondent’s Opposition Brief, filed Nov. 13, 2020 (ECF No.
69) (“Opp.”) at 6, 8–9. Dr. Fisher, Respondent’s pediatric infectious disease expert, opined that
S.M.’s clinical presentation of cough, fever, acute onset quadriparesis, spinal cord inflammation,
and limited improvement after steroid and PLEX treatments are most consistent with a diagnosis
of AFM. Id. at 9. She also identified the positive rhinovirus culture obtained on August 1, 2014 as
evidence of AFM because the respiratory panel culture does not distinguish between rhinovirus
and enterovirus, and both infections have been associated with the development of AFM. Id.Moreover, even if S.M.’s initial TM diagnosis was correct, Petitioners have failed to
preponderantly establish causation under Althen. Opp. at 10. Respondent’s immunology expert,
Dr. Kedl, identified several flaws in the proposed theory of causation. Id. at 12. First, the amino
acid sequence identified as the source of cross-reactivity is not actually found in the Hepatitis B
vaccine antigen, and the vaccine antigen sequence with the highest degree of similarity to those
found in MBP contains only four shared amino acids. Id. Dr. Kedl emphasized that this degree of
similarity is quite common throughout the human genome and can occur by random chance, and
even significant degrees of similarity do not inevitably cause meaningful pathology. Id. at 13. He
also noted that even an adaptive immune response would not be capable of producing antibody-
mediated damage to the spinal cord within the three-day timeframe proposed by Petitioners. Id.Respondent also contends that Petitioners failed to satisfy their burden in establishing a
logical sequence of cause and effect showing that the Hepatitis B vaccine was the likely source of
S.M.’s injury as is required by the second Althen prong. Opp. at 13. According to Dr. Kedl, if
22
cross-reactivity were implicated in the pathological processes leading to the development of TM,
certain clinical markers would be present. Id. But CSF studies performed within hours of S.M.’s
symptom onset did not reveal evidence of pleocytosis, and were therefore inconsistent with T cell
infiltration and damage to the spinal cord. Id.The final criticism offered by Respondent emphasized a lack epidemiological evidence
supporting Petitioners position. Opp. at 14–15. Though a number of case reports documenting
instances of TM following close in time to receipt of the Hepatitis B vaccine have been offered,
Respondent downplays their overall significance in light of several epidemiological studies which
found no association between the Hepatitis B vaccine and TM. Id.V. Applicable Legal Standards
A. Petitioner’s Overall Burden in Vaccine Program Cases
To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
he suffered a “Table Injury”—i.e., an injury falling within the Vaccine Injury Table—
corresponding to one of the vaccinations in question within a statutorily prescribed period of time
or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table
Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §
11(c)(1)(C)(ii)(I); see also 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, 1320 (Fed. Cir. 2006). 14
In this case, Petitioners do not assert a Table claim.
For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. Section 13(1)(a). That is, a petitioner must offer evidence that
leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence
before [he] may find in favor of the party who has the burden to persuade the judge of the fact’s
existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.
476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).
Proof of medical certainty is not required. Bunting v. Sec’y of Health & Hum. Servs., 931 F.2d
867, 873 (Fed. Cir. 1991). In particular, a petitioner must demonstrate that the vaccine was “not
only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.”
Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344,
1352–53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed.
Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his assertions;
14
Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Hum. Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings
concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Hum. Servs., 59 Fed. Cl. 121,
124 (2003), aff’d 104 F. Appx. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Hum. Servs., No. 13-159V,
2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).
23
rather, the petition must be supported by either medical records or by the opinion of a competent
physician. Section 13(a)(1).
In attempting to establish entitlement to a Vaccine Program award of compensation for a
Non-Table claim, a petitioner must satisfy all three of the elements established by the Federal
Circuit in Althen, 418 F.3d at 1278: “(1) a medical theory causally connecting the vaccination and
the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason
for the injury; and (3) a showing of proximate temporal relationship between vaccination and
injury.”
Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners
must provide a “reputable medical theory,” demonstrating that the vaccine received can cause the
type of injury alleged. Pafford, 451 F.3d at 1355–56 (citations omitted). To satisfy this prong, a
petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”
Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such a theory must
only be “legally probable, not medically or scientifically certain.” Id. at 549.
Petitioners may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1378–79 (Fed. Cir. 2009) (citing
Capizzano, 440 F.3d at 1325–26). Special masters, despite their expertise, are not empowered by
statute to conclusively resolve what are essentially thorny scientific and medical questions, and
thus scientific evidence offered to establish Althen prong one is viewed “not through the lens of
the laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant evidence
standard.” Id. at 1380. Accordingly, special masters must take care not to increase the burden
placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras, 121 Fed.
Cl. at 245 (“[p]lausibility . . . in many cases may be enough to satisfy Althen prong one” (emphasis
in original)).
In discussing the evidentiary standard applicable to the first Althen prong, the Federal
Circuit has consistently rejected the contention that it can be satisfied merely by establishing the
proposed causal theory’s scientific or medical plausibility. 15 See Boatmon v. Sec’y of Health &
Hum. Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019); see also LaLonde v. Sec’y of Health & Hum.
Servs., 746 F.3d 1334, 1339 (Fed. Cir. 2014) (“[h]owever, in the past we have made clear that
simply identifying a ‘plausible’ theory of causation is insufficient for a petitioner to meet her
burden of proof.” (citing Moberly, 592 F.3d at 1322)). And petitioners always have the ultimate
burden of establishing their overall Vaccine Act claim with preponderant evidence. W.C. v. Sec’y
15
Petitioners are thus consistently in error when they maintain the legal standard requires only plausibility. See, e.g.,
Boatmon, 746 F.3d at 1359. However, because Petitioners also maintain (and in my determination, have demonstrated)
that the evidence preponderantly establishes the “can cause” prong, this misstatement of the legal standard is not fatal
to Petitioners’ overall success.
24
of Health & Hum. Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted); Tarsell v.
United States, 133 Fed. Cl. 782, 793 (2017) (noting that Moberly “addresses the petitioner’s overall
burden of proving causation-in-fact under the Vaccine Act” by a preponderance standard).
The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375–77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. Servs., 956
F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions
and views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 F.3d
at 1367; Capizzano, 440 F.3d at 1326 (“medical records and medical opinion testimony are favored
in vaccine cases, as treating physicians are likely to be in the best position to determine whether a
‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury’”)
(quoting Althen, 418 F.3d at 1280). Medical records are generally viewed as particularly
trustworthy evidence, since they are created contemporaneously with the treatment of the patient.
Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).
Medical records and statements of a treating physician, however, do not per se bind the
special master to adopt the conclusions of such an individual, even if they must be considered and
carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis, conclusion, judgment,
test result, report, or summary shall not be binding on the special master or court”); Snyder v. Sec’y
of Health & Hum. Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is nothing . . . that mandates
that the testimony of a treating physician is sacrosanct—that it must be accepted in its entirety and
cannot be rebutted”). As with expert testimony offered to establish a theory of causation, the
opinions or diagnoses of treating physicians are only as trustworthy as the reasonableness of their
suppositions or bases. The views of treating physicians should be weighed against other, contrary
evidence also present in the record—including conflicting opinions among such individuals.
Hibbard v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 742, 749 (2011) (not arbitrary or capricious
for special master to weigh competing treating physicians’ conclusions against each other), aff’d,
698 F.3d 1355 (Fed. Cir. 2012); Veryzer v. Sec’y of Dept. of Health & Hum. Servs., No. 06-522V,
2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review denied, 100 Fed.
Cl. 344, 356 (2011), aff’d without opinion, 475 F. Appx. 765 (Fed. Cir. 2012).
The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the
phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant
proof that the onset of symptoms occurred within a timeframe which, given the medical
understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan
v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what
is a medically acceptable timeframe must align with the theory of how the relevant vaccine can
cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of Health & Hum.
25
Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after remand, 105 Fed. Cl. 353 (2012), aff’d
mem., 503 F. Appx. 952 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V,
2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for rev. denied (Fed. Cl. Dec. 3,
2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).
B. Legal Standards Governing Factual Determinations
The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 11(c)(2). The special master is required
to consider “all [] relevant medical and scientific evidence contained in the record,” including “any
diagnosis, conclusion, medical judgment, or autopsy or coroner’s report which is contained in the
record regarding the nature, causation, and aggravation of the petitioner’s illness, disability, injury,
condition, or death,” as well as the “results of any diagnostic or evaluative test which are contained
in the record and the summaries and conclusions.” Section 13(b)(1)(A). The special master is then
required to weigh the evidence presented, including contemporaneous medical records and
testimony. See Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (it is
within the special master’s discretion to determine whether to afford greater weight to
contemporaneous medical records than to other evidence, such as oral testimony surrounding the
events in question that was given at a later date, provided that such determination is evidenced by
a rational determination).
Medical records that are created contemporaneously with the events they describe are
presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s
health problems). Cucuras, 993 F.2d at 1528; Doe/70 v. Sec’y of Health & Hum. Servs., 95 Fed.
Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner’s testimony and his
contemporaneous medical records, the special master’s decision to rely on petitioner’s medical
records was rational and consistent with applicable law”), aff’d sub nom. Rickett v. Sec’y of Health
& Hum. Servs., 468 F. Appx. 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption
is based on the linked propositions that (i) sick people visit medical professionals; (ii) sick people
honestly report their health problems to those professionals; and (iii) medical professionals record
what they are told or observe when examining their patients in as accurate a manner as possible,
so that they are aware of enough relevant facts to make appropriate treatment decisions. Sanchez
v. Sec’y of Health & Hum. Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr.
Apr. 10, 2013); Cucuras v. Sec’y of Health & Hum. Servs., 26 Cl. Ct. 537, 543 (1992), aff’d, 993
F.2d at 1525 (Fed. Cir. 1993) (“[i]t strains reason to conclude that petitioners would fail to
accurately report the onset of their daughter’s symptoms”).
Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie, 2005 WL 6117475, at *20. Indeed, contemporaneous
medical records are generally found to be deserving of greater evidentiary weight than oral
26
testimony—especially where such testimony conflicts with the record evidence. Cucuras, 993 F.2d
at 1528; see also Murphy, 23 Cl. Ct. at 733 (citing United States v. United States Gypsum Co., 333
U.S. 364, 396 (1947) (“[i]t has generally been held that oral testimony which is in conflict with
contemporaneous documents is entitled to little evidentiary weight.”)).
There are, however, situations in which compelling oral testimony may be more persuasive
than written records, such as where records are deemed to be incomplete or inaccurate. Campbell
v. Sec’y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“like any norm based upon common
sense and experience, this rule should not be treated as an absolute and must yield where the factual
predicates for its application are weak or lacking”); Lowrie, 2005 WL 6117475, at *19 (“’[w]ritten
records which are, themselves, inconsistent, should be accorded less deference than those which
are internally consistent’”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a determination
regarding a witness’s credibility is needed when determining the weight that such testimony should
be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d 1570,
1575 (Fed. Cir. 1993).
When witness testimony is offered to overcome the presumption of accuracy afforded to
contemporaneous medical records, such testimony must be “consistent, clear, cogent, and
compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec’y of Health & Hum. Servs.,
No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In determining the
accuracy and completeness of medical records, the Court of Federal Claims has listed four possible
explanations for inconsistencies between contemporaneously created medical records and later
testimony: (1) a person’s failure to recount to the medical professional everything that happened
during the relevant time period; (2) the medical professional’s failure to document everything
reported to her or him; (3) a person’s faulty recollection of the events when presenting testimony;
or (4) a person’s purposeful recounting of symptoms that did not exist. Lalonde v. Sec’y of Health
& Hum. Servs., 110 Fed. Cl. 184, 203-04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir. 2014). In making
a determination regarding whether to afford greater weight to contemporaneous medical records
or other evidence, such as testimony at hearing, there must be evidence that this decision was the
result of a rational determination. Burns, 3 F.3d at 417.
C. Analysis of Expert Testimony
Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec’y of Health & Hum. Servs., 219 F.3d 1357,
1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to the
factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharmaceuticals,
Inc., 509 U.S. 579, 594–96 (1993). See Cedillo v. Sec’y of Health & Hum. Servs., 617 F.3d 1328,
1339 (Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195 F.3d 1302, 1316 (Fed.
Cir. 1999)). “The Daubert factors for analyzing the reliability of testimony are: (1) whether a
27
theory or technique can be (and has been) tested; (2) whether the theory or technique has been
subjected to peer review and publication; (3) whether there is a known or potential rate of error
and whether there are standards for controlling the error; and (4) whether the theory or technique
enjoys general acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2
(citing Daubert, 509 U.S. at 592–95).
The Daubert factors play a slightly different role in Vaccine Program cases than they do
when applied in other federal judicial fora (such as the district courts). Daubert factors are usually
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors
are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health
& Hum. Servs., 94 Fed. Cl. 53, 66–67 (2010) (“uniquely in this Circuit, the Daubert factors have
been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of
expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the
persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88
Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases), Daubert has not
been employed at the threshold, to determine what evidence should be admitted, but instead to
determine whether expert testimony offered is reliable and/or persuasive.
Respondent frequently offers one or more experts of his own in order to rebut a petitioner’s
case. 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, 618 F.3d at 1347 (citing Lampe, 219 F.3d at 1362). However, nothing requires the
acceptance of an expert’s conclusion “connected to existing data only by the ipse dixit of the
expert,” especially if “there is simply too great an analytical gap between the data and the opinion
proffered.” Snyder, 88 Fed. Cl. at 743 (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997));
see also Isaac v. Sec’y of Health & Hum. Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed.
Cl. Spec. Mstr. July 30, 2012), mot. for rev. denied, 108 Fed. Cl. 743 (2013), aff’d, 540 F. Appx.
999 (Fed. Cir. 2013) (citing Cedillo, 617 F.3d at 1339). Weighing the relative persuasiveness of
competing expert testimony, based on a particular expert’s credibility, is part of the overall
reliability analysis to which special masters must subject expert testimony in Vaccine Program
cases. Moberly, 592 F.3d at 1325–26 (“[a]ssessments as to the reliability of expert testimony often
turn on credibility determinations”); see also Porter v. Sec’y of Health & Hum. Servs., 663 F.3d
1242, 1250 (Fed. Cir. 2011) (“this court has unambiguously explained that special masters are
expected to consider the credibility of expert witnesses in evaluating petitions for compensation
under the Vaccine Act”).
Expert opinions based on unsupported facts may be given relatively little weight. See
Dobrydnev v. Sec’y of Health & Hum. Servs., 556 F. Appx. 976, 992–93 (Fed. Cir. 2014) (“[a]
doctor’s conclusion is only as good as the facts upon which it is based”) (citing Brooke Group Ltd.
28
v. Brown & Williamson Tobacco Corp., 509 U.S. 209, 242 (1993) (“[w]hen an expert assumes
facts that are not supported by a preponderance of the evidence, a finder of fact may properly reject
the expert’s opinion”)). Expert opinions that fail to address or are at odds with contemporaneous
medical records may therefore be less persuasive than those which correspond to such records. See
Gerami v. Sec’y of Health & Hum. Servs., No. 12-442V, 2013 WL 5998109, at *4 (Fed. Cl. Spec.
Mstr. Oct. 11, 2013), aff’d, 127 Fed. Cl. 299 (2014).
D. Consideration of Medical Literature
Both parties filed medical and scientific literature in this case, but not every filed item
factors into the outcome of this decision. While I have reviewed all the medical literature submitted
in this case, I discuss only those articles that are most relevant to my determination and/or are
central to Petitioner’s case—just as I have not exhaustively discussed every individual medical
record filed. Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322, 1328 (Fed. Cir. 2016)
(“[w]e generally presume that a special master considered the relevant record evidence even
though he does not explicitly reference such evidence in his decision”) (citation omitted); see also
Paterek v. Sec’y of Health & Hum. Servs., 527 F. Appx. 875, 884 (Fed. Cir. 2013) (“[f]inding
certain information not relevant does not lead to—and likely undermines—the conclusion that it
was not considered”).
E. Consideration of Comparable Special Master Decisions
In reaching a decision in this case, I have considered other decisions issued by special
masters (including my own) involving similar injuries, vaccines, or circumstances. I also reference
some of those cases in this Decision, in an effort to establish common themes, as well as
demonstrate how prior determinations impact my thinking on the present case.
There is no error in doing so. It is certainly correct that prior decision in different cases do
not control the outcome herein. 16 Boatmon, 941 F.3d at 1358-59; Hanlon v. Sec’y of Health &
Hum. Servs., 40 Fed. Cl. 625, 630 (1998). Thus, the fact that another special master reasonably
determined elsewhere, on the basis of facts not in evidence in this case, that preponderant evidence
supported the conclusion that vaccine X caused petitioner’s injury Y does not compel me to reach
the same conclusion in this case. Different actions present different background medical histories,
different experts, and different items of medical literature, and therefore can reasonably result in
contrary determinations.
16
By contrast, Federal Circuit rulings concerning legal issues are binding on special masters. Guillory v. Sec’y of
Health & Hum. Servs., 59 Fed. Cl. 121, 124 (2003), aff’d 104 F. Appx. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y
of Health & Hum. Servs., No. 13-159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014). Special
masters are also bound within a specific case by determinations made by judges of the Court of Federal Claims after
a motion for review is resolved.
29
However, it is equally the case that special masters draw upon their experience in resolving
Vaccine Act claims. Doe v. Sec’y of Health & Hum. Servs., 76 Fed. Cl. 328, 338-39 (2007) (“[o]ne
reason that proceedings are more expeditious in the hands of special masters is that the special
masters have the expertise and experience to know the type of information that is most probative
of a claim”) (emphasis added). They would therefore be remiss in ignoring prior cases presenting
similar theories or factual circumstances, along with the reasoning employed in reaching such
decisions. This is especially so given that special masters not only routinely hear from the same
experts in comparable cases but are also repeatedly offered the same items of medical literature
regarding certain common causation theories. It defies reason and logic to obligate special masters
to “reinvent the wheel”, so to speak, in each new case before them, paying no heed at all to how
their colleagues past and present have addressed similar causation theories or fact patterns. It is for
this reason that prior decisions can have high persuasive value—and why special masters often
explain how a new determination relates to such past decisions. 17 Even if the Federal Circuit does
not require special masters to distinguish other relevant cases (Boatmon, 941 F.3d at 1358), it is
still wise to do so.
F. Determining Matter on Record Rather Than at Hearing
After conducting the first part of a planned multi-day hearing, the parties consented to
having this case decided based on written submissions and evidentiary filings, including the
numerous expert reports that have been submitted. The Vaccine Act and Rules not only
contemplate but encourage special masters to decide petitions (or components of a claim) on the
papers rather than via evidentiary hearing, where (in the exercise of their discretion) they
conclude that the former means of adjudication will properly and fairly resolve the case. Section
12(d)(2)(D); Vaccine Rule 8(d). The Federal Circuit has recently affirmed this practice.
Kreizenbeck v. Sec’y of Health & Hum. Servs., 945 F.3d 1362, 1365–66 (Fed. Cir. 2020). It
simply is not the case that every Vaccine Act claim need be resolved by hearing—even where
the petitioner explicitly so requests.
ANALYSIS
I. Prior Decisions Involving TM and the Hepatitis B Vaccine
Claims alleging acute demyelinating conditions, like TM, following vaccination are
common in the Vaccine Program—and many have met with success. Compare Palattao v. Sec’y
of Health & Hum. Servs., No. 13-591V, 2019 WL 989380 (Fed. Cl. Spec. Mstr. Feb. 4, 2019)
17
Consideration of prior determinations is a two-way street that does not only inure to the benefit of one party. Thus,
I would likely take into account the numerous decisions finding no association between vaccination and autism when
confronted with a new claim asserting autism as an injury, and I have informed such claimants early in the life of their
case that the claim was not viable for just that reason. But I would also deem a non-Table claim asserting GBS after
receipt of the flu vaccine as not requiring extensive proof on Althen prong one “can cause” matters, for the simple
reason that the Program has repeatedly litigated the issue in favor of petitioners.
30
(denying entitlement for a claim alleging TM following receipt of several vaccines in an infant
child who experienced onset between thirty and thirty-six hours after vaccination), with Pearson
v. Sec’y of Health & Hum. Servs., No. 03-2751V, 2008 WL 5093378 (Fed. Cl. Spec. Mstr. Nov.
6, 2008) (finding in favor of a petitioner who alleged TM as a result of the Hepatitis B vaccine).
Often the nature of the causal theory proposed has made the difference in whether the claimant
was found entitled to damages. See Palattao, 2019 WL 989380, at *8 n.10 (denying entitlement
for petitioners who asserted that pathological demyelination was the result solely of the innate
immune system inducing an overwhelming proinflammatory cytokine response); Stevens v. Sec’y
of Health & Hum. Servs., No. 99-594V, 2006 WL 659525, at *1, 25 (Fed. Cl. Spec. Mstr. Feb. 24,
2006) (granting entitlement in favor of a petitioner who asserted a theory of
challenge/rechallenge). While these decisions do not bind this determination, I take note of them
and their sound analyses.
In the present matter, Petitioners’ experts propose molecular mimicry as the causal
mechanism by which the Hepatitis B vaccine can cause TM—a theory distinguishable from what
was relied upon in other cases involving the same injury. For example, the petitioners in Palattao
(who also alleged an infant’s TM was vaccine-caused) expressly rejected the theory of molecular
mimicry espoused in this case, relying instead solely on an aberrant proinflammatory cytokine
response as the disease driver. Id. at *8. I found that the petitioners had failed to “demonstrate that
cytokine upregulation in the periphery attributable to a vaccine can also trigger TM.” Id. at *36(emphasis in original).
In Stevens, the special master determined that the petitioner was entitled to compensation
for TM she developed subsequent to receiving two doses of the Hepatitis B vaccine. Stevens, 2006
WL 659525, at *25. Unlike the present case, however, the petitioner in Stevens successfully
demonstrated that her adverse reaction was due to a challenge/re-challenge rather than cross-
reactivity. Id. at *1. And in Pearson, the special master did not identify the proposed causal theory
at all, but instead relied on her prior ruling in Stevens to conclude that the Hepatitis B vaccine can
cause TM. Pearson, 2008 WL 5093378, at *3. These cases demonstrate that the evidentiary value
and persuasiveness of the causal theory can vary from case to case—resulting in disparate
outcomes even though vaccine and injury are the same.
II. Petitioners Have Established TM as S.M.’s Injury
In many cases, the first step in deciding a claim is to determine the nature of the petitioner’s
injury—especially if the causal theory is dependent on establishing that a specific injury occurred.
Broekelschen, 618 F.3d at 1345; LaPierre v. Sec’y of Health & Hum. Servs., No. 17-227V, 2019
WL 6490730, at *16–17 (Fed. Cl. Spec. Mstr. Oct. 18, 2019). That is the case here, since the
parties strenuously dispute the proper diagnosis—TM or AFM—and since Petitioners’ causation
theory wholly assumes that the former to be the correct one. Petitioners have not alleged that AFM
31
could be vaccine-caused, so a determination that this best characterized S.M.’s injury would be
fatal to their claim.
Ample evidence from the medical record supports Petitioners’ allegation that TM best
characterizes S.M.’s injury. Of great significance is the fact that S.M.’s initial treating physicians
deemed her clinical presentation consistent with TM. That diagnosis was largely based on imaging
and laboratory studies conducted within hours of her symptom onset, as well as findings present
on physical examination. See Bal Rep.; Ex. 4 at 28; Ex. 5 at 19–21, 83–86. Petitioners also
specifically note that the MRI conducted on July 17, 2014, revealed inflammation spanning the
levels of C2 through T6 and affecting both the gray and white matter of the spinal cord. Ex. 4 at
28. These findings were initially interpreted as being consistent with TM, and this interpretation
was later confirmed by the opinion of Petitioners’ radiology expert, Dr. Silverman. Id.; Silverman
Rep. at 3; Tr. at 30. Dr. Bal, S.M.’s treating infectious disease specialist, agreed with the TM
diagnosis, and he noted that CSF studies showing an elevated IgG index were consistent with
spinal cord inflammation. Bal Rep. at 2. The medical record is otherwise replete with evidence
that S.M. was experiencing motor, sensory, and autonomic dysfunction—all of which are more
characteristic of TM than AFM. See Ex. 105 at 17–18, 21, 25, 27–28.
The context in which AFM arose as a potential counter-diagnosis is also relevant. Not until
January 2017—more than two years after the initial onset of S.M.’s symptoms— did any of S.M.’s
treaters consider the possibility of AFM. Ex. 14 at 5. But even then, S.M.’s TM diagnosis remained
unchanged. Id. And while the delay in proposing this alternative diagnosis could be credited to the
fact that the AFM “outbreak” occurred in 2014 (the time period at issue here), it remains the case
that substantial record evidence is wholly consistent with the conclusion that S.M.’s injury was
TM. Although it is always reasonable when evaluating a medical record in hindsight to take into
account subsequent medical information that may not have been known at the time, the mere fact
that an AFM outbreak was temporally congruent with the onset of S.M.’s symptoms does not mean
that she suffered from AFM per se. Here, it is reasonable to infer from this record that the timing
of S.M.’s symptoms onset was the main driver for the proposed alternative diagnosis.
Respondent did cite some record evidence to rebut Petitioners’ proffered TM diagnosis
independent of the AFM outbreak. Dr. Kedl credibly noted that CSF studies conducted upon
S.M.’s admission on July 17, 2014 did not reveal pleocytosis—contrary to what would be expected
for TM (although its absence also further reduced the explanatory power of the alternative AFM
diagnosis). First Kedl Rep. at 1, 5. And S.M.’s condition did not significantly improve with steroid
or PLEX treatments, as would have been expected if she suffered from TM. First Fisher Rep. at
3–4. Beyond that, the respiratory panel results indicated S.M. was experiencing a rhinovirus
infection close in time to the onset of her condition—and as Dr. Fisher noted, rhinovirus and
enterovirus may cross-react during the respiratory panel study. Id. at 4. If S.M. was in fact suffering
from an enterovirus rather than a rhinovirus infection, this would lend support to Respondent’s
32
AFM diagnosis, because there is a known association between enterovirus—specifically the EV-
D68 strain—and the development of AFM. Id.Weighing all of the above, I find that record preponderates in Petitioners’ favor on the
contention that S.M.’s condition is best understood as TM rather than AFM. In reaching this
conclusion, I note that the opinions offered by S.M.’s treating physicians (Drs. Fantasia, Yee, and
Bal) in addition to the medical record evidence, were consistent and collectively quite
persuasive—along with the testimony of radiologic expert Dr. Silverman. And many of
Respondent’s arguments focused less persuasively on what the record actually suggested about
S.M.’s diagnosis, and more on indirect points about causes that, if established, would at best
slightly undermine the TM diagnosis. Such points had some evidentiary heft, but warranted less
weight than the record overall.
III. Petitioners Have Carried Their Burden of Proof Under Althen
A. Prong One
Petitioners’ Althen prong one showing was not especially strong, but it was nevertheless
sufficient to cross the preponderant “line.”
First, I find that both of Petitioners’ experts collectively offered enough reliable scientific
and medical evidence, bulwarked by their own personal qualifications, to provide a preponderant
“can cause” theory relating the Hepatitis B vaccine to TM. They also stated a reasonable
immunologic mechanism—molecular mimicry—to explain how the Hepatitis B vaccine can cause
TM. First Egan Rep. at 7–8; Second Steinman Rep. at 4–6; Third Steinman Rep. at 2–3. In addition
to direct treater support for a causal association (explained in more detail below), Petitioners’
experts also propped up their causal theory with references to several case reports, which have
some probative value in Program cases, even though they do not stand as particularly strong Althen
prong one evidence. Doe 93 v. Sec’y of Health & Hum. Servs., 98 Fed. Cl. 553, 568 (2011) (citing
Campbell v. Sec’y of Health & Hum. Servs., 90 Fed. Cl. 369, 385 (2009)).
Second, existing Program decisions also helped Petitioners somewhat. This is not the first
causal opinion in which a petitioner argued that the Hepatitis B vaccine can cause TM in an infant
(including those in the mini-omnibus 18 proceedings from approximately sixteen years ago), and I
18
On October 13-14, 2004, former Special Master (and later Chief Judge of the Court of Federal Claims) Margaret
Sweeney held a hearing—which became known as the “Hepatitis B – Neurological Demyelinating Omnibus
Proceeding”—to determine whether a causal association exists between the Hepatitis B vaccine and several
demyelinating illnesses (multiple sclerosis, TM, chronic inflammatory demyelinating polyneuropathy, and GBS)
alleged in four paradigm cases. Stevens, 2006 WL 659525; Werderitsch v. Sec’y of Dept. of Health & Hum. Servs.,
No. 99-638V, 2006 WL 1672884 (Fed. Cl. Spec. Mstr. May 26, 2006); Peugh v. Sec’y of Dept. of Health & Hum.
Servs., No. 99–319V, 2007 WL 1531666 (Fed. Cl. Spec. Mstr. May 8, 2007); Gilbert v. Sec’y of Dept. of Health &
Hum. Servs., No. 04–455V, 2006 WL 1006612 (Fed. Cl. Spec. Mstr. Mar. 30, 2006). These cases were then reassigned
to former Special Master Laura Millman, who found that in all four cases, the Hepatitis B vaccine was causal. Peugh,
2007 WL 1006612, at *1, 17–18.
33
give credence to those prior determinations, which constitute reasoned decisions worthy of my
consideration. See Stevens, 2006 WL 659525, at *20–25; Pearson, 2008 WL 5093378, at *3–4.
Such decisions are also distinguishable from those cases involving infants where entitlement was
denied, since molecular mimicry is here embraced as the causal mechanism. See, e.g. Palattao,
2019 WL 989380, at *33–39. Even though such prior determinations do not mandate the outcome,
I reasonably take note of them and their sound rationales.
Petitioners also buoyed their claim with substantial treater support, pointing out the extent
to which contemporaneous medical service providers deemed the Hepatitis B vaccine likely causal.
See Ex. 5 at 18; Tr. at 118–20. Even though much of this evidence bears on the diagnostic question
addressed above, or the “did cause” prong, I may also consider it under Althen prong one.
Capizzano, 440 F.3d at 1326 (“[w]e see no reason why evidence used to satisfy one of the Althen
[ ] prongs cannot overlap to satisfy another prong”).The credible testimony of S.M.’s treaters was
highly persuasive, and I afford it some weight on the “can cause” element, even if it is less detailed
and specific than what Petitioners’ causation experts proposed.
Nevertheless, much of the evidence offered by Respondent was similarly persuasive, and
it gives me pause in finding for Petitioner. In particular, Respondent’s experts have cited a number
of persuasive epidemiological studies that undercut the causal theory in this case. See, e.g., Baxter
at 1461; Hocine at 5942–43; Schattner at 3877–78. Notably, of these epidemiological studies,
Hocine (2007) and Baxter (2016) post-date the omnibus proceedings, including Stevens (2006),
and Baxter post-dates Pearson (2008). 19 Although it is unquestionably the case that Program
litigants need not offer epidemiological evidence to prevail, special masters may take notes of its
existence and consider it when determining if a claimant has met his burden of proof. See, e.g.,
D’Toile v. Sec’y of Health & Hum. Servs., 726 F. App’x 809, 811–12 (Fed. Cir. 2012). Such
evidence does undercut Petitioners’ showing—and arguments that I should give case studies great
weight, while disregarding large-scale evaluations of vaccination outcomes due to the rarity of
vaccine injuries generally, are simply not persuasive.
Petitioners’ claim was also weakened—albeit by a smaller degree—by Bogdanos, which
Petitioners themselves submitted. As Respondent correctly noted, the amino acid sequence initially
identified by Dr. Steinman as the source of homology between components of the Hepatitis B
vaccine and MBP is not actually present in Hepatitis B vaccines. Second Kedl Rep. at 4–5. And
Dr. Kedl provided credible evidence that the homology between the amino acid sequence later
identified by Dr. Steinman in supplemental reports is insufficient to generate cross-reactivity.
Second Kedl Rep. at 5–7 (citing Bogdanos at 219; Silvanovich at 252). Indeed, and as I have ruled
in other cases, simply proving sequential homology between amino acid sequences in a vaccine
component and some self-structure does not automatically make an autoimmune cross reaction
19
In a recent decision, I gave some weight to the fact that many older decisions involving vaccination and TM did
not have the benefit of review of this more-recent epidemiologic evidence. I.J. v. Sec’y of Health & Hum. Servs.,
No. 16-864, 2021 WL --- (Fed. Cl. Spec. Mstr. Jan. 4, 2021), appeal docketed Feb. 3, 2021.
34
more likely. See, e.g., Pek v. Sec’y of Health & Hum. Servs., No. 16-736V, 2020 WL 1062959, at
*16 (Fed. Cl. Spec. Mstr. Jan. 31, 2020).
Overall, after weighing all such evidence in the relevant context, I find that Petitioners have
barely met their preponderant burden on this first element. Indeed—the evidence is almost in
equipoise. But well-reasoned and controlling precedent in the Vaccine Program requires me in
such close cases to decide the matter for the petitioner. See Walther v. Sec’y of Health & Hum.
Servs., 485 F.3d, 1146, 1150 (Fed. Cir. 2007) (“[u]nder our case law, ‘close calls regarding
causation are resolved in favor of injured claimants’”) (quoting Althen, 418 F.3d at 1280)). It is
hardly settled in the Vaccine Program that the Hepatitis B vaccine can cause TM in children or
adults, and a stronger expert showing by Respondent in a future case may tilt the determination in
the other direction—especially if coupled with additional evidence. But in this case, I find the “can
cause” prong has been satisfied.
B. Prong Two
The record also supports the conclusion that the Hepatitis B vaccine likely caused S.M.’s
TM. As previously mentioned, Petitioners offered persuasive testimony from S.M.’s treating
physicians—many of whom right away considered a possible association between the Hepatitis B
vaccine S.M. received and her subsequent development of TM. While Respondent correctly
observes that the record also includes some more ambiguous statements about an association, or
may simply have over-relied on the temporal association (which is recognized in the Vaccine
Program as an insufficient basis to ascertain causation), I nevertheless discern sufficient, reliable
treater support connecting the third dose of the Hepatitis B vaccine S.M. received to her onset of
TM shortly thereafter to deem it evidentiarily sufficient.
Petitioners’ showing on the “did cause” prong was further bulwarked by the full and
extensive effort by S.M.’s treating physicians and Respondent’s experts to identify other possible
explanations for S.M.’s condition. Bal Rep. at 2–3. While petitioners may not establish entitlement
to compensation simply by eliminating other potential causes, this case presents a work-up that
was comprehensive. See Bal Rep. at 1–3. Petitioners also persuasively established that S.M. was
most likely infected with the rhinovirus during her hospital admission, diminishing the likelihood
that her pre-vaccination sickness was associated with her onset. Id. at 2. And the medical record
did not establish a likely alternative explanation (although I acknowledge that this record does
contain hints of possible alternative explanations that Respondent did not fully flesh out). 20
20
Had Respondent more directly attempted to preponderantly establish an alternative cause, I would not on this record
be able to find that burden was met. See Deshler v. Sec’y of Health & Hum. Servs., No. 16-1070V, 2020 WL 4593162,
at *22 (Fed. Cl. Spec. Mstr. July 1, 2020) (citing de Bazen v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1354
(Fed. Cir. 2008)).
35
C. Prong Three
Lastly, I find that record evidence in this matter supports the conclusion that the onset of
S.M.’s condition occurred within a medically reasonable timeframe, consistent with Petitioners’
theory. As noted above, Petitioners assert that S.M.’s symptoms began approximately seventy-
seven hours after her receipt of the third Hepatitis B vaccine—a timeframe which has consistently
been deemed medically appropriate in other cases involving demyelinating conditions, including
TM, following vaccination. See, e.g., Raymo v. Sec’y of Health & Hum. Servs., No. 11-654V, 2014
WL 1092274, at *23 (Fed. Cl. Spec. Mstr. Feb. 24, 2014) (onset of TM three to four days after
receipt of the Tdap vaccine). Petitioners’ experts also credibly explained why a facially-short
timeframe for a pathologic process driven by the adaptive immune system, as here, could occur in
an infant who had received two prior doses of the same vaccine, and thus whose adaptive response
would be inherently faster. First Steinman Rep. at 4.
In reaction, Respondent offered some persuasive evidence to suggest that the onset of
S.M.’s condition nevertheless occurred too quickly following immunization to be attributable to
an autoimmune process involving the adaptive production of autoantibodies. See First Kedl Rep.
at 5; Third Kedl Rep. at 5. Dr. Kedl also credibly highlighted that the CSF studies which were
performed within hours of S.M.’s symptoms onset were inconsistent with T cell infiltration or
cellular damage, as would have been expected under Petitioners’ proposed theory. First Kedl Rep.
at 5 (citing Ex. 4 at 64).
Dr. Kedl’s opinion was certainly reliable and well-founded, and as such, it merited careful
consideration. But in weighing this evidence against that offered by Petitioner and prior Program
cases, I find it merely (again) brought the parties closer to equipoise—supporting a determination
in Petitioners’ favor.
CONCLUSION
This matter serves as a case study for how the preponderant evidentiary standard often
functions in practice. Putting aside the parties’ dispute over the precise nature of S.M.’s injury (a
matter that was easily decided in Petitioners’ favor), it has not been established to any degree of
scientific certainty that the Hepatitis B vaccine can cause TM—especially in the fairly short
timeframe at issue here. Many of the arguments mustered by Petitioners’ experts invoke causation
contentions that either hold less and less weight as science progresses (especially in light of recent
epidemiologic studies), or reflect standard points experts nearly always assert in Program cases
(such as recitation of the magic words “molecular mimicry”) but which do not equally carry the
same weight in all cases.
36
But scientific certainty is far from the evidentiary standard to be applied in Program cases.
Indeed, Vaccine Program claimants can prevail despite the fact that considerable uncertainty
remains that they are correct. “More likely than not” is an inexact measurement to say the least.
Thus, I must conclude on the basis of Petitioners’ showing in this case that they have met
their evidentiary burden. The mix of treater support specific to S.M., plus on-point prior decisions
regarding the Hepatitis B vaccine and TM, are particularly compelling evidence, along with other
reliable science generally supporting Petitioners’ contentions. Under such circumstances, a
favorable award is legally appropriate, and consistent with the generous policy goals of the
Program. The Act expressly seeks to compensate parties like the McGrails who have needlessly
suffered, as so amply demonstrated by the facts of this case, and thus the evidence adduced herein
supports a favorable entitlement decision.
In order to guide the parties through the damages phase of the action, a separate damages
order will issue.
IT IS SO ORDERED.
/s/ Brian H. Corcoran
Brian H. Corcoran
Chief Special Master
37