Tipps v. Secretary of Health and Human Services

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 16-867V
(to be published)
************************* Chief Special Master Corcoran
KAYLON TIPPS, *
*
Petitioner, *
*
* Dated: December 9, 2022
v. *
*
*
SECRETARY OF HEALTH AND *
HUMAN SERVICES, *
*
Respondent. *
*
*************************
John R. Howie, Jr., Howie Law P.C., Dallas, TX, for Petitioner.
Jennifer L. Reynaud, U.S. Department of Justice, Washington, DC, for Respondent.
ENTITLEMENT DECISION 1
On July 22, 2016, Kay and Cathell Tipps, on behalf of their minor son, Kaylon (referred to
as ‘K.T.” at the time of filing, but now the named Petitioner) 2 filed a petition for compensation
under the National Vaccine Injury Compensation Program (the “Program”). 3 Petition (ECF No. 1)
1 This Decision 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 Decision will be available to the public in its current form. Id.
2
Mr. Tipps became the Petitioner when he turned 18, and the caption was accordingly amended. See Order, dated
May 4, 2022 (ECF No. 82).
3
The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,
100 Stat. 3758, codified as amended at 42 U.S.C. §§ 300aa-10 through 34 (2012) [hereinafter “Vaccine Act” or “the
Act”]. Individual section references hereafter will be to § 300aa of the Act (but will omit that statutory prefix).
(“Pet.”) at 1. Petitioner alleges that Meningococcal and Tetanus-Diphtheria-Acellular-Pertussis
(“Tdap”) vaccines he received on July 24, 2013, caused him to suffer meningitis and seizures.
A two-day entitlement hearing in the matter was held in Washington, D.C. on May 4–5,
2022. Having reviewed the record, all expert reports and associated literature, and listened to the
testimony at hearing, I hereby deny an entitlement award. As discussed in greater detail below,
Petitioner has not preponderantly established that the Meningococcal and Tdap vaccines were
likely causal of his subsequent illness.
I. Fact History
Vaccination and Six-Month Period Thereafter
Mr. Tipps was born on May 31, 2001. See Ex. 2 at 3. Prior to the vaccinations at issue, he
was in good health, and his medical history only establishes the existence of asthma, allergies,
eczema, and obesity. Id. at 4. On July 24, 2013, Petitioner (then twelve years old) received
Meningococcal and Tdap vaccines from his primary care physician. Id. at 5–6. The record does
not indicate that he experienced any immediate adverse reactions following the administration of
either vaccine.
On August 9, 2013 (sixteen days after his vaccinations), Petitioner was taken to the
emergency room (“ER”) at Crescent Medical Center complaining of a throbbing headache that had
persisted for over two hours. Ex. 3 at 5. His parents reported that in addition to the severe headache,
he was experiencing blurred vision. Id. at 5, 8. Upon examination, the treating physician concluded
that Mr. Tipps was dehydrated, and he was given fluids via an IV, pain medication, and discharged
home thereafter. Id. at 10.
Three days later (and shortly after midnight), on August 12, 2013, Mr. Tipps returned to
the ER at Crescent Medical Center due to episodes of starring and unresponsiveness accompanied
by a severe headache and projectile vomiting. Ex. 3 at 20. It was reported that his symptoms began
three days prior, and that he had started experiencing intense neck pain and vision changes. Id. On
exam, the treating physician observed erythema in Petitioner’s tympanic membranes,4 and
prescribed anti-seizure medication and antibiotics due to the concern for a central nervous
infection. Id at 21. Petitioner then underwent a CT scan of his head, the results of which were
unremarkable. Id. at 31. Before being transferred to Children’s Medical Center for further
evaluation, Mr. Tipps’s initial differential diagnosis included seizure disorder and mental status
change, with encephalitis ruled out. Id. at 21.
4
“Tympanic Membrane,” is defined as “the obliquely placed, thin membranous partition between the external acoustic
meatus and the tympanic cavity.” Membrana Tympanica, Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=88565 (last visited Dec. 9, 2022).
2
Petitioner arrived at the ER at Dallas Children’s Hospital around 4:00 a.m., on August 12,
2013. Ex. 4 at 1. There, his parents reported that he had been acting strangely the last three days,
recounting his ER visits at Crescent Medical Center and noting that he had a cough, runny nose,
and symptoms of an upper respiratory infection. Id. at 5. After undergoing a lumbar puncture, Mr.
Tipps’s cerebral spinal fluid (“CSF”) analysis revealed pleocytosis. 5 Petitioner’s treating
physicians felt this finding (coupled with his overall presentation) was consistent with a viral
meningoencephalitis 6 that was resolving. Id. at 25. However, because the CSF sample was
obtained in a setting in which Petitioner was receiving certain medications that might impact the
result, the CSF analysis was ultimately deemed unreliable. Id. at 27. Petitioner was discharged the
following day with a diagnosis of aseptic versus viral meningitis. Ex. 4 at 27.
On August 20, 2013, Petitioner saw pediatric neurologist, Dr. Kazi Majeed, at which time
he and his parents reported a history of prolonged, intermittent staring and unresponsiveness since
August 9th. Ex. 5 at 1. Following examination, a CT scan and an EEG were performed, both of
which resulted in normal findings— leading Dr. Majeed to propose that Mr. Tipps’s symptoms
reflected partial complex seizures. Id. at 3. Dr. Majeed recommended that Petitioner undergo a 48-
hour ambulatory VEEG 7 to try and determine a cause for the staring spells and unresponsiveness.
Id. at 3
On August 29, 2013, Mr. Tipps saw pediatric neurology physician’s assistant, Michelle
Ashcraft, PA, at the Headache Specialty Clinic at Children’s Medical Center. Based on physical
examination, recent hospitalization, and ongoing symptoms, PA Ashcraft recommended that
Petitioner be admitted to Children’s Medical Center for further neurologic evaluation, viral studies,
a brain MRI, and a possible lumbar puncture. Ex. 4 at 168–73.
The subsequently-performed lumbar puncture revealed elevated intracranial pressure
(opening pressure of 55 and a closing pressure of 19), and the brain MRI showed evidence of
5
“Pleocytosis” is defined as the “presence of a greater than normal number of cells in the cerebrospinal fluid.”
Pleocytosis, Dorland’s medical Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=39556
(last visited Dec. 9, 2022).
6
“Meningoencephalitis,” is defined as “inflammation of the brain and meninges.” Meningoencephalitis, Dorland’s
Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=30351&searchterm=meningoencephalitis (last visited Dec.
9, 2022).
7
An electroencephalogram (EEG) is a test that involves placing small metal discs, also known as electrodes, on an
individual’s scalp, in order to detect electrical brain abnormalities. A video electroencephalogram (VEEG) on the
other hand, is known as a more specialized form of an EEG, but includes the constant video monitoring of the
individual throughout the testing period. The VEEG (Video Electroencephalogram) Test Appears Useful for
Identifying Seizures, Brain Injury Association of America, https://www.biausa.org/professionals/research/tbi-model-
systems/the-veeg-video-electroencephalogram-test-appears-useful-for-identifying-seizures (last visited Dec. 9, 2022).
3
papilledema, consistent with the increased pressure. 8 Ex. 4 at 186. Petitioner was prescribed
medication for the elevated intracranial pressure and his headaches. Id. In addition, he was
evaluated by an infectious disease specialist who ruled out enterovirus, West-Nile, Arbovirus,
Varicella, and Herpes Simplex Virus (“HSV”) as potential causes for his symptoms. Id. at 186,
188. Petitioner remained at Children’s Medical Center until September 2, 2013, when his treating
physicians determined that he was stable enough for discharge. At that time, he was diagnosed
with headache, pseudotumor cerebri,9 and aseptic meningitis. Id. at 184. Petitioner was advised to
follow up with neurology and ophthalmology consults. Id. at 190.
Petitioner was taken to the ER at Methodist Charlton Medical Center on September 4,
2013, after complaining of neck pain and worsening headaches. Ex. 4 at 665. But because of his
complicated history, he was transferred to Dallas Children’s for further evaluation, where (after
his intracranial pressure medication dosage was adjusted) the severity of his symptoms subsided,
and he was later discharged. Id. at 667, 670. Then, on September 6, 2013, Mr. Tipps saw Dr.
Majeed who performed an EEG, the results of which indicated abnormal activity consistent with
encephalopathy, although no seizure activity was observed at this time. Ex. 5 at 4.
After experiencing worsening headaches and neck and back pain, Petitioner returned to the
ER on September 8, 2013, and was subsequently admitted to Medical City Dallas Hospital
(“MCDH”). Ex. 5 at 23. Upon admittance, he underwent another lumbar puncture which revealed
elevated intracranial pressure, and decreased sodium levels in the sample as well as his blood. Id.
at 47, 63. Extensive CSF studies for various possible causative agents were performed, and even
though all produced negative results, the infectious disease consultant opined that the etiology of
Mr. Tipps’s condition was nevertheless likely due to an infection “given his pleocytosis of
lymphocytosis.” Id. at 23. In addition to a hematology and oncology consult, Mr. Tipps was
examined by a neurologist who determined that his previous diagnosis of pseudotumor cerebri
from Children’s Medical Center was questionable, leading him to discontinue a diuretic and
initiate treatment with IV steroids. Ex. 7 at 55–56.
On September 13, 2013, Petitioner was experiencing significant deterioration in his vision.
During a consult with an ophthalmologist, he was now unable to make out any details or objects,
reporting that he could only see black despite the lights being on. Ex. 7 at 48–49. The
ophthalmologist noted that Petitioner’s pupils were not only significantly more dilated, but that
8
“Papilledema” is defined as “edema of the optic disk (papilla), most commonly due to increased intracranial pressure,
malignant hypertension, or thrombosis of the central retinal vein.” Papilledema, Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=36673&searchterm=papilledema (last visited Dec. 9, 2022).
9
“Pseudotumor Cerebri” is defined as “a condition of raised intracranial pressure with normal cerebrospinal fluid, in
the absence of an intracranial mass, hydrocephalus, or other identifiable cause; symptoms include headache, nausea,
vomiting, papilledema, and sometimes pulsatile tinnitus.” Pseudotumor Cerebri, Dorland’s Medical Dictionary
Online, https://www.dorlandsonline.com/dorland/definition?id=100755&searchterm=pseudotumor+cerebri (last
visited Dec. 9, 2022).
4
they were extremely sluggish and minimally reactive. Id. After consulting with other specialists
and Mr. Tipps’s family, arrangements were made for him to undergo an optic nerve sheath
fenestration in his right eye to alleviate the pressure around his optic nerve, and to return to MCDH
for further evaluation and care. Id. at 49. Dr. Zev Shulkin, a neuro-ophthalmologist, performed the
surgery that day, noting that it was necessary for him to undergo such a surgery at that time due to
the severe visual filed loss and visual acuity loss in that eye. Id. at 21.
Upon his return to MCDH, Mr. Tipps reported that his vision in his left eye had improved,
but that he did not want to open his right eye due to a burning sensation. Ex. 7 at 16. He also
complained of ongoing headaches which interfered with his ability to sleep. Id. A physical exam
was performed which indicated drainage and photophobia in both eyes, dilated and minimally
reactive pupils with swelling and slight sanguineous tearing. Id. Treating physicians determined
that he had likely experienced vision loss and impairment secondary to elevated intracranial
pressure, CF pleocytosis, peripheral leukocytosis, and thrombocytosis. Id. at 18. To address these
concerns, Petitioner underwent two lumbar punctures over the next two days, the last of which
showed an opening pressure of 27 and a closing pressure of less than 9. Id. With the hope of
alleviating some of the CSF pressure, he was restarted on certain medications. Id.
By September 16, 2013, Petitioner’s visual acuity in his left eye had become significantly
impaired, leading treaters to propose that he undergo another optic nerve sheath fenestration
(although this time in the left eye). Ex. 8 at 3–4. Dr. Shulkin performed the procedure, and
following its completion Petitioner was transferred back to MCDH for further evaluation and care.
Id. Despite the improvements in his right eye, Mr. Tipps remained unable to fully lateralize
externally in his right eye, indicating a persistent sixth nerve palsy. Ex. 7 at 12. Repeat lumbar
punctures were performed over the next several days, and by September 22, 2013, Petitioner’s
visual acuity exam and sixth nerve palsy showed significant improvement, resulting in him being
stable enough for discharge. Id. at 5. He left the hospital with diagnoses of increased intracranial
pressure, aseptic meningitis, severe papilledema, and improved vision loss. Id. at 1.
Treatment in 2015 to Present
There is a subsequent two-year records gap, revealing no treatment for Petitioner until
December 16, 2015, when he was evaluated by rheumatologist Dr. Maria Perez for his
“persistently elevated inflammatory markers over the past two years.” Ex. 10 at 312. Following an
extensive work-up, Dr. Perez opined that there was no evidence to suggest he suffered from a
rheumatic, autoimmune, or immunodeficiency illness. Id. at 61. Additional testing also revealed
no evidence of a mass or lymphadenopathy in his chest, abdomen, or pelvis. Id.
However, because of his elevated ESR/CRP, Petitioner was referred to pediatric
oncologist, Dr. Neethu Menon, due to concern for lymphoproliferative disorder. Ex. 12 at 1–4.
5
Following an exam and review of his labs, Dr. Menon opined that there was no evidence supporting
a lymphoproliferative disorder diagnosis. Id. at 5. She did, however, note the severity of his vision
impairment in his right eye, that his pupils showed impaired light reaction, and that his optic nerve
was impaired bilaterally. Id. at 8.
During a re-evaluation with Dr. Shulkin approximately six months later (on June 8, 2016),
Petitioner’s visual acuity was reported as 20/50 (-2) on the right and 20/20 on the left. Ex. 8 at 28.
At a later visit on October 31, 2016, his visual acuity was 20/40 on the right and 20/20 on the left.
Id. However, despite such improvements, Petitioner continues to have significant ongoing health-
related issues—suffering from regular headaches and general vision impairment. Ex. 1 ¶ 24.
II. Hearing Testimony
A. Petitioner’s Fact Witnesses
1. Kaylon Tipps
Petitioner was the first witness to testify at the hearing. See generally Tr. at 6–13. He
provided a brief overview of his academic studies and achievements, the extracurricular activities
he partakes in, and his plans following graduation. Id. at 6–9. He then discussed the facts and
circumstances leading up to his initial hospitalization, and the symptoms he continues to suffer
from as a result of his illness. Id. at 9–12.
Mr. Tipps recalled in particular that August 9, 2013, was very hot, and that he had been
playing out in the sun for several hours with friends. Tr. at 9–10. Aside from the asthma, allergies,
and eczema he had experienced pre-vaccination, he did not recall being sick with any sort of upper
respiratory infection on that date. Id. 10–11. Indeed, he maintained that had he been sick with an
upper respiratory infection, his mom would have wanted him to stay inside. Id. at 11. Petitioner
concluded his testimony with a brief overview of his current physical health and the problems he
continues to experience, noting that he remains partially blind in his right eye, he has diabetes
insipidus, and that the increased pressure on his brain occasionally causes him to hear “a
thundering sound.” Id. at 12.
2. Mr. Cathell Tipps
Petitioner’s father also provided live testimony. See generally Tr. at 14–29. He offered a
brief overview of Petitioner’s underlying health conditions prior to vaccination and at the time he
got sick. Id. at 16. Before the vaccination, Petitioner had suffered from asthma, allergies, and
eczema, but only took medicine as needed. Id. at 17. He recalled that Petitioner showed no signs
of an upper respiratory infection prior to his first hospitalization—and had he been suffering from
one, he would not have been permitted to play outside in the heat on August 9, 2013. Id. at 18–19.
6
He also discussed Petitioner’s first hospitalization, explaining he and his wife grew concerned for
Petitioner after they noticed he was not as responsive as he usually was, and that he began “starring
into space.” Id. at 19. He noted, however, that hospital staff evaluating Petitioner had seemed to
conclude that he might have been dehydrated from being out in the sun all day. Id. at 22.
On the morning of August 12, 2013, Mr. and Mrs. Tipps took Petitioner back to the
emergency room due to his unresponsiveness and persistent headaches. Again, Petitioner’s father
did not recall doing anything out of the ordinary the days prior to the hospitalizations, nor did he
recall Petitioner suffering from an upper respiratory infection. Tr. at 24. Later, Petitioner needed
to be transferred to a different hospital because Medical City did not have the proper equipment to
perform a spinal tap at the time. Id. at 25. Following his transfer, the spinal tap was performed to
alleviate some of Petitioner’s pain. Id. at 27. Petitioner continues to experience persistent
headaches and rarely wants to go outside and be active. Id.
B. Petitioner’s Expert Witnesses
1. Dr. Steven Lovitt, M.D.
Dr. Lovitt, a neurologist, submitted two expert reports and testified for Petitioner. See
generally Tr. at 30–96; Report, dated Feb. 5, 2018, filed as Ex. 14 (ECF No. 24-1) (“Lovitt First
Rep.”); Report, dated July 23, 2018, filed as Ex. 37 (ECF No. 32-1) (“Lovitt Second Rep.”).
Dr. Lovitt received his undergraduate degree from the University of Texas, and his medical
degree from Baylor College of Medicine. See Curriculum Vitae, filed Feb. 5, 2018 (ECF No. 24-
2) (“Lovitt CV”) at 1; Tr. at 31–32. After the completion of his fellowship in neuromuscular
diseases in 2001, Dr. Lovitt became an Assistant Professor of Medicine and Pathology at the
University of Texas Health Science Center at San Antonio, until early 2003. Lovitt CV at 2; Tr. at
32. Since then, Dr. Lovitt has been in private practice as a neurologist at The Neurology Center in
Houston, TX, and has extensive experience with the diagnosis and treatment of conditions such as
meningitis. Id. He is board certified in Neurology and Neuromuscular Medicine. Lovitt CV at 1.
Dr. Lovitt began his testimony with a brief overview of Petitioner’s diagnosis. He opined
that Mr. Tipps had suffered meningoencephalitis, with his initial headaches and unresponsive
episodes as reflecting a seizure. Tr. at 41. In so proposing, Dr. Lovitt spent some time defining
both encephalitis and meningitis, as well as discussing their diagnostic criteria.
Encephalitis, Dr. Lovitt explained, is inflammation of the brain and is generally associated
with an altered mental state and cognition persisting over 24 hours, plus some other abnormality
(i.e., abnormal spinal fluid with inflammatory cells or abnormal brain imaging). Tr. at 39–40.
Meningitis, by contrast, is inflammation of the coverings of the brain (the “meninges”). Id. at 40.
Meningitis is typically accompanied by a fever, stiff neck, confusion, or headache. Id. Dr. Lovitt
7
also explained that the diagnostic criteria for encephalitis and meningitis do not differ among
children and adults, because “the grounds for diagnosis are based on observation and based on
laboratory and ancillary testing, not [] on the age of the patients.” Id. at 36.
Dr. Lovitt next discussed the basis for his opinion that a meningoencephalitis diagnosis
was most appropriate, based on the information provided in the medical records. He first looked
at the spinal taps performed on Petitioner throughout his multiple hospitalizations, emphasizing
that each reading established an abnormal inflammatory process taking place within the brain. Tr.
at 44. In addition, Mr. Tipps also presented with a headache and an altered mental state—thus
exhibiting several of the main criteria for meningitis as defined by Dr. Lovitt. Id. While Dr. Lovitt
noted that Mr. Tipps exhibited several features indicative of encephalitis (i.e., abnormal EEG and
neuroimaging), his overall clinical presentation appeared to be more consistent with meningitis.
Id. at 45.
Mr. Tipps’s treating physicians were able to rule out a diagnosis of bacterial meningitis
based on the multiple spinal taps performed, all of which found no bacteria on the cultures. Tr. at
49; Ex. 4 at 186, 209, 213, 216. Moreover, Petitioner’s glucose levels were well within normal
range (inconsistent with a bacterial meningitis). And while Mr. Tipps was initially treated with
antibiotics (common when bacterial meningitis is suspected), he was never officially diagnosed
with bacterial meningitis, and his treating physicians ceased this course of treatment as soon as it
was determined that his clinical presentation did not fit such a diagnosis. Tr. at 49–50, 54. Thus,
Dr. Lovitt opined that Mr. Tipps more likely than not suffered from aseptic meningitis. Id.
Dr. Lovitt next explained that there are two types of aseptic meningitis: noninfectious and
infectious. Tr. at 51. Infectious aseptic, or nonbacterial meningoencephalitis, generally implies the
existence of a viral cause, like enterovirus, although there are numerous other possibly causal
viruses. Tr. at 55. Noninfectious meningoencephalitis, by contrast, can be attributable to primary
illness like cancer, an autoimmune condition that manifests due to an underlying rheumatologic
condition, or one that is confined exclusively to the central nervous system (the “CNS”). Tr. at 56.
Dr. Lovitt noted that there are different tests physicians can conduct in order to help identify the
type of aseptic meningoencephalitis an individual is suffering from. Tr. at 57. Two such common
tests are PCR 10 and antibody testing.
In Mr. Tipps’s case, extensive testing was performed to identify the presence of a virus—
including enterovirus, arbovirus, varicella virus, West Nile virus, HSV, and EBV—all of which
produced negative results. Tr. at 58; Lovitt First Rep. at 3; Lovitt Second Rep. at 3. While there
was no evidence in the medical records or the test results indicating that Mr. Tipps had a viral
10
PCR, or “Polymerase Chain Reaction,” is defined as “a type of rapid nucleic acid amplification of specific DNA or
RNA sequences, allowing small quantities of short sequences to be analyzed without cloning: oligonucleotide primers
are annealed to single-stranded nucleotide sequences, which are copied by polymerase; the number of copies is
geometrically amplified by repeated cycles of annealing and copying.” Polymerase Chain Reaction, Dorland’s
Medical Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=102447 (last visited Dec. 9,
2022).
8
infection, Dr. Lovitt acknowledged that Mr. Tipps’s treating physicians had reported two
symptoms associated with such an infection. Tr. at 58. In particular, a facial rash was documented
by treating physicians when Petitioner presented to the ER on August 12, 2013, but which was
later thought to be a manifestation of heat rash, and a cough which was described as an upper
respiratory infection (but never discussed further and ultimately dismissed). Id.
Thus, based on Mr. Tipps’s clinical presentation and in reviewing the medical records, Dr.
Lovitt opined that Mr. Tipps’s symptoms did not likely have a viral etiology. Tr. at 61. Dr. Lovitt
also deemed the unusual time course of Mr. Tipps’s symptoms, and his severe increased
intracranial pressure accompanied by seizures, as major factors weighing against a viral cause. Tr.
at 62–63. In Dr. Lovitt’s opinion and experience, cases of viral meningitis resolved within a week
or two, but Mr. Tipps’s symptoms had atypically lasted well over a month. Tr. at 65.
Dr. Lovitt next discussed the implications of an individual suffering from increased
intracranial pressure, and how that fit in with his overall opinion that Mr. Tipps more likely than
not suffered from a noninfectious form of meningoencephalitis. When an individual is suffering
from increased intracranial pressure, the consequences can be severe—the pressure can sometimes
push on the back of one’s optic nerve which can lead to vision loss, it can push on other nerves
and cause sixth nerve palsy, or it can even push the brain outside of the skull leading to herniation
which can be fatal. Tr. at 76–77. Mr. Tipps’s intracranial pressure was measured throughout the
course of his treatments and hospitalizations, and repeatedly found to be severely elevated. Id.11
As a result, Mr. Tipps’s treating physicians briefly considered the possibility of a pseudotumor
cerebri being the underlying cause of his symptoms, but the significant abnormal inflammation he
was also displaying was not consistent with that diagnosis. Id. at 68. Instead, his treating physicians
recommended that Mr. Tipps undergo an optic nerve fenestration to help alleviate the pressure and
prevent permanent vision loss. Id. at 78.
Dr. Lovitt concluded his testimony by reiterating why he had concluded that Mr. Tipps’s
vaccinations were more likely than not the cause of his meningoencephalitis. Tr. at 83–85. Mr.
Tipps had presented with a CNS inflammatory response that was accompanied with significant
increased intracranial pressure, disc edema, vision loss, and spinal fluid that demonstrated the
presence of an inflammatory process. Id. Extensive testing had been performed to identify the
presence of a viral or infectious process, yet all results were negative, and there was no other
evidence in Mr. Tipps’s medical records or clinical presentation to suggest that he was suffering
from such a process (although Dr. Lovitt admitted that negative results did not necessarily exclude
the possibility of a viral or infectious cause). Id. at 84. Dr. Lovitt strongly opined that Mr. Tipps’s
clinical course was rather atypical, based on his reviewing of the medical records as well as his
experience. Id. at 85; Lovitt Second Rep. at 3. And no other alternative explanation existed,
11
Dr. Lovitt noted that normal pressure should typically be under 20, but Mr. Tipps’s ranged from 55-90. Tr. at 68.
9
increasing (in Dr. Lovitt’s estimation) the possibility of the vaccinations received being the cause
of Mr. Tipps’s meningoencephalitis. Tr. at 89; Lovitt Second Rep. at 5.
The biggest contributing factor to Dr. Lovitt’s opinion that Mr. Tipps’s vaccinations were
causal of his meningoencephalitis was the timeframe in which his symptoms began. Tr. at 85;
Lovitt Second Rep. at 3–4. Looking at the time course of Mr. Tipps’s symptoms (headache,
photophobia, vision changes, and unresponsiveness), an onset of 16 days post-vaccination was
well within the expected timeframe to support a vaccine association. Lovitt First Rep. at 4; Lovitt
Second Rep. at 5; H. Torisu et al., Clinical Study of Childhood Acute Disseminated
Encephalomyelitis, Multiple Sclerosis, and Acute Transverse Myelitis in Fukuoka Prefecture,
Japan, 32 Brain & Development 454, 457 (2010), filed as Ex. 48 (ECF No. 34-1) (finding the
mean onset of neurological symptoms following vaccination was 17.7 days). Moreover, Mr. Tipps
suffered from severe increased intracranial pressure for over a month—atypical for viral
meningoencephalitis. Id. at 65.
2. Dr. David Axelrod, M.D.
Dr. Axelrod, an immunologist, submitted four expert reports and testified for Petitioner.
See generally Tr. at 101–58; Report, dated July 23, 2018, filed as Ex. 25 (ECF No. 29) (“Axelrod
First Rep.”); Report, dated Sept. 6, 2019, filed as Ex. 52 (ECF No. 42-1) (“Axelrod Second Rep.”);
Report, dated Mar. 5, 2021, filed as Ex. 81 (ECF No. 57-1) (“Axelrod Third Rep.”); Report, dated
June 21, 2021, filed as Ex. 102 (ECF No. 69-1) (“Axelrod Fourth Rep.”).
Dr. Axelrod received his undergraduate degree, medical degree, and graduate degree from
the University of Michigan. See Curriculum Vitae, filed July 23, 2018 (ECF No. 31-2) (“Axelrod
CV”) at 1; Tr. at 102–3. Dr. Axelrod held several academic appointments throughout his career
including Walter Reed Army Institute of Research, Medical College of Ohio, and UMDNJ-New
Jersey Medical School. Axelrod CV at 2. Dr. Axelrod was a Principal Investigator at the Walter
Reed Army Institute and participated in the study and development of a vaccine. Axelrod CV at 1;
Axelrod First Rep. at 1. Before retiring, he worked in private practice as a rheumatologist and
allergist at the Allergy and Asthma Center in Maryland, and saw patients with adult autoimmune
diseases, allergies, and occasionally immune deficiencies. Axelrod CV at 2; Tr. at 102. As a
clinician, Dr. Axelrod diagnosed and treated patients with various drug reactions. Axelrod First
Rep. at 1. He is board certified in Internal Medicine, Adult Rheumatology, Medical Laboratory
Immunology, and Allergy and Immunology, and has published several articles and abstracts over
the course of his career. Id.; Axelrod CV at 3–4.
Dr. Axelrod began his testimony with a brief overview of Petitioner’s diagnosis, agreeing
with Dr. Lovitt that Petitioner had experienced meningoencephalitis—which he in turn proposed
was more likely than not vaccine-induced. Tr. at 105–06. He then provided an explanation of the
concept of autoimmunity and the role in which molecular mimicry plays in it. Most autoimmune
10
disorders occur in individuals with a genetic predisposition and/or susceptibility to developing
such a disorder. Tr. at 109; Axelrod First Rep. at 2. As a result, Dr. Axelrod deemed it likely that
Mr. Tipps possessed some type of susceptibility to developing autoimmune meningoencephalitis.
Id. at 109–110.
However, Dr. Axelrod explained, while an individual may be predisposed to developing
an autoimmune disorder, infectious agents (including counterpart vaccines) can act as principal
environmental insults subsequently responsible for the induction of autoimmune disease. Axelrod
Second Rep. at 2; M. Cusick & R. Fujinami, Molecular Mimicry as a Mechanism of Autoimmune
Disease, 42 Clinical Rev. Allery Immunology 102, 102 (2012), filed as Ex. 55 (ECF No. 41-4)
(finding proinflammatory cytokines are critical to the clearance of pathogens, and further
suggesting that environmental factors can divert the immune response towards
immunopathogenesis).
Dr. Axelrod next proposed a theory for how the meningococcal and Tdap vaccines could
have caused Petitioner’s meningoencephalitis, focusing on the concept of “anti-idiotypic”
antibodies becoming pathogenic due to molecular mimicry. Tr. at 112; Axelrod First Rep. at 2–3;
Axelrod Second Rep. at 2–3; Axelrod Fourth Rep. at 1, 4–7. When an individual is exposed to
some external agent immunologically, a damaging, autoimmune-mediated cross-reaction can
occur via molecular mimicry. Tr. at 109–110. This can occur if the various segments of amino
acids that make up the external agent (assuming it is viral, and thus protein-based) are sequentially
or structurally similar to self-tissue sequences/structures—meaning the immune response to the
foreign antigen (whether by producing antibodies, other immune cells (meaning T cell-oriented),
or a combination thereof) can react to self, resulting in autoimmune damage and/or excessive
inflammation. Id. at 110.
In this case, Dr. Axelrod proposed that a specific kind of antibody—anti-idiotypic
antibodies—were the pathogenic drivers of this putative autoimmune process. Axelrod First Rep.
at 3. Tr. at 112–13. He defined them to be antibodies that can bind to the variable region (or
“idiotype”) of another antibody, and thus can impact immunogenicity (in potentially good and bad
ways). Axelrod First Rep. at 1. Dr. Axelrod specifically proposed that anti-idiotypic antibodies
have the ability to attach to aspects of the nervous system in a manner similar to that of the tetanus
toxoid, diphtheria toxoid, and fragments A and B of the pertussis toxin, and thereby cause
comparable harm. Thus, he theorized that autoimmune meningoencephalitis could be the result of
production of anti-idiotypic antibodies in response to vaccination. Tr. at 112.
To support his theory (and in reaction to assertions by Respondent’s expert), Dr. Axelrod
attempted to first show that the viral toxins/toxoids at issue could themselves give rise to
pathology. One article was offered to show that certain subunits of the pertussis toxin can interact
with neuronal gangliosides. Axelrod First Rep. at 3; M. Hara-Yokoyama et al., Identification of
11
Gangliosides as Inhibitors of ADP-Ribosyltransferases of Pertussis Toxin and Exoenzyme C3 from
Clostridium Botulinum, 270 J. of Biological Chemistry 8115 (1995), filed as Ex. 85 (ECF No. 57-
5) (“Hara-Yokoyama”). While Respondent’s immunologic expert, Dr. Andrew MacGinnitie,
argued (as discussed below) that Hara-Yokoyama only showed that the gangliosides can inhibit
the enzymatic activity of the pertussis vaccine, Dr. Axelrod maintained that if the pertussis toxins
can bind to the gangliosides, then anti-idiotypic antibodies can also bind to the gangliosides and
cause inflammation or damage. Axelrod First Rep. at 3; Axelrod Third Rep. at 2. Thus, Dr. Axelrod
reasoned, vaccines containing the pertussis toxin could, like their wild counterparts, cause the
production of anti-idiotypic antibodies that could interact with the neuronal ganglioside and cause
dysfunction or damage to the neurons.
Dr. Axelrod also attempted to demonstrate how anti-idiotypic antibodies might interact
with nerve gangliosides in a pathologic manner. Tr. at 117. He referenced one item of literature
that he maintained had found that gangliosides are abundantly expressed within the CNS,
constituting roughly 97% of all gangliosides in the human brain. Tr. at 120; K. Vajn et al.,
Differential Distribution of Major Bran Gangliosides in the Adult Mouse Central Nervous System,
8 PLoS ONE 1, 1 (2013), filed as Ex. 86 (ECF No. 57-6) (“Vajn”). Thus, an anti-idiotypic immune
response to the pertussis toxoid could produce a direct inflammatory response when interacting
with these gangliosides, leading to a damaging inflammatory process. Id.; S. Mangmool & H.
Krouse, Gi/o Protein-Dependent and -Independent Actions of Pertussis Toxin (PTX), 3 Toxins 884,
893 (2011), filed as Ex. 87 (ECF No. 57-7) (“Mangmool”) (establishing that the pertussis toxin
modifies cellular response by at least two signaling pathways (the A-promoter and the B-
Oligomer)); I. Gomes et al., Neuropeptide Receptors, 4 Colloquium Series of Neuropeptides 21
(2013), filed as Ex. 88 (ECF No. 57-8) (“Gomes”) (finding the highest level of G-protein-coupled
receptors (GPCRs) located within the central nervous system). Dr. Axelrod again emphasized that
since the components of various toxins—tetanus, diphtheria, or pertussis—were capable of binding
to CNS gangliosides, anti-idiotypic antibodies should have the same capacity. Tr. at 117.
Dr. Axelrod then discussed how immune system-produced antibodies (whether they
activate, complement, or direct cytotoxic cells to a particular area and respond to a specific antigen
or receptor, an inflammatory reaction) could cause either tissue damage or an exacerbation of the
inflammation. Tr. at 117. See also N. K. Jerne, Towards a Network Theory of the Immune System,
125 Annales of Immunology 373, 378 (1974), filed as Ex. 29 (ECF No. 30-4) (“Jerne”) (arguing
that idiotypes play an important role in understanding immunology because they are determined
by the same variable region that determines the antibody binding site); S. Quaglia et al., A
Functional Idiotype/Anti-Idiotype Network is Active in Genetically Gluten-Intolerant Individuals
Negative for Both Celiac Disease-Related Intestinal Damage and Serum Antibodies, 202 J.
Immunology 1079, 1081 (2019), filed as Ex. 107 (ECF No. 69-6) (“Quaglia”) (relying on the
framework set out by Jerne, and finding that the hypervariable region of an anti-idiotype antibody
can recognize the hypervariable region of the idiotype and mimic the original antigen). Because
the vaccines at issue contain antigens comparable to the wild toxins, anti-idiotypic antibodies
12
produced in response could essentially “mimic” their wild counterparts (even though that kind of
mimicry is not consistent with pure molecular mimicry between a foreign antigen and self-
structure).
Dr. MacGinnitie had contended (as discussed below) that anti-idiotype antibodies were
more likely to be protective against autoimmune conditions, but Dr. Axelrod disagreed, offering
additional literature to support his position. See e.g., L. Fernandez et al., Ganglioside Based
Vaccines and Anti-Idiotype Antibodies for Active Immunotherapy against Cancer, 2 Expert Rev.
Vaccines 817, 819–20 (2003), filed as Ex. 94 (ECF No. 58-5) (“Fernandez”) (developing an anti-
idiotype antibody by creating a monoclonal antibody with the anti-idiotype antibody, and showing
that the resulting antibody created an active immune response to damage malignant cells); M. N.
Islam et al., Biological Activity of Anti-Thyrotropin Anti-Idiotypic Antibody, 13 European J. of
Immunology 57, 59–60 (1983), filed as Ex. 75 (ECF No. 43-4) (“Islam”) (showing that anti-
thyrotropin anti-idiotype antibody can produce findings consistent with Graves Disease). 12
Dr. Axelrod further addressed the relevance of the blood-brain barrier 13 to his theory. He
acknowledged that for CNS injury to occur due to some external agent, the blood-brain barrier
would need to be breached. Tr. at 126– 27. Because Mr. Tipps had suffered from an inflammatory
response directed to his CNS, it was likely that the disease process had caused an increase of
cytokines sufficient to make this breach occur. Id. This in turn would lead to the transfer of immune
cells and antibodies into the CNS. See e.g., K. Rochfort et al., Downregulation of Blood-Brain
Barrier Phenotype by Proinflammatory Cytokines involves NADPH Oxidase-Dependent ROS
Generation: Consequences for Interendothelial Adherens and Tight Junctions, 9 PLoS ONE, Jul.
2014, at 6 (2014), filed as Ex. 90 (ECF No. 58-1) (“Rochfort”) (taking human brain microvascular
endothelial cells and exposing them to various concentrations of proinflammatory cytokines, and
finding the blood-brain barrier was resultantly more susceptible to opening); Y. Kashiwagi et al.,
Production of Inflammatory Cytokines in Response to Diphtheria-Pertussis-Tetanus (DPT),
Haemophilus Influenzae Type b (Hib), and 7-Valent Pneumococcal (PCV7) Vaccines, 10 Human
Vaccines & Immunotherapeutics 677, 679-80 (2014), filed as Ex. 91 (ECF No. 58-2)
(“Kashiwagi”) (immunization with DPT resulted in concentration of cytokines in low nanogram
12
“Graves Disease” is defined as “a syndrome of diffuse hyperplasia of the thyroid, with a female predominance; it
usually has an autoimmune etiology and has been linked to autoimmune thyroiditis.” Grave Disease, Dorland’s
Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=70364&searchterm=Graves+disease (last visited Dec. 9,
2022).
13
“Blood-brain Barrier” is defined as “the barrier system separating the blood from the parenchyma of the central
nervous system. Its anatomic component consists of unique endothelial cells in the brain capillaries, having tight
junctions without fenestrations and with few microvilli and few vesicles for fluid transport. Its physiologic component
in part consists of enzymes unique to the brain endothelia and of active transport via carrier proteins.” Blood-brain
Barrier, Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=60232&searchterm=blood-brain+barrier (last visited Dec. 9,
2022).
13
range—thus, releasing more cytokines and causing the opening of blood-brain barrier); Axelrod
Fourth Rep. at 3.
Dr. Axelrod concluded by briefly discussing the timing of Mr. Tipps’s symptoms. He
agreed with Dr. Lovitt that Petitioner’s onset (16 days post-vaccination) was consistent with the
timeframe for the development of autoimmune meningoencephalitis after a causal trigger, based
on how long he proposed it would take for the anti-idiopathic antibodies to generate. See R. Geha,
Presence of Auto-Anti-Idiotypic Antibody during the Normal Human Immune Response to Tetanus
Toxoid Antigen, 129 J. Immunology 139, 139 (1982), filed as Ex. 60 (ECF No. 41-9) (“Geha”)
(finding, based upon two-patient sample, that immunization with tetanus toxoid-containing
vaccine resulted in increase of anti-idiotypic antibodies within a couple of weeks). Dr. Axelrod
also noted that Geha demonstrated that where an individual received a booster immunization with
tetanus toxoid, anti-idiotypic antibodies could begin to increase within a couple of weeks. Geha at
142. And the vaccines received by Mr. Tipps were also boosters, like those evaluated in Geha. (As
later pointed out by Dr. MacGinnitie, however, Geha was published 40 years ago—and has not
since been updated by other literature testing its facially-limited findings). 14
B. Respondent’s Experts
1. Dr. Elaine C. Wirrell, M.D., FRCPC
Dr. Wirrell, a pediatric neurologist, testified on behalf of Respondent, and submitted three
expert reports. See generally Tr. at 164–262; Report, dated Apr. 21, 2020, filed as Ex. C (ECF No.
46-1) (“Wirrell First Rep.”); Report, dated Apr. 21, 2020, filed as Ex. D (ECF No. 46-2) (“Wirrell
Second Rep.”); Report, dated Apr. 21, 2020, filed as Ex. E (ECF No. 46-3 (“Wirrell Third Rep.”).
Dr. Wirrell largely focused her opinion on the potential impact the vaccinations had on Petitioner,
and whether they had any connection with his subsequent neurological symptoms.
Dr. Wirrell obtained her bachelor’s degree from Simon Fraser University in Burnaby,
British Columbia, followed by her medical degree at the University of British Columbia. See
Curriculum Vitae, filed as Ex. G (ECF No. 46-5) (“Wirrell CV”) at 1; Tr. at 164. Thereafter, she
completed a general pediatrics residency and child neurology fellowship at Dalhousie University
in Halifax, Nova Scotia. Wirrell CV at 1; Tr. at 165. She has been the Director of Pediatric Epilepsy
at Mayo Clinic in Rochester, Minnesota since 2007. Tr. at 165; Wirrell First Rep. at 1. She also
serves as the Director of Child and Adolescent Neurology Program Training at Mayo Clinic. Id.
She is board certified in pediatrics and neurology through the Royal College of Physicians and
Surgeons in Canada, which is the equivalent to that of a U.S. certification. Id. In addition, she has
published over 180 peer-reviewed articles and 20 book chapters, largely focused on pediatric
epilepsy and seizure disorders. Wirrell First Rep. at 1.
14
See Report, dated Apr. 16, 2019, filed as Ex. A (ECF No. 37-1) (“MacGinnitie First Rep.”) at 7.
14
Dr. Wirrell began her testimony by stating her medical opinion that the meningococcal and
Tdap vaccinations received by Mr. Tipps in July 2013 were not likely related to his
meningoencephalitis. Tr. at 168. Rather, based on Mr. Tipp’s clinical presentation, his symptoms
were most consistent with viral meningoencephalitis, denying that the criteria for an autoimmune
encephalitis diagnosis had been met. Tr. at 169–70. K. Bloch & C. Glaser, Encephalitis
Surveillance through the Emerging Infections Program, 1997-2010, 21 Emerging Infectious
Diseases 1562 (2015) (“Bloch & Glaser”).
Dr. Wirrell discussed at length the broad number of etiologies for meningoencephalitis.
Wirrell First Rep. at 13. In particular, she relied on several larger studies that looked at patients
who had clearly met the criteria for encephalitis or meningoencephalitis. Tr. at 170; Wirrell First
Rep. at 13. Bloch & Glaser, for example, identified a large number (>5,000) of patients with
encephalitis, observing that in almost half of all cases there was no identified underlying cause for
encephalitis, despite extensive infectious testing. Tr. at 170; Wirrell First Rep. at 13; Bloch &
Glaser at 3. A second study had examined 92 adult patients in Italy, finding that two thirds of cases
for aseptic central nervous system infections had no clear identifiable etiology. Tr. at 171; Wirrell
First Rep. at 13; J. Monticelli et al., Aseptic Central Nervous System Infections in Adults: What
Predictor for Unknown Etiological Diagnosis?, 39 Neurological Sci. 863, 863 (2018).
Other items of literature reached the same conclusion. See, e.g., B. George et al.,
Encephalitis Hospitalization Rates and Inpatient Mortality in the United States, 2000-2010, 9
PLoS ONE 1, 5 (2014), filed as Ex. C-9 (ECF No. 48-9) (“George”) (finding an estimated rate of
7.3 hospitalizations per 100,000 per year with over half of the cases having an unidentified cause
of etiology); K. DuBray et al., Epidemiology, Outcomes and Predictors of Recovery in Childhood
Encephalitis: A Hospital-based Study, 32 Pediatric Infectious Disease J. 839, 843 (2013), filed as
Ex. C-4 (ECF No. 48-4) (concluding that of 190 children admitted to a single California hospital
for encephalitis, roughly half of the children studied did not have an identified cause of etiology).
Moreover, where an etiology has been found, the most common (according to Dr. Wirrell) is
infectious. Wirrell First Rep. at 13.
Dr. Wirrell further disputed that the record supported a diagnosis of autoimmune
encephalitis. The most common form of an autoimmune encephalitis, she maintained, is “NDMA
receptor encephalitis.”15 But even in the absence of antibody testing (then-available in 2013) from
this case that would confirm the presence of the autoantibodies understood to drive that disease,
Mr. Tipps’s clinical presentation was inconsistent with it. Tr. at 178. Children with NMDA
15
“Anti-NDMA Receptor Encephalitis” is defined as “an autoimmune disease where the body creates antibodies
against the NDMA receptors in the brain. These antibodies disrupt normal brain signaling and cause brain swelling or
encephalitis.” Anti-NDMA Receptor Encephalitis, Center for Autoimmune Neurology, Pearlman School of Medicine,
University of Pennsylvania, https://www med.upenn.edu/autoimmuneneurology/nmdar-encephalitis html (last visited
Dec. 9, 2022).
15
receptor encephalitis typically experience pronounced psychosis and hallucinations, later
developing other symptoms such as motor dyskinesias16 and (in many cases) seizures—clinical
features that both sides’ diagnostic experts agreed were mostly absent from the record. Id at 179.
The second most common type of autoimmune encephalitis, “Acute Disseminated
Encephalomyelitis (ADEM),” usually presents with multifocal numbness, visual loss, ataxia, and
tremors. Id. at 180. And MRI readings for ADEM typically show multifocal T2 or flare
hyperintense lesions. Id.
Mr. Tipps’s MRI findings, however, were inconsistent with autoimmune encephalitis. Tr.
at 182. Dr. Wirrell recalled that Mr. Tipps had two MRIs—the first on August 29, 2013, and the
second on September 12, 2013—both of which showed a relatively small T2 hyperintensity. Id.
Such findings were more likely the result of gliosis, scarring, or a slightly larger perivascular space
around one of the blood vessels. Id. Had Mr. Tipps been suffering from an autoimmune form of
encephalitis, Dr. Wirrell opined, the T2 hyperintensities would not only be larger in size but would
also be accompanied by pronounced contrast—which the MRIs did not indicate. Id. Moreover, Dr.
Wirrell noted that she would have expected Mr. Tipps’s first MRI to show more enhancement due
to his elevated cell count (consistent with the presence of significant inflammation), but the fact
that it did not actually reduced the likelihood of an autoimmune encephalitis. Id.
Dr. Wirrell also reiterated the difference between meningitis and encephalitis as articulated
by Dr. Lovitt in his testimony, emphasizing the extent to which the medical record did contain
evidence of symptoms associated with both. Tr. at 174. Encephalitis would generally present with
behavioral changes, seizures or other focal neurological findings, and there was support in the
record for Petitioner experiencing some of these symptoms. Id. Meningitis generally features
headache, occasional neck stiffness or neck, pain, vomiting, and an elevation in CSF white count—
which Mr. Tipps presented with. Id. In addition, Mr. Tipps’s cerebrospinal fluid taps were more
indicative of viral meningoencephalitis rather than bacterial meningoencephalitis, which would
feature a very high white cell count, low glucose level, and high protein level. Id. at 175–76.
Dr. Wirrell then discussed the steroid treatments Mr. Tipps received throughout his various
hospitalizations, explaining why she believed such treatments were further evidence that Mr. Tipps
suffered from viral form of meningoencephalitis. Tr. at 184. The medical records indicated that
Mr. Tipps’s white blood cell count had significantly decreased before his treating physicians
started him on steroids—suggesting that any infectious process at work was beginning to resolve
on its own. Id. By August 19, 2013, Mr. Tipps’s WBC was 163, and by September 9, 2013, his
WBC had decreased to 43—thus, keeping more in line with a viral meningoencephalitis. Id. The
16
“Dyskinesia” is defined as “distortion or impairment of voluntary movement, as in tic, spasm, or myoclonus.”
Dyskinesia, Dorland’s Medical Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=15221
(last visited on Dec. 9, 2022).
16
purpose of the steroidal treatment was likely more to address Petitioner’s significantly increased
intracranial pressure, and the fact that he was beginning to lose his vision. Id.
Relying on several studies, Dr. Wirrell also briefly addressed the relationship between
vaccination and encephalopathy. Tr. at 188–89. One article had evaluated patients who presented
with encephalopathy or encephalitis following the Tdap vaccination. S. Chang et al., U.S.
Postlicensure Safety Surveillance for Adolescent and Adult Tetanus, Diphtheria and Acellular
Pertussis Vaccines: 2005-2007, 31 Vaccine 1447 (2013), filed as Ex. C-3 (ECF No. 48-3)
(“Chang”). Of the 20 million doses given to these patients, there were roughly 2,000 reports of
patients who reportedly presented with encephalopathy or encephalitis. Wirrell First Rep. at 11;
Chang at 1448. However, after a more in-depth review, only three of the reports were suggestive
of encephalopathy or encephalitis, and thus Chang’s findings were not consistent with the
conclusion that vaccination could lead to encephalopathy. Id. at 1450–51.
Another study sought to determine the expected rate of persons developing
encephalopathy, encephalitis, or meningitis post-vaccination as opposed to the observed rate
following receipt of the Tdap vaccine. W. Yih et al., An Assessment of the Safety of Adolescent
and Adult Tetanus-Diphtheria-Acellular Pertussis (Tdap) Vaccine, using Active Surveillance for
Adverse Events in the Vaccine Safety Datalink, 27 Vaccine 4257 (2009), filed as Ex. 70 (ECF No.
42-9) (“Yih”). But Yih determined that the observed rate specific to the Tdap vaccine was in fact
lower than the expected rate. Yih at 4257, 4262; Tr. at 191. See also T. Nakayama & K. Odona,
Vaccine Adverse Events Reported in Post-Marketing Study of the Kitasato Institute from 1994 to
2004, 25 Vaccine 570, 574 (2007), filed as Ex. 71 (ECF No. 42-10) (“Nakayama”) (reporting only
one case of encephalitis/encephalopathy out of 10.56 million doses of DPT); M. Griffin et al., Risk
of Seizures and Encephalopathy after Immunization with the Diphtheria-Tetanus-Pertussis
Vaccine, 263 J. Am. Med. Ass’n., 1641, 1643 (1990), filed as Ex. 73 (ECF No. 43-2) (“Griffin”)
(reporting the hospitalization of two children following receipt of the DPT vaccination (and hence
a different version of the Tdap vaccine), but concluding that neither had permanent sequalae and
were thus not further considered in the study).
In response to Petitioner’s expert’s proposal that molecular mimicry induced by the Tdap
and meningococcal vaccinations caused Mr. Tipp’s encephalitis and neurological symptoms, Dr.
Wirrell emphasized that there was only a single report of autoimmune encephalitis being
temporally related to a vaccine comparable to what Petitioner had received. Wirrell Second Rep.
at 2; C. Hofmann et al., Anti-NMDA Receptor Encephalitis after TdaP-IPV Booster Vaccination:
Cause or Coincidence?, 258 J. Neurol. 500 (2011), filed as Ex. C-14 (ECF No. 48-14)
(“Hofmann”) (finding a 15-year old had developed a fever within 24-hours post-vaccination which
progressed to NMDA-receptor encephalitis—and while this association could not be assumed, it
might be coincidental). And Hoffman did not even involve the form of injury that Dr. Wirrell
opined was most likely at issue.
17
Dr. Lovitt had offered a different study which he maintained reliably established that cases
of encephalitis were still observed following the introduction of the acellular pertussis-containing
vaccine (which replaced whole cell pertussis for safety reasons). H. Kuno-Sakai & M. Kimura,
Safety and Efficacy of Acellular Pertussis Vaccine in Japan, Evaluated by 23 Years of its use for
Routine Immunization, 46 Pediatrics Int’l 650, 654 (2004), filed as Ex. C-16 (ECF No. 48-16)
(“Kuno-Sakai”); Wirrell Second Rep. at 2. Kuno-Sakai reported a rate of approximately 1.3 cases
of encephalitis per 10 million children within seven days of receiving the acellular pertussis
containing vaccine. Id. However, Dr. Wirrell argued that in order to determine whether there is
any epidemiological evidence to support a causal relationship between vaccination and
encephalitis, a comparison must be done between the baseline rate of encephalitis in a population
overall, versus what is seen following vaccination. Tr. at 188; Wirrell Second Rep. at 2; Wirrell
Third Rep. at 4. Two large national studies conducted in the U.S. and the U.K. actually revealed
that the baseline rate of post-vaccination encephalitis reported in the Kuno-Sakai article was
significantly lower than the baseline rates for the general population. Tr. at 187; Wirrell Second
Rep. at 2; J. Granerod et al., New Estimates of Incidence of Encephalitis in England, 19 Emerging
Infectious Diseases 1455 (2013), filed as Ex. C-10 (ECF No. 48-10) (“Granerod”) (finding an
estimated rate of 5.23 cases of encephalitis per 100,000 per year in the U.K.); George at 5 (U.S.
study). Thus, existing epidemiologic evidence suggested less risk of encephalitis among the
vaccinated population—not more.
Dr. Wirrell was not otherwise asked to comment directly on Dr. Axelrod’s theory of
causation, deferring to Dr. MacGinnitie. Tr. at 196. But she did state that in her own clinical
background and experience, she had never come across anything supporting a relationship between
anti-idiotype antibodies and autoimmune encephalopathy. Id.17
2. Dr. Andrew J. MacGinnitie, M.D.
Dr. MacGinnitie, an attending physician and the Clinical Director for the Division of
Immunology at Boston’s Children’s Hospital, testified on behalf of Respondent, and submitted
three expert reports. See generally Tr. at 264–337; Report, dated Apr. 16, 2019, filed as Ex. A
(ECF No. 37-1) (“MacGinnitie First Rep.”); Report, dated, Apr. 21. 2020, filed as Ex. F (ECF No.
17
Dr. Wirrell also responded at some length in her reports to the “Miller” Criteria proposed by Dr. Axelrod as bearing
on whether causation can be demonstrated as a general matter of science. Wirrell Third Rep. at 2; F. Miller et al.,
Approaches for Identifying and Defining Environmentally Associated Rheumatic Disorders, 43 Arthritis &
Rheumatism 243, 244 (2000), filed as Ex. 58 (ECF No. 41-7) (“Miller”). In this regard, she contested Dr. Axelrod’s
opinion as to the Miller Criteria elements one (temporal association), two (lack of alternative explanation), and five
(biologic plausibility). Tr. at 195-96; Wirrell Third Rep. at 2–3. She also observed that Dr. Axelrod did not discuss in
detail several of the elements. Tr. at 194; Miller at 245. I do not, however, include further discussion of this aspect of
the competing expert opinions, for the simple reason that causation is determined by a legally-derived test, rather than
by factors deemed persuasive in science (even though ultimate medical or scientific reliability is very important in
assessing causation).
18
46-4) (“MacGinnitie Second Rep.”); Report, dated May 14, 2021, filed as Ex. H (ECF No. 65-1)
(“MacGinnitie Third Rep.”). Dr. MacGinnitie argued that the cause of Mr. Tipps’s
meningoencephalitis was unrelated to the Tdap and Meningococcal vaccines he had received. Tr.
at 268.
Dr. MacGinnitie received his bachelor’s degree from Yale University and then attended
the University of Chicago, Pritzker School of Medicine, where he received both an M.D. and a
Ph.D. from the Department of Pathology. See Curriculum Vitae, filed as Ex. B (ECF No. 37-2)
(“MacGinnitie CV”); Tr. at 264. He completed a residency in pediatrics in the Boston Combined
Residency Program, a joint venture of Boston Children’s Hospital and Boston Medical Center,
followed by an Allergy/Immunology fellowship at Boston Children’s Hospital. MacGinnitie CV
at 1; Tr. at 264; MacGinnitie First Rep. at 1. He is board certified in both Pediatrics and Allergy
and Clinical Immunology. Tr. at 266; MacGinnitie First Rep. at 1. Dr. MacGinnitie has also
published several articles in areas related to Allergy/Immunology, such as food allergy and vaccine
reactions. MacGinnitie First Rep. at 1.
Dr. MacGinnitie began by discussing anti-idiotype antibodies generally. MacGinnitie First
Rep. at 3. He maintained that while “theoretically appealing [,] there is little data regarding the
actual importance of anti-idiotype antibodies in human disease.” Tr. at 268–69; MacGinnitie First
Rep. at 4. Thus, he questioned whether it was credible to argue in the first place that this kind of
antibody could even be pathogenic—let alone be produced in reaction to the vaccines in question.
Tr. at 269.
Dr. MacGinnitie next scrutinized the steps implicit in Dr. Axelrod’s theory, noting how at
each stage there were evidentiary deficiencies. Tr. at 269–70; MacGinnitie Second Rep. at 2. Dr.
MacGinnitie first disputed the contention that tetanus, pertussis, and diphtheria toxins could bind
to neuronal tissues. Id. He contended that Dr. Axelrod had provided little to no evidence that the
binding causes pathology, but instead only offered evidentiary support for the idea that more
generally vaccine components can bind to neuronal tissues or gangliosides. Id. And the distinction
between the toxoids included in vaccines and their predicate toxins was highly relevant to why Dr.
MacGinnitie took issue with this aspect of Dr. Axelrod’s theory. As Dr. MacGinnitie explained,
“in the case of diphtheria, pertussis, and tetanus, they all express toxins that can lead to different
illnesses [a]nd because the toxins cause illness it [is] not advisable to vaccinate with the toxins
themselves.” Tr. at 270 (emphasis added). By contrast, a toxoid based on a toxin is either denatured
or undergoes an altered protein sequence before being included in a vaccine, greatly reducing (if
not eliminating) the risk of a pathologic reaction in any way comparable to a toxin. Id.
Moreover, Dr. MacGinnitie criticized several of the articles relied upon by Dr. Axelrod to
show the pathogenic capability of the toxins/toxoids, arguing that the data generated or relied upon
by these articles was not only outdated but irrelevant to the circumstances in this case. Tr. at 271–
19
73. Hara-Yokoyama, for example, at best established that the pertussis toxin has the capability of
interacting with neuronal tissues which can then lead to dysfunction and damage to the effected
neurons. MacGinnitie Second Rep. at 2; Yokoyama at 8118. But that study was not only based on
data that is nearly 30 years old, but its ultimate finding was more limited: that pertussis toxin can
cause inhibition of neuronal tissues and gangliosides, not that the toxin itself directly binds or
damages the neuronal tissues. Tr. at 271; MacGinnitie Second Rep. at 2. And Hara-Yokoyama
otherwise shed no light on the impact the pertussis toxoid would have on a human, and/or in an in
vivo context. Tr. at 271. He made a comparable point in reaction to other items of literature offered
by Dr. Axelrod. See also Tr. at 272; MacGinnitie First Rep. at 5; MacGinnitie Second Rep. at 2.
Vajn talks about distribution of brain gangliosides in the mouse brain, but does not deal with
binding to toxins in vaccines. Tr. at 272. Gomes explores how different neuropeptide receptors are
expressed throughout brain, but says nothing about toxins. Id. at 272–73. And Mangmool only
focused on how the pertussis toxin can act on G-proteins, without expanding to the anticipated
effect of the more-relevant toxoids included in the vaccines Petitioner received. Id. at 273.
Dr. MacGinnitie then discussed the third component of Dr. Axelrod’s theory—that the
immune system could (in reaction to vaccination) generate destructive anti-idiotypic antibodies,
maintaining that evidence relied upon for the point was not only speculative but outdated. Tr. at
270; MacGinnitie Second Rep. at 2–3. Jerne, for example, was largely theoretical in nature, with
its authors only speculating as to the importance of anti-idiotype antibodies, but providing no
actual data establishing any relevance to human disease. Tr. at 274; MacGinnitie Second Rep. at
3; Jerne at 378. Moreover, the contemporaneous evidence that does exist regarding anti-idiotype
antibodies and autoimmune diseases suggests that the antibodies are more protective than they are
causative. Tr. at 275; MacGinnitie First Rep. at 7; MacGinnitie Second Rep. at 5. Jerne was
otherwise 44 years old, and its suggestions had not been subsequently updated to show that “anti-
idiotype antibodies are involved in human disease or CNS inflammation.” MacGinnitie First Rep.
at 6.
Next, Dr. MacGinnitie discussed the articles cited by Dr. Axelrod to demonstrate a
pathogenic effect of anti-idiotypic antibodies in causing encephalomyelitis. Tr. at 276–81;
MacGinnitie Second Rep. at 4. Islam, for example, was an animal model in which rabbits were
immunized with anti-TSH antibodies, an artificial solution, finding that the resulting antibodies
could trigger symptoms similar to Graves disease. Tr. at 277; MacGinnitie Second Rep. at 4; Islam
at 57. But other than being an immune system disorder, there was nothing about Graves disease
making it comparable to encephalitis of the kind Petitioner was believed to have experienced.
Similarly, another article that featured an animal model with one human patient aimed to
demonstrate the relationship between anti-idiotype antibodies and autoimmune diseases such as
myasthenia gravis and Graves disease. Tr. at 278; B. F. Erlanger et al., Auto-Anti-Idiotype: A Basis
for Autoimmunity and a Strategy for Anti-Receptor Antibodies, 94 Immunological Reviews 23, 35
(1986), filed as Ex. 93 (ECF No. 58-4) (“Erlanger”). But Dr. MacGinnitie maintained that Erlanger
20
involved an artificial solution (purifying the antibody against a particular compound found in
myasthenia gravis) and thus showed no relation to the vaccines at issues. Tr. at 278. And
Fernandez focused on antibodies against cancer cells, as opposed to antibodies causing brain
injury. Dr. MacGinnitie also emphasized the stale nature of the data reviewed, maintaining that if
there were likely anti-idiopathic antibodies involved in myasthenia gravis or Graves disease, more
data would have come out by now. Tr. at 278–79.
Another deficiency Dr. MacGinnitie identified in Petitioner’s theory was its failure to
establish how the putatively-harmful anti-idiotypic antibodies would likely cross the blood-brain
barrier (which they would need to do to cause harm). Tr. at 287; MacGinnitie Second Rep. at 3.
Antibodies are generally excluded from the CNS as a result of the protective effect of the blood-
brain barrier; indeed, Dr. MacGinnitie noted, this is why it is difficult to employ antibody therapies
for treating various CNS diseases. Id; I. Amanna & M. Slifka, Contributions of Humoral and
Cellular Immunity to Vaccine-Induced Protection in Humans, 411 Virology 206, 212 (2011), filed
as Ex. F-6 (ECF No. 47-6). Thus, it was unlikely anti-idiotype antibodies produced by the
pertussis, diphtheria, and tetanus toxins could “get through” to cause damage to the CNS. Tr. at
287; MacGinnitie Second Rep. at 3. Moreover, in the case of Mr. Tipps, Dr. MacGinnitie observed
no evidence in his clinical presentation to suggest a breach in the blood-brain barrier had occurred.
Id.
Dr. MacGinnitie allowed, however, that there are limited exceptions where the blood-brain
barrier is breached by antibodies, and in so doing he addressed whether cytokines produced in
response to vaccines could contribute to such circumstances. Tr. at 287. He agreed that
vaccinations do generate cytokines, but argued that there was no evidence in Mr. Tipps’s clinical
presentation to suggest that he had experienced any significant elevation of cytokines. Tr. at 288;
Kashiwagi at 679, 683 (arguing that “all effective vaccines induce the production of cytokines or
chemokines, which modulate immunogenicity and are also involved in inducing adverse events,
such as systemic febrile illness and immunotoxicity”). Thus, Mr. Tipps exhibited no symptoms
(such as fever, local soreness, etc.) preceding the onset of his injury that would reflect excessive
cytokine upregulation. Another of Petitioner’s items of literature, Rochfort, was offered to show
that cytokines at nanogram levels having the ability to “disrupt the expression of certain adhesion
molecules on human brain endothelial cells,” in turn resulting in the opening of the blood-brain
barrier. MacGinnitie Third Rep. at 3; Rochfort at 2. But Dr. MacGinnitie disputed whether
Rochfort’s in vitro results were meaningful when applied to an in vivo context. Tr. at 291;
MacGinnitie Third Rep. at 4.
Dr. MacGinnitie then discussed several articles he relied on to demonstrate that the Tdap
vaccine is not linked with CNS inflammation. Tr. at 292–93. MacGinnitie First Rep. at 6. He
referred to a 1991 report cited by Dr. Lovitt in favor of causality, but noted that the report examined
the whole-cell pertussis vaccine, which Mr. Tipps did not receive. Tr. at 292; MacGinnitie First
Rep. at 6; L. Cowan et al., Acute Encephalopathy and Chronic Neurological Damage after
21
Pertussis Vaccine, 11 Vaccine 1371, 1374 (1993), filed as Ex. 16 (ECF No. 25-1) (finding that
DPT immunization was associated with an increased risk of seizures and encephalopathy within
seven days following receipt of the vaccine). More recent studies suggested no causal relationship
had ever existed with respect to the whole cell pertussis vaccine version, or the current acellular
version. MacGinnitie First Rep. at 6; P. Ray et al., Encephalopathy after Whole-Cell Pertussis or
Measles Vaccination: Lack of Evidence for a Causal Association in a Retrospective Case-Control
Study, 25 The Pediatric Infectious Disease J. 768, 773 (2006), filed as Ex. A-9 (ECF No. 38-9)
(relying on an evaluation of two million vaccinated children, no increased risk of encephalopathy
after the DTP and MMR vaccinations found); W. Huang et al., Lack of Association Between
Acellular Pertussis Vaccine and Seizures in Early Children, 126 J. of the Am. Acad. of Pediatrics
263, 266 (2010), filed as Ex. A-10 (ECF No. 38-10) (observing no increased risk in seizures after
receipt of the Tdap vaccine); L. Rorke-Adams et al., Neuropathology of Vaccination in Infants and
Children, 29 Vaccine 8754, 8758 (2011), filed as Ex. A-11 (ECF No. 38-11) (finding the
pathogenesis of the majority of the 37 infants/children studied was apparent, and thus not a
complication of the vaccination).
Dr. MacGinnitie concluded with a brief response to Dr. Axelrod’s contention that the
vaccines Petitioner received could cause production of cross-reacting anti-idiopathic antibodies
due to molecular mimicry between the vaccine antigens and self, denying that the theory was
persuasive. Tr. at 294-295. Dr. MacGinnitie argued that in order to have an autoimmune disease,
a target of autoimmunity is needed, which had not been established at all in this case by Petitioner’s
experts. Id. at 295. Moreover, Dr. MacGinnitie emphasized, there was overall a lack of evidence
presented by Petitioner’s experts to support the notion of cross-reactivity or that autoimmunity is
triggered by a vaccine component. Id. He also (parallel with Dr. Wirrell) observed a lack of
evidence that Mr. Tipps had experienced an autoimmune process. He was in fact never tested for
any of the antibodies thought to be associated with autoimmune meningoencephalitis—because
his providers did not feel it was necessary based on his clinical presentation. Id.
III. Procedural History
As noted above, this claim was initiated in early 2017, approximately five years ago, and
assigned to a different special master. Petitioner filed medical records thereafter with the statement
of completion filed in May 2017. (ECF No. 17). Respondent’s Rule 4(c) Report was filed on July
19, 2017. (ECF No. 19). Expert reports were next filed over the course of the ensuing four years.
The case was eventually reassigned to me in July 2020, and I held a status conference with the
parties, proposing a schedule for a two-day Entitlement Hearing to be held. The trial was originally
scheduled in June 2021, but was subsequently canceled and then rescheduled for the spring of
2022. The claim is now ripe for resolution.
22
IV. Applicable Legal Standards
A. Petitioners’ 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).18
In this case, Petitioner does 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;
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.”
18
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
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.
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. 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 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
24
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.
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
25
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) (determining that 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).
As noted by the Federal Circuit, “[m]edical records, in general, warrant consideration as
trustworthy evidence.” 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, Rickett v. Sec'y of Health & Hum.
Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). A series of linked
propositions explains why such records deserve some weight: (i) sick people visit medical
professionals; (ii) sick people attempt to 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 v. Sec'y of Health & Hum. Servs., No. 03–1585V, 2005 WL
6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical records
are often found to be deserving of greater evidentiary weight than oral testimony—especially
where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528; see also
Murphy v. Sec'y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff'd per curiam, 968 F.2d
1226 (Fed. Cir. 1992), cert. den'd, Murphy v. Sullivan, 506 U.S. 974 (1992) (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.”)).
However, the Federal Circuit has also noted that there is no formal “presumption” that
records are accurate or superior on their face to other forms of evidence. Kirby v. Sec’y of Health
& Hum. Servs., 997 F.3d 1378, 1383 (Fed. Cir. 2021). There are certainly situations in which
compelling oral or written testimony (provided in the form of an affidavit or declaration) 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
26
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. La Londe 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 Pharm., 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).
Under Daubert, the factors for analyzing the reliability of testimony are:
(1) whether a 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).
27
In the Vaccine Program the Daubert factors play a slightly different role than they do when
applied in other federal judicial settings, like the district courts. Typically, Daubert factors are
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable or could confuse a jury. By contrast, in Vaccine Program cases 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 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 v. Sec'y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (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. 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
review den'd, 108 Fed. Cl. 743 (2013), aff'd, 540 F. App’x. 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”).
D. Consideration of Medical Literature
Both parties filed numerous items of medical and scientific literature in this case, but not
all such items factor 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., No. 2015–5072,
2016 WL 1358616, at *5 (Fed. Cir. Apr. 6, 2016) (“[w]e generally presume that a special master
considered the relevant record evidence even though he does not explicitly reference such evidence
28
in his decision”) (citation omitted); see also Paterek v. Sec’y of Health & Hum. Servs., 527 F.
App’x 875, 884 (Fed. Cir. 2013) (“[f]inding certain information not relevant does not lead to—
and likely undermines—the conclusion that it was not considered”).
ANALYSIS
The parties seem to agree that meningoencephalitis is the proper diagnosis, although they
disputed whether Petitioner’s illness had a viral or autoimmune etiology. The record does not
permit me to conclude a virus was likely causal. Although Dr. Wirrell made several convincing
points about why she favored such an etiology (including the important fact that this illness more
often than not has a viral cause), test results never affirmatively identified any virus, and Petitioner
and his father persuasively testified that there was no evidence Mr. Tipps was ill around the time
of his onset (although this does not rule out a viral cause that simply was not identified—consistent
with an idiopathic etiology). At the same time, however, Respondent far more compellingly
established the low likelihood that Petitioner’s meningoencephalitis was autoimmune in
character—given the absence of confirming test results from the record—MRI imaging, an
inconsistent clinical presentation, and a lack of confirmation Petitioner possessed any known
autoantibodies associated with autoimmune forms of the disease, including the allegedly-causal
anti-idiotypic antibodies.
But the case turns on a more fundamental point: Petitioner’s experts did not preponderantly
establish that “more likely than not” meningoencephalitis could be caused by the Tdap or
meningococcal vaccines (with Dr. Axelrod’s focus far more on the former vaccine than the
latter). 19
Petitioner’s causation theory foundered in three primary respects. First, it relied on the
mostly-novel theoretical conception (albeit one Dr. Axelrod has unsuccessfully advanced in at
least one other recent case) 20 that anti-idiotypic antibodies could be pathologic drivers of
19
Because a vaccine injury claim must satisfy all three Althen prongs (meaning that an inability to satisfy one prong
is fatal to the entire claim), I do not discuss Petitioner’s success in establishing the third “timeframe” prong. At most,
I will observe that cases relying on vaccine-induced antibody production as driving an autoimmune process often
succeed where, as here, the span between vaccination and onset is within three weeks. But that does not assist
Petitioner if (as I am finding) the evidence does not also preponderate in favor of a conclusion that the vaccine can
result in production of antibodies leading to disease in the first place.
20
Dr. Axelrod proposed a comparable theory involving the purportedly-pathologic impact of anti-idiotypic antibodies
in an admittedly slightly-different context—a significant aggravation claim alleging that the varicella vaccine
worsened a petitioner’s preexisting peripheral neuropathy. But the theory was rejected. See generally Pavan v. Sec’y
of Health & Hum. Servs., No. 14-60V, 2020 WL 5351332 (Fed. Cl. Spec. Mstr. July 28, 2020) (denying
compensation). The special master’s determination therein was based on an extensive evaluation of the theory and its
bases, including articles like Jerne. Pavan, 2020 WL 5351332, at *12. The Pavan special master ultimately found that
the theory “does not adequately explain how the id/anti-idiotype mechanism generates an immune response” that
could have produced the complained-of autoimmune disease. Id. at *18. In addition, Pavan noted that Dr. MacGinnitie
(Respondent’s expert in that case) persuasively established that the anti-idiotype antibodies were more likely
29
autoimmune disease. But this theory (which, despite the fact it has not been advanced in the
Program often, ironically appears to arise from fairly stale items of literature, like Jerne or Geha)
seems mostly to have been proposed out of a desire to provide some link between vaccine
components and an autoimmune process. It otherwise lacks needed substantiation on several
fronts.
Thus, Dr. Axelrod’s theory assumes (incorrectly) that wild infectious toxins would function
the same as toxoids included in the Tdap vaccine (expressly because they are less likely to cause
harm, while still having a beneficial immunologic effect), and that the toxins themselves had a
pathologic capacity specific to the injury at issue. It provides little reliable support for the
conclusion that the vaccines would cause the production of any of the proposed antibodies deemed
pathologic. And it seems to presume that invocation of the concept of molecular mimicry (certainly
a scientifically-reliable theory that in other cases provides a sound causation explanation) is
enough to prevail. See Johnson v. Sec'y of Health & Hum. Servs., No. 14-254V, 2018 WL 2051760,
at *26 (Fed. Cl. Mar. 23, 2018) (stating that “when attempting to establish a causal mechanism,
“[p]etitioners cannot simply invoke the concept of molecular mimicry and call it a day”). How the
Tdap vaccine antigens would mimic CNS ganglioside structures sufficient to cause the production
of the anti-idiotypic antibodies remains no more than plausibly established—and in a loosely
sketched manner at that.
Second, the causal theory is also deficient on the “back end” of any putative autoimmune
process, because insufficient reliable evidence was offered to establish that a pathologic
autoimmune process resulting in meningoencephalitis would likely occur even if the Tdap vaccine
could cause the production of anti-idiotypic antibodies. As a threshold matter, Dr. MacGinnitie
made a number of persuasive points about the great difficulty any antibodies would have in
breaching the blood-brain barrier that were not persuasively addressed by Dr. Axelrod. But
assuming away this hurdle, Petitioner’s experts did not reliably establish how the proposed anti-
idiotypic antibodies would instigate the kind of harm needed to result in meningoencephalitis.
Thus, the target of the proposed autoimmune attack is unidentified (or merely assumed to be the
same as the toxin’s purported attack—even though the toxin is not comparable for present purposes
to the toxoid actually in the vaccine, nor was it shown likely to bind as proposed). The theory also
assumes a cross-reaction driven by a kind of antibody that Dr. MacGinnitie persuasively
established is more likely protective. And other than some case reports relying on temporal
associations—reports that should be weighed against much larger studies (cited by Dr. Wirrell)
based on greater amounts of passive surveillance reporting and which show no likely
relationship—little reliable evidence has been offered to associate the Tdap vaccine with
regulatory (and in a beneficial sense) of the immune response, and that much of the scientific authority offered in
support of the theory was quite old. Id. at *19-20.
30
meningoencephalitis. Compare Hoffman with George and Granerod; see also Chang, Yih,
Nakayama, and Griffin.21
Finally, the overall theory offered by Dr. Axelrod is facially strained. At bottom,
Petitioner’s theory posits that because vaccines implicate an immune response, they can plausibly
cause autoimmune disease—and then the theory looks for ways to reverse engineer support for
that concept. But it is not even evident that all forms of encephalitis are autoimmune in character.
Certainly, the kinds of autoimmune encephalitis discussed by Dr. Wirrell, like ADEM or Anti-
NMDA encephalitis, are not what Petitioner experienced. To argue that his meningoencephalitis
must be autoimmune simply because it post-dated vaccination is to engage in the kind of post hoc
ergo propter hac reasoning long rejected in the Vaccine Program. See Pafford v. Sec'y of Health
& Hum. Servs., No. 01-0165V, 2004 WL 1717359, at *9 (Fed. Cl. Spec. Mstr. July 16, 2004), mot.
for rev. denied, 64 Fed. Cl. 19 (2005), aff'd, 451 F. 3d 1352 (Fed. Cir. 2006).
My determination is also somewhat based on the reliability and persuasiveness of the
expert opinions, as reflected in the written reports both sides filed and testimony offered herein.
Respondent’s experts were overall not only clearer in their explanations for the deficiencies they
identified in Petitioner’s theory, but did a better job in explaining those deficiencies through their
live testimony, with far more precision and clarity. Petitioner’s experts certainly possessed the
foundational expertise needed to offer the opinions they did, but they could not breathe life into
them simply through their embrace of the opinions proposed. This was especially so with respect
to the opinions and testimony of the two immunologists in this case. Dr. MacGinnitie persuasively
and thoroughly rebutted Dr. Axelrod’s opinion.
21
Petitioner cannot persuasively shield his theory from such criticism by invoking the rarity of vaccine injuries, or the
relative paucity of evidence pertaining to the mysteries of the immune system, to excuse the limited evidence offered
herein in support of his theory. As the Court has recognized, “the standard of proof does not operate as a sliding scale
that varies depending upon the quantity and quality of the scientific evidence that is available.” Caves v. Sec'y of
Health & Hum. Servs., 100 Fed. Cl. 119, 143 (2011), aff’d, 463 F. App'x 932 (Fed. Cir. 2012).
31
CONCLUSION
A Program entitlement award is only appropriate for claims supported by preponderant
evidence. Here, Petitioner has not made such as showing, and is therefore not entitled to
compensation. I make this determination despite my strong sympathy for Mr. Tipps’s experience
in dealing with his illness.
In the absence of a motion for review filed pursuant to RCFC Appendix B, the Clerk of the
Court SHALL ENTER JUDGMENT in accordance with the terms of this Decision.22
IT IS SO ORDERED.
/s/ Brian H. Corcoran
Brian H. Corcoran
Chief Special Master
22
Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment if (jointly or separately) they file notices
renouncing their right to seek review.
32