Court Opinion

ID: 4924193
Source: CourtListenerOpinion
Date Created: 2021-09-22 13:02:28.467331+00
Date Added: 2024-06-11T08:14:12.959842
License: Public Domain

In the United States Court of Federal Claims
                                  OFFICE OF SPECIAL MASTERS
                                           No. 16-0265V
                                      Filed: August 23, 2021
                                           PUBLISHED

                                                                    Special Master Horner
    ALICIA LEANN BOHN, on behalf of her
    deceased minor child, G.B.,
                                                                    Sudden Infant Death Syndrome
                         Petitioner,                                (SIDS); Dismissal; Insufficient
    v.                                                              Proof
    SECRETARY OF HEALTH AND
    HUMAN SERVICES,

                        Respondent.

Patricia Ann Finn, Patricia Finn, P.C., Nanuet, NY, for petitioner.
Laurie Wiesner, U.S. Department of Justice, Washington, DC, for respondent.

                                                DECISION 1

       On February 25, 2016, petitioner, Alicia Bohn, filed a petition under the National
Childhood Vaccine Injury Act, 42 U.S.C. § 300aa-10-34 (2012)2 on behalf of her minor
child, G.B., alleging that several routine childhood vaccinations, including Haemophilus
influenzae type B (Hib), pneumococcal conjugate (Prevnar), rotavirus (Rotateq 3), and
Pediarix, 3 administered on March 12, 2014, “caused-in-fact” his death on March 13,
2014. (ECF No. 1.) On June 29, 2020, petitioner filed a motion for a ruling on the written
record. (ECF No. 51.) For the reasons set forth below I find that petitioner is not entitled
to compensation.

1 Because this decision contains a reasoned explanation for the special master’s action in this case, it will
be posted on the United States Court of Federal Claims’ website in accordance with the E-Government
Act of 2002. See 44 U.S.C. § 3501 note (2012) (Federal Management and Promotion of Electronic
Government Services). This means the decision will be available to anyone with access to the
Internet. In accordance with Vaccine Rule 18(b), petitioner has 14 days to identify and move to redact
medical or other information the disclosure of which would constitute an unwarranted invasion of privacy.
If the special master, upon review, agrees that the identified material fits within this definition, it will be
redacted from public access.

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

§ 300aa-10-34.
3
  Pediarix is a combined vaccine including diphtheria, tetanus, acellular pertussis, hepatis B, and
inactivated poliovirus. See https://www.fda.gov/vaccines-blood-biologics/vaccines/pediarix (last visited
August 19, 2021).
   I.     Applicable Statutory Scheme

       Under the National Vaccine Injury Compensation Program, compensation
awards are made to individuals who have suffered injuries after receiving vaccines. In
general, to gain an award, a petitioner must make a number of factual demonstrations,
including showing that an individual received a vaccination covered by the statute;
received it in the United States; suffered a serious, long-standing injury; and has
received no previous award or settlement on account of the injury. Finally – and the key
question in most cases under the Program – the petitioner must also establish a causal
link between the vaccination and the injury. In some cases, the petitioner may simply
demonstrate the occurrence of what has been called a “Table Injury.” That is, it may be
shown that the vaccine recipient suffered an injury of the type enumerated in the
“Vaccine Injury Table,” corresponding to the vaccination in question, within an
applicable time period following the vaccination also specified in the Table. If so, the
Table Injury is presumed to have been caused by the vaccination, and the petitioner is
automatically entitled to compensation, unless it is affirmatively shown that the injury
was caused by some factor other than the vaccination. § 300aa-13(a)(1)(A); § 300 aa-
11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B).

        In many cases, however, the vaccine recipient may have suffered an injury not of
the type covered in the Vaccine Injury Table. In such instances, an alternative means
exists to demonstrate entitlement to a Program award. That is, the petitioner may gain
an award by showing that the recipient’s injury was “caused-in-fact” by the vaccination
in question. § 300aa-13(a)(1)(B); § 300aa-11(c)(1)(C)(ii). In such a situation, of course,
the presumptions available under the Vaccine Injury Table are inoperative. The burden
is on the petitioner to introduce evidence demonstrating that the vaccination actually
caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d
1274, 1278 (Fed. Cir. 2005); Hines v. Sec’ of Health & Human Servs., 940 F.2d 1518,
1525 (Fed. Cir. 1991).

        The showing of “causation-in-fact” must satisfy the “preponderance of the
evidence” standard, the same standard ordinarily used in tort litigation. § 300aa-
13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 940 F.2d at 1525. Under that
standard, the petitioner must show that it is “more probable than not” that the
vaccination was the cause of the injury. Althen, 418 F.3d at 1279. The petitioner need
not show that the vaccination was the sole cause of the injury or condition, but must
demonstrate that the vaccination was at least a “substantial factor” in causing the
condition, and was a “but for” cause. Shyface v. Sec’y of Health & Human Servs., 165
F.3d 1344, 1352 (Fed. Cir. 1999). Thus, the petitioner must supply “proof of a logical
sequence of cause and effect showing that the vaccination was the reason for the
injury.” Id. at 1353. The logical sequence must be supported by “reputable medical or
scientific explanation, i.e., evidence in the form of scientific studies or expert medical
testimony.” Althen, 418 F.3d at 1278; Grant v. Sec’y of Health & Human Servs., 956
F.2d 1144, 1148 (Fed. Cir. 1992). A petitioner may not receive a Vaccine Program
award based solely on his or her assertions; rather, the petition must be supported by
either medical records or by the opinion of a competent physician. §300aa-13(a)(1).

                                             2
       In what has become the predominant framing of this burden of proof, the Althen
court described the “causation-in-fact” standard, as follows:

          Concisely stated, Althen’s burden is to show by preponderant evidence that
          the vaccination brought about her injury by providing: (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. If Althen satisfies this burden, she is “entitled to
          recover unless the [government] shows, also by a preponderance of the
          evidence, that the injury was in fact caused by factors unrelated to the
          vaccine.”

Althen, 418 F.3d at 1278 (citations omitted). The Althen court noted that a petitioner
need not necessarily supply evidence from medical literature supporting petitioner’s
causation contention, so long as the petitioner supplies the medical opinion of an
expert. Id. at 1279-80. That expert’s opinion must be “sound and reliable.” Boatmon v.
Sec’y of Health & Human Servs., 941 F.3d 1351, 1359-60 (Fed. Cir. 2019). The Althen
court also indicated, however, that a Program fact finder may rely upon “circumstantial
evidence,” which the court found to be consistent with the “system created by Congress,
in which close calls regarding causation are resolved in favor of injured claimants.”
Althen, 418 F.3d at 1280.

       In her petition, petitioner did not allege a specific fatal injury to G.B. that was
caused in fact by his March 12, 2014 vaccinations. 4 (ECF No. 1.) However, in her
motion for a ruling on the record, petitioner contends that the release of cytokines
caused “endothelial damage resulting in hemorrhaging and congestion in multiple
organs,” which caused G.B.’s death. (ECF No. 51, p. 1, 20-21.) Because these injuries
are not listed on the Vaccine Injury Table, petitioner must satisfy the above-described
Althen test for establishing causation-in-fact.

    II.      Procedural History

         Petitioner filed her petition on February 25, 2016. (ECF No. 1.) The case was
initially assigned to Special Master Laura Millman, who has since retired. (ECF No. 4.)
Petitioner subsequently filed medical records on March 10 and April 11, 2016. (ECF
Nos. 5, 8.) At the initial status conference, petitioner advised that she intended to
provide an expert report from a pediatric pathologist. (ECF No. 9.)

      On September 26, 2016, petitioner filed an expert report from Dr. Laurel Waters.
(ECF No. 12; Ex. 12.) During a second status conference, petitioner was advised that

4
 The autopsy report reflects an official cause of G.B.’s death as “probable asphyxia due to co-sleeping.”
(Ex. 4 at 1.)

                                                    3
Dr. Waters’s report did not fulfill petitioner’s burden of preponderant evidence. 5 (ECF
No. 13.) Respondent’s counsel reported that her client had retained a pediatric
immunologist to provide an opinion. (Id.) Respondent was ordered to file this expert
report, along with a Rule 4(c) report. (Id.)

       Thereafter, respondent filed his Rule 4(c) report, arguing that the evidence
presented did not meet petitioner’s burden and recommending against compensation.
(ECF No. 17.) Concurrently, respondent also filed expert reports from Dr. Christine
McCusker (immunology) and Dr. Sara Vargas (pathology). (ECF No. 17; Exs. A, C.)
Petitioner was then permitted to file a supplemental report from Dr. Waters and another
expert report from Dr. Douglas Miller. (ECF No. 22; Exs. 22, 23.) Respondent
subsequently filed a supplemental report from Dr. McCusker. (ECF No. 26; Ex. NN.)
Petitioner then filed a supplemental report from Dr. Miller. (ECF No. 28; Ex. 24.) Finally,
on November 28, 2017, respondent filed a supplemental report from Dr. Vargas. (ECF
No. 29; Ex. OO.)

       During a telephonic status conference on January 10, 2018, petitioner was
ordered to submit a demand to respondent. (ECF No. 30.) However, in a status report
dated June 11, 2018, respondent advised that, “given his strong views on the causation
issue in this matter, he does not wish to negotiate a settlement.” (ECF No. 37.) On that
same date, Special Master Millman issued an order indicating that “when this case is
transferred to another special master upon [her] retirement, the new special master will
schedule a hearing date.” (ECF No. 38.)

       After this case was reassigned to my docket on June 6, 2019 (ECF No. 42), I
ordered the parties to confer and file a joint status report confirming that the case
remained ripe for a hearing given the recent Federal Circuit ruling in Boatman v.
Secretary of Health & Human Services, 941 F.3d 1351 (Fed. Cir. 2019). (ECF No. 44.)
The parties thereafter filed a status report indicating that “they are amenable to either a
ruling on the existing record, or proceeding to a hearing in this matter, at [my]
discretion.” (ECF No. 45.) After reviewing the case, I determined that a ruling on the
written record was appropriate and ordered the parties to propose a briefing schedule. 6
(ECF No. 46.)

        Petitioner filed a motion for a ruling on the record on June 29, 2020. (ECF No.
51.) Respondent filed his response to petitioner’s motion on November 9, 2020 and
petitioner filed her reply to respondent’s response to petitioner’s motion on January 12,
2021. (ECF Nos. 56, 59.) This case is now ripe for a ruling on the record.

5
  Dr. Waters’s report will be discussed in detail below. The statement discussed during the status
conference was her conclusion that the “three different arms of the immune response which are active in
the first 24 hours [after vaccination] cause cytokine production, which could become excessive and cause
a lethal cytokine storm.” (Ex. 12 at 10 (emphasis added).)
6That is, I have concluded that the record is sufficiently developed and the parties have had a full and fair
opportunity to present their respective cases. Kreizenbeck v. Sec’y of Health & Human Servs., 945 F.3d
1362, 1366 (Fed. Cir. 2020); see also Vaccine Rule 8(d); Vaccine Rule 3(b)(2).

                                                      4
      III.     Factual History

               a. Medical Records and Petitioner’s Affidavit

       G.B. was born via c-section at 39 weeks on January 14, 2014. (Ex. 1, p. 5-6.)
There were no complications. (Id.) G.B. received his first hepatitis B vaccination on the
date of his birth. (Id. at 8.) Petitioner had a mostly unremarkable pregnancy but had
risks due to smoking, having undergone prior cesarean delivery, and having less than
one year between pregnancies. (See generally, Ex. 7.)

        On January 16, 2014, G.B. had his first newborn visit with Dr. Edward Legako.
(Ex. 2, p. 1.) At both this appointment and at another appointment on January 20, 2014,
G.B. was noted to be feeding well and gaining weight appropriately. (Id. at 3.) On
January 29, 2014, G.B. returned to Dr. Legako for diarrhea over the preceding week,
but physical examination was unremarkable. (Id. at 5.) Petitioner was reassured that
G.B.’s stool was normal for a breastfeeding infant and was advised that G.B. continued
to gain weight appropriately. (Id.) On March 12, 2014, G.B. had his two-month well
child visit with Dr. Legako, and he received routine childhood vaccinations (DTaP,
hepatitis B, IPV, HIB, pneumococcal 13, and rotavirus). (Id. at 7, 9.) During this visit,
Dr. Legako assessed G.B. with normal growth, nutrition, development, and behavior.
(Id. at 7-8.)

       In her affidavit, petitioner indicates that after G.B. received his vaccinations, he
cried “hysterically” and then “passed out” while they were still at the pediatrician’s office.
(Ex. 3 at 1.) After awakening later in the day, he continued to cry and “seemed
absolutely miserable” before falling asleep for approximately four hours. (Id. at 2.)
G.B. awoke two times during the night, during which he was crying and unwilling to
nurse more than “two to three swallows.” (Id.) After his second awakening, sometime
between 4:30 and 5:00 a.m., petitioner placed G.B. next to her in her bed. (Id.)
Petitioner awoke at 8:45 a.m. and found G.B. “lifeless.” (Id.)

       On the morning of March 13, 2014, the Sterling Volunteer Fire Department was
dispatched to petitioner’s residence pursuant to a call that G.B. was “unconscious [and]
not breathing.” (Ex. 10 at 1.) When the fire department arrived, G.B.’s father (a
member of the fire department) was already performing CPR. (Id. at 2.) CPR was
continued for approximately “20 to 25 minutes.” (Id.) A Sterling Police Department
Attended/Unattended Death Report prepared by Mike Barker 7 lists G.B.’s time of death
as 9:57 a.m. on March 13, 2014. 8 (Ex. 9 at 4.). G.B.’s body was taken directly to the
Oklahoma City Office of the Chief Medical Examiner. (Id. at 5.)

      On April 9, 2014, Petitioner completed and submitted a form to the Vaccine
Adverse Event Reporting System (VAERS). (Ex. 8 at 1.) She described the adverse
event as “death, within 24 hours.” (Id.)

7
    Mr. Barker is an officer with the Sterling Police Department. (Ex. 9 at 4.)
8
    The “Report of Investigation by Medical Examiner” lists the time of death as 9:47 a.m. (Ex. 4 at 5.)

                                                        5
          b. Autopsy Reports

        Dr. Ruth Kohlmeier of the Office of the Chief Medical Examiner of Oklahoma City
performed an autopsy of G.B. at approximately 1:00 p.m. on March 14, 2014. (Ex. 4 at
1.) The manner of death was determined to be accidental and the cause of death was
identified as “probable asphyxia due to co-sleeping.” (Id.) Post-mortem toxicology was
negative. (Id. at 1, 5.) Dr. Kohlmeier’s examination revealed no traumatic findings but
did reveal fixed livor mortis, both anteriorly and posteriorly. (Ex. 4 at 1-2; Ex. 20.)
There was purple lividity of the left side of the face and blanching of the right side of the
face. (Ex. 4 at 2.) During internal examination, G.B.’s brain, lungs, liver, and spleen
were noted to be “heavy for age.” (Id. at 2-3.) There was also a small amount of
petechial hemorrhages on the lungs; while microscopic examination showed marked
atelectasis and congestion. (Id. at 3-4.)

       Petitioner subsequently requested a second opinion from another pathologist.
Petitioner (?) sent sixteen autopsy slides and Dr. Kohlmeier’s report to Dr. Steven
Rostad. (Ex. 5.) Dr. Rostad’s findings included vascular congestion of the adrenal
gland, lungs, liver, pancreas, brain, and leptomeninges; acute hemorrhages of the
kidney and adrenal gland; acute intra-alveolar hemorrhage; atelectasis; and granular
ependymitis. (Id. at 1) Dr. Rostad further commented that “[t]ypical microscopic
findings of vaccination-related adverse reaction are not seen, however [this] does not
exclude such a cause in my opinion” and that “[o]verall, the findings are not specific but
could be explained by asphyxia.” (Id.)

   IV.    Expert Reports

          a. Petitioner’s Experts

                  i. Douglas Miller, M.D., Ph.D.

       Petitioner presented an opinion by neuropathologist, Douglas C. Miller, M.D.,
Ph.D., to support her claim. (Ex. 22.) Dr. Miller received his medical degree from
University of Miami School of Medicine in 1974 and his doctorate degree in physiology
and biophysics from University of Miami in 1978. (Ex. 21.) Dr. Miller is board certified
in anatomic pathology and neuropathology by the American Board of Pathology. (Ex.
21, p. 3.) Dr. Miller practices as a neuropathologist at University of Missouri Healthcare
and as a contract physician/consultant for the Department of Pathology at Harry S.
Truman Veterans Hospital. (Ex. 22, p. 2.) Additionally, Dr. Miller currently holds a
teaching position at University of Missouri School of Medicine. (Ex. 21 at 3.) In this
position, he acts as the neuropathologist for the Office of the Chief Medical Examiner for
two counties in Missouri and provides forensic pathology services to many counties in
Missouri that have non-physician or non-pathologist coroners. (Ex 22 at 2.) Dr. Miller
has also authored numerous publications relating to neurology and neuropathology.
(Ex. 21 at 6.)

                                              6
       In his role as a forensic pathologist for medical examiner offices, Dr. Miller is
frequently consulted in cases with sudden unexpected death of infants and young
children, so he has “considerable (and lengthy) experience in the pathological analysis
of Sudden Infant Death Syndrome (SIDS) and Sudden Unexpected Death in Childhood
(SUDC).” (Ex. 22 at 2.)

        In opining that vaccines contributed to G.B.’s death, Dr. Miller acknowledges that
the risk factors 9 that are typical in SIDS cases would statistically make SIDS the most
likely scenario in this case, but the lack of histopathological abnormalities of G.B.’s
medulla and the presence of the marked congestion and hemorrhage seen in multiple
organs argue against this conclusion. 10 (Ex. 22 at 5-6.) He therefore concludes that
“this case does not fit the most common SIDS scenarios, vaccinations or no
vaccinations (or at least as far as the autopsy evidence permits, it does not fit).” (Id. at
6.) Dr. Miller also disagrees that G.B.’s death was due to asphyxiation. (Id.)

        Instead, Dr. Miller contends that, after reviewing the autopsy slides, the findings
in G.B.’s organs “suggest a diagnosis . . . of an acute visceral microvascular bleeding
disorder, which is an abnormality that is likely mediated by cytokines, with some
similarities to primary or secondary ‘capillary leak syndromes.’” (Id. at 5). Dr. Miller
notes that Petitioner’s affidavit suggests that G.B. began to behave abnormally as soon
as he was vaccinated. (Id. at 6.) Specifically, Dr. Miller opines that “the only
reasonable hypothesis for [G.B.’s] altered behavior, including excessive sleepiness,
fussiness/crying, and refusal to feed, is a process mediated by the innate immune
system, one resulting from cytokines, which are generally regarded as the mediators of
so-called ‘sick behavior.’” (Id. at 7.) He further notes that the autopsy showed a
“widespread petechial hemorrhagic process,” which he contends is most likely the result
of cytokine actions “even if the precise mechanism remains to be elucidated.” (Id. at 7-
8.)

        Despite acknowledging the lack of explanation for the mechanism of action, Dr.
Miller postulates that the severe congestion with hemorrhages in many of G.B.’s organs
“implicates a diffuse systemic cytokine-mediated problem of small vessel (capillary)
integrity.” (Ex. 22 at 8.) He suggests that a condition known as “systemic capillary leak
syndrome” (SCLS)11 can provide insight into how it is more likely than not that G.B.’s

9
  These include prematurity, male sex, maternal smoking during pregnancy, exposure to tobacco smoke
in the dwelling, prone sleeping, hyperthermia, co-sleeping, and mild upper respiratory infections. (Ex. 22
at 5-6.)
10
  Dr. Miller characterizes G.B.’s lungs as “severely congested.” (Ex. 22 at 4.) However, as will be
discussed in more detail below, Dr. Vargas, one of Respondent’s experts, contends that G.B.’s lungs
appeared consistent with what one would expect to find in an infant who received CPR and whose cause
of death was determined to be asphyxia. (Ex. OO at 4.)
11
   SCLS was first described as an idiopathic condition in which adults had single or multiple episodes had
single or multiple episodes of otherwise unexplained swelling of the peripheral tissues (including muscle
tissue). (Robin, Eugene et al., Capillary Leak Syndrome with Pulmonary Edema, Arch. Int. Med., 1972;
130:66-71 (Ex. 34).) SCLS will be discussed in more detail below.

                                                     7
vaccinations triggered a cytokine response that resulted in his death. (Id.) Dr. Miller
indicates that the pathophysiology of SCLS has been thought to involve cytokines of the
same species documented to be secreted in response to vaccinations. (Id.) Therefore,
Dr. Miller asserts that it is plausible that G.B.’s vaccinations triggered a cytokine
response, similar to that experienced by patients with SCLS, “which for reasons
unknown set off a cascade of events” resulting in endothelial damage and the
hemorrhages and congestion in multiple organs as found at autopsy, and causing
G.B.’s death. (Id.)

       After submitting his initial expert report, Special Master Millman requested a
supplemental report discussing whether the basis for Dr. Miller’s opinion on causation
would change absent petitioner’s affidavit regarding G.B.’s behavior after he received
the vaccinations. (ECF No. 25). In a letter dated October 30, 2017, Dr. Miller states, “I
would say that the history given by [petitioner] as to [G.B.’s] abnormal behavior is of
some importance, because it suggests that there was an ongoing abnormal cytokine
response beyond that usually accepted for routine vaccinations.” (Ex. 24.) However,
he further notes that his interpretation of the autopsy findings and conclusions as to
their most likely cause, as well as the cause of death, would not change if the symptoms
and signs reported by petitioner were not present. (Id.)

                    ii. Dr. Laurel Waters, M.D.

        Petitioner also presented an opinion by Dr. Laurel Waters, a pediatric pathologist
and assistant clinical professor at the University of California at Davis School of
Medicine, Department of Pathology and Laboratory Medicine. (Ex. 11 at 1.) She
received her medical degree from the University of California at Davis and is board
certified in pediatric pathology, anatomic and clinical pathology, and nuclear medicine.
(Id.) She also has extensive clinical laboratory experience. (Id. at 2-3.)

       In her report, Dr. Waters questions the medical examiner’s assessment of G.B.’s
cause of death as probable asphyxia due to co-sleeping. (Ex. 12 at 6.) She contends
that asphyxia is difficult to diagnose from a clinical perspective, and G.B. “was not
shown by any autopsy findings to have definitely died due to asphyxia.” (Id. at 6, 10.)
Dr. Waters further asserts that co-sleeping is not a cause of death, but instead should
be characterized as a risk factor and only in the context of when an adult is impaired by
alcohol or drugs. (Id.)

       In contrast to the medical examiner’s assessment, Dr. Waters opines that the
multiple vaccinations12 administered to G.B. “massively stimulat[ed] his immune

12
   Dr. Waters initially incorrectly listed one of the vaccines received by G.B. and the expected immune
response. (Ex. 12 at 8.) Specifically, Dr. Waters reported that G.B. received Pneumovax 23, not Prevnar.
(Id.) Prevnar is a conjugated (rather than pure polysaccharide) vaccination. (Ex A at 5.) The immune
response to Prevnar is similar to that seen with the HiB vaccine, another conjugated vaccination. (Id. at
5.) Dr. Waters corrected this error in her supplemental expert report. (Ex. 23 at 2.)

                                                    8
system,” activating three different arms 13 of the immune response and causing cytokine
production. (Ex. 12 at 7-10.) She states that if an excess of cytokines occurs in any
one or any combination of the three arms, it could be enough to produce a lethal
cytokine storm. (Id. at 10.) In addition, Dr. Waters postulates that because G.B. had
previously been exposed to hepatitis B (when he was vaccinated shortly after birth), he
“likely suffer[ed] from an anamnestic response to it, causing a more serious reaction,
setting him up for a cytokine storm” when combined with the cytokines released after
the other vaccinations. (Id. at 8, 10.)

       Citing the example of dengue fever, Dr. Waters indicates that cytokine storms
can cause both increased inflammation and an increased capillary permeability
syndrome, similar to the SCLS discussed by Dr. Miller. (Ex. 12 at 9.) Dr. Waters further
suggests that susceptibility to cytokine storm is variable, such that it is impossible to
predict who will respond poorly and who will overrespond. (Id. at 10.) While Dr. Waters
acknowledges in her supplemental report that it was possible that G.B. did not suffer an
actual cytokine storm, she maintains that “the increase in cytokines precipitated by the
immunizations caused [his] death.” (Ex. 23 at 4.)

            b. Respondent’s Experts

                    i. Christine McCusker, MSc, M.D., FRCP

       Respondent’s first expert, Dr. McCusker, holds a Master of Science degree in
molecular biology and an M.D., both received from McMaster University in Ontario,
Canada. (Ex. B at 2.) She is board certified in both pediatrics and allergy and clinical
immunology. (Id. at 3.) She currently serves as an associate professor of pediatric
allergy and immunology at McGill University and as Division Director of Pediatric
Allergy, Immunology, and Dermatology at the Montreal Children’s Hospital. (Id. at 4.)

        In her initial report, Dr. McCusker specifically addresses Dr. Waters’s conclusion
that G.B. suffered from a fatal vaccine-mediated cytokine storm. (Ex. A at 4.) To begin,
Dr. McCusker acknowledges that vaccination is predicted to activate immune responses
in part through cytokine upregulation. (Id. at 6.) However, the magnitude of cytokine
responses induced by vaccination are much lower than in natural infection because the
innate system is comparatively poorly activated. (Id. at 5.)

        Dr. McCusker reports that local cytokine effects include pain and redness at the
site of inoculation and systemic cytokine effects include fever and malaise. (Ex. A at 4.)
In fact, she explains that while vaccination is predicted to activate immune responses in
part through cytokine upregulation, there is no evidence to suggest that these “post-
vaccination” cytokines exist at levels sufficient to influence the development of a
cytokine storm as hypothesized by Dr. Waters. (Id. at 6). Dr. McCusker further notes
that no literature supports Dr. Waters’s speculative statement that G.B. could have
suffered an “anamnestic response” to the hepatitis B vaccine, a point which Dr. Waters

13
  Dr. Waters classifies these three arms as the innate immune response, Type 1 hypersensitivity, and
Type 2 hypersensitivity. (Ex. 12 at 10.)

                                                   9
relies upon as further increasing the likelihood of G.B. experiencing cytokine storm. (Id.
at 5.)

        Instead, Dr. McCusker asserts that there is no evidence in the record to support
a conclusion that G.B. experienced the progressive signs of excessive cytokine
activation. (Ex. A at 7.) While petitioner reported that G.B. displayed increased
fussiness and decreased feeding in the period following vaccination, Dr. McCusker
indicates that normal clinical patterns suggest that if he had experienced excessive
cytokine activation, he “would have gotten very ill, developed very high fever and would
have exhibited symptoms, such as, respiratory distress, unrelenting irritability and rash
in the time period immediately prior to his death.” (Id.)

       Dr. McCusker also addresses Dr. Waters’ conclusion that G.B. may have
suffered Type I and Type II hypersensitivity reactions. Dr. McCusker defined Type I
hypersensitivity as an allergic reaction, including anaphylaxis, that occurs within minutes
or up to a few hours after exposure to a provoking agent, usually reaching peak severity
within 5-30 minutes. (Ex. A at 7.) Signs and symptoms of such a reaction are found in
the skin (hives and swelling), the gastrointestinal tract (e.g., vomiting and diarrhea), the
respiratory tract (e.g., throat swelling, difficulty breathing, wheezing), and the
cardiovascular system (low blood pressure). (Id.) Children who experience Type I
hypersensitivity reactions display significant skin manifestations and persistent
abdominal symptoms of pain and vomiting. (Id. at 8.) Dr. McCusker notes that G.B.
displayed “no clinical features . . . consistent with an allergic reaction that would lead to
the conclusion that his death was a result of or a component of an anaphylactic event.”
(Id.) Further, Dr. McCusker reports that there were no findings from G.B.’s autopsy that
would lead to a conclusive diagnosis of anaphylaxis. (Id.)

        As for Type II hypersensitivity, Dr. McCusker explains that such reactions occur
when IgG “auto-antibodies” are formed. (Ex. A at 8.) She notes that Dr. Waters fails to
provide any mechanism by which a Type II hypersensitivity could have contributed to
G.B.’s death, except to state that cytokines could be released in this reaction. (Id.) Dr.
McCusker explains, however, that this reaction is not caused by cytokine release and
occurs over the course of several days to weeks. (Id. at 7.) Thus, even if G.B.
experienced a Type II hypersensitivity reaction, it could not have contributed to the
cytokine storm that Dr. Waters posits as leading to G.B.’s death within 24 hours after
receiving his vaccinations. (Id. at 8.) In conclusion, Dr. McCusker contends that there
is no clinical evidence G.B. suffered a cytokine storm. (Id. at 9.) She further opines that
even if there were evidence of a cytokine storm, the mechanisms (i.e., the
hypersensitivity reactions) proposed by Dr. Waters are not consistent with the current
scientific literature. (Id.)

       Instead, Dr. McCusker concurs with Dr. Kohlmeier’s determination that G.B.’s
death resulted from “probable positional asphyxia.” (Ex. A at 9.) Nevertheless, she also
evaluated the evidence that could support SIDS as an alternative cause of G.B.’s death.
Dr. McCusker notes that epidemiological studies have identified extrinsic risk factors for
sudden infant death syndrome (SIDS), including prone or side sleeping, bed sharing,

                                             10
over-bundling, soft bedding, face covered, and recent history of upper respiratory tract
infection. (Id. at 8.) In normal infants, environmental conditions/stressors, which can
lead to transient changes in O2/CO2 balance, activate the protective mechanisms in the
brain through the 5HT system and correct the problem. 14 (Id.) However, “at risk”
children fail to correct this imbalance and suffer cardiorespiratory arrest. (Id.)

        In addition, Dr. McCusker notes that studies have demonstrated clear association
between sleep position, sleep location, and parental, especially maternal, smoking as
significant risk factors for the development of SIDS. (Ex. A at 8.) With regard to
maternal smoking, prenatal exposure to tobacco has been identified as contributing to
the intrinsic vulnerability of an infant through impairment of central chemosensitivity and
several neurotransmitter systems. (Id. at 9.) Prenatal nicotine exposure can also alter
breathing patterns and reduce the hypoxia/hypercarbia induced ventilatory
chemoreflexes. (Id.) In the case of G.B., petitioner reported that she placed him next to
her in bed after a nighttime awakening and discovered him “lifeless” several hours later.
(Ex. 3 at 2.) He was also exposed to maternal tobacco smoke during pregnancy. 15
Furthermore, Dr. McCusker explains that the location of lividity as reported in the
autopsy suggests that G.B. was at least semi-prone, possibly prone (i.e. on his
stomach), at the time of death. (Ex. A at 8.)

       With regard to an association between vaccination and SIDS, Dr. McCusker
notes that studies to analyze this connection have found no differences in the frequency
or patterns of SIDS compared with the expected frequency in the population. (Ex. A at
9.) Instead, Dr. McCusker explains that well designed studies have shown findings
against a causal association for SIDS and vaccines, providing strong epidemiological
evidence for temporal association only. (Id. citing Traversa, G. et al., Sudden
Unexpected Deaths and Vaccinations During the First Two Years of Life in Italy: a Case
Study, PLoS One 2011 6:e16363 (Ex. EE); Venneman, M. et al., Sudden Infant Death
Syndrome: No Increased Risk After Immunisation, Vaccine 2007 25:336-40 (Ex. FF);
Kuhnert, R. et al., Reanalysis of Case-Controlled Studies Examining the Temporal
Association Between Sudden Infant Death Syndrome and Vaccination, Vaccine 2012
30:2349-56 (Ex. GG). Dr. McCusker concludes by stating she “find[s] no evidence that
the vaccination[s] on March 12, 2014 contributed to [G.B.’s] death. (Id.)

                    ii. Sara Vargas, M.D.

       Respondent also provided an expert opinion from Dr. Sara Vargas, a pathologist.
(Ex. C.) Dr. Vargas serves as a pathologist at three Boston area hospitals: Children’s
Hospital, Brigham and Women’s Hospital, and the Dana Farber Cancer Institute. (Ex. D
at 2). She is also an associate professor at Harvard University. (Id.) Dr. Vargas
received her medical degree from the University of Vermont, completed a pathology
14
  The 5HT system senses changes in O2 and CO2 and is involved in regulating arousal from sleep, body
temperature, auto-resuscitation, and the laryngeal chemoreflex. (Ex. A at 8.)
15
  Petitioner’s antepartum records reflect that she was a smoker during her pregnancy with G.B. (Ex. 7 at
12-13.)

                                                   11
residency at Brigham and Women’s Hospital, and trained as a fellow in pediatric
pathology at Children’s Hospital, Boston. (Id.) She is also a diplomate of the National
Board of Medical Examiners and the American Board of Pathology (Anatomic, Clinical,
and Pediatric Pathology). (Id. at 13.)

       In evaluating G.B.’s case, Dr. Vargas initially noted that “[t]here are gaps in
available information for assessing the main differential diagnosis,” including the lack of
findings from a scene investigation, witness interviews or other detailed police
investigation, information about the position of G.B.’s body when it was found,
information about petitioner’s medications or any other ingestions proximate to G.B.’s
death, and information about the conduct of individuals at the scene. (Ex. C at 6-7.)
However, Dr. Vargas notes in her supplemental report, that she was subsequently was
provided with autopsy and scene photos. (Ex. OO at 2.) She describes these
photographs as showing “loose bedding composed of two quilted adult-sized bedcovers
and at least four pillows.” (Id.)

       Dr. Vargas states that there are a number of factors identifiable in the available
case material to support Dr. Kohlmeier’s conclusion that G.B.’s cause of death as
probable asphyxia due to co-sleeping. (Ex. C at 7.) Similar to Dr. McCusker, Dr.
Vargas notes that factors potentially contributing to asphyxiation of G.B. include
sleeping in an adult bed, sleeping with an adult, and prone sleep positioning. (Id. at 7.)
Dr. Vargas explains that postmortem lividity, which occurs as a result of blood pooling
after death, can also assist in determining body positioning at the time of death. (Id. at
6.) Scene photographs show G.B.’s body, in what appears to be an ambulance, with
postmortem lividity of the left face, back, and arms. (Ex. OO at 2.)

       Further, as discussed above, Dr. Kohlmeier’s autopsy report reflects lividity on
the anterior and posterior aspects of G.B.’s body, consistent with the photographs from
autopsy reviewed by Dr. Vargas. (Ex. 4 at 1-2; Ex OO at 2.) Dr. Vargas explains that
an infant’s body is routinely placed face-up for CPR and morgue refrigeration, which can
contribute to lividity on the posterior surfaces of the body. (Ex. C at 7.) In the case of
G.B., as noted above, CPR was performed for 20-25 minutes and he was subsequently
transported to the Oklahoma City Office of the Chief Medical Examiner, where an
autopsy was performed the next day. (Ex. 4 at 1; Ex. 10 at 2.) While a more detailed
scene investigation would be necessary to reach a definitive conclusion, Dr. Vargas
reports that “it is most likely that the anterior lividity observed in G.B.’s body stemmed
from prone positioning from the time of death until he was moved for CPR.” (Ex. C at
7.) Dr. Vargas also notes that pleural petechial hemorrhage, as was observed in G.B.,
is commonly seen at autopsy in deaths from asphyxia, which further supports Dr.
Kohlmeier’s findings regarding G.B.’s cause of death. (Id.)

       Similar to Dr. McCusker, Dr. Vargas notes that SIDS may be considered in the
differential diagnosis of G.B.’s death. (Ex. C at 8, 11.) However, SIDS is a diagnosis of
exclusion, and can only be made after asphyxia and other causes of death are ruled
out. (Id. at 8.) Nevertheless, Dr. Vargas notes that G.B. did fit the appropriate age peak
for SIDS of 1-6 months and his death apparently occurred during a period of sleep, in

                                            12
the setting of co-sleeping with an adult in an adult bed, and likely in the prone position.
(Id.) As described by Dr. McCusker, male gender and maternal smoking are risk factors
for SIDS, and pleural petechiae (as was found in G.B.) can be found in deaths due to
either SIDS or asphyxia. (Id.) In fact, Dr. Vargas states that deaths from asphyxia,
especially while occurring during a sleep period, can mimic SIDS, and if evidence
supporting asphyxia had not been recognized by Dr. Kohlmeier, then “SIDS would be a
strong diagnostic consideration in this case.” (Id.) Dr. Vargas also concurs with Dr.
McCusker’s conclusions regarding the involvement of vaccinations in this case by
stating that “[v]accinations are not known to cause or contribute to asphyxia . . . or
SIDS, and there is no evidence to suggest that they caused or contributed to G.B.’s
death.” (Id.) For reasons discussed in greater detail below, Dr. Vargas disagrees with
Dr. Miller’s interpretation of congestion and hemorrhage found during G.B.’s autopsy as
suggesting a pathological bleeding disorder. (Ex. OO, pp. 4-5.)

        Dr. Vargas also responds to the conclusions reached by Dr. Waters. (Ex. C at
8.) She agrees with Dr. Waters’s conclusion that the autopsy findings do not “definitely”
show that G.B. died of asphyxia and that there are other possibilities for a cause of
death, including SIDS. 16 (Id. at 9, 11.) However, in contrast to Dr. Waters’s statement
that “co-sleeping is not a cause of death,” Dr. Vargas indicates that infant asphyxia is a
well-known complication of bed-sharing with adults, and bed-sharing is a well-known
risk factor for SIDS. (Id. at 9.) Dr. Vargas asserts that “[a]lthough co-sleeping of course
does not always lead to death, events that occur in the course of co-sleeping are well
accepted to cause death” and “[i]t is nothing short of preposterous to state that [it]
cannot cause death or that [it] can only cause death if the adult is impaired by alcohol or
drugs,” as claimed by Dr. Waters. (Id.) Dr. Vargas indicates that it is clear from Dr.
Kohlmeier’s report that she believed that an accident from co-sleeping caused an
asphyxia death in G.B., and “for Dr. Waters to imply that such a case is not even
possible seems disingenuous.” (Id.) Finally, as for Dr. Waters’s conclusion that G.B.
suffered a lethal vaccine-mediated cytokine storm, Dr. Vargas states that such an
allegation is unsupported and that the vaccines received by G.B. have not been shown
to cause death due to cytokine storm. (Id. at 10-11.)

   V.      Discussion

       In this case, G.B.’s official cause of death as determined by the Office of the
Chief Medical Examiner of Oklahoma City is accidental death by probable asphyxiation
due to co-sleeping. Petitioner seeks to displace that finding in favor of an
immunological, cytokine-driven, explanation for G.B.’s death. Assessing petitioner’s
claim involves three overarching questions.

16
   Dr. Vargas also suggests that there is some autopsy evidence suggesting that G.B. may have suffered
from congenital pancreatic islet cell hyperplasia, causing hyperinsulinemic hypoglycemia, which could
have played a role in his death. (Ex. C at 7-8.) However, she acknowledges that without detailed scene
(of death) information, it is impossible to surmise whether asphyxia or hyperinsulinemic hypoglycemia
was the more likely cause. (Id. at 10.)

                                                  13
        First, petitioner questions the medical examiner’s decision to list asphyxiation as
a certain, accidental cause of death in what might otherwise be classified as a case of
Sudden Infant Death Syndrome (“SIDS”), i.e. an unexplained death. Deeming this a
case of SIDS is prerequisite to petitioner’s claim as it would facilitate her experts’
exploration of alternative causes of death whereas accidental asphyxiation would be a
mutually exclusive explanation of G.B.’s death. A petitioner must prove by a
preponderance of the evidence the factual circumstances surrounding her claim. 42
U.S.C. § 300aa–13(a)(1)(A). Accordingly, petitioner’s disagreement with G.B.’s
recorded cause of death poses a threshold question. For the reasons discussed below,
petitioner is not persuasive in contending that G.B.’s official cause of death is incorrect.

        Second, operating on the premise that G.B.’s death is otherwise unexplained,
petitioner advances the theory that G.B.’s vaccinations triggered a cytokine-mediated
event, causing endothelial damage that led to hemorrhaging and congestion in multiple
organs, and ultimately leading to his death. (ECF No. 51.) Petitioner’s experts opine
that what G.B. experienced was “an increased capillary permeability syndrome” (Ex. 12,
p. 9 (Dr. Waters)) or an “acute visceral microvascular bleeding disorder” similar to a
“primary or secondary ‘capillary leak syndrome.’” (Ex. 22, p. 5 (Dr. Miller)). Both experts
opine that this condition would have arisen as a consequence of an excessive cytokine
response. (Ex. 12, p. 9; Ex. 22, p. 5.) Even setting aside the question of asphyxiation,
application of the Althen test to this theory demonstrates that petitioner has not met her
burden of proof in this case.

         Third, and finally, because SIDS, though not fully understood, is believed to be
multifactorial, if petitioner were correct that G.B.’s death was better explained as SIDS
rather than as asphyxiation, this would raise a question of whether the leading model of
SIDS (the Kinney or Triple Risk Model) offered any basis for including G.B.’s
vaccinations among the multiple factors leading to his death. Confusingly, while Dr.
Miller opines on petitioner’s behalf that G.B. did not likely experience SIDS (Ex. 22, p. 6)
he also at turns characterizes this as an instance of SIDS (Id. at 7) and concludes his
initial report by directly paralleling his causal theory in this case to the causal theory he
has presented in prior SIDS cases. (Id. at 8). For her part, Dr. Waters also suggested
that a subset of SIDS cases may actually represent deaths due to immunization. (Ex.
12, p. 7.) These questions have received substantial attention in prior Program cases
and Drs. Miller and Waters are not persuasive on these points.

          a. Asphyxia is the Most Likely Cause of Death

       At first blush, there is clearly no dispute that ultimately the injury at issue in this
case is G.B.’s tragic death. Importantly, however, there is significant disagreement
regarding the correct characterization of the manner and cause of G.B.’s death. As
noted above, Dr. Kohlmeier, the medical examiner, concluded that the manner of G.B.’s
death was accidental and the cause of death “probable asphyxia due to co-sleeping.”
(Ex. 4, p. 1.) Petitioner’s experts disagree. Respondent argues, however, that “[w]hile
the autopsy report alone does not per se bind the Special Master to adopt its
conclusions (see 42 U.S.C. § 300aa-13(b)(1)), it is powerful and persuasive evidence in

                                              14
this case, particularly since the medical examiner’s findings were not rebutted by a
second review of G.B.’s pathology slides three months after his death.” (ECF No. 56,
pp. 16-17.) Respondent’s experts support the medical examiner’s conclusion. 17

        Medical records generally constitute trustworthy evidence. Cucuras v. Sec’y
Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). Moreover, although
rebuttable, the “medical records and medical opinion testimony” of treating physicians
can be “quite probative,” because “treating physicians are likely to be in the best
position to determine whether ‘a logical sequence of cause and effect show[s] that the
vaccination was the reason for the injury.’” Capizzano v. Sec’y of Health & Human
Servs., 440 F.3d 1317,1326 (Fed. Cir. 2006) (quoting Althen, 418 F.3d at 1280); accord
Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1376 (Fed. Cir. 2009). This
principle has also been applied in the context of SIDS and asphyxia because, although
not strictly speaking “treating” physicians, the opinions of coroners and medical
examiners are based on their direct autopsy examinations and role in investigating the
cause of death. Pelton v. Sec’y of Health & Human Servs., No. 14-674V, 2017 WL
1101767, at *13 (Fed. Cl. Spec. Mstr. Feb. 27, 2017). As Drs. Waters and Miller alluded
in their first reports, Dr. Kohlmeier’s conclusion draws on two sources of information, the
results of the autopsy itself and the scene information. (Ex. 12, p. 6; Ex. 22, p. 4.) Dr.
Kohlmeier is the only physician to have examined G.B.’s body post-mortem. Drs.
Rostad, Waters, Miller, and Vargas, relied on Dr. Kohlmeier’s report and on the
microscopic slides created during her examination. (Ex. 5, p. 1; Ex. 12, p. 3; Ex. 22, pp.
3-7; Ex. C, pp. 1-2.) Dr. Vargas further suggests that as the investigating medical
examiner Dr. Kohlmeier likely had access to additional scene information unavailable to
the experts in this case. (Ex. C, p. 6; Ex. OO, p. 1.) And, indeed, Dr. Kohlmeier is the
only opining physician to have had access to the investigating officers at the scene.
Accordingly, Dr. Kohlmier’s conclusion should ordinarily be entitled to significant weight.

        Petitioner’s disagreement with Dr. Kohlmeier’s conclusion stems in significant
part from a differing perspective with regard to the relationship between SIDS, co-
sleeping, and asphyxia, a question that is unsettled among pathologists. Sudden Infant
Death Syndrome is not a diagnosis per se. Rather, it is a term applied to instances of
infant death that remain unexplained. (E.g. Ex. 32, p. 1.) Accordingly, a determination
that asphyxia has occurred constitutes an explanation of death that supplants the SIDS
label. Dr. Waters explains that over time increased awareness of asphyxia as a cause
of death has explained a significant portion of the decrease in reported incidence of

17 The burden does not shift to respondent to demonstrate a factor unrelated to vaccination as the cause
of G.B.’s death unless petitioner initially meets her burden of proof under the Althen test. § 300aa-
13(a)(1)(B); Walther v. Sec’y of Health & Human Servs., 485 F.3d 1146, 1150 (Fed. Cir. 2007).
Importantly, however, respondent may also present evidence casting doubt on petitioner’s case-in-chief,
though petitioner does not bear the burden of eliminating alternative causes if she can otherwise meet her
burden of proof under Althen. de Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352-53
(Fed. Cir. 2008); Walther, 485 F.3d at 1150. When faced with disagreement among qualified experts
regarding the identification and nature of a disputed injury, the Federal Circuit has concluded that it is
“appropriate for the special master to first determine what injury, if any, [is] supported by the evidence
presented in the record before applying the Althen test to determine causation.” Lombardi v. Sec’y of
Health & Human Servs., 656 F.3d 1343, 1351-53 (Fed. Cir. 2011).

                                                   15
SIDS. (Ex. 12, p. 6.) However, in Dr. Waters’s view, because asphyxia is difficult to
diagnose pathologically, it is likely that it has been over-diagnosed. (Id.) Dr. Waters
believes that in SIDS-type cases, the cause of death should remain undetermined
rather than being identified as asphyxia. (Id.)

        Dr. Miller further explains that current forensic pathology practice in this country
is “discordant” regarding how to view the relationship between co-sleeping, asphyxia,
and SIDS. (Ex. 22, p. 6.) According to Dr. Miller, co-sleeping may be considered a risk
factor for SIDS, but the SIDS classification should not be set aside in favor of asphyxia
as the cause of death based on sleeping conditions alone. (Id.) Rather, he would
require direct evidence of entrapment (such as direct lying-over of the adult on the
baby) to conclude there was an accidental asphyxia death. (Id.) Like Dr. Miller, Dr.
Waters stresses that “if any specific lethal events occur, they should be included in the
cause of death.” (Ex. 23, p. 3.)

       Dr. Miller acknowledges, however, that “many medical examiners refuse to make
a diagnosis of SIDS in the setting of co-sleeping or even other presumed unsafe
sleeping conditions.” (Ex. 22, p.6.) Moreover, it appears that Dr. Miller is overly
stringent in his suggestion of what would constitute evidence of asphyxiation.
Describing the Triple Risk Mode of SIDS, he suggests that:

        SIDS research back to the work of Kinney and others has regarded sleeping
        conditions in carbon dioxide (“re-breathing”) as a risk factor for SIDS, not as
        an alternative diagnosis which excludes SIDS. Co-sleeping, unless there is
        demonstration of actual entrapment of the baby’s head (in the corner of a
        sofa, or under an adult’s body), is in this line of analysis therefore not
        regarded as evidence of asphyxiation separate from SIDS.

(Id.)

        For this proposition he cites Blair, et al, Major epidemiological changes in sudden
infant death syndrome: a 20-year population-based study in the UK, 367 Lancet 314
(2006) (Ex. 32). Review of that paper indicates, however, that for purposes of the study
cases were excluded from the definition of SIDS in instances of suspected overlay or
asphyxia “when the evidence on balance of probability (including histopathological
findings, review of history, and death-scene investigation), showed such a cause.”
(Blair, et al., supra, at Ex. 32, p. 2.) As described further below, this is consistent with
Dr. Kohlmeier’s report and nothing in this paper indicates that demonstrated entrapment
of the head is specifically required to evidence asphyxiation separate from SIDS as Dr.
Miller suggests.

       Additionally, although the difference between documenting a death as SIDS or
asphyxia may touch on important research or public policy considerations, there is an
extent to which, in the specific context of this case, Drs. Miller and Waters are engaging
in semantics by raising the distinction between co-sleeping as a risk factor for SIDS on
the one hand and asphyxia due to co-sleeping being a reported cause of death on the
other. Dr. Waters in particular stresses that “co-sleeping is not a cause of death.” (Ex.

                                              16
12, p. 10.) This framing of the issue has been previously criticized. Pelton, 2017 WL
1101767, at *11 (explaining that “Dr. Waters suggests that because most co-sleeping
infants do not die, co-sleeping can be considered only a risk factor and not a cause of
death. That co-sleeping does not lead to death in many or even most instances does
not preclude it from being identified as a cause of death when, as here, evidence
supports that conclusion.”) And, indeed, in this case Dr. Vargas responds sharply to
this point, indicating that “[a]lthough co-sleeping of course does not always lead to
death, events that occur in the course of co-sleeping are well accepted to cause death.
It is nothing short of preposterous to state that they cannot cause death . . .” 18 (Ex. C,
p. 8.)

        Setting aside Dr. Waters’s specific statements, Dr. Miller’s report further
illustrates the semantic issue. Dr. Miller is critical of respondent’s expert, Dr. Vargas,
because she “goes through all the risk factors for SIDS imposed on this baby by the
terminal sleeping condition, but does not explicitly deal with these as risk factors for
SIDS, instead she agrees with the ME that they suggest probable asphyxiation.” (Ex.
22, p. 6.) However, Dr. Miller also explains that under the Triple Risk Model “the
prevailing hypothesis in the SIDS research community [is] that an infant without any
medullary defects will arouse when inhaled CO2 levels cause hypercapnia, 19 even if the
hypercapnia is a consequence of the unsafe sleeping condition.” (Id. (emphasis
added).) What Dr. Miller reveals is that while the SIDS model proposes that there may
be additional underlying vulnerabilities that help explain why reduced oxygen and re-
inhaled carbon dioxide ultimately becomes fatal in these cases, even under the SIDS
model the risk posed by co-sleeping still ultimately relates to a direct relationship
between the unsafe sleeping conditions and a deficiency of breathable air, i.e.,
suffocation or asphyxia. Regardless of whether the death is labeled on a death
certificate or autopsy report as SIDS or asphyxiation, the actual hazard initially posed by
unsafe sleeping conditions is the same. Thus, standing alone, the distinction being
drawn by petitioner’s experts between asphyxiation and SIDS provides very little basis
for calling Kohlmeier’s report into question regarding her review of the circumstances
and scene.

        This point is further underscored by the literature filed by petitioner. According to
Li, et al, “[p]lacing infants to sleep on surfaces shared with another person or persons
exposes them to potentially fatal hazards. These hazards include overlay by cosleeper;
entrapment/wedging between the bedding and cosleeper or between mattress and wall,

18 It is also interesting to note that there is a degree of internal tension in Dr. Waters’s opinion. Dr. Waters
opines in effect that SIDS is now underreported due to the increase in reports of asphyxiation but also
suggests that SIDS may be overreported vis-à-vis what she considers deaths due to vaccine toxicity. (Ex.
12, pp. 6-7.) When it comes to an association between co-sleeping and death, Dr. Waters seems to
contend that the statistical association alone is not enough to implicate co-sleeping as a cause of death
via accidental asphyxiation. However, in suggesting that a subset of SIDS is actually caused by
vaccination, Dr. Waters seeks to rely entirely on the same type of associational evidence only far weaker
(in fact, relying more broadly on the overall infant mortality rate).
19Hypercapnia refers to an excess of carbon dioxide in the blood. (Dorland’s Illustrated Medical
Dictionary, p. 876 (33rd ed. 2020).)

                                                      17
head entrapment in bed railings, and suffocation on soft bedding or waterbeds.” (Li, et
al., Observations on Increased Accidental Asphyxia Deaths in Infancy While Cosleeping
in the State of Maryland, 30 Am J Forensic Med Pathol 318-321 (2009) (Ex. 13, p. 4).
This was based on a review of 102 infant deaths in Maryland. (Id. at 1.) Following a
retrospective study of nine years of infant death data from Kentucky, Knight, et al,
similarly observe with regard to co-sleeping as a risk factor for unexpected infant death
that:

       the actual hazard may also be related to confounding factors which create
       an unsafe cosleeping environment, such as cosleeping on couches and
       other unsafe surfaces (including beds too small for the number of individuals
       sleeping); soft bedding, pillows, and comforters; parental intoxication or
       exhaustion when cosleeping; cosleeping with adults who smoke; and
       cosleeping with noncaregivers, or nonelective cosleeping with a
       disinterested caregiver due to socioeconomic factors.

(Knight, et al., Cosleeping and Sudden Unexpected Infant Deaths in Kentucky, a 10-
Year Retrospective Case Review, 26 Am J Forensic Med Pathol 28-32 (2005) (Ex. 14,
p. 5.).

        Whereas Dr. Miller acknowledges co-sleeping to be a risk factor for SIDS
generally (Ex. 22, p. 6), Dr. Waters further opines that co-sleeping is not even a risk
factor absent drug or alcohol impairment. (Ex. 12, p. 10). Dr. Waters cites three articles
as support for her contention that co-sleeping is a SIDS risk factor only in the presence
of drug or alcohol impairment - the above-discussed Li, et al., and Knight, et al., as well
as a third article by Blair, et al. (Blair, et al., Bed-Sharing in the Absence of Hazardous
Circumstances: Is There a Risk of Sudden Infant Death Syndrome? An Analysis from
Two Case-Control Studies Conducted in the UK, 9(9) PLoS ONE e107799 (2014) (Ex.
15).) Only Blair, et al, directly addresses this point. Blair, et al, sought to further
investigate specific co-sleeping environments. Examining 405 infant deaths from two
prior studies, the Blair authors found that when adjusting for other SIDS risk factors, the
overall risk of SIDS for co-sleeping infants was almost four-fold. (Id. at 3.) However,
once the data was further broken down by sleeping environment and age, only those
cases associated with the hazards of drug or alcohol use, smoking, or sleeping in a sofa
or chair, remained statistically significant. (Id. at 4.) Notably, however, this study
confirms that among variables there was a strong interaction with age that
demonstrated a higher risk from co-sleeping for infants less than three months of age.
(Id. at 4.) G.B. was about two months old at the time of his death. (Ex. 2, p. 7.)

       The Blair authors also explain that “[w]e have largely established potential
associations rather than causal factors and can only interpret the findings in terms of the
factors we have recorded.” (Blair, et al., supra, at Ex. 15, p. 5.) They note that:

       [t]he combined dataset is relatively large for case-control studies and is
       population-based with very few missed deaths during the study period but
       is only large enough to look at a dichotomy of interactions amongst the

                                            18
        multiple categories of co-sleeping death and even then the numbers for
        some categories may be small as reflected by the large confidence intervals
        of risk estimates.

(Id. at 5.)

        In any event, the authors concluded that their results should further suggest that
accidental asphyxiation explains the relationship between SIDS and co-sleeping. (Id.)
Blair, et al, provides a more nuanced perspective regarding the risks of infant co-
sleeping. However, it is not in itself evidence rebutting Dr. Kohlmeier’s conclusion. Like
Li, et al, and Knight et al., it does support an overall association between co-sleeping
and infant death. Moreover, it underscores the overarching understanding that co-
sleeping is associated with SIDS precisely because of the danger of accidental
asphyxiation.

        Petitioner’s reliance on SIDS to discount Dr. Kohlmeier’s conclusion as to
asphyxia is all the more tenuous given that Dr. Miller does not actually opine that G.B.
experienced SIDS. Although he agrees that findings of pulmonary edema and pleural
petechiae are consistent with SIDS, his observation that there was congestion and
hemorrhage in other organs coupled with his inability to detect any medullary defect (a
hallmark of the Triple Risk Model of SIDS), has led him to opine that “this case does not
fit the most common SIDS scenarios, vaccinations or no vaccinations (or at least as far
as the autopsy evidence permits, it does not fit).” (Ex. 22, p. 6.) According to Dr. Miller,
under the Triple Risk Model, the presence of a medullary defect explains why an infant
may not arouse in response to hypercapnia. (Id. at 5.) This renders Dr. Miller’s opinion
inconsistent and somewhat incoherent in that it is not clear why Dr. Miller favors the
SIDS/CO2 rebreathing explanation over what he characterizes as “simple” asphyxiation
given the lack of any medullary defect consistent with that explanation.

        Instead, the thrust of the opinions offered by Dr. Waters and Dr. Miller seems to
be merely to challenge the very idea that G.B.’s death is explainable, such that their
exploration of additional hypotheses would be reasonable. In that regard they appear to
be suggesting that the risk that co-sleeping will lead to asphyxiation is not enough,
standing alone, to conclude that asphyxia due to co-sleeping was the actual cause of
G.B.’s death. Petitioner’s experts are correct that in general a statistical association is
not equivalent to proof of causation. However, they are not persuasive in suggesting
that this negates Dr. Kohlmeier’s determination of the cause of death in this case. Dr.
Kohlmeier’s conclusion cannot be reduced simply to reliance on a statistical observation
regarding the risks of co-sleeping. Nor are petitioner’s experts otherwise persuasive in
suggesting any factor specific to this case that would suggest this individual case
represents an over-use of asphyxiation as the cause of death. 20
20 Dr. Miller did note that G.B.’s brain weight was considered heavy for his age, but without evidence of

cerebral edema or brain herniations. According to Dr. Miller, this is a “common if poorly understood”
finding in SIDS cases that differentiates this case from “simple” asphyxiation. (Ex. 22, p. 6.) Dr. Miller is
unpersuasive on this point. First, Dr. Miller does not explain how or why this finding would differentiate
this case from one of asphyxia. This lack of explanation is especially notable given that Dr. Miller
acknowledges the finding to be one of poorly understood significance even in the SIDS context. Second,

                                                     19
        Dr. Kohlmeier’s reported pathology findings are consistent with SIDS, which is to
say they are also consistent with asphyxia and do not point to any other obvious cause
of death. Dr. Kohlmeier observed no trauma based on either internal or external
examination and also concluded that G.B. was a normally-developed and well-
nourished infant. (Ex. 4, p.1- 2.) Post-mortem toxicology was negative. (Id. at 1.)
There was no evidence of infection or tumor relative to either the nervous or respiratory
systems. (Id. at 2-3.) With regard to positive findings, Dr. Kohlmeier observed “a small
amount of petechial hemorrhages” in the lungs and also congestion of the lungs on
microscopic examination. (Id. at 3-4.) Both of petitioner’s experts, Dr. Waters and Dr.
Miller, agree that these petechial hemorrhages are consistent with SIDS without respect
to the specific cause of death. (Ex. 12, p. 5; Ex. 22, p. 4.) Respondent’s pathology
expert, Dr. Vargas, similarly agrees, but further stresses that the finding also supports
asphyxia specifically given the context of prone sleeping. (Ex. C, p. 6.) With regard to
the microscopic evidence of congestion, Dr. Miller and Dr. Vargas both agree that this is
also consistent with SIDS, though Dr. Miller characterizes the degree of congestion in
this case as atypically severe. 21 (Ex. 22, p. 4; Ex. C, p. 5.) Petitioner also had an
independent autopsy conducted by Dr. Rostad. (Ex. 5.) Dr. Rostad additionally agreed
that the autopsy findings were non-specific but consistent with asphyxia. (Id.)

        In the setting of pathology consistent with SIDS, the more specific conclusion that
asphyxia was the cause of death primarily derives from evidence relating to co-sleeping.
There is no dispute in this case that G.B.’s death occurred in the context of co-sleeping.
Petitioner averred that prior to his death, she had placed G.B. beside her in her bed
after a diaper change at around 4:30-5:00 a.m. (Ex. 3, p. 2.) Scene photographs also
show that G.B. had been sleeping on a bed with soft, loose bedding, which has been
identified in the relevant literature as hazardous. 22 (E.g. Shapiro-Mendoza, et al.,
Trends in Infant Bedding Use: National Infant Sleep Position Study, 1993-2010, 135
Pediatrics 1 (2015) (Ex. AA); see also Li, et al., supra, at Ex. 13, p. 4; Knight, et al.,
supra, at Ex. 14, p. 5.) Additionally, the observations on autopsy are significant for

Dr. Miller ultimately opines that he does not believe this child’s autopsy findings “fit the most common
SIDS scenarios.” (Id.) Dr. Miller cannot credibly contend that a specific finding should be viewed as
confounding the medical examiner’s assessment of asphyxia on the basis that it is consistent with SIDS
while simultaneously opining that SIDS is not the correct explanation for the child’s death. Dr. Miller
offers no explanation as to why G.B.’s brain weight supported his alternative assessment of a visceral
microvascular bleeding disorder. In any event, Dr. Vargas refutes that G.B.’s brain weight was unusually
heavy. (Ex. OO, p. 4.)

21 Dr. Waters acknowledges the finding, but did not specifically opine regarding its significance. (Ex. 12, p.
5.)
22Dr. Kohlmeier’s autopsy report does not specifically describe what she reviewed with regard to the
scene, but does confirm she was aware of the co-sleeping arrangement and was in contact with the Mike
Barker, the reporting officer. (Compare Ex. 4, p. 6 and Ex. 9, p. 5.) Petitioner subsequently filed a CD
containing “autopsy and scene photos.” (ECF No. 20.) Accompanying petitioner’s notice were 14
photographs taken in the course of the autopsy and 20 scene photographs taken by the first responders,
including photographs of G.B. on scene as well as several photos clearly documenting the sleeping
environment.

                                                     20
revealing that G.B. was likely prone at the time of death. Specifically, Dr. Miller and Dr.
Vargas both explain that the autopsy photographs confirmed the presence of both
anterior and posterior lividity, the anterior lividity indicates G.B.’s body was face down
initially while the posterior lividity is due to the post-mortem storage of his body on its
back. 23 (Ex. 22, p. 3.) Dr. Waters further observes that G.B.’s face had purple lividity
on the left and blanching on the right. (Ex. 12, p. 5.) She opines that this “suggest[s] the
right side was pressed against something and the left side was somewhat down.” (Id.)
Notwithstanding the above-discussed disagreements regarding the relationship
between SIDS, asphyxia, and co-sleeping, these factors, which suggest G.B. was co-
sleeping on soft, loose bedding and prone, face down, and with his face pressed
against something, are consistent with the medical examiner’s conclusion that the
circumstances of G.B.’s death, when combined with his autopsy results otherwise
negative for any explanation apart from SIDS, were consistent with an accidental death
due to asphyxia.

        While Dr. Waters and Dr. Miller both express concern about possible overuse of
asphyxia as a cause of death, Dr. Miller in particular acknowledges that this issue is
unsettled among forensic pathologists and that Dr. Kohlmeier would not be outside the
mainstream of the field if she refused to label the death as unexplained SIDS in the
context of an unsafe sleeping environment. (Ex. 22, p. 6.) And, in any event, even if
petitioner’s experts were persuasive in suggesting that it would be better policy for
G.B.’s cause of death to be recorded as SIDS rather than asphyxia, Dr. Miller
acknowledges that the SIDS model could still point to the unsafe sleeping conditions as
the initiating cause of the fatal hypercapnia when such conditions are present. (Id.)
Accordingly, petitioner’s experts are not persuasive in suggesting that Dr. Kohlmeier’s
report should be viewed as incorrect based on either the broader conventions of the
relevant medical community or the prevailing understanding of SIDS. 24

            b. Petitioner’s Theory of a Cytokine-Mediated Adverse Event Fails the
               Althen Test

       Instead of either asphyxiation or SIDS, petitioner argues that G.B.’s vaccinations
triggered a cytokine-mediated event, causing endothelial damage that led to
hemorrhaging and congestion in multiple organs and ultimately his death. (ECF No.
51.) Petitioner’s experts opine that what G.B. experienced was “an increased capillary
permeability syndrome” (Ex. 12, p. 9 (Dr. Waters)) or an “acute visceral microvascular

23Dr. Waters suggests that the combination of posterior and anterior lividity does not indicate which side
G.B. was on at the time of death. (Ex. 12, p. 5.) However, this does not account for Dr. Miller’s and Dr.
Vargas’s explanation that G.B. would have been kept on his back post-mortem. Dr. Waters has
previously been found unpersuasive on this point in a prior case. See Pelton, 2017 WL 1101767, at *13.

24 Of note, Dr. Miller also highlights certain pathology findings that he views as confounding as to either

asphyxia or SIDS, but which he contends support petitioner’s theory of causation. Specifically, he opined
that congestion and hemorrhaging in multiple organs supports a microvascular bleeding disorder These
findings are separately discussed in section V(b)(ii)(2), below. For the same reasons discussed therein,
they are not persuasive in calling Dr. Kohlmeier’s conclusion into question.

                                                    21
bleeding disorder” similar to a “primary or secondary ‘capillary leak syndrome’” (Ex. 22,
p. 5 (Dr. Miller)). Both experts opine that this condition would have arisen as a
consequence of an excessive cytokine response. (Ex. 12, p. 9; Ex. 22, p. 5.) For the
reasons discussed below, these opinions are inadequate to meet petitioner’s burden of
proof under the applicable three-part Althen test.

                  i. Althen Prong One

        Petitioner’s burden under the first Althen prong is to provide, by preponderant
evidence, “a medical theory causally connecting the vaccination and the injury.” Althen,
418 F.3d at 1278. Such a theory must only be “legally probable, not medically or
scientifically certain.” Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 549
(Fed. Cr. 1994). Moreover, 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.” Andreu, 569 F.3d at 1380.
However, to satisfy this prong, petitioner’s theory must be based on a “sound and
reliable medical or scientific explanation.” Knudsen, 35 F.3d at 548; Boatmon, 941 F.3d
at 1359. With this standard in mind, I conclude that upon review of Dr. Waters’s and Dr.
Miller’s reports, the literature they have cited, and Dr. Vargas’s and Dr. McCusker’s
competing opinions, petitioner has not met her burden of demonstrating a medical
theory causally linking G.B.’s death and his vaccinations.

        Both Dr. Waters and Dr. Miller opine that elevated cytokines can cause
endothelial cell dysfunction leading to some form of capillary leak or bleeding disorder.
(Ex. 12, p. 9; Ex. 22, p. 5.) As the first to opine, Dr. Waters initially relied on the concept
of a cytokine storm and indicated that such a state can produce capillary permeability
and plasma leakage as seen in dengue fever. (Ex. 12, p. 9.) Dr. Miller indicates,
however, that this is not a “prototypical” cytokine storm and instead indicates that “the
occurrence of severe congestion with hemorrhages in many organs in the absence of
any prior evidence for a coagulopathy implicates a diffuse systemic cytokine-mediated
problem of small vessel (capillary) integrity.” (Ex. 22, p. 8.) He instead analogizes
G.B.’s condition to “systemic capillary leak syndrome” (“SCLS”). (Id.) In that regard,
petitioner relies on six publications discussing SCLS. (Ex. 22 (citing Robin, supra, at
Ex. 34; Lofdahl, et al., Systemic capillary leak syndrome with monoclonal IgG and
complement alterations. A case report on an episodic syndrome, 206 Acta Med Scand.
405-12 (1979) (Ex. 35); Kawabe, et al., Capillary Leak Syndrome, 41 Int Med 211-15
(2002) (Ex. 36); Hsu, et al, Idiopathic capillary leak syndrome in children, 135 Pediatrics
e730-e735 (2015) (Ex. 37); Kulihova, et al., Fatal primary capillary leak syndrome in a
late preterm newborn, 3 Indian J. Pediatr. 1197-1199 (2016) (Ex. 38); Siddall and
Radhakrishnan, Capillary leak syndrome: etiologies, pathophysiology, and
management, 92 Kidney International 37-46 (2017) (Ex. 40)).)

       SCLS is a rare disorder in which a constellation of symptoms appear that are
related to increased permeability of capillaries to proteins. (Siddall and Radhakrishan,
supra, at Ex. 40, p. 1.) This results in edema and hypotension, and in some cases can

                                              22
lead to hypovolemic 25 shock and multiple organ failure. (Id.) There are several
conditions known to result in SCLS, including sepsis, viral hemorrhagic fevers, and
some autoimmune diseases. (Id.) It can also be drug-induced or idiopathic. (Id.) As of
2015 there had only been between 200-300 reported cases of SCLS since it was first
described in 1960. (Hsu, et al., supra, at Ex. 37, p. 1.) Petitioner filed a case report of a
newborn infant dying from suspected capillary leak syndrome. (Kulihova, et al., supra,
at Ex. 38.) However, that child died 27 days after birth with low blood pressure and
respiratory distress being observed within the first day of life. (Id. at 1-2.) No cause for
the infant’s condition was identified and there is no confirmation that any vaccines were
administered or suspected as a possible cause of the condition. (Id.)

        Some literature filed by petitioner does hypothesize that the capillary permeability
to protein underlying SCLS may be related to hypercytokinemia (Siddall and
Radhakrisnan, supra, at Ex. 40, p. 4); however, other literature cited by petitioner
cautions that the pathophysiology is unclear and cytokines are not necessarily the
leading consideration (Hsu, et al., supra, at Ex. 37, p. 5 (primarily discussing
monoclonal gammopathy and noting that “other soluble factors such as cytokines could
also have a role.”) Dr. McCusker stresses that to the extent elevated cytokines have
been observed in SCLS patients, it remains unclear whether they are pathogenic or
merely markers or manifestations of SCLS. (Ex. NN, p. 3.) Notably, SCLS is more
common in healthy young and middle-aged adults (Kawabe, et al., supra, at Ex. 36, p.
2) and among pediatric cases “the absolute levels of all cytokines were much lower in
the children tested than those seen in adults” (Hsu, et al., supra, at Ex. 37, pp. 5-6).
Importantly, while viral infection has been associated with SCLS (e.g. Kawabe, et al.,
supra, at Ex. 36, p. 2 26 ), none of the literature in this case posits or even suggests any
suspicion that vaccination could be a cause or trigger of SCLS. Dr. McCusker explains
that investigation of the cytokines elevated in SCLS suggests that a TH1 profile is
consistent with preceding viral infection. (Ex. NN, p. 3 (citing Druey and Parikh,
Idiopathic Systemic Capillary Leak Syndrome (Clarkson disease), 1430(3) J Allergy Clin
Immunol. 663-670 (2017) (Ex. NN, Tab 1)).) Conversely, Dr. McCusker cites a study by
Hingorani, et al, that demonstrated that vaccination may blunt the type of vasodilation
that precedes capillary leak, suggesting that the types of cytokines produced by
vaccination are not implicated in SCLS. (Ex. NN, p. 3 (citing Hingorani, et al., Acute
Systemic Inflammation Impairs Endothelium-Dependent Dilation in Humans, 102
Circulation 994-999 (2000) (Ex. K)).)

       Cytokines are small protein chemicals secreted by cells for the purpose of
intercellular signaling and communication. (Ex. 18 at 2; Ex. A at 4.) Their functions
include the regulation of angiogenesis and immune and inflammatory responses. (Id.)
Further, cytokines occur naturally, are present in humans in both healthy and diseased
states, and are responsible for everyday homeostasis. (Ex. C at 9; Ex. NN at 5.) Not all
25 Hypovolemia is “abnormally decreased volume of circulating blood in the body.” (Dorland’s, 33rd ed., p.

896.)
26Noting that “[a]lthough the precise mechanism of SCLS has not been elucidated, Amoura et al
suggested that viral infection might trigger the attacks because man of the patients had experienced
preceding episodes of flu-like illness.” (Ex. 36, p. 2 (citation omitted).)

                                                    23
cytokines are proinflammatory. (Ex. A, p. 3.) Thus, the simple presence of cytokines
does not imply that cytokines have caused injury. (Ex. A; Ex. C.) There is no
disagreement among the experts in this case that vaccination induces the release of
cytokines to at least some degree. (Ex. A, p. 3.) However, to the extent Dr. Waters and
Dr. Miller opine broadly that elevated cytokines could lead to a catastrophic injury, the
evidence of record does not support their conclusion that the ordinary cytokine
response to vaccination could in itself be implicated in either a cytokine storm or SCLS-
like endothelial injury. Petitioner has not filed any literature demonstrating vaccination
to be a cause or trigger of either SCLS or cytokine storm. Instead, Drs. Miller and
Waters seek to marry via their ipse dixit literature showing elevated proinflammatory
post-vaccination cytokines on the one hand with literature showing SCLS and cytokine
storm as being injurious cytokine-mediated conditions on the other. However, the
literature filed in this case demonstrates only that cytokine levels observed post-
vaccination are dramatically lower than the levels of cytokines measured in those
experiencing injurious systemic cytokine reactions. There is nothing on this record
demonstrating that the cytokines elicited by vaccination lead to uncontrolled systemic
reactions.

        For example, Hingorani, et al, injected 12 healthy subjects with a capsular
polysaccharide typhoid vaccine and compared cytokine levels based on blood samples
taken immediately before and up to eight hours after vaccination. (Hingorani, et al,
supra, at Ex. K, p. 2.) IL-1β was 4.7 pg/mL at baseline and rose to 5.0 pg/mL, a 0.3
pg/mL difference the authors characterized as “no change.” (Id. at 3 (Table).) IL-6 was
2.1 pg/mL at baseline and increased to 3.4 pg/mL. IL-1Ra was 188 pg/mL at baseline
and rose to 593.6 pg/mL. (Id. at 3 (Table).) The authors also observed that there had
been no change in concentration of TNF-α, but did not show the data. (Id. at 3.) In
contrast, Dr. McCusker cited a case study of six previously healthy control subjects from
a clinical trial who experienced a cytokine storm within 90 minutes of receiving a single
intravenous dose of a monoclonal antibody treatment, which is designed to provoke the
immune system. (Suntharalingam, et al., Cytokine Storm in a Phase 1 Trial of the Anti-
CD28 Monoclonal Antibody TGN1412, 355 N Engl J Med 10 (2006) (Ex. M).) According
to Dr. McCusker this is [t]he best documented series of clinical events that occur when
cytokines are inappropriately activated . . .” (Ex. A, p. 6.) In these cases IL-1β rose to
about 5,000 pg/mL, IL-6 rose to between 3,000 to 4,000 pg/mL, and TNF-α rose to
between 4,000 and 5,000 pg/mL. (Suntharalingam, et al., supra, at Ex M, p. 8 (Figure
3C).) Thus, for example, the increased levels of IL-1β and IL-6 during a cytokine storm
were 1,000-times the level observed post-vaccination in the Hingorani, et al, study.

        Additionally, Drs. McCusker and Miller provide competing interpretations of the
significance of a study by Kashiwagi, et al., which is a paper filed by both parties.
(Yasuyo 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(3) Human Vaccines & Immunotherapeutics
677 (2014) (Ex. 31; Ex. L).) Kashiwagi, et al, examined post-vaccination cytokine levels
in two ways. First, the study authors drew 29 blood samples from healthy children from
which peripheral blood mononuclear cells (“PBMCs”) were obtained. (Kashiwagi, et al.,

                                            24
supra, at Ex. 31, p. 3.) These PBMC cultures were then stimulated with various
combinations of diphtheria tetanus and acellular pertussis vaccine, Haemophilus
influenza b vaccine, and 7-valent pneumococcal vaccine. (Id.) Second, the study
authors obtained serum samples 24 hours post-vaccination from 61 vaccine recipients
who experienced a febrile response and 18 who did not. (Id.) These groups were
compared to each other and to a group of 18 samples taken from patients in the
influenza H1N1 outbreak and nine patients experiencing acute pneumonia. (Id.)
According to Dr. McCusker, Kashiwagi, et al., is significant for showing (1) that overall
levels of cytokines remained low post-vaccination and (2) that post-vaccination fever
developed independently of cytokine levels. (Ex. A, p. 6.) Dr. McCusker suggests this
constitutes a lack of evidence that vaccination can increase cytokine levels to an
injurious degree as seen in a cytokine storm. (Id.) Dr. Miller counters that the
significance of the Kashiwagi, et al., study is that it showed post-vaccination cytokine
levels to be comparable to the levels seen among influenza infection patients. (Ex. 22,
p. 7.) He further contends that influenza infections have in turn been documented to
induce a cytokine storm, intimating that vaccinations must therefore also be capable of
inducing a cytokine storm. (Id.)

       Although Kashiwagi, et al, did produce elevated levels of cytokines by artificially
stimulating PBMCs, they acknowledged that “an experiment in which PBMCs were
stimulated with vaccine antigen did not necessarily reflect the in vivo responses
following vaccination.” (Kashiwagi, et al, supra, at Ex. 31, p. 7.) In contrast, comparing
the febrile vaccine recipients, non-febrile vaccine recipients, and unvaccinated controls,
Kashiwagi, et al., observed:

        No detectible IL-1β was observed in sera in both febrile and non-febrile
        groups and no significant difference was observed in cytokine levels of IL-6
        and TNF-α between the two groups . . . The mean serum levels of
        inflammatory cytokines IL-1β, IL-6, and TNF-α were 0.68, 29.44, and 13.43
        pg/ml in vaccine recipients with febrile reactions after the simultaneous
        injection of three (DPT/Hib/PCV) or four vaccines (DPT/Hib/PCV+ other
        vaccine), and similar levels of inflammatory cytokines were produced in
        vaccine recipients with febrile reactions after immunization of one or two
        inactivated bacterial vaccines, also similar to those in non-febrile group. . .
        Higher levels of IL-6, Il-10, Il-12, G-CSF, IFN-γ, and TNF-α were detected
        in both febrile and non-febrile groups after vaccination in comparison with
        those in normal subjects.

(Id. at p. 4.)

        These in vivo results are far closer (by orders of magnitude) to the post-
vaccination measurements taken by Hingorani, et al., than they are to the type of
cytokine increases observed among the six confirmed cytokine storm cases discussed
above. Accordingly, Dr. McCusker’s interpretation of Kashiwagi appears sound. Dr.
Miller is also correct that the study showed post-vaccine cytokine levels comparable to
certain influenza infections; however, the authors note that cytokine levels among

                                              25
vacinees were comparable only to “mild-moderate outpatients” infected with influenza.
(Ex. 22, p. 7; Kashiwagi, et al., supra, at Ex. 31, p. 7.) Moreover, Kashiwagi, et al,
cautioned that even among their cohort of hospitalized infection patients, “extremely
serious patients were not included in the hospitalized patient group.” (Id.) And,
importantly, nothing in this paper suggests that any of the study subjects experienced
cytokine-mediated adverse events following either vaccination or infection. Thus,
although Dr. Miller suggests that some influenza infections can induce a cytokine storm,
he has not substantiated that those infections are at all comparable to the “mild-
moderate” infections studied by Kashiwagi, et al., or that those other instances had a
cytokine profile comparable to those demonstrated by Kashiwagi, et al.

         In fact, Dr. McCusker cites literature demonstrating that the levels of
inflammatory cytokines among pandemic strain influenza infections do correlate to the
severity of illness. (Zhou, et al., Avian Influenza A (H7N9) viruses isolated from patients
with mild and fatal infection differ in pathogenicity and induction of cytokines, 111
Microbial pathogenesis 402-09 (2017) (Ex. NN, Tab 8); Beigel, et al., Avian influenza A
(H5N1) infection in humans, 353 N Engl J Med 1374-85 (2005) (Ex. NN, Tab 9); Liu, et
al., The cytokine storm of severe influenza and development of immunomodulary
therapy, 13 Cellular & molecular immunology 3-10 (2016) (Ex. NN, Tab 10); Hagau, et
al., Clinical aspects and cytokine response in severe H1N1 influenza A virus infection,
14 Critical care R203 (2010) (Ex. NN, Tab 11).) In contrast, Dr. McCusker cites an
additional study, Barria, et al., which found “no predictable patterns could be detected in
the measured cytokines” following vaccination with a live attenuated influenza vaccine
(“LAIV”). (Barria, et al., Localized Mucosal Response to Intranasal Live Attenuated
Influenza Vaccine in Adults, 207 JID 115 (2013) (Ex. J, p. 6).) The authors indicated
that “in contrast to virus infection, LAIV does not appear to trigger a change in serum
cytokine profiles.”27 (Id.) While the Barria, et al., study does not negate the Kashiwagi,
et al., findings, it underscores the difficulty in attempting to extrapolate the effects of
vaccination as compared to infection, especially when juxtaposed with the above-
discussed literature relating to pandemic infections as cited by Dr. McCusker. On the
whole, Dr. Miller is not persuasive in suggesting that Kashiwagi, et al., itself provides
evidence that any vaccinations – alone or in combination – elevate cytokines to a
degree or in a manner that could be consistent with petitioner’s theory. 28

       Dr. Miller’s opinion is essentially limited to citing Kashiwagi, et al., to note the
parallel between vaccinations eliciting cytokines to any degree and SCLS being a
potentially cytokine-mediated condition. He leaves entirely unaddressed the question of

27 Dr. Miller is critical of Dr. McCusker’s reliance on this study because it measured cytokine levels three-
days post vaccination whereas he stresses that G.B. died within 24 hours of vaccination and further
stresses that cytokine levels peak between 24 and 48 hours after inoculation. (Ex. 22, pp. 7-8.) However,
the study authors indicate that they were comparing their findings to the rises in cytokines occurring
during viral infection which they indicated occurs over 48-72 hours. (Barria, et al., supra, at Ex. J, p. 6.)

28 Of note, Dr. Miller does appear to imply that his theory may be further supported by the idea that the

Triple Risk Model of SIDS accounts for otherwise trivial infections becoming fatal. (Ex. 22, p. 8.) This is
unpersuasive for the reasons discussed in Section V(c), below.

                                                     26
how an ordinarily mild cytokine response to vaccination becomes an uncontrolled and
catastrophically injurious systemic condition. (Ex. 22, pp. 7-8.) In fact, he explicitly
indicates that “in this instance the vaccinations triggered cytokine responses (as usual)
which for reasons unknown set off a cascade of events with endothelial damage in
multiple organs leading to hemorrhages and congestion found at autopsy . . .” (Id. at 8
(emphasis added).) Given that the above-discussed literature demonstrates only a mild
cytokine response to vaccination, and given that none of the SCLS literature cited by Dr.
Miller so much as suspects that vaccines trigger SCLS, Dr. Miller’s reliance on this
parallel without more would be entirely speculative even in the absence of Dr.
McCusker’s refutation.

       Dr. Waters does seek to provide some further explanation by invoking G.B.’s
multiple vaccinations, 29 possible anamnestic response from his prior Hepatitis B
exposure, and the role of Type I and Type II hypersensitivity responses. (Ex. 12, p. 8.)
However, these factors are not well explained. Moreover, Dr. McCusker notes that
G.B.’s presentation was not consistent with any Type I hypersensitivity reaction (i.e.
anaphylaxis) and a Type II hypersensitivity reaction is not consistent with petitioner’s
cytokine-mediated theory. (Ex. A, pp. 6-7.) Dr. Miller also acknowledges that G.B. had
no clinical signs or autopsy evidence of anaphylaxis. (Ex. 22, p. 7.) After challenge by
Dr. McCusker, Dr. Waters seems to indicate that the import of her initial discussion was
merely that “vaccines stimulate cytokines.” (Ex. 23, p. 2.)

       Dr. Waters also cites an article providing an overview of cytokine storms,
including their relationship to capillary permeability (most notably in relation to dengue
fever). (Tisoncik, et al., Into the Eye of the Cytokine Storm, 76(1) Microbiology and
Molecular Biology Reviews 16-32 (2012) (Ex. 18).) This article discusses some of the
susceptibilities that could help explain how a cascading cytokine response leads to a
cytokine storm; however, the article focuses on cytokine storms as following viral
respiratory infections and does not include any discussion of vaccinations. (Id.) Dr.
McCusker explains that the immune response to infection is not comparable to the
immune response to vaccination. In natural infection there are pattern recognition
receptors that upregulate gene expression of the innate immune system and

29 Kashiwagi, et al., stimulated PBMCs both with individual vaccinations and different combinations of up
to three vaccinations and examined 17 different cytokine profiles. Comparing single vaccination to
concurrent vaccination, they found no significant difference among ten of the profiles (IL-2, IL-4, IL-5, IL-7,
IL-10, IL-12, IL-13, IL-17, GM-CSF, and IFN-γ. (Kashiwagi, et al., supra, at Ex. 31, p. 5.) There were
differences among IL-1β, IL-6, G-CSF, and TFN-α; however, the results do not reflect any correlation
between the number of antigens or vaccinations and the degree of inflammation. (Id. at p. 4 (Figure 1).)
For example, mean levels of IL-1β do appear to have increased as the number of vaccines increased.
However, mean levels of IL-6 were higher for Hib alone than they were for any combination of multiple
vaccines. Combining three vaccines (DPT/Hib/PCV) resulted in lower mean IL-6 than any of the
combinations of two vaccines. Mean concentration of TNF-α was also lower when PMBCs were
stimulated with DPT, Hib, and PCV than when stimulated with only Hib and PCV. (Id.) The authors also
noted that “[c]ytokine production was examined in PBMCs culture stimulated with IPV, influenza, and MR
vaccines and very low levels of inflammatory cytokines were produced (data not shown). Therefore,
additional simultaneous immunization [is] supposed to have little influence on cytokine induction in sera.”
(Id. at p. 7.)

                                                      27
inflammatory response correlates to live virus shedding, which is not a factor in
vaccination. (Ex. A, p. 4.) Given the differing areas of specialty, Dr. McCusker is better
qualified than either Dr. Waters or Dr. Miller to speak both to the immunology underlying
cytokine storms and SCLS as well as the immune response to vaccination.

       In sum, there is inadequate evidence of record to demonstrate that petitioner’s
experts have presented a sound and reliable medical theory of causation implicating
any vaccine(s) in causing cytokine-mediated endothelial damage resulting in multiple
organ hemorrhaging. As explanation for how this may occur, petitioner advances two
conditions as proxy: a cytokine storm and/or SCLS. However, although active and
severe infections have been associated with both SCLS and cytokine storms, petitioner
has not demonstrated that vaccines have previously been implicated, or even could be
implicated, in the process of either SCLS or cytokine storms. Vaccines do elicit an
inflammatory cytokine response, but the above-discussed literature shows the ordinary
vaccine response to be mild and orders of magnitude less than what is seen in a
cytokine storm. Petitioners have not otherwise demonstrated that the mild response to
vaccination could lead to uncontrolled systemic cytokine response in the same manner
as an active infection.

                 ii. Althen Prong Two

        The second Althen prong requires proof of a logical sequence of cause and
effect connecting vaccination and injury, 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, 956 F.2d at 1148. However, medical records
and/or statements of a treating physicians 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. See 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 & Human 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”).

       Here, as discussed above, the evidence preponderates in favor of asphyxiation
as the cause of G.B.’s death as found by the investigating medical examiner, a cause of
death not consistent with petitioner’s theory. Additionally, petitioner has not
demonstrated by preponderant evidence that G.B.’s vaccinations can cause either a
cytokine storm or an SCLS-like hemorrhagic injury. These findings are fundamentally at
odds with any showing that G.B.’s vaccinations did cause his death as required under
Althen prong two. However, there are also additional significant reasons why petitioner
would be unable to demonstrate a logical sequence of cause and effect showing G.B.’s
vaccinations to be the cause of his death even in the absence of these incompatible
findings.

                                            28
                 1. G.B.’s post vaccination presentation does not indicate excessive
                    cytokine reaction.

        Initially, Dr. Waters opined that G.B. had in fact suffered a “cytokine storm.” (Ex.
12, pp. 8-10.) However, Dr. McCusker explains that a “cytokine storm” is a rare
condition that has been described in specific disease states. (Ex. A, p. 5.) Inflammation
associated with a cytokine storm begins at a local site and spreads throughout the body
via systemic circulation. (Ex. 18 at 4.) The hallmarks of acute inflammation include
rubor (redness), tumor (swelling or edema), calor (heat), dolor (pain), and “functio laesa”
(loss of function). (Id.) According to Dr. McCusker, a cytokine storm constitutes a
severe illness including not merely unrelenting irritability, but also rash, high fever, and
respiratory stress. (Ex. A, p. 6.) Those suffering a cytokine storm are “profoundly ill.”
(Id.) According to Dr. McCusker, this does not describe G.B.’s presentation prior to his
death. (Id.) Dr. Miller likewise agrees on petitioner’s behalf that a cytokine storm is not
a useful concept in this case. He notes that “[t]his is not a prototypical case of ‘cytokine
storm,’ a term used to describe fatal or near-fatal events in the setting of severe
infection with, usually, septicemia, which is clearly not the case here.” (Ex. 22, p. 8.)
Thus, in her supplemental report Dr. Waters ultimately suggests she was relying on an
increase in cytokines regardless of “whether or not there was clinical or pathological
evidence of an actual ‘cytokine storm.’” (Ex. 23, p. 4.) She does not, however, explain
on what basis G.B.’s presentation would otherwise be consistent with a systemic
cytokine response.

       Dr. Miller also initially relied on petitioner’s report that post-vaccination G.B. was
not aroused once he fell asleep, demonstrating “something more than normal sleep,” as
well as a persistent refusal to feed. (Ex. 22, p. 7 (citing Ex. 3).) Dr. Miller stressed this
as “continuously abnormal behavior of the child from the time of vaccination until death.”
(Id.) He acknowledged, however, that fussiness following a needle stick is common for
an infant and that he cannot say that what petitioner described constituted a coma. (Id.
at 6-7.) After being asked by the previously presiding special master to explain the
importance of petitioner’s description of G.B.’s post-vaccination behavior, Dr. Miller
indicates that the behavior is “of some importance,” but nonetheless explains that:

       the interpretation of the autopsy findings and my conclusions as to their
       most likely cause, and thus the cause of death, would not change if I was
       told that the symptoms and signs reported by the mother were not, in fact,
       present. Since the bulk of my conclusions are from the autopsy and not
       from the history, very little in my report would change other than to take
       away the recitation of symptoms and signs which the mother alleged the
       child exhibited.

(Ex. 24.)

       For purposes of this decision, I accept as accurate petitioner’s recollection of
G.B.’s behavior on March 12, and 13, 2014. (Ex. 3.) However, even accepting his
reported behavior as abnormal for him, the behaviors described are non-specific and

                                             29
Dr. Miller acknowledges the difficulty in drawing medical conclusions from these reports
in the absence of a medical exam. (Ex. 22, pp. 6-7; see also Ex. C, p. 6.) Ultimately,
petitioner describes G.B. as unusually sleepy, unusually fussy (“beyond fussy” and
“miserable”), crying, and uninterested in feeding. (Ex. 3, p. 2.) These behaviors were
concerning enough that petitioner contemplated contacting G.B.’s pediatrician, but not
so concerning that petitioner sought emergency care. (Id.) Again, Dr. McCusker
stresses the absence of any indication of fever or rash that would indicate cytokine
activation. (Ex. A, pp. 5-6.) She also stresses that excessive cytokine activation would
have resulted in progressive illness, including high fever and respiratory distress, which
is not the presentation described by petitioner. (Id.) Dr. Miller also acknowledges that
G.B. had no clinical signs or autopsy evidence of anaphylaxis. (Ex. 22, p. 7.)
Moreover, a case series of six pediatric cases of SCLS filed by petitioner showed that
all six children experienced flulike prodrome that consisted not merely of lethargy, but
also variously included nasal inflammation (coryzal symptoms), leg or abdominal pain,
fever, vomiting, periorbital swelling and/or headache, swelling, and in some instances
diarrhea or cough, later leading in most instances to edema and/or shock. (Hsu, et al.,
supra, at Ex. 37, p. 4 (Table 1).) G.B.’s presentation does not suggest any flulike
prodrome comparable to what was documented among the pediatric SCLS subjects.
Accordingly, there is not preponderant evidence that G.B.’s clinical presentation prior to
his death was consistent with petitioner’s theory of causation.

                    2. G.B.’s autopsy results do not indicate a SCLS-like condition.

        Dr. Miller has expressed general agreement with the observations of Dr. Rostad,
who conducted an independent review of petitioner’s autopsy for petitioner, and
stresses the severe congestion and hemorrhaging in multiple organs beyond the lungs
first noted by Dr. Rostad. (Ex. 22, p. 4.) Specifically, Dr. Miller notes congestion and
petechial hemorrhaging in the kidneys, adrenal glands, and medulla. (Id.) He describes
these as “not typical” for SIDS. (Id.) He also notes “frank” hemorrhage in the lungs,
more than could be attributed to post-mortem spillage, as well as severe congestion at
the periphery of the hepatic lobules of the liver. (Id. at 4-5.) According to Dr. Miller,
these are the findings that support the presence of a microvascular bleeding disorder.
(Id. at 5.) There are two significant reasons why Dr. Miller’s opinion is unpersuasive.

         First, Dr. Vargas explains that G.B.’s post-mortem findings are not as atypical as
Dr. Miller suggests. The hemorrhaging evidenced in G.B.’s lungs is consistent with
trauma from cardiopulmonary resuscitation. (Ex. OO, p. 4.) The blood vessels in the
lungs are especially fragile following hypoxia and death. (Id.) In contrast, SCLS is
characterized by proteinaceous fluid and alveolar damage. (Id.) Dr. Vargas further
indicates that there is a lack of evidence of inflammation or hemosiderosis 30 to suggest
that any of the bleeding happened prior to resuscitation. (Id.) Dr. Vargas additionally
cites literature demonstrating that 40% of SIDS cases have adrenal congestion and 3%
have adrenal hemorrhage. (Ex. OO, p. 5 (citing Valdes-Dapena, et al., Histopathology
Atlas for the Sudden Infant Death Syndrome, Findings derived from the National

30Hemosiderosis is “a focal or general increase in tissue iron stores without associated tissue damage.”
(Dorland’s, 33rd ed., p. 833.)

                                                   30
Institute of Child Health and Human Development Cooperative Epidemiological Study of
Sudden Infant Death Syndrome (SIDS) Risk Factors, 1993 (Ex. QQ).) Kidney
congestion is seen in 26% of SIDS cases. (Vadles-Dapena, et al., supra, at Ex. QQ, p.
9.) Twenty-eight percent of SIDS cases have congestion evidenced in the brain while
17% show perivascular hemorrhage in the brain and 16% have petechiae in the brain.
(Id.) Citing a textbook example of a normal post-mortem liver (Id. at p. 3), Dr. Vargas
disagrees that G.B.’s liver demonstrated congestion. (Ex. OO, p. 5.) For these
reasons, Dr. Vargas indicates that there is no reason for Dr. Miller to even posit a
pathologic bleeding disorder as the cause of death. (Id.) Indeed, despite noting similar
observations as those raised by Dr. Miller, Dr. Rostad concurred with Dr. Kohlmeier in
that he found the findings overall to be not specific and potentially explainable by
asphyxia. (Ex. 5, p. 1.)

        Second, respondent’s experts are persuasive in indicating that G.B.’s autopsy on
the whole is not consistent with an SCLS-like presentation. As the literature filed by
petitioner demonstrates, the “leakage” typically associated with SCLS is of plasma.
(E.g., Kawabe, et al., supra, at Ex. 36, p. 2 (noting SCLS to be characterized by
“recurrent episodes of generalized edema and hypovolemic shock.”); Kulihova et al.,
supra, at Ex. 38, p. 1 (noting SCLS to be “characterized by episodes of vascular
collapse and plasma extravasation, which may lead to multiple organ failure.”).)
Accordingly, Drs. Vargas and McCusker both explain that SCLS first and foremost
presents with edema rather than hemorrhage as suggested by Dr. Miller; however, no
edema was present upon G.B.’s autopsy. (Ex. NN, pp. 3-4; Ex. OO, p. 4.) Dr. Miller
indicates that “[s]ome cases of this syndrome have associated hemorrhages, not just
leakage of plasma,” but this explanation acknowledges hemorrhages to be a less
common manifestation of SCLS while also providing no support for the idea that SCLS
could be evidenced by hemorrhaging in the absence of edema or other indicators of
SCLS. (Ex. 22, p. 8.) Dr. McCusker in particular stresses that “the pathology of
‘visceral petechial hemorrhagic process’ described by Petitioners’ [sic] Expert has never
been described as an isolated effect of cytokine activation.” (Ex. NN, p. 4 (emphasis
original).)

                iii. Althen Prong Three

        The third Althen prong requires establishing a “proximate temporal relationship”
between the vaccination and the injury alleged. Althen, 418 F.3d at 1278. 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 & Human Servs.,
539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what is a medically
acceptable timeframe must also coincide with the theory of how the relevant vaccine
can cause an injury (Althen prong one's requirement). Id.; Shapiro v. Sec'y of Health &
Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. den'd after remand, 105 Fed. Cl.
353 (2012), aff'd mem., 503 Fed. Appx. 952 (Fed. Cir. 2013); Koehn v. Sec'y of Health
& Human Servs., No. 11–355V, 2013 WL 3214877 at *26 (Fed. Cl. Spec. Mstr. May 30,

                                           31
2013), mot. for review den'd (Fed. Cl. Dec. 3, 2013), aff'd, 773 F.3d 1239 (Fed. Cir.
2014).

        Petitioner argues that cytokine levels peak between 24-48 hours after
vaccination. (Ex. 22 at 7-8.) She asserts that because G.B. died within 24 hours of
vaccination, his adverse reaction and death fit within an appropriate timeframe for a
diffuse systemic cytokine-mediated event leading to endothelial dysfunction and
resulting in hemorrhage and congestion of the organs and subsequent death. (ECF No.
51, pp. 20-21.) Importantly, however, while Dr. McCusker filed literature suggesting that
a cytokine storm can in general occur in as little as 90 minutes, it is less clear that the
specific type of capillary leak that petitioner hypothesizes occurs so quickly. The timing
of peak cytokine levels is not necessarily equivalent to the time over which capillary leak
and hemorrhage manifest.

        Among the six cytokine storm patients described in Suntharalingam, et al., most
did not experience symptoms comparable to the capillary leak and hemorrhage
hypothesized by petitioner. (See Ex. M, pp. 6-8.) Two patients did experience
increased peripheral vascular permeability, but that presentation is described as
occurring subsequent to 48 hours. (Id. at 8.) Moreover, Dr. Waters cites dengue fever
as a relevant analogy given that hemorrhagic fever is known to be associated with
SCLS. The literature she filed with respect to cytokine storms indicated that the
increased capillary permeability seen in dengue fever typically occurs after between four
to six days of illness. (Tisoncik, et al., supra, at Ex. 18, p. 11.) In the single case report
of an infant death related to SCLS filed by petitioner, after onset of SCLS the infant
experienced a fourteen-day period of no improvement before multiple organ dysfunction
subsequently became fatal on the 27th day of life. (Kulihova, et al., supra, at Ex. 38, p.
2.) Although treatments were attempted during that period, massive capillary leak
progressed and there was no recovery stage observed during the patient’s life. (Id.) In
Hsu, et al, four out of six pediatric subjects presented with shock and/or edema after
experiencing at least 48 hours of prodromal symptoms. (See Ex. 37, pp. 2-3.) All of this
raises a question as to whether the mere fact that cytokine response is generally known
to occur rapidly is sufficient to explain a death by capillary leak and hemorrhage within
24 hours of an immune stimulus, especially in the absence of significant prodromal
symptoms.

        Both Dr. Miller and Dr. Waters are correct in noting that G.B.’s tragic death
occurred within a relatively short time period after his vaccination. However, the
significance of the temporal relationship must be tied to a reasonable theory of how the
vaccines could have caused the death and then logically how they did cause the death.
See Grant, 956 F.2d at 1144. A temporal relationship by itself is not sufficient to
establish causation, even though it may reinforce a reasonable theory and logical
explanation. See Langland v. Sec’y of Health & Human Servs., 109 Fed. Cl. 421 (2013).
In this case, neither a persuasive and reliable theory nor a logical explanation of cause
and effect were provided, leaving the potential temporal relationship standing alone.
Moreover, even the significance of that purported temporal relationship remains unclear
on this record. Accordingly, petitioner has failed to prove prong three of the Althen test.

                                             32
           c. Sudden Infant Death Syndrome Does Not Itself Otherwise Support
              Vaccine-Causation

       Petitioner is not alleging that G.B. died of SIDS. (ECF No. 51, p. 11.) And,
indeed, Dr. Miller opines on petitioner’s behalf that, while the risk factors that are typical
in SIDS cases would statistically make SIDS the most likely scenario in this case, the
lack of histopathological abnormalities of G.B.’s medulla and the presence of the
marked congestion and hemorrhage seen in multiple organs argue against this
conclusion. (Ex. 22 at 5-6.) He therefore concludes that “this case does not fit the most
common SIDS scenarios, vaccinations or no vaccinations (or at least as far as the
autopsy evidence permits, it does not fit).” (Id. at 6.)

        However, at the conclusion of his initial report, Dr. Miller suggests that his opinion
is further supported by a parallel between his opinion in this case and his opinion in
prior SIDS cases. (Ex. 22, p. 8.) Specifically, he states that:

        The occurrence of this syndrome, mediated by cytokines, following onset of
        an otherwise not life-threatening upper respiratory infection, suggests a
        parallel with the association of otherwise trivial upper respiratory infections
        with other cases of SIDS in which the pathogenesis is believed to involve
        peripherally generated cytokines interacting with developmentally defective
        medullary respiratory control systems . . .

(Id.)

       The import of this statement appears to be that, notwithstanding that Dr. Miller
does not opine that G.B. experienced SIDS, he nonetheless believes that the Kinney or
Triple Risk Model of SIDS helps to explain why otherwise safe levels of cytokine activity
could lead to death. Dr. Waters additionally indicates that in her view “[i]t is likely” that
some cases now classified as SIDS are “caused by immunizations, which are given in
quantity around the time these deaths tend to occur: 1-6 months of age.” (Ex. 12 at 7.)

       Petitioner’s specific theory in this case of how vaccination may have led to G.B.’s
death is addressed separately above. Here I note in the interest of completeness that,
even if petitioner was correct that G.B.’s death was better classified as SIDS rather than
asphyxiation, it would still not be the case that the multifactorial SIDS concept supports
any role for G.B.’s vaccinations in causing his death.

       There have been a significant number of prior cases in this Program that have
addressed allegations that one or more childhood vaccines caused or contributed to a
SIDS-labeled death. Generally, such cases have been dismissed by the presiding
special masters for insufficient evidence that any vaccine played a causal role in the
death. 31 In some instances, the parties have litigated whether SIDS presents an

 See, e.g., Olasvicky v. Sec’y of Health & Human Servs., No. 17-1806V, 2019 WL 2881009 (Fed. Cl.
31

Spec. Mstr. June 4, 2019); Nunez v. Sec’y of Health & Human Servs., No. 14-863V, 2019 WL 2462667

                                                33
alternative cause of what petitioners otherwise alleged to have been a vaccine-caused
death. See, e.g., Doe/11 v. Sec’y of Health & Human Servs., 601 F.3d 1349, 1351
(Fed. Cir. 2010) (holding that “the special master did not commit legal error in
considering evidence of SIDS, an allegedly alternative cause. Nothing in the Vaccine
Act prohibits the government from presenting evidence that the petitioner's injury was
due to “factors unrelated” to the vaccine (here, SIDS).”). However, many of these prior
cases have directly addressed at length allegations that one or more vaccines directly
caused or contributed to a child’s death within the framework of SIDS. In these prior
decisions special masters generally found that attempts to establish vaccination as an
exogenous stressor under the accepted Triple Risk (or Kinney) Model of SIDS were
unpersuasive. See, e.g., Jewell, 2016 WL 5404165 at *13; Copenhaver, 2016 WL
3456436 at *12-13; Lord, 2016 WL 806818 at *14; Cozart, 2015 WL 6746616 at *13.
Additionally, the Federal Circuit has twice considered, and rejected, Dr. Miller’s causal
theory linking vaccinations to SIDS via the Triple Risk Model. Boatmon, 941 F.3d at
1351; Nunez v. Sec'y of Health & Human Servs., 825 F. App'x 816 (Fed. Cir. 2020). I
have also addressed the significance of these prior decisions and the question of
whether vaccines contribute to the Triple Risk Model of SIDS as exogenous stressors in
two prior cases. Downing-Powers v. Sec’y of Health & Human Servs., No. 15-1043V,
2020 WL 4197303 (Fed. Cl. Spec. Mstr. June 2, 2020); Brunson v. Secretary of Health
& Human Servs., No. 17-530V, 2020 WL 5755502 (Fed. Cl. Spec. Mstr. Sept. 3, 2020).

       Several significant short-comings have prevented petitioners from relying on the
Kinney or Triple Risk Model as providing a basis for supposing under Althen prong one
that vaccination could play a role in SIDS-type deaths. The Federal Circuit explained in
Boatmon that “outside of Vaccine Act litigation, vaccinations have not been identified as
an exogenous stressor for SIDS.” Boatmon, 941 F.3d at 1360. The Federal Circuit
noted that petitioners’ “extension of the Triple Risk Model to include vaccination-induced
cytokine activity in the list of exogenous stressors” was based on “nothing more than the
assertion of [petitioner’s expert] Dr. Miller.” Id. at 1361-62. As I explained in Downing-
Powers, at least two serious obstacles remain in Dr. Miller’s prior ipse dixit effort to

(Fed. Cl. Spec. Mstr. Mar. 29, 2019), review denied 144 Fed. Cl. 540 (2019); Frady v. Sec’y of Health &
Human Servs., No. 16-148V, 2017 WL 5379391 (Fed. Cl. Spec. Mstr. Sept. 20, 2017); Pelton v. Sec’y of
Health & Human Servs., No. 14-674V, 2017 WL 1101767 (Fed. Cl. Spec. Mstr. Feb. 27, 2017); Jewell v.
Sec'y of Health & Human Servs., No. 11-138V, 2016 WL 5404165 (Fed. Cl. Spec. Mstr. Aug. 29, 2016);
Copenhaver v. Sec'y of Health & Human Servs., No. 13-1002V, 2016 WL 3456436 (Fed. Cl. Spec. Mstr.
May 31, 2016), review denied, 129 Fed. Cl. 176 (2016); Lord v. Sec'y of Health & Human Servs., No. 12-
255V, 2016 WL 806818 (Fed. Cl. Spec. Mstr. Feb. 9, 2016); Cozart v. Sec'y of Health & Human Servs.,
No. 00-590V, 2015 WL 6746616 (Fed. Cl. Spec. Mstr. Oct. 15, 2015), review denied, 126 Fed. Cl. 488
(2016); Waterman v. Sec’y of Health & Human Servs., No. 13-960V, 2015 WL 4481244 (Fed. Cl. Spec.
Mstr. June 30, 2015), review denied 123 Fed. Cl. 564 (2015); Sanchez v. Sec’y of Health & Human
Servs., No. 11-651V, 2013 WL 4476750 (Fed. Cl. Spec. Mstr. Jul. 26, 2013); Bigbee v. Sec’y of Health &
Human Servs., No. 06-663V, 2012 WL 1237759 (Fed. Cl. Spec. Mstr. Mar. 22, 2012); Nordwall v. Sec’y of
Health & Human Servs., No. 05-123V, 2008 WL 857661 (Fed. Cl. Spec. Mstr. Feb. 19, 2008); Doe/11 v.
Sec’y of Health & Human Servs., 2008 WL 649065 (Fed. Cl. Spec. Mstr. Jan. 31, 2008); Heller v. Sec’y of
Health & Human Servs., No. 96-797V, 1998 WL 408612 (Fed. Cl. Spec. Mstr. June 22, 1998); but see
Boatmon v. Sec’y of Health & Human Servs., No. 13-611V, 2017 WL 3432329 (Fed. Cl. July 10, 2017),
review granted, decision rev'd, 138 Fed. Cl. 566 (2018), aff'd on other grounds, 941 F.3d 1351 (Fed. Cir.
2019).

                                                   34
connect vaccination to that SIDS model. Studies seeking out a possible correlation
between vaccinations and SIDS have not on the whole supported any association
between the two and the evidence relied upon by Dr. Miller in linking peripheral cytokine
response to vaccination to the serotoninergic network implicated by the Triple Risk
Model is also very weak. 2020 WL 4197303 at *11-15. Thus, Dr. Miller’s ipse dixit
extension of the Triple Risk Model, which he himself previously characterized as merely
plausible, has been considered unreliable.

        Here, neither Dr. Waters nor Dr. Miller has provided information that would
resolve these deficiencies. In suggesting that some SIDS cases may be vaccine-
related, Dr. Waters cites a single study suggesting that infant mortality rates correlate
with the number of vaccines recommended in developed countries. (Ex. 12, p. 7 citing
Miller, Neil Z., and Gary S. Goldman, Infant mortality rates regressed against number of
vaccine doses routinely given: Is there a biochemical or synergistic toxicity?, 30(9)
Human and Experimental Toxicology 1420-28 (2011) (Ex. 16).) Importantly, however,
this study examines only the overall infant mortality rate for each country against the
number of vaccine doses included in the childhood immunization schedule of that
country. (Miller and Goldman, supra, at Ex. 16, p. 1.) The study authors caution that a
limitation of their study is that they did not adjust for national vaccine coverage rates
and further acknowledge that the study is susceptible to ecological bias, meaning that
“without additional data we do not know whether it is the vaccinated or unvaccinated
infants who are dying in infancy at higher rates.” 32 (Id. at 7-8.) Additionally, with
respect to his separate cytokine theory discussed above, Dr. Miller’s opinion continues
to be premised on the same Kashiwagi article (see Kashiwagi, et al., supra, at Ex. 31),
that I have previously discussed as being inadequate to demonstrate that a peripheral
cytokine reaction to vaccination would affect the central nervous system in a manner
consistent with the Triple Risk Model. Downing-Powers, 2020 WL 4197303, at *13;
Brunson, 2020 WL 5755502, at *13. No other evidence of record in this case speaks to
the issues explained by prior decisions with respect to a theory of causation based on
the Triple Risk Model. 33

32 Additionally, as in prior cases, Dr. McCusker offers competing studies that she indicates demonstrate
that there is no relationship between vaccination and SIDS. (See Ex. A, p. 9 citing Traversa, et al., supra,
at Ex. EE; Venneman, et al., supra, at Ex. FF; Kuhnert, et al., supra, at Ex. GG).)
33 Special masters reasonably draw upon their experience in resolving Vaccine Act claims. Doe v. Sec’y
of Health & Human Servs., 76 Fed. Cl. 328, 338–39 (2007) (“[o]ne reason that proceedings are more
expeditious in the hands of special masters is that the special masters have the expertise and experience
to know the type of information that is most probative of a claim”). Nonetheless, special masters are not
bound by the prior decisions of other special masters. Hanlon v. Sec’y of Health & Human Servs., 40
Fed. Cl. 625, 630 (1998). In contrast, Federal Circuit rulings concerning legal issues are binding on
special masters. Guillory v. Sec’y of Health & Human Servs., 59 Fed. Cl. 121, 124 (2003), aff’d 104 F.
Appx. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Human Servs., No. 13-159V, 2014 WL
504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014). However, the Federal Circuit has also stressed
that “[c]ausation in fact under the Vaccine Act is ... based on the circumstances of the particular case.”
Boatmon, 941 F.3d at 1358-59 (quoting Knudsen, 35 F.3d at 548). Accordingly, Federal Circuit
precedents do not automatically control the outcome of subsequent cases even when they involve the
same injury. See, e.g., Sanchez v. Sec’y of Health & Human Servs., 809 Fed. Appx. 843, 851-52 (Fed.
Cir. 2020) (citing back to a prior Federal Circuit holding in Paluck v. Secretary of Health & Human
Services involving the same injury and noting that “while there are substantial parallels between this case

                                                     35
       Also significant is that a key reason that Dr. Miller does not opine that G.B.
suffered SIDS was his observation that:

        Of particular note for a death in which at least some circumstances suggest
        SIDS, the medulla sections document a robust acruate nucleus on the
        ventral surface of each medullary phyramd (important because in some
        SIDS cases this nucleus is absent or hypolastic, and this is thought to play
        an important role in the pathophysiology of SIDS deaths in such cases).

(Ex. 22, p. 5.)

        As has been explained in prior cases, the type of medullary defect described by
Dr. Miller as important to the pathophysiology of SIDS (and absent in this case) is the
basis for his previously presented hypothesis that post-vaccination cytokines could play
a causal role in SIDS under the Triple Risk Model. See, e.g. Boatmon, 941 F.3d at 1356
(explaining that “[a]ccording to Dr. Miller's theory, ‘[w]hen the vaccines are administered
in the presence of the defects in the medulla, during the critical developmental period,
they are likely to have a similar effect as mild infection that may cause a failure of the
medullary response system and ultimately a death.’”) This also appears by extension
to be his basis for supposing that an association between trivial infections and SIDS
could be relevant to the different cytokine theory he presents in this case. However,
even assuming the medullary defect was consistent with Dr. Miller’s theory, 34 the
Federal Circuit in Boatmon held that it was an abuse of discretion for the special master
to rely for purposes of Althen prong two on the statistical probability of such a defect in
the absence of any confirmatory evidence. 941 F.3d at 1362. Here, evidence of the
defect is not merely lacking. Dr. Miller has confirmed this defect is actually absent.
Accordingly, Dr. Miller has no basis for invoking a defective medullary respiratory
control system in seeking to explain how G.B. could have been fatally susceptible to an
otherwise “usual” post-vaccination cytokine response. (Ex. 22, p. 8.) Thus, even if I
were to accept Dr. Miller’s parallel as evidence supporting his theory under Althen prong
one (which I do not), the absence of a medullary defect would then be fatal to
petitioner’s claim on Althen prong two. Accordingly, a finding that G.B. experienced
SIDS rather than asphyxiation would not lend any further support to petitioner’s claim.

and Paluck, the differences between the two cases are such that the outcome of this case is not dictated
by Paluck.”).

34 The Federal Circuit in Nunez held that it was “logical and reasonable” for the special master to

conclude that the presence of a medullary defect is contrary to Dr. Miller’s theory that cytokines can affect
the medullary serotonin system. 825 Fed. Appx. at 820. This obviously raises a further question
regarding the specifics of Dr. Miller’s reliance on the Triple Risk Model; however, it is unnecessary to
reach that question in this case.

                                                     36
            d. Respondent’s Contention of an Additional Factor Unrelated to
               Vaccination.

       In the interest of completeness, I note that in addition to all of the above,
respondent’s pathology expert, Dr. Vargas, additionally questioned whether G.B.’s
death might be explained by hyperinsulinemia hypoglycemia due to congenital
pancreatic islet cell hyperplasia. (Ex. C, p. 6.) Petitioner’s experts disagree. (Ex. 22, p.
4; Ex. 23, p. 3.) However, for all the reasons discussed above, the burden of proof did
not shift to respondent to demonstrate any factor unrelated to vaccination. § 300aa-
13(a)(1)(B). Accordingly, I do not reach the question of whether there is preponderant
evidence that G.B. suffered fatal hypoglycemia as suggested by Dr. Vargas.

     VI.    Conclusion

       G.B.’s death is tragic and a profound loss for his family. Petitioner has my
deepest sympathy. However, upon my review of petitioner’s claim, petitioner has not
established by preponderant evidence that any of G.B.’s vaccinations caused his death.
Accordingly, this petition is DISMISSED. 35

IT IS SO ORDERED.

                                                           s/Daniel T. Horner
                                                           Daniel T. Horner
                                                           Special Master

35In the absence of a timely-filed motion for review of this Decision, the Clerk of the Court shall enter
judgment accordingly.

                                                     37