Ahlum v. Secretary of Health and Human Services

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 12-763V
Filed: August 16, 2018
To be Published

*************************************
DOUG AHLUM and KARI AHLUM, *
Parents and Next of Kin to T.A., *
*
Petitioners, *
* Measles, mumps, rubella (“MMR”)
v. * vaccine; systemic inflammatory response
* syndrome (“SIRS”); double amputation.
SECRETARY OF HEALTH *
AND HUMAN SERVICES, *
*
Respondent. *
*
*************************************
Andrew D. Downing, Phoenix, AZ, for petitioners.
Debra A. Filteau Begley, Washington, DC, for respondent.

MILLMAN, Special Master

RULING ON ENTITLEMENT 1

On November 9, 2012, petitioners filed a petition under the National Childhood Vaccine
Injury Act, 42 U.S.C. § 300aa-10-34 (2012), alleging that measles, mumps, rubella (“MMR”)
vaccine administered to their son T.A. on August 11, 2011 caused him a Table encephalopathy.
Pet. Preamble. T.A. was three years old at the time. Eleven days after MMR vaccination, T.A.
was tired. Id. at ¶ 4. The following day, he had a 100-degree fever. Id. Thirteen days after his
MMR vaccination, T.A. saw his pediatrician with a rash. Id. at ¶ 5. His red platelet count was
low. That evening, T.A.’s condition worsened, his fever spiked at 103 degrees, and he had
constant vomiting and diarrhea. Id. On August 25, 2011, 14 days after MMR vaccination, T.A.
returned to his pediatrician. Id. at 6. His red platelet count was even lower and his white blood
cells were very high. Id. He was put on antibiotics and hospitalized. His legs were amputated,
at first below the knees, and then above the knees, to save his life. Petitioners’ affidavits are
consistent with their petition. Exs. 1 and 2.

1
Vaccine Rule 18(b) states that all decisions of the special masters will be made available to the public unless they
contain trade secrets or commercial or financial information that is privileged and confidential, or medical or similar
information whose disclosure would constitute a clearly unwarranted invasion of privacy. When such a decision is
filed, petitioner has 14 days to identify and move to redact such information prior to the document’s enclosure. If
the special master, upon review, agrees that the identified material fits within the banned categories listed above, the
special master shall redact such material from public access.
 On March 7, 2013, the undersigned held the first telephonic status conference with
counsel. Petitioners’ counsel said respondent was amenable to settlement and petitioners had
recently made a demand. Respondent’s counsel stated respondent was trying to put a value on
the case. Because the case was complex, respondent’s counsel had hired a life care planner.
Petitioners’ counsel said that petitioners participated in Qualchoice in Arkansas. They did not
have coverage for a period of time. T.A. was enrolled in ARKids, which is a type of Medicaid.
Petitioners had very little unreimbursable medical expenses. Petitioners’ counsel provided an
itemized Medicaid lien to respondent. T.A.’s medical treatment was mostly at Shriner’s which
does not bill for services.

One year later, on March 7, 2014, the parties still had not settled and respondent
requested petitioners file expert reports. Both parties subsequently filed expert reports.

On May 13, 2014, petitioner filed an amended petition, alleging a Table injury of
encephalopathy and a Table injury of thrombocytopenic purpura leading to systemic
inflammatory response syndrome (“SIRS”). Am. Pet. Preamble and ¶ 11.

One year later, on March 31, 2015, respondent’s counsel said respondent might possibly
settle for less than it would cost respondent to try the case. Petitioners’ counsel said he would
not recommend settling for less than costs. During a status conference on April 28, 2015,
petitioners’ counsel said his clients were interested in settling but wanted to know how far below
litigative risk that amount would be. Respondent’s counsel said she did not know if it made
sense to settle. By June 3, 2015, it was apparent the parties would not settle.

The undersigned held a three-day hearing from March 1-3, 2016. On March 4, 2016, the
undersigned issued an Order explaining the issues and encouraging settlement. During a status
conference held on May 31, 2016, respondent’s counsel said respondent was not amenable to
settlement.

After considering all the evidence, including the experts’ reports and medical literature
upon which the experts relied, and the testimony of the parents, T.A.’s pediatrician, and the
experts, the undersigned rules for petitioners on entitlement.

FACTS

Prevaccination Records

T.A. was born on March 10, 2008.

From July 25-30, 2008, T.A. was at Dell’s Children’s Medical Center of Central Texas
for acute lymphadenitis 2 with a Staphylococcus aureus infection. Med. recs. Ex. 13, at 1. T.A.

2
Lymphadenitis is inflammation of one or more lymph nodes.” DORLAND’S ILLUSTRATED MEDICAL DICTIONARY
325 (32nd ed. 2012) [hereinafter “Dorland’s”].
2
had presented with neck swelling and fever. Fluid collection was consistent with abscess. He
had incision and drainage on July 27, 2008 and was put on antibiotics. Id. at 4.

On August 30, 2008, T.A. was taken to Mercy Hospital Northwest because of a neck
abscess. Med. recs. Ex. 5, at 20. He was diagnosed with cellulitis and abscess of the neck. Id.
He was discharged on September 3, 2008. Id. at 25. T.A. had a similar problem a month before
in Austin and had to have an incision and drainage. Id. The current problem started less than
one week earlier with gradual onset. Id. Incision and drainage were performed on September 1,
2008. Id. at 31. The prior neck abscess reportedly grew Staphylococcus aureus. Id. No
organisms were detected with this neck abscess. Id. at 59.

On August 27, 2009, at 17 months, T.A.’s mother phoned the pediatrician to report that
T.A. had a rash on his feet and bottom since the day before. Med. recs. Ex. 12, at 1.

On June 22, 2011, T.A. saw Dr. L. Barry Allen, his pediatrician, for fever, vomiting, and
abdominal pain. Med. recs. Ex. 3, at 7. On physical examination, T.A. had possible early
pharyngitis. There was some exudate on his tonsils. He also possibly had early cellulitis 3 of his
eyes, 4 particularly his right eye. There was a scar over his right anterior cervical area from a
previous abscess. His white blood count (“wbc”) was normal. His platelet count was 144,000.
Hemoglobin and hematocrit were low at 10.5 and 29. Dr. Allen was concerned about
pharyngitis, possible early cellulitis. Id. Dr. Allen prescribed Augmentin 5 600 and Moxeza 6 eye
drops. Dr. Allen notes that T.A. had had anemia intermittently for at least three years. Id. The
blood count from a couple of years ago showed anemia with hematocrit of 28 or 29. Id. at 7-8.

Postvaccination Records

On August 11, 2011, T.A. saw Dr. Allen for his three-year-old well child examination.
Med. recs. Ex. 3, at 10. Dr. Allen wrote that T.A. had been doing well and had not had any
trouble up to the present time. T.A. received MMR vaccine. Id.; Ex. 4, at 1.

3
Cellulitis is “an acute, diffuse, spreading, edematous, suppurative inflammation of the deep subcutaneous tissues
and sometimes muscle, sometimes with absence formation. It is usually caused by infection of a wound, burn, or
other cutaneous lesion by bacteria, especially group A streptococci and Staphylococcus aureus, but it may also occur
in immunocompromised hosts or following erysipelas.” Dorland’s at 325. Erysipelas is “an acute superficial form
of cellulitis involving the dermal lymphatics, usually caused by infection with group A streptococci. Characteristics
include a peripherally spreading hot, bright red, edematous, brawny, infiltrated plaque with a circumscribed, raised,
indurated border.” Id. at 642.
4
Facial cellulitis is “cellultis affecting the face, sometimes produced by spread of infection from nearby or distant
foci. In children it is usually on just one cheek, and in adults it most often affects the neck; it may also occur around
the eyes. It is tender, bluish in color, and poorly demarcated, with an edematous border, and patients often have
fever, local pain, and bacteremia. Haemophilus influenzae type b, Group B streptococci, and Streptococcus
pneumoniae are etiologic agents in young children.” Dorland’s at 326.
5
Augmentin is “trademark for combination preparations of amoxicillin and clavulanate potassium.” Dorland’s at
179.
6
Moxeza is also known as moxifloxacin hydrochloride, used “in the treatment of bacterial exacerbation” of illnesses
caused by “gram-positive and gram-negative bacteria.” Dorland’s at 1184.
3
 On August 24, 2011, 13 days after MMR vaccination, T.A. returned to Dr. Allen with
fever. Med. recs. Ex. 3, at 11. The fever started the prior evening (August 23, 2011, 12 days
after MMR vaccination). T.A. had a rash with fever of 102 degrees. T.A. had a petechial 7 rash,
particularly on his neck and trunk. He had a macular 8 rash on his trunk as well. His tympanic
membranes were dull, but normal. His throat was injected without exudates. His neck was
supple, chest clear, abdomen soft, and his heart had a regular rhythm without murmurs. T.A.’s
wbc was 6,000. His platelet 9 count was 97,000. Dr. Allen prescribed Rocephin 10 750 mg
intramuscularly (“IM”) and would recheck T.A. on August 25, 2011, repeating his blood count
that day. Id. According to Dr. Allen’s lab results, T.A.’s wbc of 6,200 was within the normal
range of 6,000-17,000. Id. at 12. T.A.’s platelet count of 97,000 was below the normal range of
150,000-450,000. Id.

On August 25, 2011, T.A. returned to Dr. Allen. Id. at 14. T.A. had vomiting and
diarrhea during the night. On physical examination, Dr. Allen noted that T.A. was quite
lethargic, and at least 10 percent dehydrated. His rash had increased. T.A.’s white count rose
from 6,000 the day before to 20,000 that day. His neutrophil 11 count was 75% that day
compared to 71% the day before. His hemoglobin was 19.6 with a hematocrit of 51.5, whereas
the day before, his hemoglobin was 13 with a hematocrit of 35. T.A.’s platelet count that day
was 73,000, whereas the day before it was 97,000. Dr. Allen assessed T.A. as being extremely
dehydrated and toxic. He administered IV fluids and transferred him to the hospital for
admission. Id.

On August 25, 2011, at 11:45 a.m., T.A. was brought to Mercy Hospital Northwest.
Med. recs. Ex. 5, at 405. The history was decreased appetite, decreased activity, and fever. Id.

7
Petechia is “a pinpoint, nonraised, perfectly round, purplish red spot caused by intradermal or submucous
hemorrhage.” Dorland’s at 1422.
8
Macule is “a discolored skin lesion that is not elevated above the surface . . . .” Dorland’s at 1094. “The typical
[measles] rash consists of generalized maculopapular lesions that are at first discrete but gradually become
confluent, starting behind the ears and on the face and progressing rapidly down the trunk and onto the extremities.”
Id. at 1116. Atypical measles is “a severe form of measles occurring after . . . in some cases live attenuated measles
vaccine. It is characterized by fever, headache, myalgia, abdominal symptoms, and cough; this is followed by an
atypical rash that may be urticarial, vesicular, petechial, or maculopapular, is found on the wrists and ankles, spreads
to the palms, soles, and trunk, and later fades; there may be peripheral edema, interstitial pulmonary infiltrates, and
pleural effusion. Koplik spots are absent.” Id. “Being atypical, AMS [atypical measles syndrome] can be confused
with other entities including Rocky Mountain spotted fever, meningococcal infection, various types of pneumonia,
appendicitis, juvenile rheumatoid arthritis, etc.” Medical Definition of Atypical measles syndrome (AMS),
MEDICINENET, http://www.medicinenet.com/script/main/art.asp?articlekey=6619 (last visited July 19, 2018).
9
Platelet is “a disk-shaped structure, 2-4 µm in diameter, found in the blood of all mammals and chiefly known for
its role in blood coagulation. . . .” Dorland’s at 1459.
10
Rocephin is “trademark for a preparation of ceftriaxone sodium.” Dorland’s at 1651. Ceftriaxone sodium is “a
semisynthetic, ß-lactamase-resistant, broad-spectrum, third-generation cephalosporin effective against a wide range
of gram-positive and gram-negative bacteria; administered intravenously or intramuscularly.” Id. at 312.
11
Neutrophil is “a mature granular leukocyte that is polymorphonuclear (its nucleus having three to five lobes
connected by slender threads of chromatin, and cytoplasm containing fine granules); neutrophils have the properties
of chemotaxis, adherence to immune complexes, and phagocytosis.” Dorland’s at 1272. Leukocyte chemotaxis is
“the response of leukocytes to products formed during an immune response, whereas leukocytes are attracted to and
accumulate at the site of the reaction; it is part of the inflammatory response.” Id. at 341.
4
at 410. Dr. Allen accompanied T.A. at the bedside and an IV was started. Id. Following
stabilization, Arkansas Children’s Hospital was called and T.A. was air lifted there. Id. at 427.
Final diagnosis at Mercy Hospital Northwest was hyperglycemia, hyponatremia, ten percent
dehydration, acidosis, and probable sepsis. Id. at 428. T.A. was given dopamine for blood
pressure control and insulin. Id.

On August 26, 2011, Dr. Jose R. Romero did a consultation at Arkansas Children’s
Hospital. Med. recs. Ex. 7, at 473. The history was T.A. was in his usual state of health until
Monday, August 22, 2011, when he felt tired. Id. On Tuesday, August 23, 2011, he woke with a
temperature of 100 degrees. His mother gave him Tylenol and, after a nap in the late morning or
early afternoon, his temperature was 104 degrees. On Wednesday, August 24, 2011, T.A. saw
his pediatrician Dr. Allen at about 9:00 a.m. at which time his fever was 103 degrees. T.A. had a
non-pruritic, pinpoint rash on his upper shoulders, back and slightly on his chest. Id. Dr. Allen
told Dr. Romero that a blood culture was done, a nasopharyngeal swab was done, and a urine
culture was done, and these were negative. Id. T.A. was given a dose of ceftriazone (Rocephin)
and sent home. That evening, he vomited for an hour, slept fitfully, and developed diarrhea,
which had no blood in it. Id. On Thursday, August 25, 2011, T.A. returned to Dr. Allen with
lethargy. Id. at 474. Blood work showed an increased wbc. He was transferred immediately to
the emergency room. Blood culture was drawn, which was negative. His IgG was 204. His C4
was low. About two weeks ago, he had swelling in Beaver Lake, but no one else was ill. He had
tick exposure six weeks earlier. T.A. had a history of a separative lymphadenopathy in the neck
at four months of age, which was drained, and a second episode which recurred about one and
one-half months later, necessitating a second draining. Id. In addition he was at a fair and
petted animals. On physical examination, T.A. had gross edema in his head, eyes, neck, and
upper and lower extremities (and he was about to undergo dialysis). Id. T.A. had primarily a
truncal petechia with good capillary refill. Id. at 474-75. T.A. had anemia. Id. at 475. His
erythrocyte sedimentation rate (“ESR”) and C-reactive protein (“CRP”) were normal. His liver
enzymes were normal. His platelet count was 55,000. He had evidence of disseminated
intravascular coagulation (“DIC”). 12 Dr. Romero’s assessment was that T.A. had overwhelming
sepsis, 13 thrombocytopenia, 14 DIC, and renal failure, was on Vancomycin (an antibiotic)
although the level was low, and had low IgG, possibly hypogammaglobulinemia 15 or this could
be due to illness. Id. Dr. Romero recommended changing the Rocephin to cefepime (another
antibiotic), continuing Vancomycin, administering intravenous doxycycline (another antibiotic),
doing blood and urine cultures, taking a Rocky Mountain Spotted Fever (“RMSF”) titer, doing

12
Disseminated or diffuse intravascular coagulation is “a bleeding disorder characterized by abnormal reduction in
the elements involved in blood clotting due to their use in widespread intravascular clotting. It may be caused by
any of numerous disorders; in the late stages, it is marked by profuse hemorrhaging.” Dorland’s at 376.
13
Sepsis is “1. the presence in the blood or other tissues of pathogenic microorganisms or their toxins. 2.
septicemia.” Dorland’s at 1693.
14
Thrombocytopenia is “decrease in the number of platelets, such as in thrombocytopenic purpura.” Dorland’s at
1922.
15
Hypogammaglobulinemia is “abnormally low levels of all classes of immunoglobulins in the blood; . . . .”
Dorland’s at 901.
5
an Ehrlichia 16 polymerase chain reaction (“PCR”), and doing a Tularemia 17 titer. Id.

Also on August 26, 2011, Dr. Susan Demirel took a history and physical. Id. at 533.
T.A. was admitted to pediatric intensive care unit for shock. He had fever up to 102 degrees and
a rash. Overnight, he had persistent vomiting and diarrhea. He was dehydrated and significantly
more toxic appearing on the day of admission. The rash persisted. Chest x-ray showed a right
middle lobe infiltrate. Id. On physical examination, T.A. had prominent scleral edema in his left
eye. Id. at 534. His neck had adenopathy on the left. He had coarse breath sounds bilaterally
with decreased breath sounds on the right. Id. His abdomen was taut and distended. Id. at 535.
Dr. Demirel considered Kawasaki’s 18 as a consideration in the differential diagnosis. Id.

On August 27, 2011, Dr. Richard J. Jackson did a surgical consultation. Id. at 477. T.A.
had abdominal distension, possibly early abdominal compartment syndrome. 19 Dr. Jackson said
T.A. had developed systemic inflammatory response syndrome (“SIRS”) with diffuse capillary
leak with increasing abdominal distension. Id. The etiology was not identified. All cultures
were negative. T.A. remained thrombocytopenic. Id. Dr. Jackson decided not to perform
surgery as T.A.’s intra-abdominal hypertension/compartment syndrome was not significant. Id.
at 478.

Also on August 27, 2011, Dr. Mark J. Heulitt wrote a critical care medicine note. Id. at
486. T.A. had episodes of hypotension. The day before, he had some significant acidosis. 20 Id.
His input and output were misbalanced. Id. at 487. T.A. had low platelets of 21,000 that
morning. He continued with negative blood cultures and urine cultures. The antibiotics
cefepime, doxycycline, and vancomycin were all adjusted for T.A.’s renal failure.

16
Ehrlichia is “a genus of tick-borne bacteria. . . .” Dorland’s at 596. Tests for Ehrlichia, Staphylococcus aureus,
and Streptococcus pneumoniae were negative. Med. recs. Ex. 7, at 2239-41, 2274-75.
17
Tularemia is “a plaguelike, zoonotic disease caused by infection with the bacillus Francisella tularensis, whose
hosts include sheep and . . . rodents such as rabbits, squirrels, and muskrats. It is transmitted by the bites of
deerflies, fleas, and ticks . . . and by ingestion of contaminated food or water. [M]ost cases are characterized by
abrupt onset of fever, chills, weakness, headache, backache, and malaise.” Dorland’s at 1984.
18
Kawasaki disease is “a syndrome of unknown etiology, usually affecting infants and young children, associated
with vasculitis of the large coronary vessels and numerous other systemic signs, including fever, conjunctival
injection, changes of the oropharyngeal mucosa, cervical lymphadenopathy, and maculoerythematous skin eruption
that becomes confluent and bright red in a glove-and-sock distribution; the skin becomes indurated and edematous
and often desquamates from the fingers and toes.” Dorland’s at 537.
19
Compartment syndrome is “a condition in which increased tissue pressure in a confined anatomical space causes
decreased blood flow leading to ischemia and dysfunction of contained myoneural elements, marked by pain,
muscle weakness, sensory loss, and palpable tenseness in the involved compartment. Ischemia can lead to necrosis
resulting in permanent impairment of function.” Dorland’s at 1825.
20
Acidosis is “the accumulation of acid and hydrogen ions or depletion of the alkaline reserve (bicarbonate content)
in the blood and body tissues, resulting in a decrease in pH.” Dorland’s at 16.
6
Complement 21 studies and IgM 22 were low the day before. Id. Neurologically, T.A. was sedated
on Versed and Fentanyl. His Glasgow coma scores ranged from 3-6. Id.

On August 28, 2011, Dr. Heulitt wrote that T.A. was being managed for septic shock,
acute renal failure, and possible meningococcal septicemia, but overnight T.A. developed
demarcation in his lower extremities, bluing, and discoloration consistent with necrosis of the
skin and possible loss of those extremities. Id. at 489. He was started on Synthroid the day
before due to evidence of hypothyroidism. He was continued on mechanical ventilator support.
T.A. had bilateral chest tubes in place for pleural effusions, with increased densities in the left
lung. An echo cardiogram done the day before showed some left ventricular hypertrophy. He
was on continuous venovenous hemodiafiltration (“CVVHD”). Id. T.A.’s glucose that morning
was 229 and he was on an insulin infusion. Id. at 490. His wbc was 23,000. From an infectious
disease standpoint, all of T.A.’s cultures were negative. Dr. Heulitt was stopping T.A.’s
isolation that day. His Ehrlichia PCR, MRSA PCR, and staph pneumococcus PCR were all
negative. On examination that morning, T.A. had marked changes in his lower extremities with
blistering and further demarcation in his mid-calf area with the plan to get a formal burn
consultation to look at his wounds. Overall, T.A. remained critically ill, requiring numerous
medical interventions. Id.

Also on August 28, 2011, Burn Surgery was consulted due to discoloration of T.A.’s toes
and feet which had progressed to blisters with extension up to his ankles. Id. at 523. It was
determined that T.A. would need surgical intervention due to bilateral lower extremity limb
ischemia secondary to vasoconstriction with open wounds. Id.

On August 29, 2011, Dr. Ronald Sanders wrote a critical care medicine note stating T.A.
was being managed for four days for signs and symptoms consistent with septic shock, acute
renal failure and rhabdomyolysis. 23 Id. at 492. The nurses wrote that he was moving around a
little bit more and seemed to be responding to his loved ones. The infectious diseases specialist
said T.A.’s cultures showed no growth so far and his PCRs had not revealed any etiology for his
clinical picture. T.A. remained in acute renal failure. He remained critically ill and at high risk
of death, but he was trending in the right direction and his current clinical progression was
encouraging. Id.

21
The complement “pathway is initiated by binding of two antibody molecules to a multivalent antigen.” Dorland’s
at 394 (schematic representation). Complement “is now used to refer to the entire functionally related system
comprising at least 20 distinct serum proteins, their cellular receptors, and related regulatory proteins that is the
effector not only of immune cytolysis but also of other biologic functions including anaphylaxis, phagocytosis,
opsonization, and hemolysis.” Id. at 393.
22
IgM is “immunoglobulin M.” Dorland’s at 913. Immunoglobulin is “any of the structurally related glycoproteins
that function as antibodies, divided into five classes (IgM, IgG, IgA, IgD, and IgE) on the basis of structure and
biologic activity. … In addition to the effects produced solely by the binding of antigen by antibody, e.g., viral
neutralization or the inability of some bacteria to invade mucosal surfaces when coated by antibody, certain classes
of antibodies can trigger other processes when bound to antigen: IgM and IgG activate the classic complement
pathway. . . .” Id. at 919.
23
Rhabdomyolysis is “disintegration or dissolution of muscle, associated with excretion of myoglobin in the urine.”
Dorland’s at 1637.
7
 On September 1, 2011, Dr. Sanders wrote that T.A. had been successfully weaned off
vasopressor support. Id. at 495. Due to elevated creatinine phosphokinase (“CPK”) and the
condition of T.A.’s lower extremities, it was highly likely that T.A. was going to require bilateral
lower leg amputations. Id.

On September 2, 2011, Dr. Sanders wrote that T.A. was extubated the day before and was
off all vasopressors. Id. at 497. He was moving air equally well in both lung fields. His lower
extremities continued to be wrapped in sterile gauze. His lower extremities evidenced
gangrenous changes superficially and the Burn Service was watching him very closely. His
heart was normal. His abdomen was soft. He remained on broad spectrum antibiotics, including
vancomycin, cefepime, and doxycycline. Pediatric Infectious Diseases recommended stopping
the vancomycin that day. T.A. continued to make urine, but was not able to balance his input
and output, and remained on CVVHD. Dr. Sanders would discuss with the Renal Service how
much longer they would like to keep T.A. on CVVHD and when they planned to do intermittent
hemodialysis. T.A. remained critically ill, but was moving in the right direction. His wbc
remained elevated at 24,700. Id.

On September 3, 2011, Dr. M. Michele Moss wrote a critical care medicine note,
diagnosing T.A. with respiratory insufficiency, sepsis, and renal failure. Id. at 499. T.A.’s heart
rate increased to the 130s and 150s from the 90-100 range the day before. He was not febrile.
His eyes were somewhat sunken and his input and output remained equal to somewhat negative.
His lungs sounded clear. His lower extremities remained ischemic with wraps. His white count
was a little bit higher every day and some of that might be a leukemoid reaction, 24 although most
of the cells were actually lymphocytes. Id.

On September 4, 2011, Dr. Adnan T. Bhutta wrote a critical care medicine note,
diagnosing T.A. with septic shock, acute renal failure requiring CVVHD, and myositis 25 in the
lower extremity with associated skin ischemia. Id. at 501. The Burn Team said T.A.’s legs have
improved markedly. He was scheduled to go to the operating room for grafting. Id.

On September 5, 2011, Dr. Moss wrote that T.A. continued to show improvement. Id. at
503. T.A. was awake enough to ask for lemonade and was clearly thirsty. He was less shaky,
but remained on low-dose morphine infusion for pain. He was to go to the operating room the
next day for debridement 26 of his lower extremities. T.A. was tolerating full feeds and was
stooling. His liver function tests were improving. He had a fever that morning. Id.

24
A leukemoid reaction is “a peripheral blood picture resembling that of leukemia or indistinguishable from it on
the basis of morphologic appearance alone, with leukocytosis of varying degrees and increased numbers of
immature cells in circulation. It may be seen with infections such as tuberculosis, brucellosis, toxoplasmosis,
staphylococcal infections, and streptococcal infections; with inflammatory disorders such as glomerulonephritis,
rheumatoid arthritis, liver failure, and diabetic acidosis; with tumors and granulomatous infiltration of bone marrow;
and with intoxications such as eclampsia, severe burns, and mercury poisoning.” Dorland’s at 1600.
25
Myositis is “inflammation of a voluntary muscle. . . .” Dorland’s at 1225.
26
Debridement is “the removal of foreign material and devitalized or contaminated tissue from or adjacent to a
traumatic or infected lesion until surrounding healthy tissue is exposed.” Dorland’s at 473.
8
 On September 6, 2011, Dr. Anjay Khandelwal performed bilateral guillotine below-knee
amputations 27 on T.A. because of bilateral lower extremity limb ischemia secondary to
vasoconstriction with open wounds. Id. at 538. He had necrotic muscles of all three
compartments in the lower extremities. Id. He also had metabolic acidosis and needed to remain
intubated. Id. T.A. presented to Arkansas Children’s Hospital with evidence of sepsis. Id. In
order to perform perfusion and a blood pressure, he was started on vasopressors and
subsequently developed renal failure. Id. at 538-39. He developed significant vasoconstriction
and his vasculature clamped down, resulting in ischemia to his bilateral lower extremities. Id. at
539. When Surgery was consulted, T.A. had evidence of limb ischemia with some dry gangrene
of his toes and ischemic discoloration with blistering of his lower extremities. It was not evident
at the time that he had compartment syndrome. Id. On examination of the lower extremities, Dr.
Khandelwal noted T.A. had persistent gangrene of his toes. The dry gangrene and necrosis of his
feet had progressed and he had significantly dark, ischemic-dried gangrenous areas present on
his lower extremities, extending about ¾ proximally up his bilateral calves. Dr. Khandelwal
examined all three muscular compartments within the calf by performing a fasciotomy. 28 There
was minimal bulging of the muscle upon releasing the fascia. However, the muscle underneath
was dark and nonperfused. The muscle did not bleed and was not stimulated when Dr.
Khandelwal used a Bovie electrocautery. The muscle did not have just an ischemic appearance,
but almost a frankly necrotic appearance. There was no wet gangrene of infection. Upon
consultation with Dr. Sam Smith from Pediatric Surgery, they agreed on the need to amputate.
Id. Bilateral below-knee amputations were performed in hopes of salvaging the knees. Id. at
540. The tibia and fibula on both sides were transected using the saw. The doctors preserved as
much of the viable skin as they could. Hemostasis 29 was secured. Amputation sites were left as
guillotine amputations. Toward the end, T.A. became a little hypotensive with a bump up in his
acidosis. He was transferred back to pediatric intensive care unit intubated. Id.

On September 7, 2011, Dr. Stephen M. Schexnayder wrote a critical care medicine note.
Id. at 506. T.A. had hyperkalemia 30 after returning from the operating room from his bilateral
amputation the day before. CVVHD was started back overnight. He required some volume
resuscitation. He has had some ongoing hypotension. He was febrile overnight and vancomycin
and meropenem 31 were begun. They would keep T.A. intubated and mechanically ventilated.
Dr. Schexnayder diagnosed T.A. with hypotension and respiratory failure. Id.

On September 8, 2011, Dr. Schexnayder wrote that T.A. returned to the operating room

27
Guillotine amputation means “rapid amputation of a limb by a circular sweep of the knife and cut of the saw, the
entire cross-section being left open for dressing; done when primary closure of the stump is contraindicated, owing
to the possibility of recurrent or developing infection.” Dorland’s at 68.
28
Fasciotomy is a “surgical incision or transection of fascia, often performed to release pressure in compartment
syndrome.” Dorland’s at 685. Fascia is a sheet or band of fibrous tissue such as lies deep to the skin or forms an
investment for muscles and various other organs of the body.” Id. at 679.
29
Hemostasis means “arrest of bleeding.” Dorland’s at 843.
30
Hyperkalemia is “abnormally high potassium concentration in the blood, most often due to defective renal
excretion.” Dorland’s at 890.
31
Meropenem is “a broad-spectrum antibiotic of the carbapenem group, similar to imipenem in structure and
activity and used in the treatment of intra-abdominal infections and bacterial meningitis. . . .” Dorland’s at 1137.
9
that day for debridement of his extremities and to assess their viability. Id. at 507. His diagnosis
was sepsis with organ dysfunction. Id. Later that same day, Dr. Schexnayder wrote that T.A.
might have to be converted to bilateral above-knee amputations. Id. at 509. He was going to
request Immunology to assess T.A. because of the severe nature of illness with a negative culture
although he received IV antibiotics and this would be consistent with meningococcal infection.
Id.

On September 12, 2011, Dr. Khandelwal wrote a further operative note for bilateral lower
extremity limb ischemia secondary to sepsis and suspected Neisseria 32 meningitis, and status
post-bilateral guillotine below-the-knee amputations. Id. at 541. He performed bilateral above-
knee amputations. Id. T.A. had a complication of hypoxemia 33 requiring persistent intubation.
Id. On examination of T.A.’s stumps, Dr. Khandelwal found that the muscle was still
persistently necrotic over both lower extremities, thereby necessitating above-knee amputations.
Id. at 542. A fish-mouth incision was marked on both lower extremities above the knee with
attempts to preserve as much of the skin flap as possible as well as to preserve as much length in
the femur 34 as possible. On the right-hand side, Dr. Khandelwal made a skin incision with the
scalpel and carried it down through fat and subcutaneous tissue. For further dissection, he used
Bovie electrocautery. Dissection carried down through the muscular compartments. Once he
reached T.A.’s femur, Dr. Khandelwal used a periosteal elevator 35 to strip the periosteum from
the femur. At the beginning of the condyle, 36 Dr. Khandelwal transected the femur with the
bone saw. Id. On the left lower extremity, after making a similar fish-mouth incision, and
incising skin and fat, Dr. Khandelwal noted the quadriceps tendon was ischemic although some
of T.A.’s larger vessels appeared to have flow. The muscle appeared slightly ischemic but not
necrotic. It was very weakly contractile with the Bovie electrocautery. But some of the
musculature was not at all contractile and therefore Dr. Khandelwal excised this musculature
sharply with the Bovie electrocautery. Id. He transected the bone with the saw at a similar
length and in a similar fashion as on the right-hand side. Id. at 543. In light of the slightly
ischemic nature of the muscles, Dr. Khandelwal decided to close the wound with a wound VAC
to increase circulation and bring T.A. back to the operating room over the next several weeks to
perform an ultimate closure. Id. Dr. Khandelwal informed T.A.’s family that the length of the

32
Neisseria is “a genus of bacteria of the family Neisseriaceae, consisting of gram-negative, oxidase-positive cocci
characteristically coffee bean-shaped and paired. The organisms are aerobic or facultatively anaerobic and are part
of the normal flora of the oropharynx, nasopharynx, and genitourinary tract. The genus includes the gonococcus, the
several meningococcus types, pigmented forms occasionally associated with meningitis, and a number of
saprophytic or parasitic but nonpathogenic species.” Dorland’s at 1237. Neisseria meningitidis is “a prominent
cause of meningitis and the specific etiologic agent of meningococcal meningitis; it can also cause meningococcal
pneumonia, a type of bacterial pneumonia . . . .” Id. Meningitis is “inflammation of the meninges, usually by either
a bacterium . . . or a virus . . . .” Id. at 1132. Meninges are “the three membranes that envelop the brain and spinal
cord: the dura mater, pia mater, and arachnoid.” Id.
33
Hypoxemia is “deficient oxygenation of the blood.” Dorland’s at 908.
34
Femur is “the bone that extends from the pelvis to the knee, being the longest and largest bone in the body . . . [;]
distally, the femur, along with the patella and tibia, forms the knee joint.” Dorland’s at 688.
35
An elevator is “an instrument for lifting tissues . . . .” Dorland’s at 604. A periosteum elevator is “a flat steel bar
for separating the attachments of the periosteum to bone.” Id. Periosteum is “a specialized connective tissue
covering all bones of the body, and possessing bone-forming potentialities. . . .” Id. at 1417.
36
Condyle or condylus is “a rounded projection on a bone . . . .” Dorland’s at 402.
10
left leg might end up shorter than the right leg. Id.

Also on September 12, 2011, Dr. Parthak Prodhan wrote a critical care medicine note,
diagnosing T.A. with acute respiratory failure; septic shock meningococcemia, query; acute
kidney injury; and above-knee amputation secondary to ischemia of the lower extremities. Id. at
519. T.A. was currently not on any antibiotics. He was on steroids for relative adrenal
insufficiency. Id.

On September 13, 2011, Dr. Prodhan wrote that T.A. was slightly puffy and had pain
issues. Id. at 521. He was on fentanyl. Id.

On September 20, 2011, T.A.’s bedside nurse called social worker Esther Pipkin to say
T.A.’s bandage fell off while he was in the play room and he became upset. Id. at 1827. T.A.
was now more awake and alert. The social worker and T.A.’s family had been talking to T.A.
about his legs, but it was unclear if he understood part of his legs was removed. T.A. had looked
at the legs but not made any comments. When Ms. Pipkin entered the playroom, T.A.’s mother
was in bed with T.A. reading a book that Ms. Pipkin provided regarding a horse who lost a leg
and had a prosthetic placed. Id. T.A. turned toward his mother, crying, “Put my legs back on.”
Ms. Pipkin started talking to T.A. about his legs when T.A. stated, “I want my white legs on.”
Id. T.A.’s father arrived in the playroom and stated T.A. wanted the bandage put back on his leg.
The father explained the Burn Team was coming up to put a new bandage on T.A.’s leg. T.A.
continued to cry, stating he wanted the white bandage. Ms. Pipkin went to the nurse to see if it
was okay to put a temporary dressing on the leg until the Burn Team arrived. The nurse was
willing. Ms. Pipkin explained to T.A. that the nurse was in the playroom to put the “white leg”
back on and T.A. immediately calmed down. T.A.’s father assisted the nurse in putting the
bandage on and T.A. calmed down and went to sleep. Ms. Pipkin explained to the parents the
need for T.A. to be involved in medical play and to do express activities to assist with the loss.
T.A.’s father asked about the movie “How to Train Your Dragon” which involves the loss of a
leg and the use of a prosthetic. Ms. Pipkin encouraged T.A.’s parents to get the movie and see
how T.A. responds. Ms. Pipkin felt T.A.’s reaction to seeing his leg with an incision and no
bandage was frightening to him. She was still unsure if T.A. understood he lost part of his legs,
but once the bandage was off, he could see it and she felt it scared him. She felt T.A.’s age made
understanding his loss difficult due to children that age being magical thinkers. Her plan was to
assist with grief and loss issues. Id.

On September 22, 2011, Amelia H. Randag, a child life specialist, wrote that she met
with T.A. and his grandmother to begin a play session. Id. at 1830. T.A. had limited use of his
hands; therefore, Ms. Randag allowed T.A. to choose the colors to decorate the teaching doll,
and followed T.A.’s instructions. T.A. chose his grandmother to play the role of the doctor and
Ms. Randag to play the role of the nurse. Id. T.A. was more avoidant when the medical play
session began, not answering Ms. Randag’s questions throughout the play session, but did
answer her questions when Ms. Randag offered choices. The grandmother played through
T.A.’s admission to the prior hospital, air evacuation via Angel One, various tests and
medications that were tried to “get rid of” T.A.’s virus, and eventually the surgery when T.A.’s

11
legs were amputated. Ms. Randag explained that the medicine was not helping and the only way
to make T.A. “well” was to get rid of the part of his legs that was making him sick. She
explained that T.A. did nothing wrong to cause the amputation. T.A. turned his head away
during this portion of the play session. The grandmother took off her doctor’s hat and mask, and
Ms. Randag interpreted this as a cue to end the session. T.A. agreed to continue the play at a
later time. Ms. Randag encouraged T.A. to continue “doctoring” on the teaching doll when he
felt like it. Ms. Randag returned later that evening to follow up, but T.A. was being bathed. Ms.
Randage explained to the grandmother the goals for future play sessions: (1) to ensure T.A.
knows the amputation is not a punishment, and (2) to ensure T.A. knows that his family will still
love him and take care of him. These are common fears for this age. Id.

On September 26, 2011, Dr. Khandelwal wrote an additional operative note to revise the
right above-knee amputation with closure. Id. at 545. The muscle on top of the stump appeared
viable, but there was some fat that, although slightly ischemic, appeared to be improving over the
past several dressing changes. Id. at 545-46. He excised sharply using a scalpel some residual
tissue. Id. at 546. Dr. Khandelwal released muscle from the periosteum using a periosteal
elevator, and freeing the femur. He then resected a portion of the femur using a bone saw and
shaped the femur to prevent any sharp edges. Id.

On September 28, 2011, occupational therapist Frank H. Bregy met with T.A. to help
with hand splints, but T.A. continued to be agitated, refusing activity. Id. at 1832. T.A. was
verbalizing his requests and would state “yes” when asked if he would like to do a specific
activity, but when presented, he would refuse and begin to yell and become more upset. Id.
Later, on the same day, physical therapist Suzanne L. Shepard noted T.A. continued to be
agitated and to refuse to participate in therapist-directed activities. Id. at 1833.

On October 3, 2011, Ms. Shepard noted that T.A. was much more alert and participatory.
Id. at 1836. He could sit independently for 15 seconds at a time without upper extremity support
before requiring assistance. He did not complain of pain and was noted to be laughing or smiling
periodically. Id.

On October 4, 2011, Ms. Shepard noted T.A. could sit without upper extremity support
for 25-30 seconds. He demonstrated good weight bearing through his bilateral upper extremities
while sitting as well as transfer weight between his arms. He did not complain of pain and was
noted to be laughing or smiling periodically. Id. at 1837.

On October 5, 2011, social worker Marybeth D. Evans noted she met with T.A.’s mother
and grandmother to assess their needs and provide support for discharge issues. Id. at 1838.
T.A.’s mother said they will go home with a borrowed wheelchair. She expected they would get
a fitting for prostheses in a couple of weeks. Shriners, to whom they contributed in the past,
invited them to have T.A. assessed for services there. T.A. was looking happy “tooling down the
hallway in his little wheelchair.” Id.

On October 5, 2011, T.A. was discharged from the hospital. Id. at 523. Dr. Anjay

12
Khandelwal attended and APN Jayna C. Harper wrote the diagnosis was sepsis with bilateral
lower extremity necrosis resulting in bilateral above-knee amputation. Id. at 525, 527.
Infectious Diseases’ working differential diagnosis was tick-borne illness vs. meningococcemia
and DIC. Id. at 524. T.A. developed diffuse petechiae throughout early hospitalization. He did
not have purpura 37 or desquamation. 38 Id. His feet gradually became darker likely secondary to
vasoconstriction vs. septic emboli. Doctors determined T.A. needed surgical intervention due to
bilateral lower extremity limb ischemia secondary to vasoconstriction with open wounds. Id.

On October 7, 2011, T.A. returned to Arkansas Children’s Hospital with abdominal pain,
dehydration, drug withdrawal, and drug dependence. Id. at 987. He was discharged on October
12, 2011. Id.

On October 12, 2011, T.A. saw Dr. Jonathan Swenson and Dr. Esther H. Tomkins for a
physical medicine and rehabilitation consultation. Id. at 954. Dr. Swenson wrote that T.A. was
hospitalized due to septic shock likely due to meningococcemia. Id. T.A. was recently
discharged from Arkansas Children’s Hospital but readmitted shortly thereafter due to several
episodes of emesis and abdominal pain. He was diagnosed with opioid withdrawal and was
restarted on a slow taper of methadone. He had suspected spasticity in his left upper extremity
which might need Botox. Id. T.A. complained occasionally that his foot and ankle hurt,
consistent with phantom limb pain. Id. at 965. He had decreased functional use of his left hand
and wrist. On physical examination, he had moderate finger flexion contracture in his left hand
with atrophy of the intrinsic hand muscles on the left and some thenar 39 atrophy. The hand had
the appearance of a claw hand, but included the second and third digits. He had a mild amount
of wrist drop. The right hand was minimally affected in the same pattern distribution as the left
hand, but he could use the right hand. This could have been due to compressive neuropathy due
to his severe edema while in ICU or to positioning in bed. It appeared the compressive
neuropathy affected the ulnar and median nerves to the greatest degree and, to some degree, the
radial nerve. Id. Dr. Swenson explained to T.A.’s family that this was not likely due to a brain
problem but most likely related to focal damage of the peripheral nerves in T.A.’s forearms. Id.
Dr. Swenson recommended occupational therapy and physical therapy, stating Botox was not
indicated as T.A. did not have true spasticity. Id. at 976.

On October 18, 2011, T.A. returned to Dr. Allen after his prolonged hospitalization at
Arkansas Children’s Hospital to which he was transferred two months earlier with a diagnosis of
probable sepsis and hypovolemia. 40 Med. recs. Ex. 3, at 17.

On October 24, 2011, T.A. saw Dr. Allen. Id. at 19. Dr. Allen notes that T.A.’s legs

37
Purpura is “any of a group of conditions characterized by ecchymosis or other small hemorrhages in the skin,
mucous membranes, or serosal surfaces; causes include blood disorders, vascular abnormalities, and trauma.”
Dorland’s at 1557.
38
Desquamation is “the shedding (exfoliation) of epithelial elements, chiefly of the skin, in scales or sheets.”
Dorland’s at 501.
39
Thenar is “the mound on the palm at the base of the thumb.” Dorland’s at 1909.
40
Hypovolemia is “abnormally decreased volume of circulating blood in the body; the most common cause is
hemorrhage.” Dorland’s at 908.
13
were amputated because of ischemia 41 with possible sepsis. T.A. also had some nerve damage to
his left hand, which was fisted. He had some behavioral problems over the weekend. He threw
some paint and threw a cake; when he got upset, he became very aggressive toward anyone near
him. T.A. still did not make eye contact or smile. Id. T.A. had above-the-knee amputations
bilaterally. He had depression and behavioral problems. He was on amitriptyline, but Dr. Allen
did not know if that was effective. T.A. was tapering his methadone. Dr. Allen wrote a
prescription for Prozac. Id.

On November 14, 2011, T.A. saw Dr. Amy M. Scurlock, an allergist/immunologist, at
the Arkansas Children’s Hospital Allergy/Immunology Clinic. Med. recs. Ex. 7, at 77. Dr.
Scurlock had previously seen T.A. when he was hospitalized from August through early October
2011. Id. T.A.’s mother gave a history that about one week prior to his hospitalization, T.A.’s
feet hurt and he was more lethargic and irritable. Id. at 78. T.A. had received MMR vaccine
about two weeks prior to his hospitalization. Dr. Scurlock wrote, “With our current data that we
have now, I cannot clearly implicate or not implicate the vaccine.” Id. Dr. Scurlock states,
“Unfortunately we were unable to clearly identify an infectious etiology. It is a presumed
infectious etiology but he did receive some antibiotics prior so we were unable to culture
anything.” Id. T.A.’s mother said that, in comparison with T.A.’s brothers, he seemed to pick
up infections more easily. Id. On lab testing, T.A.’s natural killer cell count was elevated. Id. at
79. Dr. Scurlock wrote that T.A. never developed the true purpura, although he did have
petechiae. Id. T.A. also had a history of lymphopenia 42 while hospitalized which continued to
improve, and he had an abnormal immune test. Id.

On December 2, 2011, T.A. saw Dr. Perry Schoenecker at Shriners Hospitals for
Children for evaluation for prosthetic care. Med. recs. Ex. 14, at 1. Dr. Shoenecker writes that a
physician told T.A.’s mother that T.A. could have had an immunologic response to vaccination
vs. possible meningococcemia, but it would never be able to be proven. Id. Dr. Schoenecker
comments that T.A. has had some difficulties with sleeping because he went to sleep when he
had his amputations and when he woke up, he had no legs. He has become very apprehensive
about sleep. He mostly scoots around. Id.

On February 6, 2012, T.A. saw Dr. Barbara Saunders for a habilitation consultation.
Med. recs. Ex. 7, at 44. She described him as status post-bilateral transfemoral amputation
secondary to infection, likely meningococcemia. Id. During his hospitalization, he developed a
compressive neuropathy with radial nerve injuries bilaterally. The left hand seems to be more
affected than the right. He kept his left hand in a loose fist but easily opened it when reminded.
T.A. tended to crawl on the heel of his hand and his wrist to push his wheelchair. He had
difficulty with balance during transfers because of keeping his hand held in this position. Id.
T.A. was an active, well-appearing little boy. He showed off his break dancing skills during the
physical examination. Id.

41
Ischemia is “deficiency of blood in a part, usually due to a functional constriction or actual destruction of a blood
vessel.” Dorland’s at 961.
42
Lymphopenia is lymphocytopenia which is “reduction in the number of lymphocytes in the blood. . . .” Dorland’s
at 1085.
14
 On May 14, 2012, T.A. saw Dr. Scurlock again for an evaluation. Med. recs. Ex. 7, at
27. Her diagnosis was abnormal immune disorder, lymphopenia. Id. at 21. As an infant, T.A.
had a staphylococcal infection at age 5-6 months. Id. at 28. T.A.’s mother said he had been
sicker than other children. Id. On lab testing that day, T.A.’s AST was 58, whereas the normal
range is 15-50. Id. at 28-29. His ALT was 44, whereas the normal range is 10-25. Id. at 29. Dr.
Scurlock sent panels to Cincinnati, including an ALPS 43 panel, because one of T.A.’s brothers
has an increased double negative T cell count and he did have “this response” (the brother tested
positive to the ALPS panel). Id. Dr. Scurlock’s impression was that T.A. has a history of
abnormal immune studies with lymphopenia (reduction in the number of lymphocytes in the
blood) primarily. Id. at 29. Her differential diagnoses for T.A. included: (1) infection, status
post-vasopressors, 44 and (2) infection and meningococcemia. She found it interesting, however,
that he never developed a true purpura, although he did have some petechiae with
meningococcemia. 45 Id.

Also on May 14, 2012, Dr. Scurlock had Arkansas Children’s Hospital do laboratory tests
on T.A. Id. at 3. In special immunology studies, T.A. had a high percentage of gamma delta
cells, i.e., 10, when the normal range is 1-5. Id. at 6. He had a low percentage of CD4 T helper
cells, 46 i.e., 31, when the normal range is 35-51. Id. T.A. had a low percentage of alpha beta T
cells, i.e., 90, when the normal range is 95-97. Id. at 7. He had a high percentage of CD45RA T
SUPRS, i.e., 92, when the normal range is 60-90, but a low percentage of CD45RO T SUPRS,
i.e., 8, when the normal range is 10-40. Id. Dr. Terry Harville, Medical Director of the Special
Immunology Laboratory, concluded T.A. exhibited an essentially normal immunophenotype. He
could not identify the cause of T.A.’s recurrent infections by specific immunodeficiency. T.A.
had a low normal-for-age CD4 T lymphocyte count. Id. at 14. T.A. was given an ALPS test for
which he tested normal. Id. at 17. He was given a cytotoxic T-lymphocytes (“CTL”) 47 function
test and the result was decreased CTL function. Id. at18.

On July 25, 2012, T.A. returned to Dr. Schoenecker at Shriners Hospitals for Children
because he may have gotten a splinter in his right stump while crawling through the grass the day
before without any protection or prosthetic on. Med. recs. Ex. 14, at 4. His right stump was
warm, red, and swollen. Id. The doctor found a single puncture wound in the middle of the
erythema. Id. at 5. The doctor admitted T.A. to the hospital and placed him on IV antibiotics.

43
ALPS is “autoimmune lymphoproliferative syndrome.” Dorland’s at 54. Autoimmune lymphoproliferative
syndrome is “a hereditary disorder of lymphocyte apoptosis that results in the accumulation of large numbers of
mature lymphocytes in the lymph nodes and spleen, appearing during childhood and characterized by massive
lymphadenopathy, splenomegaly, and autoimmune hemolytic anemia and other cytopenias.” Dorland’s at 1822.
44
A vasopressor is a “1. stimulating contraction of the muscular tissue of the capillaries and arteries. 2. an agent that
stimulates contraction of the muscular tissue of the capillaries and arteries.” Dorland’s at 2027.
45
Meningococcemia is “invasion of the bloodstream by meningococci.” Dorland’s at 1133.
46
Helper T cells are “differentiated T lymphocytes whose cooperation (help) is required for the production of
antibody against most (T-dependent) antigens. . . . [H]uman helpers cells [are marked ] by the CD4 antigen.”
Dorland’s at 318.
47
Cytotoxic T lymphocytes are “differentiated T lymphocytes that can recognize and lyse target cells bearing
specific antigens recognized by their antigen receptors. . . . These lymphocytes are important in . . . killing of . . .
virus-infected host cells. . . . Called also killer or killer T cells.” Dorland’s at 1084.
15
Id. On July 26, 2012, Dr. Schoenecker did irrigation and debridement on T.A.’s right stump. Id.
at 8. A large pocket of fluid was seen mostly straw-colored with a few purulent areas. Id. at 9.
T.A. was discharged on July 27, 2012 on oral antibiotics. Id. at 11.

On October 11, 2016, T.A. had a test for Neisseria meningitidis Ag. Med. recs. Ex. 54.
The test result was negative. 48 Id. at 1.

On February 9, 2018, petitioners filed a HIPPA amendment to Arkansas Children’s
Hospital discharge diagnosis. Ex. 56. Petitioners requested T.A.’s medical records be revised.
Id. at 3. On August 30, 2017, petitioners met with Chief Medical Officer Dr. Jayant Deshpande,
infectious diseases specialist Dr. Jose Romero, and two risk management liaisons to discuss their
concerns about T.A.’s medical records and what they wanted amended. Id. Subsequently, Dr.
Deshpande wrote an addendum to T.A.’s chart, stating he would modify T.A.’s final discharge
diagnosis to read: “(1) sepsis syndrome with bilateral lower extremity necrosis; (2) bilateral
above-knee amputations.” Id. at 5.

On May 29, 2018, petitioners filed e-mail correspondence between the surgeon Dr. Anjay
Khandelwal and themselves. Ex. 57. Dr. Khandelwal writes that his “strong belief” is that the
necrosis of T.A.’s skin and muscle was likely from the pressors and his overall illness. Id. at 3.
“They are not typical for purpura fulminans 49 as seen with meningitis – in fact in my initial
consult, I remarked that I did not think the diagnosis was purpura fulminans.” Id.

Medical Expert Reports

Petitioners filed a statement from Dr. L. Barry Allen, T.A.’s treating pediatrician, in
which he says that, on August 11, 2011, T.A. came to his office for his three-year-old well child
examination. Ex. 18, at 1. T.A. was doing well and did not have any problems. T.A. received
MMR vaccine on that date. Thirteen days later, T.A. returned to Dr. Allen’s office with a fever
of 102 degrees and a macular and petechial rash. His platelets were low and his white blood cell
count was normal. He gave T.A. Rocephin and requested T.A. return the next day. On August
25, 2011, T.A. returned and was quite lethargic. His white blood cell count was elevated and his
platelets lower than the day previous. Dr. Allen thought he had either an infection or an adverse
reaction to MMR vaccine since the timing of the vaccination two weeks before was a red flag for
causation. Id. Numerous tests failed to identify a bacterial or viral etiology. Id. at 2. Dr. Allen
concludes that MMR vaccine probably caused T.A.’s symptoms, not only because the timing

48
The cover page to this filing states it is antibody testing, but the test result refers only to N. meningitidis Ag. Med.
recs. Ex. 54, at 1. “Ag” means “antigen.” Dorland’s at 37. The undersigned has no idea if more than five years
after T.A. became ill, if he had been exposed to Neisseria meningitidis, the antigen would still be present in his
body. Moreover, the undersigned has no idea if the absence of Neisseria meningitidis antigen equals negative
antibody to it. Petitioners never filed a doctor’s report to explain the significance of Exhibit 54. Therefore, the
undersigned does not base any finding upon this test result.
49
Purpura fulminans is “a form of nonthrombocytopenic purpura seen mainly in children, usually following an
infectious disease such as scarlet fever or varicella; characteristics include fever, shock, anemia, and sudden and
rapidly spreading symmetrical skin hemorrhages of the lower limbs, often with extensive intravascular thromboses
and gangrene.” Dorland’s at 1557.
16
was perfect, but also because an adverse reaction to MMR vaccine would cause an increase in
white blood cells and neutrophils and a reduction in leukocytes. Id. Dr. Allen attributes T.A.’s
ultimate bilateral amputations and permanent neurological deficits to his adverse reaction to
MMR vaccination. Id.

Petitioners filed an initial opinion of their expert pediatric neurologist Dr. David J.
Siegler, dated October 4, 2012. Ex. 10. He states that T.A. had a vaccine-induced encephalitis,
indicating a vaccine-related adverse event. Id. at 1. T.A.’s depressed level of consciousness
with fever and rash developing 12 days after MMR vaccination supports causation. Id. At the
time he wrote his expert report, Dr. Siegler maintained a clinical practice as well as acted as
Clinical Assistant Professor at Oklahoma University State College of Osteopathic Medicine,
Department of Pediatrics. Ex. 11, at 1.

Respondent filed a report of his expert pediatric neurologist Dr. Lawrence W. Brown,
dated July 24, 2013. Ex. A. Dr. Brown states he has had almost 35 years of experience
managing critically ill children with neurological disease. Id. at 1. T.A. presented with fatigue
and low-grade fever followed quickly by spiking fever, petechial rash, vomiting, diarrhea, and
rapid decline with multisystem involvement, i.e., septic shock. He received MMR vaccine about
10 days before the onset of illness. Id. In the hospital, T.A. had a markedly abnormal complete
blood count with dramatic shift to the left, thrombocytopenia (platelets 23,000), and signs of
coagulopathy. Id. at 2. Over his first few days of PICU, T.A. was comatose, but improved
within days. T.A. did not have signs of meningitis or focal neurologic deficits. Id. T.A.’s
doctors never considered T.A. had meningoencephalitis by obtaining a lumbar puncture or T.A.’s
central nervous system to be a primary target of his illness by doing an EEG or MRI. Id. The
doctors did an extensive and comprehensive infectious diseases search considering everything
from meningococcemia as the most likely cause to Ehrlichia, rickettsia, MRSA, pneumococcus,
and tularemia. Id.

Dr. Brown’s opinion is that the combination of fever, vomiting, petechial rash with
thrombocytopenia, hypotension despite adequate fluid resuscitation, oliguria, 50 hypoxia, and
coma is most consistent with septic shock. He states, “It is unfortunate that no definitive
organism was found. . . .” Id. Dr. Brown states that T.A. did not have acute measles
encephalitis, which typically presents with headache, irritability, somnolence, seizures and coma
with occasional ataxia, chorea or focal deficits. It does not start with diarrhea, vomiting,
petechial rash, and shock. Cerebral spinal fluid (“CSF”) pleocytosis is the rule. The only
symptom that T.A. had that would be consistent with MMR encephalitis was altered awareness.
Id. The attending physicians never considered T.A. had encephalitis. Id. at 3. Only in
December 2011 when T.A. was in Shriner’s Hospital being evaluated for prostheses was
immunization first implicated. Dr. Perry Schoenecker wrote that T.A.’s parents were told T.A.’s
condition could have been an immunologic response to MMR or meningococcemia, but the
etiology could not be proven. Id. Dr. Brown concludes by saying that no specific etiology was
found for T.A.’s illness. Id. He notes that septic shock is a syndrome that many viruses or
bacteria can cause, but vaccinations are not a “known etiology.” Id.

50
Oliguria is “diminished urine production and excretion as compared with fluid intake. . . .” Dorland’s at 1318.
17
 Dr. Brown’s CV shows extensive training, clinical experience, academic appointments,
numerous awards, honors, memberships in honorary and scientific societies, and extensive
publications. Ex. A, Tab 1.

Respondent filed a report of his pediatric infectious diseases expert Dr. Jerome O. Klein,
dated April 25, 2013. Ex. B. Dr. Klein writes T.A. had septic shock, a multisystem disease
associated with acute respiratory failure, acute renal failure, DIC, and vascular insufficiency of
the lower extremities resulting in ischemia followed by extensive tissue damage necessitating
above the knee amputations. Id. at 3. Dr. Klein states septic shock is usually due to extensive
bacterial infection such as meningococcemia or pneumococcal or streptococcal bacteremia. He
says it is likely that the intramuscular injection of ceftriaxone on August 24, 2011 had
bactericidal concentrations in the blood sufficient to suppress growth of the causative organisms.
It is also possible that a tick-borne disease such as Rocky Mountain spotted fever caused T.A.’s
septic shock. Id. Dr. Klein denies that T.A. had encephalopathy. Dr. Klein states he knows of
no similar case in which MMR caused septic shock. Id. Even though T.A. received MMR
vaccine eleven days prior to onset of his septic shock, “there are no data that would indicate
MMR could be a causative factor in developing of septic shock and the sequelae of tissue
damage requiring amputations.” Id. at 4. He denies that T.A. had SIRS from MMR vaccine
because SIRS occurs within minutes to hours after administration of the provocative agent. Dr.
Klein states, “It is biologically implausible that administration of MMR on August 11 would be
responsible for a cytokine storm 11 days after vaccination.” Id. Dr. Klein says
thrombocytopenia is one of many features of organ dysfunction associated with sepsis syndrome,
but it is the result, not the cause, of the coagulopathy that sepsis causes. The thrombocytopenia
was responsible for the ischemia of T.A.’s tissues leading to lower limb amputations. Pathogens
responsible for sepsis syndrome include pneumococcus, meningococcus, and streptococcus
which the antibiotic T.A. receive on August 24th, i.e., ceftriaxone, inhibited. Therefore, Dr.
Klein states, when doctors cultured T.A.s blood, he still had a concentration of ceftriaxone in his
blood sufficient to suppress growth of these organisms, leading to a negative result. Id.

Dr. Klein’s CV shows extensive training, clinical experience, academic appointments,
numerous awards, honors, memberships in honorary and scientific societies, and extensive
publications. Ex. B, Tab 1. Respondent later filed Dr. Klein’s updated CV as Exhibit J.

Respondent filed a supplemental expert report from Dr. Brown, pediatric neurologist,
dated February 11, 2014, stating that since an infectious septic shock unrelated to MMR vaccine
caused T.A.’s altered mental status, T.A.’s medical complications do not qualify as a Table
encephalopathy. Ex. C, at 1. Dr. Brown states there is no doubt that T.A. had encephalopathy
within the time frame after MMR immunization, but his encephalopathy was just one component
of septic shock. Id. at 3. Dr. Brown agreed that the live attenuated virus in measles vaccine can
cause encephalopathy. Id. T.A.’s petechiae were completely different from the morbilliform 51
rash seen in a measles reaction. Id.

51
Morbilliform means “like measles; resembling the eruption of measles.” Dorland’s at 1180.
18
 Respondent filed a supplemental expert report from Dr. Klein, infectious diseases
specialist, dated February 11, 2014. Ex. D. Dr. Klein states the rash that T.A. had was not red,
blotchy, beginning on his head and progressing to his feet within three days. Id. at 5. T.A. had a
petechial rash, which is small hemorrhages in the skin. T.A. did not have a rasping cough,
conjunctivitis, or Koplik spots 52 characteristic of measles. Id. Dr. Klein concludes T.A. did not
have vaccine-induced measles. Id. Dr. Klein notes that T.A. had thrombocytopenia which his
sepsis caused. The thrombocytopenia did not cause the sepsis. Id. Dr. Klein states that only
blood-borne bacteria can cause sepsis. Id. at 6. The reason cultures of T.A.’s blood were
negative is because he had received the antibiotic ceftriaxone. Id.

Petitioners filed an expert report from Dr. Alan S. Levin, an immunologist, dated May 6,
2014. Ex. 19. He writes that he has treated over 100 patients with septic shock, systemic
inflammation, organ dysfunction, and organ failure. Id. at 1. His opinion is that T.A. did not
have septic shock but SIRS. Id. at 2. He agrees with Dr. Klein that T.A.’s receipt of ceftriaxone
on August 24, 2011 would have suppressed growth of a bacterium initially, but given the
protracted course and worsening of T.A.’s SIRS, subsequent histopathology specimens and
cultures would have indicated a bacterial etiology if there were one. Thus he states T.A. did not
likely have bacteria-induced septic shock. Dr. Levin’s opinion is that MMR caused T.A.’s
encephalopathy and SIRS. Id. He explains that inflammation 53 is a body’s response to a
nonspecific insult that can have various causes, including vaccines, since vaccination provokes
an immune response and cytokine release. Id. at 1. Cytokine release overwhelmingly leads to
activation of the endothelial system and loss of circulatory integrity, resulting in end organ
dysfunction. Id. The time period between T.A.’s August 11, 2011 MMR vaccination and his
onset of symptoms on or before August 24, 2011 is appropriate for the occurrence of an immune
response. Id.

Petitioners filed a supplemental expert report from Dr. Siegler, pediatric neurologist,
dated May 9, 2014. Ex. 22. Dr. Siegler states that T.A.’s history suggests non-infectious,
autoimmune-mediated shock syndrome which MMR vaccine triggered. Id. at 2. He developed
fever, macular rash, and thrombocytopenia 13 days after MMR vaccination, followed the next
day by diarrhea and encephalopathy. Id. Dr. Siegler said strong consideration should be given
to systemic inflammatory response syndrome (“SIRS”), a clinical syndrome describing shock
and multiple organ dysfunction responses to a nonspecific insult due to either infectious
(bacterial, viral, fungal, parasitic) or non-infectious (trauma, dehydration, drug reactions,
autoimmune disorders) causes. He writes MMR was the known autoimmune trigger of T.A.’s
SIRS 12-14 days post-vaccination. Id. There was no diagnostic evidence for bacterial etiology.

52
Koplik sports are “small, irregular, bright red spots on the buccal and lingual mucosa, with a minute bluish white
speck in the center of each; seen in the prodromal state of measles.” Dorland’s at 1756.
53
Inflammation is “a localized protective response elicited by injury or destruction of tissues, which serves to
destroy, dilute, or wall off (sequester) both the injurious agent and the injured tissue. It is characterized in the acute
form by the classical signs of pain (dolor), heat (calor), redness (rubor), swelling (tumor), and loss of function
(functio laesa). Histologically, it involves a complex series of events, including dilatation of arterioles, capillaries,
and venules, with increased permeability and blood flow; exudation of fluids, including increased permeability and
blood flow; exudation of fluids, including plasma proteins; and leukocytic migration into the inflammatory focus.”
Dorland’s at 936.
19
Id.

Respondent filed an expert report from Dr. J. Lindsay Whitton, who is not a practicing
clinician, but a virologist and pathologist, dated August 4, 2014. Ex. E (C.V. at Ex. E, Tab 1.)
Dr. Whitton states that T.A.’s very rapid and profound rise in his neutrophil count is completely
consistent with a bacterial infection. Ex. E, at 2. On August 24, 2011, T.A.’s proportion of
neutrophils was higher than normal, but the absolute number of neutrophils was normal.
Neutrophils are a type of white blood cell that combats bacterial infections. Id. at 1. T.A.’s wbc
continued to rise extremely rapidly. Id. at 2. Sepsis can and in this case did very quickly lead to
shock in which blood pressure declines and the blood supply to arms and legs is seriously
compromised. Id. T.A. did not have encephalitis. T.A. did have encephalopathy. T.A. had a
reduced level of consciousness because he was in shock. Id. Dr. Whitton states that culture-
negative sepsis is very common. Id. at 3. Dr. Whitton states it can be extraordinarily difficult to
grow bacteria in an artificial environment, resulting in a positive result only 50 percent of the
time. Sepsis is a clinical diagnosis. Dr. Whitton said that T.A.’s fever, petechial rash, and
thrombocytopenia were consistent with an MMR vaccine etiology, but were also consistent with
sepsis. Id. at 4. Dr. Whitton states that the three attenuated viruses in MMR vaccine replicate to
activate the immune response, which includes triggering cytokines. Id. Dr. Whitton states that
the vast majority of viral infections do not cause cytokine storm. Id. at 5. He concludes that
SIRS is more closely related to the innate immune response (occurring within two days of a
trigger) than to the adaptive immune response. Id. at 6. Dr. Whitton disagrees with T.A.’s
pediatrician Dr. Allen that MMR vaccine can cause an explosive increase in neutrophils 14 days
after vaccination. Id. at 8.

Respondent filed a second supplemental expert report from Dr. Klein, dated August 19,
2014. Ex. F. He states if a vaccine were to induce SIRS, it would appear as anaphylaxis and
immediately after the vaccination, not 13 days later as petitioners’ expert Dr. Levin posited. Id.
at 1. Dr. Klein states he has treated hundreds of cases of bacterial sepsis and T.A.’s onset,
clinical course, and recovery are completely consistent with that diagnosis. Id.

Respondent filed a second supplemental expert report of Dr. Brown, which is undated.
Ex. G. Dr. Brown states that “sepsis” refers only to a condition that bacterial infections cause.
Id. at 1. Dr. Brown denies that MMR vaccine caused T.A.’s encephalopathy. Id.

Petitioners filed an expert report from Dr. David Axelrod, an immunologist, dated
October 3, 2014. Ex. 24. He states that T.A. reacted to MMR vaccine 12 days after vaccination,
with lethargy and fever, evolving to what became SIRS. Id. at 1. Dr. Axelrod writes that
etiology of SIRS may be septic or non-septic. He states elevated levels of mannose-binding
lectin (“MBL”) 54 are associated with noninfectious SIRS with multiple organ failure, whereas
low MBL is associated with multiple organ failure in infectious SIRS. Id. Dr. Axelrod says that

54
Mannose-binding lectin is “a protein that is structurally similar to complement component C1 and recognizes
many microorganisms, including bacteria, fungi, parasites, and viruses. It initiates the lectin pathway of
complement activation, without the presence of antibody, by binding to carbohydrates on the microbial surface and
activating C3.” Dorland’s at 1017.
20
T.A.’s MBL levels were high, suggesting T.A. had a noninfectious form of SIRS. Id. Moreover,
T.A. suffered evidence of activation of the complement pathways with subsequent multiple
organ failure as part of the SIRS. Id. at 3.

Respondent filed a supplemental expert report from Dr. Whitton, dated February 11,
2015. Ex. H. Dr. Whitton terms Dr. Axelrod’s report “a series of unsubstantiated suppositions”
and says Dr. Axelrod made “numerous errors of fact.” Id. at 1. Dr. Whitton says that since
MMR vaccine contains live vaccine, it is infectious. Id. at 2. Therefore, Dr. Axelrod makes no
sense when he writes that T.A.’s SIRS had a noninfectious cause, yet was due to MMR vaccine.
Id. He accuses Dr. Axelrod of failing to explain and/or misrepresenting the biological function
of MBL. Dr. Whitton writes that MBL is a pattern recognition molecule that recognizes sugar-
like structures present on the surfaces of some bacteria and viruses. Id. at 2. MBL is synthesized
mainly in the liver and is readily detectable in most healthy people, usually above a level of
~1,000 µg/ml. Id. Dr. Whitton says measurement of MBL function, rather than level of MBL
alone, may be a more reliable parameter to determine disease susceptibility. Id. at 2-3. MBL
can sometimes rise in response to infection, but the rise is usually quite modest. Id. at 3. He
notes that in a study of levels of MBL during sepsis in humans, the subjects had a relatively
stable MBL level mostly. Id. Dr. Whitton says MBL appears to play a role in very early (innate)
immune response to several infections. T.A.’s treating doctors were trying to see if T.A. had
immunodeficiency when they tested his serum MBL levels, knowing he had a history of
recurrent infectious. Id. Dr. Whitton noted that the two times T.A.’s MBL levels were tested,
the results (1,384 µg/ml on September 9, 2011 and 522 µg/ml on November 14, 2011) were
normal. But Dr. Whitton notes that the doctors did not evaluate T.A.’s MBL function. Id. Dr.
Whitton states that having a high MBL is misleading because that number does not reflect an
abnormality. Id. at 4. Dr. Whitton accepted that vaccination can cause transient fever and that
fevers are cytokine-related. Id. at 6. Dr. Whitton explained the dramatic rise of T.A.’s blood
neutrophil count indicated an acutely active process, rather than a delay of 12 days since MMR
vaccination. Id. at 7. He states viruses associated with SIRS “cytokine storm” have the
respiratory tract as a primary site of infection, but none of MMR vaccine’s three viruses targets
this tissue. Id.

Respondent filed a third supplemental report from Dr. Klein, dated February 19, 2015.
Ex. I. He agrees with Dr. Whitton’s report criticizing petitioner’s expert Dr. Axelrod’s report.
Id. at 1. Dr. Klein states T.A.’s multi-organ failure was a result of bacterial sepsis. Id. Dr. Klein
reiterates Dr. Whitton’s point that since T.A. had a history of frequent staphylococcal infections,
MBL tests were performed because MBL deficiency has been associated with recurrent
infections. Id. at 2. Dr. Klein states that Dr. Axelrod’s claim that a high level of MBL
distinguishes between infectious and noninfectious causes is without foundation or recognition
within the medical community. Id.

Petitioners filed a supplemental expert report from Dr. Levin, dated February 25, 2016.
Ex. 43. Dr. Levin deals with timing in his supplemental report. Id. at 1. He states that T.A.
received his first MMR vaccination on August 11, 2011 and it is well accepted that an initial
immune response to measles vaccine usually takes weeks to develop. Id. Citing the numerous

21
attempts of T.A.’s hospital treaters to detect a bacterial infection by conventional cultures and
PCR testing, Dr. Levin states their failure to find any bacterium makes it more probable than not
that MMR vaccine caused T.A.’s SIRS. Id.

Respondent filed a third supplemental report from Dr. Brown, dated August 2, 2017. Ex.
M. This was after the three-day hearing. He attributes all of T.A.’s clinical signs to likely
“meningococcal encephalitis.” Id. at 1. Both medication and infectious septic shock caused
T.A.’s altered mental status. Id. Dr. Brown does not believe T.A. had acute encephalopathy
persisting for 24 hours. Id. at 2. Lethargy, which T.A. had on September 25, 2011, is not
evidence itself of an encephalopathy. When T.A. entered Mercy Hospital on September 25,
2011, he answered questions appropriately and responded to external stimuli until medication
made him unresponsive and he entered a medically-induced coma. Id. Since T.A. recovered full
consciousness and was fully responsive to his environment, he did not have a chronic
encephalopathy for six months, although, to Dr. Brown, it is “possible” T.A. had an
encephalopathy when he was septic, intubated, and struggling with multiple system issues as he
was in acute multisystem organ failure that bacterial sepsis caused. Id. at 3. T.A. did not clearly
have an acute encephalopathy for 24 hours before he was intubated. Id.

Petitioners filed a second supplemental report from Dr. Siegler, dated October 23, 2017.
Ex. 55. Dr. Siegler posits that T.A. developed clinical signs of acute encephalopathy beginning
on Tuesday, August 23, 2011 and before sedation the afternoon of Thursday, August 25, 2011.
Id. at 1. He agrees with respondent’s expert that T.A. had encephalitis, i.e., brain inflammation.
Id. He states that T.A.’s brain inflammation was the likely pathologic process explaining T.A.’s
encephalopathy. Dr. Siegler notes that on August 24, 2011, T.A.’s wbc and absolute neutrophil
count were normal, when both are typically elevated in bacterial infections. Id. at 2. Dr. Siegler
does not think T.A.’s answering questions appropriately at Mercy Hospital on August 25, 2011
rules out an acute encephalopathy because it can present as alternate levels of consciousness. Id.
at 3. Dr. Siegler does not mention chronic encephalopathy in his report.

Respondent filed a fourth supplemental report from Dr. Brown, dated December 15,
2017. Ex. N. Dr. Brown states that he meant to write “meningococcal infection” in his third
supplemental report, not “meningococcal encephalitis.” Id. at 1.

Medical Articles

Respondent filed as Exhibit B, Tab 3, to his infectious diseases specialist Dr. Klein’s
expert report (Ex. B) chapter 64 from a medical text entitled NELSON TEXTBOOK OF PEDIATRICS
(Robert M. Kliegman et al. eds.,19th ed. 2011), although the undersigned cannot find in Dr.
Klein’s report that he referred to it: David A. Turner 55 & Ira M. Cheifetz, 56 Shock, 305-14. Ex.

55
Dr. David A. Turner is Associate Director, Pediatric Critical Care Fellowship Program; Medical Instructor,
Department of Pediatrics, Division of Pediatric Critical Care Medicine, Duke University Medical Center, Durham,
North Carolina. Contributors, NELSON TEXTBOOK OF PEDIATRICS xxx (Robert M. Kliegman et al. eds., 19th ed.
2011).
56
Dr. Ira M. Cheifetz is Professor of Pediatrics; Chief, Pediatric Critical Care Medicine; Medical Director, Pediatric
22
B, Tab 3. The authors write under the subheading “Pathophysiology” the following:

An initial insult triggers shock, leading to inadequate oxygen
delivery to organs and tissues. Compensatory mechanisms attempt
to maintain blood pressure by increasing cardiac output and
systemic vascular resistance. The body also attempts to optimize
oxygen delivery to the tissues by increasing oxygen extraction and
redistributing blood flow to the brain, heart, and kidneys (at the
expense of the skin and gastrointestinal tract). These responses
lead to an initial state of compensated shock, in which blood
pressure is maintained. If treatment is not initiated or is inadequate
during this period, decompensated shock develops with
hypotension and tissue damage that may lead to multisystem organ
dysfunction and ultimately to death. . . .

Id. at 2 (internal page 305).

The authors also define SIRS:

The systemic inflammatory response syndrome (SIRS) is an
inflammatory cascade that is initiated by the host response to an
infectious or noninfectious trigger (Table 64-5). This
inflammatory cascade is triggered when the host defense system
does not adequately recognize and/or clear the triggering event.

Id. at 4 (internal page 307). Table 64-5, to which this excerpt refers, is entitled, “Differential
Diagnosis of Systemic Inflammatory Response Syndrome.” Id. at 6 (internal page 309).
Included in the sub-category “Infection” are the following:

Bacteremia or meningitis (Streptococcus pneumoniae,
Haemophilus influenza type b, Neisseria meningitidis, group A
streptococcus, S. aureus)
Viral Illness (influenza, enteroviruses, hemorrhagic fever group,
herpes simple[x] virus, respiratory syncytial virus,
cytomegalovirus, Epstein-Barr virus)
Encephalitis (arboviruses, enteroviruses, herpes simplex virus)
Rickettsiae (Rocky Mountain spotted fever, Ehrlichia, Q fever)
Syphilis
Vaccine reaction (pertussis, influenza, measles)
Toxin-mediated reaction (toxic shock, staphylococcal scalded
skin syndrome)

ICU; Medical Director, Pediatric Respiratory Care & ECMO Programs, Duke Children’s Hospital, Durham, North
Carolina. Contributors, NELSON TEXTBOOK OF PEDIATRICS x (Robert M. Kliegman et al. eds., 19th ed. 2011).
23
Id. (emphasis added). The authors also add other causes of SIRS under separate sub-categories:
cardiopulmonary, metabolic-endocrine, gastrointestinal, hematologic, neurologic, and other. Id.

This chapter on shock in the well-recognized NELSON TEXTBOOK OF PEDIATRICS supports
the view that the pediatric medical community considers one of the causes of SIRS is a reaction
to measles vaccine.

Petitioners’ counsel referred to the same chapter’s Table 64-7 in cross-examination of Dr.
Whitton. Table 64-7 is on page 8 of Ex. B, Tab 3 (internal page 311):

Table 64-7 – INTERNATIONAL CONSENSUS DEFINITIONS FOR PEDIATRIC SEPSIS

Infection Suspected or proven infection or a clinical syndrome associated with high
probability of infection

Systemic 2 out of 4 criteria, 1 of which must be abnormal temperature or abnormal
inflammatory leukocyte count:
response 1. Core temperature >38.5˚C or <38˚C (rectal, bladder, oral, or central
catheter)
syndrome
2. Tachycardia: Mean heart rate >2 SD above normal for age in absence of
(SIRS) external stimuli, chronic drugs or painful stimuli OR Unexplained
persistent elevation over 0.5-4 hr OR in children <1 year old, persistent
bradycardia over 0.5 hour (mean heart rate <10th percentile for age in
absence of vagal stimuli, ß-blocker drugs, or congenital heart disease)
3. Respiratory rate >2 SD above normal for age or acute need for
mechanical ventilation not related to neuromuscular disease or general
anesthesia
4. Leukocyte count elevated or depressed for age (not secondary to
chemotherapy) or >10% immature neutrophils

Sepsis SIRS plus a suspected or proven infection

Severe Sepsis plus 1 of the following:
Sepsis 1. Cardiovascular organ dysfunction, defined as: •Despite >40 mL/kg of
isotonic intravenous fluid in 1 hour: ́•Hypotension <5th percentile for age
or systolic blood pressure <2 SD below normal for age OR •Need for
vasoactive drug to maintain blood pressure OR •2 of the following:
•Unexplained metabolic acidosis: base deficit >5 mEq/L; •Increased
arterial lactate: >2 times upper limit of normal; •Oliguria: urine output
<0.5 mL/kg/hr; •Prolonged capillary refill: >5 sec; •Core to peripheral
temperature gap >3˚C
2. Acute respiratory distress syndrome (ARDS) as defined by the presence
of a PaO2/F102 ratio ≤300 mm Hg, bilateral infiltrates on chest
radiograph, and no evidence of left heart failure OR Sepsis plus 2 or

24
 more organ dysfunctions (respiratory, renal, neurologic, hematologic, or
hepatic)

Septic shock Sepsis plus cardiovascular organ dysfunction as defined above

Multiple Presence of altered organ function such that homeostasis cannot be maintained
organ without medical intervention
dysfunction
syndrome
(MODS)

Respondent filed as Exhibit C, Tab 1, to Dr. Brown’s supplemental expert report (Ex. C)
the following medical article: Derek C. Angus & Tom van der Poll, Severe Sepsis and Septic
Shock, 369 N ENGL J MED 9:840-51 (2013). The authors state that “signs of a systemic
inflammatory response, such as tachycardia or an elevated white-cell count, occur in many
infectious and noninfectious conditions . . . .” Id. at 840. This medical article supports the view
that the medical community accepts non-infectious causes of SIRS.

Respondent filed as Exhibit C, Tab 2, the following untitled chapter from RED BOOK:
2009 REPORT OF THE COMMITTEE ON INFECTIOUS DISEASES (Larry K. Pickering et al. eds., 28th
ed. 2009) (missing internal page numbers, but respondent numbered pages 1-6). The authors
state in the category of adverse events a fever of 103 degrees or higher occurring between 6-12
days after MMR vaccination. Id. at 4. Transient rashes and thrombocytopenia have been
reported. Id. Thrombocytopenia has occurred between two to three weeks after MMR
vaccination. Id. at 5. This report supports the view that reactions of fever, rash, and
thrombocytopenia occur at least almost a week or two after MMR vaccination.

Respondent filed as Exhibit E, Tab 2, to Dr. Whitton’s expert report (Ex. E) the following
medical article: Jason Phua et al., Characteristics and outcomes of culture-negative versus
culture-positive severe sepsis, 17 CRITICAL CARE R202 1-12 (2013) doi:10.1186/cc12896.
Although bacteria are known to cause 50 percent of severe sepsis cases, less is known about the
other half of severe cases for which etiologic agents have not been discovered. Id. at 1. The
authors state that “severity of illness and mortality are not significantly affected by
microbiological documentation in sepsis. . . .” Id. They posit that some of the culture-negative

25
sepsis patients might have had nonbacterial sepsis. Id. at 9. They also consider that some of
these patients might not have had actual sepsis. Id. This article supports the view that
nonbacterial sepsis may be just as severe as bacterial sepsis.

Respondent filed as Exhibit E, Tab 6, to Dr. Whitton’s expert report (Ex. E) the following
medical article: Steven D. Burdette, Systemic Inflammatory Response Syndrome, MEDSCAPE
(updated: Jan. 29, 2014) https://emedicine.medscape.com/article/168943-overview (last visited
July 23, 2018). 57 The author states that “SIRS is not always related to infection.” Id. at 1. He
also states, “Although not universally accepted terminology, severe SIRS and SIRS shock are
terms that some authors have proposed. These terms suggest organ dysfunction or refractory
hypotension related to an ischemic or inflammatory process rather than to an infectious
etiology.” Id. at 2. The author states, “Systemic inflammatory response syndrome (SIRS),
independent of the etiology, has the same pathophysiologic properties, with minor differences in
inciting cascades. Many consider the syndrome a self-defense mechanism. Inflammation is the
body’s response to nonspecific insults that arise from chemical, traumatic, or infectious stimuli.”
Id. The author lists as one of the noninfectious causes of SIRS: “drug reaction.” Id. at 4. The
author states, “Of the SIRS patients without infection, the clinical characteristics were similar to
those with positive cultures.” Id. at 5. This medical article supports the view that the medical
community accepts that non-infectious causes such as drug reaction can cause SIRS and the
clinical characteristics of SIRS do not differ whether the cause is infectious or non-infectious.

Respondent filed as Exhibit E, Tab 7, to Dr. Whitton’s expert report (Ex. E) pages 75-76
from a chapter entitled “Evaluating Biological Mechanisms of Adverse Events” and a subchapter
entitled “Immune-Mediated Mechanisms,” and pages 218-21 from the book ADVERSE EFFECTS
OF VACCINES. EVIDENCE AND CAUSALITY (Kathleen Stratton et al. eds., 2012). This excerpt from
the Institute of Medicine (“IOM”) states subtle imbalances of proinflammatory and anti-
inflammatory cytokines may follow immunization against rubella, citing four medical articles.
Id. at 76. Moreover, the IOM considered that a vaccinee’s unique immunogenetic makeup might
predispose him to an exaggerated cytokine imbalance following immune stimulation such as
vaccine administration. Id. The IOM took a neutral stance as to whether or not vaccinations can
result in oversecretion of cytokines. Id.

Respondent filed as Exhibit H, Tab 4, to Dr. Whitton’s supplemental expert report (Ex.
H) the following medical article: Damon P. Eisen & Robyn M. Minchinton, Impact of Mannose-
Binding Lectin on Susceptibility to Infectious Diseases, 37 CLIN INFECTIOUS DIS 1496-1505
(2003). The authors show that low mannose-binding lectin (“MBL”) is related to greater risk of
infection. In discussing Neisseria meningitidis, the authors state MBL stimulates phagocytosis
of this disease by neutrophils, macrophages, and monocytes, and increases the rate of killing of
the organism while modulating the immune response through reduced production of
proinflammatory cytokines. Id. at 1499. T.A.’s doctors tested T.A.’s MBL levels to find out if

57
Respondent did not provide an electronic citation for this 2014 version. The updated version is dated May 7, 2018
and the author is Lewis J. Kaplan. Petitioners filed the same article as Exhibit 41 but updated to Mar. 30, 2015 with
the author as Lewis J. Kaplan and the same electronic citation the undersigned notes in the text of this opinion.
Petitioners’ and respondent’s pagination are identical, and the undersigned cites this pagination.
26
he were deficient since he had a history of staphylococcal infections. T.A.’s levels were not
deficient.

Petitioners filed as Exhibit 36 an excerpt from CENTERS FOR DISEASE CONTROL AND
PREVENTION. EPIDEMIOLOGY AND PREVENTION OF VACCINE-PREVENTABLE DISEASES (Jennifer
Hamborsky et al. eds., 13th ed., 2015). The CDC state:

The immune response to a live attenuated vaccine is virtually
identical to that produced by a natural infection. The immune
system does not differentiate between an infection with a
weakened vaccine virus and an infection with a wild virus.

Id. at 5 (petitioners’ page 16).

Petitioners filed as Exhibit 44 to Dr. Levin’s supplemental expert report (Ex. 43) the
following medical article: Rita F. Helfand et al., Timing of Development of Measles-Specific
Immunoglobulin M and G after Primary Measles Vaccination, 6 CLIN DIAGN LAB IMMUNOL
2:178-80 (1999). The authors tested 209 children to determine when, after measles vaccination,
they had the greatest positive IgM results. Id. at 178. The answer was the second and third
weeks after measles vaccination. Id. This article supports the opinion that immunity after
measles vaccination takes two to three weeks to develop.

TESTIMONY

Before testimony began, the undersigned had a discussion on the record with counsel
during which respondent’s counsel stated there was an issue of more than six months of sequelae
should the undersigned rule in favor of petitioners. Tr. at 6-7. The undersigned explained for the
benefit of the petitioners sitting in the hearing room that this discussion was in the context of
petitioners’ proving a Table acute encephalopathy which must be followed by a chronic
encephalopathy lasting more than six months and proving a Table thrombocytopenic purpura
which must be followed by more than six months of sequelae. Id. at 9. In addition, petitioners
were alleging causation in fact SIRS. Id. The undersigned said that if the undersigned ruled
MMR vaccine caused in fact T.A.’s SIRS, no one was going to doubt there were more than six
months of sequelae. Id. at 9.

Petitioner Mr. Ahlum testified first. Tr. at 41. T.A. received MMR vaccine on August
11, 2011. Id. at 45. T.A. started getting sick on Tuesday, August 23, 2011 because he had a
fever. Id. at 46. No one else in the family was ill. Id. His wife called the pediatrician and the
staff recommended using Tylenol and ibuprofen and scheduled an appointment with Dr. Allen
the next morning. Id. at 47. T.A. was a little irritated. Id. at 48. When T.A. came home from
seeing Dr. Allen, T.A. was worse. Id. at 50. In the late evening, he was throwing up and had
diarrhea. Id. T.A. was lethargic, and defecated in his pants. Id. at 51. Dr. Allen called an
ambulance to start IVs on the way to Mercy Hospital. Id. at 52. Dr. Allen cleared his schedule
for the rest of the day. Id. at 53. T.A. perked up with the IV fluid and said he wanted something

27
to drink and maybe watch a little television. Id. at 54. T.A. became much worse and plans were
made around 4:00 or 5:00 p.m. to airlift him to Arkansas Children’s Hospital. Id. at 55. The
anesthesiologist came in to intubate T.A. and put him to sleep. Id. T.A. freaked out and was
scared. Id. at 56. To Mr. Ahlum, it looked as if T.A. was essentially doing okay; he was still
breathing fine. Id. Dr. Allen was really concerned about T.A.’s insulin level. Id.

When the staff at Arkansas Children’s Hospital finally let Mr. Ahlum into T.A.’s room
around 11:30 p.m., T.A. had multiple tubes in him and he was leaking fluids out of every orifice.
Id. at 58. None of the staff was wearing a mask and he was not either. Id. He was with T.A.
every night for the weeks T.A. was at Children’s. Id. at 60. There was not a moment that
someone in the family was not at his bedside. Id. Immediately after the hospital discharged
T.A., it readmitted him the next day. Id. This readmission lasted one week and T.A. was with
his mother because Mr. Ahlum went back to work with Mr. Ahlum visiting on the weekends. Id.
at 60-61. As Mr. Ahlum put it, T.A. did “some crazy things.” Id. T.A. would stand up on his
stumps, run on his bed, try to jump off, and lash out at his mother. Id. That behavior continued
in the weeks after petitioners and T.A. returned home. It felt as if T.A. were possessed. He was
“just completely out of his mind on many occasions.” Id. When T.A. went back to Dr. Allen’s
clinic, it was “a life-altering experience for everyone in their clinic.” Id. at 62. They had a cake
for him and nice things, but it was a terrible experience. Id. at 63. T.A. was angry that it was
happening and he destroyed the cake in front of everyone. Id. T.A. had no eye contact. He
would look around with just a dead stare. Id. Before all this happened, T.A. was the life of the
party for himself and his older brother. Id. at 64. That was no longer T.A. after this experience.
Id. Also, after this experience, T.A. was no longer potty trained. Id. at 65. When Thanksgiving
came, T.A. was off in his little room. Id. It broke Mr. Ahlum’s mother’s heart. Id.

Mr. Ahlum said T.A. hated to go to therapy. Id. at 67. He does pretty well in school. Id.
He has home school two days a week and goes to a private school two days a week. Id. at 68.
T.A.’s reading level is a grade behind. Id. T.A. puts things in his mouth, like his T-shirt edge or
a Lego. Id. at 69. He does not want to go outside and play, and he mutters. Id. at 70. Early on,
T.A. was having “unbelievably terrible night terrors.” Id.

Dr. Barry Allen, T.A.’s treating pediatrician, testified next. Id. at 104. He has been in
practice since 1976, or 40 years at the time of the hearing. Id. at 105. T.A. received his first
MMR vaccination on August 11, 2011. Id. at 107, 108. Dr. Allen next saw T.A. 13 days later on
August 24, 2011, because T.A. had fever and a rash. Id. at 108. T.A. had a fever of 102 degrees
and a petechial rash. Id. T.A. also had a macular rash on his neck and trunk. Id. at 109. His
white blood cell count was 6,000, which is normal. His platelet count was low. Dr. Allen gave
T.A. Rocephin. Id. When the undersigned asked Dr. Allen what was the difference between a
macular rash and a petechial rash, he replied a macular rash is a red rash and a pectechial rash
little blood spots on the skin. Id. Dr. Allen gave T.A. an antibiotic because he was concerned
that T.A. could have an infection because of his low platelet count and fever. Id.

Dr. Allen has had patients who had an adverse reaction to MMR vaccine. Id. at 110. The
typical time frame after vaccination was a week to several weeks. Id. T.A. returned to Dr. Allen

28
the next day, on August 25, 2011, and was very seriously ill. Id. He was 10 percent dehydrated
and had vomited during the night. Id. His platelet count had dropped to 73,000. Id. at 110-11.
His white blood cell count had risen from 6,000 to 20,000. Id. at 111. Dr. Allen’s concern was
to get T.A. out of a shock-like state. He started an IV on T.A. in the office and transferred him to
the hospital and then to Arkansas Children’s Hospital. Id. Dr. Allen considered the diagnostic
possibilities to be sepsis and thus putting T.A. on IV fluids and IV antibiotics, but also T.A.
could be reacting to MMR vaccination because of the time interval. Id. He went in the
ambulance with T.A. to the hospital. Id.

During T.A.’s time at Arkansas Children’s Hospital, T.A. was on multiple antibiotics, on
medication to maintain his blood pressure, and on dialysis. Id. at 112. T.A. had multiple blood
tests, multiple cultures, and PCRs to identify a bacterial cause, and the results were all negative.
Id. Rocephin is a broad-based antibiotic that covers meningococcus, pneumococcus, and
streptococcus. Id. It works within minutes to hours. Id. at 113. T.A. did not improve after
being on Rocephin. Id. In light of the failure of the cultures and PCR to find a bacterial cause,
Dr. Allen reassessed the timing of the MMR vaccination considering the onset of T.A.’s illness.
Id. Dr. Allen testified, “I have thought about him obviously several times over the past years,
and I have to think that the MMR was the etiology of his illness.” Id.

When Dr. Allen saw T.A. on October 24, 2011, T.A. had not returned to his neurological
baseline because he still did not make eye contact or smile, and this was a week after he was
discharged from the hospital. Id. at 114. He also had some aggressive behavior. Id. It could
indicate depression and even some neurological problems. Id. T.A. has not received a second
MMR vaccination. When asked if he would recommend T.A. receive a second MMR
vaccination, Dr. Allen replied, “Well, that would be a very difficult decision for me. I would
probably recommend the other immunizations, but I would be very reluctant to recommend an
MMR for T.A.” Id.

On cross-examination, Dr. Allen agreed that the standard of care for a patient with
bacterial sepsis is the administration of antibiotics and when he saw T.A. on August 24, 2011, he
suspected T.A. had a possible bacterial infection. Id. at 115. Dr. Allen admitted he is not an
infectious diseases specialist. Id. at 118. He also admitted that a macular rash and a petechial
rash can indicate an infectious process, including meningococcus. Id. at 120. T.A.’s symptoms
were consistent with a meningococcal infection. Id. at 124. Dr. Allen’s initial concern on
August 24, 2011 was sepsis, but T.A. did not have purpura. Id. Dr. Allen said that his records
do not reflect his considering a reaction to MMR because he was primarily concerned initially
about an infection, but the fact that T.A. had MMR only came to light later. Id. He did not note
it in his record for August 25, 2011 because T.A. was very ill, dehydrated, and hypovolemic. Id.
at 125. He does not know why he did not dictate the role of MMR vaccine when he wrote the
discharge summary at Mercy Hospital. Id. After T.A. was transferred to Arkansas Children’s
Hospital, Dr. Allen went back and looked through T.A.’s record and became aware that he had
received MMR vaccine. Id. at 126. Dr. Allen said, “We were trying to save his life at the time
he was transferred, Ma’am.” Id. Dr. Allen did, after the initial day, have phone conversations
with the doctors at Arkansas Children’s Hospital. Id. It does not surprise Dr. Allen that his

29
phone conversations with the doctors at the hospital are not reflected in their records. Id. at 128.
He does remember telling the doctors that T.A. had received MMR vaccine two weeks before.
Id. He is aware that except for a reference in the hospital records to SIRS, the diagnosis
throughout the other records at Arkansas Children’s Hospital is to bacterial shock and sepsis. Id.
at 129. Dr. Allen stated again that his focus on MMR vaccine as the cause was the two-week
interval between vaccination and T.A.’s illness, and the negative results of the PCRs and
cultures. Id. at 132. Dr. Allen never diagnosed T.A. as having encephalopathy. Id. at 133-34.

Petitioner Mrs. Ahlum testified next. Id. at 143. After T.A. received MMR vaccine on
August 11, 2011, he was fine the week afterwards. Id. at 145. On Monday, he was tired. On
Tuesday, he ran a low-grade fever in the morning. He was tired. Later in the evening, he ran a
higher temperature. She called the local walk-in clinic and the nurse told her to use ibuprofen
and Tylenol, and to see the doctor in the morning. Id. at 145. On August 24, 2011, she took him
to Dr. Allen. Id. at 146. T.A. had a 102 fever, a small pinpoint rash plus another kind of rash,
low platelets, and was very sick. Dr. Allen gave him a shot of Rocephin and told them to come
back the next day. Id. That night, T.A. got worse. He started throwing up and had diarrhea. Id.
They went back to Dr. Allen earlier than their appointment and T.A. was lethargic. Id. at 147.
T.A.’s platelets were lower and his white blood cell count was higher. She rode in the
ambulance with T.A. and Dr. Allen. Id. T.A. seemed to perk up in Mercy Hospital, but his
insulin level started skyrocketing to 400 and then to 661. Id. at 148. The doctors thought T.A.
was going into diabetic shock. Then T.A. started crashing. Id. No one in T.A.’s room including
her and her four-month-old baby wore protective garb to protect them from a virus or bacterium.
Id. at 149.

When Mrs. Ahlum arrived at Arkansas Children’s Hospital, T.A. was in the PICU and
not isolated from anyone else. Id. at 150. The only time personnel were really concerned about
wearing a mask was after T.A.’s legs turned purple and were blistered and the Burn Team came
in to make sure his legs did not get infected. Id. at 151. The next day, Mrs. Ahlum told two
infectious diseases doctors that the family had gone to a petting zoo at the state fair and she had
washed T.A.’s hands and put antibacterial spray on them. Id. at 151. The doctors had no idea
what the cause of T.A.’s illness was. Id. at 152.

Dr. Alan S. Levin testified next for petitioners. Id. at 175. He is board-certified in
allergy, immunology, pathology, and emergency medicine. Id. at 178. He is a member in the
American Academy of Allergy, Immunology. Id. He used to teach medical students medicine
and immunology. Id. at 179. He testified he is very familiar with vaccines in general and the
immunology of vaccines. Id. at 180. He has treated about a hundred patients with SIRS. Id. He
spends about 95 percent of his time working as a lawyer. Id. at 183. The other five percent of
time he treats patients. Id. Since 1993, the majority of his time has been spent practicing law.
Id. at 184. He practices toxic torts. Id. at 185. He became a lawyer because “toxic tort litigation
is the single-most powerful tool to advance science.” Id. at 186. Respondent did not object to
Dr. Levin as an expert in immunology. Id. at 196.

Dr. Levin testified that when T.A. saw Dr. Allen on August 11, 2011, he did not have an

30
infection when he received MMR vaccine. Id. at 198. Dr. Levin said that an adverse reaction to
MMR vaccine is very rare. Id. at 198-98. He stated measles virus is not very pathogenic
compared to influenza. Id. at 199. MMR does not have enough of the receptor molecules on the
cell surface to provoke the immune system. Id. Killed measles virus vaccine did not work.
Then the manufacturers created attenuated measles virus vaccine so that it could replicate, but it
did not replicate as quickly and aggressively as wild measles virus. Id. The attenuated measles
virus vaccine is safer than having wild measles, but it does not provoke an immune response as
rapidly as wild measles virus. Id. at 199-200. The immune response that the attenuated measles
virus provokes in a naïve patient, i.e., one who has not received measles vaccine before such as
T.A., takes roughly two weeks to have an immune response. Id. at 200. Although the attenuated
measles virus vaccine provokes the innate immune system a little bit, Dr. Levin said the vaccine
primarily reacts against the adaptive immune system. Id.

Dr. Levin explained that the innate immune system recognizes patterns of molecules and
serves as a gate guard. Id. It is the original protector of the body and responds within hours.
The adaptive immune system functions by having receptors identify the tertiary structure of an
antigen. Molecules signal the cells to secrete antibodies or cytokines. The adaptive immune
system responds in weeks. Respondent’s experts ask why T.A. did not become ill in the first 48
hours after his MMR vaccination. The answer is that the vaccination did not provoke the innate
immune system enough to cause him to be sick. Id. After two weeks, then the adaptive immune
system starts working against the vaccine and we see the cytokine storm that T.A. suffered. Id.
at 201. Dr. Levin cited the Helfand article (Ex. 44) as support for at least a week or two weeks
before an immunological response to a first MMR vaccination occurs. Id. at 203.

Dr. Levin explained SIRS. Id. at 204. People have only a few ways of responding to an
immunologic insult. SIRS is the way that people respond to bacteria, viruses, fungi, toxic
chemicals, and vaccines. Id. Once SIRS is triggered, it goes on spontaneously in the body as
happened in T.A. Id. In SIRS, there is an overreaction of pro-inflammatory or anti-
inflammatory cytokines and other agents that cause inflammatory response. Id. at 205. Certain
molecules, such as interleukin-6 and sometimes interleukin-1, can reach endothelial cells or the
cells that bind capillaries of the blood vessels and cause the cells that have fused together to
separate. Then plasma comes out and causes edema, which happened in T.A.’s arms and
probably in his brain. Id. Edema causes all kinds of problems in the central nervous system and
circulation. Then there is clotting of blood, platelets sticking together, intervascular coagulation,
and thrombocytopenia in which the level of platelets decreases, causing blood clots, which
happened to T.A.’s legs. The reason the legs are vulnerable is they are far from the heart and
they die first. Id. Interleukin-1 and Interleukin-6 are small protein molecules secreted by
macrophages primarily and increase inflammation. Id. at 205-06. Although it is called an
immune system, Dr. Levin prefers to call it a system of growth and differentiation, i.e., part of
the system destroys and the other part of the system heals. Id. at 206. Dr. Levin said life is
homeostasis. 58 Id. In T.A.’s case, it was the pro-inflammatory cytokines that caused the harm.
Id. T.A.’s maculopapular rash, petechial rash, 103 degree fever, vomiting, and diarrhea were

58
Homeostasis is “a tendency to stability in the normal body states (internal environment) of the organism. It is
achieved by a system of control mechanisms activated by negative feedback. . . .” Dorland’s at 867.
31
consistent with a reaction going out of control. Id. at 208-09. Those symptoms are what make
the reaction systemic. Id. at 209.

In Dr. Levin’s opinion, T.A.’s fever on August 23, 2011 was due to MMR vaccination.
Id. The pro-inflammatory cytokines triggered T.A.’s fever. Id. Dr. Levin said that T.A.’s white
cell count rising from 6,000 on August 24, 2011 to 20,000 on August 25, 2011 was very typical
of a SIRS reaction to bacteria, viruses, toxic chemicals, and/or vaccines. Id. at 210. The spleen
“spits out” all kinds of cells. Id. T.A.’s decrease in platelet counts from 97,000 on August 24,
2011 to 73,000 on August 25, 2011 were partially responsible for the petechial rashes and little
blood clots, and were also a response to MMR vaccine. Id. Dr. Levin said that because T.A.’s
titers were positive to measles, he had a local reaction which was the predicate of a systemic
reaction to the vaccine. Id. at 212-13. The local reaction is a good thing, not an adverse
reaction. Id. at 214. Dr. Levin said that the adaptive immune system can cause SIRS and did so
in T.A. Id. at 215. The appropriate time for a SIRS reaction is one to three weeks post-
vaccination. Id.

Dr. Levin noted that, although T.A. received the antibiotic Rocephin on August 25, 2011,
the antibiotic did not work and T.A. became much sicker. Id. at 216. The failure of Rocephin to
help T.A. mitigates against T.A. having a bacterial infection that caused his SIRS. Id. at 216-17.
Dr. Levin stated that meningococcus is exquisitely sensitive to Rocephin and the failure of
Rocephin to work means T.A. probably did not have meningococcus. Id. at 217. In T.A.’s case,
the most probable cause of T.A.’s SIRS was the MMR vaccine because the doctors could not
find a pathogen. Id. at 219. Dr. Levin said that the immunology unit of the Arkansas Children’s
Hospital is one of the best immunology units in the United States. Id. at 220.

Dr. Levin said that all SIRS is the same, whether the trigger is bacteria or a vaccination.
Id. at 224. He said humans have a limited repertory of responses to insults. Id. Dr. Levin called
NELSON TEXTBOOK OF PEDIATRICS (Ex. B, Tab 3) the bible of pediatrics. Id. at 225. The chapter
from NELSON that respondent filed as an exhibit lists measles vaccine as a cause of SIRS. Id. at
223-24. The chapter includes measles vaccine as part of its list of infections. Dr. Levin said that
since attenuated measles vaccine replicates, measles virus vaccine is an infection. Id. at 225.
SIRS leads to sepsis by replicating an infectious organism causing a disease process. Id. at 227.
T.A. had a fever, tachycardia, respiratory distress, elevated neutrophils, all indicative of SIRS on
August 25, 2011. Id. at 228. Elevated neutrophils are not indicative of bacterial infection; rather
they are a criterion for SIRS no matter what the cause. Id.

Dr. Levin’s opinion is that T.A. had SIRS which MMR vaccine probably triggered. Id. at
236. He also believes that T.A. did not have meningococcus because Rocephin did not help T.A.
get better. Id.

On cross-examination, Dr. Levin agreed that Neisseria meningitidis is a very infectious
disease process. 59 Id. at 255. It is one of the most common causes of SIRS. Id. at 256. On

59
The undersigned recalled Mrs. Ahlum to testify if she or her baby got sick since they were purportedly exposed to
what respondent’s experts and Dr. Levin agreed is a very infectious disease process. The undersigned asked Mrs.
32
redirect, Dr. Levin noted that T.A. also had a nasal culture which was negative. Id. at 263. Dr.
Levin thinks that T.A.’s having a staph infection on his neck which formed a cyst and had to be
drained when he was an infant is relevant because T.A. may have had some immune
dysregulation prior to being vaccinated against MMR in 2011. Id. at 267. Dr. Levin said that
T.A. had an immune workup after his SIRS, which indicated a very subtle immune
dysregulation. Id. at 268. Whether or not T.A. has an immune deficiency does not affect Dr.
Levin’s opinion that MMR vaccine caused T.A.’s SIRS. Id. at 302.

Dr. David Siegler testified next for petitioners. Id. at 304. He is a pediatric neurologist.
Id. at 305. He is familiar with how MMR vaccine initiates the immune response. Id. at 314.
The three viruses making up the vaccine are attenuated, i.e., engineered to be less virulent. Once
injected in the recipient, the viruses replicate but not to the degree that a live, wild virus would.
The viral replication induces the immune system to develop a response to produce immunity. Id.
Twelve days after T.A. received MMR vaccine, he had symptoms. Id. An adverse reaction to
MMR takes days because the immune response needs to gear up. Id. at 315. The Vaccine Injury
Table puts the Table duration as five to 15 days. Id. T.A.’s having fever 12 days after MMR
vaccination followed by the other symptoms fits perfectly in the timing of what is expected for
an adverse reaction to MMR vaccine. Id. The adverse reaction is systemic, causing
inflammation which can affect all organs. Id. at 316. On August 24, 2011, T.A. saw Dr. Allen
and had a fever of 102 degrees, petechial rash over his neck and trunk, macular rash on his trunk,
low platelet count, and a normal white blood cell count. Id. at 317. The low platelet count can
be caused by either MMR vaccine or inflammation resulting in clotting. Id.

Dr. Siegler said that Rocephin administered intramuscularly works quickly on a bacterial
infection. Id. at 319. The Rocephin did not work which means either T.A. did not have a
bacterial infection or the antibiotic was not the correct one to use. Id. at 320. Dr. Siegler said
that on August 25, 2011, T.A. was manifesting signs and symptoms of encephalopathy. Id. at
322. T.A. was quite lethargic, meaning he had a depressed level of consciousness, which is a
sign of encephalopathy. Id. T.A. was so depressed in consciousness that he had no normal
response to his need to defecate and stooled in his pants. Id. at 323. Dr. Siegler said T.A.’s
decreased level of consciousness lasted more than 24 hours. Id. He said T.A.’s change in mental
status was not related to medication. Id.

Dr. Siegler’s opinion is that T.A. had an adverse reaction to MMR vaccine. Id. at 337.
There was no other explanation and he did not improve on the various antibiotics he received.
Id. at 338. Dr. Siegler agrees with the diagnosis of SIRS. Id. Dr. Siegler believes that T.A.’s
behavioral peculiarities are due to his acute encephalopathy. Id. at 342. He thinks T.A.’s
petechiae were due to his low platelet count from his MMR reaction and the macular rash was
due to the MMR reaction. Id. at 348. Dr. Siegler said that the first neurologic symptom in shock
regardless of the cause is poor perfusion which leads to a depressed level of consciousness. Id.
at 366. Then comes ischemia, cranial nerve dysfunction, edema, bleeding, and possible strokes

Ahlum if, after the night between August 24 and 25, 2011, when she had T.A. in bed with her on one side and her
four-month-old baby on the other side, and T.A. was vomiting and had diarrhea all night, if she or her four-month-
old baby got sick. She said no. Id. at 304.
33
and seizures. Id. at 367. Ischemia is decreased blood flow that can cause tissue injury due to
lack of nutrients or oxygen to an area. If blood flow is diminished too long to the extremities,
necrosis occurs. Id. In the hospital, doctors had to give T.A. pressors to increase his blood
pressure and get blood moving to his brain. Id. at 368. Muscles have a greater metabolic
demand for nutrients and oxygen which is why T.A.’s leg muscles died before his skin. Id.
T.A.’s kidneys shut down and he was on dialysis, but the kidneys came back. Id. T.A.’s liver
function tests were very elevated. Id. at 369. Dr. Siegler explained that a depressed level of
consciousness means that the brain is impaired. Id. at 370.

Dr. Siegler’s opinion is that T.A. had an adverse reaction to MMR that presented initially
with fever and petechiae, followed by encephalopathy. Id. at 374. T.A.’s first symptoms were a
systemic inflammatory event that ultimately resulted in multi-organ dysfunction, the earliest
being brain dysfunction or encephalopathy from a depressed level of consciousness. Id. The
initial reaction to MMR vaccine was begun in the immune system and, in the course of that
immunologic reaction, he had symptoms of encephalopathy. Id. The first signs of T.A.’s
reaction to MMR occurred on August 23, 2011 with fever and rash. Id. at 377. He was not
encephalopathic at the time. Id. T.A. did not have a consultation with a neurologist. Id. at 383.
Dr. Seigler said that T.A.’s encephalopathy began on August 25, 2011. Id. at 386. When T.A.
arrived at Mercy Hospital, he perked up and wanted lemonade and to watch cartoons, meaning
his encephalopathy was improved. Id. at 389. Prior to T.A.’s transport by helicopter, he was
intubated at 4:30 p.m. and sedated at 4:25 or 4:30 p.m. at Mercy Hospital. Id. at 386, 408, 409.

Dr. J. Lindsay Whitton testified next for respondent. Id. at 440. He is a full professor at
the Scripps Research Institute working on the immune response to viral and bacterial infections.
Id. at 441-42. He also works on vaccines. Id. at 442. He studies the interface between viruses
and immunology in live animals. He infects animals with viruses and studies how their immune
systems respond to the viruses. Id. Dr. Whitton does not have patients. Id. at 442-43. His
funding come from National Institutes of Health grants. Id. at 444. He is an editor of the journal
Virology. Id. at 449. Essentially all of his work relates to the immune system and how viruses
and/or bacteria cause disease. Id. at 452-53. He works on Group B streptococcus and
Staphylococcus aureus. Id. at 453. He does not work on fungi in the lab. Id. at 454. When he
works with rats, rabbits, and mice, he is trying to induce an inflammatory response by
introducing either a virus or a bacterium. Id. Dr. Whitton has not ever qualified to practice
medicine in the United States because he wanted to do research. Id. at 464.

Dr. Whitton said the immune system is smart enough to recognize the type of invader of
a bacterium or a virus and then mount the type of immune response that is best suited to deal
with the invader. Id. at 455. Dr. Whitton has done research on vaccines. Id. at 457. He does
not work on measles in the lab because it is hard to get a great animal model for measles. Id. at
458.

Dr. Whitton said that T-cells help to control viral infection by secreting cytokines. Id. at
460. Cytokines are very toxic molecules and dangerous. Id. Whereas antibodies recognize free
viruses floating in the blood, T-cells recognize intact cells that are infected with viruses. Id. T-

34
cells make cytokines which are in direct contact with the virus-infected cell and, after direct
contact, the T-cell shuts down cytokine production. Id. at 461. There is a constant balance
between pro-inflammatory and anti-inflammatory cytokines. Id. at 462. When things get out of
control, there is cytokine storm. Id. at 463.

Dr. Whitton said that measles is a viral infection. Id. at 465. Dr. Whitton’s opinion is
that MMR vaccine did not play any role in T.A.’s shock syndrome. Id. at 472. He defined SIRS
as systemic inflammatory response syndrome, reflecting a body-wide response to the release of
cytokines. Id. at 474. There are varying degrees of SIRS. Id. at 475. Sepsis is bacterial
infection in the bloodstream. Id. at 477. Viruses and fungi can cause cytokine storm. Id. at 477-
78. In Dr. Whitton’s view, it is a semantic issue. Id. at 478. He said, “I think of sepsis as
bacterial, and I’m perfectly happy to accept a redesignation of sepsis to include other infections,
but for me, the way I was trained, it’s a bacterial infection entering the bloodstream.” Id.

Dr. Whitton defined septic shock as when bacteria in the bloodstream, often called
septicemia have caused sufficient stimulation of the innate immune response to trigger vast
release of cytokines, both pro-inflammatory and anti-inflammatory, which leads to other signs
and symptoms. Id. at 478-79. Bacterial septic shock is a type of cytokine storm. Id. at 479. The
terms “sepsis,” “septic shock,” “SIRS,” and “cytokine storm” overlap. Id. Dr. Whitton
proceeded to draw a schematic (marked as Exhibit K). Id. at 482. He said that many bacterial
infections exist in the absence of SIRS. Id. They do not trigger much of an immune response.
Sometimes bacterial infections become a little bit more severe, and they begin to enter the
domain of SIRS. Id. Some bacteria enter the bloodstream and this is sepsis. Id. at 483. Some
move on to severe sepsis and some move on to septic shock. Id. All SIRS means is systemic
inflammatory response which does not say anything about the clinical severity of that response.
Id. Dr. Whitton prefers to talk about mild SIRS and severe SIRS and then SIRS shock. Id. at
484. One could get SIRS shock from nonbacterial causes and this means not all SIRS shock
would be septic shock. Id.

Dr. Whitton moved on to viruses. Id. Many viruses do not cause even mild SIRS, but “a
bunch of them” do. Id. Some viruses move into the mild SIRS category. Some viruses go out to
cause septic shock, but this is semantics. The viruses cause what Dr. Whitton would call
cytokine storm, but he has no objection whatsoever to calling it septic shock or virus-induced
shock or SIRS shock. Id. But, he explained, “[H]ere we see that there is not a precise
equivalence between SIRS shock and septic shock because if you have a SIRS shock caused by
virus, it’s not septic shock.” Id. at 484-85. SIRS shock is the umbrella term Dr. Whitton would
use. Id. at 485. He would “happily” also use cytokine storm because the two terms are basically
synonymous. Id. All septic shock is SIRS shock. Id.

Dr. Whitton did not put measles vaccine on his chart. Id. He said that vaccines do not
always induce SIRS, but they can certainly induce mild SIRS. Id. at 486. He stated, “I contend
that vaccines do not induce SIRS shock or cytokine storm.” Id. He knows of no literature to
show that vaccines can induce cytokine storm. He says it is very difficult to understand how a
vaccine could induce a shock syndrome. With MMR vaccine, Dr. Whitton sees no possible

35
biological reason to suspect it caused the catastrophically severe symptoms T.A. suffered. Id.
He is basing his opinion on 30 years of knowledge and the medical literature. Id. Dr. Whitton
said he has never worked with humans, but routinely vaccinates animals. Id. at 488. He stated
vaccination induces the protective component of memory lymphocytes, part of the adaptive
immune system. He also relies on literature but the literature petitioners filed on behalf of their
experts does not suggest vaccines can cause shock. Id. Vaccines can cause fever, a bit of
tachycardia, which would put the vaccinee in the mild SIRS category. Id. at 489.

Respondent’s counsel asked Dr. Whitton if the chapter on shock from NELSON
TEXTBOOK OF PEDIATRICS (Ex. B, Tab 3), “provide[d] a mechanism or state[d] that vaccines
could cause cytokine storm” to which Dr. Whitton replied he did not recall. Id. at 491-92.
Respondent’s counsel then asked him whether the same chapter stated vaccines could cause
severe SIRS or septic shock to which Dr. Whitton replied “certainly not severe SIRS or septic
shock because I’m not aware of any evidence that they do.” Id. at 492. [Table 64-5 on page 6 of
Ex. B, Tab 3, is replicated in part earlier in this decision.]

Dr. Whitton then discussed how the immune system reacts to a bacteria. Id. Components
of the bacterium called pathogen-associated molecular patterns (“PAMPS”) activate the innate
immune response. Id. Two of the common activators that bacteria carry which very strongly
and explosively activate the innate immune response are a sugary lipid called lipopolysaccharide
(“LPS”) or endotoxin. Id. at 492-93. The innate immune system comprises a lot of different
sensors that have a degree of specificity. Id. at 493. Either the LPS or endotoxin interact with a
sensor. Id. One group of sensors is called the toll-like receptor of which there are 11 or 13.
Bacterial endotoxin triggers toll-like receptor 4 (“TLR4”). Not all bacteria carries an endotoxin,
but Streptococcus pneumoniae and Neisseria meningitidis do carry endotoxin. Id. The
molecules combine with a signal through TLR4 and cause an explosive innate immune response
with the production of cytokines. Id. Bacteria contain a second danger signal which is their
DNA, although not all viruses and all bacteria contain DNA. Bacterial DNA differs from human
DNA. Id. Bacterial DNA contains a higher proportion of CpG motifs. Id. at 493-94. Another
of the TLRs, i.e., TLR9, has evolved to recognize DNA containing CpG motifs. Id. at 494. If a
bacterium with endotoxin infects a person and causes septicemia, the innate immune system
profoundly activates through TLR4 with endotoxin and TLR9 with bacterial DNA. Id.

Subsequently the adaptive immune system steps in and responds. Its response to bacteria
differs from its response to viruses. The immune system responds to bacteria by activating B-
lymphocytes which produce antibodies but also one subset of T-cells called CDR4-positive T-
cells. Id. The innate immune response is dose-dependent in that a lot of bacteria produce a
stronger response. The adaptive immune response is only dose-dependent until a threshold is
reached and then it is activated. Id. at 496.

Viruses are similar in that the innate immune system contributes toll-like receptors and
sensor molecules that are different than with bacteria. The innate response usually lasts for three
to five days and then transits into the developing adaptive response which actually begins about
day three but is so small, it is hard to detect. Id. By day 14, the adaptive begins to decline to

36
enter the memory phase which provides protective immunity. Id. at 497.

Another profound difference between viruses and bacteria is in the adaptive response
because the adaptive response to viruses not only includes B-cells and CD4 T-cells, which
collaborate to produce antibodies, but also very strong CD8-positive T-cells, which are very
important for controlling viruses. Id. Dr. Whitton said the immune response is not monolithic.
It responds differently to viruses and bacteria. Id. Genetic deficiencies of the immune system
respond differently to bacteria than to viruses. Id. at 498.

When bacteria invade a host, triggering an innate immune response and its sensors,
including mainly TLR4 and TLR9, cytokine storm can occur. Id. Some bacteria encode very
specialized molecules called superantigens. Id. at 499. Superantigens act through the adaptive
immune system, not through the innate immune system. Id. The adaptive immune system is
highly specific. Id. at 500. If influenza or measles enters, it triggers maybe 100-200 of 10
million cells that are able to respond to that specific antigen. Id. This takes a matter of days to
develop. Id. at 501. The reason it takes the adaptive immune response time to develop is it starts
at a very low number of specific cells and takes about a week or two to develop the full
complement of flu- or measles-specific cells. Id. By the end of 14 days after infection, the host
has multiplied those 100-200 cells about 15-16 times and they begin to die, leaving memory cells
which are the cornerstone of vaccination. That is the normal adaptive immune response. Id.

Dr. Whitton said there is no evidence that that can cause cytokine storm. But
superantigens can act on these cells to cause cytokine storm. Superantigens do not active T-cells
in a specific manner. They activate T-cells in a fairly nonspecific manner. Staphylococcal
superantigen binds to molecules on the surface of T-cells and activates 10-15 percent of all T-
cells, which is a large number. Id. Dr. Whitton said bacteria can induce a very rapid cytokine
storm by this mechanism, the key to which is its rapidity. Id. at 502. With endotoxins, cytokine
storm evolves rapidly because of stimulation of the innate immune system. Id.

Dr. Whitton said there is no evidence that MMR vaccine contains a superantigen. Even if
it did, the vaccine would have triggered cytokine shock within two or three days not weeks later.
Id. The innate immune system gets triggered within minutes but not noticeably until a few
hours. Id. at 503. In a bacterial infection, if someone administers Rocephin, it acts very quickly
to stop bacterial replication. Id. at 504. Even if the antibiotic kills the bacteria, the bacteria’s
DNA remains. Id. at 505. DNA can stimulate the innate immune response through CpG motifs.
Id. The spleen clears membranes of the bacteria in 24-36 hours. Id.

Dr. Whitton stated that superantigens do not trigger the innate immune response; they
inappropriately trigger the adaptive immune response. Id. at 507. Viruses differ in their capacity
to trigger the innate immune response. Id. at 512. A superantigen would impact the adaptive
immune system while an endotoxin would impact the innate immune system. Id. at 513. MMR
does not contain a superantigen. Id. at 514.

The undersigned asked petitioners’ immunologic expert Dr. Levin if he agreed with Dr.

37
Whitton’s statement that only a superantigen can impact the adaptive immune system but MMR
does not contain a superantigen. Id. at 515-16. Dr. Levin stated that Dr. Whitton was incorrect.
Id. at 516. Medical literature describes cytokine storm involving a monoclonal antibody, not a
superantigen, which affected the adaptive immune system causing a cytokine storm. Id. Dr.
Whitton responded not only a superantigen but some drugs such as monoclonal antibodies can
activate the adaptive immune system. Id. at 518.

Dr. Whitton stated that vaccines always cause a release of cytokines in the innate immune
system. Id. at 519. Attenuated live viral vaccines cause an innate immune response although
quantitatively probably a little bit less than wild viruses because they replicate much less than
wild-type and there is less of the viral DNA or RNA to start triggering the innate response. Id. at
520. There are two purposes for the cytokines. The innate immune response to live viruses
largely rests upon release of molecules called interferons, because they interfere with virus
infection. These interferons act upon neighboring uninfected cells to alert them to the coming
virus and these cells alter their physiology to make them more resistant to the viral infection.
The other task of cytokines is to facilitate the development of the adaptive immune response. Id.
The innate immune system cytokines last three to five days in mice. Id. As the adaptive immune
response increases in cell numbers, those cells will make cytokine if they encounter viral antigen.
Id. at 522. How long the adaptive immune response lasts depends on the type of viral infection.
Id. at 523.

With MMR vaccine, the host has a primary infection. Id. at 524. Dr. Whitton stated, “I
have no objection to the notion that the adaptive immune response to MMR in this specific case
was occurring at around the time that T.A. developed his signs and symptoms. . . .” Id. at 527.
Dr. Whitton thought that T.A.’s pediatrician Dr. Allen’s opinion that T.A.’s petechiae, lethargy,
and fever could be due to a bacterial infection or to an MMR reaction was reasonable. Id. at
527-28. T.A.’s loss of platelets was due to sepsis, septic shock, and DIC rather than due to
MMR vaccine. Id. at 528. Dr. Whitton said that an injected throat (as T.A. had on August 24,
2011) “is certainly part of measles.” Id. at 529. He did not think that T.A.’s injected throat was
due to MMR vaccine because T.A. did not have Koplik spots. Id. at 529-30. Dr. Whitton said
that T.A. had petechial hemorrhages and stated, “Unquestionably, MMR can cause petechial
hemorrhages.” Id. at 530. MMR can cause fever and T.A. had fever. Id. at 531. He thinks what
happened to T.A. afterwards was due to a bacterial infection. Id. In his view T.A. had a normal
adaptive immune response to MMR because it was the correct time frame. Id. at 533.

Dr. Whitton said that meningococcemia would have caused a fever, DIC,
thrombocytopenia, and a spike in neutrophils. Id. at 535. He said the Rocephin did its job by
killing the bacteria which maybe explains why it was not detectable. Id. But Rocephin does not
remove the materials which stimulate the innate immune system. Id. The following colloquy
occurred:

THE COURT: Now, if he [T.A.] had a bacterial infection that
brought him to the – to Dr. Allen on August 24th, 2011, why was
his white count normal? It was only 6000 on August 24th, 2011.

38
 THE WITNESS: I confess, I am surprised by that. I would have
expected an earlier elevation in his white count. . . . I’m surprised
by that.

Id. at 536.

Dr. Whitton attributed all the catastrophic events that ensued from this date to T.A.’s
innate immune response and not to his adaptive immune response. Id. at 539. He called it septic
shock, or SIRS shock, or cytokine storm. Id. Dr. Whitton stated, “I almost cannot comment on
whether or not there was an adaptive immune response. There may have been.” Id. at 540. Dr.
Whitton said that, possibly, T.A. did not mount an adaptive immune response because he
received IVIG and steroids which suppress the immune response, but he also stated the
suppressive response would tend to limit T.A.’s capacity to mount an adaptive response. Id. at
540-41. Dr. Whitton thinks a bacterium entered T.A. around seven days before the onset of his
symptoms. Id. at 543.

Dr. Whitton, in responding to the Table time onset of 5-15 days for encephalopathy after
MMR vaccine or 7-30 days for thrombocytopenia after MMR vaccine, said those intervals reflect
the adaptive immune response to MMR vaccine. Id. at 548. He is unaware that a normal
adaptive immune response ever causes cytokine storm. Id. at 549.

Dr. Whitton testified that there were two overlapping immune responses occurring at the
time T.A. became sick. First was T.A.’s normal adaptive immune response to measles vaccine.
Second was his innate immune response to the bacterium Neisseria meningitidis, causing
cytokine storm and disseminated intravascular coagulation, which caused thrombocytopenia. Id.
at 551. Dr. Whitton said he could not identify the biological infection T.A. had because it was
not identified. Id. at 552. But he said T.A.’s symptoms were consistent with Neisseria
meningitidis, particularly the petechiae and macular rash. Id. Respondent’s counsel asked Dr.
Whitton by what day after August 11, 2011 when T.A. received MMR vaccine would T.A.’s
innate immune system have returned to normal. Id. at 554. Dr. Whitton responded, “Probably
four or five days post-vaccination, somewhere around there.” Id. He said cytokine storms can
occur in the absence of an increase in neutrophils. Id. Neutrophils are generally a response to
bacterial infection, not viral infection. Id. at 555. One can have cytokine storm without an
elevation of neutrophils. Id. at 558. On August 24, 2011, T.A.’s absolute neutrophil count was
4.39, a normal value. Id. at 561. But on August 25, 2011, T.A.’s absolute neutrophil count rose
to 15.11. Id.

The following colloquy occurred:

THE COURT: [T]here may have been immune modulation from
the two antigenic attacks at the same time. You could say four,
because the measles/mumps/rubella—

39
 THE WITNESS: Yeah.

THE COURT: -- vaccine is three antigens. So, you’ve got three
attenuated live viral antigens working on the immune system to
produce a response, while he’s also fighting off a bacterial
infection that’s trying to provoke another response, and the
immune system is not going – when it’s got too much to deal with,
it may not deal appropriately and neutrally with the bacterial
attack. Is that consistent with your answer?

THE WITNESS: I – I cannot exclude that possibility. I think it’s
an interesting suggestion.

Id. at 567. Respondent’s counsel asked Dr. Whitton if he was aware of reliable evidence to
support the conclusion that that was more likely than not, to which Dr. Whitton replied, “No.”
Id.

Dr. Whitton said if someone had a mild reaction to measles vaccine, he would not require
Koplik spots. Id. at 574. Dr. Whitton said he believed in Occam’s razor, that is, if there might
be two explanations for something, it is better to have one explanation because it is simple. Id. at
576. That is why he attributes all of T.A.’s symptoms to Neisseria meningitidis. Id. He looked
up the incubation period of meningococcus and it is two to ten days. Id. at 577. Usually, it is
three to four days. Id. at 578.

Dr. Whitton said that antigen does not drive the adaptive immune response. Id. at 594. It
triggers it. Id. The innate immune system feeds cytokines to the adaptive immune system to
facilitate the development of the adaptive immune system. Id. at 595. Dr. Whitton stated that
MMR vaccine does replicate, and this is an infectious process. Id. at 607. He admitted that the
immune response to a live attenuated vaccine is similar to that produced by a natural infection.
Id. at 608. He said that as the incoming genetic material in the vaccine virus replicates, the
amount of viral RNA increases and provides a stronger trigger to the innate immune system. Id.
at 614. The replication of this virus is extraordinarily limited, amounting to only about 20 times
compared to thousands of times for the wild virus. Id. The tripping of the innate immune system
would be more likely as the abundance of viral RNA continues to increase due to replication. Id.
at 615. A twelve-day onset to symptoms such as fever and thrombocytopenia after MMR
vaccination is a “perfectly reasonable” time frame to assume a vaccine reaction has occurred. Id.
at 618. The following colloquy occurred:

MR. DOWNING: I am at Exhibit B, Tab 3, page 6. . . . [D]oes
Table 64.5 list a large grouping of differential possibilities for
systemic inflammatory response syndrome?

DR. WHITTON: It does.

40
 MR. DOWNING: Is measles [vaccine] listed as one of the
potential infectious causes of systemic inflammatory response
syndrome?

DR. WHITTON: It is, and so it should be.

Id. at 619-20.

Dr. Whitton said that shock syndrome is undoubtedly attributable to cytokines without
question. Id. at 635. Dr. Whitton denied that MMR vaccine can get the immune system to that
level. Id. Dr. Whitton said he was not sure that MMR vaccine can cause encephalopathy even
though HHS considers it a Table injury. Id. at 639. He said he does not know what the primary
cause of measles encephalopathy is. Id. He said he does not know what the underlying
biological mechanism of measles encephalopathy is. Id. at 640.

Petitioners’ counsel then asked Dr. Whitton if T.A.’s illness satisfied the criteria in Table
64-7 of the chapter on shock [replicated earlier in this decision] from NELSON TEXTBOOK ON
PEDIATRICS (Ex. B, Tab 3). Id. at 643. The heading of Table 64-7 is “International Consensus
Definitions for Pediatric Sepsis.” It has a left-hand column proceeding from infection →
systemic inflammatory response syndrome (SIRS) → sepsis → severe sepsis → septic shock →
multiple organ dysfunction syndrome. Next to each level are definitions of each category. In the
category of SIRS, petitioners’ counsel asked Dr. Whitton since T.A. had fever, tachycardia,
respiratory distress, and leukocytosis, can we skip sepsis, severe sepsis, and septic shock because
there was no infection and end up at multiple organ dysfunction syndrome. Id. at 644. Dr.
Whitton replied, “Absolutely” and offered to explain why. Id. He said there are noninfectious
causes of shock. Id. at 645. Dr. Whitton said someone could absolutely end up in MODS by
skipping sepsis and severe sepsis in pancreatitis or trauma. Id. at 646. Dr. Whitton agreed that
on August 25, 2011, T.A. had SIRS according to the definition of Table 64-7. Id. at 648. But he
said T.A.’s extensive illness was not caused by MMR vaccine. Id. Dr. Whitton said T.A.
developed shock. Id. Dr. Whitton admitted that MODS involves a lot of the same problems
reflected under severe sepsis such as loss of cardiovascular integrity. Id. at 650. Dr. Whitton
said T.A. had a suspected infection, but Dr. Whitton does not mean this was MMR infection
because that virus would not be there anymore. Id. at 651, 683. He said he was talking about the
bacterial infection that T.A. almost certainly had. Id. at 651.

T.A. had culture-negative sepsis. Id. at 669. Dr. Whitton admitted someone could have
elevated neutrophils and SIRS without an infection. Id. at 677. Elevated levels of neutrophils
are more likely produced in the context of bacterial infection rather than viral infection because
neutrophils do not play a key role in clearing a virus. Id. at 677. He said lymphopenia (lowering
the number of lymphocytes) is not unusual when there is ongoing profound inflammation. Id. at
680. Dr. Whitton said that cytokines can drive down leukocytes or lymphopenia. Id. at 682.
Replication of MMR vaccine virus would occur in the first 72 hours. Id. at 684. Dr. Whitton
believes that T.A.’s lethargy and fever resulted from bacterial stimulation of his innate immune
response which subsequently developed into septic shock. Id. at 695. Dr. Whitton said “there’s

41
no rational biological explanation for the vaccine having . . . trigger[ed] the cytokine storm.” Id.
at 697. T.A.’s fever showed his immune system was beginning to respond to a bacterial
infection which progressed very rapidly. Id. The fever represented the very early stage of the
innate response to bacterial lipopolysaccharide. Id. at 698. Dr. Whitton thinks the same events
would have occurred even if T.A. had not received MMR vaccine. Id. at 704. He called measles
vaccine a “crippled virus.” Id. He thinks it unlikely that the adaptive immune response to MMR
vaccine was going to interfere in any way with T.A.’s antibacterial response mainly because he
did not have “a stunningly strong measles virus infection.” Id.

Dr. Jerome Klein testified next for respondent. Id. at 718. He has been professor of
pediatrics at the Boston University School of Medicine since 1974. Id. at 719. He is board-
certified in pediatrics and consults in pediatric infectious diseases. Id. at 720-21. He has been
teaching pediatric infectious disease since 1961. Id. at 722. He is an associate editor of Clinical
Infectious Diseases, which he described as the most important infectious disease journal in the
U.S. Id. at 724. Dr. Klein stopped seeing patients in 2010. Id. at 726.

In Dr. Klein’s over 50-year practice, he would see two to three patients each year with
bacterial sepsis. Id. at 728. The most challenging were those with meningococcal infections. Id.
Some patients progressed to septic shock, particularly those with meningococcemia. Id. His
opinion in this case is that T.A. suffered a catastrophic complication of meningococcal infection.
Id. at 731. One of the bases of his opinion is that the Arkansas Children’s Hospital physicians
diagnosed T.A. with sepsis, septic shock, and meningococcemia based on all the information
available to them, and managed T.A. as a meningococcemia case. Id. at 732. Another basis of
his opinion is his own clinical experience. He has seen “this tragic circumstance a number of
occasions.” Id. In addition, the clinical and laboratory signs point to meningococcemia. Lastly,
the lack of a microbiological diagnosis is readily explainable. Id.

Dr. Klein said that meningococcal colonization of the upper respiratory tract is relatively
common. Id. at 733. T.A. was probably infected days before the parents noted he was tired on
August 22, 2011. Id. at 734. As the organisms proliferated in the upper respiratory tract, at
some point, they invaded T.A.’s blood. On August 23, 2011, he was febrile and sleeping most of
the day, probably indicative of a systemic infection. Id. On August 24, 2011, T.A. had a
petechial rash and a decreased platelet count of 97,000. Id. Normal platelet count would have
been 150,000. Id. at 735. Dr. Allen gave T.A. 750 mg of ceftriaxone intramuscularly because he
was concerned about a systemic bacterial infection. Id. Ceftriaxone is a cephalosporin antibiotic
introduced in the 1990s and used against common bacterial organisms responsible for pediatric
and adult diseases, including pneumococcus, streptococcus, staphylococcus, and meningococcus.
Id. Dr. Klein said the unique feature of ceftriaxone was its long half-life. A dose would promote
substantial antibacterial activity for more than 24 hours. However, Dr. Allen should have taken a
culture of blood prior to administering ceftriaxone to T.A. Id. A blood culture would guide
further management because it would be either positive the next day or negative and, then, the
doctor would know this was not a systemic bacterial infection. Id. at 735-36. All the blood
cultures that Arkansas Children’s Hospital did were negative. Id. at 736. The hospital did PCR
for other organisms, which were negative, but did not do PCR for meningococcal infection. Id.

42
 T.A.’s petechial rash was an alarming feature because it may indicate bacterial invasive
disease causing those hemorrhages in the skin. Id. at 739. This could be due not only to
meningococcus, but also to pneumococcus, staphylococcus, and group A streptococcus. In
addition, T.A. had a macular rash on his trunk. Id. Macules are discrete, small, red rashes. The
typical rash of measles is called morbilliform rash, a blotchy rash which is not small maculars,
but very extensive. Id. By the evening of August 24, 2011, T.A. had a higher temperature of
103 degrees and was vomiting and had diarrhea. Id. at 740. T.A. was toxic. He had significant
fluid losses, what Dr. Allen described as 10 percent. Dr. Klein said that 10 percent is huge on
the spectrum of dehydration. T.A. needed intravenous fluids and hospitalization. Id.

By August 25, 2011, T.A. was sufficiently ill so that Dr. Allen sent him to Mercy
Hospital where he received another dose of ceftriaxone plus doxycycline. He was in severe
respiratory distress and his oxygen saturations declined to 80, necessitating his being put on a
ventilator. That evening, between 8:00 and 10:00 p.m., he was transferred to Arkansas
Children’s Hospital. Id.

Dr. Klein traced the trajectory of the disease from multiplying in the upper respiratory
tract for the first three or four days and then, for unknown reasons, invading T.A.’s bloodstream.
Id. at 741. Meningococcus has toxins that are responsible for stimulating white cells, including
macrophages, monocytes, and lymphocytes to produce cytokines resulting in SIRS syndrome.
Doctors use ceftriaxone to sterilize the blood but at the same time the antibiotic is killing the
organism, it is also breaking open the envelope, releasing endotoxins. Id. The toxins then flood
the system, releasing a burst of cytotoxins which is what happened to T.A. after he received
ceftriaxone on August 24, 2011. Id.

T.A.’s white cell count was initially 6,000 on August 24, 2011 and then the infection
stimulated the bone marrow to release more white cells, particularly neutrophils, so that on
August 25, 2011, the total number of white blood cells was 20,000. Id. at 742. T.A.’s platelets
were being consumed. His platelets in the peripheral blood decreased from 97,000 on August
24, 2011 to 73,000 on August 25th, both times at Dr. Allen’s office, to 27,000 when he was at
Arkansas Children’s Hospital. Id. T.A. had disseminated (widespread) intravascular (within
blood vessels) coagulopathy (clotting problem) or DIC. Id. at 742-43. The clotting may
progress to complete obstruction of the arteries. Id. at 743. Since there is no blood going
through the distal extremities (the feet, the hands), there is the potential for gangrene, which
causes those tissues to die. Id. at 743. This is a recognized part of meningococcemia which Dr.
Klein has seen on multiple occasions. Id. Usually capillary refill occurs in three seconds, but
here it took more than six seconds. Id. at 744.

T.A. was in great distress, transferred to Arkansas Children’s Hospital, and managed as a
patient in septic shock with multisystem manifestations, including: renal failure, resulting in
dialysis; respiratory failure, resulting in ventilation support; and the dreaded complication of
DIC. Id. Dr. Klein said T.A.’s disease progression was a well-recognized complication of
meningococcal infection. Id.

43
 Dr. Klein said the five strains of meningococcus can be cultured, but T.A. received prior
antibiotics before cultures were done and the culture of other fluids such as spinal fluid would
have had to be done. Id. at 745. Because T.A. had coagulopathy and decreased platelets, the
doctors were concerned about bleeding with a needle stick into his spinal fluid and, thus, T.A.
did not receive a lumbar puncture. Id. Dr. Klein said he was “hypothesizing that [T.A.] had
meningococcemia when he received the Rocephin on the 24th and that the blood culture that was
taken on the 25th was negative.” Id. When T.A.’s blood was cultured, the meningococcus was
no longer available to be isolated. Id.

Dr. Klein’s opinion is that MMR vaccine had nothing to do with T.A.’s disease, but he
would not recommend that T.A. receive a second MMR vaccination because of the parents’
anxiety over their associating his first MMR with his devastating event. Id. at 746. Dr. Klein
regards the information about MMR being responsible for this sepsis event as speculative, but he
is “almost certain” that T.A. had a tragic consequence as a complication of meningococcemia.
Id. at 747. Dr. Klein said he has never heard and cannot find any medical literature to cause him
to believe that a vaccine could cause septic shock and amputations. Id.

Dr. Klein said that the onset of T.A.’s meningococcal infection was August 22, 2011
when T.A.’s parents noted T.A. was not himself. Id. at 750. No PCR assay was done for
meningococcal bacteria in T.A. Id. at 756. Dr. Klein described Arkansas Children’s Hospital as
a very highly progressive institution and Dr. Klein knows the infectious disease director there.
Dr. Klein imagines that the staff had reasons not to do PCR testing and the PCR test availability
was probably limited at the hospital. Id. The staff was very complete in looking at a variety of
organisms such as Ehrlichia and rickettsia and they identified none of them. Id. at 757.

As for Table 64-5 (Ex. B, Tab 3), the chapter on shock from NELSON TEXTBOOK OF
PEDIATRICS, which Dr. Klein gave respondent to file into evidence, Dr. Klein said he had no idea
why the authors of chapter 64 included measles vaccine as a cause of SIRS. Id. at 759. Dr.
Klein said that NELSON TEXTBOOK OF PEDIATRICS was not an authoritative source. Id. at 760.
He does not recall why he gave this chapter to respondent’s counsel to file into evidence. He
admitted he uses NELSON TEXTBOOK OF PEDIATRICS in teaching. Id. He stated NELSON
TEXTBOOK OF PEDIATRICS is an excellent textbook but that does not mean everything in it “has
been presented with sufficient evidence to provide those indications.” Id. at 761. He thinks the
editors of this text “missed” and the reference to measles vaccine in the chapter on shock “was
included without any sufficient evidence to support it.” Id. Dr. Klein’s opinion is that the
chapter is right on all the other infectious causes the authors list except vaccinations. Id. at 763.
Dr. Klein regards Table 64-5 as a “salad” with things that do not belong in that salad. Id.

Dr. Klein said that on August 24, 2011, T.A. was bacteremic, that is, the organism had
invaded his blood. Id. at 771. T.A.’s petechial rash was due to the organism lodging in small
blood vessels, producing a hemorrhage. Id. at 772. T.A.’s white blood cell count on August 24,
2011 was not elevated because the organism was in the process of stimulating T.A.’s bone
marrow to produce more white blood cells, particularly neutrophils, which showed up in testing

44
on August 25, 2011. Id. at 772-73. Dr. Klein said he agreed with Dr. Whitton that SIRS is a
spectrum. Id. at 782. Dr. Klein said he was quite confident that T.A. had meningococcemia with
unfortunate complications that led to amputation. Id. at 784.

DISCUSSION

To satisfy their burden of proving causation in fact, petitioners must prove by
preponderant evidence: “(1) a medical theory causally connecting the vaccination and the injury;
(2) a logical sequence of cause and effect showing that the vaccination was the reason for the
injury; and (3) a showing of a proximate temporal relationship between vaccination and injury.”
Althen v. Sec’y of HHS, 418 F.3d 1274, 1278 (Fed. Cir. 2005). In Althen, the Federal Circuit
quoted its opinion in Grant v. Secretary of Health and Human Services, 956 F.2d 1144, 1148
(Fed. Cir. 1992):

A persuasive medical theory is demonstrated by “proof of a logical
sequence of cause of and effect showing that the vaccination was
the reason for the injury [,]” the logical sequence being supported
by a “reputable medical or scientific explanation[,]” i.e., “evidence
in the form of scientific studies or expert medical testimony[.]”

418 F.3d at 1278.

Without more, “evidence showing an absence of other causes does not meet petitioner’s
affirmative duty to show actual or legal causation.” Grant, 956 F.2d at 1149. Mere temporal
association is not sufficient to prove causation in fact. Id. at 1148.

Petitioners must show not only that but for MMR vaccine, T.A. would not have had SIRS
and the complications leading to amputation of T.A.’s legs, but also that MMR vaccine was a
substantial factor in causing T.A.’s SIRS and the complications leading to amputation of T.A.’s
legs. Shyface v. Sec’y of HHS, 165 F.3d 1344, 1352 (Fed. Cir. 1999).

Change in Focus on the Issues in this Case

The undersigned’s March 4, 2016 Order described the change in focus to petitioners’
three assertions: (1) on-Table encephalopathy; (2) on-Table thrombocytopenic purpura; and (3)
causation in fact SIRS. Respondent defends, asserting that petitioners do not satisfy the
Qualifications and Aids to Interpretation (“QAI”) for the Vaccine Injury Table for their two on-
Table allegations, and that there is a known factor unrelated to the MMR vaccine, i.e., bacterial
infection, which was the cause in fact of T.A.’s SIRS, shock, and bilateral amputation of his legs,
as well as other injuries. Petitioners defend against respondent’s claim of a known factor
unrelated to the MMR vaccine by stating that test results were negative for any bacterial
infection. Therefore, petitioners assert, respondent cannot satisfy his burden of proving there
was a known factor unrelated to the administration of the vaccine that caused T.A.’s SIRS,
shock, and bilateral amputation of his legs, as well as other injuries. Respondent counters

45
petitioners’ defense by asserting that T.A.’s clinical symptoms (fever, petechiae, encephalopathy,
thrombocytopenia, and shock) are classic for bacterial infection, specifically meningococcus, and
although measles vaccine can cause a mild form of SIRS, it has never been known to be so
severe as to cause shock.

On-Table Encephalopathy

The QAI for an on-Table encephalopathy require a vaccinee to have an acute
encephalopathy for at least 24 hours. For someone older than 18 months of age, the QAI require,
among other things, that a vaccinee’s significantly decreased level of consciousness not be
attributed to the effects of medication, such as sedation. 42 C.F.R. § 100.3(c)(2)(i)(B). 60

T.A. received his first MMR vaccination on August 11, 2011. He again saw his
pediatrician, Dr. L. Barry Allen, on August 23, 2011, at which time, he was not acutely
encephalopathic. When he returned to Dr. Allen on August 24, 2011, he was much worse,
transferred by ambulance to Mercy Hospital, and sedated by 4:25 p.m. Sedation affects one’s
level of consciousness. In order to have an on-Table encephalopathy between days five and 15
(the Table time interval) following MMR vaccination on August 11, 2011, T.A. would have had
to have the onset of his acute encephalopathy no later than 4:24 p.m. on August 23, 2011. Since
T.A. was consistently sedated for days after 4:25 p.m. on August 24, 2011, the only greater-than-
24-hour period required to satisfy the on-Table encephalopathy QAI would have had to have
occurred between August 23 and 24, 2011. Petitioners have not presented evidence that T.A.
had an acute encephalopathy by 4:24 p.m. on August 23, 2011. Thus, petitioners have not
satisfied the QAI for an on-Table encephalopathy after MMR vaccination.

Because the undersigned finds petitioners have not proven an on-Table encephalopathy,
the undersigned will not discuss the opinions of petitioners’ expert neurologist Dr. Siegel and
respondent’s expert neurologist Dr. Brown regarding a Table encephalopathy. The undersigned
notes that the issue of encephalitis momentarily surfaced in this case, but this is not a credible
diagnosis as no medical record supports T.A.’s having encephalitis. There is one notation in
Arkansas Children’s Hospital that T.A. had meningitis, but the undersigned regards that as an
inadvertent error since T.A. did not have meningitis.

On-Table Thrombocytopenic Purpura

The QAI for an on-Table thrombocytopenic purpura require that the thrombocytopenic
purpura not be “associated with disseminated intravascular coagulation, as observed with
bacterial and viral infections.” 42 C.F.R. § 100.3(c)(7). 61 T.A. was consistently noted to have

60
(2) Encephalopathy. (i) Acute encephalopathy. … (B) For adults and children 18 months of age or older, an acute
encephalopathy is one that persists at least 24 hours and is characterized by at least two of the following: (1) A
significant change in mental status that is not medication related (such as a confusional state, delirium, or
psychosis); (2) A significantly decreased level of consciousness which is independent of a seizure and cannot be
attributed to the effects of medication; and (3) A seizure associated with loss of consciousness.
61
(7) Thrombocytopenic purpura. This term is defined by the presence of clinical manifestations, such as petechiae,
significant bruising, or spontaneous bleeding, and by a serum platelet count less than 50,000/mm with normal red
46
disseminated intravascular coagulation (“DIC”). Petitioners assert that T.A. did not have either a
bacterial or a wild viral infection and, therefore, this proscription is inapplicable to their case.
However the wording of the QAI for an on-Table thrombocytopenic purpura does not link the
DIC to a bacterial and viral infection as a prerequisite. The link is “as observed with bacterial
and viral infections.” Thus, because T.A. had DIC, petitioners have not satisfied the QAI for an
on-Table thrombocytopenic purpura after MMR vaccination.

The Meaning of “Known” Factor Unrelated

Respondent defends with a known factor unrelated to vaccine of a bacterial infection,
probably Neisseria meningitidis. Petitioners deny that T.A. had a bacterial infection because
blood cultures, urine cultures, tissue stains, and PCR assays have all been negative. Respondent
states that, based on clinical symptoms and course of disease, T.A. had the signs and symptoms
of a bacterial SIRS, and numerous doctors at Arkansas Children’s Hospital wrote that T.A. had a
meningococcal infection or meningococcemia in the medical records. The determination of who
is legally correct depends on an interpretation of 42 U.S.C. § 300aa-13(a)(2)(A) and (B).
Petitioners’ burden is to prove their allegations by a preponderance of the evidence. Section
300aa-13(a)(1)(A). If petitioners put on a prima facie case, the burden then shifts to respondent
to show that the vaccinee’s illness “is due to factors unrelated to the administration of the
vaccine. . . .” Section 300aa-13(a)(1)(B).

The Vaccine Act further defines what are “factors unrelated to the administration of the
vaccine.” Section 300aa-13(a)(2). Factors unrelated to the vaccine do not include “any
idiopathic, unexplained, unknown, hypothetical, or undocumentable cause . . . .” Section 300aa-
13(a)(2)(A). Factors unrelated to the vaccine may include “infection, toxins, trauma . . ., or
metabolic disturbances . . . .” Section 300aa-13(a)(2)(B).

Petitioners argue that § 300aa-13(a)(2)(A) applies in this case because all of the blood
cultures, tissue stains, and PCR assays were negative for bacteria. Respondent argues that §
300aa-13(a)(2)(B) applies because clinical signs and symptoms and the course of the illness
indicate that T.A. had a bacterial infection and, therefore, the factor unrelated to the MMR
vaccine was not unexplained, unknown, or undocumentable. Dr. Jerome Klein, respondent’s
expert, relies on decades of experience as a pediatric infectious disease specialist in concluding
T.A. had a bacterial SIRS. Dr. Whitton, respondent’s immunologic expert, testified that this
most likely was meningococcemia. He cannot imagine the specific biological mechanism to
explain how MMR vaccine could cause multiorgan failure although he accepts that MMR
vaccine can, and did, in this case cause T.A. to have SIRS.

Respondent’s Argument that SIRS has to start immediately

and white blood cell indices. Thrombocytopenic purpura does not include cases of thrombocytopenia associated
with other causes such as hypersplenism, autoimmune disorders (including alloantibodies from previous
transfusions) [,] myelodysplasias, lymphoproliferative disorders, congenital thrombocytopenia or hemolytic uremic
syndrome. Thrombocytopenic purpura does not include cases of thrombocytopenia associated with disseminated
intravascular coagulation, as observed with bacterial and viral infections.
47
 Dr. Whitton and Dr. Klein stated that underlying SIRS is the heightened activity of
cytokines which must happen immediately after the triggering event.

An analysis of respondent’s own view as to when an immunologic reaction to MMR
vaccine occurs is instructive. When formulating what should be the appropriate timing for a
Table encephalopathy after MMR vaccination, respondent’s view of onset changed from the
inception of the Vaccine Program on October 1, 1988 until his first revision of the Vaccine
Injury Table on February 8, 1995, effective March 10, 1995. Initially, the onset interval for a
Table encephalopathy after MMR vaccine was 0-15 days. However, except in the case of
anaphylaxis, after this first Table Revision in 1995, respondent required at least a five-day
interval from vaccination to onset to have a Table encephalopathy. This change in on-Table
onset after MMR vaccine from the original Table onset of 0-15 days to the revised Table onset of
5-15 days in the case of a Table encephalopathy was based on respondent’s realization that viral
replication of at least five days was necessary:

Since viral replication is required for a viral vaccine-associated
encephalopathy, a window for the expected time of onset is
appropriate. The onset of vaccine-related illness following MMR
(or any of its components) is generally from 7 to 14 days[;] thus a
time interval of 5 to 15 days would be all-inclusive.

National Vaccine Injury Compensation Program Revision of the Vaccine Injury Table, 60 Fed.
Reg. 7678, 7692 (Feb. 8. 1995, effective Mar. 10, 1995) (to be codified at 42 C.F.R. § 100.3(a)).

Thus, respondent recognizes that immunologically a Table encephalopathy is not going to
constitute an adverse reaction to MMR vaccine if it occurs immediately after vaccination. As for
SIRS, petitioners’ filing of the medical article by Helfand, Timing of Development of Measles-
Specific Immunoglobulin M and G after Primary Measles Vaccination (Ex. 44), showing that
IgM mostly develops two to three weeks after MMR vaccination is support for Dr. Allen’s and
Dr. Levin’s testimony that the onset of T.A.’s SIRS occurred at the most appropriate time post-
vaccination to reflect an immunologic challenge. On his first day of testimony, Dr. Whitton
thought it possible and an interesting suggestion that T.A. could have both an MMR-induced
SIRS coupled with a bacterial infection, but on his second day of testimony, he rejected this
suggestion and instead preferred the Occam’s razor or “unity” theory, i.e., one explanation is
much simpler and preferable to two explanations. The Federal Circuit, however, rejected the
“unity” theory in Knudsen, 35 F.3d at 550 (in Knudsen, respondent said the baby had a cold
which must have caused her encephalopathy under this “unity” theory, whereas the Federal
Circuit saw no difficulty in holding that the baby had both a cold and a DPT-caused
encephalopathy).

The point however for this decision is that respondent’s expert Dr. Whitton accepts that
SIRS is appropriate, even reasonable, 12 days after MMR vaccination. Dr. Whitton does not
accept that T.A.’s MMR vaccine-induced SIRS, if he had it, led to shock, multiorgan dysfunction

48
syndrome, and bilateral amputation. The undersigned finds that the evidence and testimony best
support the conclusion that SIRS does not have to occur immediately post-MMR vaccination,
and that an onset nearly two weeks later is immunologically reasonable, as Dr. Whitton initially
testified.

Respondent’s Defense

Respondent has two defenses to petitioners’ allegations of causation in fact from MMR
vaccine: (1) although he admits that T.A. had SIRS, Dr. Whitton does not know the underlying
biological mechanism to explain how MMR vaccine-caused SIRS led to the catastrophic
condition T.A. experienced, ultimately necessitating amputation of his legs; and (2) neither Dr.
Whitton nor Dr. Klein knows of any medical literature that supports petitioners’ allegation that
MMR vaccine-induced SIRS can lead to the catastrophic condition ultimately causing
amputation of T.A.’s legs.

These defenses fail in light of the Federal Circuit’s decisions in Knudsen v. Sec’y of
HHS, 35 F.3d 543 (Fed. Cir. 1994), and Capizzano v. Sec’y of HHS, 440 F.3d 1317 (Fed. Cir.
2006). Petitioners do not have the burden of proving a specific biological mechanism or
providing medical literature in support of their allegations:

As the Federal Circuit stated in Knudsen, 35 F.3d at 549:

Furthermore, to require identification and proof of specific
biological mechanisms would be inconsistent with the purpose and
nature of the vaccine compensation program. The Vaccine Act does
not contemplate full blown tort litigation in the Court of Federal
Claims. The Vaccine Act established a federal “compensation
program” under which awards are to be “made to vaccine-injured
persons quickly, easily, and with certainty and generosity.” House
Report 99-908, supra, at 3, 1986 U.S.C.C.A.N. at 6344.

The Court of Federal Claims is therefore not to be seen as a vehicle for
ascertaining precisely how and why DTP and other vaccines sometimes
destroy the health and lives of certain children while safely immunizing
most others.

As the Federal Circuit stated in Capizzano, 440 F.3d at 1325:

[W]e conclude that requiring either epidemiologic studies,
rechallenge, the presence of pathological markers or genetic
disposition, or general acceptance in the scientific or medical
communities to establish a logical sequence of cause and effect is
contrary to what we said in Althen . . . . We think such an
approach is inconsistent with the use of circumstantial evidence.

49
 Id. The Federal Circuit stated in Althen, 418 F.3d at 1280, that
“the purpose of the Vaccine Act’s preponderance standard is to
allow the finding of causation in a field bereft of complete and
direct proof of how vaccines affect the human body.”

The undersigned respects the sterling credentials of both Dr. Whitton and Dr. Klein.
However, the undersigned finds that under the law as the Federal Circuit has interpreted it, their
testimony does not vitiate petitioners’ proof. Dr. Whitton not only denied that MMR vaccine-
induced SIRS could lead to T.A.’s catastrophic illness because Dr. Whitton does not know what
is the underlying biological mechanism, but also he denied the validity of respondent’s including
encephalopathy as a Table injury within 5-15 days of MMR vaccination because he does not
know what is the underlying biological mechanism for MMR-induced encephalopathy. The
undersigned finds his position opposing the Table injury of encephalopathy after MMR
vaccination remarkable because HHS does not create a Table injury without scientific and
medical input and HHS changed the Table onset for MMR vaccine encephalopathy from 0-15
days to 5-15 days based on scientific and medical input. See, e.g., 42 U.S.C. § 300aa-2(a)(7).
Evaluating the need for and the effectiveness and adverse effects of vaccines and
immunization activities:

The Director of the Program shall, through the plan issued under
section 300aa-3 of this title [preparation and issuance of a plan for
the implementation of responsibilities; the plan shall establish
priorities in research and the development, testing, licensing,
production, procurement, distribution, and effective use of
vaccines], coordinate and provide direction to the National
Institutes of Health, the Centers for Disease Control and
Prevention, the Office of Biologics Research and Review of the
Food and Drug Administration, the National Center for Health
Statistics, the National Center for Health Services Research and
Health Care Technology Assessment, and the Health Care
Financing Administration in monitoring the need for and the
effectiveness and adverse effects of vaccines and immunization
activities.

(emphasis added).

In addition, Dr. Whitton, as he frequently stated at the hearing, does not see medical
patients. He is not a clinician in any specialty. He is not licensed to practice medicine in the
United States. His extensive knowledge about immunology derives from animal research.

In contradistinction to Dr. Whitton’s acceptance of measles vaccine as a cause of SIRS,
Dr. Klein does not accept MMR vaccine as a cause of SIRS for two reasons: (1) the lack of
medical literature to support that assertion, and (2) he has not seen patients with MMR vaccine-
induced SIRS in his own clinical experience. But the Federal Circuit in Althen, 418 F.3d at

50
1280, states that requiring medical literature as part of petitioners’ proof “contravenes section
300aa-13(a)(1)’s allowance of medical opinion as proof.” The Federal Circuit in Capizzano, 440
F.3d at 549, states petitioners do not have to prove general acceptance in the scientific or medical
communities. Moreover, a rare adverse reaction to a vaccine would be unlikely to appear in a
clinician’s practice.

Dr. Klein in his testimony disparaged the chapter on shock in NELSON TEXTBOOK OF
PEDIATRICS, which lists measles vaccine as an infectious cause of SIRS, even denying the
textbook is an authoritative source. But then, on cross-examination, Dr. Klein admitted he uses
this very same textbook when he teaches. Dr. Klein undercut his own credibility. Dr. Levin,
petitioners’ expert immunologist, called NELSON TEXTBOOK OF PEDIATRICS the bible of
pediatrics.

The undersigned finds Dr. Whitton’s acceptance of measles vaccine as a cause of SIRS
more credible than Dr. Klein’s denial of measles vaccine as a cause of SIRS, particularly since
the two authors of the chapter on shock are accomplished pediatricians involved in critical care
medicine at Duke. These accomplished pediatricians are: (1) Dr. David A. Turner, Associate
Director, Pediatric Critical Care Fellowship Program; Medical Instructor, Department of
Pediatrics, Division of Pediatric Critical Care Medicine, at Duke University Medical Center,
Durham, North Carolina, and (2) Dr. Ira M. Cheifetz, Professor of Pediatrics; Chief, Pediatric
Critical Care Medicine; Medical Director, Pediatric ICU; Medical Director, Pediatric Respiratory
Care & ECMO Programs, at Duke Children’s Hospital, Durham, North Carolina. At the end of
the chapter on shock, these co-authors offer to the reader a complete bibliography at
www.expertconsult.com. Undoubtedly this website has changed since the 2011 date of
publication of the 19th edition because it advertises the 20th edition which was published in 2016.
The website states:

After more than 75 years, Nelson Textbook of Pediatrics remains
the indispensable source for definitive, state-of-the-art answers on
all aspects of pediatric care. This classic reference provides
essential information that practitioners and other care providers
involved in pediatric health care need to understand to effectively
address the enormous range of biologic, psychologic, and social
problems that children and youths may face. Regular online
updates personally selected by Dr. [Robert M.] Kliegman ensure
that you have the most recent information on diagnosis and
treatment of pediatric diseases based on the latest
recommendations and methodologies.

https://expertconsult.inkling.com/store/book/kliegman-nelson-textbook-pediatrics-20/ (last
visited August 8, 2018).

The undersigned notes that both Dr. Whitton and Dr. Klein explained the lack of a
positive blood or urine culture detecting meningococcus based on their assumption that Dr.

51
Allen, T.A.’s pediatrician, administered Rocephin to T.A. before any cultures were done, and
thus the antibiotic eliminated the successful detection of meningococcus. However, Dr. Allen
told Dr. Joseph R. Romero, an infectious diseases consultant at Arkansas Children’s Hospital, on
August 26, 2011 that Dr. Allen had performed a blood culture, a nasopharyngeal swab, and a
urine culture, all of which were negative, before he gave T.A. Rocephin on August 24, 2011. 62
Exhibit 7, at 473. If Dr. Whitton’s and Dr. Klein’s opinion that T.A. had meningococcemia or
another bacterial infection were valid, one or all of those tests should have been positive. In fact,
Dr. Klein emphasized that meningococcus resides in many people’s nasal passages. He said he
himself had a problem with meningococcus in his own nasal passages and developed petechiae
which with medication became better. But when Dr. Allen did a nasopharyngeal swab of T.A.’s
nasal passages, the result was negative, as were the blood and urine cultures prior to Dr. Allen’s
administration of Rocephin.

This contemporaneous medical record on August 26, 2011 reporting Dr. Allen’s
conversation with Dr. Romero just two days after Dr. Allen performed the blood culture,
nasopharyngeal swab, and urine culture before administering Rocephin makes respondent’s
experts’ explanation of the subsequent negative blood and urine cultures, as well as other tests,
done at Mercy Hospital and Arkansas Children’s Hospital not credible. The undersigned notes
that Dr. Allen testified by telephone at the hearing and, when he was finished, hung up. He
never got to hear Dr. Whitton’s and Dr. Klein’s testimony (and it is unclear if he ever read their
expert reports) that the blood and urine cultures at Mercy Hospital and Arkansas Children’s
Hospital were negative because Dr. Allen had not performed any testing on T.A.’s blood, urine,
or nasopharyngeal passages before administering Rocephin. The undersigned also reflects that
some of the other medical doctors note in the Arkansas Children’s Hospital records that, even
though T.A. was repeatedly tested, the administration of Rocephin and other antibiotics was
probably the cause of the negative test results. The undersigned assumes these busy doctors did
not comb through T.A.’s voluminous hospital records to see if Dr. Allen had told a doctor in the
hospital that Dr. Allen had administered Rocephin after he did a blood culture, nasopharyngeal
swab, and urine culture.

Thus, respondent’s known factor unrelated to MMR vaccine that T.A. had in fact

62
The undersigned cannot find in the filing of Dr. Allen’s pediatric records for August 24, 2011 that he noted the
blood culture, nasopharyngeal swab, and urine culture or the actual test results on a different page than the pediatric
notes for the visit of August 24, 2011. The undersigned however credits Dr. Allen’s history to Dr. Romero because
the undersigned has heard Dr. Allen testify and finds him eminently credible and is aware that sometimes medical
record notes are incomplete and lab test results do not make their way into medical records that counsel files.
Moreover, Dr. Allen would have had no idea that Dr. Romero was including in the hospital records the history Dr.
Allen gave Dr. Romero since Dr. Romero dictated his notes later. Med. recs. Ex. 7, at 476. Since this was a
conversation during an emergency admittance with a little boy’s life on the line (and not in the context of litigation),
Dr. Allen would have been motivated to give Dr. Romero every piece of information he could from T.A.’s visit two
days earlier plus the day before that would help Dr. Romero treat this little boy. The undersigned is cognizant that
on August 25, 2011, Dr. Allen cancelled all of his appointments that day in order to accompany T.A. to Mercy
Hospital by ambulance, stayed with him throughout his stay there, and signed the Angel One Transport Medical
Necessity Form to enable T.A. to proceed by helicopter to Arkansas Children’s Hospital the night of August 25,
2011. Med. recs. Ex. 6, at 6. Since the conversation he had with Dr. Romero occurred on August 26, 2011, Dr.
Allen must have driven to Arkansas Children’s Hospital where he joined petitioners in speaking to Dr. Romero.
52
meningococcemia or another bacterial infection, undetected because of prior administration of
antibiotics, which caused in fact his SIRS and its sequelae fails. Even if, however, Dr. Romero
dictated his notes on August 26, 2011 incorrectly, i.e., Dr. Allen told him he did a blood culture,
nasopharyngeal swab, and urine culture after not before he administered Rocephin to T.A.,
respondent’s known factor unrelated to MMR vaccine fails because the numerous and varied
antibiotics T.A. received did not improve his condition. The undersigned is convinced that the
medical staff at Arkansas Children’s Hospital diagnosed T.A. with meningococcemia because it
is a well-accepted cause of SIRS, sepsis, septic shock, and multiorgan dysfunction syndrome and
most, if not all, of the doctors were unaware that T.A. had received MMR vaccine almost two
weeks before he became ill. Even if they had known of the preceding MMR vaccination, the
rarity of this catastrophic reaction would have eliminated MMR vaccine as a cause from their
minds, just as it did from Dr. Whitton’s and Dr. Klein’s minds. But the rarity of an occurrence
does not mean it is non-existent.

Petitioners’ Proof of Causation in Fact

Respondent filed two of the most important pieces of medical literature that benefit
petitioners. The first is the chapter on shock in NELSON TEXTBOOK OF PEDIATRICS. The second
is the Medscape article by Steven D. Burdette on SIRS, Systemic Inflammatory Response
Syndrome (Ex. E, Tab 6), which states that SIRS is not always related to infection and that
whatever the etiology of SIRS, it has the same pathophysiologic properties with minor
differences in inciting cascades. The author states that inflammation is the body’s response to
nonspecific insults that can include a reaction to a drug. He also states both infectious and non-
infectious SIRS have similar clinical characteristics. Although respondent filed Exhibit E, Tab 6,
to Dr. Whitton’s expert report, its conclusions undercut Dr. Whitton’s testimony that MMR-
induced SIRS can never be as severe as bacterial SIRS.

Petitioners filed an excerpt from a Centers for Disease Control and Prevention (“CDC”)
publication on prevention of vaccine-preventable diseases (Ex. 36) which states that the immune
response to a live attenuated vaccine is virtually identical to the immune response to a natural
infection because the immune system does not differentiate between an infection with an
attenuated viral vaccine and a wild viral infection. The CDC is part of HHS. This publication
undercuts the credibility of both Dr. Whitton and Dr. Klein, who insist that MMR vaccine can
never cause the severe sequelae that happened to T.A., although Dr. Whitton concedes MMR
vaccine can cause SIRS, but it will always be mild, and Dr. Klein denies that MMR vaccine can
even cause SIRS.

Dr. Allen testified that he has had patients who had adverse reactions to MMR vaccine.
He testified that he has thought about T.A. several times over the past years and he has to think
MMR was the cause of T.A.’s illness in light of timing after vaccination and the failure of the
cultures and PCR to find a bacterial cause. He said he would be very reluctant to recommend
that T.A. receive a second MMR vaccination: “Well, that would be a very difficult decision for
me. I would probably recommend the other immunizations, but I would be very reluctant to
recommend an MMR for T.A.” Tr. at 114. “A treating doctor’s recommendation to withhold a

53
particular vaccination can provide probative evidence of a causal link between the vaccination
and an injury a claimant has sustained.” Andreu v. Sec’y of HHS, 569 F.3d 1367, 1376 (Fed.
Cir. 2009 (citing Capizzano, 440 F.3d at 1320, 1326).

Dr. Levin, whom respondent accepted as an expert in immunology, testified based on the
Helfand article, Timing of Development of Measles-Specific Immunoglobulin M and G after
Primary Measles Vaccination (Ex. 44), showing that IgM mostly develops two to three weeks
after MMR vaccination, that one would not expect an immunological response to a first MMR
vaccination until at least a week or two weeks. He explained SIRS by saying that people have
only a few ways of responding to an immunologic insult, and SIRS is a way people respond to
bacteria, viruses, fungi, toxic chemicals, and vaccines. Once SIRS is triggered, it proceeds
spontaneously as it did in T.A. He said there is an overreaction of pro-inflammatory or anti-
inflammatory cytokines and other agents that cause an inflammatory response. In T.A.’s case,
the pro-inflammatory cytokines caused the harm. T.A.’s maculopapular rash, petechial rash,
103-degree fever, vomiting, and diarrhea were consistent with a systemic reaction going out of
control. Dr. Levin testified that MMR vaccine caused T.A.’s fever on August 23, 2011 due to
pro-inflammatory cytokines. His white cell count rose from 6,000 to 20,000, a typical SIRS
reaction to bacteria, viruses, toxic chemicals, and vaccines. The petechial rashes and little blood
clots were due both to the decrease in platelet counts and to MMR vaccine. Titers were taken
that showed T.A. was positive to measles. Dr. Levin noted that Rocephin, the antibiotic, did not
work and T.A. became much sicker. Dr. Levin ascribes the failure of Rocephin to help T.A. as
an indication that T.A. did not have a bacterial infection, noting that meningococcus is
exquisitely sensitive to Rocephin. Dr. Levin called the immunology unit of Arkansas Children’s
Hospital one of the best in the country. He said the reason those doctors could not find a
pathogen was probably because MMR vaccine caused T.A.’s SIRS. Dr. Levin said all SIRS is
the same whether the trigger is bacterial or a vaccinal. This is because people have a limited
repertory of responses to immunologic insults.

Considering the Opinions of Treating Physicians

The Federal Circuit in Capizzano, 440 F.3d at 1326, emphasized that the special masters
are to evaluate seriously the opinions of petitioner’s treating doctors since “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.” See also Broekelschen v. Sec’y of
HHS, 618 F.3d 1339, 1347 (Fed. Cir. 2010); Andreu v. Sec’y of HHS, 569 F.3d 1367, 1375
(Fed. Cir. 2009).

The undersigned takes seriously Dr. Allen’s opinion that T.A. had an adverse reaction to
MMR vaccination which led to his thrombocytopenia, necessitating amputation of T.A.’s legs.
Dr. Allen is T.A.’s treating pediatrician who had 36 years of experience when the 2011 events
occurred. When he testified, Dr. Allen had 40 years of experience as a pediatrician. The
undersigned recognizes that initially Dr. Allen thought T.A. might have a bacterial infection
which is why he initially gave T.A. Rocephin. The undersigned is also aware that the doctors at
Mercy Hospital, where T.A. was initially taken, diagnosed him with sepsis, and the doctors at

54
Arkansas Children’s Hospital diagnosed T.A. with sepsis, septic shock, or meningococcemia.
The undersigned contrasts the time that Dr. Allen has had since 2011 to reflect on what caused
T.A.’s illness versus the emergency situation prevailing at Mercy Hospital and Arkansas
Children’s Hospital where T.A. was on the verge of death. No doubt, the treaters at both
hospitals saw more cases of sepsis and meningococcemia than of MMR vaccine-induced SIRS.
That a reaction is rare does not mean it never occurs. As the Federal Circuit stated in Knudsen,
35 F.3d at 550:

The bare statistical fact that there are more reported cases
of viral encephalopathies than there are reported cases of DTP
encephalopathies is not evidence that in a particular case an
encephalopathy following a DTP vaccination was in fact caused by
a viral infection present in the child and not caused by the DTP
vaccine.

Moreover, if someone were to view Dr. Allen’s opinion and the treating doctors’
opinions at Mercy Hospital and Arkansas Children’s Hospital as in equipoise, and thus cancel
each other out, the Federal Circuit states that Congress, in passing the National Childhood
Vaccine Injury Act, envisioned a system “in which close calls regarding causation are resolved
in favor of injured claimants.” Althen, 418 F.3d at 1280.

Althen Analysis

Prong One

The undersigned has narrowed the issues to one issue: can MMR vaccine cause SIRS
followed by sequelae of shock and amputation. Based on the evidence submitted, the
undersigned finds the answer is yes. Dr. Whitton, respondent’s immunologic expert, accepts that
measles vaccine can cause SIRS, although Dr. Klein, respondent’s infectious diseases expert,
denies that. However, Dr. Whitton denies that a MMR-vaccine-induced SIRS can lead to the
sequelae of shock and multiorgan dysfunction syndrome. Petitioners’ immunological expert Dr.
Levin testified that MMR vaccine can cause on rare occasions SIRS leading to shock and
multiorgan dysfunction syndrome.

The medical literature that respondent filed, particularly chapter 64 on shock from the
19th edition of NELSON TEXTBOOK OF PEDIATRICS, supports petitioners’ allegation that MMR
vaccine can cause SIRS. Respondent also filed an article from the online site Medscape by
Steven D. Burdette on SIRS, Systemic Inflammatory Response Syndrome (Ex. E, Tab 6), that
states that SIRS is not always related to infection and that whatever the etiology of a particular
case of SIRS, SIRS has the same pathophysiologic properties with minor differences in inciting
cascades. The author states that inflammation is the body’s response to nonspecific insults that
can include a reaction to a drug. He also states both infectious and non-infectious SIRS have
similar clinical characteristics. Both these pieces of literature are consistent with petitioners’
expert immunologist Dr. Levin’s testimony.

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 Petitioners filed an excerpt from a CDC publication on prevention of vaccine-preventable
diseases (Ex. 36) which states that the immune response to a live attenuated vaccine is virtually
identical to the immune response to a natural infection because the immune system does not
differentiate between an infection with an attenuated viral vaccine and a wild viral infection.
This excerpt is consistent with petitioners’ expert Dr. Levin’s testimony.

The undersigned finds that as to Althen Prong One, petitioners’ expert Dr. Levin is more
credible than respondent’s experts Dr. Whitton and Dr. Klein and that the medical literature
supports Dr. Levin’s testimony and refutes respondent’s experts’ testimony. The undersigned
finds that MMR vaccine can on rare occasions cause SIRS, shock, and multiorgan dysfunction
syndrome, leading to bilateral amputation.

Prong Two

Based on the undersigned’s finding above for petitioners on Prong One and the
discussion below finding for petitioners on Prong Three, the undersigned finds that petitioners
have proved that MMR vaccine did cause in fact T.A.’s SIRS, shock, multiorgan dysfunction
syndrome, and bilateral amputation based on the testimony of Dr. Levin and the medical
literature described above in the discussion of Prong One.

Prong Three

The timing for an immune challenge (not including anaphylaxis) after MMR vaccine is
one to two weeks, according to both HHS in its Table injury of encephalopathy, and two to three
weeks according to the Helfand article, Timing of Development of Measles-Specific
Immunoglobulin M and G after Primary Measles Vaccination (Ex. 44), showing that IgM mostly
develops two to three weeks after MMR vaccination and that one would not expect an
immunological response to a first MMR vaccination until at least a week or two weeks. T.A.’s
onset of SIRS was on either August 23 or 24, 2011, that is, either 12 or 13 days after his MMR
vaccination. The timing of his illness fits perfectly within the onset interval that doctors
(including respondent’s Dr. Whitton) would say is causally related to MMR vaccine. Dr. Levin
relied on this article as support for his opinion that T.A.’s onset of SIRS, followed by shock and
multiorgan dysfunction syndrome, was consistent with an immunologic challenge resulting in an
adverse reaction.

Petitioners have successfully proved a prima facie case of causation in fact. Respondent
has failed to satisfy the criteria for proving a known factor unrelated to MMR vaccine caused in
fact T.A.’s SIRS, shock, multiorgan dysfunction syndrome, and bilateral amputation.

CONCLUSION

This is a tragic case involving a little boy who had an adverse reaction to MMR vaccine,
including rash, fever, lethargy, and irritability 12 or 13 days later, a medically appropriate time

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for such a reaction, and whose worsened condition resulted in SIRS, shock, multiorgan
dysfunction syndrome, and bilateral amputation of his legs. Based on the evidence submitted
and the testimony of the experts at the hearing, the undersigned rules that petitioners are entitled
to compensation.

The undersigned encourages the parties to proceed diligently to settle damages.
Petitioners merit $250,000.00 in pain and suffering. Petitioners must ascertain the amount of the
Medicaid lien pertaining to T.A.’s illness and sequelae, and provide that information and
documentation of unreimbursable medical expenses to respondent.

The undersigned will set a telephonic status conference soon to discuss how the parties
are proceeding in settling damages.

IT IS SO ORDERED.

Dated: August 16, 2018 /s/ Laura D. Millman
Laura D. Millman
Special Master

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