Williams v. Secretary of Health and Human Services

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: April 25, 2022

* * * * * * * * * * * * * * *
CAYLIN WILLIAMS, * No. 16-553V
*
Petitioner, * Special Master Sanders
*
v. * Ruling on Entitlement; Tetanus-Diphtheria-
* Acellular Pertussis (“TDaP”); Human
SECRETARY OF HEALTH * Papillomavirus (“HPV”); Meningococcal
AND HUMAN SERVICES, * Vaccines; Interstitial Pulmonary Fibrosis;
* Acute Respiratory Failure
Respondent. *
* * * * * * * * * * * * * * *
Michael G. McLaren, Black McLaren, et al., PC, Memphis, TN, for Petitioner.
Dhairya D. Jani, United States Department of Justice, Washington, DC, for Respondent.

RULING ON ENTITLEMENT 1

On May 5, 2016, Donna Williams (“Mrs. Williams”) filed a petition for compensation
pursuant to the National Vaccine Injury Compensation Program, 2 on behalf of her then-minor
daughter Caylin Williams (“Petitioner”). Pet. at 1, ECF No. 1; 42 U.S.C. §§ 300aa-1 to -34 (2012).
The petition alleges that tetanus, diphtheria, and pertussis (“TDaP”), human papillomavirus
(“HPV”), and meningococcal vaccines that Petitioner received on July 29, 2014, caused her to
suffer from interstitial pulmonary fibrosis (“IPF”) 3 and acute respiratory failure. 4 Pet. at 1.

1
This Ruling shall be posted on the United States Court of Federal Claims’ website, in accordance with the
E-Government Act of 2002, 44 U.S.C. § 3501 note (2012) (Federal Management and Promotion of
Electronic Government Services). In accordance with Vaccine Rule 18(b), a party has 14 days to identify
and move to delete medical or other information that satisfies the criteria in § 300aa-12(d)(4)(B). Further,
consistent with the rule requirement, a motion for redaction must include a proposed redacted Ruling. If,
upon review, I agree that the identified material fits within the requirements of that provision, such material
will be deleted from public access.
2
National Childhood Vaccine Injury Act of 1986, Pub L. No. 99-660, 100 Stat. 3755. Hereinafter, for ease
of citation, all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. § 300aa
(2012).
3
Interstitial pulmonary fibrosis (“IPF”) is defined as “chronic inflammation and progressive fibrosis of the
pulmonary alveolar walls, with steadily progressive dyspnea, resulting finally in death from oxygen lack or
right heart failure.” Dorland’s Illustrated Medical Dictionary 1, 704 (32nd ed. 2012) [hereinafter
“Dorland’s”].
4
Acute respiratory failure is “a [sudden] condition resulting from respiratory insufficiency, in which there
is persistent abnormally low arterial oxygen tension (Pao2) or abnormally high carbon dioxide tension
(Paco2).” Dorland’s at 678.
 After carefully analyzing and weighing all the evidence and testimony presented in this
case in accordance with the applicable legal standards, 5 I find that Petitioner has met her burden
and presented preponderant evidence that her vaccinations were the but-for cause of her IPF and
acute respiratory failure.

I. Procedural History

Mrs. Williams filed a petition for compensation on behalf of Petitioner on May 5, 2016.
Pet. at 1. Mrs. Williams filed a motion to amend the case caption on November 9, 2020, indicating
that Petitioner had reached the age of majority. ECF No. 66. I granted Mrs. Williams’ request, and
the case caption was amended. ECF No. 67. Prior to the change in case caption, on May 17, 2016,
Mrs. Williams filed a notice of intent to file an affidavit and medical records on a compact disc.
ECF No. 7. The following day, the clerk’s office received the compact disc, along with a statement
of completion. Pet’r’s Exs. 1–6, ECF No. 8.

Respondent filed his Rule 4(c) report on August 3, 2016, recommending that compensation
be denied. Resp’t’s Report at 1, ECF No. 11. The presiding special master held a status conference
pursuant to Vaccine Rule 5 on August 24, 2016. See Min. Entry, docketed Aug. 24, 2016.
Following the conference, the presiding special master ordered Petitioner to file an expert report
addressing three pertinent issues. Sched. Order at 1, ECF No. 12. Specifically, Petitioner’s expert
was to address whether the fact that Petitioner was born seven to eight weeks premature had
implications for her later development, the causal relevance of Petitioner’s MRSA infection 6 in
July of 2014, and which, if any, of the three vaccines identified are alleged to have been causal.
Id. Prior to filing an expert report, Petitioner submitted an additional medical record on November
7, 2016. Pet’r’s Ex. 7, ECF No. 15. On December 9, 2016, Petitioner filed a status report indicating
that she was consulting with experts in immunology and pulmonology and requesting an extension
for filing her report. ECF No. 16. The presiding special master extended Petitioner’s deadline.
Non-PDF Order, docketed Dec. 12, 2016. This case was transferred to me on January 9, 2017.
ECF Nos. 17–18.

On February 8, 2017, Petitioner filed an expert report from Eric Gershwin, M.D., and
supporting medical literature. Pet’r’s Exs. 8–48, ECF Nos. 22-1–26-6. Respondent filed his
responsive expert report from Gary Rachelefsky, M.D., on June 28, 2017. Resp’t’s Ex. A, ECF
No. 31. On June 5, 2017, Respondent filed a notice of intent to file medical literature on a compact

5
While I have reviewed all of the information filed in this case, only those filings and records that are most
relevant to the decision will be discussed. Moriarty v. Sec'y of Health & Hum. Servs., 844 F.3d 1322, 1328
(Fed. Cir. 2016) (“[w]e generally presume that a special master considered the relevant record evidence
even though he does not explicitly reference such evidence in his decision.”) (citation omitted); see also
Paterek v. Sec'y of Health & Hum. Servs., 527 F. App'x 875, 884 (Fed. Cir. 2013) (“[f]inding certain
information not relevant does not lead to—and likely undermines—the conclusion that it was not
considered.”).
6
A MRSA infection is an infection caused by the “methicillin-resistant Staphylococcus au’reus.” Dorland’s
at 1184. Staphylococcus au’reus is defined as “a species comprising the yellow-pigmented, coagulase-
positive pathogenic forms of the genus; it causes serious suppurative infections and systemic disease,
including impetigo bullosa, staphylococcal pneumonia, and staphylococcal scalded skin syndrome, and has
developed resistance to nearly all classes of antibiotics.” Id. at 1765.

2
disc. ECF No. 32. The following day, the clerk’s office received the compact disc. Resp’t’s Exs.
C–JJ.

I held a status conference with the parties on July 25, 2017. See Min. Entry, docketed July
25, 2017. During the conference, I discussed Respondent’s request to submit a second responsive
expert report regarding the immunological aspects of Petitioner’s causation theory. Sched. Order
at 1, ECF No. 33. Petitioner indicated that she would not reply to Respondent’s first report, but
she requested the right to respond to Respondent’s second report. Id. I ordered Respondent to
submit a second expert report and for Petitioner to submit a status report regarding her intention
to file a supplemental report thereafter. Id.

Respondent submitted a second responsive expert report from Christine McCusker, M.D.,
on September 8, 2017. Resp’t’s Exs. KK, LL, ECF Nos. 34-1, 34-2. Petitioner filed a status report
on September 25, 2017, indicating that she did not wish to file a supplemental expert report and
requesting this matter be set for an entitlement hearing. ECF No. 35. Respondent submitted
medical literature on October 18, 2017. Resp’t’s Exs. MM–QQ, ECF Nos. 37-1–37-5.

I scheduled this matter for an entitlement hearing to take place on December 18–19, 2019.
Hearing Order, ECF No. 39. Petitioner filed her pre-hearing brief on August 19, 2019. Pet’r’s Br.,
ECF No. 43. Respondent filed his pre-hearing response brief on September 17, 2019. Resp’t’s Br.,
ECF No. 44. On October 11, 2019, Petitioner refiled highlighted medical literature. Pet’r’s Exs.
49–59, ECF Nos. 45-1–45-12. Respondent refiled highlighted medical literature on October 16,
2019. Resp’t’s Exs. RR–WW, ECF Nos. 46-1–46-6. Petitioner filed a notice of intent to file
exhibits on a compact disc on December 5, 2019. ECF No. 51. The next day, the clerk’s office
received photograph and video exhibits documenting Petitioner’s condition. Pet’r’s Exs. 60–69.
The entitlement hearing was held as scheduled on December 18–19, 2019. See Min. Entry,
docketed Dec. 19, 2019.

Following the entitlement hearing, I ordered Respondent to file the medical literature
regarding the impact of multiple infiltrates on the immune system, which was referenced by his
expert during the hearing. Sched. Order at 1, ECF No. 52. On December 26, 2019, Petitioner filed
a photograph exhibit depicting the whiteboard which was displayed during the hearing. Pet’r’s Ex.
70, ECF No. 53. On January 6, 2020, Respondent filed additional medical literature exhibits.
Resp’t’s Exs. XX–AAA, ECF Nos. 54-1–54-4.

Petitioner filed an opening post-hearing brief and supporting documentation on April 30,
2020. Pet’r’s Br., ECF No. 62. On June 29, 2020, Respondent filed his post-hearing response brief.
Resp’t’s Resp., ECF No. 64. Petitioner filed her post-hearing reply brief on July 13, 2020. Pet’r’s
Reply, ECF No. 65. This matter is now ripe for consideration.

II. Evidence

A. Medical Records

Petitioner’s medical record, diagnosis, and treatment are not in dispute in this case.
Petitioner’s symptom presentation and complaints to medical personnel are also not disputed by

3
either party. While I have reviewed the entire record, the records most relevant to Petitioner’s
symptomology and progression are discussed herein. 7

1. Pre vaccination

Petitioner was born premature at thirty-two weeks on November 8, 2002. Pet’r’s Ex. 6 at
426. In August of 2011, Petitioner was prescribed Desonide cream, a topical corticosteroid, to treat
eczema 8 and skin hypersensitivity. Pet’r’s Ex. 2 at 5–6. She continued to take steroids for
dermatological concerns into 2014. See Pet’r’s Ex. 2. She had no relevant medical conditions as a
result of her prematurity and no other relevant health concerns until July of 2014. Id. On July 21,
2014, she presented to her pediatrician for a painful lesion on her left inner thigh that appeared two
days prior. Id. at 37. Petitioner’s pediatrician ordered testing on a cultured sample, which came
back positive for MRSA. Id. at 94. She was started on a ten-day course of Bactrim. 9 Pet’r’s Ex. 4
at 2307.

On July 28, 2014, Petitioner was evaluated for eczema and lichen simplex chronicus. 10
Pet’r’s Ex. 2 at 45–46. The next day, on July 29, 2014, Petitioner presented for her twelve-year-
old well-visit and noted no significant issues. Id. at 47. An examination of Petitioner’s lungs
showed that her chest was clear with “no wheezing or rales” 11 and she exhibited symmetric air
entry throughout both lung fields. Id. at 53. She received the TDaP, HPV, and meningococcal
vaccinations during this visit. Id. Petitioner’s pediatrician encouraged her to remain in the clinic
for twenty minutes following her vaccinations and to report any adverse reaction. Id. at 47. Her
pediatrician indicated “[n]o sign[s] and symptoms of [an] allergic reaction [that were] noted or
reported at the time of vaccination.” Id.

2. Post vaccination

On July 31, 2014, Petitioner was seen by Renee Quinton, M.D., with complaints of fever,
abdominal pain, vomiting, fatigue, and back pain lasting for two days. Id. at 57. The review of

7
See supra, note 5.
8
Eczema is “any of various pruritic, papulovesicular types of dermatitis occurring as reactions to
endogenous or exogenous agents. In acute types there may be erythema, edema, inflammatory infiltrates in
the dermis, vesiculation, crusting, and scaling. In chronic types there may be lichenification, skin
thickening, signs of excoriation; and areas of hyperpigmentation or hypopigmentation.” Dorland’s at 592.
9
Bactrim is “the trademark for combination preparations of trimethoprim and sulfamethoxazole.”
Dorland’s at 194. Trimethoprim is “an antibacterial closely related to the antimalarial pyrimethamine,
acting by inhibiting a step in bacterial folate biosynthesis and effective against various gram-negative and
gram-positive bacteria; administered orally in the prophylaxis and treatment of urinary tract infections and
the treatment of pneumocystis pneumonia.” Id. at 1968. Sulfamethoxazole is “a sulfonamide used as an
antibacterial active against various gram-negative and gram-positive organisms, especially for the treatment
of acute urinary tract infections[.]” Id. at 1801.
10
Lichen simplex chronicus is “eczema caused by repeated itching and rubbing or scratching of the skin; it
may arise spontaneously or be associated with other dermatoses. Characteristics are sharply demarcated,
circumscribed, scaling patches of thickened, furrowed skin, usually on the face, neck, limbs, or anogenital
region.” Dorland’s at 1034.
11
A rale is “a discontinuous sound consisting of a series of short nonmusical noises, heard primarily during
inhalation; called also crackle.” Dorland’s at 1576.

4
symptoms was significant for emesis, 12 lethargy, sore throat, chills, some cough, and no nasal
congestion. Id. at 57–58. Dr. Quinton’s examination of Petitioner was normal, but the visit notes
indicate that Petitioner was “mild ill appearing.” Id. at 58. Dr. Quinton determined that Petitioner
likely had a viral illness, but that a reaction to her HPV vaccine could not be ruled out in light of
her fever and vomiting. Id.

On August 2, 2014, Petitioner went to the emergency room (“ER”) with complaints of a
continued fever and respiratory difficulty. Pet’r’s Ex. 3 at 8. Petitioner reported a cough, swollen
tonsils without purulence, 13 and bilateral anterior cervical lymphadenopathy, 14 but no shortness of
breath. Id. at 6–7; see also Pet’r’s Ex. 2 at 58. An examination of Petitioner’s lungs was normal
with normal breath sounds. Pet’r’s Ex. 3 at 8.

By the next day, August 3, 2014, Petitioner had developed a significant cough, chest pain,
and respiratory distress and therefore presented to the Children’s Hospital of Atlanta (“CHOA”) –
Hughes Spalding. Pet’r’s Ex. 4 at 4360. She was initially placed on a high frequency nasal cannula
(“HFNC”), 15 but was transitioned to bilevel positive airway pressure (“BiPAP”) 16 when her
oxygen levels decreased from 100% saturation to the high 80s. Id.; see also Pet’r’s Ex. 2 at 62.
Petitioner was prescribed a course of Rocephin, 17 but due to the severity of her condition, she was
transferred the same day to Scottish Rite, a level two trauma center within the CHOA network.

12
Emesis is another term for vomiting. Dorland’s at 608.
13
Purulence refers to pus or discharge. Dorland’s at 1558.
14
Lymphadenopathy is “a disease of the lymph nodes, usually with swelling[.]” Dorland’s at 1083.
15
A high frequency nasal cannula (“HFNC”) is a potent “cannula that fits into the nostrils for delivery of
oxygen therapy.” Dorland’s at 281.
16
Bilateral positive airway pressure (“BiPAP”) is a machine that “use[s] pressure to push air into the lungs
. . . improving the level of oxygen in the blood and decreasing the carbon dioxide.” What is a BiPAP
Machine and What’s it Used For?, HEALTHLINE https://www.healthline.com/health/what-is-a-bipap-
machine (last visited Apr. 11, 2022).
17
Rocephin is the “trademark for a preparation of ceftriaxone sodium.” Dorland’s at 1651. Ceftriaxone
sodium is “a semisynthetic, β-lactamase–resistant, broad-spectrum, third-generation cephalosporin
effective against a wide range of gram-positive and gram-negative bacteria; administered intravenously or
intramuscularly.” Id. at 312.

5
Pet’r’s Ex. 4 at 4360. Petitioner was “started on [A]lbuterol, 18 [S]olumedrol, 19 [a] ketamine drip,20
magnesium sulfate, 21 and [she] received a terbutaline drip 22 overnight.” See id.

Her respiratory virus panel came back negative, and on August 5, 2014, Petitioner was
prescribed a second course of Rocephin and a five-day course of Zithromax. 23 Pet’r’s Ex. 2 at 64.
A chest scan performed on August 6, 2014, showed “ground[-]glass opacities 24 with mild
interlobular septal thickening within dependent portions of the lower lobes. There was no alveolar
consolidation, or bronchiectasis 25 seen. No enlarged hilar or mediastinal lymph nodes seen either.”
Pet’r’s Ex. 4 at 2341. The attending physician weaned Petitioner to HFNC on August 8, 2014, and
then to a low-flow nasal cannula on August 11, 2014. Id. Petitioner then “[a]cutely” developed
worsening respiratory distress and she was placed back on BiPAP. Id. On August 12, 2014,
Petitioner was afebrile and improving on BiPAP, but her symptoms then began to worsen. Id.
Petitioner was restarted on Bactrim. Id. at 2312. Cultures were taken, but none were positive for
bacterial infection. Id. at 2311. Petitioner underwent an immunology work-up, which showed
decreased T cells and NK cells, but normal B cells. Id. at 2319. Her treaters noted that these results
were “of unclear significance in this child.” Id. Petitioner’s medical records document “an
extensive infectious work[-]up given her isolated lung findings and fever, though she does not

18
Albuterol is “a β-adrenergic agonist . . . ; administered by inhalation as a bronchodilator for the treatment
and prophylaxis of bronchospasm associated with . . . chronic obstructive airway disease, the treatment of
asthma-associated bronchospasm, and the prophylaxis of exercise-induced bronchospasm.” Dorland’s at
45.
19
Solumedrol is the “trademark preparation of methylprednisolone sodium succinate.” Dorland’s at 1731.
Methylprednisolone sodium succinate is “the 21-succinate sodium salt of methylprednisolone, having
actions and uses similar to those of the base; it is highly soluble in water and is chiefly used for the rapid
achievement of high blood levels of methylprednisolone in short-term emergency treatment; administered
by intramuscular or intravenous injection.” Id. at 1154.
20
Ketamine hydrocholoride is “a rapid-acting general anesthetic and anesthesia adjunct, administered
intramuscularly and intravenously.” Dorland’s at 983.
21
Magnesium sulfate is “MgSO4·xH2O, a salt used as an anticonvulsant in the prophylaxis and treatment
of seizures associated with toxemia of pregnancy; also used as an electrolyte replenisher; administered
intramuscularly and intravenously.” Dorland’s at 1096.
22
Terbutaline sulfate is “a β2-adrenergic receptor agonist, used as a bronchodilator for the treatment of
asthma-associated bronchospasm and the treatment and prophylaxis of bronchospasm associated with
chronic bronchitis, pulmonary emphysema, or other chronic obstructive airway disease; administered by
oral inhalation, subcutaneously, or orally. It is also used as a tocolytic in the prevention of premature labor;
administered intravenously.” Dorland’s at 1883.
23
Zithromax is “the trademark for preparations of Azithromycin.” Dorland’s at 2092. Azithromycin is “an
antibiotic, derived from erythromycin, that inhibits bacterial protein synthesis, effective against a wide
range of gram-positive, gram-negative, and anaerobic bacteria; used in the treatment of mild to moderate
infections caused by susceptible organisms, administered orally and intravenously.” Id. at 187.
24
Ground-glass generally refers to “having a filmy, hazy appearance, as in radiographs of a lung containing
excess fluid.” Dorland’s at 808. Ground-glass opacities is “a radiological term indicating an area of hazy
increased lung opacity through which vessels and bronchial structures may still be seen.” See M. Infante,
et al., Differential Diagnosis and Management of Focal Ground-glass Opacities, 33 EURO. RESPIRATORY
J. 821–27 (2009).
25
Bronchiectasis is “chronic dilatation of the bronchi marked by fetid breath and paroxysmal coughing,
with the expectoration of mucopurulent matter. Types are distinguished according to the nature of the
dilatations.” Dorland’s at 252.

6
have much evidence of systemic inflammation.” Id. A chest CT showed Petitioner had developed
interstitial pneumonia, 26 and she had to be intubated and transferred to CHOA-Egleston, a level
one trauma center. Id. at 2315.

Petitioner was admitted to the pediatric intensive care unit (“PICU”) at Egleston on August
15, 2014. Id. A chest X-ray showed worsening interstitial 27 opacities, pneumomediastinum, 28 and
subcutaneous air. Pet’r’s Ex. 2 at 73. Dr. Dawn Simon, a pediatric pulmonologist, noted that
Petitioner was “admitted with respiratory failure and progressive interstitial lung disease 29
concerning for acute interstitial pneumonitis.” 30 Pet’r’s Ex. 4 at 2472.

On August 16, 2014, Petitioner underwent a bronchoscopy 31 and lung biopsy. Id. at 2341.
Her bronchoscopy revealed “active bleeding with lavage,” 32 causing treaters to consider
“vasculitis 33 [as] a potential etiology.” Id. at 2340. Petitioner’s pattern was “also consistent with
hypersensitivity pneumonitis[,] 34 however[, Petitioner’s condition] ha[d] not improved in the
hospital[,] which is typical when patients are removed from the offending agent found in their
home environment.” Id. Petitioner’s preliminary biopsy results showed “diffuse interstitial fibrosis
[with a] chronic, non-infectious process.” Id. at 2430. The histology of Petitioner’s lung biopsy
revealed “severe, advanced diffuse alveolar damage[,] however[,] no trigger ha[d] been
identified.” Id. at 2472. Petitioner was placed on extracorporeal membrane oxygenation
(“ECMO”) 35 on August 17, 2014. Id. at 2351.

26
Interstitial pneumonia is “1. any of various types of pneumonia characterized by thickening of the
interstitial tissue. 2. idiopathic pulmonary fibrosis.” Dorland’s at 1473.
27
Interstitial means “pertaining to or situated between parts or in the interstices of a tissue.” Dorland’s at
951.
28
Pneumomediastinum is “the presence of air or gas in the mediastinum, which may interfere with
respiration and circulation and may lead to such conditions as pneumothorax or pneumopericardium. It may
occur as a result of trauma or a pathologic process, or it may be induced deliberately as a diagnostic
procedure. Called also Hamman disease [] and mediastinal emphysema.” Dorland’s at 1472.
29
Interstitial lung disease is “a heterogeneous group of noninfectious, nonmalignant disorders of the lower
respiratory tract, affecting primarily the alveolar wall structures but also often involving the small airways
and blood vessels of the lung parenchyma; slowly progressive loss of alveolar-capillary units may lead to
respiratory insufficiency and death.” Dorland’s at 536.
30
Pneumonitis is “inflammation of the lungs.” Dorland’s at 1475.
31
A bronchoscopy is an “examination of the bronchi through a bronchoscope.” Dorland’s at 253.
32
Lavage is “1. the irrigation of an organ, such as the stomach or bowel. 2. to wash out, or irrigate.”
Dorland’s at 1009.
33
Vasculitis is “inflammation of a blood or lymph vessel[.]” Dorland’s at 2026.
34
Hypersensitivity pneumonitis is “a respiratory hypersensitivity reaction to repeated inhalation of organic
particles, usually in an occupational setting, with onset a few hours after exposure to the allergen.
Characteristics include fever, fatigue, chills, unproductive cough, tachycardia, and tachypnea; in the chronic
form there is interstitial fibrosis with collagenous thickening of the alveolar septa. There are many specific
types . . . . Called also allergic or extrinsic allergic alveolitis.” Dorland’s at 1475.
35
Extracorporeal membrane oxygenation (“ECMO”) is also called extracorporeal life support. Dorland’s
at 590. It is defined as “the provision of respiratory support by circulating the blood through an artificial
lung consisting of two compartments separated by a gas-permeable membrane, with the blood on one side
and the ventilating gas on the other[.]” Id. at 1805.

7
 By August 18, 2014, Petitioner’s treaters were considering several etiologies for her
condition, including an “idiosyncratic Bactrim reaction, [an] infectious etiology ([but] all
evaluations so far [were] negative), rheumatologic [causes] (however[,] inflammatory markers
[were] only mildly elevated), [and] inhalational/toxin exposure.” Id. at 2472. Dr. Simon noted that
the family questioned Petitioner’s vaccinations as being responsible for her condition, “in
particular the HPV [vaccine.]” Id. Dr. Simon wrote that “in reviewing the VAERS [database, she
found] no description of lung injury.” Id. She did “not believe a second bronchoscopy w[ould]
shed any further light on the etiology[]” for Petitioner’s condition. Id. at 2473. Petitioner’s treaters
at Egleston described her condition as “an end[-]stage irreversible injury,” and informed her
parents that “her only chance for survival [wa]s lung transplantation.” Id. at 2472. They also noted
that Petitioner was “[status post] pulse steroid without significant improvement.” Id. Progress
notes dated August 18, 2014, list Petitioner’s diagnoses as status asthmatics, pneumonia, acute
respiratory failure, hypoxemia, 36 hyponatremia, 37 pneumomediastinum, pneumothorax 38 on right,
and idiopathic pulmonary fibrosis. 39 Id. at 2407.

On August 24, 2014, Petitioner was transferred to the University of Kentucky for possible
lung transplantation. Pet’r’s Ex. 2 at 75. The admission note for this procedure listed her diagnosis
as acute respiratory failure with an unclear etiology. See Pet’r’s Ex. 5 at 245. Approximately one
month later, on September 25, 2014, Petitioner underwent a successful bilateral lung
transplantation. Id. at 1115, 1462. She was discharged from the hospital on October 16, 2014. Id.
at 1462. During post-surgical follow up on October 21, 2014, Petitioner’s treaters noted that she
was tolerating her immunosuppressive therapies well and was able to play and walk without
dyspnea. 40 Pet’r’s Ex. 6 at 2. Petitioner underwent a repeat bronchoscopy and lung biopsy on
November 3, 2014, and the results showed no evidence of rejection. Id. at 139. Petitioner’s filed
medical records to-date detail Petitioner’s extensive follow up care, therapies, and recovery. 41
Petitioner has not filed additional medical records.

B. Witness Statements

Mr. and Mrs. Williams both testified about their daughter’s health prior to her July 29,
2014 vaccinations, and her rapid deterioration immediately thereafter. Their testimony was
consistent with the medical record and each other. They provided additional information about
Petitioner’s symptoms at home and their encounters with medical personnel while they were
attempting to obtain a diagnosis for her condition. Mrs. Williams testified that Petitioner did not
have any residual effects from prematurity with respect to her lungs or pulmonary function. Tr.
16:22–25. She stated that Petitioner had received vaccinations from birth up until her last
scheduled round of immunizations on July 29, 2014. Tr. 17:19–20.

36
Hypoxemia means “deficient oxygenation of the blood[.]” Dorland’s at 908.
37
Hyponatremia is the “deficiency of sodium in the blood.” Dorland’s at 903.
38
Pneumothorax is “an accumulation of air or gas in the pleural space . . . .” Dorland’s at 1476.
39
Pulmonary fibrosis is the “chronic inflammation and progressive fibrosis of the pulmonary alveolar walls,
with steadily progressive dyspnea, resulting finally in death from oxygen lack or right heart failure.”
Dorland’s at 702. Also called Hamman-Rich syndrome and interstitial pulmonary fibrosis. Id.
40
Dyspnea is “breathlessness or shortness of breath; difficult or labored respiration.” Dorland’s at 582.
41
See supra, note 5.

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 Mrs. Williams explained that the entire family went on a trip to Busch Gardens in the days
before Petitioner’s vaccinations. Tr. 19:23–25. During the vacation, Petitioner did not express any
concerns or exhibit any signs that she was in respiratory distress. Tr. 20:10–12. Upon the family’s
return from the trip, Petitioner received the vaccinations at issue in this case. Tr. 21:2. Mrs.
Williams testified that Petitioner did not have any breathing issues on the day of her vaccinations.
Tr. 21:6–7. She noted that Petitioner received the TDaP and meningococcal vaccines in her left
arm and the HPV vaccine in her right arm. Tr. 23:3–8. The next day, she noted that Petitioner ran
a fever of 105 degrees Fahrenheit. Tr. 21:17. Mrs. Williams also noted that Petitioner had swelling
in her left arm. Tr. 22:11. Mrs. Williams testified that she tried unsuccessfully to break Petitioner’s
fever by following her sister’s advice to alternate between Tylenol and Motrin. Tr. 23:15–17.

From there, Mrs. Williams described how medical professionals initially reacted to her
daughter’s symptoms. The first time Mrs. Williams and her husband took Petitioner to the ER,
“[t]hey put us in a room and we waited.” Tr. 27:25. Eventually, “they swabbed [her] for strep,”
and then “they sent us home.” Tr. 23:20–21. Petitioner was given “a prescription for antibiotics,”
but “[t]hey didn’t [identify] a diagnosis or anything.” Tr. 28:1–2. Meanwhile, Petitioner had
developed breathing problems and she wasn’t getting better. Tr. 28:9–12. Mrs. Williams noted that
Petitioner’s symptoms had started the day after vaccination with arm swelling and a fever. Tr.
24:11–13. She stated that soon thereafter, Petitioner “would just lay around and she wouldn’t eat.”
Tr. 27:4. Petitioner “would just stay in bed.” Tr. 27:5. Once Petitioner started having breathing
problems, “[s]he just would do this rapid breathing and she really became confined to [her] bed.”
Tr. 28:15–16.

Mrs. Williams explained that the first ER they went to was WellStar, a local facility in
Austell, Georgia. Tr. 29:22–23. After Petitioner’s symptoms worsened, Mrs. Williams and her
husband took Petitioner to Hughes Spalding Children’s Hospital in Atlanta. Tr. 29:23–24. Mrs.
Williams stated that Petitioner was airlifted from Hughes Spalding to CHOA – Scottish Rite and
was then placed in the intensive care unit (“ICU”). Tr. 30:16–17, 31:9. After she was placed in the
ICU for a couple of days, Petitioner’s condition started to improve, and Scottish Rite was preparing
to release her. Tr. 31:24–25. However, when Petitioner “tried to get up and she fell,” they
reconsidered. Tr. 32:3–5. Shortly thereafter, medical personnel told Petitioner’s parents that “they
had done all they could do at Scottish Rite and [they] needed to take her to Egleston for more
testing and stuff.” Tr. 32:6–8. Mrs. Williams stated that after Petitioner was transferred to Egleston,
she was placed in a coma. Tr. 32:11.

Mr. Williams recounted much of Mrs. Williams’ account. He noted that ER personnel did
“pretty much nothing as far as [he was] concerned.” Tr. 55:22–23. He described how they
“wouldn’t give [Petitioner] an X-ray.” Tr. 55:23. They “gave [Petitioner] medicine,” and “watched
her for a couple of hours and then they released her.” Tr. 55:23–25. Mr. Williams remembered that
on the following Sunday, they were on the way to church and “she was really panting a lot.” Tr.
56:6–8.

Both of Petitioner’s parents noted that she is no longer recommended for vaccination. See
Tr. 37:17–18. Mrs. Williams did not offer a reason, but Mr. Williams stated that, Petitioner’s
“immune system is weakened due to the medication[]” she is on. Tr. 37:17–18, 82:20–21.

9
 Petitioner’s testimony was brief and consistent with her parents’ accounts. She identified
the first symptom she remembers as “not having any energy to do anything.” Tr. 69:20–21. She
stated that she felt like she “had a cold maybe but ten times worse.” Tr. 69:22–23.

Lastly, Petitioner’s aunt Mrs. Nina Lagarde, testified. She noted that when Petitioner was
in the ICU, her treaters “tried to say she had asthma.” Tr. 85:14. Petitioner’s aunt noted that she is
an ER nurse practitioner, and she was the one who told medical personnel about the vaccines as a
possible cause. Tr. 85:20–21. She noted that “nothing else made sense” and asked the attending to
“just scan [Petitioner’s] arm” and to “do an echo.” Tr. 85:21–24. Mrs. Lagarde emphasized that
she is a nurse practitioner, not a medical doctor and she is not testifying as an expert. Tr. 86:4–8.
Although she was upfront with hospital staff about her belief that Petitioner’s condition was
vaccine caused, they never identified a cause, “[t]hey just said something attacked . . . .” Tr. 85:20–
21, 93:7–8.

C. Medical Literature

i. ChILD

Interstitial lung disease in children (“chILD”) is an umbrella term for a group of respiration
disorders that are “characterized by inflammatory and fibrotic changes that affect alveolar walls.”
Pet’r’s Ex. 17 at 1, ECF No. 23-1. 42 A chILD syndrome diagnosis requires:

the presence of at least [three] of the following [four] criteria in the absence of other
known disorders: (a) respiratory symptoms (cough, rapid breathing, or exercise
intolerance), (b) signs (resting tachypnea, 43 crackles, retractions, digital clubbing,
failure to thrive, or respiratory failure), (c) hypoxemia, and (d) diffuse chest
infiltrates on chest X-ray or computed tomography (CT) scan.

Pet’r’s Ex. 10 at 3, ECF No. 22-3. 44 There have been several different systems that have been
developed for the classification of lung diseases in children. In the late 1990s, researchers
developed “four histopathologically distinct subgroups of idiopathic interstitial pneumonias: usual
interstitial pneumonia (“UIP”), desquamative interstitial pneumonia (“DIP”) and a closely related
pattern termed respiratory bronchiolitis-associated ILD, acute interstitial pneumonia (formerly
Hamman-Rich syndrome), and non[-]specific interstitial pneumonia (“NSIP”).” Pet’r’s Ex. 17 at
1. ChILD cases have also been categorized more recently by diagnosticians into the following
groupings: “1) exposure-related ILD; 2) systemic disease-associated ILD; 3) alveolar structure
disorder-associated ILD; and 4) ILD specific to infancy.” Id.

42
A. Clement, et al., Interstitial Lung Diseases in Children, 5 ORPHANET J. RARE DISEASES 1–24 (2010).
43
Resting tachypnea is the “excessive rapidity of breathing[]” while at rest. Dorland’s at 1868.
44
J. Soares, et al., Childhood Interstitial Lung Diseases: An 18-year Retrospective Analysis, 132
PEDIATRICS 684–91 (2013).

10
 Another classification system first groups such conditions into “‘Disorders More Prevalent
in Infancy’ and ‘Disorders not Specific to Infancy.”’ Pet’r’s Ex. 15 at 3, ECF No. 22-8. 45 This type
of “classification strategy recognizes that some disorders present largely in infancy, but may also
develop later in childhood or even adulthood, whereas the second category acknowledges that
infants can develop conditions that are more common in older children and adults.” Id. The
diseases seen more often in older children include, “systemic diseases, idiopathic disorders [DIP,
UIP, NSIP and lymphoid interstitial pneumonia [(“LIP”)], unclassifiable ILD[,] and also infectious
disorders.” Pet’r’s Ex. 17 at 2. Although these conditions are iterations of lung disease, the
classifications are important for treatment. Id. In some cases where there is clear evidence of
inflammation, corticosteroids can be quite effective. Id. In other cases, steroids can exacerbate the
injury. Id. In the most severe chILD cases, such as in Petitioner’s case, a lung transplant is the only
viable treatment option. Early identification of the nature of a patient’s condition can expedite
treatment, particularly in cases where organ donation and transplantation are needed. See id.

The rarity of chILD cases has limited the ability of researchers to conduct clinical trials or
epidemiological studies. Pet’r’s Ex. 14 at 5, ECF No. 22-7. 46 Due to the wide spectrum of the
syndrome, the outcome for cases “is highly variable with a mortality rate around 15%.” Resp’t’s
Ex. H at 1; 47 see also Pet’r’s Ex. 17 at 1. In general, “[a]n overall favorable response to
corticosteroid therapy is observed in around 50% of cases, often associated with sequelae such as
limited exercise tolerance or the need for long-term oxygen therapy.” See id. There is much more
information on the etiology, progression, and treatment of ILD in adults, which is sometimes used
to help understand and characterize chILD cases. ILD in adults is classified by histology; however,
these schemes “are not satisfactory for [all] pediatric cases which seem to comprise a broader
spectrum of disorders.” Pet’r’s Ex. 17 at 1.

ii. Pulmonary Fibrosis

Fibrosis occurs when tissue repair is dysregulated and “the excess accumulation of
extracellular matrix components (“ECM”)” leads to scarring. Pet’r’s Ex. 47 at 1, ECF No. 26-4. 48
Pulmonary fibrosis (“PF”) is a condition that includes acute, treatment-resistant disease and
involves “the progressive and irreversible destruction of lung architecture caused by scar formation
that ultimately leads to organ malfunction[] and death from respiratory failure.” Id. While
idiopathic pulmonary fibrosis (“IPF”) is a type of ILD seen in adults, there are some studies that
suggest that IPF is “not believed to occur in children.” Pet’r’s Ex. 13 at 5, ECF No. 22-6. 49 A study
by Nathan et al. states that pulmonary fibrosis has not been identified as a distinct child entity with
diagnostic criteria. N. Nathan, et al., Review: Pulmonary Fibrosis in Children, 8(9) J. CLIN. MED.
1–15 (2019). The authors found “that adult radiologic and histologic lung fibrosis patterns partially

45
G. Kurland, et al., An Official American Thoracic Society Clinical Practice Guideline: Classification,
Evaluation, and Management of Childhood Interstitial Lung Disease in Infancy, 188 AM. J. RESPIRATORY
CRIT. CARE MED. 376–94 (2013).
46
T. Vece, et al., Diagnosis and Management of Diffuse Lung Disease in Children, 12 PED. RESPIRATORY
REV. 238–42 (2011).
47
See Clement, et al., supra note 42.
48
T.A. Wynn, Integrating Mechanisms of Pulmonary Fibrosis, 208 J. EXP. MED. 1339–50 (2011).
49
J. Popler, et al., New Coding in the International Classification of Diseases, Ninth Revision, for
Children’s Interstitial Lung Disease, 142 CHEST 774–80 (2012).

11
fail to precisely describe pediatric PF lesions and that [in usual interstitial pneumonia], the most
common aspect of IPF, is exceptionally or never observed in childhood.” Id. at 2. The few
identified cases of PF in children exhibit “a different pattern than in adults, with more
inflammatory cell recruitment and less fibroblast recruitment and ECM deposition.” Id. at 7. The
authors contended that “pediatric PF . . . may have a different meaning in children, than in adults,
with more cellular recruitment, less collagen deposition, and less parenchymal 50 destruction.” Id.
at 10.

Most studies indicate that patients with IPF “ha[ve] an [sic] life expectancy of 2–6 [years]
after diagnosis.” Pet’r’s Ex. 47 at 1; 51 see also Resp’t’s Ex. TT at 1, ECF No. 46-3. 52 “The majority
of patients demonstrate a slow, gradual progression over many years.” Resp’t’s Ex. I at 11. 53 The
mortality rate is high, because “the only effective treatment available for progressive lung fibrosis
is lung transplantation.” Pet’r’s Ex. 47 at 1. This is compounded by the fact that “pathological
mechanisms that account for disease progression are poorly understood but likely involve
alterations in innate inflammatory cells, epithelial cells, and fibroblasts.” Pet’r’s Ex. 56 at 1, ECF
No. 45-8. 54 It can occur following viral infections, exposure to toxins, following chemotherapy, or
accompanying autoimmune disease. Pet’r’s Ex. 47 at 1.

There is debate surrounding the role of inflammation in the development of pulmonary
fibrosis. Id. at 2. Dr. Thomas Wynn contended that “inflammatory mediators clearly play a role in
both the initiation and progression of some forms of pulmonary fibrosis.” Id. at 3. Dr. Wynn noted
that “many forms of the disease are believed to be induced, at least initially, by a strong
inflammatory response.” Id. at 2. This is based on elevated levels of TNF in some patients with an
idiopathic etiology and mice models that show an over-expression of cytokines in the lungs. Id.
While animal studies provided some support for the role of inflammation, “it remains unclear
whether any of the experimental models truly duplicate the idiopathic form of the disease that is
commonly seen in humans.” Id.

Immediately following tissue damage in humans, epithelial cells “release inflammatory
mediators . . . that trigger[] clotting and [the] development of provisional ECM.” Id. This process
results in “[p]latelet aggregation and subsequent degranulation” to “promote[] blood vessel
dilation and increased permeability” and allows the “efficient recruitment of inflammatory cells.”
Id. These cells, including neutrophils and macrophages, “eliminate any invading organisms.” Id.
Cytokines are also produced, and they “amplify the inflammatory response and trigger fibroblast
proliferation.” Id. Fibroblasts are “highly responsive to growth factors/cytokines,” such as TGF-

50
Parenchyma refers to “the essential or functional elements of an organ[.]” Dorland’s at 1382.
51
See Wynn, supra note 48.
52
D. Galati, et al., Peripheral Depletion of NK Cells and Imbalance of the Treg/Th17 Axis in Idiopathic
Pulmonary Fibrosis Patients, 66 CYTOKINE 119–26 (2014).
53
G. Raghu, et al., An Official ATS/ERS/JRS/ALAT Statement: Idiopathic Pulmonary Fibrosis: Evidence-
based Guidelines for Diagnosis and Management, 183 AM. J. RESPIRATORY CRIT. CARE MED. 788–824
(2011).
54
D.N. O’Dwyer, et al., Influences of Innate Immunity, Autophagy, and Fibroblast Activation in the
Pathogenesis of Lung Fibrosis, 311 AM. J. PHYSIOL. LUNG CELL MOL. PHYSIOL. 590–601 (2016).

12
beta, IL-1beta, IL-6, IL-13 and IL-33.” Resp’t’s Ex. UU at 2, ECF No. 46-4. 55 Studies on the role
of cytokines in the development of pulmonary fibrosis have suggested that TGF-beta is the
“prototypical ‘profibrotic’ mediator.” Id. at 5.

TGF-beta1 “promotes ECM accumulation, . . . drives phenotypic changes of fibroblasts,”
and “promotes fibroblast proliferation in patients with IPF.” Id. These cytokines “are recruited
from a variety of sources,” and once activated, they initiate regeneration of the damaged tissue by
a process where “epithelial/endothelial cells divide and migrate over the temporary matrix to
regenerate the damaged tissue.” Pet’r’s Ex. 47 at 2. Scars can result at any stage of this process,
“likely explaining the complex nature of pulmonary fibrosis.” Id.

In clinical trials, TNF inhibitors were effective “but, because TNF can inhibit collagen
synthesis in myofibroblasts, TNF antagonists might have the undesired effect of worsening the
disease.” Id. at 3. Evidence of increased TNF levels alongside IL-1beta induced fibrosis suggests
a connection. See id. Chemokines and profibrotic cytokines are increased by IL-1beta “illustrating
how [an] acute lung injury initiated by proinflammatory cytokines and neutrophils can quickly
evolve[] to a progressive fibrotic response.” Id.

Alternatively, IPF is “often characterized as exhibiting highly progressive fibrotic disease
in the absence of detectable inflammation.” Id. at 2. Unlike other forms of ILD, evidence that “an
active inflammatory response is not a strict prerequisite[,] likely explains why standard
autoinflammatory therapies, including corticosteroids and cytotoxic agents[,] have shown little
efficacy.” Id.; see also Resp’t’s Ex. TT at 8. 56 Additionally, “[d]epletion of NK and Th17 cells
along with a[n un]compromised [regulatory T lymphocyte] compartment delineate the existence
of an ‘immune profile’ in IPF that may be more closely assimilated to that observed in the cancer
model.” Resp’t’s Ex. TT at 8. The Galati et al. study sought to “investigate the distribution of
peripheral immune subsets in patients affected by clinically stable idiopathic pulmonary fibrosis.”
Id. at 5. The author’s “exclusion criteria were acute disease exacerbation, and systemic
administration of corticosteroids, and/or immune-suppressive drugs at enrollment or in the
previous [sixty] days.” Id. at 2. They found a significant decrease in the number of NK cells in IPF
patients, which is contrary to a previous, smaller study. Id. at 5. Potential reasons for this difference
include different diagnostics for IPF, different exclusionary criteria, and “the inclusion [of a]
control group of patients affected by other interstitial lung diseases instead of healthy subjects.”
Id. Although there was a difference in NK cell levels in IPF patients, “there are [sic] no information
addressing dynamics of NK and NKT cells in IPF pathogenesis for any comparison with our data.”
Id. There is so much we don’t know about “the nature of how or which inflammatory immune cells
may be contributing to pathogenesis,” that “it is likely that the immunosuppressive agents we have
used to date may not have effective[ly] targeted the profibrotic actions of innate immune cells.”
Pet’r’s Ex. 56 at 4. 57

There have been several potential “triggers [identified] that initiate and maintain fibrotic
pulmonary remodeling” but they are controversial. See Resp’t’s Ex. UU at 1. These include

55
S. Kolahian, et al., Immune Mechanisms in Pulmonary Fibrosis, 55:3 AM. J. RESPIRATORY CELL MOL.
BIOL. 309–22 (2016).
56
See Galati, et al., supra note 52.
57
See O’Dwyer, et al., supra note 54.

13
infections, environmental and occupational pollutants, obesity, diabetes mellitus, pulmonary
hypertension, gastroesophageal reflux, and connective tissue diseases/autoimmune disorders. Id.
There is evidence that “immune cells have more opportunity to cross talk with structural cells of
the lung than was previously appreciated.” Pet’r’s Ex. 56 at 8. Researchers have discovered the
“release of IL-17 from neutrophils promotes fibroblast proliferation.” Id. Other literature suggests
that “neutrophils can activate TGF-beta,” and “further promote fibrogenesis by blocking
autophagy and increasing ECM deposition.” Id. Fibroblasts, if activated by dysregulation, can be
“highly responsive to growth factors/cytokines, such as connective tissue growth factor,
(“CTGF”), platelet-derived growth factor (“PDGF”), [TGF-beta, various interleukins,] as well as
aberrantly activated profibrotic pathways, . . . that maintain fibrotic tissue transformation.”
Resp’t’s Ex. UU at 2.

iii. Immune Response

While there are conflicting perspectives on the role of the immune system in the
development of IPF, there is also disagreement on the effect of multiple immune triggers occurring
simultaneously within the body. In the Boyce et al. 58 study, researchers tested whether there is “an
association between recent vaccination with a pertussis-containing vaccine and increased severity
of respiratory syncytial virus (“RSV”) 59 infection.” Resp’t’s Ex. VV at 1, ECF No. 46-5. This
study focused on the pertussis vaccination because the acellular pertussis vaccine contains a
toxoid. Id. Even in this inactivated form, the authors found that the pertussis toxin “enhances the
magnitude of the antibody response to the simultaneously delivered antigens.” Id. at 2. Researchers
hypothesized that evidence “to support the role of the host immune response as a determinant of
RSV disease severity,” would have included a more severe RSV disease course in “[i]nfants
immunized with an experimental formalin-inactivated RSV vaccine [when compared to an
unvaccinated group],” following exposure to the wild virus. Id. The authors found that in mice,
“exposure to [the] pertussis toxoid (which is a component of all pertussis vaccines) was associated
with an altered cellular and humoral immune response to RSV infection and with increased
mobility and mortality.” Id. at 4. This “suggest[s] that enhanced illness was the result of selection
activation of type 2 CD4+ [Th] lymphocytes, leading to altered cytokine and immunoglobulin
production.” Id. Ultimately, the authors noted that the results from the murine model were not
duplicated in children. Id. Researchers found that receipt of a recent pertussis vaccination did not
increase illness severity or likelihood of hospitalization. Id. The authors cautioned that “[t]he
reason for the disparity between the animal data and [human subjects] is unknown.” Id.

The McDonald et al. 60 study sought to answer the question, “[h]ow do cells of the innate
immune system find their way to sites of sterile inflammation?” Pet’r’s Ex. 48 at 3, ECF No. 26-
5. The authors defined sterile inflammation as an immune system process that occurs where there

58
T. Boyce, et al., Pertussis Vaccination and the Risk of Respiratory Syncytial Virus-Association
Hospitalization, 23 J. PEDIATRIC INFECT. DIS. 897–901 (2004).
59
Respiratory syncytial virus (“RSV”) refers to “any of a group of viruses belonging to the genus
Pneumovirus, isolated originally from chimpanzees . . . . In humans, they cause respiratory disease that is
particularly severe in infants, in whom it causes bronchiolitis [] and sometimes pneumonia.” Dorland’s at
2064.
60
B. McDonald, et al., Innate Immune Cell Trafficking and Function During Sterile Inflammation of the
Liver, 151 GASTROENTEROLOGY 1087–95 (2016).

14
is cell death in the absence of infection. Id. at 1. This process “is required for processes that include
organ development, tissue repair[,] and host defense.” Id. The researchers focused on liver disease
and noted that “there are few treatments beyond liver transplantation for patients with end-stage
disease.” Id. They cautioned that “molecular mechanisms that control immune cell trafficking
during sterile inflammation may be organ and tissue specific.” Id. at 7. In other words, “lessons
learned from the skin or kidney are not necessarily applicable to the liver microvasculature.” Id.
They used information from prior recent studies that described “cellular and molecular
mechanisms of immune cell recruitment to damaged tissues, as well as the cell types that mediate
tissue repair and homeostasis.” Id.; see also Pet’r’s Ex. 58 at 3, ECF No. 45-10. 61 The McDonald
et al. study revealed “the molecular mechanisms that enable immune cells to traffic to sites of
sterile inflammation in the liver[,] as well as the contributions of innate immune cells during tissue
repair.” Pet’r’s Ex. 48 at 1. It also showed that neutrophils respond to the liver injury by
“infiltrating the site of injury within minutes.” Id. at 3. The release of damage associated molecular
patterns (“DAMPs”) “from dead cells[,] stimulates [the] endothelium to present adhesion
molecules and chemokines on their surface to draw neutrophils out of the mainstream of blood and
initiate a well-described recruitment cascade.” Id. Still within the context of sterile inflammation,
“neutrophils migrate via intravascular channels rather than into the parenchyma[,] and through the
interstitium.” Id. at 4. This “neutrophil influx is focused precisely into areas of tissue injury where
they are observed to exhibit swarming behavior.” Id. The authors noted that this swarming “has
been observed in multiple models of sterile inflammation[,] as well as infections.” Id.

The authors of the McDonald et al. 62 article further noted that macrophage infiltration at
the site of sterile inflammation also occurred one- to- two- days after the neutrophils arrive. Id. at
5. They continued that “[m]onocytes have many functions, . . . including production of
inflammatory mediators, clearance of dead neutrophils, stimulation of extracellular matrix
production, regeneration of parenchymal cells, and angiogenesis.” Id. In addition to inflammatory
monocytes, anti-inflammatory monocytes are produced that “promote resolution (IL-10,
transforming growth factor beta, and VEGF) to shift the [] response from active inflammation
toward resolution and restitution.” Id. The “in situ reprogramming [of inflammatory monocytes to
an anti-inflammatory phenotype] was induced by local production of anti-inflammatory cytokines
(IL-10 and IL-4) and was required for clearance of necrotic debris and deposition of new
extracellular matrix scaffolding in the healing wound.” Id. Lastly, they noted that “monocytes have
been found to patrol the microvasculature monitoring for danger[, and ]monocytes have been
observed to continuously crawl throughout tissue micro-vessels.” Id. at 6. The authors found that
“[u]pon encountering infection or tissue injury, these monocytes rapidly exit the blood vessels and
begin producing cytokines and chemokines to summon other immune cells.” Id.

III. Experts

A. Expert Backgrounds

1. Petitioner’s Expert, Eric Gershwin, M.D.

61
V. Colmenares, et al., Human Papillomavirus Immunization is Associated with Increased Expression of
Different Innate Immune Regulatory Receptors, 19:7 CLIN. & VACCINE IMMUNOLOGY 1005–11 (2012).
62
See McDonald, et al., supra note 60.

15
 Dr. Gershwin received his medical degree from Stanford University in 1971. Pet’r’s Ex. 9
at 1, ECF No. 22-2. He is licensed to practice in several states, including California, and holds
board certifications in internal medicine, internal medicine with a subspecialty in rheumatology,
and allergy and clinical immunology. Id. at 2. Dr. Gershwin has an honorary doctorate, or “Honoris
Causa,” from the University of Athens, Greece, in recognition of his lifetime contributions in
immunology and medicine. Id. at 1. Dr. Gershwin has also been awarded the AESKU Prize in
Autoimmunity for his lifetime contribution in immunology and the Vasco Da Gama Prize for “a
lifetime of deep explorations in immunology to benefit mankind.” Id.

Dr. Gershwin’s post-doctoral training includes a two-year residency at the Tufts-New
England Medical Center in Boston, Massachusetts, two years as a clinical associate in immunology
at the National Institutes of Health in Bethesda, Maryland, and two years as an Assistant Professor
of Medicine in Rheumatology and Allergy at the University of California School of Medicine in
Davis, California (“UC Davis”). Id. at 2. Dr. Gershwin then went on to become the Director of the
Special Immunology Diagnostic Laboratory at UC Davis. Id. He has been a Professor of Medicine,
specializing in Rheumatology and Allergy, at UC Davis since 1981 and a Chief of the Division of
Rheumatology/Allergy and Clinical Immunology since 1982. Id. at 1.

Dr. Gershwin is also a fellow with the American Academy of Allergy and Immunology,
the American College of Physicians, and the American College of Rheumatology. Id. at 3–4. He
currently serves as the editor-in-chief for the Journal of Autoimmunity and Clinical Reviews in
Allergy, as co-editor-in-chief for Autoimmunity Reviews, and as co-editor for Reviews in
Autoimmunity. Id. at 5. Dr. Gershwin’s curriculum vitae lists numerous books, book chapters, and
research papers of which he is a listed author. See id. at 8–125.

During the hearing, he noted that he has testified in the Program before. Tr. 97:19–21. He
also stated that he has “seen and treated patients with immunological issues for nearly [fifty]
years.” Tr. 100:8–9. Dr. Gershwin highlighted that he has published “nearly 1,000 papers, books[,]
and reviews” during that time. Tr. 100:10–11. He noted that he has “been funded by the [National
Institute of Health] for basic and clinical research in immunology without interruption
continuously since 1975[.]” Tr. 100:14–16. Dr. Gershwin testified that he has consulted on
approximately five to seven chILD cases throughout the course of his career, as they are
“exceedingly rare” cases. Tr. 102:13–23.

Dr. Gershwin submitted one expert report and testified during the entitlement hearing. See
Pet’r’s Ex. 8, ECF No. 22-1; Tr. 97–169, 285–318. Petitioner offered Dr. Gershwin as an expert
in immunology without objection, and I recognized him as such. Tr. 103:11–15.

2. Respondent’s Expert, Dr. Gary S. Rachelefsky, M.D.

Dr. Rachelefsky received his medical degree from Washington University in St. Louis,
Missouri in 1967. Resp’t’s Ex. B at 1, ECF No. 28-2. Dr. Rachelefsky completed a residency in
pediatrics at Johns Hopkins University in Baltimore, Maryland in 1970. Id. He completed
fellowships in epidemiology and allergy and immunology at the Center for Disease Control and
the UCLA School of Medicine in 1972 and 1974, respectively. Id. He holds board certifications in
pediatrics and allergy and immunology. Id. Dr. Rachelefsky currently serves as a Professor of
Allergy and Immunology at the David Geffen School of Medicine at UCLA. Id. He is also the

16
Associate Director of the Allergy-Immunology Training Program at the UCLA’s medical school.
Id. Dr. Rachelefsky serves as the Director of the Executive Care Center for Asthma, Allergy &
Respiratory Diseases at UCLA. Id. Dr. Rachelefsky holds memberships in numerous professional
societies, committees, and advisory boards dedicated to pediatrics, allergy and immunology, and
asthma. Id. at 5–10. Dr. Rachelefsky’s curriculum vitae lists numerous books, book chapters, and
research papers of which he is a listed author. See id. at 13–35. He submitted one expert report and
did not testify at the entitlement hearing. See Resp’t’s Ex. A.

3. Respondent’s Expert, Christine McCusker, M.D.

Dr. McCusker received her medical degree from McMaster University Medical School in
Ontario, Canada in 1993. Resp’t’s Ex. LL at 1, ECF No. 34-2. Dr. McCusker completed a
residency in pediatrics at Montreal Children’s Hospital in Quebec, Canada in 1996. Id. at 2. She
also completed a fellowship in allergy and immunology at McGill University in Quebec, Canada
in 1999. Id. Dr. McCusker completed a post-doctoral research fellowship in immunology at the
same institution in 2000. Id. Dr. McCusker has been a physician in the emergency department of
Montreal Children’s Hospital and McGill University since 1999. Id. at 5. She has been the Director
of the Clinical Immunology Laboratory at the same institution since 2004. Id. Since 2009, Dr.
McCusker has also served as an Associate Professor of Allergy and Immunology in the Pediatrics
Department of McGill University. Id. at 3. She currently serves as the Research Director of
Meakins-Christie Laboratories. Id. Dr. McCusker is board-certified in pediatrics and holds several
professional credentials in allergy and immunology. Id. at 2–3. She has received numerous honors
and has delivered a plethora of national and international lectures. Id. at 4–7. She is a member of
several academic committees and societies. Id. at 13–15. Her curriculum vitae lists extensive
publications, including articles, abstracts, book chapters, and editorials of which she is a listed
author. See id. at 20–26. Some of the articles address cytokine activity. Tr. 174:22–24.

During the hearing, Dr. McCusker explained that as part of her clinical practice, she spends
half of her time seeing patients and the other half “either in research or in administration or in
teaching[.]” Tr. 172:10–17. She testified that the patients she treats in her immunology clinic are
referred to her by specialists. Tr. 173:1–12. Dr. McCusker stated that she sees pediatric patients
with pulmonary fibrosis and has treated approximately four patients with chILD. Tr. 173:22–25,
174:11.

Dr. McCusker submitted one expert report and testified at the entitlement hearing. See
Resp’t’s Ex. KK; Tr. 170–238, 243–284. Respondent offered Dr. McCusker as an expert in
pediatric immunology, pediatric clinical allergy/immunology, and pediatrics without objection,
and I recognized her as such. Tr. 176:6–14.

B. Expert Review

1. Petitioner’s Expert, Eric Gershwin, M.D.

In general, Dr. Gershwin’s practice was approximately 10% focused in pediatrics. Tr.
130:11–12. Over the course of his practice, he has “seen hundreds of patients in a given year,
particularly with immune deficiencies.” Tr. 130:14–15. He noted that he “actually wrote or edited

17
the first textbook of pediatric rheumatology.” Tr. 130:12–13. He explained that “[t]he prevalence
[of chILD cases] is about one in a million per children under the age of [sixteen].” Tr. 130:19–20.
In the past ten years, Dr. Gershwin has seen pediatric patients with connective tissue disease and
lupus, in addition to two with “a disease like this [case].” Tr. 131:7–11.

Dr. Gershwin was qualified as an expert in immunology, and he provided a brief overview
of the immune system and “two major types of immunity.” Tr. 103:25, 104:1–2. The innate system,
Dr. Gershwin explained, is analogous to a first responder. Tr. 104:5. When a person is vaccinated,
innate system cells “produce cytokines that facilitate the immune system.” Tr. 104:6–7. Indeed,
Dr. Gershwin noted that “[t]he FDA requires that you show that vaccines produce cytokines.” Tr.
121:16–17. He continued that there are different types of cytokines that are produced in different
bodily systems. Dr. Gershwin described them as signal transmitters and said they are “responsible
for cell health” and “cell pathology in some cases.” Tr. 104:18–21. Proinflammatory cytokines
“will facilitate or promote scarring or connective tissue repair.” Tr. 105:8–9. Dr. Gershwin testified
that the process of inflammation, “might be local or it might be systemic.” Tr. 105:24–25. He
added that an inflammatory response does not have to occur in a vacuum. Dr. Gershwin stated that
inflammation can coincide with “something else happening in a different part of the body,” to
produce a result different or more severe than if the body was only confronted with one type of
stress. Tr. 106:4–25, 107:1. For example, Dr. Gershwin explained that someone that suffers from
food allergies may try to “avoid those foods [because] they might produce itching [or] maybe even
some hives.” Tr. 106:15–16. This same person, “if they happen to exercise around the same time
they’re eating that food, they may have a life-threatening allergic reaction.” Tr. 106:16–19. The
combination of those two stressors on the body, the allergic reaction and the exercise, “can cause
an entirely different reaction than if they just had the food and sat back and watched a movie.” Tr.
106:20–23. Similarly, Dr. Gershwin opined that Petitioner’s chILD developed due to immune
system dysregulation “caused by the vaccine and an underlying viral infection” acting in
combination on the immune system. Tr. 109:11–12.

According to Dr. Gershwin, the logical sequence of cause and effect in this case began with
Petitioner’s “underlying predisposition” due to her prematurity. Tr. 109:18. He testified that
“chILD is extremely rare[,] and we should discuss that, but . . . it is true that being born premature
will make you more susceptible.” Tr. 109:19–22. Dr. Gershwin noted “that the use of steroid cream
and ointment [from approximately 2011 to 2014] did lead to some T cell suppression in [Petitioner]
and likely a dysregulation, and also would have been a predisposing factor if she faced the right
challenge to getting interstitial [lung] disease in the future.” Tr. 110:1–6. Dr. Gershwin continued
that Petitioner “had a really intense innate immune response against the vaccine.” Tr. 110:7–9. He
characterized Petitioner’s swollen arm as a local reaction. Tr. 110:9. Petitioner’s fever, however,
he did “not believe [was] a response [to vaccination],” and stated that “it[ was] part of the
interstitial lung disease.” Tr. 110:12. Dr. Gershwin noted Petitioner’s sore throat, “pharyngitis and
some evidence of a viral infection.” Tr. 110:13–14. He explained that “[Petitioner] had her own
innate immune response against that virus, as you would expect it,” but he added that “this occurred
in combination with a really high intense first responder response against the vaccine.” Tr. 110:17–
20. Specifically, in “a regional lymph node [there was] an intense up-regulation of molecules
involved in the innate response to vaccination.” Tr. 110:22–24. According to Dr. Gershwin,
Petitioner was “a predisposed host [with] a viral infection” in an instance of “an incredibly fast
onset of [chILD].” Tr. 110:25, 111:1–4. He added that this process “[wa]s being driven and

18
amplified by the bystander events by the cognate cells of [Petitioner’s] immune system.” Tr.
111:5–6.

In his written report, Dr. Gershwin likened this concept to sterile inflammation, which was
discussed in the McDonald et al. 63 article. Pet’r’s Ex. 8 at 5; see also Pet’r’s Ex. 48. He wrote,
“[i]n other words, [there is] inflammation in the absence of infection to a tissue injury which leads
to chronic perpetuation of an immune response.” Pet’r’s Ex. 8 at 5. Later in this report, Dr.
Gershwin explicitly incorporated the process of sterile inflammation into his theory. He wrote that
Petitioner, “more likely than not, was undergoing a mild drug or viral-induced reaction that should
have been reversible were it not for the sterile inflammation and abnormal healing characterized
by fibrosis that was induced by her vaccinations.” Id. During his testimony, Dr. Gershwin again
analogized Petitioner’s case to “acute sterile inflammation [that] is activated in response to
podocyte death during [hepatitis].” Tr. 299:17–19. When discussing the migration of innate cells
to a bodily injury, he noted that “[c]ells will go to areas of injury. Whether it’s a sterile splinter,
whether it’s a nonbacterial infection, a viral infection, they will go there.” Tr. 299:24–25, 300:1.

Dr. Gershwin noted that Petitioner “didn’t have an underlying connective tissue disease,”
and “[s]he didn’t have a family history of [ILD].” Tr. 111:21–23. Therefore, the quick progression
of Petitioner’s chILD “was guided and driven by cognate immune cells that result from the
vaccination as bystanders pushing ahead what her own immune response was to [the] virus.” Tr.
111:24–25, 112:1–2. He concluded, “[s]o it’s not the virus that produced the [ILD]. It’s her own
immune system.” Tr. 112:3–4. When asked what role the virus or Petitioner’s Bactrim regiment
had on the development of her chILD, Dr. Gershwin stated that the viral or Bactrim process would
be the same. He explained that Petitioner “produced an innate or bystander response.” Tr. 113:20.
This “response became incredibly magnified [and] produced large numbers of cytokines because
[Petitioner] got three vaccines.” Tr. 113:23–25. Dr. Gershwin stated that he was unable to identify
the cytokines produced in Petitioner’s case because there was a virus involved and “they didn’t do
any cytokine measurements[,] and they didn’t do immunohistochemistry of her lung tissue during
the biopsy of August 15th.” Tr. 114:3–6. He conceded that he was more familiar with the functions
of specific cytokines in mice than in humans. However, Dr. Gershwin named TGF beta, IL-1 alpha
and IL-17 as cytokines that could have been upregulated in response to Petitioner’s vaccinations.
Tr. 114:12–24.

In Petitioner’s case, Dr. Gershwin opined that these and other cytokines acted as
inflammatory mediators from macrophages to myofibroblasts that then “produce[d] scarring” and
“release[d] connective tissue disease” in Petitioner’s lung. Tr. 116:16–18. He explained that a
fibroblast, or the “cell that wreaks havoc on the alveolar epithelial cell,” can be found all over the
body to heal damaged tissue and produce scars. Tr. 122:24–25, 123:1. These scars “will push out
any [healthy or damaged] cells or tissue in the area and destroy it.” Tr. 123:6–7. In the case of
chILD, “the lung thinks it’s got an injury that requires a scar.” Tr. 116:18–19. He continued that
the “scarring pushes out and removes the alveolar epithelial cells, which are the air sacs that we
depend on to breathe.” Tr. 123:7–9. This can occur because the cells “become[] susceptible to
[inflammatory] mediators produced by macrophages, T cells, and to a lesser extent to neutrophils,
including for example, IL-1, TGF beta, IL-13, and TNF.” Tr. 116:10–13. Dr. Gershwin testified
that “[t]he end result is [that] the lung turns basically to scar tissue. Instead of alveolar cells, it ends
63
See McDonald, et al., supra note 60.

19
up with basically a wound.” Tr. 118–21. Dr. Gershwin noted that due to the rare occurrence rate
of chILD, “[s]o much of this data is based on our understanding of pulmonary fibrosis in other
diseases.” Tr. 117:13–14. He concluded that when this occurs “there has to be an abnormality in
cytokines in the inflammatory response.” Tr. 118:1–2.

Dr. Gershwin made the argument that the body mounts “an intense response” to
vaccination that is analogous to “a civil war.” Tr. 118:24. He referred to the Chatziandreou et al. 64
article that seeks to “examine the role of lymph node macrophages in the induction of the cytokine
storm triggered by [an] inactivated influenza virus vaccine.” Pet’r’s Ex. 51 at 1, ECF No. 45-3.
This article is a study of the influenza vaccine, but Dr. Gershwin argues that the authors illustrate
an “intense cytokine response and chemokine response following vaccination.” Tr. 119:1–2. In the
present case, Petitioner “had an intense local response, an extremely intense fever following
response, in very close proximity to a viral infection.” Tr. 119:8–10. Dr. Gershwin explained that
“[i]t’s not the virus that’s wiping out her lung. It’s the immune response.” Tr. 119:17–18. He
described the “autoinflammatory response” as “extremely intense” and “very short-lived.” Tr.
119:19–22. Dr. Gershwin asserted that the response is “going to all be over in three to four days.”
Tr. 119:23–24. He noted that Petitioner was vaccinated on July 29, 2014, and had a fever and
swollen arm the next day. Tr. 119:24–25. By July 31, 2014, Petitioner had developed a cough and
“[b]y the 2nd of August, she’s got further evidence of a viral infection and even a higher fever.”
Tr. 120:1–3. Dr. Gershwin asserted that a biopsy during this period would have revealed
“inflammatory cells in the lung.” Tr. 120:10. Petitioner’s deterioration continued, and Dr.
Gershwin testified that Petitioner had pulmonary effusion by August 5, 2014, and nothing but “scar
tissue” left by August 15, 2014. Tr. 120:4, 11–12.

Dr. Gershwin explained that while “[t]he FDA requires [a showing] that vaccines produce
cytokines,” the over production of cytokines in this case is indicative of a pathological, intense
immune response. Tr. 121:16–17. Dr. Gershwin stated by way of example, “[i]f you get infected
with [the] Ebola virus . . . and die, it’s not because the virus has taken over the lungs.” Tr. 124:1–
3. Rather, “[i]t’s because your immune system has gone astray[,] and it’s become dysregulated . .
. it’s not as if you find sheets of virus there. It’s our own immune response, . . .which has gone
astray.” Tr. 124:3–8. He noted that he did not find any analogous case studies, because Petitioner’s
course is “an extremely rare event.” Tr. 122:15. She is, he concluded, “a perfect storm where
someone who happens to be born premature, who has a cold, has an infection, also has a very
intense reaction to a vaccine . . . all within that same short period of time.” Tr. 122:16–20.

Petitioner’s prematurity, according to Dr. Gershwin, may have affected “the matrix of her
lung,” and resulted in “lower levels of molecules known as trefoils, which are found in tissue
repair.” Tr. 124:14–15. He did not believe that her prematurity had resulted in surfactant defects,
because that would have manifested “much earlier in [her] life.” Tr. 125:3–4. Dr. Gershwin did
not identify any other predisposing factors aside from Petitioner’s prematurity. Tr. 125:10–11. In
response to my questioning, Dr. Gershwin stated that as a practical matter, Petitioner’s prematurity
is not a significant factor for predisposition. Tr. 159:14. He confirmed that there was no indication
that Petitioner suffered from any illness that was associated with prematurity, and it had not played

64
N. Chatziandreou, et al., Macrophage Death Following Influenza Vaccination Initiates the Inflammatory
Response that Promotes Dendritic Cell Function in the Draining Lymph Node, 18 CELL REPORTS 2427–
40 (2017).

20
any role in her development up until the point that she developed chILD. Tr. 159:2–5. He reasoned
that Petitioner’s vaccinations were a substantial factor in causing her injury. Tr. 126:7–8. He added
that he did not “believe that vaccinations will produce pulmonary fibrosis,” and Petitioner’s
condition was multifactorial. Tr. 126:9–11.

Dr. Gershwin ended his direct testimony by noting that “part of this serendipit[ous,] very
rare event is that these two events, the vaccination and the viral infections, were very, very close
in proximity to each other.” Tr. 127:8–11. He noted the immune response to the virus would have
been elicited at the same time as the response to the vaccine. Tr. 127:11–13. Ultimately, “the injury
to [Petitioner’s] lung [wa]s caused by her own innate immune system involving cytokines which
ultimately [] target[ed] fibroblasts, which [] lead [sic] to scarring.” Tr. 127:15–18. Dr. Gershwin
noted that the progression of events in this case occurred “much more rapidly than the average
patient in the literature with this symptomatology[.]” Tr. 127:19–21. Specifically, “that within days
[Petitioner] had evidence of respiratory involvement, [and] ultimately within a period of a month
or so[,] into end[-]stage respiratory failure.” Tr. 127:21–24.

On cross examination, Dr. Gershwin broke down his theory into steps. First, Petitioner
mounted an innate immune response against components of the vaccine that “occur[ed] at the local
site to the regional lymph node and it [] spread.” Tr. 132:10–11. He continued that the lymphocytes
were activated and “cytokines [] travel[ed] through the blood.” Tr. 132:16–17. This all happened
while Petitioner was “having the same response at the same time to the virus.” Tr. 134:5–6. He
explained that the immune response to the virus was happening “in [Petitioner’s] respiratory tract.”
Tr. 134:8–9. Dr. Gershwin noted he has “never testified that a vaccine by itself is going to produce
a [specific organ injury].” Tr. 135:10–11. He continued, that patients “can get lymphadenopathy
all over the body if [they] get a different kind of reaction known as serum sickness where you can
get a diffuse lymphadenopathy all over the body if you happened to have that.” Tr. 135:12–16. Dr.
Gershwin testified that cytokines were being produced in multiple areas of the body and that
Petitioner’s pulmonary fibrosis proved they were being produced in the lung. Tr. 135:22–23. He
opined that Petitioner’s fever is proof that cytokines were also being produced in her blood and
brain. Tr. 136:2–3.

When asked to identify the vaccine responsible for Petitioner’s cytokine response, Dr.
Gershwin stated that “it’s more likely the tetanus [vaccine] that produced it because [he] suspects
she received a tetanus vaccination early in life.” Tr. 136:13–15. He would not rule out Petitioner’s
other vaccinations and stated that “the HPV [vaccine] would have also produced cytokine[s],
meaning that all of [her vaccines] would have been involved.” Tr. 137:7–9. “The quantitative
nature of which might have been more involved than others will depend on the intensity of the
innate first responder response against the vaccines.” Tr. 139:14–17. Dr. Gershwin was then asked
what cytokines were produced by this intense immune response. He responded that cytokine
responses differ by age, individual, time of measurement, and other factors. Tr. 141:25, 142:1–3.
He also noted that “there are different units, sub-units, that may be produced, for example, to each
of these vaccines.” Tr. 142:5–6. Dr. Gershwin was unable to opine as to an appropriate timeframe
“on an epidemiologic perspective” for his theory, “because this [wa]s such an unusual event.” Tr.
146:2–4. He stated that Petitioner’s timeframe “occurred a lot more rapidly than the average
survival of children with chILD.” Tr. 146:5–6. Dr. Gershwin testified that “the onset [of

21
Petitioner’s chILD] would be when she began to have worsening pulmonary symptoms, which
looks to be [on] approximately the 3rd of August.” Tr. 149:20–22.

Dr. Gershwin conceded that it is possible that Petitioner could have developed chILD
without her vaccinations. Tr. 151:15. He noted the accelerated progression and late age of onset of
her injury compared to other cases as evidence that the vaccines played a role. Tr. 151:16–22. Dr.
Gershwin clarified that this is not an autoimmune response, but an autoinflammatory one. Tr.
165:24. I asked Dr. Gershwin if he routinely checks for the presence of cytokines to detect
inflammation. He noted it was not practical to test for cytokines as a clinician. Tr. 159:23–24.
However, he did reiterate that there is a relationship between cytokine upregulation and
inflammation. He explained that cytokines are upregulated by the vaccines and they “further
activate the mononuclear cells in the lung that are responding to the virus.” Tr. 162:12–16. He
added that they “produce other inflammatory bystander cells that will traffic into the lung and
further amplify the response.” Tr. 162:16–18. Dr. Gershwin summarized his position by noting
that the “virus is in her respiratory tract.” Tr. 164:6–7. “If the virus wasn’t there, there wouldn’t
be mononuclear cells in the lung.” Tr. 164:9–11. He concluded,“[i]f the mononuclear cells were
not in the lung, there’d be nothing for the cytokines produced by the vaccination to amplify.” Tr.
164:11–13.

Dr. Gershwin referred to the Kashiwagi et al. 65 article to establish that cytokine production
increases post vaccination. Pet’r’s Ex. 54 at 1, ECF No. 45-6. He noted that cytokine levels “are
anywhere from a few hundred to nearly 1,000 percent higher than [in] unvaccinated people,”
depending on the number of vaccines an individual receives. Tr. 288:1–2. He then noted that
Petitioner received one viral and four bacterial vaccines. Tr. 288:6–7. She was also suffering from
a virus severe enough to “develop a clinically significant immune response.” Tr. 307:9–10. Dr.
Gershwin contended that Petitioner had a local response to her vaccines that “proceed[ed] to the
lymph node,” and “travel[ed] throughout the lymphatics and [entered] the lung as [an] activated
cell in response to an injury.” Tr. 308:12–15. Dr. Gershwin explained that cytokines produced as
a result of one specific injury can adapt and respond to a different injury that occurred in a different
area of the body, despite a different cause. Tr. 309:25. The combination of vaccinations and
infection generated an immune response that ultimately caused Petitioner’s case to be the fastest
progressing chILD Dr. Gershwin has ever seen. Tr. 304:16.

Lastly, Dr. Gershwin clarified the effect of introducing multiple immune stimuli at one
time. In theory, if a child that is already infected with a virus is vaccinated, “you would enhance
the immune response to [the] virus and the child would get better faster against the virus.” Tr.
315:19–22. He then cautioned that “[i]f your immune response to that virus cross-reacted with a
self-antigen and you enhance that response, you’d enhance whatever molecular mimicry is taking
place.” Tr. 316:3–6. Because “there are some viruses that just have other properties that may cause
other diseases,” it is not worth enhancing the chance that a boosted immune response could prompt
the development of an autoimmune disease. Tr. 318:1–3.

65
Y. Kashiwagi, et al., Production of Inflammatory Cytokines in Response to Diphtheria-Pertussis-Tetanus
(DPT), Haemophilus Influenzae Type B (Hib), and 7-valent Pneumococcal (PCV7) Vaccines, 10:3 HUMAN
VACCINES & IMMUNOTHERAPEUTICS 677–85 (2014).

22
 2. Respondent’s Expert, Dr. Gary S. Rachelefsky, M.D.

Dr. Rachelefsky did not testify but he provided a written expert report that Respondent
relied on, at least in part, to defend against Petitioner’s claim. Resp’t’s Ex. A. Dr. Rachelefsky
began his report with a chronological summary of Petitioner’s relevant medical history pre
vaccination. Id. at 1. He then provided a detailed account of Petitioner’s symptoms, medical
examinations, and treatment immediately prior to her vaccinations, and thereafter. See id. at 2–11.
Dr. Rachelefsky noted that he was unable to review “the actual report of the lung biopsies and the
CAT scans and chest X-rays performed at [Petitioner’s] initial evaluations in Atlanta,” because
they were unavailable. Id. at 1.

For background, Dr. Rachelefsky conducted a review of the VAERS and VSD databases
and found “no literature or epidemiologic investigations that associated the administration of [the]
HPV [vaccine] to children and the development of interstitial lung disease.” Id. at 12. Dr.
Rachelefsky did note “one case report in an adult with [a] questionable association of [the] HPV
vaccination and interstitial lung disease.” Id. He concluded that “[v]accines are rarely associated
with ILDs, except some cases of influenza or [Bacillus Calmette–Guérin] vaccines.” Id.

Dr. Rachelefsky wrote that ILD is “characterized by inflammatory and fibrotic changes
that affect alveolar walls.” Id. at 13. He continued that “[i]diopathic interstitial pneumonias are
diffuse parenchymal lung diseases, of which IPF is the most common type of fibrotic lung disease.”
Id. Dr. Rachelefsky conceded that “the exact nature of the initiating injury and the subsequent
cascade of mechanistic events needs to be elucidated.” Id. He explained IPF pathogenesis to the
extent it is known:

[I]t is now clear that the interaction of growth factors, cytokines, and other
mediators with cells resident in the lung[,] is important to the evolution of the
fibrotic response in IPF. Resident epithelial cells, fibroblasts, and endothelial cells
within the lung produce an array of cytokines and growth factors that stimulate
fibroblast proliferation and matrix synthesis. Following epithelial injury, fibrosis is
believed to progress due to an imbalance between many groups of molecules that
include pro-inflammatory and anti-inflammatory cytokines, fibrogenic and
antifibrogenic polypeptides, oxidant-antioxidants, and angiogenic and angiostatic
molecules.

Id.

He asserted that “[t]rue idiopathic pulmonary fibrosis, defined pathologically by the
characteristic fibroblastic foci and temporal heterogeneity of usual interstitial pneumonia, has not
been reported in children.” Id. He reiterated, “IPF, a common idiopathic interstitial pneumonia in
adults that has a very poor prognosis, does not occur in children.” Id. at 14. He noted that “there
are forms of diffuse lung disease (DLD) that are either unique to young children or having differing
manifestations as compared with adults.” Id. These conditions fall under the umbrella term chILD,
which “differs from ILD in adults in that it is much rarer and, includes pathologies that are unique
to infants and young children (e.g., pulmonary interstitial glycogenosis [or] genetic abnormalities
that cause ILD in childhood.” Id. at 15. “Conversely,” he added, “common adult ILD[,] such as

23
usual interstitial pneumonia[,] is rarely described in children.” Id. ChILDs “are divided into three
subtypes according to the origin of the primary condition involving pulmonary conditions: ILD
specific to infancy []; ILD related to a primary systemic disease; and exposure-related ILDs.” Id.
Dr. Rachelefsky estimated that the frequency of chILD is estimated as low, at 1.3 cases per
1,000,000 in one study of children less than seventeen years old. Id. He noted, however, that “it is
difficult to fix a precise number for the frequency of chILD.” Id. Ultimately, ILD can progress “to
severe irreversible fibrosis of the lung. In such cases, lung transplantation can be used as a final
option in children of all ages.” Id. As such, chILD “has been associated with considerable
morbidity and mortality.” Id.

Dr. Rachelefsky opined that Petitioner suffered from an acute interstitial pneumonia
(“AIP”), otherwise known as Hamman-Rich syndrome. Id. at 16. AIP is a type of idiopathic acute
respiratory distress syndrome that “is classified as an idiopathic interstitial pneumonia” with the
“most acute onset and rapidly progressive course.” Id. Dr. Rachelefsky acknowledged that
“[c]ontrolled prospective studies on the treatment of AIP are not available[, which is] not
surprising since AIP is so uncommon.” Id. He noted that AIP “generally affect[s] previously
healthy individuals without a prior history of lung disease,” and “has the histopathologic
appearance of diffuse alveolar damage (“DAD”).” Id. at 16–17.

Accelerated IPF is a potential differential diagnosis for AIP, however, Dr. Rachelefsky
explained that in the former, there is evidence of “bilateral ground-glass opacities.” Id. at 17. In
AIP, “[t]he rapid onset of a widespread injury pattern suggests a single insult as an initiating
factor.” Id. at 18. He continued, “[a]lveolar epithelial cell damage and death lead to elaboration
and release of mediators. Recruitment of neutrophils into the alveolar spaces and alveolar septal
leads to further cellular damage, possibly via [the] release of toxic oxygen radicals and proteases.”
Id. The symptoms of AIP appear quickly, “with a prodromal illness that typically lasts 7 to 14 days
prior to presentation, the most common presenting signs and symptoms are fever, cough, and
progressive, severe shortness of breath.” Id. Biopsy results will show “an acute and/or organizing
form of [DAD].” Id. at 19. Dr. Rachelefsky wrote that “[t]he diagnosis of [AIP] is based upon two
findings: the presence of a clinical syndrome of idiopathic acute respiratory distress syndrome []
and pathologic[al] confirmation of diffuse alveolar damage.” Id. at 20.

Dr. Rachelefsky then discussed chILD in the context of Petitioner’s condition and
responded to Dr. Gershwin’s report. He began by asserting that Dr. Gershwin’s IPF discussion is
misplaced because it does not relate to the disease that Petitioner has, “which is acute interstitial
pneumonia.” Id. In fact, Dr. Gershwin has also improperly lumped the diseases together, because
“[t]he literature is quite clear that [ILD] in infants (and related to prematurity) is different than in
childhood, which is then different from what one sees in adults.” Id. at 22. He continued “the lack
of evidence in the literature of association [between the HPV vaccine and ILD] is ample evidence
that there is no relationship whatsoever between the two. This also relates to meningococcal
vaccination and to TDaP.” Id.; see also Resp’t’s Ex. D. 66 Dr. Rachelefsky also opined that
“[Petitioner’s] onset of [her] pulmonary disease at age [eleven] has nothing to do with her
premature birth.” Resp’t’s Ex. A at 24. Dr. Rachelefsky acknowledged that “it’s plausible that the
intravenous administration of the Bactrim may have enhanced its pulmonary toxicity,” but
66
Y. Yamamoto, et al., Interstitial Lung Disease Associated with Human Papillomavirus Vaccination, 16
RESPIRATORY MED. CASE REPORTS 15–17 (2015).

24
maintained that “[t]he unknown factor is whether [Petitioner] was exposed to some infectious
agent or toxic substance that caused her disease [] prior to the onset of her symptoms.” Id. at 23.

As to Dr. Gershwin’s theory of causation, Dr. Rachelefsky asserted “the predominant
response to the non-live vaccines is B-cell induced [] and has nothing to do with [sterile
inflammation or a similar immune response].” Id. Dr. Gershwin’s explanation, according to Dr.
Rachelefsky, is “an overstatement of the actual immunologic response to the vaccines.” Id. As
support, he noted that the “lessons learned from the skin or kidney are not necessarily applicable
to the liver microvasculature.” Id.

3. Respondent’s Expert, Dr. McCusker

Dr. McCusker was admitted as an expert in the fields of pediatric immunology, pediatric
clinical allergy and immunology, and pediatrics. Tr. 175:8–11. She began with a general overview
of interstitial lung disease. She explained that the clinical diagnosis is based on a patient presenting
with “low oxygen saturation [and] an X-ray picture that is quite specific.” Tr. 175:22–23. Dr.
McCusker also identified associated risk factors including, prematurity, “mutations in the genes
involved in formation and functioning of surfactant,” and “telomeres which [have] to do with
factors affecting cell life.” Tr. 177:3–8. Specific to chILD, Dr. McCusker noted that patients “will
have a history and a relatively recent antecedent history of infection.” Tr. 177:13–15. She added
that it is not clear why some patients will develop chILD and others do not, but “[w]e know that
there are certain immunodeficiencies” and “particulates in the airway [that] are associated with the
development of interstitial lung disease.” Tr. 177:16–19.

Dr. McCusker testified that there is no literature that relates the HPV vaccination and
chILD, aside from a temporal association. Tr. 178:12–14. The Yamamoto et al. 67 study referenced
by Dr. Rachelefsky is not analogous to this case, according to Dr. McCusker. See Tr. 178–79; see
also Resp’t’s Ex. D. She noted that the patients were not the same age, and in the case study, “the
responsiveness to corticosteroids was clear in this patient whose symptoms resolved completely.”
Tr. 179:20–23. Petitioner did not respond similarly to corticosteroid treatment, and Dr. McCusker
concluded that the patient in the case study was an adult suffering from a different disease. Tr.
179:24–25.

Dr. McCusker also wanted to clarify that “the gold standard for a vaccine is clinical
protection from disease. It doesn’t matter how many cytokines you produce.” Tr. 182:19–22. The
outcome measures used as the gold standard for vaccine clinical protection are the “levels of
protective antibodies and/or evidence of [a] protective adaptive T cell response.” Tr. 183:1–2. Dr.
McCusker explained that “[t]he cytokines – the purpose of the inflammatory response at the site
is to attract cells to the area.” Tr. 183:9–11. These cells, she continued, “contain the inflammation
at the site and for the antigen presenting cells to pick up those antigens and travel back to the
draining lymph node.” Tr. 183:14–17. This process continues for approximately four days, before
there is “[m]ovement outside of the lymph node.” Tr. 184:12. The cells will then circulate “back
to the site of the original inflammation,” thereby triggering an adaptive immune response. Tr.
184:16–19. Dr. McCusker testified “that there’s actually very little cytokines that circulate in the
peripheral circulation post vaccination.” Tr. 184:24–25, 185:1.
67
See Yamamoto, et al., supra note 66.

25
 Turning to the Boyce et al. 68 study, Dr. McCusker explained that the authors sought to
answer, “does [receipt of a vaccination] worsen the acute viral infection in a real[-]world study.”
Tr. 186:11–13. The authors looked at children who were hospitalized with RSV “proximal to
getting the pertussis vaccination.” Tr. 186:20–21. Ultimately, “what they found was that a recent
immunization with pertussis was not a risk factor for hospitalization.” Tr. 187:3–5. Additionally,
Dr. McCusker testified that the study found that “pertussis in the arm does not worsen what’s going
on in the lungs.” Tr. 187:24–25. She continued that line of reasoning to note another study that
revealed “no increased episodes of inflammatory events post vaccination in patients who have
underlying autoimmune [autoinflammatory] disease.” Tr. 188:21–24 (citing Resp’t’s Ex. WW,
ECF No. 46-6). 69

Dr. McCusker also sought to clarify the concept of sterile inflammation. She defined the
term as “an inflammatory event that would occur in the absence of – technically it’s an exogenous
antigenic trigger.” Tr. 191:19–20. She then referenced the McDonald et al. 70 article, submitted by
Petitioner, that discusses how sterile inflammation leads to tissue injury, followed by normal
healing. Tr. 192:22–24. Dr. McCusker explained that “inflammation and healing are two sides of
the same coin.” Tr. 192:8–9. In cases where there is “an inflammatory event and there’s a problem
or disconnect between inflammation and then healing, you end up with damage.” Tr. 192:12–14.
In the McDonald et al. article, there is localized sterile inflammation that stays at the initial site.
Tr. 193:5–6. Dr. McCusker noted “it’s not like you get sterile inflammation of the liver[,] and the
kidney inflames.” Tr. 193:6–7. There is “no evidence here in this article that there’s trafficking to
other organs.” Tr. 193:10–11. Furthermore, Dr. McCusker asserted that “[b]ecause vaccine[s]
provide antigen[s],” they are not sterile. Tr. 193:18–21. Cell damage is the usual trigger for sterile
inflammation and “when a cell dies by necrosis, the wrong way, and it releases its cellular contents,
those cellular contents are actually inflammatory.” Tr. 194:4–6. In Petitioner’s case, “the signaling
for the inflammation [wa]s the release of self-molecules that are normally not seen [outside of the
cell by the immune system].” Tr. 194:11–12. This concept, Dr. McCusker asserted, is completely
different from vaccinations. She stated that the vaccine components are “foreign in the first place,
. . . and [are] also designed to activate the immune system in the form of the microbes themselves
and the adjuvants that go with. So that’s not sterile.” Tr. 194:15–19.

Next, Dr. McCusker discussed cytokines. She defined them as small communication
molecules with different functions, different receptors, and “each with their own regulatory
pathway.” Tr. 195:4–5. She noted that “[t]here are at least 80-plus, probably over 100 now[,]
cytokines that have been defined.” Tr. 195:2–3. They can vary wildly in origin, function, and form.
Tr. 195:15–17. One type of cytokine, Dr. McCusker explained, is released by epithelial cells when
they are damaged. Tr. 195:22. Those “cytokines tell the local area that cells are being damaged.”
Tr. 195:22–23. She described preformed mediators, which are “formed inside cells and they’re
ready to — ready to rock when the cell opens up.” Tr. 196:2–3. Cells can also signal to other cells
signaling for additional cytokines as needed to address the damage. Tr. 196:4–7. When asked how
this happens when chILD develops, Dr. McCusker admitted that “we don’t know.” Tr. 196:25.
She noted that TGF-beta is one cytokine that is released by epithelial cells and has also “been

68
See Boyce, et al., supra note 58.
69
J. Westra, et al., Vaccination of Patients with Autoimmune Inflammatory Rheumatic Diseases, 11
NATURE REVIEWS RHEUMATOLOGY 135–46 (2015).
70
See McDonald, et al., supra note 60.

26
implicated in the development of fibrosis.” Tr. 197:1–2. Specifically, TGF-beta is released by
some types of T cells and myofibroblasts. Tr. 197:6–7. Dr. McCusker cautioned that animal
models show “excessive amounts of TGF[-]beta in addition to an inflammatory insult,” but “it is
not clear who’s the boss in terms of getting that TGF[-]beta released.” Tr. 197:10–15.

Dr. Gershwin and Dr. McCusker agree that animal models show “the inciting event leading
to pulmonary fibrosis is epithelial cell damage.” Tr. 199:20–22. During the healing process, “you
end up restricting the lung differently from the original lung and you end up with a lung that is no
longer able to do its job, which is to exchange air.” Tr. 199:24–25, 200:1–2. Dr. McCusker
explained that adult literature is used for comparison due to the rarity of chILD. Tr. 200:4–5. She
testified that “there is some evidence” that ILD responds to corticosteroids, which “implies that
it’s inflammatory.” Tr. 200:6–8. The best immune response following vaccination is a regulatory
response that does not involve inflammation. Tr. 201:14–17. Dr. McCusker characterized Dr.
Gershwin’s discussion of pro-inflammatory and anti-inflammatory T cells as “concepts in the early
2000s[ and noted that] we’ve moved on from there a long time ago.” Tr. 201:25, 202:1–2.

In response to Dr. Gershwin’s reliance on medical literature to establish that “exogenous
cytokines com[e] from someplace else . . . and act as factors to promote more inflammation,” Dr.
McCusker walked through some of the same articles he used. Tr. 205:17–19. She noted that the
article by Wynn 71 provides “an overall big picture about how you end up with pulmonary fibrosis.”
Tr. 203:8–9 (citing Pet’r’s Ex. 47). The “first step in pulmonary fibrosis is epithelial cell injury.”
Tr. 203:10. That leads directly to “the release of inflammatory mediators” coming from the inside
of the injured cells. Tr. 203:11–14. Dr. McCusker continued that these “inflammatory mediators
induce migration of cells from the periphery into the area of cell damage.” Tr. 203:20–21. They
are “now in the milieu looking at or being triggered or stimulated by the inflammatory mediators
and by whatever else is in the environment.” Tr. 203:24–25, 204:1. They are also producing
cytokines. Tr. 204:1–2. These cytokines would normally initiate the repair response; however, the
repair does not go as it should. Tr. 204:6. Dr. McCusker explained that the first stage of lung repair
is to lay down the “extracellular matrix.” Tr. 204:20–21. Everything is great “[i]f all this is done
in a relatively short order where you kind of rebuild the structure, reset everything up[,] and stop
the repair[.]” Tr. 204:23–25. Fibrosis occurs when “that matrix continues to be laid and you don’t
actually get that stop. So now instead of having relaying of the matrix and them allowing []
everything to heal, you end up with cement in the lung.” Tr. 205:9–11. Dr. McCusker testified that
“the problem with fibrosis isn’t more inflammation. It’s more repair.” Tr. 205:20–21. She agreed
that “while TGF-beta is one of the cytokines . . . it’s a cytokine that’s being released and acting
locally and the dysregulation is local.” Tr. 205:21–24. She asserted that “in the case of chILD, at
least in theory, you would have that inflammation, that cell death of the epithelial cells, and then
just ongoing progression of fibrosis instead of the stop.” Tr. 206:12–15. Respondent filed the
Kolahian et al. 72 article to support Dr. McCusker’s contention that the idiopathic pulmonary
fibrosis is not the result of too much inflammation or stimulation. Tr. 220:21–23 (citing Resp’t’s
Ex. UU). She stated, “once you switch to healing the process [] — that’s where the fibrotic process
take[s] hold and takes off.” Tr. 220:23–25. Dr. McCusker added that premature infants and babies
with genetic variations in surfactant [may be] particularly at risk [because] their pulmonary
vasculature and the structure of their regulatory tree never fully forms.” Tr. 206:17–20.

71
See Wynn, supra note 48.
72
See Kolahian, et al., supra note 55.

27
 The Chatziandreou et al. 73 article that Dr. Gershwin referenced was not thoroughly
explained according to Dr. McCusker. Tr. 208:4–6 (citing Pet’r’s Ex. 51). She noted this article
tried “to understand how the influenza vaccine can craft an influenza-specific response” by
injecting mice with the flu vaccine. Tr. 208:6–12. The lymph nodes from the mice were then
isolated so that researchers could “watch the cells talk to one another in the lymph node and try to
figure out what [wa]s going on.” Tr. 208:16–18. Dr. McCusker explained that “you could maybe
translate this — vaccinate [] mice in their muscle, the components of the vaccine are taken up and
brought to the local lymph node[,] and there’s a lot of activity in that lymph node.” Tr. 209:19–22.

Turning next to the Kashiwagi et al. 74 article, Dr. McCusker stated the researchers found
that blood samples taken from children within 24 hours of vaccination revealed the production of
cytokines; but she noted, “[t]hat is not evidence that cytokines circulate at 24 hours.” Tr. 210:15–
23 (citing Pet’r’s Ex. 54). In fact, when looking at “circulating serum cytokine profiles” in
vaccinated children that were febrile vs. non febrile, “there was actually very little cytokine[s] that
circulated.” Tr. 211:3–8. Dr. McCusker stated that she “was not able to find literature that would
say that inflammation in the arm would lead to upregulation of cytokines in the lung.” Tr. 212:4–
7. She asserted that the immune system, even when exposed to a vaccine, “works in a
compartmental fashion.” Tr. 212:7–9. She conceded that while there are “‘systemic symptoms’
such as fever and sickness behaviors, the mechanisms of those are not through the circulation of
cytokines through the blood stream.” Tr. 212:11–14. Dr. McCusker could not reconcile how to
“walk the cytokines from the arm to the lung.” Tr. 212:14–15.

Petitioner’s typical clinical presentation of chILD was another factor that Dr. McCusker
identified as evidence that Petitioner’s vaccination had nothing to do with how her condition
developed and progressed. Tr. 212:16–19. She testified that:

[b]ecause I can’t walk the cytokines to the lungs from the arm or the draining lymph
node, and I don’t — I can’t — I do not have any literature that says that that
happens. And the disease in and of itself occurs in the sequence of events that it
occurred in this case in the absence of vaccination. It’s exactly what happens. This
is chILD.

Tr. 213:1–7.

When asked about Dr. Gershwin’s concept of concurrent processes, Dr. McCusker asserted
that this theory doesn’t work by using Dr. Gershwin’s analogy of exercise and food allergies. Tr.
213:25. She explained that “the mechanism by which exercise increases the severity of [a] food
allergy is not related to the circulation of cytokines.” Tr. 213:25, 214:1–2. That mechanism is
completely different and “has to do with the activation of mast cell mediators and the increase in
the basal metabolic rate.” Tr. 214:2–4.

73
See Chatziandreou, et al., supra note 64.
74
See Kashiwagi, et al., supra note 65.

28
 Dr. McCusker then continued her discussion of Petitioner’s filed literature. She noted that
the Tempark et al. 75 article describes “adrenal suppression and [asserts] that there’s increased risks
for difficultly of the immune system to generate a good response to [an] infection” that is
“associated with the use of topical corticosteroids.” Tr. 218:12–18 (citing Resp’t’s Ex. SS, ECF
No. 46-2). Dr. McCusker then addressed the Galati et al. 76 article. Resp’t’s Ex. TT. This article
suggests that “in idiopathic pulmonary fibrosis, there’s evidence of T cell dysregulation.” Tr.
219:18–20. Taken together, Dr. McCusker asserted that “corticosteroids could affect T cells and
T cell development and that idiopathic pulmonary fibrosis might be a disease of T cell
dysregulation.” Tr. 219:21–23. However, Dr. McCusker also conceded that there is some debate
regarding this theory. Tr. 219:23–25.

She discussed these articles in the context of Petitioner’s case. Dr. McCusker noted that
Petitioner “was using a fairly high potency corticosteroid . . . from eight years to [eleven.]” Tr.
218:24–25, 219:1. Dr. McCusker explained that Petitioner’s steroid use could have led to her
“immune dysregulation.” Tr. 219:4. She also noted that Petitioner showed evidence of
dysregulation, specifically that “her NK cells were low[,] and she had ‘lowish’ T cells.” Tr. 220:4–
6. This is especially possible in Petitioner’s case because her infection could have served as an
exciting event. Tr. 220:19–20. Dr. McCusker concluded that Petitioner’s infection, “coupled with
the recent history of the chronic topical steroid use, you put those together and you have your
perfect situation for dysregulation.” Tr. 220:12–15.

The biggest contention Dr. McCusker had with Dr. Gershwin’s theory is that it would
require a “change in how the immune system works.” Tr. 221:15. She gave the example of a cut
on a patient’s thumb in tandem with a virus. According to Dr. Gershwin, “if I have a cut on my
thumb, I’m going to have inflammation in my thumb and I’m going to have inflammation in my
nose because I’ve got, you know, some stimulation of the immune system in my nose.” Tr. 221:17–
21. Dr. McCusker asserted that it “doesn’t work that way because if the signal in my nose is saying,
yeah, you got a little cold, don’t worry about it, but my thumb is saying, listen this is going to get
infected; you want to focus your attention to the thing that’s more dangerous.” Tr. 221:23–25,
222:1–2. This, Dr. McCusker explained, is “the containment concept.” Tr. 222:7. Dr. Gershwin’s
example of serum sickness is a systemic immune response. However, Dr. McCusker clarified that
it is “a Type III hypersensitivity reaction.” Tr. 222:12–15. This type of reaction involves
“antibodies that are floating around bound to antigen[s] and they get caught in small capillaries
and create inflammation.” Tr. 222:16–18. The circulation of these antibodies “isn’t the same as a
cytokine being produced in one lymph node[,] circulating[,] and affecting the immune response in
the lung.” Tr. 222:20–23. She testified that it is “really not the same.” Tr. 222:23. Dr. McCusker
continued that even if “these two things connected, which I can’t connect in my mind, then you
still need [to get to] the fibrosis.” Tr. 223:15–17.

Dr. McCusker identified three factors to explain why cytokines do not circulate. First, she
stated that they “act over short distances.” Tr. 269:4–5. Cytokines look for and find their receptors
immediately. Tr. 269:7–8. Those receptors hold them, and cytokines don’t then “bounce from one
receptor to another.” Tr. 269:9–10. Second, “there’s a regulation loop” that “doesn’t really allow

75
T. Tempark, et al., Exogenous Cushing’s Syndrome due to Topical Corticosteroid Application: Case
Report and Review Literature, 38 ENDOCR. 328–34 (2010).
76
See Galati, et al., supra note 52.

29
for significant . . . amplification.” Tr. 269:13–18. Lastly, the half-life of cytokines would not
support that process. Tr. 269:21–23. Dr. McCusker noted that “one of the cytokines that keeps
getting discussed is IL-1 beta.” Tr. 269:22–23. With a half-life of nineteen minutes, “they do their
thing and then they’re deactivated.” Tr. 269:25, 270:1. Dr. McCusker mentioned signal
transduction, whereby a fever can result from a localized inflammatory event because “the nerves
that are innervated are triggered at the site of the lymph node by the release of those cytokines.”
Tr. 270:10–16. She went on to say that the trigger that moves to the hypothalamus and “says turn
on fever” does not involve the movement of cytokines. Tr. 270:16–18. She identified other
examples of systemic signs of inflammation but noted that “the circumstances that are predicated
to occur with a vaccination under this case scenario does [sic] not — allow for it.” Tr. 271:10–12.
She also noted literature that studied the interaction between the pertussis vaccination and RSV.
See Resp’t’s Ex. VV. 77 The literature indicated that “if there was an interaction, it would be to sort
of tamp down the immune response.” Tr. 279:3–5.

Turning to Petitioner’s medical record, Dr. McCusker discussed what she identified as the
“wide net of ideologies” that Petitioner’s treaters explored. Tr. 227:1–2. She noted that on August
18, 2014, “they talked about [an] idiosyncratic reaction to Bactrim, . . . the potential for an
infectious ideology . . . an inflammatory ideology or rheumatologi[c] ideology but found no
significant persistent elevation in the inflammatory markers of the body.” Tr. 227:2–7 (citing
Pet’r’s Ex. 4 at 2472). Although Petitioner exhibited an elevated C-reactive protein (“CRP”),
which is indicative of systemic inflammation when Petitioner was admitted to the hospital, by that
time, treaters were more concerned about addressing Petitioner’s failing lungs. Tr. 227:8–10.

Dr. McCusker noted that Petitioner’s treaters took “into account the family’s concerns that
the vaccines may have played a role[]” in her condition. Tr. 227:19–20. Although there are
disadvantages with relying on VAERS reporting that Dr. McCusker acknowledged, she stated that
they “found there was no reported association” between the HPV vaccine and ILD. Tr. 227:21–
25. Instead, an immunological examination revealed a “decrease in total T cells and the decrease
in — specifically in T helpers and NK cells for age, which is consistent with other children or other
individuals who have interstitial lung disease.” Tr. 228:14–17. Looking at her entire medical
record, Dr. McCusker concluded that Petitioner “followed a clinical course that was consistent
with other children who had chILD[,] and [she] did not have features that would distinguish her
[case] as [a] vaccine-mediated event as opposed to anybody else who developed chILD.” Tr.
228:21–15. This is a rare disease, Dr. McCusker admitted, but she opined that Petitioner’s case
was classic. Tr. 229:1.

Dr. McCusker stated that redness, swelling, and site pain are common symptoms of a
“large local reaction” to a vaccination. Tr. 229:5–7. A fever lasting 24 hours and “an elevation in
the C-reactive protein” are also symptoms of a large local reaction. Tr. 229:14–17. Petitioner in
the present case suffered from a fever and localized arm inflammation, which Dr. McCusker
characterized as “normal responses to her vaccine.” Tr. 182:11–12. However, Dr. McCusker noted
that during Petitioner’s July 31, 2014 medical visit, there was no mention of arm swelling upon
her physical examination. Tr. 212:19 (citing Pet’r’s Ex. 2 at 57–58). This suggests that Petitioner’s
immune stimulus “that had started locally was gone.” Tr. 233:8–9. Dr. McCusker testified that a
strep screen would have been her first course of action given Petitioner’s symptoms of “swollen
77
See Boyce, et al., supra note 58.

30
tonsils, the sore throat, big tonsils, swollen lymph nodes[,] and high fever.” Tr. 276:2–3. Following
a negative strep test, “most likely the reason for this constellation of symptoms is that your child
has a virus.” Tr. 276:9–10. She identified Epstein-Barr virus (“EBV”) 78 because it is “one of the
factors that is associated with chILD.” Tr. 277:7–8. Dr. McCusker was unable to identify an
etiology. She also admitted that it was unclear “when [Petitioner] presented with the cough and
the hypoxia and the real story of hardcore [symptoms].” Tr. 281:8–10. Dr. McCusker was unable
to unequivocally identify an onset date for Petitioner’s chILD. Tr. 234:10. She reasoned that based
on an account of Petitioner’s mild cough, July 31, 2014, would be a good estimate. Tr. 235:3. She
admitted her uncertainty, but stated that “on the 31st, . . . there were already signs, which means
that you kind of have to back up — yeah, probably pre vaccine in order for the series of events to
reach symptomatic by the 31st.” Tr. 283:1–5. Immediately following that statement, she noted that
she was “very hesitant to time out the pathophysiology because, yeah, it is apparently very sudden
onset.” Tr. 283:10–12. Dr. McCusker described a recent patient who went from healthy, to having
a fever with cough two days later, and then needed ventilation by day four. Tr. 283:15–22. In that
case, Dr. McCusker noted that the patient “grew two viruses on her culture . . . , so of course people
sa[id], oh, it must [have] be[en] the virus that caused all this.” Tr. 283:23–25, 284:1. That patient
notwithstanding, Dr. McCusker asserted that “the process that led to [Petitioner’s respiratory
distress] was not 24, 48, 72, or even 96 hours in going. It was probably a much longer process
before you g[o]t to that.” Tr. 281:15–18. As support, she explained that “the lungs of children are
generally healthy,” and that “it takes a significant amount of compromise for the child to
deteriorate.” Tr. 281:25, 282:1–2.

IV. Applicable Legal Standards

A. Causation

The Vaccine Act was established to compensate vaccine-related injuries and deaths. §
10(a). “Congress designed the Vaccine Program to supplement the state law civil tort system as a
simple, fair and expeditious means for compensating vaccine-related injured persons. The Program
was established to award ‘vaccine-injured persons quickly, easily, and with certainty and
generosity.’” Rooks v. Sec’y of Health & Hum. Servs., 35 Fed. Cl. 1, 7 (1996) (quoting H.R. Rep.
No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).

To receive compensation under the Act, a petitioner must demonstrate either that: (1) the
petitioner suffered a “Table injury” by receiving a covered vaccine and subsequently developing
a listed injury within the time frame prescribed by the Vaccine Injury Table set forth at 42 U.S.C.
§ 300aa-14, as amended by 42 C.F.R. § 100.3; or (2) that petitioner suffered an “off-Table injury,”
one not listed on the Table, as a result of his receiving a covered vaccine. See 42 U.S.C. §§ 300aa-
11(c)(1)(C); Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010);
Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1319–20 (Fed. Cir. 2006). Petitioner
does not allege a Table injury in this case; thus, she must prove that her injury was caused-in-fact
by a Table vaccine.

78
Epstein-Barr is also referred to as human herpesvirus 4. Dorland’s at 2061. Human herpesvirus 4 is a
virus of the genus lymphocryptovirus that causes infectious mononucleosis[.]” Id. at 852–53.

31
To establish causation-in-fact, a petitioner must demonstrate by a preponderance of the evidence
that the vaccine was the cause of the injury. 42 U.S.C. § 300aa-13(a)(1)(A). A petitioner is required
to prove that the vaccine was “not only a but-for cause of the injury but also a substantial factor in
bringing about the injury.” Moberly, 592 F.3d at 1321–22 (quoting Shyface v. Sec’y of Health &
Hum. Servs., 165 F.3d 1344, 1352–53 (Fed. Cir. 1999)). Shyface clarifies “[i]t is not necessary that
it be the cause, using the word “the” as meaning the sole and even the predominant cause.” 165
F.3d at 1352.

In the seminal case of Althen v. Sec’y of the Dept. of Health & Hum. Servs., the Federal
Circuit set forth a three-pronged test used to determine whether a petitioner has established a causal
link between a vaccine and the claimed injury. See 418 F.3d 1274, 1278–79 (Fed. Cir. 2005). To
that end, the Circuit noted that a petitioner need not necessarily supply evidence from medical
literature supporting petitioner’s causation contention, so long as the petitioner supplies
the medical opinion of an expert. Id. at 1279–80. A special master may rely upon “circumstantial
evidence,” which the court found to be consistent with the “system created by Congress, in which
close calls regarding causation are resolved in favor of injured claimants.” Id. at 1280.

The Althen test requires petitioners to set forth: “(1) a medical theory causally connecting
the vaccination and the injury; (2) a logical sequence of cause and effect showing that the
vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship
between vaccination and injury.” Id. at 1278. To establish entitlement to compensation under the
Program, a petitioner is required to establish each of the three prongs of Althen by a preponderance
of the evidence. See id.

A petitioner who satisfies all three prongs of the Althen test has established a prima facie
showing of causation. Hammitt v. Sec’y of Health & Hum. Servs., 98 Fed. Cl. 719, 726 (2011). A
petitioner who demonstrates by a preponderance of the evidence that he suffered an injury caused
by vaccination is entitled to compensation unless the respondent can demonstrate by a
preponderance of the evidence that the injury was caused by factors unrelated to the vaccination.
See Althen, 418 F.3d at 1278; Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 547 (Fed.
Cir. 1994). Consequently, when and if a petitioner establishes a prima facie case, the burden then
shifts to the government to prove that an alternative cause, unrelated to the administration of the
vaccine, was the “sole substantial factor” in causing the alleged injury. See de Bazan v. Sec’y of
Health & Hum. Servs., 539 F.3d 1347, 1354 (Fed. Cir. 2008); see also Hammitt, 98 Fed. Cl. at 726
(explaining that the respondent’s burden is to show that the “factor unrelated” was the “sole
substantial factor” in causing the injury). Additionally, a factor unrelated “may not include ‘any
idiopathic, unexplained, unknown, hypothetical, or undocumentable cause, factor, injury, illness
or condition.’” 42 U.S.C. § 300aa-13(a)(2); see also Doe v. Sec’y of Health & Hum. Servs., 601
F.3d 1349 (Fed. Cir. 2010) (opining that an idiopathic diagnosis cannot be a “factor unrelated,” as
it is idiopathic).

B. Significant Aggravation

Petitioners must establish causation in all off-Table cases; however, petitioners may
establish they are entitled to compensation based on a claim that a vaccination significantly
aggravated a pre-existing condition. The Vaccine Act defines significant aggravation as “any

32
change for the worse in a pre[-]existing condition which results in markedly greater disability,
pain, or illness accompanied by substantial deterioration of health.” § 300aa-33(4). When a
petitioner makes this argument, the evidentiary burden is expanded. See Loving v. Sec’y of Health
& Hum. Servs., 86 Fed. Cl. 135, 144 (2009). In Loving, the Court of Federal Claims set forth a six-
factor test, which requires establishing the following:

(1) the person’s condition prior to administration of the vaccine, (2) the person’s
current condition (or the condition following the vaccination if that is also
pertinent), (3) whether the person’s current condition constitutes a “significant
aggravation” of the person’s condition prior to vaccination, (4) a medical theory
causally connecting such a significantly worsened condition to the vaccination,
(5) a logical sequence of cause and effect showing that the vaccination was the
reason for the significant aggravation, and (6) a showing of a proximate
temporal relationship between the vaccination and the significant aggravation.

Loving, 86 Fed. Cl. at 144.

The Loving analysis requires the special master to “evaluat[e] whether the vaccine made
the person worse than the person would have been but for the vaccination. In doing so, the natural
course of the disease must be considered.” Locane v. Sec’y of Health & Hum. Servs., No. 99-589V,
2011 WL 3855486 at *10 (Fed. Cl. Spec. Mstr. Feb. 17, 2011), mot. for review den’d, 99 Fed. Cl.
715 (2011), aff’d, 685 F.3d 1375 (Fed. Cir. 2012); see also Hennessey v. Sec’y of Health &
Hum. Serv., No. 01-190V, 2009 WL 1709053, at *41–42 (Fed. Cl. Spec. Mstr. May 29, 2009), mot.
for review den’d, 91 Fed. Cl. 126 (2010). However, a petitioner is not required “to demonstrate an
expected outcome and that her current post vaccination condition was worse than such expected
outcome.” Sharpe v. Sec’y of Health & Hum. Servs., 964 F.3d 1072, 1081 (Fed. Cir. 2020).

V. Discussion

Petitioner’s theory of causation must generally establish that one or more of the vaccines
at issue is the but-for cause of the type of injury alleged. Her petition sought relief for two related
injuries, IPF and acute respiratory failure. ChILD syndrome covers a wide range of conditions that
includes IPF to the extent that it occurs in children. However, there is so much that remains
unknown about the etiology and pathogenesis of IPF, especially in the extremely rare pediatric
cases. Furthermore, the literature filed in this case does not paint a clear picture of Petitioner’s
diagnosis. After careful consideration of Petitioner’s medical history, expert reports, and filed
medical literature, Petitioner has provided preponderant evidence that she suffered from IPF that
ultimately lead to acute respiratory failure. Given her age, Petitioner’s condition would fall under
the umbrella syndrome of chILD. I will consider Petitioner’s causation theory in light of this injury.

Petitioner’s expert’s argument that her otherwise mild, viral illness was worsened by
vaccination and ultimately developed into chILD is reconcilable with Respondent’s expert’s
argument that Petitioner was likely suffering from a viral infection pre vaccination and that was
the cause of her acute respiratory failure. Both experts characterize Petitioner’s clinical course as
a worsening of an otherwise manageable infection. The heart of the issue then becomes whether
one or more of her vaccines was a substantial cause of the worsening. This analysis requires

33
consideration of the Shyface “substantial factor” standard in bringing about the harm, and the
significant aggravation factors detailed in the Loving decision. Petitioner has not explicitly
identified her claim as one of significant aggravation, but Dr. Gershwin made that argument. He
testified that the onset of her chILD “would be when she began to have worsening pulmonary
symptoms.” Tr. 149:20–21. Furthermore, Respondent’s expert indicated that was her
understanding of Petitioner’s theory. She testified, “[Dr. Gershwin] feels that those two things
came together in the lungs because cytokines worsened her pulmonary disease leading to her
chILD.” Tr. 181:14–16. I must consider the evidence presented to reach my decision in conjunction
with counsel’s framing of the claim in Petitioner’s filings. Therefore, I find that there is
preponderant evidence of a post-vaccination change for the worse in Petitioner’s condition, which
resulted in markedly greater illness accompanied by a substantial deterioration of her health.

In addition to preponderant evidence of a worsened condition, a significant aggravation
claim must still establish by a preponderant standard all three Althen factors: general causation,
specific causation, and timing. It is not entirely clear if Petitioner’s condition is the result of an
aberrant immune response to multiple stimuli including a wild virus and vaccinations (causation-
in-fact). Alternatively, Petitioner’s condition could be the result of vaccine-caused dysregulation
of the immune system’s response to a respiratory virus that had already begun to cause lung
damage (significant aggravation). In either instance, Petitioner has established by a preponderant
standard that her vaccinations were a substantial, but not necessarily the sole or predominant cause
of her IPF, acute respiratory failure, and need to undergo a bilateral lung transplant. See Shyface,
165 F.3d at 1352–53.

A. Loving Prong One – Condition Prior to Vaccination

There is no dispute that Petitioner was generally healthy in the days leading up to her
vaccination. Her prematurity had not resulted in any chronic respiratory condition, and her
wellness check immediately prior to vaccination did not reveal any pulmonary concerns. Petitioner
did have a years-long history of chronic corticosteroid use for dermatological conditions that lasted
up until the month of her vaccinations. She was also prescribed antibiotics for a viral infection in
mid-to-late July of 2014, but there were no indications of sequela post treatment. Petitioner’s
medical record also does not include symptoms or a diagnosis of lung disease prior to July 29,
2014. Instead, the medical record illustrates how quickly Petitioner’s condition worsened from
symptoms consistent with a mild viral infection that manifested just hours post vaccination.

Dr. Gershwin’s theory begins with the premise that Petitioner’s “vaccination(s) provided a
mechanism of exacerbation of an already ongoing ‘starter’ cause.” Pet’r’s Br. at 6. Her expert Dr.
Gershwin asserted in his written expert opinion that although vaccinations were the but-for cause
of Petitioner’s ILD, “more likely than not, [she] was undergoing a mild drug or viral-induced
reaction that should have been reversible were it not for the sterile inflammation and abnormal
healing characterized by fibrosis that was induced by her vaccination.” Pet’r’s Ex. 8 at 5. He
admitted that Petitioner could have developed chILD without her vaccinations but noted the
severity and rapid progression of her case to support his opinion on vaccine-causation.

Respondent’s expert testified that “children who present with chILD will have a history
and a relatively recent antecedent history of infection.” Tr. 177:13–25. Dr. McCusker also noted

34
the sudden onset of Petitioner’s symptoms and testified that “you kind of have to back up yeah,
probably pre vaccine in order for the series of events to reach symptomatic by the 31st.” Tr. 283:2–
5. Both experts explained the clinical progression of ILD with supporting literature that identified
infection as a possible trigger.

Traditionally, the Loving factors have been applied to cases where, pre vaccination, the
petitioner has symptoms consistent with the ultimate diagnosis or where the petitioner has already
been diagnosed. See Tomsky v. Sec’y of Health & Hum. Servs., No. 17-1132V, 2020 WL 5587365
(Fed. Cl. Spec. Mstr. Aug. 24, 2020) (applying the Loving analysis in a case where the petitioner’s
alleged vaccine-caused injury was chronic inflammatory demyelinating polyneuropathy (“CIDP”)
and where he exhibited symptoms consistent with CIDP, including lower extremity and facial
weakness, pre vaccination); Maciel v. Sec’y of Health & Hum. Servs., No. 15-362V, 2018 WL
6259230 (Fed. Cl. Spec. Mstr. Oct. 12, 2018) (applying the Loving analysis in a case involving a
petitioner who had already been diagnosed with multiple sclerosis and was alleging the significant
aggravation of the same); see also L.Z. v. Sec'y of Health & Hum. Servs., No. 14-920V, 2018 WL
5784525 (Fed. Cl. Spec. Mstr. Aug. 24, 2018); Bubb v. Sec’y of Health & Hum. Servs., No. 01-
721V, 2005 WL 1025707 (Fed. Cl. Spec. Mstr. Apr. 29, 2005).

In this case, Petitioner does not present evidence that she was suffering from chILD at the
time of vaccination. Dr. McCusker suggested this during her testimony, but her explanation was
limited to the timing of Petitioner’s progression. She was unable to point to any evidence in the
medical record that Petitioner had begun to develop lung disease prior to vaccination. However,
given the immediacy of Petitioner’s respiratory symptoms following vaccination, it is reasonable
that some latent period must be accounted for. Assuming that infection and symptom onset are not
instantaneous, Petitioner’s assertion that she had developed a mild respiratory illness that would
not have worsened and led to severe chILD absent vaccination, is consistent with her medical
presentation prior to vaccination. Petitioner has established by a preponderance of the evidence
that she had been infected with a virus and was asymptomatic or exhibiting mild symptoms
immediately prior to or around the time of vaccination.

B. Loving Prongs Two and Three – Post-Vaccination Condition/Significant
Aggravation

While there are sub-classifications of chILD syndrome, the urgent need for treatment in
some cases prevents the comprehensive testing needed for diagnostics. Petitioner’s medical
records are not in dispute in this case, but her rapid clinical progression did not allow for
differential exclusions. Petitioner was asymptomatic or exhibiting mild symptoms at the time of
her vaccinations. She was coughing later that day, seen by a doctor two days later, admitted to the
hospital four days later, and completely unable to use her lungs two weeks later. When Petitioner
was transported to Kentucky for her lung transplant in late August of 2014, she had been diagnosed
with acute respiratory failure. Her record also listed idiopathic pulmonary fibrosis and interstitial
pneumonia as diagnoses.

The heterogenous nature of chILD makes sub-classification extremely difficult.
Petitioner’s condition shares some features with adult IPF, but there is disagreement within the
medical community regarding whether IPF is seen in children at all. Petitioner’s condition does

35
not answer that question as it does not neatly fit into either category. Petitioner’s test results
included evidence of active bleeding, small hemorrhagic areas, interstitial fibrosis, collagen
deposition, alveoli destruction, diffuse petechiae, interstitial opacities, pneumomediastinum, and
subcutaneous air. Some of these are commonly seen in chILD, while some symptoms are very rare
in children, but common with adult IPF. The medical personnel at CHOA realized fairly quickly
that identifying Petitioner’s specific condition would be of no consequence absent immediate
treatment. They secured her a place at a lung transplant facility, and Petitioner ultimately received
a life-saving bilateral lung transplant. The hospital where Petitioner received her transplant did
note her diagnosis, but her admission paperwork generally lists “acute lung failure.”

The medical literature filed by both parties details how ILD generally and IPF specifically
result from the immune system’s unsuccessful attempt to repair injury to the lung. The majority of
patients then experience a gradual deterioration over several years, but there are some exceptions
where onset is acute and severe. Petitioner and Respondent both filed medical literature that sets
the life expectancy post diagnosis between two and six years without a lung transplant. Even on
the shorter end of the range, treatment was discussed in terms of months. Petitioner’s medical
history, when compared with the filed medical literature, would place her in an extremely rare
class of chILD cases characterized by a high mortality rate, the failure to respond to treatment, and
an absolute inability to recover absent lung transplantation. The Clement et al. 79 article, filed by
Respondent, explains that the “outcome [for chILD] is highly variable with a mortality rate around
15%,” but “[a]n overall favorable response to corticosteroid therapy is observed in around 50% of
cases.” Resp’t’s Ex. H at 1. In this case, the experts testified that Petitioner’s deterioration was
rapid and extreme. The rapid deterioration of Petitioner’s condition, measured in days and weeks,
was noted by her treaters and both experts.

In Petitioner’s case, her medical records note that test results, including her lung biopsy,
could not identify the cause of Petitioner’s extensive fibrosis. Her treaters noted that additional
testing would be of no use to determine etiology and their focus shifted to life-saving treatment.
The difference between Petitioner’s initial mild viral symptoms and later need for ECMO,
underscores the disparity between her pre vaccination and post vaccination condition. While
chronology alone is not sufficient to prevail, it is necessary to establish an appropriate timeline.
Dr. Gershwin, in arguing that Petitioner’s respiratory illness was worsened by her vaccinations,
made a significant aggravation argument. He asserts explicitly that Petitioner would have
recovered if not for the amplified immune response that was partly due to her vaccines. I find there
is preponderant evidence that Petitioner’s condition post vaccination constitutes a significant
aggravation of both her asymptomatic status and her mild viral symptoms at the time of or
immediately preceding her vaccinations.

C. Loving Prong Four/Althen Prong One – Medical Theory

Under the first prong of Althen, a petitioner must offer a scientific or medical theory that
answers in the affirmative the question: “can the vaccine[] at issue cause the type of injury
alleged?” See Pafford v. Sec’y of Health & Hum. Servs., No. 01-0165V, 2004 WL 1717359, at *4
(Fed. Cl. Spec. Mstr. July 16, 2004), aff’d, 64 Fed. Cl. 19 (2005), aff’d, 451 F.3d 1352 (Fed. Cir.
2006). To satisfy this prong, a petitioner’s theory must be based on a “sound and reliable medical
79
See Clement, et al., supra note 42.

36
or scientific explanation.” Knudsen, 35 F.3d at 548. Such a theory must only be “legally probable,
not medically or scientifically certain.” Id. at 548–49. A petitioner is not required to identify
“specific biological mechanisms” to establish causation, nor are they required to present
“epidemiologic studies, rechallenge[] the presence of pathological markers or genetic disposition,
or general acceptance in the scientific or medical communities.” Capizzano, 440 F.3d at 1325
(quoting Althen, 418 F.3d at 1280). However, as the Federal Circuit has made clear, “simply
identifying a ‘plausible’ theory of causation is insufficient for a petitioner to meet her burden of
proof.” LaLonde v. Sec’y of Health & Hum. Servs., 746 F.3d 1334, 1339 (Fed. Cir. 2014) (citing
Moberly, 592 F.3d at 1322). Rather, “[a] petitioner must provide a reputable medical or scientific
explanation that pertains specifically to the petitioner’s case.” Moberly, 592 F.3d at 1322. In
general, “the statutory standard of preponderance of the evidence requires a petitioner to
demonstrate that the vaccine more likely than not caused the condition alleged.” LaLonde, 746
F.3d at 1339.

Furthermore, establishing a sound and reliable medical theory connecting the vaccine to
the injury often requires a petitioner to present expert testimony in support of her claim. Lampe v.
Sec’y of Health & Hum. Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000). The Supreme Court’s
opinion in Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993), requires that
courts determine the reliability of an expert opinion before it may be considered as evidence. “In
short, the requirement that an expert’s testimony pertain to ‘scientific knowledge’ establishes a
standard of evidentiary reliability.” Id. at 590 (citation omitted). Thus, for Vaccine Act claims, a
“special master is entitled to require some indicia of reliability to support the assertion of the expert
witness.” Moberly, 592 F.3d at 1324. The Daubert factors are used in the weighing of the reliability
of scientific evidence proffered. Davis v. Sec’y of Health & Hum. Servs., 94 Fed. Cl. 53, 66–67
(2010) (“uniquely in this Circuit, the Daubert factors have been employed also as an acceptable
evidentiary-gauging tool with respect to persuasiveness of expert testimony already admitted.”).
Where both sides offer expert testimony, a special master’s decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe, 219 F.3d at 1362). And nothing requires the acceptance of an expert’s conclusion
“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
great an analytical gap between the data and the opinion proffered.” Snyder v. Sec’y of Health &
Hum. Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146
(1997)).

Petitioner is placed in a difficult position in this case. She must establish a theory that
cannot be systemically tested, due to the uncommon nature of the disease, nor can it be
methodically observed, due to the speed at which irreversible and fatal damage occurs following
onset. Petitioner’s expert has presented a causation theory that has evolved over time. Throughout
this case, however, Petitioner’s expert never suggested that the vaccines at issue were the sole
cause of the alleged condition. Petitioner’s theory depends on multiple immune triggers, including
long-term corticosteroid use, antibiotic treatments, viral illness, and, finally, vaccines. Had
Petitioner’s explanation of vaccine causation ended here, Respondent would be correct that
Petitioner’s claim fails. This overview of Petitioner’s theory must be supported by indicia of
reliability. I have cautioned petitioners in the past that the mere mention of upregulated cytokines
is not the same as an articulated biological mechanism. See, e.g., Nunez v. Sec’y of Health & Hum.

37
Servs., No. 14-863V, 2019 WL 2462667, at *41 (Fed. Cl. Spec. Mstr. Mar. 29, 2019) (finding that
the petitioners failed to present a biological mechanism connecting the vaccination to the alleged
injury because their theory involving the increase in cytokine production levels did not involve
evidence of an active transportation mechanism to cause said injury.). This case involves a
condition (like others in the Program) that medical professionals have classified as idiopathic.
Indeed, it is not surprising that Petitioner’s expert was unable to provide a detailed and exact
biological mechanism to explain how one or more of the vaccines at issue in this case can cause
chILD. That is not the standard. Dr. Gershwin was ultimately able to articulate a medical theory
that causally connects the vaccinations at issue to IPF and acute respiratory failure. Therefore, I
find that Petitioner has met her burden with respect to Althen prong one/Loving prong four.

Respondent’s expert asserts that Dr. Gershwin’s theory must fail, because it involves a rare
disease that cannot be studied epidemiologically. Furthermore, Petitioner’s theory lacks a practical
testing methodology, and it has not been proposed by anyone in the medical community. Both
experts repeatedly agreed that IPF is an extremely rare form of the already rare chILD. Its high
mortality rate compounds that. In fact, some of the literature submitted argued that children do not
suffer from IPF. As a result, there are no studies that have been done that explicitly study
vaccinations and IPF in children. Petitioner submitted literature that provided varying perspectives
on ILD generally, chILD, and IPF. Petitioner’s submitted literature explained the role of cytokines
in the development of lung disease. Petitioner also submitted literature that successfully
established that there is an increase in cytokine production post vaccination. The conclusions from
these studies, when put together, support Petitioner’s theory of causation.

The ineffectiveness of autoinflammatory therapies has fueled significant debate within the
medical community about whether IPF is the result of a systemic inflammatory response. Dr.
McCusker explained that IPF does not develop as a result of inflammation or the body’s disarming
of an offending antigen. The dysregulation that leads to IPF occurs during the repair phase. She
likened the relationship between inflammation and repair to opposites sides of the same coin. If
that is the case, however, it would stand to reason that the two would be directly correlated to each
other. An intense immune response could cause severe damage and increase the possibility for
something to go wrong during a substantial repair phase. Dr. Gershwin does not undertake to
explain how cytokines produced as a response to vaccination miscommunicate with cells in the
lung. He does, however, identify some of the relevant proteins and explain their intended role.
Specifically, TNF-beta and several interleukins are instrumental in fibroblast proliferation and the
development of ECM. It is reasonable that these cytokines, if improperly upregulated or
dysregulated, could prevent tissue repair following lung damage. Dr. Gershwin argues that the
inciting agent (a virus), vaccinations, and potentially Bactrim, could all overload the immune
system resulting in cytokine miscommunication. He has presented preponderant evidence that this
process could occur. The remaining piece of his causation theory is how these cytokines that are
responding to immune stimuli in other parts of the body are able to migrate to the lung.

Petitioner’s mechanism is based on the concept of bystander activation and circulation. Dr.
Gershwin argues that Petitioner’s IPF developed due to the migration of bystander cells summoned
by circulating cytokines that called because they were reacting to a multifactorial, immune
stimulus event. Petitioner has presented preponderant evidence of cytokine upregulation following

38
vaccination, cytokine migration to injured tissue, and cytokine involvement in disease
development.

Dr. McCusker was asked to respond to Dr. Gershwin’s description of the role of cytokines,
specifically TFG-beta, and she agreed with his explanation. Her dissent lies in Dr. Gershwin’s
assertion that the cytokines migrate. Dr. McCusker testified that she “can’t walk the cytokines
from the arm to lung.” Tr. 212:14–15. Despite this, Dr. McCusker later testified that in a systemic
immune response, there are antibodies “floating around bound to antigen[s] and they get caught in
small capillaries and create inflammation,” but, she noted that this is not the same as migrating
cytokines. See Tr. 222:15–23.

Dr. Gershwin’s explanation of sterile inflammation in this context is confusing. At one
point, he incorporated sterile inflammation directly into his causation theory. At another point, he
testified that this reference is an analogy to explain the concept of cell migration. Sterile
inflammation was defined in the literature as cell death in the absence of inflammation. Pet’r’s Ex.
48 at 1. Petitioner filed literature that described IPF as a “highly progressive fibrotic disease in the
absence of detectable inflammation.” Pet’r’s Ex. 47 at 3. Dr. McCusker clarified that sterile
inflammation occurs in the absence of “an exogenous antigenic trigger.” Tr. 191:19–20. There is
no evidence in the record, however, that IPF or acute respiratory failure can develop from sterile
inflammation pursuant to Dr. Gershwin’s theory. Vaccines, viral infections, and even Bactrim
exposure are all exogenous antigens. Furthermore, as Dr. McCusker noted, the McDonald et al. 80
article cited by Dr. Gershwin does not discuss multi-system injury where there are simultaneous
immune system responses. The article does, however, explain how “[r]ecent studies of models of
sterile injury in the liver have uncovered cellular and molecular mechanisms of immune cell
recruitment to damaged tissues as well as the cell types that mediate tissue repair and homeostasis.”
Pet’r’s Ex. 48 at 3. Dr. Gershwin appears to be using this article to provide an example of immune
cells ‘figuring out’ where the damage is and that they are needed in the absence of inflammation.
It may not be a perfect analogy, but it is an exception to Dr. McCusker’s blanket rule of ‘no
migration.’ The potential migration of neutrophils and monocytes via intravascular channels to
tissue that has been injured can be supported potentially by evidence of vasculitis. Furthermore,
evidence of severe diffuse fibrosis tracks the process in the McDonald et al. study of monocytes
producing cytokines and chemokines to summon other immune cells and stimulate extracellular
matrix production. This can result in the overproduction of ECM and the dysregulation of lung
repair.

Indeed, Petitioner may have taken a “kitchen sink approach” with a mechanism that
involves cytokine production, bystander activation, and molecular mimicry. Ultimately, Dr.
Gershwin’s theory narrowed subject to cross-examination and further questioning. Dr. Gershwin
shifted his theory and provided vague and extremely tentative answers. It is noteworthy that Dr.
McCusker was likewise vague and tentative at times. Petitioner has therefore met her burden with
respect to Althen prong one/Loving prong four.

D. Loving Prong Five/Althen Prong Two – Actual Causation

80
See McDonald, et al., supra note 60.

39
 Under the second prong of Althen, a petitioner must prove that the vaccine actually did
cause the alleged injury in a particular case. See Pafford, 2004 WL 1717359, at *4; Althen, 418
F.3d at 1279. The second Althen prong requires proof of a logical sequence of cause and effect,
usually supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278;
Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. Servs., 956 F.2d 1144, 1148 (Fed.
Cir. 1992). A petitioner does not meet this obligation by showing only a temporal association
between the vaccination and the injury; instead, the petitioner “must explain how and why the
injury occurred.” Pafford, 2004 WL 1717359, at *4 (emphasis in original). The Court in Pafford
noted petitioners “must prove [] both that her vaccinations were a substantial factor in causing the
illness . . . and that the harm would not have occurred in the absence of the vaccination.” 2004 WL
1717359, at *4 (citing Shyface, 165 F.3d at 1352). A reputable medical or scientific explanation
must support this logical sequence of cause and effect. Hodges v. Sec’y of Health & Hum. Servs.,
9 F.3d 958, 961 (Fed Cir. 1993) (citation omitted). Nevertheless, “[r]equiring epidemiologic
studies . . . or general acceptance in the scientific or medical communities . . . impermissibly raises
a claimant’s burden under the Vaccine Act and hinders the system created by Congress . . . .”
Capizzano, 440 F.3d at 1325–26. “[C]lose calls regarding causation are resolved in favor of injured
claimants.” Althen, 418 F.3d at 1280.

In Program cases, contemporaneous medical records and the opinions of treating
physicians are favored. Capizzano, 440 F.3d at 1326 (citing Althen, 418 F.3d at 1280). This is
because “treating physicians are likely to be in the best position to determine whether ‘a logical
sequence of cause and effect show[s] that the vaccination was the reason for the injury.’” Id. In
addition, “[m]edical records, in general, warrant consideration as trustworthy evidence. The
records contain information supplied to or by health professionals to facilitate diagnosis and
treatment of medical conditions. With proper treatment hanging in the balance, accuracy has an
extra premium. These records are also generally contemporaneous to the medical events.”
Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). While a special
master must consider these opinions and records, they are not “binding on the special master or
court.” 42 U.S.C. § 300aa-13(b)(1). Rather, when “evaluating the weight to be afforded to any
such . . . [evidence], the special master . . . shall consider the entire record . . . .” Id. The record
often includes “evidence of possible sources of injury” that can show alternate causes for the
alleged vaccine-related injury. See Stone v. Sec’y of Health & Hum. Servs., 676 F.3d 1373, 1379
(Fed. Cir. 2012).

In order to apply Petitioner’s presented causation theory (Loving prong four/Althen prong
one) to Petitioner’s clinical presentation and condition (Loving prongs 1–3), my analysis pursuant
to Loving prong five/Althen prong two must begin with the specifics of Petitioner’s condition.
Because it is difficult to align IPF histology with typical chILD cases, it is necessary to determine,
based on Petitioner’s history, where her condition fits within the expert opinions and the medical
literature.

During Petitioner’s initial urgent care visit on July 31, 2014, her symptoms were not
indicative of lung disease. Petitioner’s medical history included no signs of asthma or other
respiratory distress. Initially, medical personnel believed Petitioner was suffering from a viral
illness, or possibly an adverse vaccine reaction. By the time the severity of Petitioner’s condition
was discovered, she was unable to breathe on her own. Both experts in this case testified that while

40
prematurity is a risk factor for ILD, Petitioner had no known respiratory issues resulting from her
prematurity. Petitioner’s Bactrim course in the days prior to her vaccinations had not led to any
respiratory issues, and her lung examination at the time of her vaccinations on July 29, 2014, was
normal. Dr. Gershwin and Dr. McCusker agreed that Petitioner was suffering a viral infection at
the end of July of 2014, but neither expert was able to definitively identify Petitioner’s symptom
onset. Because Petitioner’s July 31, 2014 complaints of fever, vomiting, sore throat, and fatigue
are all potential symptoms of a Bactrim reaction, virus, and/or ILD, and one or more of these
conditions all manifested at the same time, it is impossible to assign any specific symptom to any
one condition. Furthermore, treaters never ruled out a reaction to the HPV vaccine. Petitioner’s
medical record also indicates she suffered swollen tonsils and bilateral anterior cervical
lymphadenopathy following vaccination. This is all evidence that Petitioner’s immune system had
initiated a strong response to one or more of these possible triggers.

Petitioner’s rapid deterioration hindered her treaters’ ability to rule out differential
diagnoses of ILD. In essence, Petitioner’s lungs were destroyed by a force similar to a fire in speed
and severity. The damage was total, irreversible, and opaque. A chest scan performed on August
6, 2014, showed ground-glass opacities consistent with Dr. Rachelefsky’s description of
accelerated IPF. Pet’r’s Ex. 4 at 2341; see also Resp’t’s Ex. A. Her biopsy also revealed severe,
advanced diffuse alveolar damage with little indication of the stages of injury and fibrosis. Pet’r’s
Ex. 4 at 2472. According to Dr. Rachelefsky, this is consistent with acute interstitial pneumonia.
Her treaters specifically listed IPF as a diagnosis on August 18, 2014. Id. at 2407. And, Petitioner’s
medical records note diffuse fibrosis with no other findings. Petitioner did have some
inflammatory markers. However, they were slight. Furthermore, she was treated with steroids that
are designed to fight inflammation. The rapid progression of Petitioner’s condition makes it
difficult to determine how all of these factors affect each other. Because her condition deteriorated
so quickly, Petitioner’s treaters were forced to shift their focus entirely from pathogenesis to
treatment. As with many cases where patients experience acute and irreversible respiratory failure,
it is difficult, if not impossible, to retroactively determine etiology in Petitioner’s case. Based off
the opinions of Petitioner’s treaters as documented in her medical records, the expert opinion
evidence, and the medical literature filed in this case, I find there is preponderant evidence that
Petitioner suffered from IPF and subsequent acute respiratory failure.

i. Immune Response

Dr. Gershwin asserts that in the wake of her vaccinations, Petitioner’s immune system was
dysregulated, and her lungs were unable to recover following a mild respiratory illness, due to the
immune system’s over-production of cytokines needed to initiate tissue healing and regulate repair.
Dr. McCusker relied on two factors to argue that vaccinations did not lead to Petitioner’s immune
system dysregulation and her development of chILD. First, Petitioner’s immunological testing
revealed decreased T and NK cells. This finding is consistent with the Galati et al. 81 article’s
conclusion that because IPF patients in severe cases have a decreased number of NK cells, the
disease itself it not the result of an overactive immune system upregulating the production of killer
cells. Additionally, Petitioner’s rheumatological testing did not uncover significantly elevated
inflammatory markers, they were merely slightly elevated. Petitioner’s treaters noted the presence
of fever and severe lung tissue damage, but they determined that there was little evidence of
81
See Galati, et al., supra note 52.

41
systemic inflammation. Dr. Gershwin countered that Petitioner’s persistent fever and CRP
elevation is some evidence of systemic inflammation. He further argued that Petitioner’s treatment
course, including an extended course of anti-inflammatory drugs, had severely impacted the
integrity of any testing to identify inflammation.

Dr. Gershwin’s theory does not rely on a sustained, heightened immune response in the
face of anti-inflammatory or immuno-suppressive treatment. I do not find here any evidence of
cytokine storm. Petitioner’s disease, as both testifying experts pointed out, resulted from an error
in repair facilitated by the immune system. The immune system is regulated by cytokines. In this
case, Petitioner’s immune response is evidenced by her local immune reaction at the vaccination
site and her fever that exceeded 102 degrees Fahrenheit. Dr. McCusker did not rebut Dr.
Gershwin’s contention the Petitioner’s body was attempting to develop antibodies pursuant to
vaccination, fight off her mild viral illness, stave off further cell damage, and initiate lung tissue
repair. Even acting in a compartmentalized manner, these stressors more likely than not had an
additive, if not synergistic, effect on Petitioner’s immune system.

In accordance with Shyface, I find that all of these competing factors: Bactrim; viral
infection; and TDaP, HPV, and meningococcal vaccines, collectively played a role in this child’s
development of IPF. The vaccinations were a substantial factor in the severity of her condition. If
not for the vaccines Petitioner received on July 29, 2014, she would not have suffered a rapid and
life-threatening condition requiring a bilateral lung transplant. I must emphasize that the causation
in this case is extremely fact specific. It is difficult to imagine how Petitioner’s theory would be
applicable to another individual, given her age, the rarity of her condition, the rapid progression of
her disease following vaccination, her contemporaneous illness, and her prior antibiotic use.

ii. Rapid Progression of Disease

All agree that by July 31, 2014, Petitioner was exhibiting signs of respiratory distress.
Approximately two weeks later, her treaters had determined that she would need a bilateral lung
transplant immediately to save her life. By all measures, this would appear to be an extremely
rapid progression of disease. Respondent’s expert testified that she had a similar patient who went
from healthy to ventilator in four days. However, Dr. McCusker did not file any literature to
support her contention that a range from 4–14 days from time of diagnosis to respiratory failure is
expected. In fact, Dr. McCusker stated plainly that she did not know what an appropriate timeframe
is. She described Petitioner’s case as “classic” and “very sudden” without additional context from
the medical literature. She then testified that chILD takes longer than several days to process and
hypothesized that Petitioner likely began to develop chILD prior to vaccination. Ultimately,
Respondent was unable to provide persuasive evidence to counter the medical literature provided
by both parties, and Dr. Gershwin’s testimony regarding the timeframe for a chILD patient to
advance to respiratory failure. Therefore, I find that Petitioner has provided persuasive evidence
that her rapid progression is evidence there were compounding triggers for her disease.

Petitioner and Respondent also agree that Petitioner was born premature but that her
medical records to do not reveal a history of respiratory issues. Both experts testified at some point
that Petitioner’s prematurity is a risk factor, but also likely played no role in the pathogenesis of
her disease. Lastly, both parties noted that Petitioner’s Bactrim use and upper respiratory infections

42
are known triggers of some forms of interstitial lung disease. Petitioner asserts that her
predisposition and additional causal factors led to an exacerbated version of her disease and severe
outcome. Respondent counters that vaccinations do not cause chILD, and any one of Petitioner’s
other issues could be the sole cause of her chILD; alternatively, it could be idiopathic.

I do not accept Respondent’s contention that any of Petitioner’s other immune stimuli could
be the trigger, but due to the rarity of the disease, we cannot include vaccines in that list.
Petitioner’s clinical course is truly one in a million, but the mechanism submitted by Dr. Gershwin
is consistent with the facts in this case. Therefore, I find that Petitioner has met her burden with
respect to Althen prong two/Loving prong five.

E. Loving Prong Six/Althen Prong Three – Temporal Relationship

Under the third prong of Althen, a petitioner must show that the timing of the injury fits
with the causal theory. See Althen, 418 F.3d at 1278. For example, if a petitioner’s theory involves
a process that takes several days to develop after vaccination, an injury that occurred within a day
of vaccination would not be temporally consistent with that theory. Conversely, if the theory is
one that anticipates a rapid development of a reaction post vaccination, the development of the
alleged injury weeks or months post vaccination would not be consistent with that theory. See de
Bazan, 539 F.3d at 1352. Causation-in-fact cannot be inferred from temporal proximity alone. See
Grant, 956 F.2d at 1148; Thibaudeau v. Sec’y of Health & Hum. Servs., 24 Cl. Ct. 400, 403–04
(1991); see also Hasler v. United States, 718 F.2d 202, 205 (6th Cir. 1983) (“Without more, [a]
proximate temporal relationship will not support a finding of causation.”).

Petitioner exhibited symptoms consistent with an errant reaction immediately following
her vaccinations. She described swelling on her arm at the injection site and fever the same day.
She began to experience respiratory issues within 48 hours of vaccination and was diagnosed with
acute respiratory failure two weeks later. Dr. Gershwin explained that the stress on Petitioner’s
innate immune system due to the virus and the culmination of vaccinations happened during the
peripheral circulation of proinflammatory cytokines. The testimony by both experts established
that there was a window of up to four days for this to occur. The onset of Petitioner’s chILD around
July 31, 2014, is within this timeframe. Therefore, I find that Petitioner has established by a
preponderance of the evidence that the temporal relationship between her July 29, 2014
vaccinations and symptoms is appropriate based on her causation theory. She has therefore met
her burden with respect to Althen prong three/Loving prong six.

F. Alternative Causation

If a petitioner presents a prima facie case, the Federal Circuit has held that the burden of
proof shifts to the government, and Respondent must prove that the “‘injury . . . described in the
petition is due to factors unrelated to the . . . vaccine.’ 42 U.S.C. § 300aa-13(a)(1)(b).” Knudsen, 35
F.3d at 547. Yet, a petitioner’s failure to prove any element of his prima facie case mandates that
the Court deny entitlement. See id. Under such circumstances, the burden of proof does not shift
to the respondent to establish an alternate cause for the petitioner’s claimed injury. Althen, 418
F.3d at 1278; see also Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d 1570, 1575 (Fed. Cir.
1993).

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 In this case, Petitioner has established a prima facie case for compensation under Loving
and Althen. Therefore, Respondent has the burden to prove Petitioner’s injury was caused by
something other than her July 29, 2014 vaccinations. See LaLonde, 746 F.3d at 1340. However,
Respondent has been unable to do so. Dr. McCusker contends that Petitioner’s chILD developed
because her corticosteroid treatment may have somehow disrupted her immune system and then
she got sick. This process, according to Dr. McCusker, was unaffected by Petitioner’s multiple
vaccines, which are designed to engage the immune system. There is no biological mechanism
articulated here. Respondent argues that Petitioner is an isolated case with no known cause and no
cure. Petitioner is, according to Dr. McCusker, “the perfect situation for dysregulation,” and her
fibrosis is the result of the inability of the immune system to properly shift from fighting infection
to tissue repair. Dr. Gershwin goes a step further than Dr. McCusker and offers a logical
explanation as to why Petitioner’s immune system was unable to shift. The immune system’s
signalers were unable to properly relay a message of repair. This explanation is reasonable and
persuasive. Dr. McCusker did not identify a biological mechanism of causation, a potential trigger
for Petitioner’s ILD, or an appropriate symptom-onset date to counter Dr. Gershwin’s theory.
Therefore, Respondent has failed to show by preponderant evidence that Petitioner’s acute
respiratory failure has an alternative cause.

VI. Conclusion

Petitioner has suffered an unimaginable injury that brings with it life changing effects. She
is to be commended for her bravery and resolve. The determination of her immediate family is
undoubtably the reason she is here today, and their continued support is a ray of light in stormy
weather. As I stated during the entitlement hearing in this case, I do not allow sympathy to sway
the outcomes in these cases. However, it is endearing on those occasions when the Program is used
as it was intended, to provide compensation with certainty and generosity, to the rare few who
establish that they suffered a vaccine-caused injury. This is one such occasion. Petitioner has
shown by a preponderance of the evidence that one or more of her vaccinations was a substantial
factor and a but-for-cause of her IPF and acute respiratory failure. She is therefore entitled to
compensation and a subsequent damages order will issue.

IT IS SO ORDERED.

s/Herbrina D. Sanders
Herbrina D. Sanders
Special Master

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