Delgado v. Secretary of Health and Human Services
17-1382V
| Fed. Cl. | Nov 17, 2025|
Check Treatment|
Docket
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: October 23, 2025
* * * * * * * * * * * * * * *
NAOMI DELGADO, *
*
Petitioner, * No. 17-1382V
*
v. * Special Master Young
*
SECRETARY OF HEALTH *
AND HUMAN SERVICES, *
*
Respondent. *
* * * * * * * * * * * * * * *
Jeffrey S. Pop, Jeffrey S. Pop & Associates, Beverly Hills, CA, for Petitioner.
Mitchell Jones, United States Department of Justice, Washington, DC, for Respondent.
ENTITLEMENT DECISION1
On September 29, 2017, Naomi Delagado (“Petitioner”) filed a petition for compensation
pursuant to the National Vaccine Injury Compensation Program.2 Pet. at 1, ECF No. 1; 42 U.S.C.
§§ 300aa-1 to -34 (2018). Petitioner alleges that the Prevnar 13 vaccine she received on June 15,
2015, was the cause-in-fact of her asthma, “a condition she did not previously have.” Pet. at 1.
Petitioner amended her petition on November 11, 2019, to allege “[i]n the alternative, the
Petitioner’s pre-existing asthma which was stable and controlled was substantially aggravated by
the Prevnar 13 vaccination.” Am. Pet. at 10, ECF No. 36.
A careful analysis and weighing of all the evidence and testimony presented in this case
in accordance with the applicable legal standards,3 reveals that Petitioner has failed to provide
1
Because this Decision contains a reasoned explanation for the action taken in this case, it must be made
publicly accessible and will be posted on the United States Court of Federal Claims’ website, and/or at
https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government Act
of 2002. 44 U.S.C. § 3501note (2018) (Federal Management and Promotion of Electronic Government Services). This means the Decision will be available to anyone with access to the internet. In accordance with Vaccine Rule 18(b), Petitioner has 14 days to identify and move to redact medical or other information, the disclosure of which would constitute an unwarranted invasion of privacy. If, upon review, I agree that the identified material fits within this definition, I will redact such material 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 (2018). 3 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
preponderant evidence that the Prevnar 13 vaccine she received on June 15, 2015, was the cause-
in-fact of her asthma or a significant aggravation of her asthma. Accordingly, Petitioner is not
entitled to an award of compensation.
I. Procedural History
Petitioner filed her petition on September 29, 2017. Pet. She filed an affidavit and medical
records on October 24, 2017. Pet’r’s Exs. 1–3, ECF No. 8. On March 23, 2018, Petitioner filed an
expert report from Hermes J. Garban, M.D., Ph.D., and supporting medical literature. Pet’r’s Exs.
4–13, ECF No. 13. Petitioner filed additional medical records on June 22 and July 12, 2018. Pet’r’s
Exs. 14–15, ECF Nos. 17, 19. Respondent filed his Rule 4(c) report arguing against compensation
on October 11, 2018. ECF No. 23.
On December 28, 2018, Petitioner filed another expert report from Dr. Garban and medical
literature. Pet’r’s Exs. 16–18. On May 22, 2019, Respondent filed an expert report from Emil
Bardana, Jr., M.D., and supporting medical literature. Resp’t’s Exs. A–B, ECF No. 27. Petitioner
filed an expert report from Petitioner’s treating physician, Stasha Novakovic, M.D., on November
1, 2019. Pet’r’s Exs. 19–20, ECF No. 30. Medical literature supporting Dr. Novakovic’s opinions
was filed on November 4, 2019. Pet’r’s Exs. 21–36, ECF Nos. 31–32. Petitioner filed an amended
petition on November 11, 2019. Am. Pet.
Respondent filed supplemental expert reports from Dr. Bardana and medical literature on
February 18, 2020. Resp’t’s Exs. C–D, ECF No. 44. Petitioner filed additional medical records on
June 2, 2020. Pet’r’s Exs. 40–41, ECF No. 48. On June 3, 2020, Petitioner filed a supplemental
expert report from Dr. Novakovic and medical literature. Pet’r’s Exs. 42–46, ECF No. 49. And on
July 20, 2020, Petitioner filed a supplemental report from Dr. Garban. Pet’r’s Exs. 47–48, ECF
No. 51. On November 25, 2020, Respondent filed a supplemental report and medical literature
form Dr. Bardana, and an expert report from Derek E Byers, M.D., Ph.D, and supporting medical
literature. Resp’t’s Exs. E–G, ECF No. 54–55. On March 10, 2021, Petitioner filed supplemental
expert reports and medical literature from Dr. Garban and Dr. Novakovic. Pet’r’s Exs. 49–55, ECF
No. 57.
On March 15, 2022, I held a Rule 5 conference where I told Petitioner that her theory
pursuant to Althen prong one was unclear. ECF No. 59. Petitioner requested sixty days to clarify
her theory. Id. On May 23, 2022, Petitioner filed declarations from her husband and daughter.
Pet’r’s Exs. 56–57, ECF No. 61. On June 1, 2022, Petitioner filed a supplemental expert report
from Dr. Garban and medical literature. Pet’r’s Exs. 58–65, ECF Nos. 62, 64. Respondent filed a
supplemental expert report from Dr. Byers on December 19, 2022. Resp’t’s Ex. H, ECF No. 69.
On June 28, 2023, an entitlement hearing was scheduled for October 2024. ECF No. 70.
Petitioner filed additional medical records and medical literature on June 24, September 30,
October 2, October 3, and October 11, 2024. Pet’r’s Ex. 66, ECF No. 72; Pet’r’s Exs. 69–87, ECF
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.”).
2
Nos. 77, 79, 85, 88. On July 5, 2024, Petitioner filed her pre-hearing brief. Pet’r’s Br., ECF No.
74. Respondent filed his responsive pre-hearing brief on September 17, 2024. Resp’t’s Br., ECF
No. 76. Petitioner filed a reply brief on October 3, 2024. Pet’r’s Reply, ECF No. 84. An entitlement
hearing was held on October 10 and 11, 2024. Min. Entry, docketed Oct. 11, 2024. No post-hearing
briefs were filed.
II. Factual Background
A. Medical Records
Petitioner’s pre-vaccination medical history is significant for a pulmonary disease. See
Pet’r’s Ex. 40 at 2. On December 23, 2003, Petitioner was seen in urgent care for diabetes
complications. Pet’r’s Ex. 40 at 168. During that visit, she also complained of shortness of breath
(“SOB”), and cough. Id. She was diagnosed with bronchitis, and instructed to use “an Albuterol
inhaler, two puffs four times daily to improve her breathing.” Id. at 162. Petitioner continued to
complain of this cough during a January 16, 2004 visit to the emergency department (“ED”), and
noted that it had been productive for three weeks. Id. at 165. She was diagnosed with “recurrent
bronchitis” and the albuterol medication was continued. Id. at 166.
One of the earliest mentions of “possible asthma” was within a medical record from a
primary care physician (“PCP”) visit, dated October 24, 2007. Pet’r’s Ex. 14 at 534. In her medical
history, it was noted that she complained of chronic cough for two months and SOB without
wheezing. Id. at 531. The record also noted no history of asthma. Id. She was prescribed an
albuterol inhaler and instructed to “use [two] puffs by mouth every [six] hours for [SOB].” Id. at
532. A medical record dated March 23, 2008, from the West Palm Beach VA Medical Center
(“WPBVAMC”), noted ‘asthma’ under nursing discharge instructions with general information
and a warning that “[r]epeat attacks are common.” Id. at 456–57. Petitioner presented to the ED
on April 4, 2008, with complaints of coughing and wheezing. Pet’r’s Ex. 14 at 449. She reported
that she had been to the ED multiple times for the same complaints. Id. “When she is given
albuterol, steroids, and antibiotics she improves but relapses when weaned off steroids.” Id. Treater
impressions included chronic cough, wheezing, and seasonal allergies. Id. at 452. She was referred
to a pulmonologist. Id.
On April 14, 2008, Petitioner was seen by Dr. Sateesh Veeramachaneni for a pulmonary
consultation. Pet’r’s Ex. 14 at 432. She had complaints of “cough with productive sputum
approximately [seven] months duration and wheezing of [six] weeks duration.” Id. Petitioner had
been to the ED multiple times and been treated with steroids and antibiotics. Id. Petitioner reported
that she was a former smoker with a history of gastroesophageal reflux disease (“GERD”) and had
a penicillin allergy. Id. Her active medications included an albuterol inhaler and prednisone for
exacerbation of chronic obstructive pulmonary disease (“COPD”)/asthma; flunisolide nasal spray
and loratadine for allergies; mometasone furoate for breathing and guaifenesin for cough; and
additional medications for infection, pain, and diabetes. Id. at 432–33. Physical examination
revealed “hazy density throughout the upper mid and lower lung zone,” which Dr.
Veeramachaneni noted was “most likely secondary to a poor inspiratory effort or lack of ability to
cooperate with inspiration.” Id. at 434. Dr. Veeramachaneni also noted “subtle peripheral septal
thickening in the subpleural region in the upper mid and lower lung zones [and] mild
3
bronchiectasis [] at the lung bases posteriorly.” Id. She assessed Petitioner with bronchiectasis and
reactive airway disease.4 Id. at 435.
On May 16, 2008, Petitioner was seen at WPBVAMC for a follow-up for her
bronchiectasis. Pet’r’s Ex. 14 at 426. Pulmonary function testing (“PFT”) revealed restrictive
disease “most probably secondary to obesity,” and a chest computed tomography (“CT”) showed
pleural changes and increased size of pulmonary arteries. Id. Notes from Petitioner’s PCP dated
July 8, 2008, indicated that she was seeing a pulmonologist for her bronchiectasis but that “[h]er
cough ha[d] resolved, and she [was] no longer needing albuterol.” Id. at 417. An ophthalmology
note for an unrelated examination, dated May 19, 2009, listed Petitioner’s medical history,
including diabetes (on insulin) and COPD/asthma. Id. at 351.
The following chart summarizes Petitioner’s pre-vaccination pulmonary history.5 See
Pet’r’s Ex. 14 at 126–548.
Date/Location Symptoms Assessment/Diagnosis Treatment
10/24/07 Chronic cough, SOB, Cough- likely due to Albuterol inhaler
PCP fatigue GERD, possible asthma
03/14/08 Cough with yellow sputum, Bronchitis Inhaler, antibiotics,
ED wheezing, SOB, low grade steroid
fever
03/22/08 Persistent productive cough, Asthma exacerbation Nebulized
ED wheezing, SOB bronchodilators,
intravenous steroids
04/05/08 Coughing and wheezing Hypersensitive Inhaler and steroids
ED pneumonitis rule out
bronchial asthma
04/15/08 Cough and wheezing Bronchiectasis, reactive Steroid inhaler,
Pulmonary airway disease allergy medication,
specialist cough suppressant
07/08/08 No complaints Bronchiectasis without Off albuterol
Pulmonary acute exacerbation
specialist
On June 15, 2015, Petitioner received a pneumococcal vaccine “with no noted adverse
reactions.” Pet’r’s Ex. 3 at 907. Four days later, on June 19, 2015, Petitioner reported to the ED
with complaints of “wheezing and coughing since Tuesday[, June 16, 2015].” Id. at 900. Petitioner
continued that she was also experiencing “productive cough, chills, SOB and vomiting since
Tuesday[,] a day after receiving the [pneumococcal] shot, [she was] currently [a]febrile although
having a hard time breathing.” Id. Petitioner stated that the evening of her vaccination, “she began
developing generalized malaise,” and that she “ha[d] never experienced symptoms this severe in
the past.” Id. at 887. Petitioner denied a history of asthma. Id. Dr. Bijal Asrani diagnosed Petitioner
4
Reactive airway disease refers to “any of several conditions characterized by wheezing and allergic
reactions; the most common ones are asthma, bronchiolitis, and chronic obstructive lung disease.”
Reactive Airway Disease, DORLAND’S MED. DICTIONARY ONLINE.
5
This is also discussed by Petitioner’s expert, Dr. Novakovic, during his testimony. Tr. 58–73
4
with “[S]tatus asthmaticus: in the setting of recent viral [upper respiratory tract infection
(“URI”)].” Id. at 889. Other diagnoses included tachycardia, leukocytosis, and hyperglycemia in
the setting of type two diabetes mellitus. Id. at 890. She was administered nebulizer and steroid
treatments. Id. Petitioner was admitted to the hospital and underwent an intensive care unit (“ICU”)
consultation for noninvasive positive pressure ventilation. Id. There was “no evidence of
respiratory fatigue.” Pet’r’s Ex. 15 at 9. Petitioner was “clinically improved/resolved, no longer
tachypneic and able to ambulate without [SOB].” Id. She was discharged on June 23, 2015. Id.
Petitioner was treated again at the ED for “increasing wheezing and cough with occasional
white phlegm and shortness of breath,” on July 4, 2015. Pet’r’s Ex. 3 at 794. She was diagnosed
with bronchiectasis and treated with steroids. Id. On July 9, 2015, a high-resolution CT scan of the
chest showed borderline bronchiectasis. Id. at 136–37. She returned to the ED on July 19, 2015,
with worsening SOB after her steroid treatment concluded. Id. at 764. Petitioner was admitted and
underwent a pulmonary consult with Dr. Stasha Novakovic, who recommended treatment with IV
steroid, an IV antibiotic, and frequent scheduled bronchodilators. Id. at 757. He also advised
Petitioner of the importance of avoiding triggers, optimal medications, and proper inhaler
technique. Id. She was discharged home on July 25, 2015. Pet’r’s Ex. 15 at 5–8.
On August 12, 2015, Petitioner saw Dr. Novakovic in the pulmonary clinic. Pet’r’s Ex. 3
at 636. Dr. Novakovic noted that “though she carrie[d] a diagnosis of bronchiectasis, a CT of the
thorax from July show[ed] barely increased dilatation of the airways with no other parenchymal
abnormalities or complications of bronchiectasis.” Id. Petitioner reported that she felt better since
her discharge but had not returned to her baseline. Id. at 637. The assessment was “newly
diagnosed, and uncontrolled asthma. She ha[d] a minimal component of bronchiectasis but this
[was] not the primary issue.” Id. Petitioner returned to the pulmonary clinic on September 22,
2015, and reported that she “had an exacerbation for the past week. Though she was better that
day, she was still short of breath and had a persistent cough.” Id. at 621. Imaging did “not show
any pulmonary abnormalities.” Id. at 622.
Two days later, on September 24, 2015, Petitioner came into the ED with an asthma attack
that began the previous day and had worsened. Pet’r’s Ex. 3 at 616. She had a consultation with
Dr. Novakovic who noted that “after not having respiratory symptoms for [eight] years, this [was]
her third exacerbation requiring hospitalization in the last three months.” Id. at 607. Dr. Novakovic
further noted that Petitioner’s IgE was high and would qualify her for Xolair. Id. at 608. She
improved with treatment and was discharged home on September 28, 2015. Id. at 539.
Petitioner had an allergy consult on October 21, 2015. Pet’r’s Ex. 3 at 529. She reported a
history of “recent asthma onset since she received her first Prevnar-13 shot on June 15, 2015.” Id.
“Problems started that night with her arm hurting and then she started having problems breathing.”
Id. Petitioner had “[h]igh total IgE” and a skin test positive to dust mites. Id. at 532. She was
diagnosed with recent onset bronchial asthma. Id.
Since September 2015, Petitioner has continued to be seen regularly in the Pulmonary
Clinic at the VA Medical Center. See generally Pet’r’s Exs. 3, 15. She was started on Xolair on
October 26, 2015. Pet’r’s Ex. 3 at 526. A medical record dated April 27, 2018, detailed how
Petitioner “was asymptomatic until she received a Prevnar shot in June 2015. This seems to have
5
triggered her asthmatic symptoms.” Pet’r’s Ex. 15 at 33. Petitioner reported that she had “mild
intermittent exacerbations, but overall [she was] doing much better than before.” Id. Her Xolair
dosage had been decreased from biweekly to monthly since January 2015, and she used a rescue
inhaler about three times per day. Id.
B. Lay Witnesses
1. Petitioner’s Affidavit & Fact Testimony
Petitioner submitted an affidavit dated September 25, 2017. Pet’r’s Ex. 1. She stated that
prior to her June 15, 2015 Prevnar 13 vaccine, she “did not have any asthmatic symptoms.” Id. at
¶ 4. Petitioner acknowledged “a respiratory issue diagnosed as bronchiectasis without exacerbation
that resolved by approximately October 2007.” Id. She noted that her diagnosis was reclassified
from active to nonactive. Id.
The affidavit described how shortly after her vaccination, that same day, Petitioner
“developed a rash and itching.” Pet’r’s Ex. 1 at ¶ 5. Her additional symptoms including coughing,
wheezing, and breathing difficulties started the next day. Id. Petitioner provided a chronology of
her symptoms and treatment consistent with her medical record post vaccination. See id. at ¶¶ 2–
6. She noted that any “[c]itations to the medical records are from [her] attorneys’ review of the
medical records. Many of the dates referred to are based on those records.” Id. at ¶ 3.
Petitioner testified at the hearing on October 10, 2024. Tr. 12–32. She explained that prior
to 2007, her medical history included diabetes, neuropathy, bronchiectasis, and pulmonary
hypertension. Tr. 14. She also noted her chronic back pain and history of GERD. Tr. 15. Despite
Petitioner’s history, she asserted that from December 19, 2008, through the time of her Prevnar 13
vaccine, she never had a problem that necessitated the use of her inhaler. Tr. 19–20. Petitioner
stated that she kept the prescription filled, although she “never had a problem.” Tr. 19. After the
vaccination, Petitioner detailed how she developed what she characterized as severe asthma. Tr.
23–28. She acknowledged that she “wasn’t perfectly healthy, but the asthma did a job on [her]. Tr.
28. She noted that at the time of her testimony that she was having breathing difficulties due to the
weather. Tr. 28. She also described the inability to breathe when encountering lingering second-
hand smoke residue, cleaning agents, and certain perfumes and deodorants. Tr. 26–27. Before her
vaccination, Petitioner stated that “was a lot happier, [] and doing things before [she] got asthma.”
Tr. 28.
2. Andres Delgado, Sr.’s Declaration & Fact Testimony
Mr. Delgado, Sr., Petitioner’s husband, submitted a declaration on May 23, 2022. Pet’r’s
Ex. 56. He noted that the “[c]itations to the medical records are from [his] wife’s attorney’s review
of the medical records.” Id. at ¶ 4. Mr. Delgado, Sr., described how for several years pre
vaccination his wife “did not have any noticeable asthmatic symptoms or respiratory problems.”
Id. at ¶ 5. Less than an hour and a half post vaccination, on June 15, 2015, Petitioner complained
to him of itching at the injection site that began immediately after the shot. Id. at ¶ 7. The location
was also red and welting. Id. He noted that “[w]ithin approximately an hour, she started coughing.
Id. Mr. Delgado, Sr., continued that “the following day, [Petitioner] did not improve and she was
6
wheezing along with coughing.” Id. at ¶ 8. He ultimately took her to the ED after four days of her
symptoms worsening, on June 19, 2015. Id. at ¶ 12. He described her as “wheezing heavily, had
more trouble breathing[,] and even had trouble speaking.” Id.
Petitioner’s husband also testified at the entitlement hearing. Tr. 33–50. He stated that he
was unaware of any occasions that Petitioner saw a health care provider for any breathing issues
from 2010 up to her Prevnar 13 vaccination. Tr. 38. He added that there were no environmental
changes during that time, nor did she develop any allergy symptoms, including sneezing or runny
eyes. Tr. 39. Mr. Delgado, Sr., briefly described the days immediately following Petitioner’s
vaccination, and his account was consistent with the medical records and Petitioner’s testimony.
He testified that currently, Petitioner still has breathing issues, and she has difficulty around
chemicals that did not affect her pre vaccination. Tr. 43–44. On cross examination, Mr. Delgado,
Sr., explained that in 2015, Petitioner’s daughter, Ms. Delgado lived with them, and she was a
smoker. Tr. 46. He explained that she only smoked outside, but that she would come into the home
wearing clothes that were exposed to her smoking. Id.
3. Maria Delgado’s Declaration
Maria Delgado is the adult daughter of Petitioner, and she provided a declaration dated
May 23, 2022. Pet’r’s Ex. 57. Ms. Delgado remembered that Petitioner complained of arm pain
after her vaccination, and later that evening, Petitioner “thought she was having a reaction to the
vaccination.” Id. at ¶ 5. Ms. Delgado noted that her mother’s health changed after her vaccine. Id.
at ¶ 6. She described how, “[s]ince that time, she has had some trouble breathing and asthma.” Id.
Prior to her mother’s vaccination, Ms. Delgado “was not aware that [Petitioner] had asthma or had
trouble breathing.” Id. at ¶ 7.
III. Experts
A. Expert Qualifications
1. Petitioner’s Expert, Hermes J. Garban, M.D., Ph.D.
Dr. Garban is a biomedical scientist. Tr. 130. He received his M.D. from the Central
University of Venezuela and his Ph.D. from the Department of Microbiology, Immunology and
Molecular Genetics at the University of California, Los Angeles. Pet’r’s Ex. 4 at 2. His “fields of
expertise are in molecular immunology, immunotherapy and vaccine development,
molecular/medical pharmacology.” Id. He currently consults and advises companies and
institutions on scientific and clinical direction. Pet’r’s Ex. 67 at 1; Tr. 135–36.
2. Petitioner’s Expert, Stasha B. Novakovic, M.D.
Dr. Novakovic is board certified in internal medicine and pulmonary and critical care.
Pet’r’s Ex. 19 at 1. He received his M.D. from St. George’s University School of Medicine and
subsequently completed a fellowship in pulmonary critical care at Jackson Memorial University.
Pet’r’s Ex. 68 at 1; Tr. 52–53. He is currently a full-time pulmonary and critical care physician at
the Miami VA Medical Center. Tr. 54. Dr. Novakovic was Petitioner’s treating clinician. Tr. 52.
7
3. Respondent’s Expert, Emil J. Bardana, Jr., M.D.6
Dr. Bardana is board certified in allergy and immunology. Resp’t’s Ex. B at 3. He received
his M.D. from McGill University Faculty of Medicine and subsequently completed an internship
at University of California Medical Center and an internal medicine residency at Oregon Health
Sciences University. Id. at 1. He retired from active practice in 2014 and is currently a Professor
Emeritus at Oregon Health Sciences University. Id. at 2. He has numerous publications in the field
of allergy and immunology. See id. at 21–40.
4. Respondent’s Expert, Derek E. Byers, M.D., Ph.D.
Dr. Byers is a board-certified pulmonary and critical care physician. Resp’t’s Ex. F at 1.
He received his M.D. from University of Texas Southwestern Medical School and his Ph.D. in
immunology from University of Texas Southwestern Graduate School. Resp’t’s Ex. G at 1. He is
currently a professor of medicine at Washington University and a practicing physician. Tr. 219.
He specializes in lung transplantation. Id. His research focuses on cellular immunology and T-cell
reactions. Tr. 220.
B. Expert Reports and Testimony
1. Petitioner’s Expert, Dr. Garban
Dr. Garban summarized Petitioner’s medical record pre and post vaccination, along with
her declaration, and opined that “[b]ased on the provided [information], there is significant
evidence to support the medical theory of vaccine-triggered allergic sensitization leading to the
onset of severe asthma.” Pet’r’s Ex. 4 at 9. He then provided background information on Prevnar
13 and characterized asthma as complex, multifactorial, and heterogeneous. Id. at 10. Dr. Garban
explained that asthma is a common, chronic, non-communicable disease with variable respiratory
symptoms and air flow limitations among patients. Id. The type and intensity of airway
inflammation is also heterogenic in presentation. Id. Referring to Petitioner’s status asthmaticus
diagnosis, Dr. Garban quoted Papiris et al.7 to explain that this diagnosis “relates severity to
outcome and has been used to define a severe asthmatic exacerbation that does not respond to
and/or perilously delays the repetitive or continuous administration of short-acting inhaled β2-
adrenergic receptor agonists (SABA) in the emergency setting.” Id. (citing Pet’r’s Ex. 8 at 1). The
article noted that the clinical presentation can include “episodes of increased breathlessness,
cough, wheezing, chest tightness[,] or some combination of these symptoms.” Pet’r’s Ex. 8 at 3.
Development may be abrupt or progressive, and exacerbations “are always related to decreases in
expiratory (and in severe cases also in inspiratory) airflows that should be quantified objectively
by lung function measurements.” Id. Cases of severe asthma are life-threatening, and progression
can occur over minutes and hours or days and weeks. Id. The authors cautioned that a severe
exacerbation may occur during the lifetime of any asthmatic person. Id. Furthermore,
“[o]ccasionally, acute severe asthma may present as a new problem in a patient who is unaware of
his or her asthma, and diagnosis needs to be established in the [ED].” Id.
6
Dr. Bardana did not testify at the hearing.
7
Spyros A. Papiris et al., Acute Severe Asthma, 69 DRUGS 2363 (2009).
8
The Papi et al.8 seminar paper sought to “provide a clinically focused overview of asthma,
including epidemiology, pathophysiology, clinical diagnosis, asthma phenotypes, severe asthma,
acute exacerbations, and clinical management of disease.” Pet’r’s Ex. 9 at 1. The authors noted
that “[e]sinophilic high type 2 airway inflammation is present in around 50% of adults with
asthma.” Id. at 2. Where there is inflammation, Dr. Garban explained that “airway edema [consists
of] cellular infiltration by eosinophils (and in some cases neutrophils), activated CD4+ T
lymphocytes and mast cells, and intra-luminal mucous plugs composed of mucin glycoproteins,
plasma proteins, epithelial and inflammatory cells, and cellular debris.” Pet’r’s Ex. 4 at 10. Dr.
Garban further explained that “allergic sensitization and consequent stimulation by dendritic cells
adaptive T helper 2 (Th2) cells produce interleukin[s . . .]. IL-4 drives B-cell isotype switching
and IgE synthesis, which binds to mast cell high-affinity IgE receptors, leading to mast cell
activation.” Id.
The Papi et al. paper also discussed non-eosinophilic asthma and described a “neutrophil-
predominant [version of the] disease with release of cytokines from [T helper cells], lymphoid
cells, with activation of macrophages and release of neutrophil chemokines.” Pet’r’s Ex. 9 at 2.
The authors noted, “with bronchiectasis as a common comorbidity of severe asthma in adults, a
neutrophilic response could reflect bacterial colonisation or effects of corticosteroids on promotion
of neutrophil survival and suppression of type 2 immunity, leading to the upregulation of type 1
or type 17 immunity.” Id. at 2. Dr. Garban addressed Petitioner’s bronchiectasis diagnosis,
describing it as a long-term lung condition characterized by wider than normal airways. Pet’r’s Ex.
4 at 11. This disease “clinically may be associated with symptoms of chronic cough and
expectoration, as well as a tendency to infections.” Id. at 11. The accompanying airway obstruction
“contribute[s] to obstructive airflow limitation, and accordingly [bronchiectasis] is also a
differential diagnosis to asthma.” Id. Therefore, Dr. Garban explained, “bronchiectasis is
associated in high co-morbidity with severe asthma and should be consider as part of the
differential diagnosis. However, both conditions on illnesses differ significantly in their
pathophysiology and etiology.” Id.
Dr. Garban also explained that Prevnar 13 includes aluminum phosphate, an adjuvant that
“enhance[es] uptake by antigen presenting cells for presentation of the protein component to CD4+
T helper cells and the tendency to induce IgE-mediated immune responses.” Pet’r’s Ex. 4 at 10.
He reasoned that Petitioner’s positive response to omalizumab, an anti-IgE monoclonal antibody,
“suggested a strong IgE connection between her allergic sensitization and her asthma condition,”
triggered by her Prevnar 13 vaccine. Id.
Dr. Garban opined that Petitioner’s sensitization began as a type I allergy “characterized
by specific IgE, a typical Th2 skewing associated with IL-4, IL-13 cytokines, sometimes
accompanied by eosinophilic inflammation.” Pet’r’s Ex. 4 at 11. He highlighted the presence of
aluminum phosphate and the “[u]ndesired properties of aluminum adjuvants [that] comprise acute
and chronic inflammation at the injection site, its Th2 immune stimulatory capacity and potential
allergenic outcome.” Id. Although he did not identify an appropriate temporal relationship, Dr.
Garban asserted that Petitioner’s “allergic sensitization leading to the onset of severe asthma []
appeared to be within a medically accepted time frame to infer causation.” Id. at 12.
8
Alberto Papi et al., Asthma, 391 LANCET 783 (2018).
9
A supplemental expert report dated December 20, 2018, clarified Dr. Garban’s
characterization of Petitioner’s reaction as a vaccine-mediated allergic sensitization and not an
IgE-mediated hypersensitivity. Pet’r’s Ex. 16. The Galli et al.9 article provided the following
relevant definitions:
1. Allergy- An abnormal adaptive immune response directed against
non-infectious environmental substances (allergens), including non-
infectious components of certain infectious organisms.
2. Allergen- Type I: any non-infectious environmental substance that
can induce IgE production (thereby ‘sensitizing’ the subject) so that
later re-exposure to that substance induces an allergic reaction. Type
II: a non-infectious environmental substance that can induce an
adaptive immune response associated with local inflammation but is
thought to occur independently of IgE.
3. Allergic inflammation- The inflammation produced in sensitized
subjects after exposure to a specific allergen(s). A single allergen
exposure produces an acute reaction, which is known as an early-phase
reaction or a type I immediate hypersensitivity reaction. In many
subjects, this is followed by a late phase reaction.
i. Early-phase reaction- An IgE-mediated type I immediate
hypersensitivity reaction that can occur within minutes of
allergen exposure. *Reactions can be localized (for example,
acute asthma attacks).
ii. Late-phase reaction- A reaction that typically develops after
2–6 h[ours] and peaks 6–9 h[ours] after allergen exposure. It is
usually preceded by a clinically evident early-phase reaction
and fully resolves in 1–2 days.
4. Chronic allergic inflammation- Persistent inflammation induced by
prolonged or repetitive exposure to specific allergens, typically
characterized not only by the presence of large numbers of innate and
adaptive immune cells (in the form of leukocytes) at the affected site
but also by substantial changes in the extracellular matrix and
alterations in the number, phenotype and function of structural cells in
the affected tissues.
Pet’r’s Ex. 62 at 2.
Dr. Garban asserted that unlike a hypersensitivity, which manifests after re-exposure to an
initial sensitizing agent, the mechanism at play here “involved an initial adjuvant-mediated
immunoreactivity–triggered by the aluminum phosphate contained in the [Prevnar 13]–for primary
immunization and priming (sensitizing) the immune system to further responses.” Pet’r’s Ex. 16
at 2. Petitioner’s reaction hours following her vaccination, instead of immediately thereafter,
“suggests an inflammatory-allergic-reaction following [Prevnar 13] vaccination.” Id. “IgE-
mediated sensitization, which is the propensity to develop IgE antibodies against common
9
Stephen J. Galli et al., The Development of Allergic Inflammation, 454 NATURE 445 (2008).
10
environmental allergens, is associated with a lymphocyte [Th2] skewed immune response and a
high risk of allergic respiratory disease.” Id. Dr. Garban asserted that “IgE sensitization was
associated with a higher risk of asthma.” Id.
The Galli et al. article identified many factors that “affect the likelihood of developing
clinically significant sensitization: host genotype, type of allergen, allergen concentration in the
environment and [presences of enhancing agents], [and] the pattern of contact of the immune
system with allergens.” Pet’r’s Ex. 62 at 4. In addition to defining key terms, the authors further
explained the differences between the types of allergic inflammation. Id. at 5. Early phase or type
I immediate hypersensitivity reactions “mainly reflect the secretion of mediators by mast cells at
the affected site.” Id. The mast cells in susceptible individuals “already have allergen-specific IgE
bound to their surface high-affinity IgE receptors.” Id. Galli et al. continued that this preformed
mediator release “contributes to the acute signs and symptoms,” and can include “contraction of
bronchial smooth muscle (producing airflow obstruction and wheezing), and increased secretion
of mucus (exacerbating airflow obstruction in the lower airways and producing a runny nose).” Id.
The authors next explained that late-phase reactions occur when “mast cells responding to
IgE and allergen also release a broad range of newly synthesized cytokines, chemokines and
growth factors,” that “are released more slowly than the preformed mediators.” Pet’r’s Ex. 62 at
5. They acknowledged that “[i]t is not understood why [this does] not develop in all sensitized
subjects,” and noted that when it does occur, “there may be no clear clinical demarcation between
the end of the early phase and the onset of the late phase.” Id. at 7. In asthma patients, the late
phase reaction is found in the lower airways and involve Th cells, eosinophils and monocytes. Id.
Lastly, the authors explained how continuous or repetitive allergen exposure leads to persistent
inflammation, and “changes in the structural cells at the affected sites” to cause chronic allergic
inflammation. Id. There is no clear understanding of this process, but the authors noted this process
occurs in chronic asthma patients. Id.
The complex interactions between affected airway epithelial cells and the
underlying mesenchymal cells, which together are known as the ‘epithelial–
mesenchymal trophic unit’ and are thought to regulate the tissue remodeling
characteristic of chronic allergic inflammation of the airways, have been likened to
those at a persistent wound. In patients with asthma, mast cells can appear in
increased numbers in the smooth muscle of the airway, placing this potent source
of mediators that can influence smooth muscle function in intimate proximity to
this crucial target-cell population. This may contribute to the development of ‘non-
specific airway hyperreactivity’ to agonists such as histamine, cys-LTs and
methacholine, which is a hallmark of asthma.
Id. at 8. The authors identified respiratory viruses including, rhinoviruses, influenza virus,
and respiratory syncytial virus as common infections which “can produce a marked
exacerbation of the signs and symptoms of asthma.” Id. Furthermore, “[t]he increased
levels of IgE observed in many allergic subjects can drive another amplification
mechanism in allergic disorders.” Id. at 8.
11
Dr. Garban also cited the Johansson et al.10 article that explained revisions to the
nomenclature re: allergic and allergy-like reaction proposed by the World Allergy Organization
(“WAO”) in 2003. Pet’r’s Ex. 16 at 2 (citing Pet’r’s Ex. 17). The article provided definitions for:
(1) hypersensitivity- “objectively reproducible symptoms or signs initiated by exposure to a
defined stimulus at a dose tolerated by normal persons,” (2) allergy- “a hypersensitivity reaction
initiated by specific immunologic mechanisms,” and (3) atopy- “a personal and/or familial
tendency, usually in childhood or adolescence, to become sensitized and produce IgE antibodies
in response to ordinary exposures to allergens.” Id.
According to the WAO, generally an allergy is not defined by increased IgE levels;
although, a symptomatic inflammatory reaction that is IgE initiated may be dominated by allergen-
specific monocytes. Pet’r’s Ex. 17 at 2. “Asthma resulting from immunological reactions should
be called allergic asthma.” Id. A second article filed by Dr. Garban noted that a “higher risk of
asthma associated with IgE sensitization is well known,” but the authors also suggested that
“reverse causation, i.e. infection/airway disease having an influence on IgE sensitization status,”
could be occurring. Pet’r’s Ex. 18 at 9.11 “[I]t is possible that, in persons with lower chronic airway
disease, IgE sensitization does confer an increased risk of hospital admission due to exacerbation
of disease.” Id.
Dr. Garban’s second supplemental report clarified that his theory is applicable to Petitioner
to explain causation-in-fact, but he added that even “assuming [Petitioner] had controlled asthma,
the evidence that the vaccine substantially aggravated her asthma turning it into a chronic condition
of severe asthma is compelling.” Pet’r’s Ex. 37 at 2. A third supplemental report re-presented
several arguments previously made and reiterated the significance of Petitioner’s extreme
exacerbation of symptoms following her vaccination. See Pet’r’s Ex. 47. Dr. Garban also noted
that Petitioner “did not have hypereosinophilia at any point in her life and she did not have elevated
IgE until after hospitalized for severe asthma in 2015.” Id. at 4. In a short follow-up report, Dr.
Garban narrowed his biological mechanism to a vaccine-caused aggravation of Petitioner’s (pre-
existing and stable) asthmatic condition. Pet’r’s Ex. 55 at 3. He noted that his theory is illustrated
by Petitioner’s vaccination to symptom temporality and “[c]linical evidence including positive
therapeutic response.” Id. Lastly, Dr. Garban advocated for “examin[ing Petitioner’s] case in its
singularity and not dilute it on a series of arguments and discussions pertaining to a generalization
of the potential severe effects of a vaccine.” Id.
A final supplement report filed by Dr. Garban was focused on “providing a single, cohesive
theory to explain and address solely Althen prong one regarding how the Prevnar-13 can cause an
allergic inflammatory reaction and aggravation of Petitioner’s asthmatic stable condition.” Pet’r’s
Ex. 58 at 1. He summarized his hypothesis with Figurine 1, reproduced below:
10
S.G.O. Johansson et al., Revised Nomenclature for Allery for Global Use: Report of the Nomenclature
Review Committee of the world Allergy Organization, October 2003, 113 J. Allergy Clinical Immunology
832 (2004).
11
Tea Skaaby et al., IgE Sensitization to Inhalant Allergens and the Risk of Airway Infection and Disease:
A Population-Based Study, 12 PLOS ONE (2017).
12
Id. at 4.
Dr. Garban continued to explain the specifics of Petitioner’s injury during his testimony.
See Tr. 130–210. He asserted that Petitioner suffered a Type 1 hypersensitive reaction “in the mild
spectrum.” Tr. 158. When asked if Petitioner’s reaction would qualify as anaphylaxis, Dr. Garban
stated that he “wouldn’t call anaphylaxis what she had,” but later added, “when she increased in
the events that took her to a respiratory component, it could be an anaphylactic reaction that is not
taken to the extreme side of very severe. It could be a mild anaphylaxis.” Tr. 158–59. According
to Dr. Garban, Petitioner “initially had a Type 1 hypersensitivity[, a]nd she manifest[ed], and it
was documented that she started having itching, redness, the warm rash,” and some inflammation.
Tr. 159. Her symptoms “extended to the loss of function not only in the local area,” known as an
atopic reaction, but also to other areas, including asthma. Tr. 141. Dr. Garban explained that “acute
or early phase of hypersensitivity, of hypersensitivity reaction happens from seconds, minutes and
can be extended to hours.” Tr. 141. Following this initial allergic inflammatory response, “in the
later hours of development or days of development immediate to the vaccination, you have the
late-phase development, which is the persistent cough that she started manifesting, . . . and also
that hard time breathing.” Tr. 159–60.
Vaccine-associated hypersensitivity reactions “are not uncommon,” according to Dr.
Garban, but he added that “severe hypersensitivity as anaphylaxis, for instance, they are really,
really rare.” Tr. 147. Indeed, “serious acute onset, presumably IgE-mediated or IgG and
complement-mediated anaphylactic or serious delayed onset T-cell-mediated systemic reactions
are considered extremely rare.” Tr. 148. Dr. Garban asserted that any vaccine component “[f]rom
the antigen that has been used to generate a specific target, also to the adjuvant and also to the
stabilizing agent, the hard part of that,” can cause a hypersensitivity reaction. Tr. 149. He
specifically noted “the material that is the CRM 197, the aluminum phosphate or aluminum
compounds in general and also the polysorbate [80].” Tr. 150.
13
The aluminum phosphate was of particular concern for Dr. Garban, because of its role “to
not only enhance the immune response in terms of the vaccine, but also it serves as a depot to
maintain a localized content of the vaccine in the site of injection in order to favor the immune
response.” Tr. 153. He asserted that there is new research on “the use of aluminum compounds in
order to redirect the immune response toward a Th2-type of response that will elicit the production
of cytokines,” including IgE. Id. Dr. Garban continued, asserting that “aluminum phosphate will
somehow bring the immune cells.” Tr. 154. Some of those cells are there to generate cytokines
that will switch IgG to IgE and lead to “induction of B-cells that are the ones that produce the
immunoglobulins to the production of IgE.” Id. This process is articulated in the HogenEsch12
paper. See Pet’r’s Ex. 7. HogenEsch asserted that “[a]luminum compounds can further enhance
the immune response by direct or indirect stimulation of dendritic cells, activation of complement
and by inducing the release of chemokines.” Pet’r’s Ex. 7 at 1. The depot effect, initially
“suggested that the slow release of alum-precipitated antigens from the injection site resulted in
prolonged exposure of the immune system to vaccine antigens” and it was thought that in the case
of alum-precipitated diphtheria toxoid, “some antigen is retain[ed] at the injection site for at least
[seven] weeks.” Id. at 2. HogenEsch noted that later challenges to this theory “suggest that
sustained release of antigen from a depot site over days or weeks is unlikely to contribute to the
adjuvant effect of aluminum compounds.” Id. Although Dr. Garban noted that CRM 197,
polysorbate 80, and aluminum phosphate can work together to cause an immune-mediated
response, in Petitioner’s case, a hypersensitivity reaction “can turn into a[n] entirely different
process that is modulating the immune system in order to acquire a different reactivity to a different
component that w[as] not present even in the vaccine but to other environmental triggers and
substance.” Tr. 156.
The Verstraelen et al.13 paper described “the mechanism and cell types involved in allergic
asthma.” Pet’r’s Ex. 25 at 1. The authors described the disease as clinical and “characterized by
airway obstruction, airway inflammation and airway hyperresponsiveness to a variety of stimuli.”
Id. The process begins with “[a]irway hyperresponsiveness and bronchial inflammation
[following] the inhalation of an antigen.” Id. at 3. The article explained how the allergen is
intercepted by antigen presenting cells that activate helper T cells and lead to lymphocyte
activation, including B cells. Id. “Allergic asthma is characterized by increased IgE production by
B cells.” Id. The authors asserted that the link between IgE and airway hyperresponsiveness is
mast cells. Id. They explained that “[i]n the lungs, mast cells are found in bronchial airway
connective tissues and in peripheral intra-alveolar spaces . . . and their numbers increase after
allergen exposure.” Id. Asthma patients have an increased number of localized mast cells “within
the bronchial smooth muscle bundles and the bronchial epithelium, and infiltrate in the airway
mucous glands.” Id. Once re-exposed to the allergen, “cross-linking of antigen by mast cell IgE
antibodies” on the receptor cell occurs. Id. “This cross-linking has been well documented to trigger
activation of signaling cascades and causes mast cell degranulation and synthesis of
proinflammatory molecules.” Id. at 3–4. “Mediators produced by mast cells are categorized into
preformed mediators, . . . [and t]hey cause the symptoms of immediate-type hypersensitivity.” Id.
at 4.
12
Harm HogenEsch, Mechanisms of Stimulation of the Immune Response by Aluminum Adjuvants, 20
VACCINE 534 (2002).
13
S. Verstraelen et al., Cell Types Involved in Allergic Asthma and Their Use in In Vitro Models to Assess
Respiratory Sensitization, 22 TOXICOLOGY IN VITRO 1419 (2008).
14
Once an early-phase asthmatic reaction occurs, “a more severe and prolonged late-phase
asthmatic reaction” may follow. Pet’r’s Ex. 25 at 4. The article then explained how a
hypersensitivity reaction can evolve into a chronic condition.
In general, mast cell-derived mediators induce airway constriction, increase
vascular permeability, enhance [airway hyperresponsiveness], induce mucus
secretion, and promote the recruitment of inflammatory cells into the airways after
several hours of allergen challenge, especially eosinophils, but also T cells,
macrophages, basophils, neutrophils, and structural cells like epithelial cells,
fibroblasts, endothelial cells, and [airway smooth muscle] cells. These
inflammatory cells can produce a vast array of inflammatory mediators, namely
chemokines, cytokines and [leukotrienes], that act either directly on the airway or
indirectly through neural mechanisms, promoting the chronic characteristic of the
airway inflammation after repeated allergen exposure. As a result of this chronic
inflammation, airway tissue is continuously being injured and healed, leading to
structural changes of the airways that may account for the decline in airway
function seen in patients over the years. These structural changes are collectively
referred to as airway remodeling.
Id. (internal citations omitted).
Dr. Garban described this secondary process as the adaptive Th2 response “that will
produce immune mediators that will redirect the cells of the immune system to produce now
immunoglobulin E. And this [] IgE, starts acting whenever they recognize the triggering substance
that, again, [he] must emphasize, not necessarily are the same component of the vaccine.” Tr. 161.
Because the immune system is now sensitized according to Dr. Garban, “once it gets engaged,
then it starts binding to these cells called mast cells through the high affinity receptor for IgE and
so in that case trigger an allergic response.” Id. This activity initiates “that bronchoreactivity, the
bronchial reactivity that is a hallmark of the asthmatic response.” Id. Dr. Garban was asked whether
this Th2 cell activation occurred in the immediate or late phase of Petitioner’s immune system
response. Tr. 165. He stated, “what you have is probably on the late/early phase start,” and
continued, that “definitely in the first hours you have that window of engaging or engagement of
a Th2 type of response. And this can last for days.” Id. Without the vaccine, this IgE sensitivity
would not have occurred. Id. Dr. Garban asserted that this hyperreactivity can cause an acquired
sensitivity to new environmental triggers and “an allergic response, and in this case, an asthmatic
atopic response.” Tr. 162. He further argued that Petitioner’s clinical management provided
evidence of IgE mediation, “because then when she was treated with Xolair, that even a specific
antibody that blocks that IgE, the binding of IgE to the mast cell, then the disease was a fairly
controlled.” Tr. 163.
Outside the context of vaccines, Dr. Garban testified about “examples in the scientific
literature of aluminum salts inducing sensitization to substances that might not normally be
considered as antigens.” Tr. 163. This “possible indirect adjuvanticity” is also related to food
allergies. Id. Dr. Garban suggested that a sensitivity reaction may have also been influenced by
exposure to previous adjuvants or vaccine components. Tr. 166–67. Specifically, “in the case of
15
[Petitioner] somehow the presence of these adjuvants or components of vaccines of previous
vaccine, might result or more likely than not resulted into that sensitization.” Tr. 167. The period
of four days between Petitioner’s vaccination and her relevant symptoms “leading to the drastic
aggravation of asthma symptoms suggested the engagement of a reactive Type 2 Th2 IgE-mediated
inflammatory response responsible for the worsening of the respiratory symptoms and therefore
setting the stage for a deteriorating chronic asthmatic condition.” Tr. 169.
Dr. Garban summarized his causation theory as applied to Petitioner’s case. He stated that
Prevnar 13 vaccine components triggered an “allergic Type 1 hypersensitivity immune response.”
Tr. 170. During that response, Petitioner experienced “inflammatory signs, redness, swelling, heat,
et cetera.” Id. Dr. Garban asserted that Petitioner’s reaction to her vaccination developed into “a
more severe or a more elaborated allergic response” or atopy. Tr. 170–71. This included “another
set of immune reactions that were happening there surrounding this event that promote an allergic
sensitization . . . in the sight of the injection, but also it starts being more systemic.” Tr. 171. Dr.
Garban also described this process as a “chronic type of reactivity where then the deterioration of
function or loss of function will -- of the immune system start having this reactivity to other kind
of antigen.” Id. There were no viral or bacterial infections identified in Petitioner’s medical history
that may have played a role in her symptoms. Tr. 172. Dr. Garban did note that Petitioner’s pre-
existing conditions and a “contributing comorbidity [] might [have] took that route that was
triggered by the vaccine.” Id. However, for Dr. Garban, Petitioner’s “period of seven years without
any respiratory event and after the vaccination, you start having cardinal signs and symptoms that
start happening that’s suggestions of an allergic reaction to the vaccination.” Tr. 172–73. He
described that reaction time as immediate, stating, “it’s seconds to minutes that happen that kind
of reactivity.” Tr. 173.
Dr. Garban described the two stages of Type 1 hypersensitivity: immediate reactions and
late-phase reaction. Tr. 174. The former, initial phase is “a sudden response within minutes of
exposure to the allergen, while the late phase may develop [four] to 12 hours post early phase
reaction and can last for up to 24 to 73 hours.” Tr. 174. In Petitioner’s case, “you have a clear Type
1 hypersensitivity exhibiting very beautiful distinction between the early and late phases of both
and also the evolution into a possible or more likely than not circle where chronicity will establish
then further sensitization.” Tr. 174–75. Petitioner’s cough and asthma exacerbation also provide
clear evidence of vaccine causation, according to the Haber et al.,14 article filed by Dr. Garban.
See Pet’r’s Ex 50 at 4. This article documented “adverse events reports following [Prevnar 13] in
adults aged ≥19 years reported to the [VAERS] from June 2012 to December 2015.” Id. at 1. There
was one account each of cough, asthma exacerbations, and bronchospasm out of 138 medical
conditions in non-death serious reports in persons aged ≥ 65 years following Prevnar 13 in
VAERS. Id. at 4. The authors noted “the limitations of VAERS, which may include
underreporting, varying quality of reports, and the lack of an unvaccinated comparison group.” Id.
at 5.
In response to my questioning, Dr. Garban asserted that Petitioner’s status asthmaticus
diagnosis from June 19, 2015, was the result of her increased sensitivity following her vaccination
14
Penina Haber et al., Post-Licensure Surveillance of 13-Valent Pneumococcal Conjugate Vaccine
(PCV13) in Adults Aged ≥19 Years Old in the United States, Vaccine Adverse Event Reporting System
(VAERS), June 1, 2012–December 31, 2015, 34 VACCINE 6330 (2016).
16
and any subsequent asthmatic event would also relate back to her vaccination. Tr. 192. He clarified
that any post-vaccination allergic reaction that Petitioner suffers affects the “reactivity of her
airway” and is consistent with her June 19, 2015 presentation and could be rightly attributed to her
vaccine. Tr. 208.
2. Petitioner’s Expert, Dr. Novakovic
Petitioner’s treater, Dr. Novakovic provided multiple expert reports and testimony in
support of her claim. In his first report, Dr. Novakovic opined that “[t]he temporal relationship
between the administration of the vaccine and the drastic worsening of [Petitioner’s] asthma
supports the conclusion that these two events are related.” Pet’r’s Ex. 19 at 3. He described how
she first experienced symptoms of an adverse reaction to the vaccine “within an hour,” and as her
breathing worsened, “she had no choice but to seek help in the [ED].” Id. Dr. Novakovic noted
that “there were no significant events affecting [Petitioner’s] medical history or her respiratory
system in the weeks and months prior to June 2015.” Id. He specified that pre vaccination, there
were no new respiratory symptoms; no “new environmental triggers, allergens, noxious fumes or
inhalational toxins;” and no travel or address change. Id. “Following the vaccination, she became
[Dr. Novakovic’s] sickest asthma patient for a period of time and continues to struggle with her
disease more than four years later.” Id. Dr. Novakovic noted Petitioner’s improvement but stated
that she still requires injections and intermittent steroids. Id. He opined that “there is no medical
basis to attribute her sudden decompensation in respiratory status to anything other than the
vaccination.” Id. Dr. Novakovic acknowledged “[e]ven though the facts of [Petitioner’s] case
strongly suggest a causative relationship, there have not been very many reported cases of asthma
as a direct result of a pneumonia vaccine.” Id. at 4.
Dr. Novakovic categorized Petitioner’s urticaria, cough, wheezing and SOB as indicative
of a type I hypersensitivity reaction to the vaccine. Pet’r’s Ex. 14 at 4. He asserted that Petitioner’s
respiratory symptoms and ensuing “hypersensitivity reactions with manifestations centered in the
lung” have been reported following exposure to injected allergens. Id. These reactions are
generally short lived; however, Petitioner’s asthma symptoms continue years later. Id. That is
because “[t]he specific mediators generated by the [P]revnar vaccine, in contrast to traditional
pneumococcal vaccines, turn out to be vital in the allergic response typical of asthma.” Id. The
conjugated nature of Prevnar 13 “elicit[s] a stronger immune response and activate[s] a cascade
that is dependent on T-cells, in contrast to the T-independent responses of unconjugated vaccines.”
Id. at 5. T cells in turn drive production of antibodies, eventually IgE. Id. at 4. Dr. Novakovic
stated that “[i]t is widely believed that Th2 cells play a pivotal role in the pathogenesis of asthma.
These cells influence antibody production towards the generation of IgE.” Id. at 4–5. Dr.
Novakovic asserted that because of asthma’s association with an IgE-reaction in almost all cases,
“the sensitization to environmental triggers which is fundamental in asthma is [likewise] an IgE-
driven process.” Id. at 5. Conversely, exposure to allergens such as pet dander or dust mites is not
a risk factor for individuals without IgE antibodies. Id. In lifelong asthmatics, “[t]he consistent
allergic response caused by IgE over time is due to both the long life of IgE-secreting B cells as
well as the stability of mast cells in the soft tissues.” Id.
Dr. Novakovic argued that Petitioner’s elevated IgE levels three months post vaccination
“lends support to the argument that her immune system by that time was altered on a permanent
17
basis, since levels of IgE are generally not abnormally elevated in patients without pathology.”
Pet’r’s Ex. 19 at 5. Her high levels are evidence of over sensitization “to common environmental
triggers, leading to allergic and asthmatic symptoms.” Id. This cycle of 1) sensitization, 2) trigger
or infection, and 3) symptom manifestation that reinforces the sensitization, is “a lifelong process”
in patients like Petitioner. Id.
The Cockcroft15 book chapter on allergens was filed with Dr. Novakovic’s report and cited
to support his assertion that injected allergens can trigger respiratory reactions. See Pet’r’s Ex. 23.
Cockcroft asserted that ingested and injected allergens can trigger an isolated bronchial asthma
that manifests as a type I-mediated hypersensitivity. Id. at 14. He offered that these reactions are
occasionally “centered primarily within the lung.” Id. However, he added that “[it] is likely that
these most often represent systemic allergic reactions in asthmatic individuals who have a
preexisting high level of airway hyperresponsiveness and therefore develop disproportionately
severe bronchospasm.” Id. Cockcroft listed nut/shellfish allergies and insect bites as examples of
ingested and injected allergens, respectively, “as the cause of severe unexplained status
asthmaticus.” Id.
A supplemental report filed by Dr. Novakovic made it clear that he is “willing once again
to accept the assumption that [Petitioner] had asthma back to 2008.” Pet’r’s Ex. 42 at 2. “Rather
than try to disprove that the patient had any evidence of asthmatic respiratory disease prior to that
event, [he] tried to convey the abruptness and the severity of its worsening.” Id. Dr. Novakovic
discounted the opinion of the medical resident that attributed Petitioner’s June 15, 2015 asthmatic
attack to a viral infection. Id. He opined that “infections are generally overdiagnosed as a cause of
exacerbations of asthma” and added that non-infectious triggers are often overlooked. Id. at 3. In
Petitioner’s case, Dr. Novakovic did not identify “typical findings of a respiratory infection that
generally include sick contacts, fever, characteristic bandemia in her bloodwork (excess of white
cells released by the bone marrow usually signifying infection) or radiographic changes.” Id. He
noted the difficulty in proving or disproving a viral infection in the ED but asserted that “if this
was in fact the case, we would have to accept the unlikely happenstance that the infection triggered
her symptoms at the exact same time that the vaccine was administered, in the absence of the
typical clinical manifestations of a virus.” Id.
Dr. Novakovic also included a table listing Petitioner’s eosinophil levels as detailed in her
medical records from September 2, 2003, through February 19, 2020. Pet’r’s Ex. 42 at 7–8. He
noted that Petitioner’s recorded levels were between 140 and 220 from 2003 until March 14, 2008,
and April 5, 2008, when her levels jumped to 960 and 830 respectively. Id. at 7. Petitioner’s levels
went back down to 250 on July 8, 2008, and again remained below 220 (April 14, 2009 reading)
until June 19, 2015, when she reached 400. Id. On July 4 and 19, 2015, Petitioner’s eosinophil
count jumped back up to 900 and 800 respectively. Id. She dropped to 300 on September 22, 2015,
before having one more spike to 900 on September 24, 2015. Id. Petitioner’s levels then fell, and
she consistently tested at 400 in February and May of 2016, 300 through August 1, 2017, and back
down to 200 beginning November 21, 2017, through February 19, 2020. Id. at 7–8. Although her
levels were higher than her baseline in 2008 and again in 2015, during these peak counts,
15
D.W. Cockcroft, Allergens, in ASTHMA: BASIC MECHANISMS AND CLINICAL MANAGEMENT, 507 (3rd
ed. 1998).
18
Petitioner’s test results did not reveal levels that would indicate hypereosinophilia (over 1500) or
even a medically significant elevated eosinophil count. Id. at 4.
In his second supplemental report, Dr. Novakovic reiterated that Petitioner had pre-existing
asthma but stressed that the nature of her condition pre vaccination differed dramatically from her
flare in 2015. See Pet’r’s Ex 49. He noted that from 2008 until 2015, Petitioner’s treatment
consisted of intermittent mometasone use, and she “avoided any exacerbations severe enough to
result in medical visits and trips to the [ED] for about seven years.” Id. at 1. In comparison, from
2015 to 2017, “her asthma was not controlled despite maximal doses of Symbicort, frequent steroid
courses, rescue inhaler use several times daily and monoclonal antibody injections.” Id. He
asserted that “both her condition as well as the medication requirements were so much worse after
June of 2015 that they cannot objectively be compared in any way to anything she experienced
prior.” Id. at 2. Dr. Novakovic conceded that Petitioner’s “medical comorbidities as well as certain
environmental and social triggers [can be] complicating factors in the patient’s asthma.” Id.
However, he argued that Petitioner had these factors prior to her 2015 vaccination and remained
stable. Id. Therefore, they “cannot be blamed for [Petitioner’s] sudden deterioration.” Id.
During his testimony, Dr. Novakovic distinguished Petitioner’s history of bronchiectasis
and pulmonary dysfunction with her post-vaccination asthma. He defined bronchiectasis as dilated
airways, explained pulmonary hypertension, and characterized asthma largely by noting
respiratory symptoms that indicate a “limitation in expiratory air flow.” Tr. 57. Dr. Novakovic
explained that all three conditions “can coexist in the same patient, but they are caused by different
pathophysiological properties.” Tr. 58. Going through Petitioner’s medical records pre
vaccination, Dr. Novakovic stated that Petitioner was diagnosed with a URI and acute bronchitis
in 2007, bronchitis and asthma exacerbation in March of 2008. Tr. 58–60. On April 5, 2008,
Petitioner was diagnosed with hypersensitivity pneumonitis, which Dr. Novakovic defined as “an
allergic disease that is directed towards a very specific allergen and results in a very abnormal
chest imaging.” Tr. 61. He noted the significance of this diagnosis based in part on Petitioner’s
elevated eosinophil count “suggesti[ng] that the patient’s disease process may be related to an
allergy.” Id. Petitioner’s treatment for her conditions included care from a pulmonologist, and her
IgE levels were measured in April of 2009 with normal results. Tr. 63. Based on this test, Dr.
Novakovic determined that Petitioner “may have had Type 2 asthma, but her IgE levels were
normal at the time.” Tr. 64. He explained that her asthma may still be IgE-mediated, “but it sill
means that IgE was not a prominent component of her disease at the time.” Id. Relying on literature
from the Global Initiative for Asthma, Dr. Novakovic asserted that Petitioner’s treatment,
“includ[ing] as-needed inhaled steroids or daily low-dose inhaled steroids,” was successful in
controlling her asthma. Tr. 65. Dr. Novakovic contrasted this treatment regimen with Petitioner’s
course in 2015 of long-acting beta antagonists, which is used to treat severe asthma that is
otherwise uncontrolled. Id.
Dr. Novakovic noted that Petitioner’s IgE levels were elevated in 2015, but he asserted that
“her total serum IgE was also elevated throughout her life because of her continued allergic
response to tree pollen and house dust mites.” Tr. 66. He referred to Petitioner’s history of allergic
rhinitis dating back into childhood and hypereosinophilia in 2008, but Dr. Novakovic
acknowledged testing of IgE levels in 2008, was also within normal limits. Tr. 68. He opined that
Petitioner’s pre-existing respiratory condition was episodic asthmatic symptoms and disagreed
19
with her hypersensitivity pneumonitis diagnosis. Tr. 71. Furthermore, notwithstanding Petitioner’s
episodes, Dr. Novakovic did not believe that Petitioner suffered from asthma from 2007 through
2009. Tr. 72. Regarding Petitioner’s symptoms in 2007, 2008, and 2009, Dr. Novakovic testified
that she “exhibited wheezing, cough and [SOB] prior to 2015, but there was a drastic difference in
the severity of symptoms.” Tr. 75. He described the severity, noting “her requirement for
medication, steroids, [ED] visits, just the escalation of therapy needed just to keep her out of the
hospital as well as the fact that there is a change in the IgE levels prior and after that.” Tr. 85.
Although not an immunologist, Dr. Novakovic highlighted in his education “pulmonary
boards [] represented by asthma, and that component includes the biology, the immunology and
the allergic Type 2 eosinophilic asthma as well.” Tr. 87–88. He presented the theory that a Prevnar
13 component, “most likely, aluminum, but also possible the protein pneumococcal polysaccharide
primed her immune system which then resulted in this severe hypersensitivity reaction which
occurred in June 2015.” Tr. 88. Dr. Novakovic named the reaction an IgE-mediated response and
described it as “a very brisk allergic, rapid type of response to a perceived allergen or a danger
signal by the body.” Id. He relied on the HogenEsch paper to assert that when the body processes
aluminum adjuvant in the Prevnar 13 vaccine, NLRP3, a receptor protein linked to chronic disease,
activates. Tr. 89. Dr. Novakovic testified about “studies suggest[ing] that aluminum adjuvants
induced a differentiation of Th2 cells that drive an eosinophilic inflammatory response and TSH
cells that stimulate antibody production,” and referenced HogenEsch, Batista-Duharte et al.,16 and
Guimaraes et al.17 Tr. 89–92.
Dr. Novakovic asserted that “[a]luminum compounds persist for up to [eight] to 11 years
post vaccination the human body. This fact, combined with repeated exposure, may account for a
hyperactivation of the immune system and subsequent chronic inflammation.” Tr. 92. In
Petitioner’s case, Dr. Novakovic noted four total previous vaccinations “which contained
aluminum in the 11 years preceding her [Prevnar 13] vaccine in June of 2015.” Tr. 93. He
explained that “any one of these vaccines could have primed her immune system to develop IgE
against this compound.” Id.
I asked Dr. Novakovic to clarify his position as it relates to the nature of Petitioner’s
hypersensitivity. He agreed that Petitioner was not anaphylactic; however, asserted that hers was
“not a typical manifestation of anaphylaxis, but . . . that it worked along the same mechanisms.”
Tr. 123. The mechanism, overproduction of IgE due to the introduction of an aluminum adjuvant,
“activates the chronic inflammasome system.” Tr. 125. He noted that he did not “have a definitive
answer because [he has not] seen it explained in the medical literature either.” Id. Dr. Novakovic
also clarified that it was likely Petitioner “had some degree of asthma prior to 2015.” Tr. 127. In
the several years preceding her vaccination, the condition was controlled, and she was
asymptomatic. Tr. 127. He reiterated that the re-emergence of her symptoms, and to that degree of
severity, would not have occurred without her June 15, 2015. Id.
16
Alexander Batista-Duharte et al., Systemic Immunotoxicity Reactions Induced by Adjuvanted Vaccines,
20 INT’L IMMUNOPHARMACOLOGY 170 (2014).
17
Luisa Eca Guimaraes et al., Vaccines, Adjuvants and Autoimmunity, 100 PHARMACOLOGICAL RSCH.
190 (2015).
20
3. Respondent’s Expert, Dr. Bardana
Dr. Bardana began his first submitted expert report with a detailed recount of Petitioner’s
medical record and witness statement. See Resp’t’s Ex. A at 1–26. He then indicated his
disagreement with Petitioner’s theory of the case and progression of her illness, asserting that “Dr.
Garban essentially undervalue[d] from consideration the medical history prior to vaccination on
June 15, 2015.” Id. at 26. Most importantly for Dr. Bardana is the “significant recorded evidence
that [Petitioner] developed adult-onset asthma on the heels of an acute viral bronchitis in
September of 2007.” Id. He added that pre vaccination, Petitioner had “established adult-onset,
intermittent asthma and allergic rhinitis controlled” by an inhaled corticosteroid and a steroid nasal
spray. Id. at 28.
On the day of Petitioner’s vaccine, she experienced a localized reaction, which Dr. Bardana
characterized as a common event that occurs in approximately 10% of recipients. Resp’t’s Ex. A
at 28. He noted that when Petitioner was seen at the ED four days after her vaccination, her
diagnosis was status asthmaticus in the setting of a recent viral URI. Id. He acknowledged that
Petitioner was eventually treated with antibiotics, suggesting that her bronchitis may not have been
viral, as originally believed by her treaters. Id. at 29. Dr. Bardana opined that Petitioner’s
symptoms were more likely due to “a deep seated, possibly resistant, pathogen which had
precipitated severe asthma.” Id. He criticized the use of the phrase of “reactive airways disease”
in Petitioner’s medical records, explaining that this phrase is synonymous with asthma and is
otherwise unhelpful. Id. at 30. “The term is nonspecific and has no clinical meaning. It does not
have a specific ICD code and is not a diagnosis.” Id. Furthermore, Dr. Bardana took issue with the
identification of Petitioner’s obesity as the causal factor. Id. He listed a “variety of other co-morbid
factors which have played a potentially negative role in her asthmatic illness, i.e., prior tobacco
abuse, vitamin D deficiency, allergic rhinitis and allergies to housedust mite and tree pollen,
possible obstructive sleep apnea, GERD, etc.” Id. Alternatively, Dr. Bardana was unable to find
any reports of IgE-mediated reactions, including asthma, that were “ascribed to Prevnar 13 and/or
aluminum hydroxide.” Id. at 33. He countered Dr. Garban’s assertion that Petitioner’s response to
Omalizumab is indicative of an IgE sensitization by noting that Petitioner meets the clinical
requirement for Omalizumab use, namely a (pre-existing) allergy to a perennial allergen. Id.
In a supplemental report, Dr. Bardana reiterated many of his initial opinions. See Resp’t’s
Ex. C. He opined that Petitioner’s medical records revealed that “she was diagnosed with [asthma],
responded to treatment[,] and had confirmatory physical findings.” Id. at 4. Dr. Bardana further
stated that “[t]he apparent lack of continuity of care and perhaps unavailability of records made it
appear her providers were unmindful about her primary condition.” Id. The plethora of diagnoses,
including GERD, asthma, and hypersensitivity pneumonitis, suggested to Dr. Bardana that
Petitioner’s treaters were unable to ascertain the true nature of her condition. Id. He was therefore
unsure why “between 2007 and 2017 there were only two attempts to conduct pulmonary function
studies, neither of which is available.” Id. at 5.
Dr. Bardana agreed with the admitting ED physician’s 2015 diagnosis of status-
asthmaticus in the setting of recent viral URI, despite Petitioner’s assertion at the time that her
21
illness was related to her Prevnar 13 vaccine. Resp’t’s Ex. C at 5. Noting that Dr. Novakovic’s
June 2015 asthma diagnosis based on Petitioner’s “symptoms ([SOB], wheezing, coughing, chest
tightness and difficulty with exertion, her physical exam findings (wheezing, limited air movement
and prolonged expiratory phase) and her appropriate though generally short-lasting response to
aggressive asthma management,” Dr. Bardana identified these same symptoms in medical records
from 2007 through 2009. Id. He then questioned why Dr. Novakovic was hesitant to accept asthma
as a diagnosis during those previous flare ups. Id.
According to Dr. Bardana, Petitioner’s condition is more specifically defined as “Type 2-
like-eosinophilic asthma.” Resp’t’s Ex. C at 7. He explained that this phenotype is more common
in adult-onset asthma patients and usually “require[s] glucocorticosteroids to maintain control.”
Id. He also disputed any evidence of hyperreactivity. Id. Dr. Bardana suggested that because
Petitioner “never had the demonstration of variable expiratory airflow obstruction which is a sine
qua non in verifying the diagnosis of asthma,” her diagnosis is best characterized as presumptive
based on her clinical presentation. Id.
In a brief supplemental follow-up, Dr. Bardana asserted that Petitioner’s treatment regimen
between 2009 and 2015 included “Mometasone (Asmanex) by inhaler on a daily basis with stand-
by Albuterol.” Pet’r’s Ex. D at 2. Dr. Bardana also asserted that Petitioner had not been exposed
to Prevnar 13 prior to her 2015 vaccination; therefore, she could not have been pre-sensitized,
leading to an immediate allergic reaction. Id. Dr. Bardana did not discount Petitioner’s localized
itchy rash with swelling immediately following vaccination at the injection site. Id. He
characterized this as a nonspecific irritant reaction and argued that “[i]t does not signify the
presence of IgE-sensitization.” Id. Further, Petitioner’s cough, wheezing, and SOB that same day
“reflected the later onset of an acute viral infection” which precipitated her asthmatic symptoms
four days later. Id. Dr. Bardana asserted “that [Petitioner’s] total serum IgE was also elevated
throughout her life because of her continued allergic response to tree pollen and housedust mite.”
Id. at 3. Accordingly, there is no medical or scientific evidence that she suffered from sensitization.
Id. at 4.
A third supplemental report continued to explain the nuance of Petitioner’s diagnosis. See
Resp’t’s Ex. E. Dr. Bardana asserted that most often, asthma manifests in childhood, but “[a]fter
40 years of age, most new-onset asthma cases are non-allergic.” Id. at 1. He continued that “[i]n
the older age group, asthma usually begins during or after a[ URI].” Id. at 2. “In 2007 [Petitioner]
suffered an acute onset of asthma attributed to a viral infection which precipitated three [ED] visits
and commitment to chronic controller/reliever medication until the acute symptoms of 2015 which
were also attributed to an acute viral infection.” Id. Dr. Bardana maintained that the association of
symptom onset with Petitioner’s vaccine is “based on a subjective belief” that relies wholly on
chronology. Id. He clarified that Petitioner’s comorbidities compromised her ability to cope with
her viral infection and exacerbated her asthma flare. Id.
To support his contention that Petitioner’s condition was precipitated by an infection, Dr.
Bardana argued that her condition was refined from an initial characterization as a viral URI to
viral bronchitis followed by secondary infection to bacterial bronchitis. Resp’t’s Ex. E at 4.
Knowing that URIs are the most common asthma trigger, Petitioner’s “providers unanimously felt
22
she had an infectious process (viral followed by bacterial) and treated her with aggressive antibiotic
management.” Id.
Dr. Bardana agreed with Dr. Novakovic in that Dr. Bardana improperly used the term
hypereosinophilia. Resp’t’s Ex. E at 5. He clarified that he “should have used the phrase elevated
peripheral blood eosinophils.” Id. He further noted that “eosinophilia is associated with
[Petitioner’s] atopic condition,” and the presence of eosinophils can be suppressed by exogenous
corticosteroids, stress and some types of infections. Id. Dr. Bardana conceded that “neither [he]
nor Dr. Novakovic can make definitive statements regarding [Petitioner’s] total serum IgE,” due
to sparse testing. Id. at 6.
4. Respondent’s Expert, Dr. Byers
In his first written expert report, Dr. Byers asserted that “the central tenet” of Dr. Garban’s
biological mechanism for causation “is that an ‘immediate early reaction’ would require pre-
formed, allergen-specific IgE to be present in [Petitioner’s] skin and airways on June 15, 2015 that
was directed to some putative component in the [Prevnar 13] vaccine.” Resp’t’s Ex. F at 7. Relying
on literature (Nials & Uddin)18 filed by Petitioner, Dr. Byers asserted that acute sensitization
“usually require[s] multiple systemic administrations of the allergen in the presence of adjuvant”
and takes 14 to 21 days. Id. at 7. The Nials and Uddin article defined human asthma as “a chronic
inflammatory disorder of the airways [that] is characterised by airway inflammation, persistent
airways hyperresponsiveness (AHR) and intermittent, reversible airways obstruction.” Pet’r’s Ex.
13 at 1. Noting that the underlying cellular and biochemical processes underlying chronic asthma
are poorly understood, the authors looked to mouse models in lieu of human models with
substantial ethical considerations. Id. Ultimately, they found that “[c]hronic allergen exposure
[reproduced] allergen dependent sensitisation, a Th2-dependent allergic inflammation
characterised by eosinophilic influx into the airway mucosa, and AHR.” Id. at 3.
Dr. Byers argued that “[i]f Petitioner had pre-formed IgE of the scale to induce an
immediate allergic reaction and allergic sensitization as Dr. Garban suggested, then her skin
reaction at the time of vaccination would have been much more profound” than the common,
nonspecific symptoms that Petitioner experienced post vaccination. Resp’t’s Ex. F at 7. Dr. Byers
expressed certainty that Dr. Garban “would agree that the development of de novo IgE within a
few days sufficient to lead to severe and persistent allergic asthma like [Petitioner] experienced
would require a much longer time frame than a few hours to days of exposure.” Id. He noted that
Petitioner had never received the Prevnar 13 vaccine. Id. However, Petitioner had received several
vaccines with aluminum adjuvant from 2003 through 2016, “including two that also contained
pneumococcus antigens, with no side effects and no evidence of a sensitization process that would
be required for an ‘immediate early or acute’ hypersensitivity response.” Id. at 7.
Dr. Byers conceded in his report that “elevations in IgE, eosinophilia, and type 2 cytokines
are all biomarkers of allergic disease,” but he cautioned that they “do not necessarily impart
causation for asthma.” Resp’t’s Ex. F at 8. He surmised that one plausible explanation would be
that some undetermined environmental factor that Petitioner was continually exposed to and at the
18
Anthony T. Nials & Sorif Uddin, Mouse Models of Allergic Asthma: Acute and Chronic Allergen
Challenge, 1 DISEASE MODELS & MECHANISMS 213 (2008).
23
time of vaccination acted as a trigger. Id. at 8. “Through the process of vaccination, she then
became immunologically primed to the undetermined environmental trigger that persisted in her
local environment and resulted in . . . the pathological manifestations of severe asthma.” Id. Dr.
Byers described this theory as “superficially compelling but an unlikely hypothesis with no
medical evidence.” Id. at 9. These opinions are also held in Dr. Byers’s supplemental report filed
December 19, 2022. See Resp’t’s Ex. H. He noted that “Dr. Garban’s opinion has remained
consistent in that the temporal relationship of vaccination and development of severe persistent
asthma within days following vaccination provides enough evidence for cause-and-effect.” Id. at
1. Likewise, he “restate[d his] original conclusion that it is not biologically plausible to ascribe the
severe acute asthma exacerbation to the vaccination that was received just days before.” Id. at 4.
At hearing, Dr. Byers testified that there is no dispute that Petitioner suffered from severe
asthma and asserted that “the crux of the case really rests upon what the likelihood is of a Prevnar
vaccination to have led to severe asthma.” Tr. 230. He explained that asthma is “a heterogeneous
disease that’s characterized by variable episodes of obstructed airflow characterized clinically by
cough, [SOB,] and wheezing.” Tr. 230. Dr. Byers testified that the condition “ebbs and flows due
to whatever [inhaled] trigger contributes to the asthma.” Tr. 235. Under the umbrella of asthma,
Dr. Byers described endotypes that occur in different populations or are distinguished by the
presence or absence of Type 2 inflammation. Tr. 232–33. He identified Type 2 as the same as “so-
called Th2” and noted that it indicates “a type of cytokine pathway that’s produced by CD4 T-
cells.” Tr. 233. However, Dr. Byers continued, it “is not just about cytokine, and there’s overlap
with other inflammatory pathways.” Id. The Type 2 inflammation occurs and “it’s really IL-4, IL-
5 and IL-13 are sort of the center of activity that then induces a number of other Type 2
inflammatory-type cells like eosinophils, basophils, mast cells that are involved in the allergic
response or the Type 2 response.” Tr. 234. This production of IgE production “leads to things like
airway hyperreactivity, smooth muscle hyperplasia and mucus production [that] are the
characteristics of asthma.” Id. And “typically Type 2 inflammation [is] characterized by this sort
of IgE eosinophil, if you want to look at biomarkers of inflammation.” Id. Dr. Byers noted that
“Type 2 inflammation can happen anywhere. This isn’t a unique lung issue.” Id.
In Petitioner’s case, Dr. Byers stated “[i]t’s hard to say if this specifically was an IgE-
mediated process or not.” Tr. 236. He noted that although this was Petitioner’s first Prevnar 13
vaccine, she had been exposed to components of the vaccine through prior vaccinations with “no
reported history of escalating hyperreactivity to any of these components.” Id. Assuming that there
was a Type 1 hypersensitivity, he stated that they “resolve fairly quickly. So the likelihood of
having long-term persistent symptoms as a result of that [would] invoke two different pathways
that a single vaccine could induce.” Tr. 237. He asserted that hypothesis would require him to
“ignore the effect of the respiratory inhaled stimulus and triggers that really promoted her disease
process.” Id. Dr. Byers acknowledged that the cause of asthma remains unknown, despite
advancements in treatment through the use of biologics. Id. He stressed the difference between
identifying the cause of asthma generally and a trigger. Tr. 238. The cause is “a combination of
environmental exposure and genetic predisposition” that is seen in “all severe, complex, chronic
diseases.” Id. Triggers, conversely, are identifiable. Id. They include perfumes, animal dander,
smoke, or maybe be exercise- or cold-induced; “[b]ut all of these triggers or stimuli are things that
are inhaled into the airways.” Id.
24
Dr. Byers expressed hesitation about linking asthma to vaccines without any supporting
studies “because asthma is so common and vaccines are so common, ascribing a specific cause
and effect from a single vaccination to lead to asthma is more likely to happen by chance than to
have true cause and effect.” Tr. 239. He did not see the link between the vaccine and the production
of IgE. Tr. 239–40. Dr. Byers argued that it is not biologically plausible in the period asserted for
highly specific IgE production “through the process of B-cell development and affinity
maturation,” that then “binds to the surface of these cells that then release all the inflammatory
mediators that cause asthma.” Tr. 240. He referenced one epidemiological study “that talked about
the development of asthma within 60 days after vaccination,” but then stated that it “warrants
further study.” Tr. 241. Even in mouse models where they have been sensitized using aluminum,
Dr. Byers explained that “[i]t’s only after [the mice] are subjected to the ovalbumin through the
airways that you get an asthma effect.” Id.
Another point that Dr. Byers contested was how this acute IgE response is intertwined with
chronic asthma, because this presentation involves an “acute phase where she came to the
emergency room in an acute flare within four days following the vaccination versus the long-term,
severe, persistent asthma.” Tr. 242. Dr. Byers agreed with Dr. Garban that Type 1 hypersensitivity
is applicable here. Tr. 243. “Type 1 hypersensitivity defines how we can develop pre-existing IgE
in our body.” Id. He noted that “[i]t doesn’t have to be in our lungs,” and “upon re-exposure, there
is a response that occurs within minutes to hours to that re-exposure to that allergen.” Id.
Dr. Byers also took issue with the contention that Petitioner’s alleged asthma trigger was
not inhaled. Tr. 277. He asserted that “asthma attacks occur from something you inhale.” Id.
Anaphylaxis and bronchospasm can occur “from having exposure to something that’s not
necessarily in the airways,” but Dr. Byers did not think that is what occurred here or in any instance
where the diagnosis is asthma. Id. In the case of an inhaled trigger, Dr. Byers conceded that “an
acute respiratory tract infection can alter forever the airways.” Tr. 284. Consequently, it is possible
that some sort of inhaled allergen could cause a permanent change and make Petitioner’s asthma
worse again. Id. Dr. Byers did not see any evidence that a vaccine, specifically Prevnar 13, could
do that. Id.
C. Petitioner’s Rebuttal Testimony
1. Dr. Novakovic
On rebuttal, Dr. Novakovic discussed the differences and similarities between aluminum
hydroxide and aluminum phosphate in the context of adjuvants. He submitted the Zhang et al.19
paper and asserted that although “the authors stated that there’s a much more robust neutrophilic
response with aluminum hydroxide,” he did not think which adjuvant was used “plays much role
in the mechanism” that Petitioner’s experts presented. Tr. 294. Both adjuvants “function through
the same mechanism . . . activating NLRP3, which then shifts the immune response toward the
Th2 pathway and then generates the class switch that Dr. Garban talked about to IgE.” Tr. 295. He
continued, “[f]rom an immunological perspective, aluminum-containing adjuvants induce IgE-
mediated hypersensitivity reactions.” Tr. 296. Dr. Garban noted that Petitioner received two
19
Ting Zhang et al., Research Progress of Aluminum Phosphate Adjuvants and Their Action Mechanisms,
15 PHARAMACEUTICS 1756 (2023).
25
vaccines containing an aluminum adjuvant in February and June of 2015, diphtheria and
pneumococcal respectively. Tr. 297, 299. He agreed that when Petitioner received the first
adjuvanted vaccine in February, there was no evidence of an allergic reaction. Tr. 304.
2. Dr. Garban
Dr. Garban used the Galli et al. paper to better explain “the late phase in the inflammatory
allergic inflammation and the allergic response after that early phase that happened and the release
of cytokines and activation of the immune response.” Tr. 306. He asserted that the figure within
the article shows how the “Th2 cells are orchestrating the whole molecular and cellular
phenomenon here and resulting in the activation of cellular factors and also humeral factors such
as immunoglobulin E or IgE, affecting, at the end, the airway.” Tr. 307 (citing Pet’r’s Ex. 62).
Furthermore, the figure shows lung damage that “will then sensitize that area to another kind of
triggering.” Id. These injured lung cells, according to Dr. Garban, “are more sensitive to other kind
of stimuli such as smoke, viral infection or other type of things that will then trigger the asthmatic
event, and this contributes to the severity.” Tr. 308. He continued, the increased IgE levels with
increased levels of the receptor or the surface of B-cells “will cause that in the absence of the
antigen, this reaction, this cross-linking happened and the activation of cells, and again, further
damage [] in the system.” Id. Dr. Garban described it as “a vicious cycle.” Tr. 309.
Next, Dr. Garban described the depot effect of the aluminum phosphate in Prevnar 13. He
testified it will bring together antigens in the vaccine, including different strains of streptococcus
and CRM 197 to stimulate the immune system. Tr. 309. Dr. Garban explained “that depot effect,
at least they last for weeks and months and it has been even reported, years, where it’s still
remaining – complexes have been found in the site of injection.” Tr. 309–10.
I asked how the pathogenic nature of IgE sensitization following the introduction of an
inhaled antigen relates back specifically to the Prevnar 13 vaccine, an injectable. Dr. Garban stated
that “the allergic inflammatory response that we have described upon vaccination is going to
generate a more systemic effect than we described and respiratory effect in this case and causing
these asthma related symptoms.” Tr. 311. He continued that this process continues in perpetuity
and “some of these generation of these factors that are not what we desire, as we call an allergic
reaction is a nondesire or a very extreme, unusual phenomenon that happen upon the challenge
with a targeted antigen.” Id. Ultimately, the perpetuation is caused by the depot effect. Id.
IV. Applicable Legal Standards
A. Standard of Adjudication—Burden of Proof
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).
26
Petitioner’s burden of proof is by a preponderance of the evidence. § 13(a)(1). The
preponderance standard requires a petitioner to demonstrate that it is more likely than not that the
vaccine at issue caused the injury. Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y of Health & Hum. Servs.,931 F.2d 867, 873
(Fed. Cir. 1991).
B. Standard of Adjudication—Factual Issues
A petitioner must prove, by a preponderance of the evidence, the factual circumstances
surrounding her claim. § 13(a)(1)(A). To resolve factual issues, the special master must weigh
the evidence presented, which may include contemporaneous medical records and testimony. See
Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (explaining that a special
master must decide what weight to give evidence including oral testimony and contemporaneous
medical records).
In Program cases, contemporaneous medical records and the opinions of treating
physicians are favored. Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1325, 1326(Fed. Cir. 2006) (citing Althen v. Sec’y of Health & Hum. Servs.,418 F.3d 1274, 1280
(Fed. Cir. 2005)). Indeed, when reviewing the record, a special master must consider the opinions of treating physicians. Capizzano,440 F.3d at 1326
. 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.” § 13(b)(1). Rather, when “evaluating the weight to be afforded to any
such . . . [evidence], the special master . . . shall consider the entire record . . . .” Id. There is no
presumption that medical records are accurate and complete as to all the patient’s physical
conditions. Kirby v. Sec’y of Health & Hum. Servs., 997 F.3d 1378, 1383 (Fed. Cir. 2021) (finding
that “[b]ecause a reasonable fact finder could conclude that [Petitioner’s] testimony [wa]s not
inconsistent with her medical records . . . it was not arbitrary and capricious for the special master
to credit [Petitioner’s] testimony” over her medical records).
Where there are inconsistencies, special masters are within their discretion to award
contemporaneous medical records greater weight than later conflicting testimony. See Cucuras,
993 F.2d at 1528(holding that the special master’s reliance on contemporaneous medical records over conflicting oral testimony given after the fact was not arbitrary or capricious); see also Burns,3 F.3d at 417
(holding that the decision of whether to accord greater weight to contemporaneous
medical records or later given testimony is “uniquely within the purview of the special master”).
Indeed, the Court of Federal Claims has outlined four potential explanations for inconsistencies
between contemporaneously created medical records and later testimony: (1) a person’s failure to
recount to the medical professional everything that happened during the relevant time period; (2)
27
the medical professional’s failure to document everything reported to her or him; (3) a person’s
faulty recollection of the events when presenting testimony; or (4) a person’s purposeful
recounting of symptoms that did not exist. LaLonde v. Sec’y of Health & Hum. Servs., 110 Fed.
Cl. 184, 203–04 (2013), aff’d,746 F.3d 1334
(Fed. Cir. 2014).
Despite the weight afforded to medical records, special masters are not bound rigidly by
those records in determining onset of a petitioner’s symptoms. Valenzuela v. Sec’y of Health &
Hum. Servs., No. 90-1002V, 1991 WL 182241, at *3 (Fed. Cl. Spec. Mstr. Aug. 30, 1991); see also Eng v. Sec’y of Health & Hum. Servs., No. 90-1754V,1994 WL 67704
, at *3 (Fed. Cl. Spec.
Mstr. Feb. 18, 1994) (“[Section 13(b)(2)] must be construed so as to give effect also to § 13(b)(1)
which directs the special master or court to consider the medical records (reports, diagnosis,
conclusions, medical judgment, test reports, etc.), but does not require the special master or court
to be bound by them.” (emphasis omitted)).
C. Standards for Adjudication—Causation
To receive compensation through the Program, Petitioner must prove either (1) that she
suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding to a
vaccine that she received, or (2) that she suffered an injury that was actually caused by a
vaccination. See §§ 11(c)(1), 13(a)(1)(A); Capizzano, 440 F.3d at 1319-20. Because Petitioner does not allege she suffered a Table Injury, she must prove a vaccine she received caused her injury. To do so, Petitioner must establish, by preponderant evidence: “(1) a medical theory causally connecting the vaccination and the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship between vaccination and injury.” Althen,418 F.3d at 1278
.
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), mot. for rev. denied,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 or scientific explanation.” Knudsen v. Sec’y of Health & Hum. Servs.,35 F.3d 543, 548
(Fed. Cir. 1994). Such a theory must only be “legally probable, not medically or scientifically certain.”Id.
at 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
). Scientific and “objective confirmation” of the medical theory with additional medical documentation is unnecessary. Althen, 418 F.3d at 1278–81; see also Moberly,592 F.3d at 1322
. Petitioner need not make a specific type of evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of pathological markers or genetic predisposition, or general acceptance in the scientific or medical communities to establish a logical sequence of cause and effect.” Capizzano,440 F.3d at 1325
. However,
Petitioner cannot establish entitlement to compensation based solely on his assertions; rather, a
vaccine claim must be supported either by medical records or by the opinion of a medical doctor.
§ 13(a)(1). Furthermore, 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
28
of Health & Hum. Servs., 746 F.3d 1334, 1339(Fed. Cir. 2014) (citing Moberly,592 F.3d at 1322
). Testimony that merely expresses the possibility—not the probability—is insufficient, by itself, to substantiate a claim that such an injury occurred. See Waterman v. Sec’y of Health & Hum. Servs.,123 Fed. Cl. 564
, 573–74 (2015) (denying Petitioner’s motion for review and noting that a possible causal link was not sufficient to meet the preponderance standard). While certainty is by no means required, a possible mechanism does not rise to the level of preponderance. Moberly,592 F.3d at 1322
; see also de Bazan v. Sec’y of Health & Hum. Servs.,539 F.3d 1347, 1351
(Fed. Cir. 2008). 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
.
Next, 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
. 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). In particular, Petitioner must prove that the vaccine was “not only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.” Moberly,592 F.3d at 1321
(quoting Shyface v. Sec’y of Health & Hum. Servs.,165 F.3d 1344
, 1352–53 (Fed. Cir. 1999)); see also Pafford v. Sec’y of Health & Hum. Servs.,451 F.3d 1352
, 1355 (Fed. Cir. 2006). The received vaccine, however, need not be the predominant cause of the injury. Shyface,165 F.3d at 1351
. The special master 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).
Lastly, 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 v. Sec’y of Health & Hum. Servs.,956 F.2d 1144
, 1148 (Fed. Cir. 1992); 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) (“[w]ithout more, [a] proximate temporal relationship will not support a finding of
causation”).
D. Standards for Adjudication—Significant Aggravation
Additional analysis is required to determine whether Petitioner’s vaccination significantly
aggravated her pre-existing injury. The elements of an off-Table significant aggravation case are
set forth in Loving. See Loving, 86 Fed. Cl. at 142-44; see also W.C. v. Sec’y of Health & Hum.
Servs., 704 F.3d 1352, 1357 (Fed. Cir. 2013) (holding that “the Loving case provides the correct
framework for evaluating off-table significant aggravation claims”). The Loving court combined
the Althen test, which defines off-Table causation cases, with a test from Whitecotton. Whitecotton
29
v. Sec’y of Health & Hum. Servs., 17 F.3d 374(Fed. Cir. 1994), rev’d sub nom., Shalala v. Whitecotton,514 U.S. 268
(1995) (concerning on-Table significant aggravation cases). The
resultant test has six components, which are:
(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 significant 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 statute defines “significant aggravation” as “any change for the worse in a pre-existing
condition which results in markedly greater disability, pain, or illness accompanied by substantial
deterioration in health.” § 33(4).
In determining whether Petitioner is entitled to compensation, the special master shall
consider all materials in the record, including “any . . . conclusion, [or] medical judgment . . .
which is contained in the record regarding . . . causation.” § 13(b)(1)(A). The undersigned must
weigh the submitted evidence and the testimony of the parties’ proffered experts and rule in
Petitioner’s favor when the evidence weighs in her favor. See Moberly, 592 F.3d at 1325-26(“Finders of fact are entitled—indeed, expected—to make determinations as to the reliability of the evidence presented to them and, if appropriate, as to the credibility of the persons presenting that evidence.”); Althen,418 F.3d at 1280
(noting that “close calls” are resolved in Petitioner’s favor). A petitioner who satisfies her burden is entitled to compensation unless Respondent can prove, by a preponderance of the evidence, that the vaccinee’s injury is “due to factors unrelated to the administration of the vaccine.” § 13(a)(1)(B). However, if a petitioner fails to establish a prima facie case, the burden does not shift. Bradley v. Sec’y of Health & Hum. Servs.,991 F.2d 1570, 1575
(Fed. Cir. 1993).
In considering the reliability of a petitioner’s evidence of a prima facie case, the special
master may consider alternative causes for a petitioner’s condition that are reasonably raised in the
record, even if the respondent does not pursue a formal alternative cause argument. Doe v. Sec’y
of Health & Hum. Servs., 601 F.3d 1349, 1358(Fed. Cir. 2010). Thus, in weighing a petitioner’s case-in-chief, a special master may consider evidence that the petitioner’s alleged injury could have been caused by alternative causes.Id.
E. Standards for Adjudication—Alternative Causation
A petitioner who satisfies all three prongs of the Althen test (or all six prongs of the
Loving test) has established a prima facie showing of causation. Hammitt v. Sec’y of Health &
Hum. Servs., 98 Fed. Cl. 719, 726 (2011). Where a petitioner demonstrates by a preponderance
of the evidence that she suffered an injury caused by vaccination, the government must not
30
merely prove the existence of an alternative cause, but that such an alternative actually caused
the injury. Knudsen, 35 F.3d at 549. Additionally, a factor unrelated “may not include ‘any idiopathic, unexplained, unknown, hypothetical, or undocumentable cause, factor, injury, illness or condition.’” § 13(a)(2); see also Doe,601 F.3d 1349
(opining that an idiopathic diagnosis
cannot be a “factor unrelated,” as it is idiopathic).
“Regardless of whether the burden ever shifts to the [R]espondent, the special master may
consider the evidence presented by the [R]espondent in determining whether the [P]etitioner has
established a prima facie case.” Flores v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 157, 162- 63 (2014); see also Stone v. Sec’y of Health & Hum. Servs.,676 F.3d 1373, 1379
(Fed. Cir. 2012) (“[E]vidence of other possible sources of injury can be relevant not only to the ‘factors unrelated’ defense, but also to whether a prima facie showing has been made that the vaccine was a substantial factor in causing the injury in question.”); de Bazan,539 F.3d at 1353
(“The government, like any
defendant, is permitted to offer evidence to demonstrate the inadequacy of the [P]etitioner’s
evidence on a requisite element of the [P]etitioner’s case-in-chief.”); Pafford, 451 F.3d at 1358-59
(“[T]he presence of multiple potential causative agents makes it difficult to attribute ‘but for’
causation to the vaccination. . . . [T]he Special Master properly introduced the presence of the
other unrelated contemporaneous events as just as likely to have been the triggering event as the
vaccinations.”).
V. Discussion
A. Loving Factor One: What was Petitioner’s Condition Prior to Administration of the
Vaccine?
Petitioner’s medical record provides the best evidence of the nature of her condition prior
to vaccination. As early as October 30, 2007, Petitioner’s symptoms gave one treater the
impression of “possible asthma.” Pet’r’s Ex. 14 at 534. Nursing discharge instructions from a
March 23, 2008 trip to the ED, included a substantial section on asthma with general information
on the condition, a list of several potential triggers: “pollen, dust, animal dander, molds, some
foods, respiratory infections, exposure to smoke, exercise, or emotional stress[; and a note that
r]epeat attacks are common.” Id. at 456–58. Also included were symptoms to be concerned about
in the case of a recurrence and circumstances that would warrant a return to the ED. Id. One month
later in April, Petitioner’s active medications included an inhaler and steroids for the exacerbation
of COPD/asthma. Id. at 433.
Although there was initial disagreement among the experts about the onset of Petitioner’s
condition, they all eventually agreed that Petitioner likely suffered from asthma prior to her
vaccination. Petitioner’s experts, Drs. Garban and Novakovic, both assumed that Petitioner had
pre-existing asthma in their second supplemental expert reports, submitted on November 12, 2019,
and March 10, 2021, respectively. See Pet’r’s Exs. 37, 49. Respondent’s expert Dr. Bardana noted
that Petitioner had intermittent asthma that developed in 2007. See Resp’t’s Ex. A. Dr. Byers
likewise asserted that Petitioner suffered from asthma prior to her vaccination with a flare that
occurred in 2015. See Resp’t’s Ex. F.
Despite preponderant evidence that Petitioner suffered from asthma for several years prior
to her vaccination, Petitioner asserted that she did not suffer from pre-existing asthma. Petitioner
31
was definitive in her written declaration, stating that she did not have asthmatic symptoms before
she received the vaccine. Petitioner maintained in her amended petition that following her June
15, 2015 vaccination, Petitioner “developed asthma, a condition she did not previously have.” Am.
Pet. at 1. She continued that her asthma was “caused-in-fact” by her vaccination. Id. In her
prehearing brief, filed on July 5, 2024, Petitioner continued to assert that she “ha[d] provided
persuasive evidence establishing that onset of her asthma following administration of the Prevnar
13 vaccine was within a medically appropriate timeframe to infer causation.” Pet’r’s Br. at 7.
Petitioner also testified that she was diagnosed with asthma following her July 15, 2015
vaccination, and prior to that she suffered from pulmonary hypertension. Tr. 16.
Because Petitioner’s condition was described as asthma as early as 2007 by her treaters, it
could not have been caused by a subsequent vaccine seven years later. Furthermore, both of
Petitioner’s experts ultimately abandoned any assertation that Petitioner did not suffer from asthma
pre vaccination. Therefore, Petitioner has not presented preponderant evidence of a causation
claim. A petitioner cannot succeed on a claim of causation-in-fact where the alleged condition
preexisted the vaccination. See W.C., 704 F.3d at 1354–55 (affirming the special master’s denial
of compensation of a claim of causation-in-fact because “[i]f a petitioner has a disorder before
being vaccinated, the vaccine logically cannot have caused the disorder”). Alternatively, Petitioner
submitted that she “may have had controlled asthma prior to the Prevnar 13 vaccination of June
15, 2015. If so, the vaccination substantially aggravated the controlled asthma into a severe and
uncontrolled asthma.” Am. Pet. at 1. Petitioner described the possibility of pre-existing asthma, in
the alternative to her causation claim, as “mild and controlled.” Pet’rs Br. at 7.
Despite agreement about the diagnosis, there is much dispute about the severity of
Petitioner’s condition. The last medical record that mentions pulmonology concerns pre
vaccination, is a July 8, 2008 record, that noted at that time, Petitioner was no longer in need of
her inhaler. Pet’r’s Ex. 17 at 417. Prior to that, beginning as early as 2003 and certainly by October
of 2007, Petitioner presented to the ED and to other medical providers on multiple occasions with
pulmonary symptoms consistent with asthma. She complained of productive cough and SOB, and
Petitioner necessitated treatment including steroids and antibiotics. During a series of medical
visits beginning in 2007, asthma repeatedly appeared as a potential diagnosis, alongside
bronchiectasis. Petitioner’s own expert, Dr. Garban, acknowledged that “bronchiectasis is
associated in high co-morbidity with severe asthma and should be considered as part of the
differential diagnosis.” Pet’r’s Ex. 4 at 11. Notably on April 4, 2008, Petitioner reported that her
condition was uncontrolled, and the medical record states that “when she [was] given albuterol,
steroids, and antibiotics she improve[d] but relapse[d] when weaned off steroids.” Pet’r’s Ex. 14
at 449. Petitioner reported that these symptoms had been over the course of the preceding year. Id.
There is preponderant evidence that during this timeframe, Petitioner was suffering from asthma
symptoms that were more severe than in other times pre vaccination.
Following this series of episodes, Petitioner insisted that she did not require treatment for
any asthmatic symptoms for the next seven years from 2008 through 2015. Furthermore, Petitioner
testified at hearing that she continued to fill her prescription during that time (although she did not
take her prescribed dose) to keep unexpired treatment on hand in the case of need. While there is
preponderant evidence in Petitioner’s medical record to support Respondent’s claim that Petitioner
suffered from asthma before 2015, including at least one significant flare in 2007-2008,
32
Petitioner’s asthma was stable and possibly asymptomatic for several years before her Prevnar 13
vaccination.
B. Loving Factor Two: What is Petitioner’s Current Condition (or Her Condition
Following the Vaccination, if Also Pertinent)?
Petitioner presented to the ED four days post vaccination with complaints of coughing and
wheezing since the day after her vaccine. Pet’r’s Ex. 3 at 900. Similar to her 2008 complaints,
Petitioner reported productive cough, wheezing, and SOB, with the additional symptoms of
vomiting and chills. Petitioner’s medical record again provides the best evidence of the nature of
her condition during this time. In the ED, Petitioner stated that she had never had such severe
symptoms before. She was admitted to the hospital on June 19, 2015, and remained for four days.
Pet’r’s Ex. 15 at 9. During her hospitalization, Petitioner was diagnosed with status asthmaticus in
the setting of recent viral URI. In the ensuing days and weeks, Petitioner was seen several times
in the ED and diagnosed with bronchiectasis. Similar to March and April of 2008, Petitioner was
treated with steroids and bronchodilators. By September 24, 2015, Petitioner was treated for a
severe asthma attack and her doctor noted it was her third incident in as many months. Pet’r’s Ex.
3 at 607. She was placed on Xolair and sent home upon improvement. Petitioner remained on
Xolair to manage her bronchial asthma. Petitioner’s medical records illustrate a clear exacerbation
of her asthma, following an asymptomatic period, around the time of her vaccination.
Furthermore, Petitioner’s filed literature provides additional context to the severity of
status asthmaticus. Noting that the phrase could be problematic due to “a number of limitations []
concerning the quantification of unresponsiveness,” the Papiris et al. article suggested the
nomenclature, acute severe asthma. Pet’r’s Ex. 8 at 1. This phrase “relat[es] severity mostly to a
combination of the presenting signs and symptoms and the severity of cardiorespiratory
abnormalities observed.” Id. 1–2. These patients require “close observation plus aggressive
administration of bronchodilators (SABAs plus ipratropium bromide via a nebulizer driven by
oxygen)[,] and oral or intravenous corticosteroids are necessary to arrest the progression to severe
hypercapnic respiratory failure . . . that requires [ICU] admission.” Id. at 2. This definition is
consistent with the treatment and concerns documented in Petitioner’s medical record of her
treatment in June of 2015. Furthermore, this aggressive treatment is more severe than Petitioner’s
presentation during her care in 2008.
C. Loving Factor Three: Does Petitioner’s Current Condition (or Condition After
Vaccination) Constitute a “Significant Aggravation” of Her Condition Prior to
Vaccination?
To determine whether there is a “significant aggravation” of Petitioner’s condition, it is
necessary to compare her condition before vaccination to her condition after vaccination. The
statute defines “significant aggravation” as “any change for the worse in a pre-existing condition
which results in markedly greater disability, pain, or illness accompanied by substantial
deterioration in health.” § 33(4). There is no dispute between the parties that Petitioner’s condition
worsened, beginning in June of 2015, although there is disagreement about the role of vaccination,
and the extent to which it may have permanently altered the nature of her asthma. Petitioner had
steadily decreased her treatments and testified that she had not used her inhaler in the years prior
33
to the 2015 exacerbation. Furthermore, she had not complained of the symptoms commonly
associated with asthma to a medical provider for the same period of years prior to her vaccination.
The reemergence of symptoms, the series of ED visits and hospitalization, and the introduction of
Xolair and other treatments used for severe forms of asthma, provide preponderant evidence of
significant aggravation of Petitioner’s asthma in the days following her June 15, 2015 vaccination.
D. Loving Factor Four/Althen Prong One: Medical Theory of Causation
The theory of causation that Petitioner presented has evolved somewhat over the course of
several rounds of written expert reports and testimony. In his first report, Dr. Garban opined that
Petitioner suffered a vaccine-triggered allergic sensitization that began as type I allergy resulting
in IgE upregulation. He filed literature that defined a type I allergy as a reaction to the initial
exposure to an allergen “that can induce IgE production so that later re-exposure to that substance
induces an allergic reaction.” Pet’r’s Ex. 62 at 3. Dr. Garban reasoned that the aluminum adjuvant
in the vaccine is an allergen that can cause acute and chronic inflammation, T helper cell response,
and production of IgE leading to asthma exacerbation.
Despite Dr. Bardana’s conflation of Dr. Garban’s use of the “type I” modifier, the literature
that Dr. Garban filed distinguished a type I allergen (a substance that can induce IgE production)
and a type I allergic inflammation (a process that is IgE mediated, also referred to as a type I
immediate hypersensitivity reaction). Dr. Garban’s attempt to address this confusion is where
things become unclear. Dr. Garban wrote that “his potential causal mechanism on the matter of
[Petitioner] involved an initial adjuvant mediated immunoreactivity.” Pet’r’s Ex. 16 at 2. He
suggested, without explicitly stating, that this is unlike a hypersensitivity that “involve[s] an initial
sensitizing exposure to an antigen followed by a subsequent re-exposure.” Id. However, Dr.
Garban does not define immunoreactivity. Dorland’s defines immunoreaction as “the reaction that
takes place between an antigen and its antibody or between an antigen and an immunocyte
sensitized to it.” Immunoreaction, DORLAND’S MED. DICTIONARY ONLINE. This definition is broad
enough to cover any and all immune responses that the experts have discussed and is therefore
unhelpful. It lends credibility to Dr. Bardana’s argument that Dr. Garban is asserting a
hypersensitivity reaction, while simultaneously arguing a primary exposure to the allergen. At this
point, it seems Dr. Garban was characterizing Petitioner’s reaction as an initial response to
aluminum phosphate and not the result of a re-exposure. He asserted that the primary exposure of
aluminum adjuvant in the Prevnar 13 vaccine sensitized Petitioner’s immune system to overreact
to later exposure to antigens. Dr. Garban does not identify the kinds of later antigens to which he
refers but noted that “common environmental allergens” are at play. Pet’r’s Ex. 16 at 2. This initial
adjuvant mediated immunoreactivity theory is vague and does not find support, even in theory, in
the medical literature that Petitioner filed.
In his final written report, Dr. Garban submitted a figure to illustrate his asserted causation
theory. The chart breaks down the pathogenesis of Petitioner’s asthma exacerbation into three
steps: 1. Allergic Inflammatory Reaction- type I hypersensitivity (localized itching/swelling)
followed by type II late phase reaction (coughing/wheezing); 2. Allergic Sensitization- IgE
synthesis leading to mast cell activation; and 3. Aggravation and Perpetuation- bronchial
hyperreactivity. Pet’r’s Ex. 58 at 1. This explanation is in direct contrast to his prior assertion that
Petitioner did not suffer from a type I hypersensitivity. Dr. Garban confirmed this development
34
when he testified that Petitioner suffered from an allergic response—a (non-anaphylactic) type 1
hypersensitivity, with a systemic, respiratory manifestation. Tr. at 199–200. He then used a
snowball metaphor to explain an “increasing in terms of catching up on the sensitivity to other
antigens that then will result in the increasing frequency of asthmatic events and chronicity and
severity of these asthmatic events.” Tr. at 200. Ultimately, Dr. Garban asserted that Petitioner’s
reaction was a sort of type 1 hypersensitivity reaction that developed into a self-perpetuating
chronic condition.
Although Dr. Garban was initially equivocal when characterizing the acute allergic
inflammatory reaction in Petitioner’s case, Dr. Novakovic always categorized Petitioner’s reaction
as a type 1 hypersensitivity. As noted, a hypersensitivity is an expedited response to a re-exposure.
This definition and the first iteration of Dr. Garban’s theory are mutually exclusive, and it appears
that Dr. Garban eventually abandoned any argument that Petitioner’s Prevnar 13 vaccine was her
primary/initial exposure to aluminum adjuvant. Therefore, I do not find that Petitioner has
presented preponderant evidence of a biological mechanism that includes an allergic, acute
reaction, absent a re-exposure.
Dr. Garban highlighted the role of aluminum adjuvants in enhancing an immune response
of Th2 production of IgE cytokines, which are central to an allergic asthmatic response.
Petitioner’s and Respondent’s experts agree that IgE has been linked to the development of allergic
asthma. See Tr. 243. Furthermore, Dr. Byers described “the roles of aluminum salt in terms of
caus[ing] allergic reactions,” as “enticing.” Tr. 244. He conceded that adjuvants ignite antibody
responses in Type 2 inflammation and acknowledged Th2 cells in the role of asthma. Notably Dr.
Byers acknowledged “some cases that where asthma flares might have occurred after the vaccine,
but [he asserted], there is not conclusive evidence that it was causative.” Tr. 245. Petitioner is not
required to submit conclusive evidence of causation. She submitted a theory supported by medical
literature, that identifies several components of the Prevnar 13 vaccine that potentially contribute
to the upregulation of IgE cytokines.
Dr. Garban was also equivocal about whether the aluminum adjuvant was the cause of
Petitioner’s reaction, noting the potential role of polysorbate 80 and CRM 197. When asked
directly if he believed the aluminum adjuvant is the responsible antigen, he testified, “I don’t know
in this case.” Tr. 198. Dr. Garban suggested that it could be one or a combination of any of the
components of Prevnar 13. He acknowledged, he “[did not] know and [could not] guarantee . . .
which component of the vaccine start[s] the whole process in terms of triggering or was the
allergen that triggered the disease.” Tr. 200. Dr. Novakovic identified CRM 197 at the potential
initiator of Petitioner’s allergic response. He noted that the Prevnar 13 vaccines’s conjugated
nature and use of the carrier protein “elicit[ed] a stronger immune response and activate[d] a
cascade that is dependent on T cells.” Pet’r’s Ex. 19 at 4. Dr. Novakovic’s theory then dovetails
with Dr. Garban with his assertion that T cells “drive[] B cell differentiation into Ig-secreting
plasma cells,” producing, among other antibodies, IgE. Id. Both experts rely on the ability of
specific antigens to “cause some rare events of anaphylaxis or allergic response,” and “[d]efinitely
type I hypersensitivity.” Tr. 200. Petitioner has presented preponderant evidence that the Prevnar
13 vaccine, via one or more components including aluminum phosphate and CRM 197, could
trigger an allergic inflammation, IgE-mediated type I immediate hypersensitivity reaction.
35
However, Petitioner’s theory does not end there. Petitioner further asserted that the Prevnar 13
vaccine can cause the “onset and persistence of status asthmaticus.” Pet’r’s Ex. 16 at 2.
Dr. Novakovic testified that a hypersensitivity reaction can permanently alter the immune
system due to the sustained high IgE levels over an extended period of time. Pet’r’s Ex. 19 at 5.
This sensitization is reinforced over the lifetime of the patient, resulting in asthmatic symptoms
following exposure to common environmental triggers. Id. The Galli et al. article described how
chronic allergic inflammation can occur “[w]hen allergen exposure is continuous or repetitive,
inflammation persists, and many innate and adaptive immune cells derived from the blood can be
found in the tissues at sites of allergen challenge.” Pet’r’s Ex. 62 at 5. This leads to structural
changes “with marked altered function of the affected organs.” Id. Furthermore, Petitioner’s filings
that explained the nature of allergic inflammation all noted that hypersensitivity reactions are
temporary: hours to days in case of an early phase reaction and days in late phase reactions.
Petitioner’s theory does not persuasively explain how a hypersensitivity reaction that is
precipitated by a contained, single vaccination constitutes a repetitive or continuous exposure to
an antigen extensive enough to cause chronic inflammation.
Petitioner’s experts both rely on the IgE mediated nature of allergic asthma to assert that
the Prevnar 13 vaccine caused Petitioner’s antibody upregulation and continued sensitization to
common, environmental substances. The theory follows that these allergens then trigger asthma
attacks that are more severe and occur more often. This argument suggests that elevated IgE levels
are necessary for ongoing airway hyperactivity. While the medical literature does provide evidence
for this process occurring upon continuous exposure to triggering allergens, there is not
preponderant evidence presented that the vaccine causes increased IgE levels for an extended
period of time to cause hyperreactivity. The flow chart that Dr. Garban created to illustrate his
proposed biological mechanism described the vaccine-mediated allergic sensitization leading to
the perpetuation of asthma. See Pet’r’s Ex. 58 at 1. “Adaptive [Th2] cells produce soluble immune
mediators driving IgE synthesis, which binds to mast cell high-affinity IgE receptors, leading to
mast cell activation.” Id. Dr. Garban does not discuss mast cell activation syndrome (“MCAS”)
specifically, and his testimony is limited to the conclusion that this process generates an allergic
reaction. He does not explain how mast cell activation, a process that produces mediators that
“cause the symptoms of immediate-type hypersensitivity” lead to ongoing airway hyperactivity.
See Pet’r’s Ex. 25 at 4. However, the Verstraelen et al. article explained the process: 1) mast cells
that are circulating in bronchial airway connective tissue; 2) re-exposure to a triggering allergen
“causes mast cell degranulation and synthesis of proinflammatory molecules;” and 3) this mediator
release manifests as a hypersensitivity.” Id. at 3–4. The hypersensitivity is followed by a late phase
reaction, and the newly recruited “inflammatory cells can produce a vast array of inflammatory
mediators,” that promote chronic airway inflammation “after repeated allergen exposure.” Id. at
4–5. Again, the key link is repeated exposure to the allergen. During his testimony, Dr. Garban
referred to the depot effect to assert the prolonged exposure to aluminum following a Prevnar 13
vaccination, but he did not address HogenEsch’s caution “that sustained release of antigen from a
depot site over days or weeks is unlikely to contribute to the adjuvant effect of aluminum
compounds.” Pet’r’s Ex. 7 at 2.
Dr. Byers contested Petitioner’s assertion that Petitioner could develop an asthma
exacerbation from an injected antigen but acknowledged that bronchospasms “can occur from
36
having exposure to something that’s not necessarily in the airways.” Tr. 277. The Verstraelen et
al. paper, filed by Petitioner, described chronic asthma following repeated re-exposure to an
inhaled allergen. The authors did not contemplate an injected allergen as a trigger for airway
hyperreactivity. Dr. Garban relied on the Cockcroft chapter to assert that an injected allergen can
cause a respiratory reaction, despite its rare occurrence. Indeed, Cockcroft wrote that “[i]solated
bronchial asthma induced by allergens introduced into the body via routes other than inhalation is
uncommon but has been reported.” Pet’r’s Ex. 23 at 14. He also noted that “these most often
represent systemic allergic reactions in asthmatic individuals who have a preexisting high level of
airway hyperresponsiveness and therefore develop disproportionately severe bronchospasm.” Id.
This would suggest that an injected allergen would only have this type of effect on someone who
is already hyperresponsive, as opposed to the argument presented in this case that the allergen
could cause such a condition. Cockcroft also discussed chronic airway hyperreactivity, but in the
context of continued exposure to inhaled allergens. He named occupational hazards and
environmental triggers, such as dust mites, and asserted that an “IgE--antigen reaction occurring
continuously in the airways will lead to exacerbation of clinical asthma.” Id. at 12. Cockcroft also
acknowledged that other immunological reactions may be responsible for bronchial and
parenchymal destruction, with the development of (proximal) bronchiectasis.” Id. at 13. Unlike
Petitioner’s experts, Cockcroft also highlighted the importance of repeated exposure to an inhaled
allergen for a chronic condition to develop. Dr. Byers ultimately conceded that “a single exposure
to some sort of respiratory viral illness can cause lifelong change in the airways . . . and so it is
possible that she could come back into contact with some sort of inhaled allergen or inhaled trigger
that can make her asthma worse again.” Tr. 284. However, repeated exposure would be needed
following the initial hypersensitivity. Dr. Byers argued that he could “find no evidence in [his]
review of the literature that support[s] a Prevnar 13 vaccination causing asthma.” Tr. 280.
Dr. Byers also highlighted the absence of large-scale studies to support Petitioner’s theory
in this case. However, such evidence is not required for a claim to be successful and are rarely
done, if even possible. Petitioner has identified several avenues for a potential biological
mechanism; however, each one fails to connect the injected vaccine to a hyperreactive airway
susceptible to chronic, severe asthma attacks.
1. Petitioner’s experts have abandoned any mechanism that does not rely on a type 1
hypersensitivity reaction, which by definition, involves re-exposure.
2. Petitioner’s experts have not explained how a type 1 hypersensitivity extends beyond
a late phase reaction, without repeated exposure to the offending allergen or a pre-
existing hyperreactivity.
3. Petitioner’s experts have not explained how a single Prevnar 13 vaccination, four
months after a prior aluminum adjuvanted vaccine, constitutes repeated exposure
substantial enough to trigger sustained elevated IgE levels.
4. Petitioner’s experts have not explained how an injected allergen can cause a severe
asthma flare necessary for structural change, absent pre-existing levels of
hyperreactivity.
While Petitioner’s theory has pieces that make sense under certain circumstances, such as
the ability of an inhaled allergen to cause a respiratory reaction, and the ability for an acute
hypersensitivity reaction to develop into chronic allergic asthma, they do not all fit together to
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create a cohesive theory. Furthermore, the hyperreactivity necessary for an injected allergen to
trigger a severe bronchospasm would also need to predate the vaccine, precluding but-for causation
of the significant aggravation. While Petitioner has presented preponderant evidence that the
Prevnar 13 vaccine can cause a type 1 hypersensitivity reaction, she has not presented preponderant
evidence that the vaccination is the catalyst for the type of allergen re-exposure necessary for
chronic, severe asthma.
E. Loving Factor Five/Althen Prong Two: Logical Sequence of Cause and Effect
Petitioner described the nature of her symptoms in 2015 as more severe than ever before,
and the medical records support that assertion. However, Petitioner’s medical records first
mentioned Petitioner’s pulmonary symptoms in 2003. While she was diagnosed with bronchitis
and not asthma at that time, the medication prescribed included a daily inhaler in response to
sustained symptoms that did not immediately improve. She was on this medication for several
weeks and eventually stabilized for several years until she had another acute respiratory event in
2008 that was significantly worse than 2003. Her cough and SOB returned, more severe, and this
time, those symptoms were associated with asthma. In addition to steroids and an inhaler,
Petitioner was prescribed antibiotics as a part of her treatment, indicating a possible infectious
trigger. Petitioner’s 2015 presentation arc is then parallel to her exacerbation in 2008. Petitioner
had an acute pulmonary symptoms, specifically productive cough, wheezing, and SOB, and all
symptoms were again more severe than the previous flares. She went to the ED several times, and
her treaters considered several differential diagnoses before ultimately developing a treatment plan
consistent with asthma. Specifically, Petitioner was diagnosed in the ED with asthma pursuant to
a URI. Petitioner’s symptoms returned when she initially attempted to wean off daily medication
(similar to 2008), but eventually she stabilized, and her symptoms eased. These acute respiratory
events are similar in their presentation, treatment, symptom course, and suspected infectious
trigger, with a progressively more severe iteration each time. Petitioner has provided preponderant
evidence that her symptoms worsened in June of 2015, but Petitioner further bears the burden of
providing preponderant evidence of the vaccine’s role in this progression of her pre-existing
condition.
Petitioner’s causation theory must be applicable to the facts and circumstances in her case.
The theory relies on the premise that exposure to components of the Prevnar 13 vaccine, including
aluminum phosphate, can cause a hypersensitivity reaction. Again, the evolution of Dr. Garban’s
opinion must be noted. In his report, he was initially adamant that Petitioner did not suffer a
hypersensitivity reaction, because this 2015 Prevnar 13 vaccine was the primary exposure to
whatever antigen triggered her asthmatic exacerbation. Specifically, he suggested that the Prevnar
13 sensitization or priming resulted in the onset and persistence of IgE-mediated allergic asthma,
unrelated to any previous exposure to an aluminum adjuvant and without the need for re-exposure.
Pet’r’s Ex. 16 at 3. During his testimony however, Dr. Garban stated “the presence of these
adjuvants or components of vaccines of previous vaccine, might result or more likely than not
resulted into [her] sensitization.” Tr. 167. Dr. Garban stated that immediately post vaccination,
Petitioner demonstrated a “systemic manifestation, like respiratory manifestation” that
“demonstrates that whatever was in that vaccine triggered an allergic response.” Tr. at 199. He
described it as a mild, type 1 hypersensitivity without anaphylaxis. Tr. 138. Dr. Novakovic also
testified that Petitioner’s reaction “was a type I hypersensitivity [that] just happened not to
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manifest with severe vasodilation,” and while not “a typical manifestation of anaphylaxis, []
worked along the same mechanisms.” Tr. 122–23.
Drs. Garban and Novakovic both opined that in Petitioner’s case, the aluminum adjuvant
in her June 15, 2015 vaccine was most likely the culprit allergen. Pet’r’s Ex. 4 at 11–12; Tr. 88.
However, they both acknowledged that a hypersensitivity reaction necessitates a prior exposure
for sensitization. Furthermore, hypersensitivity reactions are replicable. Respondent’s expert, Dr.
Byers noted that Petitioner had received at least four previous vaccines that contained aluminum:
Pneumovax in 2004 and 2013, and TdaP in 2005 and February of 2015. Resp’t’s Ex. F at 11. None
of these vaccinations occurred close in time to Petitioner’s 2003 or 2007 manifestations of
respiratory symptoms. Dr. Byers took issue with attributing Petitioner’s acute, localized reaction,
immediately post vaccination, as a type I hypersensitivity and countered that Petitioner “tolerated”
four previous instances of aluminum adjuvanted vaccinations, “including two that also contained
pneumococcus antigens, with no side effects and no evidence of a sensitization process.” Id. at 7.
Dr. Novakovic asserted that Petitioner’s previous vaccinations, containing aluminum and
pneumococcal polysaccharide, “primed her immune system which then resulted in this severe
hypersensitivity” in June of 2015. Tr. 88. Dr. Garban pointed to Petitioner’s “itching, redness, the
warm rash and some inflammatory site [] swelling,” as evidence of an early-phase, allergic reaction
followed by a chronic asthma exacerbation that left her susceptible to more frequent and severe
asthma attacks in the future. Tr. at 159–60.
However, both of Petitioner’s experts acknowledged that Petitioner’s initial reaction on
June 15, 2015, was mild with no evidence of respiratory symptoms until the late phase reaction
that occurred hours later. Petitioner’s IgE levels then jumped to 900 and 800 in July of 2015, and
the only other time in Petitioner’s medical history when her levels had been that high was in March
and April of 2008. It is during this time period that Petitioner had first been diagnosed with status
asthmaticus. This exacerbation was not associated with any of Petitioner’s previously received
adjuvanted vaccines. Similar to what occurred in 2008, following ED visits and inpatient treatment
in 2015, Petitioner’s IgE levels returned to counts of 400 and lower. Although Petitioner remained
on medication to control her symptoms beyond 2015, she was likewise prescribed a daily inhaler
to control her asthma in 2008. The medical literature filed by Petitioner suggests that it is possible
for an injected allergen to cause a severe, systemic respiratory hypersensitivity reaction, such as
an asthma attack, in cases where a person already suffers from hyperreactivity. Petitioner’s 2008
reaction, with a similar clinical presentation, clear worsening respiratory symptoms from a
previous acute, respiratory condition, and elevated IgE levels is persuasive evidence that
Petitioner’s 2015 reaction is a continuation of the progression of her asthma following allergen
exposure. It is evidence of a pre-existing airway hyperreactivity that was triggered in or around
the time of her vaccination. There is also evidence in the medical record to suggest that Petitioner’s
treaters in 2008 (antibiotics prescription) and 2015 (status asthmaticus in the setting of URI
diagnosis) believed her triggers to be infections. This is consistent with the medical literature’s
explanation of progressively worsening reactions following re-exposure to an allergen.
There is clear evidence, conceded by both sides, that Petitioner suffered from an allergic
reaction immediately following her vaccination on June 15, 2015. However, there is not
preponderant evidence that Petitioner suffered from chronic allergic inflammation due to the
Prevnar 13 vaccine. There is preponderant evidence that she was already sensitized and susceptible
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to an isolated bronchial asthma attack as described by Cockcroft. The filed medical literature
further explained how Petitioner’s localized reaction evolved into systemic injury was in the
context of acute bronchial asthma. The clear differences between Petitioner’s symptoms
immediately following her vaccination (localized, redness, itching, swelling) and four days later
(systemic, wheezing, coughing, SOB) do not, without explanation, support one extended process.
Dr. Garban did not persuasively address the effect of the previous vaccine(s) on the sensitization
process or how Petitioner’s medical history of a prior asthma exacerbation in 2008 would fit into
his theory. His simple dismissal of her 2008 incident as too remote in time to contribute to her
2015 exacerbation, eight years later, is unpersuasive and undercuts his assertion that Petitioner’s
future allergic reactions that involve the reactivity of her airways can be traced back to a vaccine
administered over eight years prior. Petitioner presented preponderant evidence that she suffered
from an acute vaccine-caused reaction; however she did not present preponderant evidence that
any one or combination of the Prevnar 13 components discussed at the hearing caused her to
develop a more systemic chronic asthma.
Dr. Novakovic’s reliance on timing is insufficient to establish causation when balanced
against the filed literature that repeatedly discussed the random nature of asthma attacks in people
with severe and chronic allergic asthma. Notably, Petitioner did not file literature that links the
Prevnar 13 vaccine to chronic allergic asthma, although other environmental triggers that
Petitioner was exposed to on a daily basis were identified.
F. Loving Factor Six/Althen Prong Three: Proximate Temporal Relationship
There is no dispute between the parties that Petitioner’s initial reaction shared an
appropriate temporal relationship with her Prevnar 13 vaccine. However, Respondent contested
any assertion that this immediate, localized reaction was an early phase, hypersensitization.
Petitioner’s contention that the immediate reaction developed into a late phase, inflammatory
reaction is also contested by Respondent. The Galli et al. article explained that “[l]ate-phase
reactions typically develop [two to six hours] after allergen exposure and often peak after [six to
nine hours].” Pet’r’s Ex. 62 at 1. Furthermore, a late-phase reaction “is usually preceded by a
clinically evident early-phase reaction and fully resolves in [one to two] days.” Id. That is
inconsistent with Petitioner’s assertion that her late-stage reaction continued to cause new
reactions years later. Petitioner has not presented preponderant evidence that her asthmatic
symptoms that began on or around June 19, 2015, have an appropriate temporal relationship with
her vaccination to be consistent with a late-phase reaction or chronic allergic inflammation.
Additionally, Petitioner has not presented preponderant evidence that her subsequent asthma flares
in response to new environmental factors have an appropriate temporal relationship to her June 15,
2015 vaccination to support causation. Petitioner’s vaccine-caused initial, localized reaction is
insufficient, without a late phase reaction or chronic allergic inflammation link, to meet the
temporality burden.
V. Conclusion
After a careful review of the record, Petitioner has failed to provide preponderant evidence
that her June 15, 2015 Prevnar 13 vaccine caused or significantly aggravated her status
asthmaticus, resulting in more severe and more frequent asthma flares that can be related back to
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her vaccination. Accordingly, Petitioner’s claim is DENIED. Absent a timely motion for review,
the Clerk is directed to enter judgment dismissing this case for insufficient proof in accordance
with Vaccine Rule 11(a). 20
IT IS SO ORDERED.
s/Herbrina D. S. Young
Herbrina D. S. Young
Special Master
20
Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint filing of a notice
renouncing the right to seek review.
41