“there is nothing ... that mandates that the testimony of a treating physician is sacrosanct—that it must be accepted in its entirety and cannot be rebutted”
How later courts described this case
- “there is nothing ... that mandates that the testimony of a treating physician is sacrosanct—that it must be accepted in its entirety and cannot be rebutted”
- explaining that although the Shyfaces did not prove that the DPT vaccine was the only or predominant cause of his death, the requirements of the Vaccine Act are met prima facie upon proof of the substantial factor criterion.
- stating that “the petitioner generally has the burden on causation, but where there are multiple independent potential causes, the government has the burden to prove that the covered vaccine did not cause the harm.”
Written by the judges who cited it.
The opinion
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 16-808V
Filed: October 20, 2020
PUBLISHED
DOLORES SOLTERO ARIAS, Special Master Horner
Petitioner,
v. Causation in fact; Guillain Barre
Syndrome (GBS); Influenza
SECRETARY OF HEALTH AND (Flu) Vaccination; Factor
HUMAN SERVICES, Unrelated; Cytomegalovirus
(CMV) infection
Respondent.
Kelly Danielle Burdette, Burdette Law, PLLC, North Bend, WA, for petitioner.
Mallori Browne Openchowski, U.S. Department of Justice, Washington, D.C., for
respondent.
RULING ON ENTITLEMENT 1
On July 7, 2016, petitioner, Dolores Soltero Arias, filed a petition under the
National Childhood Vaccine Injury Act, 42 U.S.C. § 300aa-10-34 (2012), 2 alleging that
she suffered acute inflammatory demyelinating polyneuropathy (“AIDP”) or Guillain
Barre Syndrome (“GBS”) as a result of her November 16, 2015 influenza vaccination. 3
For the reasons set forth below, I conclude that petitioner is entitled to an award of
compensation for this injury.
1 Because this decision contains a reasoned explanation for the special master’s action in this case, it will
be posted on the United States Court of Federal Claims’ website in accordance with the E-Government
Act of 2002. See 44 U.S.C. § 3501 note (2012) (Federal Management and Promotion of Electronic
Government Services). This means the decision will be available to anyone with access to the
Internet. In accordance with Vaccine Rule 18(b), petitioner has 14 days to identify and move to redact
medical or other information the disclosure of which would constitute an unwarranted invasion of privacy.
If the special master, upon review, agrees that the identified material fits within this definition, it will be
redacted from public access.
2All references to “§ 300aa” below refer to the relevant section of the Vaccine Act at 42 U.S.C. § 300aa-
10-34.
3 For purposes of this decision, the terms AIDP and GBS will be used interchangeably.
1
I. Applicable Statutory Scheme
Under the National Vaccine Injury Compensation Program, compensation
awards are made to individuals who have suffered injuries after receiving vaccines. In
general, to gain an award, a petitioner must make a number of factual demonstrations,
including showing that an individual received a vaccination covered by the statute;
received it in the United States; suffered a serious, long-standing injury; and has
received no previous award or settlement on account of the injury. Finally – and the key
question in most cases under the Program – the petitioner must also establish a causal
link between the vaccination and the injury. In some cases, the petitioner may simply
demonstrate the occurrence of what has been called a “Table Injury.” That is, it may be
shown that the vaccine recipient suffered an injury of the type enumerated in the
“Vaccine Injury Table,” corresponding to the vaccination in question, within an
applicable time period following the vaccination also specified in the Table. If so, the
Table Injury is presumed to have been caused by the vaccination. § 300aa-13(a)(1)(A);
§ 300 aa-11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B).
In many cases, however, the vaccine recipient may have suffered an injury not of
the type covered in the Vaccine Injury Table. In such instances, an alternative means
exists to demonstrate entitlement to a Program award. That is, the petitioner may gain
an award by showing that the recipient’s injury was “caused-in-fact” by the vaccination
in question. § 300aa-13(a)(1)(B); § 300aa-11(c)(1)(C)(ii). In such a situation, of course,
the presumptions available under the Vaccine Injury Table are inoperative. The burden
is on the petitioner to introduce evidence demonstrating that the vaccination actually
caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d
1274, 1278 (Fed. Cir. 2005); Hines v. Sec’y of Health & Human Servs., 940 F.2d 1518,
1525 (Fed. Cir. 1991).
In this case, petitioner alleges that she suffered Guillain Barre Syndrome or
“GBS” following her influenza vaccination. Currently, GBS is a Table Injury for the
influenza vaccination if it occurs between three and 42 days after vaccination. 42
C.F.R. § 100.3(a)(XIV). However, the petition in this case, dating back to July of 2016,
was filed prior to the March 21, 2017 addition of GBS to the Vaccine Injury Table. See
National Vaccine Injury Compensation Program: Revisions to the Vaccine Injury Table,
Final Rule, 82 Fed. Reg. 6294, Jan. 19, 2017; National Vaccine Injury Compensation
Program: Revisions to the Vaccine Injury Table, Delay of Effective Date, 82 Fed. Reg.
11321, Feb. 22, 2017 (delaying the effective date of the final rule until March 21, 2017).
Accordingly, petitioner must bear the burden of demonstrating causation-in-fact without
the benefit of a presumption of causation. § 300aa-14(c)(4) (explaining that
modifications to the Vaccine Injury Table “apply only with respect to petitions for
compensation under the Program which are filed after the effective date of such
regulation”).
The showing of “causation-in-fact” must satisfy the “preponderance of the
evidence” standard, the same standard ordinarily used in tort litigation. § 300aa-
13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 940 F.2d at 1525. Under that
2
standard, the petitioner must show that it is “more probable than not” that the
vaccination was the cause of the injury. Althen, 418 F.3d at 1279. The petitioner need
not show that the vaccination was the sole cause but must demonstrate that the
vaccination was at least a “substantial factor” in causing the condition, and was a “but
for” cause. Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344, 1352 (Fed. Cir.
1999). Thus, the petitioner must supply “proof of a logical sequence of cause and effect
showing that the vaccination was the reason for the injury[,]” with the logical sequence
being supported by “reputable medical or scientific explanation, i.e., evidence in the
form of scientific studies or expert medical testimony.” Althen, 418 F.3d at 1278; Grant
v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). A petitioner
may not receive a Vaccine Program award based solely on his or her assertions; rather,
the petition must be supported by either medical records or by the opinion of a
competent physician. § 300aa-13(a)(1).
In what has become the predominant framing of this burden of proof, the Althen
court described the “causation-in-fact” standard, as follows:
Concisely stated, Althen’s burden is to show by preponderant evidence that
the vaccination brought about her injury by providing: (1) a medical theory
causally connecting the vaccination and the injury; (2) a logical sequence
of cause and effect showing that the vaccination was the reason for the
injury; and (3) a showing of proximate temporal relationship between
vaccination and injury. If Althen satisfies this burden, she is “entitled to
recover unless the [government] shows, also by a preponderance of the
evidence, that the injury was in fact caused by factors unrelated to the
vaccine.”
Althen, 418 F.3d at 1278 (citations omitted). The Althen court noted that a petitioner
need not necessarily supply evidence from medical literature supporting petitioner’s
causation contention, so long as the petitioner supplies the medical opinion of an
expert. Id. at 1279-80. The court also indicated that, in finding causation, a Program
fact-finder may rely upon “circumstantial evidence,” which the court found to be
consistent with the “system created by Congress, in which close calls regarding
causation are resolved in favor of injured claimants.” Id. at 1280.
Generally, respondent bears the burden of demonstrating the presence of any
alternative cause by preponderant evidence only if petitioner satisfies her prima facie
burden. § 300aa-13(a)(1)(B); Walther v. Sec’y of Health & Human Servs., 485 F.3d
1146, 1150 (Fed. Cir. 2007). Respondent may also present evidence relating to an
alternative cause to demonstrate the inadequacy of petitioner’s evidence supporting her
case in chief, but petitioner does not bear the burden of eliminating alternative causes
where the other evidence on causation is sufficient to establish a prima facie case under
Althen. de Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352-53 (Fed.
Cir. 2008); Walther, 485 F.3d at 1150.
3
II. Procedural History
Based on the allegations in the petition, this case was initially assigned to the
Special Processing Unit (“SPU”) for potential discussions regarding settlement or
proffer. (ECF No. 5.) Soon thereafter petitioner filed medical records marked as
Exhibits 1 through 3 and a statement of completion. (ECF Nos. 7-14.) Additional
records were later filed as Exhibits 4 through 6. (ECF Nos. 16, 21.)
Respondent confirmed in September of 2016 that he was not amenable to
pursing settlement discussions in this case (ECF No. 18) and later filed his Rule 4(c)
report on February 17, 2017 (ECF No. 24). In his report, respondent argued that
petitioner’s medical records do not provide preponderant evidence in satisfaction of
petitioner’s prima facie burden of proof because the records document a
cytomegalovirus (“CMV”) infection, which is an established prodrome for GBS. (ECF
No. 24, p. 10.) Accompanying respondent’s report, he filed an expert report by
immunologist Kenneth Fife, M.D. (ECF No. 25; Exhibit A.)
Based on these filings, the case was removed from the SPU and reassigned to
Special Master Millman. (ECF No. 27.) Special Master Millman held a status
conference in which she explained the parties’ respective burdens of proof regarding
the significance of petitioner’s CMV infection and urged the parties to settle the case.
Respondent again declined to pursue settlement discussions and petitioner was
instructed to file an expert report responding to Dr. Fife. (ECF Nos. 30, 33.)
Subsequently, petitioner filed additional medical records marked as Exhibit 7
(ECF No. 31) and an expert report by neurologist Mary Reif, M.D. (ECF No. 36 (Ex. 8).)4
Thereafter, the parties exchanged several expert reports by Drs. Fife and Reif. (ECF
No. 40 (Ex. C); ECF No. 41 (Ex. 33); ECF No. 43 (Ex. D).) In August of 2018, petitioner
filed, but then moved to strike a third report by Dr. Reif due to incorrect exhibit
designations. (ECF Nos. 44-46.) That report was not immediately refiled.
The case was reassigned to me on June 7, 2019. (ECF No. 49.) On January 14,
2020, I issued a Scheduling Order in which I indicated that based upon my review of the
docket, respondent had not been prompted to revisit his position regarding settlement
since petitioner had filed her expert reports. (ECF No. 51.) I briefly addressed the
substance of the case and noted that the issues in the case appeared to be both narrow
and well addressed by the expert reports. (Id. at 3.) I advised that if the parties did not
wish to resolve this case informally, I may resolve the case on the written record. (Id.)
4 Confusingly, petitioner filed her expert report at ECF No. 36 without any exhibit designation and marked
the accompanying attachments (a curriculum vitae and medical literature) as Exhibits A through X.
However, petitioner had previously been using Arabic numeral designations and respondent alphabetic
designations. Accordingly, Special Master Millman issued an order redesignating petitioner’s filings as
Exhibits 8 through 32 respectively. (ECF No. 37.) Accordingly, references in this decision to Exhibit 8
refer to petitioner’s expert report filed as the main document at ECF No. 36. References to Exhibits 9-32
refer respectively to the attached documents as ECF No. 36-1, et seq, which appear incorrectly on the
docket as Exhibits A-X.
4
On June 18, 2020, respondent confirmed that he still was not amenable to settlement
discussions. (ECF No. 56.)
On June 24, 2020, I advised the parties that I intend to resolve this case based
on the written record pursuant to Vaccine Rule 8(d). (ECF No. 57.) I provided the
parties 60 days to file simultaneous briefs supporting their respective positions and a
further 30 days to file rebuttal briefs, if any. However, petitioner subsequently was
permitted to refile her previously struck expert report, which was then filed on August
13, 2020 and the parties’ briefing deadline was extended. 5 (ECF Nos. 58, 59 (Ex. 35).)
The parties filed their initial briefs on September 18, 2020. They were then
allowed until October 19, 2020, to file rebuttal briefs, but no rebuttal briefs were filed.
Based on review of the parties’ briefs, as well as the record as a whole, I have
concluded that the record is fully developed and that the parties have had a full and fair
opportunity to present their respective cases. Kreizenbeck v. Sec’y of Health & Human
Servs., 945 F.3d 1362, 1366 (Fed. Cir. 2020); see also Vaccine Rule 8(d); Vaccine Rule
3(b)(2). Accordingly, this case is now ripe for a ruling resolving entitlement.
III. Factual History
a. Prior to Petitioner’s November 16, 2015 Flu Vaccination
Petitioner received the flu vaccination at issue in this case on November 16,
2015. (Ex. 4, p. 1.) Before November of 2014, petitioner was a relatively healthy forty-
nine-year-old woman except for a history of hyperlipidemia, obesity, and an abnormal
cervical cytology. (Ex. 2, p. 1.) Petitioner received the flu shot every year since 2007
except for 2009 without any adverse effects. (Ex. 1, p. 1.)
On September 3, 2014, petitioner complained about arthritis in her hands and
was recommended fish oil and ibuprofen as needed. (Ex. 2, pp. 9-13.) During this visit,
the physician noted that petitioner suffered from occasional right upper arm pain and
pain in the right second finger, left fifth finger, and occasionally in the distal phalanx.
(Id. at 11.) However, petitioner’s pain was not severe enough to require any
medication. (Id.)
On November 24, 2014, petitioner was seen for mild-to-moderate right shoulder
pain that was described as intermittent but worsening. (Id. at 26.) Petitioner noted that
this pain was not preceded by any injury and was aggravated by lifting. (Id.)
Petitioner’s physical examination showed tenderness of her right shoulder in the upper
humerus in the lateral aspect. 6 (Id. at 28.) Petitioner’s examination also showed that
she was not suffering from any pain at the clavicle or scapula, but that she had a
5 In completing this filing, petitioner incorrectly duplicated the previously used designation of Exhibit 33. In
an order issued September 23, 2020, I redesignated this report as Exhibit 35. (ECF No. 63.)
6Although the physical exam compares the “left shoulder” to the “left arm,” it is suspected that this was a
mistake and that the physician incorrectly listed the results of petitioner’s right arm exam under the
comments of the “left arm” exam. (See Ex. 2, p. 28.)
5
decreased active range of motion. (Id.) Petitioner received a flu vaccination following
her physical examination during this visit and was diagnosed with bursitis of the right
shoulder. (Id. at 26, 29.) Petitioner was prescribed nabumetone b.i.d. and pendulum
exercises. Petitioner did not seek additional consultation for her bursitis. (Id.)
Petitioner was next seen by her physician on April 14, 2015 for a cough lasting
three weeks. (Id. at 30.) Petitioner was taking black cohosh and omega fatty acid at
this time and was recommended guaifenesin for her cough. (Id. at 31.)
On July 22, 2015, petitioner was seen for complaints about new right shoulder
pain that arose without injury and had lasted for around two months. (Ex. 2, p. 33.)
Petitioner was told to use ice or heat, over the counter painkillers, and physical therapy
to manage her pain. (Id.) Petitioner also complained of a burning sensation on the
inside and outside of her lips, as well as swelling and dryness of her lips. Petitioner’s
physician believed that petitioner’s lip condition was caused by her new toothpaste.
(Id.)
Although there is no record of the clinical visit for petitioner’s November 2015 flu
vaccination, a patient chart summary printed on June 23, 2017 indicates that she
received a flu vaccine on November 16, 2015 around 11 a.m. (Ex. 4, p. 1; Ex. 7, p. 2.)
b. After Petitioner’s November 16, 2015 Flu Vaccination
Petitioner reported to the emergency room on November 29, 2015, about two
weeks after she received the vaccination at issue in this case. (Ex. 3, p. 52.) She was
seen for generalized body aches, numbness all over, and a subjective fever that had
lasted four days. (Id.) Petitioner denied focal weakness, headache, coughing, sore
throat, and had not measured her temperature. (Id.) Petitioner was found to have 1+
occult blood in her urine and negative leukocyte esterase. (Id. at 54.) Her absolute
lymphocyte count was elevated while her white blood cell count was normal. (Id.)
Petitioner’s liver function was tested; her SGOT/AST was 402, elevated over the normal
maximum of 40. (Id. at 55.) Her SGP/ALT was 381, also elevated over the normal
maximum of 60. (Id.) Nursing triage noted a headache and diminished appetite. (Id. at
57.) Petitioner was treated with Toradol and IV fluids and anti-nausea medications. (Id.
at 56.) Petitioner was discharged with plans to follow up with her primary care provider
regarding the results of a hepatitis panel. (Id.) Petitioner tested negative for hepatitis A,
B, and C. (Id. at 66.) Petitioner was diagnosed with aches and elevated liver enzymes,
however there was an additional notation in this record that listed “viral syndrome” as
the diagnosis. (Id. at 80.)
On November 30, 2015, one day after she visited the emergency room, petitioner
reported to her primary care physician, Dr. Laurel, at Healthpoint Clinic. (Ex. 2, p. 38.)
Petitioner reported five days of sweats and chills, numbness of the upper and lower
extremities, headache, nausea, weakness, lack of appetite, posterior headache, and
mouth numbness. (Id. at 38, 40.) Dr. Laurel suspected that petitioner’s symptoms were
6
“probably [a] sign” of GBS, meningitis, or other acute illness. (Id. at 38.) Dr. Laurel
referred Petitioner to the ER. (Id.)
Following her visit to Dr. Laurel, petitioner reported to Auburn Medical Center
emergency department on November 30, 2015 for ataxia, nausea, and headache. (Id.
at 77.) She described to the attending physician a one-week course of night sweats,
fever, headache, and body aches. (Id.) Petitioner denied cough or runny nose, had a
normal head CT scan, and normal cerebral spinal fluid levels of 29 mg/dl. (Ex. 2, pp.
80, 85.) Petitioner received a neurological consult from Dr. Ashish Trivedi on November
30, 2015 while she was at the emergency room. (Ex. 3, p. 268.) Dr. Trivedi’s exam
noted absent ankle jerks and that abdominal reflexes were difficult to obtain.
Petitioner’s toes were pointing down, her reflexes were -1 in the upper extremities and
2+ at the knees. (Id. at 270.) Dr. Trivedi noted complaints of saddle distribution,
paresthesia in the feet and hands, and generalized weakness. (Id. at 269.) Dr. Trivedi
suggested a potential sensory level on the trunk at T6, and some diminished vibration in
the distal one third of the feet. (Id.) Subsequent to her neurology consult, petitioner
was deemed appropriate for admission with weakness and suspected GBS. (Ex. 2, pp.
81-82.)
Petitioner was then admitted. (Ex. 3, pp. 83, 85-86.) The attending physician
was concerned that that petitioner was suffering from acute inflammatory demyelinating
polyradiculopathy (“AIDP”), ordered a neurology consult, and prescribed five days of
gammaglobulin. (Id. at 96.) Dr. Lisa M. Soehren assessed petitioner with “saddle
anesthesia, paresthesia of the upper and lower extremities, elevated liver enzymes,
fever, and headache.” (Ex. 2, p. 85.) Petitioner’s fever was attributed to a “possible
viral illness in the last week,” and petitioner was suspected of having GBS or “other
ascending neurological disorder, myopathy, or autoimmune process.” (Id. at 85-86.)
On December 1, 2015, petitioner’s bloodwork revealed elevated liver function. (Id. at
87.) At this time, Petitioner tested negative for Epstein-Barr virus, but tested positive for
cytomegalovirus (“CMV”) at a level of 1100 IU/ml. (Ex. 3, p. 686-87.)
By December 3, 2015, petitioner was suffering additional cranial nerve problems
including right lower facial droop, bilateral lid lag, and worsening weakness of her left
upper extremities. (Ex. 2, p. 92.) Petitioner could barely open her mouth and was
having hypertensive crisis with a blood pressure of 220/120. (Id.) Tachycardia and
hyponatremia were also noted. (Id. at 88.) Petitioner’s initial exam included MRIs of
her brain and spine, performed on December 2, 2015, both of which were normal. (Id.
at 91.) Petitioner was seen by Dr. Trivedi again on this date. (Ex. 3, p. 360.) Dr.
Trivedi noted that petitioner was areflexic at the knees and that she could not get her
head off of the bed, but that she had a normal shoulder shrug. (Id.) Dr. Trivedi started
petitioner on IVIG. (Id. at 361.) IVIG was administered from December 3, 2015 to
December 7, 2015. (See id. at 361, 467.) On December 4, 2015, petitioner required
intubation. (Id. at 272.) She remained intubated until December 10, 2015. (Id. at 259.)
Petitioner was examined by Dr. Soehren on December 4, 2015. Her examination
was negative for Epstein-Barr PCR, rheumatoid factor, SSA/SSB, HIV, and
7
antimitochondrial antibodies. (Ex. 2, p. 94.) Dr. Soehren noted that petitioner’s CMV
positivity “possibly indicating cause for GBS variant.” (Id.) Petitioner was not tested for
other potential causes of GBS/AIDP including Campylobacter Jejuni, mycoplasma
pneumonia, Haemophilus influenzae, Zika, hepatitis E, and HSV.
Petitioner also underwent an electrodiagnostic test performed by Dr. Trivedi on
December 4, 2015. (Ex. 3, p. 189.) This test showed slowing on motor nerve
conductions into 15 to 30 meters per second (M/s) compared to the normal range of 40
to 60 M/s. (Id.) Dr. Trivedi performed an EMG on a limited number of petitioner’s
muscles, showing no active denervation at that time, but noted that petitioner’s results
were consistent with demyelinating polyneuropathy and diagnosed petitioner with
“presumed post viral, AIDP.” (Id. at 189, 379.) Petitioner’s vital signs subsequently
dropped, mainly worsening respiratory reserve, and she was moved to the intensive
care unit (“ICU”). (Ex. 2, p. 100-01.) At the time she was moved to the ICU, petitioner
was complaining of band-like sensation around lower chest/abdomen, increased
numbness of her lower extremities, and significant right-side mouth droop. (Id. at 100.)
On December 5, 2015, day three of five of IVIG treatment, Dr. Triveldi assessed
petitioner with AIDP and noted that petitioner was able to move all four extremities and
had gained somewhat better strength. (Ex. 3, p. 398.)
On December 6, 2015, Dr. Rizwana Khan noted that petitioner was being treated
with ceftriaxone, metronidazole, fentanyl, propofol, ranitidine, DOS, Senna, enoxaparin,
and immune globulin. (Ex. 3, p. 392.) Dr. Khan noted that petitioner had an acute
respiratory failure and that the weakness in petitioner’s upper extremities seem stable
although still areflexic. (Id. at 396.) Labs performed on December 8, 2015 showed
normal white blood cell count, slightly reduced platelet count of 136,000, and a slightly
elevated absolute lymphocyte percentage which returned to normal by December 13,
2015. (Ex. 2, p. 123.) Petitioner was discharged from the ICU on December 12, 2015,
but remained in acute hospital care until December 23, 2015. (Id. at 109; Ex. 3, p. 246.)
Petitioner’s primary diagnosis throughout her hospitalization was AIDP. (Ex. 2,
pp. 108, 120, 126.) Petitioner’s physicians consistently noted her elevated liver function
and blood pressure. (Id. at 109.) Resident physician, Sowmya Paturi, DO assessed
petitioner on December 15, 2015. (Id. at 143.) Dr. Paturi noted that petitioner was on
day fifteen of her hospitalization for AIDP and that the etiology was CMV versus
influenza vaccination. (Id.) Cecelia Dinh, DO noted on December 17, 2015 that she
suspected that petitioner’s “AIDP is possibly due to [her] recent flu vaccine or CMV as
evident in blood studies on 12/1/15.” (Id. at 153.) Dr. Dinh explained that she was
reporting petitioner’s case to the CDC so that she could “hopefully . . . be compensated
for her medical care.” (Id.; Ex. 3, p. 472-74.) Petitioner’s physician filed a report with
the Vaccine Adverse Event Reporting System (“VAERS”) on December 20, 2015. 7 (Ex.
5; Ex. 2, p. 179.)
7 The VAERS form filed by petitioner as Exhibit 5 is actually a photograph of a computer screen
displaying a website confirmation of the VAERS submission. It is too blurry to discern the details of the
report. However, Dr. Dinh separately recorded in petitioner’s medical records a confirmation that the
VAERS submission was completed online. (Ex. 2, p. 179.) According to Dr. Dinh’s note, it was reported
8
By December 22, 2015, petitioner’s attending physician noted that she was
“stable for transfer to in-patient rehab.” (Ex. 2, p. 191.) Petitioner was subsequently
transferred to Good Samaritan Hospital for rehabilitation on December 23, 2015. (Id. at
217; Ex. 3, p. 246.) Petitioner’s elevated liver enzymes gradually decreased upon
sequential testing until normalizing in mid-January 2016. (Ex. 3, p. 2766.) On January
5, 2016, petitioner’s physical therapist noted that she was able to drive an electric
wheelchair, but that she would not require the chair at discharge. (Id. at 2678.)
Petitioner was also using a left ankle foot orthosis during her rehab. (Id.) Petitioner’s
physical therapist indicated that she might benefit from bilateral ankle-foot orthoses. At
this point, petitioner was able to walk 70 feet with a front-wheeled walker, and a
moderate assist for hip alignment and balance. (Id.) Petitioner was discharged from
the Good Samaritan rehabilitation unit on January 26, 2016. (Id. at 3986.) At the time
she was discharged, petitioner was able to walk with a front-wheeled walker and had
near-independence in many daily life activities including cooking, light cleaning,
showering, and using the bathroom. (Id. at 3990.)
Petitioner began outpatient physical therapy with a consultation on February 18,
2016. (Ex. 6, pp. 2, 12.) Her diagnosis was GBS. (Id. at 12.) Petitioner complained of
left upper extremity weakness, left shoulder pain, weakness in her hands, difficulties
performing household chores, difficulties squatting, and that she became easily
fatigued. (Id.) She had 2/5 manual muscles testing strength in ankle plantarflexion, 3/5
with hip abduction and extension, 4/5 ankle dorsiflexors, and 4-/5 bilateral knee flexion.
(Id. at 42.) On that same day petitioner’s left-hand grip strength was 15 to 19 pounds
and 25 to 28 pounds on the right. (Id. at 43.) Petitioner continued her occupational
therapy until at least March 1, 2016 where petitioner’s physical therapist noted that most
mild exercises targeting petitioner’s rotator cuff caused her a great deal of pain. The
physical therapist recommended evaluation by an orthopedic surgeon.
On February 29, 2016, petitioner reported continued “tingling and burning” to her
primary care physician, Dr. Laurel. (Ex. 2, p. 43.) Dr. Laurel’s primary diagnosis was
GBS following vaccination, adhesive capsulitis of the left shoulder, and peripheral
neuropathy due to inflammation which she characterized as “secondary to GBS.” (Id.)
Dr. Laurel noted that petitioner was no longer using assistive devices despite continued,
but improved, tingling and numbness in her hands and feet. (Id.) Petitioner’s gait was
observed to be “slow, but steady” during this visit. (Id. at 47.)
Petitioner sought treatment from Dr. Laurel for her continuing left shoulder pain
on March 2, 2016. (Id. at 49.) Dr. Laurel believed that petitioner’s left frozen shoulder
pain was due to the fact that her left side was most affected by her GBS. (Id.) Dr.
Laurel observed no significant improvement in petitioner’s shoulder on March 14, 2016,
and referred her back for additional outpatient physical therapy. (Id. at 53.)
Petitioner’s left shoulder pain was evaluated on March 25, 2016. (Ex. 3, p.
4365.) Dr. Patrick Nguyen noted “dramatic improvement in terms of [petitioner’s GBS]
that petitioner received a flu vaccine on November 16, 2015, and experienced “[f]atigue, weakness, and
fever” that started November 25, 2015. (Id.)
9
where she is able to walk on her own and needs no assistive device.” (Id. at 4366.) At
this time, petitioner was only taking vitamins, sleep medicine, and nortriptyline for nerve
pain. (Id.) Dr. Nguyen believed that petitioner’s shoulder pain was not due to
musculoskeletal injury, but was most likely due to the fact that she was “still recovering
from [GBS].” (Id. at 4366-67).
On May 10, 2016, petitioner returned to Dr. Nguyen for a follow up exam on her
shoulder. (Id. at 4378.) Petitioner reported that she still experienced occasional eye
and mouth symptoms and limitation in the range of motion of her left shoulder. (Id. at
4378.) Dr. Nguyen recommended that petitioner continue her exercises and did not
recommend taking a flu shot. (Ex. 3, p. 4379-80.) Petitioner averred as of the time she
filed her petition that she continued to suffer from the ill effects of GBS. (Ex. 1, ¶ 6.)
Subsequent records show that peripheral neuropathy secondary to GBS remained on
petitioner’s active problems list as of June 2017 and that she continued to take
nortriptyline at that time. (Ex. 7.)
IV. Expert Opinions
In this case, respondent presented the first expert opinion along with his Rule 4
report. Respondent filed a report by Dr. Kenneth H. Fife, M.D. Ph.D to support his
contention that petitioner’s GBS was likely caused by a CMV infection and not her
November 16, 2015 flu vaccination. Dr. Fife is board certified in internal medicine and
board eligible in infectious diseases. 8 (Ex. A, p. 1.) In response, petitioner presented
an opinion by neurologist Dr. Mary Reif to support the claim that her GBS was caused
by her November 16, 2015 flu vaccination. 9 (Ex. 8.)
a. Dr. Fife’s Initial Report
Dr. Fife notes that when petitioner was initially hospitalized for her AIDP, she
presented with elevated liver enzymes, a finding he suggests is not usually associated
with AIDP. (Ex. A, p. 3.) Based on her elevated liver function, petitioner was tested and
found positive for CMV. (Id.) Dr. Fife points out that CMV infections often involve the
liver and that half of GBS patients associated with CMV present with elevated liver
enzymes. (Id.) Dr. Fife concludes, based on these facts, that petitioner’s elevated liver
enzymes strongly suggest an ongoing CMV infection. (Id.) Dr. Fife explains that after
petitioner’s positive PCR assay for CMV, her attending physicians began to note a
potential link between her GBS and November 16th flu vaccination relative to the
8 Dr. Fife is currently Professor of Medicine in the Division of Infectious Diseases and holds appointments
in the Departments of Microbiology & Immunology and Pathology at the Indiana University School of
Medicine. (Ex. A, p. 1.) Dr. Fife is a fellow of the American College of Physicians and a Fellow of the
Infectious Diseases Society of America. (Id.) His bibliography includes 144 peer-reviewed publications, 8
of which relate to vaccine development and testing. (Id.)
9 Dr. Reif received her medical degree in 1978 from the University of Iowa. (Ex. 9, p. 1.) She is licensed
by the National Board of Medical Examiners and the State of Washington. (Id.) She has researched
neurological conditions, with an emphasis on multiple sclerosis, since 1995. (Id. at 2.) Currently, Dr. Reif
serves as a neurologist for Swedish Medical Group in Seattle. (Id. at 1.)
10
potential for compensation. (Id.) Dr. Fife does not suggest any impropriety based on
these notes but concludes that “there is certainly no medical justification for narrowing
the petitioner’s diagnostic possibilities down to a single entity.” (Id.)
Dr. Fife concludes that petitioner’s GBS was most likely caused by her CMV
infection and not by the flu vaccine. (Id.) According to Dr. Fife, GBS has been linked to
influenza vaccines, however, “the vast majority” of those cases were linked to the
A/New Jersey vaccination administered in the United States from 1976-77. (Ex. A, p.
3.) Dr. Fife states that since that time, GBS cases following flu vaccines are rare and
may be purely coincidental. (Id.) Dr. Fife contrasts these statistics with the fact that
CMV is associated with 10-15% of GBS cases. (Id.) Based on the potentially
coincidental nature of vaccine-induced GBS, and the rate of CMV-associated GBS
cases, Dr. Fife concludes that it is over 100 times more likely that petitioner’s GBS was
the result of a CMV infection than an adverse reaction to the flu vaccine. (Id.)
b. Dr. Reif’s Initial Report
Dr. Reif notes that petitioner’s GBS began on approximately November 25, 2015,
about ten days after her flu vaccination. (Ex. 8, p. 6.) According to Dr. Reif, a
“stimulus,” either infectious or immune stimulating, is found prior to onset in two-thirds of
GBS cases. (Id.) Dr. Reif indicates that although the antecedent stimulus is self-limiting
in GBS cases, it creates a “cascade of immune events” which cannot be stopped once
started that ultimately lead to GBS. (Id. (citing Emily J. Woo, Scott K. Winiecki, & Alan
C. Ou, Motor Palsies of Cranial Nerves (Excluding VII) After Vaccination. Reports to US
Vaccine Adverse Event Reporting System, 10 HUMAN VACCINES AND
IMMUNOTHERAPEUTICS 301-05 (2014) (Ex. 20).).) This cascade phenomenon is believed
to be caused by molecular mimicry and other unknown immunological factors, including
the host’s genetic markers. (Ex. 8, p. 6.) Additionally, Dr. Reif explains that petitioner’s
onset of weakness was 1-2 weeks post immunization, consistent with the standard
onset following an antecedent event in all cases of GBS regardless of etiology. (Id.)
Dr. Reif explains that CMV is nearly as ubiquitous as Herpes Type 1, meaning
there is a high likelihood that Petitioner had contracted the virus at some point prior to
her vaccination. (Id.) CMV is a virus that remains dormant once the host is infected.
(Id. at 7.) Dr. Reif notes that because an IgG antibody test for CMV was never
performed, it is impossible to determine precisely whether petitioner’s CMV was a
chronic or primary infection. (Id.) Dr. Reif notes that while petitioner was positive for
CMV, she never presented with a sore throat, the most common presentation of a
primary CMV infection and was not caring for grandchildren nor any other infants which
Dr. Reif explains is the “main vector” in primary CMV infections in late adulthood. (Id.
(citing Awad Al-Omani et al., Cytomegalovirus Infection in Immunocompetent Critically
Ill Adults: Literature Review, 6 ANNALS OF INTENSIVE CARE 110 (2016) (Ex. 15.)).) Dr.
Reif believes that petitioner’s positive CMV assay was the result of a reactivation of a
chronic infection and not a primary infection. (Id.) In support of that position, Dr. Reif
cites a study finding that 36% of ICU patients have reactivated CMV infections due to
extreme physiologic stress. (Ex. 8, p. 7; Al-Omani et al., supra, at Ex. 15.) Dr. Reif
11
notes that although petitioner was CMV positive prior to being admitted to the ICU, she
had been extremely ill and was therefore under levels of stress comparable to the ICU
patients in the study. (Id.)
Although CMV infection can be accompanied by disturbed liver function, Dr. Reif
explains that GBS can also be accompanied by disturbed liver function when no
etiologic agent is defined. (Id.) Dr. Reif cites a study finding 38 out of 100 GBS patients
had abnormal liver function tests, but only 10 out of that 100 were CMV positive. (Id.
(citing Peter G. Oomes et al., Liver Function Disturbances in Guillain-Barre Syndrome:
A Prospective Longitudinal Study in 100 Patients, 46 NEUROLOGY 96 (1996) (Ex. 16.)).)
Finally, Dr. Reif also proposes that the presence of CMV will improve the immune
response to influenza. This means that petitioner’s reactivated CMV could add to her
increased immune response to the flu vaccine and increase the likelihood of a
cascading immune response leading to GBS. She explained that numerous viral
reactivations and neurological conditions can occur after flu vaccinations including HSV-
1, HSV-2, Herpes Zoster, transverse myelitis, and cranial nerve palsies. (Id.) She also
proposes that even seasonal flu shots can generate not only the seasonal antibodies
that they are intended to generate, but also polyclonal varied neutralizing antibodies that
can cross react with prior vaccinations such as H1N1 or H5N1, which can be more
pathological for the molecular mimicry associated with GBS. (Ex. 8, p. 8 (citing Davide
Corti et al., Heterosubtypic Neutralizing Antibodies are Produced by Individuals
Immunized with a Seasonal Influenza Vaccine, 120 J. OF CLINICAL INVESTIGATION 1663
(2010) (EX. 14.)).) Based on these findings, Dr. Reif concludes that it is possible for the
flu vaccine to reactivate CMV. (Ex. 8, p. 8.)
c. Dr. Fife’s First Supplemental Report
In his second report, Dr. Fife notes that while it took at least ten days from
admission for ICU patients with reactivating CMV to reach a viral load of 1000 in the
ICU study cited by Dr. Reif, petitioner reached that viral load in a matter of days after
being admitted to the ICU. (Ex. C, pp. 1-2.) Dr. Fife suggests that petitioner’s rapid
viral load increase is more indicative of a primary CMV infection. (Id. at 2.) He further
indicates that “[i]t is not possible to determine when the petitioner was first infected with
CMV, so it remains plausible that she had a primary CMV infection at the time of the
neurological illness. In addition, although most studies that associate CMV with
AIDP/GBS focus on primary CMV infection, it is not known whether reactivated CMV
infection can trigger AIDP/GBS. Many of the studies of CMV and AIDP/GBS were done
before the advent of sensitive molecular techniques that can detect CMV reactivation.”
(Id.at 1.) Dr. Fife also asserts that while elevated liver function can occur without a
primary CMV infection, the alternative explanations offered by petitioner are less likely
than a primary CMV infection to have caused her elevated liver enzymes. (Id.)
Although some cases have linked the flu vaccine to reactivation of herpesviruses, these
studies fail to establish a causal relationship. (Id.)
12
d. Dr. Reif’s First Supplemental Report
In her second report, Dr. Reif notes that there is no data available to support the
idea that reactivated CMV can cause GBS. (Ex. 34, p. 1.) Further, Dr. Reif states that if
it were true that reactivated CMV caused GBS, there would be a noticeable trend in the
ICU and neurological communities. Because there has been no such trend, Dr. Reif is
confident concluding that reactivated CMV cannot trigger GBS. (Id.)
Dr. Reif disagrees with Dr. Fife’s suggestion that petitioner’s CMV titer levels
were too high too quickly in comparison to the subjects of the ICU study cited in her
prior report. (Ex. 34, p. 1.) In the ICU study, viral loads of reactivated CMV in ICU
patients took at least ten days to exceed 1000 titers. (Al-Omani et al., supra, at Ex. 15.)
Dr. Reif stresses, however, that the study did not correlate titer levels with severity of
illness. (Id.) Dr. Reif further explains that petitioner’s viral load was ultimately within the
boundaries of typical reactivation cases regardless of the rate at which she developed
that viral load. (Id. at 1-2.) Dr. Reif concludes that the rapid increase in petitioner’s viral
load does not eliminate the possibility that petitioner’s CMV was the result of
reactivation. (Id. at 2.)
e. Dr. Fife’s Final Supplemental Report
Dr. Fife’s final supplemental report agrees that petitioner was at high risk of
contracting CMV early in her life, but notes that there is still a small chance that this was
her first CMV infection. (Ex. D, p. 1.) Dr. Fife cites several reports which found that
reactivated CMV caused GBS in organ transplant patients to counter Dr. Reif’s
argument that there is no evidence that reactivated CMV can cause GBS. (Id.) Dr. Fife
restates his argument regarding petitioner’s CMV viral load, stating that “the fact that the
petitioner had levels above 1000 on her second hospital day suggests that the CMV
[reactivation] . . . occurred before hospitalization and the acute neurological illness,
again consistent with CMV as a cause of the neurologic illness.” (Id. at 1-2.)
Dr. Fife notes that while Dr. Reif has provided a variety of explanations beside
CMV for petitioner’s elevated liver function, elevated liver function is nonetheless
strongly associated with CMV. (Id. at 2.) Dr. Fife explains that petitioner’s liver enzyme
elevation was 8.3 times the upper limit of normal which is common with CMV infection
but much less common in AIDP. (Id.) Based on these facts, Dr. Fife concludes that
CMV remains the most likely cause of petitioner’s elevated liver function. (Id. at 2.)
Dr. Fife concludes his report stating that “it is plausible that the petitioner had a
CMV reactivation rather than a primary CMV infection at the time of her hospitalization.”
But because reactivated CMV has been shown to cause AIDP, he opines that CMV
infection remains “the most probable cause” of petitioner’s GBS. (Id. at 2.)
13
f. Dr. Reif’s Final Supplemental Report
Dr. Reif’s final report addresses Dr. Fife’s later assertion that CMV reactivation
can trigger GBS. Dr. Reif notes that the first study he cited focuses on organ transplant
patients who are clearly immunodeficient, a cohort that petitioner is not in. (Ex. 35, p.
1.) The second study focuses on organ transplant patients and HIV positive patients,
who are also clearly immunocompromised. Dr. Reif concludes that because there is no
evidence that petitioner was immunocompromised, neither of these studies are relevant
to petitioner’s case. (Id.)
V. Analysis of Petitioner’s Prima Facie Showing Under Althen
As explained above, petitioner’s burden is to demonstrate by preponderant
evidence each of the three Althen prongs for determining causation-in-fact (i.e. a
medical theory, a logical sequence of cause and effect, and a proximate temporal
relationship). Althen, 418 F.3d at 1278. Provided petitioner can affirmatively meet this
burden, she bears no burden of eliminating alternative causes. Walther, 485 F.3d at
1150; de Bazan, 539 F.3d at 1352. Importantly, however, respondent may present
evidence relating to an alternative cause to demonstrate the inadequacy of petitioner’s
evidence supporting her case in chief. de Bazan, 539 F.3d at 1353.
a. Althen Prong One
Petitioner’s burden under the first Althen prong is to provide, by preponderant
evidence, “a medical theory causally connecting the vaccination and the injury.” Id. at
1278. Such a theory must only be “legally probable, not medically or scientifically
certain.” Knudsen v. Sec’y of Human & Health Servs., 35 F.3d 543, 549 (Fed. Cir.
1994). Here I find that petitioner has presented preponderant evidence pursuant to
Althen prong one that the influenza vaccine can cause GBS.
Dr. Reif persuasively opined that the influenza vaccine can cause GBS. 10 (Ex. 8,
pp. 7-8.) This is based on several factors. First, Dr. Reif explains that it is generally
accepted that GBS constitutes a post-infectious or post-inflammatory autoimmune
reaction affecting the peripheral nerves. It is also generally accepted that this
autoimmune process likely results from molecular mimicry. (Id. at 6.) Moreover, studies
have confirmed that certain formulations of the influenza vaccination, most notably the
1975-76 swine flu and 2009 H1N1 vaccines, have been clearly associated with
increased incidents of GBS. Additionally, although the strongest evidence has related
to pandemic formulations, seasonal influenza vaccinations have also been shown to
10Notably, Dr. Reif’s opinion is also consistent with prior Program cases. Even before inclusion of GBS
on the Vaccine Injury Table, prior decisions had concluded that the association between influenza
vaccination and GBS satisfies Althen prong one’s “can cause” requirement. See, e.g., Stitt v. Sec'y of
Health & Human Servs., No. 09–653V, 2013 WL 3356791 (Fed. Cl. Spec. Mstr. May 31, 2013); Stewart v.
Sec'y of Health & Human Servs., No. 06–777V, 2011 WL 3241585, at *16 (Fed. Cl. Spec. Mstr. July 8,
2011); see also Barone v. Sec'y of Health & Human Servs., No. 11–707V, 2014 WL 6834557 (Fed. Cl.
Spec. Mstr. Nov. 12, 2014).
14
demonstrate some increase in incidences of GBS. (See e.g., L.H. Martin Arias et al.,
Guillain-Barre Syndrome and Influenza Vaccines: A Meta-Analysis, 33 VACCINE 3773
(2015) (Ex. 12); Woo, Winiecki & Ou., supra, at EX. 20.)
Much of Dr. Fife’s opinion stresses that there is a stronger association between
CMV infection and GBS than between influenza vaccination and GBS. (Ex. A). This
does not refute petitioner’s demonstration of a medical theory connecting the influenza
vaccine to GBS under Althen prong one. Since GBS is generally accepted to be
associated with multiple different antecedent events, the fact that an unrelated trigger
potentially explains a greater number of cases does not in itself necessarily diminish the
evidence favoring a connection between GBS and vaccination. Accord Knudsen, 35
F.3d at 550 (observing in a different context that “[t]he bare statistical fact that there are
more reported cases of viral encephalopathies than there are reported cases of DTP
encephalopathies is not evidence that in a particular case an encephalopathy following
a DTP vaccination was in fact caused by a viral infection present in the child and not
caused by the DTP vaccine.”).
b. Althen Prong Two
The second Althen prong requires proof of a logical sequence of cause and
effect usually supported by facts derived from a petitioner's medical records. Althen,
418 F.3d at 1278; Andreu, 569 F.3d at 1375–77; Capizzano, 440 F.3d at 1326; Grant v.
Sec'y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). However,
medical records and/or statements of a treating physician do not per se bind the special
master to adopt the conclusions of such an individual, even if they must be considered
and carefully evaluated. See Section 13(b)(1) (providing that “[a]ny such diagnosis,
conclusion, judgment, test result, report, or summary shall not be binding on the special
master or court”); Snyder v. Sec'y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67
(2009) (“there is nothing ... that mandates that the testimony of a treating physician is
sacrosanct—that it must be accepted in its entirety and cannot be rebutted”).
In this case, petitioner’s correct diagnosis is undisputed. Petitioner’s treating
physicians and both experts all agree that petitioner suffered GBS. With regard to the
cause of that condition, however, onset of petitioner’s GBS occurred approximately ten
days after her flu vaccination, but also in the course of an apparent viral illness. During
her hospitalization she later tested positive for the CMV virus on PCR assay. (Ex. 3, p.
686.) Petitioner’s treating physicians were unwilling to rule out either her influenza
vaccination or a CMV infection as the cause of her GBS. Although petitioner’s
physicians initially suspected a post-viral etiology, they also later completed a VAERS
report (Ex. 5) and included a diagnosis of vaccine-caused GBS in her assessment (Ex.
2, p. 153). 11 Ultimately, when petitioner was released to rehabilitation her diagnosis
11 Dr. Fife stresses notations in petitioner’s medical records indicating that her treating physicians were
aware that petitioner may be entitled to compensation if her injury was caused by her vaccination. (Ex. A,
p. 3.) Although he is careful to note he is not suggesting impropriety, he nonetheless intimates that the
notations linking petitioner’s GBS to her influenza vaccine may not have been motivated purely by
medical judgment. (Id.) Respondent also implicitly argues that the earlier impression of a post-viral
etiology should be more persuasive because “[t]here was no subsequent testing or medical explanation
15
was AIDP “possibly due to recent flu vaccine or CMV as evidenced in blood studies.”
(Ex. 2, p. 187.)
For her part, Dr. Reif similarly explained that the onset and course of petitioner’s
GBS is “very standard” and consistent with an antecedent event occurring one to two
weeks prior, regardless of whether that event was viral, bacterial, or otherwise immune
stimulated (i.e. by vaccination). (Ex. 8, p. 6.) Dr. Reif indicated that petitioner’s lab
results are inadequate to “forensically” determine the cause of her GBS. (Id. at 6.) She
did, however, indicate that petitioner’s presentation with a viral illness lacked any
indication of a sore throat, which she characterized as a hallmark of an active CMV
infection. (Id. at 7.) In contrast, Dr. Fife suggested that petitioner’s own clinical course,
with severe sensory deficits, respiratory involvement, and prolonged recovery period, is
consistent with the same subgroup of GBS that is typically associated with CMV. (Ex.
C, p. 3.) This was also considered by the treating neurologist. (Ex. 2, p. 95.)
While Dr. Fife’s observation regarding petitioner’s clinical presentation potentially
provides some evidence supportive of CMV as a possible cause of petitioner’s injury, it
does not establish CMV as a more likely cause. Although Dr. Fife suggests that CMV-
caused GBS has a tendency toward a certain clinical presentation, he has not asserted,
let alone substantiated, that this presentation represents any contrast to the expected
presentation for a vaccine-caused GBS. 12 In that regard, the same literature Dr. Fife
cites for the concept of a CMV-infection subtype cautions that “none of the associations
is perfect.” (Frans Van Der Meche et al., Diagnostic and Classification Criteria for the
Guillain-Barre Syndrome, 45 EUR. NEUROLOGY 133 (2001) (Ex. C, Tab 7, p. 2).) That
article includes a Venn diagram showing that the subtypes of GBS overlap. (Id. at Fig.
1.) And, despite having specifically considered whether petitioner’s clinical picture best
for the changes in her diagnosis after petitioner’s discharge from the hospital.” (ECF No. 62, p. 15 (citing
petitioner’s primary care record at Ex. 2, p. 43).) Upon my own review, I do not believe that the medical
records support this skepticism of the treating physicians for several reasons. First, Dr. Fife’s suspicion is
prompted in part by his own apparent confidence in CMV as the more likely cause of petitioner’s GBS, but
this is not a confidence shared by petitioner’s treating physicians. The records stress that petitioner’s
physicians felt her GBS was only “presumed” to be post-viral or that a post-viral etiology was “possibly”
indicated and never expressed full confidence in CMV infection as the cause of her GBS. (Ex. 3, p. 379;
Ex. 2, p. 153.) Additionally, and to respondent’s related point, the records are clear that post-vaccination
GBS was part of petitioner’s assessment during her hospitalization and not merely after the fact. Second,
the specific notations at issue are explicit in expressing that an adverse vaccine event report would be
submitted only in good faith. Specifically, Dr. Dinh recorded that “[s]uspect that pt’s AIDP is possibly due
to recent flu vaccine or CMV as evident in blood studies on 12/1/15. If this is the case, will report pt’s case
to CDC and pt may be able to be compensated for her medical management.” (Ex. 3, p. 474 (emphasis
added).) Third, petitioner’s hospital discharge records show that her physicians maintained CMV as a
possible cause of petitioner’s GBS even after discussing that an adverse vaccine event may be reported.
(Ex. 2, p. 187.) For these reasons, I see no basis for suggesting that petitioner’s potential for
compensation influenced her physicians’ clinical impressions, changed their diagnostic assessments, or
that their consideration of vaccine causation otherwise constituted an unexplained afterthought.
12
For example, the Qualifications and Aids to Interpretation for the Vaccine Injury Table identifies GBS as
a spectrum of four subtypes any one of which may be entitled to a causal presumption as a Table Injury.
See 42 C.F.R. § 100.3(c)(15).
16
fit post-CMV GBS, the treating physicians still remained unwilling to rule out petitioner’s
vaccination as the cause. (Ex. 2, p. 153.) “[T]reating physicians are likely to be in the
best position to determine whether ‘a logical sequence of cause and effect show[s] that
the vaccination was the reason for the injury.’” Capizzano, 440 F.3d at 1326 (quoting
Althen, 418 F.3d at 1280).) In any event, Dr. Fife also agreed that there is no “definitive
proof” regarding the etiology of petitioner’s GBS. (Ex. A, p. 3.) Further, in discussing
the evolution of petitioner’s diagnosis and certain notations that leaned more heavily in
favor of petitioner’s vaccination as the cause of her GBS, Dr. Fife stressed that “[t]here
is certainly no medical justification for narrowing the petitioner’s diagnostic possibilities
down to a single entity.” 13 (Id.)
Without more, this would suggest that petitioner has met her initial burden, as
she has presented both treating physician and expert opinion directly linking her
vaccination to her injury as one of two medically reasonable causes that cannot be
distinguished. Because petitioner’s clinical history presents a logical sequence of cause
and effect consistent with vaccine causation, she need not eliminate CMV infection as
an alternative cause. Walther, 485 F.3d at 1151 (stating that “the petitioner generally
has the burden on causation, but where there are multiple independent potential
causes, the government has the burden to prove that the covered vaccine did not cause
the harm.”). Even if the viral illness and flu vaccine operated in conjunction to cause
petitioner’s GBS, petitioner would still be able to meet her burden of proof. 14 Shyface,
165 F.3d at 1353 (explaining that although the Shyfaces did not prove that the DPT
vaccine was the only or predominant cause of his death, the requirements of the
Vaccine Act are met prima facie upon proof of the substantial factor criterion.).
However, in addition to discussing her clinical presentation as a whole, Dr. Fife did also
raise two discrete points regarding petitioner’s own clinical presentation which he felt
evidenced CMV as the more likely cause of petitioner’s GBS in preference to
vaccination. These issues warrant further discussion; nevertheless, Dr. Reif’s opinion
supporting vaccine causation satisfactorily accounts for both points.
First, Dr. Fife stressed the fact of the positive CMV finding itself. He noted that “a
serum PCR assay for cytomegalovirus (CMV) (a test that detects the presence of viral
genetic material in the blood) was sent and it was positive, documenting the presence of
virus in the bloodstream.” (Ex. A, p. 3.) Dr. Reif persuasively explained, however, that
CMV infection is prevalent among the adult population, especially among Hispanic
women, and that once infected a person retains the virus in latency throughout life. (Ex.
8, pp. 6-7.) Although petitioner’s PCR assay showed that she had the virus circulating
13 To be clear, Dr. Fife’s statement was intended to convey in response to notations regarding vaccination
as a possible cause that CMV infection could not reasonably be ruled out as a cause of the GBS.
Nonetheless, this statement is also operates as an explicit ratification of the treating physicians’ inclusion
of both the CMV and flu vaccine as potential causes.
14 Dr. Reif suggested not only that petitioner’s influenza vaccination could have reactivated her latent
CMV infection, but also that her CMV positivity could have been an enhancing factor that contributed to
her risk of developing GBS as a response to her influenza vaccination. (Ex. 8, p. 8.) For all the reasons
discussed herein I did not find it necessary to reach that question.
17
in her bloodstream, physiological stress from illness or trauma has been shown to
reactivate the virus. (Id.) For example, Dr. Reif cited a study showing positive PCR
assays among ICU patients. (Id. at 7.) Accordingly, Dr. Reif opined that petitioner’s
positive PCR assay is more likely a further consequence of her post-vaccination
condition than a separate cause of her GBS. 15 (Id. at 8.)
Although he continued to maintain that reactivated CMV could still be a cause of
petitioner’s GBS (discussed separately in Section VI below), Dr. Fife ultimately agreed
that petitioner’s PCR assay was more likely to be explained by reactivation and that
there is only a “small chance” that she was experiencing a primary CMV infection at the
time of her PCR assay. (Ex. D, p. 1.) Dr. Fife did not dispute Dr. Reif’s opinion that the
physiological stress of acute illness can cause viral reactivation, but he did question the
timing in this case. (Ex. C, pp. 1-2.) He indicated that based on the study cited by Dr.
Reif, it takes at least ten days of acute illness for patients to develop a CMV load
comparable to what was measured in petitioner. (Id.) However, the evidence does not
support Dr. Fife’s suggestion of any identifiable threshold interval for the presence of a
significant viral load. Petitioner’s PCR assay was collected on December 1, two weeks
following her influenza vaccination and about one week following onset of both her
possible viral illness and GBS. (Ex. 3, p. 686.) This remains consistent with Dr. Reif’s
opinion that reactivation followed vaccination and illness. 16
15 Notably, if petitioner’s positive finding for CMV was only a downstream consequence of her post-
vaccination condition, that leaves the etiology of her presumed viral syndrome unclear. That would refute
several points raised by Dr. Fife but would not preclude the presumed viral illness from being a possible
cause of petitioner’s GBS even if it were not CMV. Significant to that point, as noted above, Dr. Reif
opined that petitioner’s presentation is consistent with a prior antecedent event whether bacterial, viral, or
otherwise immune. (Ex. 8, p. 6.) This would still be consistent with the idea that petitioner suffered GBS
the etiology of which cannot be distinguished as between vaccination and unspecified viral illness, which,
as explained above, is consistent with petitioner’s burden of proof.
16
Specifically, Dr. Fife derives the ten-day period from a chart he highlighted from a review article. (Ex. C,
p. 2 (Ajit P. Limaye & Michael Boeckh, Cytomegalovirus (CMV) in Critically-Ill Patients: Pathogen or
Bystander?, 20 REV. MED. Virol 372 (2010) (Ex. C, Tab 2).) This chart is based on a single study not
otherwise a part of the record and speaks only to the probability that a CMV load will be detected in a
patient and does not purport to create a threshold of what is physiologically possible. Moreover, Dr. Reif
contends that the study findings do not correlate titer levels to severity of illness, making it impossible for
Dr. Fife to suggest that high titer levels necessarily indicate a primary infection. (Ex. 34, pp. 1-2.) The
review paper itself otherwise notes that time to detectable levels of CMV can be as little as three days.
(Limaye and Boeckh, supra, at Ex. C, Tab 2, p. 3 (Table 4).) However, separate figures are not provided
for the higher loads Dr. Fife referenced. (Id.) In any event, the authors of the review paper caution that
prior studies have suffered significant limitations, including small population size and variations in findings
based on the sensitivity of the method of detection. (Limaye and Boeckh, supra, at Ex. C, Tab 2, p. 2.) A
separate review paper, which examined the same study among others, suggested that CMV disease
occurs at any time “within the first 2 weeks of critical illness” and further explained that PCR detection is
the most sensitive diagnostic test for CMV. (Al-Omani et al., supra, at Ex. 15, p. 10.) Dr. Fife’s point is
well taken to the extent that these studies tend to show that it generally appears likely that it takes longer
to reach a higher viral load, but these studies are inadequate to assert that any specific timeframe is
necessary to reach such viral loads.
18
Second, Dr. Fife indicated that “CMV infection often involves the liver, and over
half of patients with Guillian-Barre syndrome (or AIDP) associated with CMV infection
present with elevated liver enzymes. The fact that the patient presented with elevated
liver enzymes and continued to have liver enzyme elevations until Jan 13 in the
absence of any other apparent cause strongly suggests that she had ongoing CMV
infection.” (Id.) In that regard, Dr. Reif explained that while liver dysfunction can be
associated with CMV infection, it is also present among GBS patients even in the
absence of any known cause. (Ex. 8, p. 7.) Dr. Reif cited a study of 100 GBS patients.
(Id. (citing Peter G. Oomes et al., Liver Function Disturbances in Guillain-Barre
Syndrome: A Prospective Longitudinal Study in 100 Patients, 46 NEUROLOGY 96 (1996)
(Ex. 16.)).) Thirty-eight subjects had evidence of liver dysfunction while only 10 of those
subjects were positive for CMV infection. The remaining 28 were negative for other
known causes of liver damage. (Oomes et al., supra, at Ex. 16, p. 1.) The study also
found that treatment with IVIG “significantly increased” liver function disturbances. (Id.
at 6.) The authors concluded “that in GBS some [liver function disturbances] may be
transiently present without obvious cause and that treatment with [IVIG] may increase
these abnormalities.” 17 (Id.)
Dr. Fife responded by noting that petitioner’s own enzyme elevations were 8.3
times the upper limit for normal whereas most of the study subjects had enzyme
findings of no more than four times the upper limit. (Ex. C, p. 2.) While Dr. Fife is
correct that this would place petitioner with a minority of the test subjects, he also
acknowledged that eight study subjects had enzyme findings in excess of four times the
normal limit and only half of those subjects in this higher category were CMV-infected.
(Id.) Accordingly, Dr. Fife confirms that petitioner’s degree of elevation still potentially
fits the study’s findings even in the absence of CMV-caused GBS.
Nonetheless, Dr. Fife contends that the fact that half of the relevant subset of
study subjects had CMV infection represents a “strong association.” (Ex. D, p. 2.) This
is unpersuasive in the context of the study. It is not disputed that CMV infection can be
associated with liver function disturbances. Yet this study demonstrates that,
regardless of how often liver dysfunction follows CMV infection, CMV infection does not
conversely explain liver function disturbances among a majority share of GBS patients
who exhibit such disturbance, even including some with significantly elevated enzymes.
Dr. Fife also noted that one possible explanation for the study findings was under-
reporting of CMV infections. (Ex. D, p. 2.) However, the authors also posited a direct
immune-mediated explanation for the liver dysfunction and ultimately concluded that the
17 Among the group of patients receiving IVIG, the study saw a significant increase in the number of
patients experiencing liver function disturbances, from 35% at admission to 69% after IVIG treatment.
The increase in incidences of liver function disturbances dropped significantly by four weeks post
treatment, but did not fall to below the rate seen among the control group until fourteen weeks post-
treatment. (Oomes et al., supra, at Ex. 16, p. 3.) Overall, liver function disturbances peaked at either two
weeks post-admission or one-week post-IVIG. (Id. at 6.) In this case, petitioner was found to have
elevated liver enzymes upon admission which decreased during the course of her hospitalization. (Ex. 2,
p. 88.) They had returned to normal range by January 13, 2016, approximately six weeks after her initial
hospitalization. (Ex. 3, p. 2766.) Potentially consistent with this study, an autoimmune process affecting
the liver was suspected. (Ex. 2, p. 88.)
19
liver dysfunction is present “without obvious causes.” (Oomes et al., supra, at Ex. 16, p.
6.)
When examined in detail, the expert presentations in this case underscore why
petitioner’s treating physicians were unable to definitively identify her GBS as either
CMV-caused or vaccine-caused. Ultimately, Dr. Fife was correct to suggest that “[t]here
is certainly no medical justification for narrowing the petitioner’s diagnostic possibilities
down to a single entity.” (Ex. A, p. 3.) Although Dr. Fife highlights some points
potentially supportive of CMV as a cause of petitioner’s GBS, for the reasons discussed
above, none of these points are able to outweigh Dr. Reif’s competing opinion that
petitioner’s clinical course was nonetheless also consistent with vaccine-causation.
In light of all of the above, I find that petitioner has presented preponderant
evidence of a logical sequence of cause and effect, based on her own clinical history,
demonstrating that her influenza vaccination did cause or substantially contribute to her
GBS. Accordingly, she has satisfied her burden of proof under Althen prong two.
c. Althen Prong Three
The third Althen prong requires establishing a “proximate temporal relationship”
between the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term
has been equated to the phrase “medically-acceptable temporal relationship.” Id. Here,
the timing in this case is not controversial and I find that there is preponderant evidence
of a proximate temporal relationship between petitioner’s influenza vaccination and her
GBS. Dr. Reif explained that the onset of petitioner’s GBS, which occurred between
one to two weeks following her vaccination, is consistent with current understanding of
GBS onset following an antecedent event. 18 (Ex. 8, pp. 6, 8.) Although Dr. Fife
preferred CMV as the cause of petitioner’s GBS based on petitioner’s clinical picture, he
did not raise any question as to a medically acceptable temporal relationship in this
case between the vaccination and onset of petitioner’s GBS. (See Exs. A, C, and D
generally.)
VI. Analysis of Respondent’s Presentation of Factors Unrelated to
Vaccination
Based on the analysis above, petitioner has presented a prima facie case that
her GBS was, in fact, caused by her influenza vaccination by demonstrating each of the
three Althen prongs by preponderant evidence. Once petitioner has satisfied her own
18 This is also consistent with prior cases which have generally identified a relevant medically reasonable
period of onset for GBS. Daily v. Sec’y of Health & Human Servs., No. 07-173V, 2011 WL 2174535, at *9
(Fed. Cl. Spec. Mstr. May 11, 2011) (accepting two weeks as an appropriate latency for post-vaccination
GBS); Barone v. Sec’y of Health & Human Servs., No. 11-707V, 2014 WL 6834557, at *13 (Fed. Cl.
Spec. Mstr. Nov. 12, 2014) (accepting a latency for GBS of up to six to seven weeks post-vaccination);
Accord Aguayo v. Sec’y of Health & Human Servs., No. 12-563V, 2013 WL 441013, at *3 (Fed. Cl. Spec.
Mstr. Jan. 15, 2013) (rejecting a latency of three- and one-half months for GBS); Corder v. Sec’y of Health
&Human Servs., No. 08-228V, 2011 WL 2469736, at *27-29 (Fed. Cl. Spec. Mstr. May 31, 2011)
(rejecting a four-month onset for GBS).
20
burden pursuant to the Althen test, the burden shifts to respondent to demonstrate that
her injury was caused by factors unrelated to vaccination. § 300aa-13(a)(1)(B);
Deribeaux v. Sec’y of Health & Human Servs., 717 F.3d 1363, 1367 (Fed. Cir. 2013).
In order to meet his burden, respondent must demonstrate by preponderant
evidence “that a particular agent or condition (or multiple agents/conditions) unrelated to
the vaccine was in fact the sole cause (thus excluding the vaccine as a substantial
factor).” de Bazan, 539 F.3d at 1354. As with petitioner’s burden under Althen,
respondent must show a logical sequence of cause and effect linking the injury to the
proposed factor unrelated. Deribeaux, 717 F.3d at 1369. It need not be scientifically
certain but must be legally probable. Id. Conditions or other factors that are “idiopathic,
unexplained, unknown, hypothetical, or undocumentable” cannot defeat a petitioner’s
claim. § 300aa-13(a)(2); Knudsen, 35 F.3d at 548. Significantly, the Federal Circuit has
rejected the contention that the presence of a viral infection can per se be considered a
factor unrelated to vaccination. Knudsen, 35 F.3d at 548-50. Rather, respondent bears
a burden of proving not only that there was a viral infection, but also that the infection
was principally responsible for causing petitioner’s injury. Id.
In this case, respondent cannot meet this burden based on his contention that
petitioner’s CMV infection caused her GBS. As explained above, petitioner’s physicians
were unwilling to conclude that petitioner’s GBS was CMV-caused rather than vaccine-
caused. (Ex. 2, p. 187.) In fact, Dr. Fife likewise explicitly opined that “[t]here is
certainly no medical justification for narrowing the petitioner’s diagnostic possibilities
down to a single entity.” (Ex. A, p. 3.) Nonetheless, he initially opined that “[a]lthough
there is no definitive proof, the probability is over a hundred times higher that the
petitioner’s neurologic condition was a result of the CMV infection than the influenza
immunization.” (Id.) Significantly though, Dr. Fife subsequently acknowledged that it is
not possible to know when petitioner was first infected with CMV and further that there
is only a small chance that this was her first CMV infection. (Ex. C, p. 1; Ex. D, p. 1.)
He agreed that it was more likely a reactivation of a latent infection. (Ex. D, p. 1.) He
also conceded, at least initially, that it is unknown whether reactivated CMV infection
can trigger GBS. (Ex. C, p. 1.)
Subsequently, however, Dr. Fife did suggest that reactivated CMV can cause
GBS, citing for example a paper describing five case reports of CMV-positive transplant
patients who developed AIDP. (Ex. D, p. 1.) He contended that this is evidence that
CMV reactivation, and not only primary infection, can be associated with GBS.
Significantly though, case reports are not strong evidence. Moreover, Dr. Reif
reasonably questioned whether the context of organ transplant recipients was
sufficiently analogous to petitioner (otherwise previously healthy and not known to be
immune compromised) to be illuminating. (Ex. 35, p. 1.) Indeed, Dr. Reif’s skepticism
is supported by another paper cited by Dr. Fife, Steininger et al. That paper cautioned
that organ transplant patients may be uniquely or unusually susceptible to CMV viremia.
(Christoph Steininger et al., Primary Cytomegalovirus Infection in Patients with Guillain-
Barre Syndrome, 183 J. OF NEUROIMMUNOLOGY 214 (2007) (Ex. A, Tab 4, p. 2).) The
paper studied 46 GBS patients and found that almost 25% of those patients were
21
suffering a primary CMV infection, while 59% had detectable levels of CMV-DNA
attributable to either primary infections, reactivation, or reinfection. Although the study
confirms an association between CMV and GBS, it focuses principally on primary
infection and does not definitively conclude that reactivated CMV infections are
significantly associated with GBS. Instead, Steininger et al, cast doubt on whether the
mechanism by which CMV is believed to cause GBS can be said to apply equally to
cases of CMV reactivation. Specifically, the authors explained that “[m]olecular
mimicry, which was proposed to be a relevant mechanism in the pathogenesis of GBS,
and cross-reactivity of CMV-specific antibodies with neuronal structures would be
expected to be more likely in primary CMV infection than in the course of virus
reactivation because of the lower antibody-specificity and -affinity early after infection.” 19
(Steininger et al., supra, at Ex. A, Tab 4, p. 2.)
Accordingly, Dr. Fife’s repeated assertion that CMV is a far more likely cause is
not persuasive given the evidence of record in this case. These assertions rely on the
much stronger evidence regarding primary CMV infection, but Dr. Fife ultimately
acknowledged that this is not likely what petitioner experienced in this case. Moreover,
Dr. Fife has acknowledged that there is no medical justification for narrowing the cause
of petitioner’s GBS to a single entity and, for all the reasons discussed above, petitioner
has presented a prima facie case, inclusive of both expert and treating physician
opinions, otherwise supporting influenza vaccination as a cause of her injury. Thus,
although CMV remains one possible factor explaining petitioner’s injury, respondent has
not met his burden of providing preponderant evidence that CMV infection was the sole
cause of petitioner’s injury to the exclusion of her vaccination.
VII. Conclusion
For all the reasons discussed above, I find that petitioner is entitled to
compensation for her vaccine caused GBS. Specifically, I find that petitioner has
established by preponderant evidence that her GBS was caused-in-fact by her
November 16, 2015 influenza vaccination and further that respondent has not presented
preponderant evidence that her injury was due to factors unrelated to her vaccination.
A separate damages order will be issued.
IT IS SO ORDERED.
s/Daniel T. Horner
Daniel T. Horner
Special Master
19
Notably, Dr. Reif has also suggested that vaccination itself can cause reactivation of latent viral
infection, suggesting petitioner would again point back to the influenza vaccine as at least one substantial
contributing factor among others in causing petitioner’s GBS, even if reactivation of the CMV infection
was the immediately preceding cause. (Ex. 8, p. 8.) However, for all the reasons discussed herein, I do
not reach that question.
22