               In the United States Court of Federal Claims
                                 OFFICE OF SPECIAL MASTERS
                                     Filed: February 19, 2020


* * * * * * * * * * * * * *                   *
JAMES F. DUNN,                                *       PUBLISHED
                                              *
               Petitioner,                    *       No. 16-1506V
                                              *
v.                                            *       Special Master Dorsey
                                              *
SECRETARY OF HEALTH                           *       Tetanus-Diphtheria-Acellular Pertussis
AND HUMAN SERVICES,                           *       Vaccine (“Tdap”); Varicella Zoster Virus
                                              *       (“VZV”) Infection; Meningoencephalitis;
               Respondent.                    *       Reactivation; Alternative Factor Unrelated
                                              *       to Vaccine
* * * * * * * * * * * * * *                   *

Jeffrey A. Golvash, Brennan, Robins & Daley, P.C., Pittsburgh, PA, for petitioner.
Darryl R. Wishard, United States Department of Justice, Washington, DC, for respondent.

                                           DECISION1

I.     INTRODUCTION

       On November 14, 2016, James F. Dunn (“petitioner”) filed a petition under the National
Vaccine Injury Compensation Program (“Vaccine Act” or “the Program”),2 42 U.S.C. § 300aa-
10 et seq. (2012), alleging that as a result of receiving a Tetanus-diphtheria-acellular pertussis

1
  Because this decision contains a reasoned explanation for the undersigned’s action in this case,
the undersigned intends to post this decision on the website of the United States Court of Federal
Claims, in accordance with the E- Government Act of 2002, 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. As provided by Vaccine
Rule 18(b), each party has 14 days within which to request redaction “of any information
furnished by that party: (1) that is a trade secret or commercial or financial in substance and is
privileged or confidential; or (2) that includes medical files or similar files, the disclosure of
which would constitute a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b).
2
 The National Vaccine Injury Compensation Program is set forth in Part 2 of the National
Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended,
42 U.S.C. §§ 300aa-10 to -34 (2012). All citations in this decision to individual sections of the
Vaccine Act are to 42 U.S.C. § 300aa.



                                                  1
(“Tdap”) vaccine on December 2, 2014,3 he developed meningoencephalitis. Petition at
Preamble; Joint Prehearing Submission (“Joint Sub.”), filed May 23, 2019, at 1 (ECF No. 59).

        Petitioner asserts that the Tdap vaccination he received in December 2014, caused an
“immune-mediated inflammatory response, such as occurs with normal antibody production
post-Tdap vaccination” resulting in meningoencephalitis. Petitioner’s Prehearing Submission at
6 (ECF No. 53). Respondent argues against awarding compensation, stating that petitioner failed
to provide preponderant evidence that his illness was caused by the Tdap vaccine. Respondent’s
Report at 9. Respondent also contends that petitioner’s meningoencephalitis was caused by a
varicella zoster virus (“VZV”) infection, an alternative factor, unrelated to the Tdap vaccine.
Respondent’s Pre-Hearing Brief at 1 (ECF No. 58).

        Petitioner suffered a very serious and significant illness which required hospitalization in
an intensive care unit. He suffered respiratory failure requiring intubation and ventilation, and
other sequela, which had a profound impact on his life, for which the undersigned extends her
sympathy. However, after carefully analyzing and weighing all of the evidence and testimony
presented in this case in accordance with the applicable legal standards, the undersigned finds
that petitioner is not entitled to compensation.

       Even assuming that petitioner provided preponderant evidence of causation, the
undersigned finds that respondent proved by preponderant evidence that petitioner’s
meningoencephalitis was caused by VZV infection reactivation, an alternative factor unrelated to
his Tdap vaccination. Therefore, petitioner is not entitled to compensation, and his case must be
dismissed.

II.    PROCEDURAL HISTORY

        Petitioner, James F. Dunn, filed for compensation under the National Vaccine Injury
Compensation Program on November 14, 2016. Petitioner alleged that he developed viral
encephalopathy/aseptic meningitis, which was caused-in-fact by the Tdap vaccination he
received on December 2, 2014. Petition at Preamble. Petitioner alleged that he “suffered from
the residual effect and/or complication from his viral encephalopathy/aseptic meningitis for more
than six (6) months.” Id. at ¶ 14. Petitioner filed medical records on January 9, 2017.
Petitioner’s Exhibits (“Pet. Exs.”) 2(a)-5(b). Respondent filed his Rule 4(c) Report on March 8,
2017, recommending against compensation. Respondent’s Report at 9 (ECF No. 12).

       Petitioner filed additional medical records on May 5, 2017. Pet. Exs. 6-8. On August 28,
2017, petitioner filed the expert report of Dr. George Small, a neurologist, and respondent filed
the expert report by Dr. Subramanian Sriram, a neurologist, on November 9, 2017. Pet. Ex. 9;
Respondent’s Exhibit (“Resp. Ex.”) A. Petitioner filed a responsive expert report from Dr. Small
on January 9, 2018. Pet. Ex. 10.

3
 The parties later stipulated that petitioner received the Tdap vaccine on either December 2, or
December 4, 2014. Joint Sub., filed May 23, 2019, at 1 (ECF No. 59). For purposes of this
decision, December 2, 2014 will be referred to as the date of vaccination.


                                                 2
       On February 5, 2018, respondent filed a second expert report from Dr. Sriram, including
responses to questions the special master posed during the January 25, 2018 Status Conference
and responses to Dr. Small. Resp. Exs. E, M. During this period, the parties discussed
settlement of this matter but were unable to resolve the case informally. Respondent’s Status
Report, filed Mar. 7, 2018 (ECF No. 40). Petitioner then filed responses to questions the special
master posed and a responsive expert report from Dr. Small on May 18, 2018. Pet. Exs. 13, 19.
Both parties filed medical literature referenced by their respective experts.

        Petitioner filed additional medical records on October 15, 2018. Pet. Ex. 21. On October
19, 2018, respondent filed a supplemental expert report from Dr. Sriram. Resp. Ex. N.
Petitioner filed a third expert report from Dr. Small on April 25, 2019, and respondent filed
another expert report from Dr. Sriram in response on May 23, 2019. Pet. Ex. 22; Resp. Ex. P.

        The parties filed a joint stipulation of facts on May 23, 2019, in which they agreed that
the petitioner received the Tdap vaccination in December 2014 (either on December 2, 2014 or
December 4, 2014) in the United States, and that he was diagnosed with meningoencephalitis in
December 2014. Joint Sub., filed May 23, 2019, at 1 (ECF No. 59). The parties disagreed on the
significance of the VZV test performed on the petitioner during his admission at Allegheny
General Hospital (“AGH”) in December 2014. Id. at 2.

         An entitlement hearing was held on June 26, 2019 in Pittsburgh, Pennsylvania. Dr. Small
testified on behalf of the petitioner. Dr. Sriram testified on behalf of respondent. Post-hearing,
petitioner and respondent both continued to file additional exhibits, including medical literature
and expert reports until the record was closed on November 26, 2019. Petitioner filed a fourth
expert report from Dr. Small on November 15, 2019. Pet. Ex. 38. Respondent filed a final
expert report from Dr. Sriram on November 26, 2019. Resp. Ex. S.

       The matter is now ripe for adjudication.

III.   ISSUES TO BE DECIDED

       The parties dispute causation.4 Petitioner asserts that his Tdap vaccination caused him to
suffer meningoencephalitis and maintains that he has proven by preponderant evidence the
standards articulated in Althen. See Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274,
1280 (Fed. Cir. 2005), Joint Sub., filed May 23, 2019, at 2 (ECF No. 59). Respondent disagrees.
Moreover, respondent contends that even if petitioner has met his burden under Althen, there
was an alternate cause for petitioner’s illness, unrelated to his vaccination. Respondent
“contends that petitioner’s VZV infection was the likely cause of his meningoencephalitis.” Id.


4
 In addition, the respondent disagrees with the tentative findings set forth in an Order filed April
6, 2017, as to whether petitioner’s evidence meets the severity requirements under the Act. See
42 U.S.C. §§ 300aa-11(c)(1)(D)(i), (iii); Joint Sub., filed May 23, 2019 at 2 (ECF No. 59). This
decision makes that tentative finding not relevant. The parties also dispute the significance of
petitioner’s testing regarding VZV infection. That issue will be discussed in the context of the
experts’ opinions and causation analysis.


                                                  3
      For purposes of this decision, the undersigned assumes that petitioner has proven his case,
and that the burden then shifted to respondent to show that a factor unrelated to the vaccination
caused petitioner’s meningoencephalitis. Therefore, the causation analysis relates only to
respondent’s theory of causation and does not include an analysis of petitioner’s causation claim.

IV.      FACTUAL SUMMARY

             A. Summary of Facts

        In his Prehearing Memorandum, petitioner sets forth a summary of facts which the
undersigned finds generally accurate, with some additions and explanations. Petitioner’s
Prehearing Memorandum, filed Apr. 25, 2019, at 1-4 (ECF No. 53). The summary below is
largely derived from petitioner’s summary.5

        At the time petitioner received the vaccination at issue in this case, he was forty-four
years old, active, and working. On November 14, 2013, petitioner weighed 348 pounds, and was
diagnosed as morbidly obese. His blood pressure was elevated at 137/97. Pet. Ex. 2(a) at 1, 2,
175. Petitioner’s past medical history was significant for ocular stroke,6 obstructive sleep apnea,
post-traumatic stress disorder, and hyperlipidemia. Pet. Ex. 4(a) at 118, 123, 126.

         On December 2, 2014, petitioner received a Tdap vaccine at the Veteran’s Administration
Hospital (“VA”). Pet. Ex. 3. On or about December 12, 2014, he began to experience
headaches. Petition at ¶ 4. Approximately on December 18, 2014, petitioner began to have flu-
like symptoms including fever, chills, headache, and mild nausea. Id.; Pet. Ex. 5(b) at 298. On
December 19, 2014, petitioner awoke feeling warm, fatigued, and generally not himself. Petition
at ¶ 5; Pet. Ex. 4(a) at 8, 118, 123, 126, 129. Petitioner went to work but left work early to return
home. Petition at ¶ 5; Pet. Ex. 4(a) at 8, 118, 123, 126, 129. When petitioner’s wife arrived
home, petitioner was unable to respond to questions or commands. Petition at ¶ 5; Pet. Ex. 4(a)
at 8, 118, 123, 126, 129. She dialed 911 for emergency medical assistance and petitioner was
taken by ambulance to AGH for evaluation and treatment. Petition at ¶ 5; Pet. Ex. 4(a) at 8, 118,
123, 126, 129.

       When petitioner arrived at the emergency room, he was nonverbal and nonresponsive,
could open his eyes to painful stimuli, but was otherwise encephalopathic. Pet. Ex. 4(a) at 8,
118, 121, 123. CT and MRI of head and chest X-ray were unremarkable. Due to his altered
mental status (“AMS”), a lumbar puncture (“LP”) was performed. Pet. Ex. 4(a) at 8, 118-19,
121, 123, 126-27. Cerebral spinal fluid (“CSF”) analysis revealed elevated white blood cells of
16 and elevated protein of 63 and glucose of 83. Pet. Ex. 4(d) at 741. Bacterial antigens and
Gram stain were negative. Polymerase chain reaction (“PCR”) for herpes simplex virus (“HSV”)
5
    Petitioner’s summary for events occurring after November 2015 is not included here.
6
  A brain MRI done October 23, 2013 showed small old lacunar infarct in the right superior
frontal periventricular white matter. Pet. Ex. 2(a) at 21. On October 25, 2013, petitioner was
diagnosed with central retinal artery occlusion and acute vision loss of his left eye. Id. at 48.



                                                 4
and VZV were also negative. Id. at 741-42. Influenza type A, B, and A-H1N1 were all negative.
Id. Cryptococcal antigen was negative. Pet. Ex. 4(a) at 8, 118-19, 126-27; 129-31; Pet. Ex. 4(d)
at 741-42.7 Blood cultures were also negative. Petitioner was started on empiric antiviral and
antibiotic therapy with acyclovir, ceftriaxone, and vancomycin. Pet. Ex. 4(a) at 8, 118, 126, 129.
He was transferred to ICU for continued evaluation and treatment. Id. at 126. Impression was
altered mental status likely secondary to viral encephalitis/aseptic meningitis. Id. at 127.

        Petitioner was seen by an infectious disease specialist on December 20, 2014. He was
observed to be nonresponsive and otherwise encephalopathic. Pet. Ex. 4(a) at 119. He had no
evidence of skin rash. Id. Assessment was encephalopathy secondary to toxic ingestion versus
nicotine toxicity versus viral encephalitis, possible meningoencephalitis, abnormal cerebrospinal
fluid, and hypoxia. Id. at 21, 119. The infectious disease specialist suspected abnormal CSF
findings were reactive in nature as petitioner did not have any evidence of infection. Id. at 119.
Petitioner was also seen by a neurologist on December 20, 2014. Id. at 130. Temperature was
37.8 ºC and the petitioner was noted to be confused, nonverbal, unable to track, exhibiting non-
purposeful movements but without seizures, and there was no evidence of skin rash. Id. The
neurologist assessment was altered mental status, likely viral encephalitis considering the CSF.
Id. at 130-31.

        Petitioner remained in the ICU through December 24, and was nonresponsive, unable to
follow commands, unable to verbalize, hyper-reflexive, and encephalopathic. Pet. Ex. 4(a) at 25-
28. Due to acute respiratory failure, he underwent bronchoscopy on December 23, 2014. Id. at
132. A biopsy of the lung Gram stain, bacterial culture, and viral culture were all negative. Pet.
Ex. 4(d) at 761. Following his bronchoscopy, petitioner continued to be followed and monitored
in the ICU. Petitioner remained encephalopathic as he continued to be nonverbal without
showing any signs of understanding. Pet. Ex. 4(a) at 44, 140. His differential diagnosis was
encephalitis/aseptic meningitis.8 Id. at 37, 47. On December 23, 2014, a bilateral rash was
subsequently observed and swabs were sent for testing.9 Id. at 36, 140. He had a PICC line
inserted on December 24, 2014 for fluid and medications. Id. at 42. Petitioner remained
nonresponsive and noncommunicative with intermittent body tremors.

       On December 25, 2014, petitioner’s mental status began to improve. He awoke on that
day and was alert and oriented as to time, place, and person. The antivirals and antibiotics were
discontinued. Pet. Ex. 4(a) at 140.




7
 Urine toxicology screen was positive for benzodiazepines and cannabinoids. It was noted that
petitioner used cannabis daily and that he vaped nicotine. Pet. Ex. 4(a) at 8; Pet. Ex. 4(d) at 739.
8
 Aseptic meningitis is defined as “any of several mild types of meningitis, most of which are
caused by viruses.” Dorland’s Illustrated Medical Dictionary 1117 (33rd ed. 2020).
9
 Additional details about petitioner’s rash and swab testing are set forth below in section ii:
“Additional Facts Regarding Rash and Diagnostic Testing.”


                                                 5
        Given his continued improved mental state, petitioner was discharged from the hospital
on December 27, 2014 with instructions to follow up with his primary care physician. Pet. Ex.
4(a) at 62, 140. At the time of discharge, petitioner’s differential diagnosis was altered mental
status secondary to encephalitis/aseptic meningitis and acute respiratory failure secondary to
encephalitis/aseptic meningitis. Id. at 57, 62. On December 26, 2014, the infectious disease
physician wrote, “encephalopathy resolved—suspect nicotine overdose initially followed by
withdrawal.” Id. at 60. The discharge summary dated December 27, stated “leukocytosis
concerning for viral etiology” and PCR for VZV and HSV were negative. Id. at 140. (The
reference to PCR here applies to CSF.) The discharge note does not reference the PCR swab test
for petitioner’s rash. See Pet. Ex. 4(d) at 758. At the time of discharge, petitioner had word-
finding difficulty, general fatigue, and some short-term memory lapses. Petition at ¶ 8.

                   i.   Subsequent Care

        On January 13, 2015, petitioner was seen in follow-up by his primary care physician,
Derek Pae, M.D., at the VA. Dr. Pae noted petitioner’s recent hospitalization for altered mental
status and presumptive diagnosis of viral encephalitis. Pet. Ex. 5(b) at 303-04. Petitioner
reported a depressed mood, cognitive/short term memory deficiency, and that he generally felt
“clouded,” which affected his ability to function. Id. Dr. Pae recommended further consult and
evaluation by an infectious disease specialist. Id.

        Petitioner was seen by Jae Ho Hong, M.D., an infectious disease specialist at the VA, on
January 28, 2015. Pet. Ex. 5(b) at 296. During the visit, Dr. Hong noted, “Most likely the cause
was viral encephalitis. However, on reviewing the chart, he received Tdap vaccine on the
beginning of December. . . . Post-vaccination ADEM [acute disseminated encephalomyelitis]
has been associated with several vaccines such as rabies, diptheria?tetanus? . . . . Anyway, he is
clinically improving and no need for further testing or treatment.” Id. at 297. Subsequently on
February 4, 2015, Dr. Hong prepared an allergy and immunology adverse event note. In the
adverse event note, Dr. Hong reported that petitioner had a Tdap vaccine on December 2, 2014
and that petitioner was hospitalized on December 19, 2014 with altered mental status and aseptic
meningitis.10 Id. at 296, 357.

        On March 24, 2015, petitioner was again seen by Dr. Pae. Petitioner continued to have
short-term memory lapses and lethargy. Pet. Ex. 5(b) at 292-93. The short-term memory lapses
impacted petitioner’s ability to perform everyday living activities. Id. Dr. Pae suspected that
petitioner’s cognitive defects and short-term memory loss was caused by his hospitalization and
worsened by depression. Id. Dr. Pae prescribed an antidepressant (sertraline). Id. at 292-93,
364. On May 12, 2015, petitioner presented to Dr. Pae in follow-up. Petitioner’s cognitive
defects, memory loss, and depression had improved since taking sertraline. Pet. Ex. 5(a) at 95.




10
  Adverse Event Note states: “PT was admitted to AGH on 12/19/2014 with AMS. LP shows
aseptic meningitis result. Had Tdap vaccine on 12/2/14.” Pet. Ex. 5(b) at 357.


                                                6
        Petitioner next saw Dr. Pae on November 10, 2015. Pet. Ex. 5(a) at 93. Dr. Pae wrote: “I
am [] concerned because after his hospitalization for encephalitis, no known cause found and per
ID [infectious disease], most likely 2/2 [secondary to] tetanus vaccine. He is understandably
reluctant about future vaccines.” Id. at 94.

       On November 25, 2015, petitioner sought emergency care for fever and chills. His prior
medical history noted his previous hospitalization for encephalitis, which may have been
secondary to Tdap vaccine. Petitioner was discharged the next day with his symptoms resolved.
Pet. Ex. 5(a) at 20-21.

        Petitioner was seen in follow-up by Dr. Omran on December 2, 2015. Petitioner’s past
medical history was significant for “encephalitis in 2014, temporal link to tetanus vaccine” and
“adverse reaction/allergy to Tdap”. Pet. Ex. 5(b) at 191-92. At that time, petitioner was still
taking sertraline for his depression. Id.

        On May 6, 2016, petitioner was seen by a rheumatologist at the VA. His prior medical
history was significant for aseptic encephalitis/meningitis that may be Tdap vaccine related. Pet.
Ex. 5(b) at 99. Petitioner was still taking sertraline. Id. By July 13, 2016, approximately one
and half years after his initial hospitalization, initial mental slowing, progress notes reflect that
petitioner’s cognitive/memory impairment had resolved. Id. at 119.

                 ii.   Additional Facts Regarding Rash and Diagnostic Testing

       In addition to the facts set forth above, the following facts are relevant and pertinent.

        On the date of vaccination, petitioner presented to Dr. Pae on December 2, 2014, for a
routine follow-up visit. On that date, Dr. Pae noted that Mr. Dunn had “a truncal rash which
does not itch or cause pain.” This problem had been treated in the past with medication. Pet. Ex.
5(b) at 371. Dr. Pae also documented that petitioner had “another separate lesion on his right
arm which is different and itchy. He has always had ‘skin problems’ in the past but this is new.”
Id. Dr. Pae diagnosed Mr. Dunn’s truncal rash as “suspect[ed] tinea corporus” (fungus) and the
lesion on his right arm as eczema. Id. Mr. Dunn received the Tdap vaccine at this visit. Id. at
373.

       On December 19, 2014, petitioner was taken to the AGH emergency department with
decreased mental status and admitted for evaluation and treatment. Lab work testing included
blood work for VZV IgG, which was positive: VZV IgG: ˃4000.11 Pet. Ex. 4(a) at 189.

      Diagnostic testing was ordered on December 20, 2014, including CSF tests by PCR for a
number of viruses, including HSV, VZV, enterovirus, West Nile virus, Lyme Disease, syphilis,
human immunodeficiency virus, and others. Pet. Ex. 4(a) at 189. The results of the PCR tests on

11
  Petitioner’s result was greater than 4,000 units. A positive result is generally greater than 165
units. Pet. Ex. 4(d) at 746.



                                                 7
the petitioner’s cerebrospinal fluid were ultimately reported back as negative, including the test
for VZV.12 Id.; Pet. Ex. 4(d) at 741-42.

        On December 23, 2014, an infectious disease physician documented the presence of skin
vesicles on petitioner’s left chest and left upper extremity where the cardiac monitor pad and BP
cuff had been placed. Pet. Ex. 4(a) at 36. The vesicles looked like “contact dermatitis” as they
were not in a dermatomal distribution. Id. “However, given possible viral
meningitis/encephalitis, shingle/herpetic lesions should be ruled out.” Id. “Blister in LUE [left
upper extremity] and chest—not typical appearance of shingles but [] and fever, droplet
precautions given that patients next room are immunosuppressed. Skin lesions in VZV
encephalitis may develop after AMS even during tx [treatment].” Id. 35.

        The physician ordered droplet isolation, and a PCR swab test from the left wrist blister
for herpes simplex virus and VZV. Pet. Ex. 4(a) at 35. The physician also ordered to continue
IV acyclovir (antiviral) until the cerebrospinal fluid and blister swab results were returned. Id.
The PCR of the blister subsequently tested positive for VZV. Pet. Ex. 4(d) at 758.

         Petitioner’s medical records do not state when the results of the positive VZV blister test
were received or whether his physicians were notified of the results. There is no reference to the
results in the physicians’ progress notes or petitioner’s discharge summary. The test results
appear in the laboratory reports section of the petitioner’s medical records. Pet. Ex. 4(d) at 758.
During the hearing, upon review of the lab reports, it was noted that the swab PCR
(“miscellaneous fluid”) was performed at LabCorp, an outside laboratory. Pet. Ex. 4(d) at 758;
Transcript (“Tr.”) 170. After the hearing, petitioner obtained the report from LabCorp, which
notes that the test was drawn on December 23, 2014 and reported on December 30, 2014. The
results were positive for VZV; “varicella zoster virus DNA [was] detected.” Pet. Ex. 39 at 2.

                iii.   Petitioner’s Testimony

      Mr. Dunn was born October 24, 1970. He testified that as a child he had chickenpox. Tr.
30. He received the Tdap vaccine at issue in this case on December 2, 2014. Tr. 8.

        On December 12, 2014, Mr. Dunn started having headaches. Tr. 11. On the evening of
December 18, 2014, he had nausea, dizziness, fever, and chills. Id. The next day, December 19,
2014, he felt ill, and left work and drove home at noon. Tr. 12. When he arrived home, he went
upstairs to lie down. Id. That is his last memory until December 25, 2014, when he came out of
a coma. Tr. 16.
12
   Varicella virus testing described in this decision includes serological antibody testing of
peripheral blood, and viral DNA PCR testing of cerebrospinal fluid and of a fluid filled vesicle.
Petitioner’s VZV IgG test was positive, indicating that he tested positive for antibodies to the
varicella virus. See Mosby’s Manual of Diagnostic and Laboratory Tests 712-75 (Kathleen D.
Pagana & Timothy J. Pagana eds., 6th ed. 2018). Varicella virus DNA proteins can be detected
by PCR. Id. at 713. Here, petitioner had PCR analysis of his CSF on December 20, and then of
fluid in a vesicle on December 23. The PCR on the CSF was negative. The PCR of the vesicle
fluid was positive.


                                                 8
        Based on information shared with him by his wife, petitioner testified that on December
19, 2014, when Ms. Dunn arrived home, she found her husband ill, and she called 911. Tr. 12.
Mr. Dunn was taken by ambulance to AGH. Id. Mr. Dunn explained that he had not told his
wife that he received the Tdap vaccine, and she did not inform petitioner’s health care providers
of his history of Tdap vaccination when petitioner was taken to the hospital. Tr. 14.

        Petitioner was questioned regarding Dr. Pae’s medical records, specifically, the entry
dated December 2, 2014, which documented that petitioner had a truncal rash. See Pet. Ex. 5(b)
at 371. Petitioner explained that he told Dr. Pae that in the past he had taken medication for the
rash and it cleared up. Tr. 24. Dr. Pae’s records also note that petitioner had a separate lesion on
the right arm which was “different and itchy.” Id.; Pet. Ex. 5(b) at 371. Dr. Pae stated that Mr.
Dunn had skin problems in the past, but this was a new problem. Pet. Ex. 5(b) at 371.

        Petitioner testified that he had a history of sensitive skin, and a nickel allergy, along with
a long history of skin allergies. Tr. 29. He testified, however, that he had never sought treatment
for a painful rash. Tr. 30. Petitioner also testified that he did not have a painful skin rash
between December 2, 2014 and December 19, 2014. Tr. 10.

        Significantly, Mr. Dunn testified that while he was a patient at AGH, no one ever told
him that he tested positive for shingles (VZV). Tr. 31. Further, when he was discharged from
the hospital, he was not informed of his positive shingles test or VZV diagnosis. Tr. 21.
Petitioner did not become aware that he had a positive PCR test for shingles until his lawyer told
him during the pendency of this claim. Id.

                iv.    Contemporaneous Treating Physician Assessments

        During petitioner’s admission to AGH in December 2014, he was initially seen by an
emergency room physician and then followed by several specialists, including neurology,
infectious disease, and while in the ICU, critical care physicians. The following is a chart with
the daily assessments charted by these physicians.

     Date                              Clinical impression                          Pet. Ex. 4(a) at
   12/19/14           Initial progress note – altered mental status (AMS)                  9
                 encephalitis/meningitis/intoxication . . . intoxication unlikely
    12/20                       Likely viral meningoencephalitis                           10
    12/20                             Most likely infectious                               16
    12/20                  ? etiology appears to have viral infection.                     22
                                           LP WBC 16
    12/21                           Could be viral meningitis                              12
    12/21           Etiology unclear ? nicotine toxicity ? viral encephalitis              14
    12/21         Possible meningoencephalopathy but also consistent with                  15
                                          toxic exposure
    12/22                        Concern for infectious etiology                           25
    12/22                         Infectious vs. encephalopathy                            25
    12/22                            Likely viral encephalitis                             32

                                                 9
    12/23       ID noted some vesicles left chest, LUE… shingles/herpetic               36
                               lesions should be ruled out
    12/23        Aseptic meningitis CT [continue] Acyclovir follow PCR                  37
    12/24           AMS – unclear etiology most likely viral etiology                   50
    12/25                 AMS – unclear etiology. Likely viral                          52
    12/25              AMS 2/2 [secondary to] HSV encephalitis ?                        54
                                CSF HSV PCR negative
    12/26                 Encephalitis 2/2 [secondary to] viral ?                       57
    12/26                       Encephalopathy resolved.                                59
                           Abnormal CSF w/ viral pleocytosis
    12/26       Encephalopathy resolved, suspect nicotine overdose initially            60
                                 followed by withdrawal
    12/27                 AMS secondary to aseptic meningitis                           62

            B. Expert Qualifications and Opinions

                 i.   Expert Qualifications

                          a. Petitioner’s Expert, Dr. George Allen Small

        Dr. George Allen Small is a board-certified neurologist and is the Director of Allegheny
General Hospital’s EMG Laboratory and Neuromuscular Service. Pet. Ex. 9 at 5-6. Dr. Small is
also an Associate Professor of Neurology at Drexel University School of Medicine and at the
Temple University School of Medicine. Id. at 5; Tr. 37. Dr. Small received his M.D. from
Jefferson Medical College and completed his residency at the Neurological Institute of New
York. Pet. Ex. 9 at 5. He also serves as the Program Director for the Clinical Neurophysiology
Fellowship. Id. Dr. Small has published numerous articles. Id. at 9-11.

        Dr. Small has treated hundreds of patients with encephalitis, and of those, most did not
have a recognized or known etiology for their illness. He testified that the most common viral
cause is the herpes virus type one (HSV). Tr. 102. Dr. Small has also seen cases of
postvaccination encephalitis, but “not very many.” Id.

       Dr. Small has privileges to practice at AGH, the hospital where petitioner was admitted
and received care in December 2014, but he does not recall caring for or treating petitioner. Tr.
111

                          b. Respondent’s Expert, Dr. Subramaniam Sriram

        Dr. Subramaniam Sriram is a board-certified neurologist with a focus in
neuroimmunology. See Resp. Ex. Q at 2. He obtained a Bachelor of Medicine and a Bachelor of
Surgery from the University of Madras in Madras, India. Id. at 1. He then served as an intern
and resident at Wayne State University and completed a residency in neurology at Stanford
University, where he also served as chief resident and eventually completed a post-doctoral
fellowship in neuroimmunology. Id. Currently, Dr. Sriram serves as the William Weaver
Professor of Experimental Neurology at Vanderbilt University Medical Center. Id. at 2; Tr. 140.

                                                10
He also holds a joint appointment as Professor of Pathology, Microbiology, and Immunology.
Resp. Ex. Q at 2. Dr. Sriram’s clinical practice includes seeing patients two days a week. Tr.
140.

        Like Dr. Small, Dr. Sriram has treated patients with meningoencephalitis, including cases
caused by VZV. He has also authored a paper about a patient with VZV encephalitis. Resp. Ex.
Q at 19; Tr. 142. That patient had CSF findings consistent with VZV, but had abnormal eye
movements (ocular findings) and did not present with encephalitis or meningitis. Tr. 142. Of
note, two to three weeks later, the patient developed a shingles lesion. Id.

                   ii.   Expert Opinions

                             a. Petitioner’s Expert, Dr. Small13

        Dr. Small opined that petitioner’s meningoencephalitis was due to a reaction to the Tdap
vaccine that he received on December 2, 2014. Tr. 73-74, 106. Dr. Small defined
meningoencephalitis as altered mental status for greater than twenty-four hours with “objective
evidence of inflammation in the brain” and spinal fluid. Tr. 60. He further explained that
meningoencephalitis encompasses aseptic meningitis (inflammation of meninges as evidenced
by cerebrospinal fluid analysis) and encephalitis (inflammation of the brain as evidence by
dysfunction of the brain). Tr. 69. He further explained that aseptic meningitis also suggests that
no viral or bacterial organism is found in the spinal fluid. Tr. 70-71.

        Petitioner’s cerebrospinal fluid showed elevated white blood cells and protein. Pet. Ex.
4(d) at 741. Cultures and PCR testing of the CSF did not reveal a specific virus or bacteria. Tr.
50, 55-56. Dr. Small explained that the CSF was “reactive,” meaning that the tests suggested an
inflammatory and immunological reaction to some agent. Tr. 52. However, according to Dr.
Small, the CSF results ruled out the possibility of active viral or bacterial meningoencephalitis.
Tr. 55-57.

        With regard to Althen Prong One, Dr. Small posits that the Tdap vaccine causes the
following immunological reaction: The bacterial antigen in the vaccine initiates an immune
response (T cells interacting with B cells) that results in the production of protective antibodies
against the bacterial antigen. Tr. 76; Pet. Ex. 9 at 2. The immune response also results in the
production of proinflammatory cytokines, including interleukin 6 (Il-6), and tumor necrosis
factor-α (TNF-α). Tr. 76. According to Dr. Small, these cytokines break down the blood brain
barrier, which normally protects the brain from noxious material, and allows for inflammation of
the central nervous system and brain to occur. Tr. at 77-78. The inflammation causes abnormal
function, including altered mental status. Id. Dr. Small testified that the inflammation causes
damage to the brain, and the waste products of that damage elevate the protein level in the
cerebrospinal fluid. Tr. at 80. The “immunization-promoted inflammatory response becomes
exuberant and spills over into the central nervous system.” Pet. Ex. 9 at 3.


13
     Petitioner filed six expert reports authored by Dr Small. Pet. Exs. 9, 10, 13, 19, 22, 38.



                                                   11
         Dr. Small cited several medical articles in support of his proposed causal mechanism. He
cited the Kashiwagi14 article to support his position that cytokines IL-6 and TNF-α are produced
in response to the DPT, Hib, and PCV vaccines and that “brain cells can be abrogated by
inflammation.” Tr. 81-84; see Pet. Ex. 25 at 3. Dr. Small explained that the Rochfort15 article
also describes how cytokines IL-6 and TNF-α cause a breakdown of “tight junctions” that keep
bacteria and toxins away from the central nervous system. Tr. 87-88; Pet. Ex. 26. Dr. Small
testified that “substances get into parts of the brain where they shouldn’t be” due to the presence
of these cytokines. Tr. 88.

        Dr. Small also cited Hiraiwa-Sofue,16 a case report of a child who had encephalitis caused
by a pertussis infection. Tr. 89; Pet. Ex. 27 at 3. The child had a seizure and encephalopathy
eighteen days after the onset of a pertussis infection. MRI showed “marked demyelination.”
Pet. Ex. 27 at 1. There was no evidence of direct infection of the pertussis bacteria in the central
nervous system. The authors suggested several possible mechanisms, including immune
mediation, proinflammatory cytokine production, pertussis toxin effect on the blood brain
barrier, and inflammation of the central nervous system. Id. at 3. The authors also stated that
proinflammatory cytokines were “associated with the development of acute encephalitis.” Id.
They also noted that levels of IL-6 and another cytokine, IL-10, were higher in the CSF than in
the blood, suggesting they played a role in the cause of encephalitis. Id.

        Another article cited by Dr. Small is Aydin,17 a case report of an infant who presented
with seizures and abnormal neurological findings six days after receipt of the whole cell DTP
vaccination. Pet. Ex. 28. The child was diagnosed with acute necrotizing encephalopathy.
Possible causal mechanisms included breakdown of the blood brain barrier, “alteration of vessel
wall permeability,” or “vessel wall necrosis.” Pet. Ex. 28 at 2. The authors hypothesized that the
vaccine caused increased levels of IL-6 and TNF-α which may have altered “vessel wall
permeability and local breakdown of the [blood brain barrier].” Id.

       Based on the articles cited, Dr. Small testified that an active infection with bacteria is not
required in order to have meningoencephalitis; cytokines may be elevated in the cerebrospinal
14
  Yasuyo Kashiwagi et al., Production of Inflammatory Cytokines in Response to Diphtheria-
Pertussis-Tetanus (DPT), Haemophilus Influenzae Type b (Hib), and 7-Valent Pneumococcal
(PCV7) Vaccines, 10 Hum. Vaccines & Immunotherapeutics 667 (2014).
15
  K.D. Rochfort et al., Downregulation of Blood-Brain Barrier Phenotype by Proinflammatory
Cytokines Involves NADPH Oxidase-Dependent ROS Generation: Consequences for
Interendothelial Adherens and Tight Junctions, 9 PLoS One e101815 (2014).
16
 Ayako Hiraiwa-Sofue et al., Pertussis-Associated Encephalitis/Encephalopathy with Marked
Demyelination in an Unimmunized Child, 320 J. Neurological Sci. 145 (2012).
17
  Hale Aydin et al., Acute Necrotizing Encephalopathy Secondary to Diphtheria, Tetanus
Toxoid and Whole-Cell Pertussis Vaccination: Diffusion-Weighted Imaging and Proton MR
Spectroscopy Findings, 40 Pediatric Radiology 1281 (2010).



                                                 12
fluid which cause encephalopathy.18 Tr. 89-91. According to Dr. Small, it is the promotion of
cytokines, not bacteria, that breaks down the blood brain barrier, causing meningoencephalitis.
See Tr. 97.

        Next, Dr. Small opined regarding Althen Prong Two, the logical sequence of cause and
effect—how the Tdap vaccine caused petitioner’s meningoencephalitis. Dr. Small testified that
prior to vaccination, the petitioner was generally healthy. Petitioner received the vaccine on
December 2, 2014, and approximately fifteen to sixteen days later became lethargic and
unresponsive. Tr. 99; Pet. Ex. 9 at 3. He was admitted to the hospital where diagnostic testing
of his cerebrospinal fluid showed a “clear aseptic meningitis picture” and he was diagnosed with
meningoencephalitis. Tr. 99. Again, according to Dr. Small, aseptic meningitis indicates an
inflammatory reaction in the spinal fluid. Tr. 64-65. In support of his opinions, Dr. Small cited
the petitioner’s treating neurologist who stated that petitioner had meningoencephalitis of
“unknown cause.” See Pet. Ex. 4(a) at 130-31; Tr. 56. Dr. Small also cited a reference in
petitioner’s medical record stating that petitioner had aseptic meningitis, which Dr. Small
explained indicated an inflammatory reaction in the spinal fluid without the presence of virus or
bacteria. Tr. 64-65.

        Dr. Small further opined that while test results were pending, petitioner was treated
empirically “for the most common causes of infectious encephalitis” with antivirals and
antibiotics. Tr. 99. Petitioner had respiratory depression, required a bronchoscopy, but then
improved. Tr. 100. After discharge, he had depression and cognitive issues. Tr. 100. Dr. Small
opined that the only “clear and inciting event” was “the proximate relationship of the Tdap
vaccine.” Id. He opined that “[c]onsidering Mr. Dunn’s prior medical history and subsequent
medical workup, there is no other suggestive or explainable cause for his meningoencephalitis
but-for his Tdap vaccination.” Pet. Ex. 9 at 3.

        On cross-examination, Dr. Small conceded that petitioner here did not have evidence of
demyelination or a pertussis infection, both of which distinguish petitioner’s case from the case
presented in Hiraiwa-Sofue, described above. Tr. 115; Pet. Ex. 27. Dr. Small agreed that having
a pertussis infection is very different than receiving the acellular pertussis vaccine that petitioner
received. Tr. 115. Dr. Small also conceded that the patient in the Aydin case report had
hemorrhagic necrosis of the deep brain, which petitioner here did not have. Id.; Pet. Ex. 28.

        With regard to Althen Prong Three, Dr. Small opined that the temporal association
between vaccination and onset of petitioner’s illness was appropriate. He testified that “[i]t takes
time for the inflammatory reaction to develop” and it is not unusual for an immune response like
the one he proposes here to take a week or two to occur. Tr. 100-01. The two cases reported in
Aydin and Hiraiwa-Sofue had onset of six and eighteen days. Therefore, Dr. Small believes that
petitioner’s onset of fifteen to sixteen days post-vaccination is within the range of expected onset
given his proposed theory. Tr. 103-04.


18
   Dr. Small explained that generally there are no commercial tests available to test for cytokines
in cerebrospinal fluid. Tr. 91.



                                                 13
         Dr. Small was asked to provide medical literature regarding reports of encephalitis and
meningitis following the Tdap vaccination. See Pet. Ex. 13 at 1-2. In response, he cited an
article by Dalmau,19 in which the authors discuss encephalitis associated with antibodies against
the N-methyl-D aspartate receptor (“NMDAR”). Pet. Ex. 11. The pathogenic mechanism of the
illness is thought to be immune mediated. The article makes a reference to a patient who
developed anti-NMDAR encephalitis following receipt of the TDaP-IPV (Polio) booster
vaccination. Pet. Ex. 11 at 5. Dr. Small conceded that petitioner here did not have anti-NMDAR
encephalitis. Tr. 111.

       Dr. Small also referenced the Baxter study.20 Pet. Ex. 13 at 2; Pet. Ex. 18. That article
describes acute demyelinating events following vaccines, including acute disseminated
encephalomyelitis (“ADEM”) after the Tdap vaccine. Dr. Small conceded that petitioner did not
have ADEM, and that petitioner’s MRI did not show any evidence of demyelination. Tr. 78, 97,
111-12, 114.

        Dr. Small conceded that there was no epidemiology support for an association between
the Tdap vaccine and meningoencephalitis. Tr. 114. In an article cited by Dr. Small, authored
by Singh,21 the most common cause of encephalitis in 139 cases was viral infection (48%),
followed by autoimmune (22%), and unknown/other (30%). Pet. Ex. 37 at 2. The most common
viral infection was herpes simplex virus (HSV) at 38.9%, followed by varicella zoster virus
(VZV) at 23.2%. Id. at 3. Vaccines were not listed in the Singh article as a cause of
encephalitis.

        As for respondent’s position that petitioner’s illness was caused by reactivation of a prior
varicella infection, Dr. Small testified that in order to attribute petitioner’s illness to varicella
reactivation, he would need evidence that petitioner was “infected with varicella-zoster at the
time of his neurological presentation.” Tr. 107-08. Also, Dr. Small does not believe that
varicella was the cause of petitioner’s meningoencephalitis because his CSF tested negative for
the virus. Tr. 107. Additionally, the note by Dr. Hong, stating that the vaccine was the cause of
petitioner’s illness, influenced Dr. Small’s opinion. Tr. 108.

        On cross-examination, Dr. Small conceded that varicella infection can involve the central
nervous system. Tr. 112. He also agreed that a patient can first have central nervous system
involvement with a varicella infection without having any skin lesions. Id. When asked whether
a patient can have central nervous system involvement with a varicella infection followed by
19
  Josep Dalmau et al., Clinical Experience and Laboratory Investigations in Patients with Anti-
NMDAR Encephalitis, 10 Lancet Neurology 63 (2011) (Petitioner filed this article as Exs. 11
and 16).
20
 Roger Baxter et al., Acute Demyelinating Events Following Vaccines: A Case-Centered
Analysis, 63 Clinical Infectious Diseases 1456 (2016).
21
  Tarun D. Singh et al., The Spectrum of Acute Encephalitis: Causes, Management, and
Predictors of Outcomes, 84 Neurology 359 (2015).


                                                 14
skin lesions, Dr. Small answered that he did not know. He deferred to an infectious disease
physician to answer the question. Id.

      Dr. Small confirmed that the petitioner’s vesicular skin lesions were swabbed on
December 23, 2014, and that the PCR analysis was positive for the varicella zoster virus. Tr.
130. He did not know how long it took to obtain the results of the PCR test. Id.

        Importantly, Dr. Small testified that petitioner’s clinical course was “completely
consistent” with meningoencephalitis caused by varicella. Tr. 123. He also agreed that
respondent’s theory of causation, varicella infection reactivation, is a known cause of
encephalitis. Tr. 124. Dr. Small described the mechanism of reactivation very similarly to the
explanation given by Dr. Sriram. Compare Pet. Ex. 13 at 1-2, with Resp. Ex. E at 1.

        Further, Dr. Small agreed that petitioner’s cerebrospinal fluid showed an elevated white
blood cell count and elevated protein, and that patients with varicella infection can have these
findings. Tr. 120. Dr. Small also agreed that petitioner’s varicella zoster IgG was elevated. Tr.
118-19. Initially, he testified that petitioner’s clinical course was milder than patients he has
seen with varicella infection and that his patients with the illness had higher white blood cell
counts, more elevated protein cerebrospinal fluid counts, shingles along the course of nerves in
the head, and significant brain swelling. Tr. 123-27. However, he later admitted that he also had
patients with a milder clinical course, like that of petitioner. Tr. 128.

        Lastly, Dr. Small discussed whether AGH and the VA have the ability to share a patient’s
electronic medical records. He testified that as recent as three months ago it was impossible for
the two hospitals to share records electronically and this has made treating patients “very
difficult.” Tr. 119-20.

                            b.   Respondent’s Expert, Dr. Sriram22

        Dr. Sriram agrees with Dr. Small as to petitioner’s diagnosis of meningoencephalitis but
does not believe that petitioner’s Tdap vaccine caused his illness. Tr. 147. Instead, Dr. Sriram
opines that reactivation of petitioner’s VZV infection caused his meningoencephalitis. Tr. 146;
Resp. Ex. A at 3.

        Dr. Sriram defined meningoencephalitis as “a clinical diagnosis based to some extent on
[] laboratory data.” Tr. 146. A patient will have altered mental status which may be associated
with focal deficits such as hand or leg weakness, speech problems, or seizures. Tr. 147. The
cerebrospinal fluid may show elevated lymphocytes and protein which indicate inflammation of
the meninges. Id.

       With regard to petitioner’s theory of causation, Dr. Sriram disagreed with Dr. Small that
the Tdap vaccine can cause a cytokine reaction which increases the permeability of the blood
brain barrier. Dr. Sriram testified that there is no evidence to support this hypothesis. See Tr.
152. Further, Dr. Sriram did not agree that the medical articles cited by Dr. Small support
22
     Respondent filed six expert reports authored by Dr. Sriram. Resp. Exs. A, E, M, N, P, S.


                                                 15
petitioner’s causal theory. Dr. Sriram explained that the Kashiwagi study was done to examine
the effects of the DPT, Hib, and PCV7 vaccines on lymphocytes in peripheral blood. Tr. 148.
Since the article has nothing to do with the brain, Dr. Sriram does not believe that it supports Dr.
Small’s theory as it relates to the effect of cytokines on the blood brain barrier. Id. Moreover,
Dr. Sriram testified that in Kashiwagi, the DTP vaccine decreased cytokine levels, except for a
marginal increase of IL-6. Id.; Pet. Ex. 25 at fig.1. On cross-examination, however, Dr. Sriram
agreed that the DTP vaccine caused an elevation of cytokines TNF-α and IL-6, and that he was
previously mistaken when he testified that there was a decrease in cytokines. Tr. 210.

       As for the Rochfort article cited by petitioner, Dr. Sriram noted that it was an in vitro
experiment, and thus, it does not speak to what may happen in humans. Tr. 150-52. Rochfort
was an in vitro experiment where human microvascular endothelial cells were treated with
cytokines IL-6 and TNF-α, and then studied. Pet. Ex. 26. According to Dr. Sriram, very large
amounts of cytokines were used. Tr. 150-52. Dr. Sriram testified that researchers have not
studied whether the blood brain barrier is permeable if a person is injected with high doses of
cytokines. See Tr. 152.

        Next, Dr. Sriram explained why the Hiraiwa-Sofue and Aydin articles do not support
petitioner’s theory. He opined that Hiraiwa-Sofue is not relevant because petitioner did not have
evidence of demyelination, and petitioner is not pursuing a theory based on demyelination. Tr.
153. The Aydin study involved whole cell pertussis, and here petitioner did not receive a
vaccine that contained whole cell pertussis, only acellular pertussis. Tr. 154. Moreover,
petitioner here did not have hemorrhage necrotizing encephalitis, like the patient in Aydin. Id.

         Dr. Sriram emphasized that none of the literature cited by petitioner states that the Tdap
vaccine can cause a syndrome even close to what petitioner had—Mr. Dunn did not have ADEM
or NMDAR encephalitis. Tr. 155. Further, Dr. Sriram did not agree that cytokines can cause
encephalitis. Tr. 214. He explained that cytokines are associated with encephalitis but “are not
causally connected to it.” Id. Dr. Sriram testified that he has not seen any support in the
literature to prove that cytokines cause a breakdown of the blood brain barrier in humans. Tr.
218.

        Next, Dr. Sriram turned his focus to testifying in support of respondent’s position that
petitioner’s meningoencephalitis was caused by an alternative factor unrelated to his Tdap
vaccine—petitioner’s VZV infection. General information about VZV infections is set forth in
the Nagel and Gilden article23 filed by respondent. Resp. Ex. H. VZV is a virus in the herpes
family. Primary VZV infection generally occurs in childhood among non-vaccinated children
and is known as chickenpox. Id. at 1. After primary infection, the virus becomes latent in nerve
ganglia. Id. VZV infection reactivation may cause herpes zoster, also known as shingles. Id.
VZV reactivation may also cause vasculopathy, meningoencephalitis, cerebellitis, and other
neurological illnesses. Id. “VZV can reactivate and infect the meninges, brain parenchyma and
nerve roots to produce a VZV meningoencephalitis.” Id. at 4.


23
  Maria A. Nagel & Don Gilden, Neurological Complications of Varicella Zoster Virus
Reactivation, 27 Current Opinion Neurology 356 (2014).


                                                 16
         With regard to Althen Prong One, a medical theory of causation, Dr. Sriram’s opinions
were consistent with the information about VZV set forth in Nagel and Gilden. He explained
that the herpes zoster virus is present in the ganglion cells of the body. Tr. 156. The virus
resides in the neurons of the ganglion cells, and for reasons that are not clearly understood, the
virus becomes activated. Id. One trigger for activation is immunosuppression, which is more
common in persons as they become older, and also is “classic” in those between ages forty-five
to fifty. Id. The virus that resides in the ganglion cells can either “come forward and cause
infection of the skin or they go backwards and infect the meninges and the brain.” Tr. 157.
Persons who had chickenpox have the virus in their nerve cells, and it remains present
throughout life. The virus can become activated and travel “proximally into the spinal cord or []
brain or distally out into the skin.” Tr. 157-58. It is not uncommon for viral reactivation to
cause both encephalitis and meningitis. Id. Dr. Sriram further explained that with herpes zoster
reactivation, the virus can affect both the skin and nervous system. Id. VZV is a known cause,
and the second leading cause of, viral encephalitis.24 Resp. Ex. E at 2.

        In support of his theory of causation, Dr. Sriram cited several medical articles. A number
of which support his opinion that VZV can cause central nervous system illnesses, including
encephalitis and meningitis, through the mechanism of reactivation. In Grahn and Studahl,25 the
authors state that VZV is the “second most common infectious etiology of encephalitis after the
herpes simplex virus.” Resp. Ex. F at 2. The authors describe the mechanism as follows: VZV
is a herpes virus that may become latent in neurons in the dorsal root, autonomic, and cranial
ganglia. Id. Reactivation of the virus may infect the skin, and central nervous system, causing
encephalitis and meningitis. Id. And in Nagel and Gilden, the authors state that VZV can travel
to the central nervous system to produce meningoencephalitis, as described by Dr. Sriram. Resp.
Ex. H at 1; Tr. 160.

       Dr. Small also recognizes the theory of herpes zoster reactivation, and his explanation of
the mechanism did not differ from that provided by Dr. Sriram. See Pet. Ex. 13 at 1-2; Tr. 171.

         With regard to Althen Prong Two, a logical sequence of cause and effect, Dr. Sriram
testified that petitioner had herpes zoster which infected his central nervous system, causing
encephalitis and meningitis (meningoencephalitis), via the mechanism of viral reactivation. Tr.
156. Dr. Sriram provided several reasons why the evidence supported his opinion that
petitioner’s VZV infection was the more likely cause of his meningoencephalitis. First,
petitioner had acute encephalopathy and his cerebrospinal fluid revealed elevated lymphocytes
and protein consistent with VZV meningoencephalitis. Tr. 163-64. Dr. Sriram cited the
24
   See Don Gilden et al., Varicella Zoster Virus Vasculopathies: Diverse Clinical Manifestations,
Laboratory Features, Pathogenesis, and Treatment, 8 Lancet Neurology 731 (2009); T. De
Broucker et al., Acute Varicella Zoster Encephalitis Without Evidence of Primary Vasculopathy
in a Case-Series of 20 Patients, 18 Clinical Microbiology Infection 808 (2011).
25
  Anna Grahn & Marie Studahl, Varicella-Zoster Virus Infections of the Central Nervous
System – Prognosis, Diagnostics and Treatment, 71 J. Infection 281 (2015).



                                                17
Gregoire study26 to establish that there can be a wide range in the number of lymphocytes present
in the cerebrospinal fluid of patients with meningoencephalitis. Resp. Ex. C at 2 tlb.1. In
Gregoire, one patient had 13 and another patient had 358 lymphocytes in their CSF. Id.; Tr. 162-
63. Dr. Sriram explained that the presence of and number of lymphocytes (indicating
inflammation) in the CSF depends at what point in the illness the spinal fluid is drawn. Tr. 163.

        The second basis for Dr. Sriram’s Althen Prong Two opinion is that petitioner had a rash
on his chest noted December 23, and a swab of the rash tested by PCR was positive for VZV.27
Dr. Sriram cited medical articles which supported his position that a patient can have central
nervous system symptoms with no rash, or the neurological symptoms can be followed by the
rash. In Nagel,28 the authors addressed the issue of whether the herpes zoster rash must be
present for the virus to cause illness. Resp. Ex. O. The authors reviewed 30 cases of VZV
vasculopathy, which caused stroke due to viral infection of the cerebral arteries. Id. at 1. A
herpes zoster rash occurred in 19 out of the 30 cases. The authors concluded that the herpes
zoster rash was “not required to diagnose varicella zoster virus vasculopathy.” Id.

        A positive CSF PCR is not required to find that a patient has VZV encephalitis. The
Gilden article states, “[a]lthough a positive PCR for VZV DNA in CSF is helpful, a negative
PCR does not exclude the diagnosis . . .” Resp. Ex. T at 3. Dr. Sriram explained that “[w]hile
the specificity of [a] PCR assay for VZV is 100% [there are no false positive PCR values], the
sensitivity varies.” Resp. Ex. E at 2. A PCR done either very early or very late during the
clinical course of encephalitis may be negative. Id. A negative PCR study does not exclude the
diagnosis of VZV encephalitis. Resp. Ex. N at 2; see also Resp. Ex. T at 3.

        Dr. Sriram cited a paper by De Broucker. Resp. Ex. G. There, four out of twenty
patients had a negative cerebrospinal fluid PCR for VZV but had a herpes zoster rash before or
after onset of acute VZV encephalitis. Id. at 1. As it relates to the timing of the herpes zoster
rash, the authors state that “neurological presentations can also appear with, precede, or follow
herpes zoster.” Id. Dr. Sriram also cited the Grahn and Studahl article, which states that “the
central nervous system manifestations might occur before the skin eruptions.” Resp. Ex. F at 2.

       Dr. Sriram agreed that based on the criteria set forth in De Broucker, petitioner would not
have qualified as a “confirmed” case of VZV encephalitis because he did not have a positive
cerebrospinal fluid PCR for VZV. Tr. 199. Dr. Sriram affirmed that in De Broucker, the authors
26
  S. S. Gregoire et al., Polymerase Chain Reaction Analysis and Oligoclonal Antibody in the
Cerebrospinal Fluid from 34 Patients with Varicella-Zoster Virus Infection of the Nervous
System, 77 J. Neural Neurosurgery Psychiatry 938 (2006).
27
  Dr. Sriram believes it is likely that petitioner had the zoster rash before December 23, but it
was not detected. Tr. 164, 225. However, even if the zoster rash was not present until it was
seen on December 23, Dr. Sriram’s opinion would be the same. Tr. 225.
28
  Maria A. Nagel et al., The Varicella Zoster Virus Vasculopathies: Clinical, CSF, Imaging, and
Virologic Features, 70 Neurology 853 (2008).



                                                 18
stated that the only way to confirm VZV is by a positive CSF PCR or evidence of antibodies to
VZV.29 Tr. 201. In Arruti,30 the authors distinguish between “confirmed” and “probable” or
“suspected” VZV-caused illness. Resp. Ex. J at 2. While a confirmed case is defined as one
with positive cerebrospinal fluid PCR testing, a patient probably has VZV infection if there is a
simultaneous rash or a rash that occurs shortly after illness onset and there are inflammatory
markers in the CSF. Tr. 203.

        In Arruti, the authors studied the clinical characteristics of central nervous system
infections caused by VZV in 280 older patients (over age 65). Resp. Ex. J at 1. The authors
discussed the incidence of varicella zoster central nervous system infections, stating that “VZV is
a common viral agent causing central nervous system infections in the adult population, using
ranking behind HSV.” Id. at 7. The authors also discuss the incidence of skin lesions in the
context of central nervous system infections caused by VZV:

       Previous studies have shown that neurological complications of HZ [herpes
       zoster] can occur without skin lesions, such complications being observed in 38 to
       69% of patients with no skin involvement (cites omitted). In our study, only
       16.7% of patients had no signs of skin involvement. Hence, our data indicate that
       HZ [herpes zoster] occurring simultaneously or shortly after CNS [central nervous
       system] neurological symptoms suggests causality in a high percentage of cases in
       the elderly. . . . In the eight patients with probable VZV encephalitis and no viral
       confirmation [PCR negative for VZV], the clinical syndrome in combination with
       skin involvement [the presence of an HZ rash] together with imaging and/or
       cerebrospinal fluid findings supported the diagnosis and suggested a causative
       link.

       Id. Thus, based on Arruti, Dr. Sriram opines that petitioner would fall into the probable
category. Tr. 203.

       Lastly, Dr. Sriram testified that petitioner’s elevated VZV titer ˃4000, was a value
considered to be a striking elevation and confirmed recent activation of the varicella virus.31 Tr.
167-70.



29
   Dr. Sriram filed the Gregoire article to support his testimony that if a PCR of cerebrospinal
fluid is negative for VZV, an anti-VZV specific antibody test may be performed to confirm
diagnosis, but this test was not ordered for petitioner. Tr. 161-62; Resp. Ex. C at 1.
30
  Maialen Arruti et al., Incidence of Varicella Zoster Virus Infections of the Central Nervous
System in the Elderly: A Large Tertiary Hospital-Based Series, 23 J. Neurovirology 451 (2017).
31
  Dr. Sriram testified that although the VZV titer is high, because he does not know petitioner’s
baseline level, this fact alone does not form the basis of his causation opinion but is consistent
with it. Tr. 224.



                                                19
         When asked how long it would take to perform swab PCR test, Dr. Sriram answered that
if the test is sent to an outside laboratory, it would take three to five days to obtain the results.
Tr. 170. Dr. Sriram testified that based on petitioner’s medical records, it appeared that the PCR
swab test was sent out LabCorp in North Carolina on December 23. See Pet. Ex. 4(d) at 758.

         As for Althen Prong Three, Dr. Sriram opined that the timing between vaccination and
illness onset was appropriate for the VZV to cause petitioner’s meningoencephalitis. Tr. 170-71.
Dr. Sriram emphasized that when a person with shingles and altered mental status also has
cerebrospinal fluid that shows inflammation, “the preponderance of the clinical opinion would be
this is a zoster meningoencephalitis.” Tr. 171. Dr. Sriram cited the study by Science,32 which
studied eighty-four children with VZV neurological complications. Resp. Ex. U at 2. Children
were included in the study if the onset of their neurological symptoms occurred four weeks
before or after the VZV rash. Id. The “median interval between onset of rash and onset of
neurological manifestations was 5 days (range 6 days before to 16 days after the appearance of
the rash).” Id. at 3.

         On cross-examination, Dr. Sriram was questioned about the note made by Dr. Hong, one
of petitioner’s treating physicians at the VA. Dr. Sriram did not agree that the following note by
Dr. Hong was an opinion that the Tdap vaccine caused petitioner’s illness. On February 4, 2015,
the title of Dr. Hong’s note is “Allergy & Immunology Adverse Event Note.” Pet. Ex. 5(b) at
296. It states that petitioner “was admitted to AGH on 12/19/2014 with AMS. LP shows aseptic
meningitis result. Had Tdap vaccine on 12/2/2014.” Id. Dr. Sriram did agree that this note and
other entries in the VA records referenced that petitioner had an allergy or adverse drug reaction
to Tdap. Tr. 188.

     Dr. Sriram explained that according to the AGH records, the PCR swab test of petitioner’s
vesicle was sent out for testing on December 23. December 25 was a holiday, and petitioner was
discharged on December 27.33 Dr. Sriram testified that it was “highly unlikely” that the PCR test
results (positive for VZV) would have come back the day after Christmas in time for someone to
review it and make an assessment or recommendation about the diagnosis prior to the patient’s
discharge.34 Tr. 189.




32
   Michelle Science et al., Central Nervous System Complications of Varicella-Zoster Virus, 165
J. Pediatrics 779 (2014).
33
  During his testimony, Dr. Sriram stated petitioner was discharged on December 26. Tr. 189.
Petitioner was actually discharged on December 27.
34
  After the hearing, the PCR swab test results from LabCorp were filed. Pet. Ex. 39. They
showed the test report date was December 30, 2014. Thus, it appears Dr. Sriram was correct that
the results were not available before the petitioner’s hospital discharge on December 27.


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V.     LEGAL FRAMEWORK

           A.   Standards for Adjudication

        The Vaccine Act was established to compensate vaccine-related injuries and deaths. §
300aa-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 & Human 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).

        Petitioner’s burden of proof is by a preponderance of the evidence. § 300aa-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 & Human Servs., 592
F.3d 1315, 1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v.
Sec’y of Health & Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). In particular, petitioners
must prove that 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 & Human Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999)); Pafford v. Sec’y of
Health & Human Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). A petitioner who satisfies this
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.” § 300aa-13(a)(1)(B).

           B. Causation

        To receive compensation under the Program, petitioner must prove either: (1) that he
suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding to a
vaccine that he received, or (2) that he suffered an injury that was actually caused by a
vaccination. See §§ 300aa-13(a)(1)(A) and 11(c)(1); Capizzano v. Sec’y of Health & Human
Servs., 440 F.3d 1317, 1319-20 (Fed. Cir. 2006). Petitioner must show that the vaccine was “not
only a but-for cause of the injury but also a substantial factor in bringing about the injury.”
Moberly, 592 F.3d at 1321 (quoting Shyface, 165 F.3d at 1352-53).

        Because petitioner does not allege that he suffered a Table injury, he must prove that the
vaccine he received caused his injury. To do so, he must establish, by preponderant evidence:
(1) a medical theory causally connecting the vaccine and injury (“Althen Prong One”); (2) a
logical sequence of cause and effect showing that the vaccine was the reason for the injury
(“Althen Prong Two”); and (3) a showing of a proximate temporal relationship between the
vaccine and injury (“Althen Prong Three”). § 300aa-13(a)(1); Althen, 418 F.3d at 1278.

        The causation theory must relate to the injury alleged. Thus, petitioner must provide a
reputable medical or scientific explanation that pertains specifically to this case, although the
explanation need only be “legally probable, not medically or scientifically certain.” Knudsen v.
Sec’y of Health & Human Servs., 35 F.3d 543, 548-49 (Fed. Cir. 1994). Petitioner cannot
establish entitlement to compensation based solely on assertions. Rather, a vaccine claim must

                                                21
be supported either by medical records or by the opinion of a medical doctor. § 300aa-13(a)(1).
In determining whether petitioner is entitled to compensation, the special master shall consider
all material contained in the record, including “any . . . conclusion, [or] medical judgment . . .
which is contained in the record regarding . . . causation.” § 300aa-13(b)(1)(A). The
undersigned must weigh the submitted evidence and the testimony of the parties’ offered experts
and rule in petitioner’s favor when the evidence weighs in his 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”); see also Althen, 418 F.3d at 1280 (providing “close calls” are
resolved in petitioner’s favor).

        Another important aspect of the causation-in-fact case law under the Vaccine Act
concerns the factors that a special master should consider in evaluating the reliability of expert
testimony and other scientific evidence relating to causation issues. In Daubert v. Merrell Dow
Pharmacy, Inc., 509 U.S. 579 (1993), the United States Supreme Court listed certain factors that
federal trial courts should utilize in evaluating proposed expert testimony concerning scientific
issues. In Terran v. Secretary of Health & Human Services., 195 F.3d 1302, 1316 (Fed. Cir.
1999), the Federal Circuit ruled that it is appropriate for special masters to utilize Daubert’s
factors as a framework for evaluating the reliability of causation-in-fact theories actually
presented in Program cases.

        The Daubert factors for analyzing the reliability of testimony are: (1) whether a theory or
technique can be (and has been) tested; (2) whether the theory or technique has been subjected to
peer review and publication; (3) whether there is a known or potential rate of error and whether
there are standards for controlling the error; and (4) whether the theory or technique enjoys
general acceptance within a relevant scientific community. Terran, 195 F.3d at 1316, n.2 (citing
Daubert, 509 U.S. at 592-95). In addition, where both sides offer expert testimony, a special
master’s decision may be “based on the credibility of the experts and the relative persuasiveness
of their competing theories.” Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339,
1347 (Fed. Cir. 2010) (citing Lampe v. Sec’y of Health & Human Servs., 219 F.3d 1357, 1362
(Fed. Cir. 2000)). However, nothing requires the acceptance of an expert’s conclusion
“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
great an analytical gap between the data and the opinion proffered.” Snyder v. Sec’y of Health
& Human Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146
(1997)).

        In deciding the issues in this case, the undersigned has considered the record as a whole.
§ 300aa-13(a)(1). The undersigned has reviewed and relied on statements in the medical records,
as medical records are generally viewed as trustworthy evidence, since they are created
contemporaneously with the treatment of the vaccinee. Cucuras v. Sec’y of Health & Human
Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). In addition, the treating physicians’ opinions are
“quite probative,” as treating physicians are in the “best position” to evaluate the vaccinee’s
condition. Capizzano, 440 F.3d at 1326. However, no treating physician’s views bind the
special master, per se; rather, their views should be carefully considered and evaluated. § 300aa-
13(b)(1); Snyder, 88 Fed. Cl. at 745 n.67. Each opinion from a treating physician should be
weighed against other, contrary evidence present in the record—including conflicting opinions

                                                 22
from other treating physicians. Hibbard v. Sec’y of Health & Human Servs., 100 Fed. Cl. 742,
749 (2011), aff’d, 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec’y of Health & Human Servs.,
100 Fed. Cl. 119, 136 (2011), aff’d, 463 F. App’x. 932 (Fed. Cir. 2012); Veryzer v. Sec’y of
Health & Human Servs., No. 06-522V, 2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29,
2011), mot. for rev. denied, 100 Fed. Cl. 344 (2011).

           C. Alternative Causation

       A petitioner who satisfies his burden of proof under the standards set forth above 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.” § 300aa-
13(a)(1)(B). Therefore, in this case, even if petitioner met his burden of proof on causation, he is
not entitled to compensation where the respondent has proven by preponderant evidence that a
factor unrelated to the vaccination caused his meningoencephalitis. See Doe v. Sec’y of Health
& Human Servs., 601 F.3d 1349, 1358 (Fed. Cir. 2010) (“[Petitioner] Doe never established a
prima facie case, so the burden (and attendant restrictions on what ‘factors unrelated’ the
government could argue) never shifted.”). The Vaccine Act provides that “factors unrelated to
the administration of the vaccine,” are those “which are shown to have been the agent . . .
principally responsible for causing the petitioner’s illness, disability, injury, condition or death.”
§ 300aa-13(a)(2)(B).

       In Munn, the Federal Circuit affirmed the special masters’ findings of alternate causation.
The special master “concluded that ‘[petitioner] succumbed to infection’ and thus that the
pneumonia led to her death” not the encephalopathy alleged to be caused by the vaccination.
Munn v. Sec’y of Health & Human Servs., 970 F.2d 863, 872 (Fed. Cir. 1992).

       Here, respondent has identified an alternative cause of petitioner’s illness: Reactivation of
VZV infection. Thus, the undersigned undertakes an analysis based on the Althen prongs as to
whether VZV reactivation—a factor unrelated to petitioner’s vaccination—caused petitioner’s
meningoencephalitis. See Forrest v. Sec’y of Health & Human Servs., No. 14-1046V, 2019 WL
925495, at *1 (Fed. Cl. Spec. Mstr. Jan. 28, 2019) (finding respondent showed by preponderant
evidence that a VZV infection was responsible for petitioner’s injury).

VI.    Alternative Factor Analysis

           A. Althen Prong One: Respondent’s Medical Theory

        Under Althen Prong One, respondent must set forth a medical theory explaining how
VZV infection reactivation can cause meningoencephalitis. Andreu v. Sec’y of Health & Human
Servs., 569 F.3d 1367, 1375 (Fed. Cir. 2009); Pafford, 451 F.3d at 1355-56. The theory of
causation must be informed by a “sound and reliable medical or scientific explanation.”
Knudsen, 35 F.3d at 548; see also Veryzer v. Sec’y of Health & Human Servs., 98 Fed. Cl. 214,
223 (2011) (noting that special masters are bound by both § 300aa-13(b)(1) and Vaccine Rule
8(b)(1) to consider only evidence that is both “relevant” and “reliable”). If respondent relies
upon a medical opinion to support his theory, the basis for the opinion and the reliability of that
basis must be considered in the determination of how much weight to afford the offered opinion.

                                                 23
See Broekelschen, 618 F.3d at 1347 (“The special master’s decision often times is based on the
credibility of the experts and the relative persuasiveness of their competing theories.”); Perreira
v. Sec’y of Health & Human Servs., 33 F.3d 1375, 1377 n.6 (Fed. Cir. 1994) (“Expert opinion is
no better than the soundness of the reasons supporting it.” (citing Fehrs v. United States, 620
F.2d 255, 265 (Ct. Cl. 1980))).

        Respondent’s proposed mechanism of causation is varicella zoster viral reactivation. The
mechanism is not disputed by petitioner’s expert. Further, the experts do not disagree with
petitioner’s diagnosis, meningoencephalitis, and they both agree that VZV infection can cause
this illness. Respondent’s proposed mechanism is a sound and reliable explanation of
pathogenesis as illustrated by the testimony of both experts and the medical literature filed by
respondent. Therefore, the undersigned finds that respondent has established by preponderant
evidence that VZV reactivation can cause meningoencephalitis.

           B. Althen Prong Two: Logical Sequence of Cause and Effect

        Under Althen Prong Two, respondent must prove by a preponderance of the evidence that
there is a “logical sequence of cause and effect showing that the vaccination was the reason for
the injury.” Capizzano, 440 F.3d at 1324 (quoting Althen, 418 F.3d at 1278). Respondent must
show “that the vaccine was the ‘but for’ cause of the harm . . . or in other words, that the vaccine
was the ‘reason for the injury.’” Pafford, 451 F.3d at 1356 (citations omitted).

     The central issue here is not whether VZV reactivation can cause meningoencephalitis, but
whether it did in petitioner’s case. The undersigned finds that respondent has proven by
preponderant evidence that it did for the following reasons.

        Petitioner had chickenpox as a child. His clinical course was consistent with
meningoencephalitis caused by VZV. Petitioner had altered mental status, his CSF analysis was
consistent with inflammation caused by a viral infection, he had an abnormal and elevated VZV
titer, and he had skin vesicle which tested positive for the virus. Moreover, the medical literature
shows that next to the herpes simplex virus, VZV is the second leading cause of viral
meningoencephalitis. And further, Dr. Small agreed that petitioner’s clinical course was
“completely consistent” with VZV infection. Tr. 123.

       Dr. Small testified that in order to diagnose petitioner with VZV caused illness, he would
need to see evidence that petitioner was infected with the virus at the time he presented with
neurological symptoms. When asked whether a patient could first have central nervous system
involvement, followed by a skin rash, Dr. Small stated that he did not know. Medical literature
filed by respondent answered the question. Articles by De Broucher, Grahn and Studhal, and
Arruti all state that neurological manifestations may occur before the skin vesicles of herpes
zoster appear. The fact that several articles address this issue suggest that the factual
circumstances here, where the rash occurs after the neurological symptoms, is not unique to this
petitioner.

      Petitioner’s onset of altered mental status was December 19, and his herpes zoster rash
was present on December 23, while petitioner was still encephalopathic. Thus, he had

                                                24
neurological symptoms and a rash at the same time. The Arruti article speaks to this exact
scenario. Their patient data indicated that the herpes zoster rash occurred either “simultaneously
or shortly after CNS [central nervous system] neurological symptoms.” Resp. Ex. J at 7.

       In addition to the support from medical articles, the petitioner’s medical records also offer
support for Dr. Sriram’s position that the rash can follow central nervous system symptoms. On
December 23, an infectious disease physician charted that, “skin lesions in VZV encephalitis
may develop after AMS even during [treatment].” Pet. Ex. 4(a) at 35. This contemporaneous
note is persuasive evidence in support of respondent’s position.

       With regard to medical record entries by Dr. Hong and Dr. Pae, attributing petitioner’s
illness to the Tdap vaccine, the undersigned finds these references are not persuasive evidence of
causation based on the totality of the facts and circumstances. Dr. Hong and Dr. Pae could not
have been informed by the petitioner that he had a positive skin test for herpes zoster, because at
the time the petitioner saw these doctors, he did not know that information. Neither of these
physicians saw nor treated the petitioner while he was a patient at AGH. Dr. Hong and Dr. Pae
treated the petitioner after his discharge from AGH, when he presented for follow-up care at the
VA. Neither of these physicians reference the positive PCR skin test results in their records.
Based on Dr. Small’s testimony, it would have been difficult, if not impossible, for them to
review the petitioner’s AGH record. Tr. 119. If Dr. Hong or Dr. Pae had reviewed the
petitioner’s positive VZV skin test results, which was very important and relevant data that could
inform their opinions as to causation, it is likely that at least one of them would have noted the
results. Lastly, the LabCorp report date is December 30, three days after petitioner’s discharge
from AGH. Based on the available record, it does not appear the report was seen by either Dr.
Hong or Dr. Pae.

       The undersigned generally finds opinions of a treating physician to be persuasive evidence
of causation, but for all of the reasons stated above, Dr. Hong’s statement about Tdap causation
is not persuasive here. The far more sound and reliable evidence as to causation specific to
petitioner’s case is that offered by respondent and Dr. Sriram.

       The undersigned does find the contemporaneous records created by the physicians at AGH
to be persuasive. On approximately twelve occasions, the treating physicians suggest that the
etiology of petitioner’s illness is “likely viral” or “infectious.” See, e.g. Pet Ex. 4(a) at 9-62.
This information, along with all of the reasons discussed above, combine to provide
preponderant evidence that petitioner’s illness was caused by VZV infection reactivation.

           C. Althen Prong Three: Proximate Temporal Relationship

        Under Althen Prong Three, respondent must provide “preponderant proof that the onset
of symptoms occurred within a timeframe for which, given the understanding of the disorder’s
etiology, it is medically acceptable to infer causation-in-fact.” De Bazan v. Sec’y of Health &
Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The acceptable temporal association will
vary according to the particular medical theory advanced in the case. See Pafford, 451 F.3d at
1358. A temporal relationship between a vaccine and an injury, standing alone, does not
constitute preponderant evidence of vaccine causation. See, e.g., Veryzer, 100 Fed. Cl. at 356

                                                 25
(explaining that “a temporal relationship alone will not demonstrate the requisite causal link” and
there must be “a medical theory causally connecting the vaccine and injury”).

       The onset of petitioner’s altered mental status occurred on December 19, and his herpes
zoster skin rash was present on December 23. Based on testimony of Dr. Sriram, and the journal
articles by Arruti, De Broucker, Grahn and Stadahl, and Science, the timeline of illness and rash
is consistent with the clinical course of VZV meningoencephalitis occurring with viral
reactivation. Thus, the undersigned finds the respondent has proven by preponderant evidence
that the temporal association between the mechanism of reactivation on the onset of illness is
appropriate.

VII.   CONCLUSION

       It is clear from the medical records that Mr. Dunn suffered as a result of his illness, and
the undersigned extends her sympathy to him. However, this case cannot be decided based upon
sympathy but rather by an analysis of the evidence.

        For all of the reasons discussed above, the undersigned finds that respondent has
established by preponderant evidence a factor unrelated to vaccination caused petitioner’s illness.
Therefore, petitioner is not entitled to compensation and his petition must be dismissed. In the
absence of a timely filed motion for review pursuant to Vaccine Rule 23, the Clerk of the Court
SHALL ENTER JUDGMENT in accordance with this Decision.


            IT IS SO ORDERED.


                                                     s/Nora Beth Dorsey
                                                      Nora Beth Dorsey
                                                      Special Master




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