In the United States Court of Federal Claims
                          OFFICE OF SPECIAL MASTERS

**********************
MARI BOURCHE,                        *
As Personal Representative of the    *     No. 15-232V
Estate of JOSEPH BOURCHE,            *     Special Master Christian J. Moran
                                     *
                  Petitioner,        *     Filed: January 7, 2020
                                     *
v.                                   *     Entitlement, hepatitis B vaccine,
                                     *     vasculitis, IgA nephropathy,
SECRETARY OF HEALTH                  *     endocarditis, vancomycin.
AND HUMAN SERVICES,                  *
                                     *
                  Respondent.        *
**********************
Andrew D. Downing and Courtney Van Cott, Van Cott & Talamante, PLLC,
Phoenix, AZ, for petitioner;
Sherry D. Soanes and Lisa Watts, United States Dep’t of Justice, Washington, DC,
for respondent.

                PUBLISHED DECISION DENYING COMPENSATION1

      Mari Bourche was married to Joseph Bourche, who was born in 1959. In
2014, Mr. Bourche was suffering from two significant health problems – poor
functioning in his kidneys for which he was receiving dialysis and heart trouble for
which he had a pacemaker implanted. He received a dose of the hepatitis B
vaccine in April 2014. In May 2014, Mr. Bourche suffered a serious infection for
which he was hospitalized for five days. In October 2014, Mr. Bourche required


       1
          The E-Government Act, 44 U.S.C. § 3501 note (2012) (Federal Management and
Promotion of Electronic Government Services), requires that the Court post this decision on its
website (http://www.cofc.uscourts.gov/aggregator/sources/7). Anyone can access this decision
once it is posted to the website. Pursuant to Vaccine Rule 18(b), the parties have 14 days to file
a motion proposing redaction of medical information or other information described in 42 U.S.C.
§ 300aa-12(d)(4). Any redactions ordered by the special master will appear in the document
posted on the website.
another heart operation. Unfortunately, Mr. Bourche declined and eventually died
in January 2016.

       As the administrator of her deceased husband’s estate, Ms. Bourche is
pursuing a claim that the hepatitis B vaccination led to the infection, which, in turn,
set off a series of events ultimately shortening her husband’s life. To assist with
her claim, Ms. Bourche retained two doctors, Thomas Zizic, a rheumatologist; and
Robert Stark, a cardiologist. Ms. Bourche also presented reports and testimony
from a nephrologist who cared for Mr. Bourche, Thomas Mooney.
      The Secretary disagreed with the claim that the hepatitis B vaccination
caused any adverse consequences to Mr. Bourche. The Secretary also retained two
doctors who have the same specialties as the doctors Ms. Bourche retained. These
are Mehrdad Matloubian (rheumatologist) and Shane LaRue (cardiologist).
      These five doctors as well as Ms. Bourche testified at a hearing on April 23–
24, 2018. Following the hearing, the parties submitted additional evidence and
post-hearing briefs.
       As presented in the testimony as well as in pre-hearing and post-hearing
briefs, Ms. Bourche is seeking recovery through a multi-step theory. She
maintains the following: (1) the April 23, 2014 hepatitis B vaccination caused Mr.
Bourche to develop vasculitis before he entered the hospital on May 23, 2014 by
inducing the production of immune complexes, (2) the vasculitic skin lesions
allowed bacteria to enter Mr. Bourche’s body and this bacterial infection
necessitated the hospitalization, (3) bacteria, which the vaccination-induced
vasculitic skin lesions permitted, seeded an infection on a heart valve, further
weakening Mr. Bourche’s cardiac function, (4) this decreased cardiac function was
a substantial factor in Mr. Bourche’s death on January 16, 2016.
       The Secretary challenges Ms. Bourche’s theory. The Secretary disputes that
the hepatitis B vaccine can cause vasculitis. The Secretary argues that Mr.
Bourche developed vasculitis after (not before) the May 2014 hospitalization and
further argues that the vasculitis could have been a consequence of the provoking
infection or a medication, vancomycin, used to treat the infection. The Secretary
disputes the allegation that any vasculitic skin lesion was the portal of entry for the
bacteria because the bacteria could have entered Mr. Bourche’s body during
dialysis. The Secretary questions the sequence of the vasculitis and the heart-valve
infection, noting that the infection of the heart valve could have occurred before
the vasculitis. Finally, the Secretary contends that the heart-valve infection was
not a substantial factor in Mr. Bourche’s death.

                                              2
       The evidence does not preponderate in Ms. Bourche’s favor. The primary
flaw is that the evidence, taken as a whole, shows Mr. Bourche did not form the
immune complexes Dr. Zizic’s theory predicted. In addition, the evidence does not
support a finding that Mr. Bourche developed vasculitis before his hospitalization.
Because a finding that Mr. Bourche developed vasculitis before his hospitalization
is necessary to link Mr. Bourche’s April 2014 hepatitis B vaccination to his
subsequent decline in health, the remainder of Ms. Bourche’s case becomes
untenable. This sequence of events is more compatible with a cause, such as a
reaction to vancomycin, other than the hepatitis B vaccination. Finally, Ms.
Bourche has not persuasively established that any complication of the hepatitis B
vaccination hastened her husband’s death. Thus, as explained in more detail
below, Ms. Bourche is not entitled to compensation.
I.    Events in Mr. Bourche’s Life

       Due largely to Mr. Bourche’s pre-existing conditions, his case presents one
of the most challenging and complicated cases the undersigned has reviewed.
      A.    Pre-existing Kidney Disease

       Mr. Bourche’s relevant medical history begins a relatively long time before
the 2014 hepatitis B vaccination. In 2000, Dr. Mooney began treating Mr. Bourche
for a disease known as IgA nephropathy.
                                 IgA nephropathy
       The basic meaning of “nephropathy” is a disease of the kidneys. Dorland’s
Illustrated Medical Dictionary 1241-42 (32d ed. 2012). “IgA” refers to a type of
immunoglobulin. Dorland’s at 919-21; Tr. 258. In IgA nephropathy, the tubes in
the kidneys that filter waste products become inflamed, a condition known as
glomerulonephritis. Dorland’s at 786; Tr. 379.
       The cause of IgA nephropathy is partially known. A person with IgA
nephropathy produces abnormal IgA. The specific problem is a defective sugar
moiety in a region of the IgA known as the hinge. Because the abnormal IgA is
not expected, the body makes antibodies to the abnormal IgA. When the
antibodies attack the abnormal IgA, they form immune complexes that clog the
tubes in the kidneys leading to kidney damage. Tr. 267-69; see also Tr. 147, 200.
For a more in-depth explanation of the pathogenesis of IgA nephropathy, see




                                            3
exhibit A-8 (Wyatt) at 2404.2 However, why some people produce abnormal IgA
molecules is not known. Tr. 208.
       In the context of discussing the pathogenesis of IgA nephropathy, Wyatt
links IgA nephropathy to another disease, Henoch-Schönlein purpura (“HSP”).
“Patients with Henoch-Schönlein purpura nephritis and those with IgA
nephropathy have many of the same laboratory abnormalities . . . and pathological
features of renal-biopsy specimens. These similarities have led to proposals that
the two entities represent opposite ends of the clinical spectrum characterizing a
single disease process.” Exhibit A-8 (Wyatt) at 2406. Other evidence also
connects IgA nephropathy with HSP. See Tr. 98, 151, 271; exhibit A-9
(Knoppova). As discussed below, later in Mr. Bourche’s course, some doctors
propose that Mr. Bourche suffered from HSP.
       IgA is a chronic condition that medicine cannot cure. Tr. 97, 327. The
problem is that the body cannot stop making the defective IgA without a drastic
intervention such as a bone marrow transplant. Tr. 330.
      One consequence of IgA nephropathy can be hypertension. Tr. 99. As IgA
nephropathy progresses, patients require kidney dialysis. Tr. 82, 97.
       Dr. Mooney, the nephrologist primarily responsible for treating Mr.
Bourche’s IgA nephropathy, explained the dialysis process. Tr. 103-10. The
dialysis center where Mr. Bourche went is a public place containing approximately
20 chairs. People undergoing dialysis remain in their usual clothes and sit in a
reclining chair. A nurse conducts an examination focused on the systems involved
in dialysis.
       A needle is inserted through a fistula and this needle draws blood out of the
patient’s arm. A second needle is inserted higher up in the arm to return the
cleansed blood to the patient. A dialysis fistula “is a natural connection between
an artery and a vein that is covered with your own skin.” Tr. 110. With a sterile
technique, the insertion of needles is extremely unlikely to introduce bacteria. In
the facility that Dr. Mooney supervised, bacterial infections were “extremely rare.”
Tr. 110.
       The removed blood is processed to remove the waste. Dialysis also removes
fluids that have accumulated in the patient’s body due to the lack of kidney
function. The removal of fluids causes dehydration, which is difficult to tolerate.

       2
        The complete bibliographical information for all articles cited in the decision appears in
the appendix.

                                                    4
The dialysis process can cause itchiness. Tr. 62, 161, 330; exhibit A-1
(Ankudowicz) at 1436. Mr. Bourche experienced itchiness during his dialysis. Tr.
34.
       The dialysis process takes approximately four hours. Mr. Bourche required
dialysis three times per week. Dr. Mooney or one of his doctor-partners examined
patients “pretty rarely,” although the doctors were available for more thorough
consultations. Tr. 108; see also Tr. 87.
       Dr. Mooney initiated dialysis for Mr. Bourche in December 2004. Exhibit
14 at 1. He remained on dialysis until he received a kidney transplant in February
2006. Exhibit 7 at 306.
      In October 2009, Mr. Bourche developed shortness of breath, chest pain,
hypertensive urgency, a fever, headache, cough and nausea. He underwent a
kidney biopsy. Exhibit 9 at 628-29.
       Sections of the kidney were stained for immunofluorescence.
Immunofluorescence is a process by which a pathologist can determine the
presence (or absence) of various antibodies and other components of the immune
system. Dorland’s at 919. For Mr. Bourche, the pathologist (Patrick Walker)
identified IgA and IgM but not IgG. Exhibit 9 at 629. Dr. Matloubian opined that
Mr. Bourche was having a recurrence of his IgA nephropathy. Tr. 273, 326, 378.
        With respect to the recurrence of IgA nephropathy in Mr. Bourche, Dr.
Matloubian’s opinion conflicts with the view of Dr. Mooney. Dr. Mooney testified
that Mr. Bourche did not have a recurrence of IgA. Tr. 84. Although treating
physicians are usually entitled to deference, their views are not sacrosanct. On this
point, Dr. Matloubian is more persuasive than Dr. Mooney. First, the biopsy report
states under diagnosis “IgA nephropathy, Recurrent.” Exhibit 9 at 628. Second,
the literature supports the recurrence of IgA nephropathy after a transplant.
Exhibit A-8 (Wyatt) at 2408; exhibit A-9 (Knoppova) at 3. Third, Dr. Zizic also
supported the idea of a recurrence of IgA nephropathy. Tr. 385 (“[L]et me start off
by saying that it would not be surprising to see some IgA deposition in the
transplanted kidney.”).
     The transplanted kidney was removed on September 2, 2011. Exhibit 7 at
95. Dr. Mooney indicated that Mr. Bourche had rejected the kidney. Tr. 65; see




                                             5
also Tr. 150, 328-29, 386.3 However, there appears to be no biopsy of the rejected
kidney to determine whether the IgA nephropathy had occurred again. Tr. 378.
       B.      Events from Kidney Removal to Pacemaker Implantation

       On April 12, 2012, Mr. Bourche was having a problem with his skin. Tr. 28.
He underwent a biopsy and the results were consistent with prurigo nodularis.
Exhibit 6 at 9; see also Tr. 160, 274. Prurigo nodularis is “a chronic, intensely
pruritic [itchy] form of neurodermatitis… Characteristics include single or
multiple, firm nodules that are red, brown, or pink… Scratching or rubbing of the
nodules often makes the condition worse.” Dorland’s at 1539. According to Ms.
Bourche, prurigo nodularis is related to chronic kidney disease. Pet’r’s Posth’g Br.
at 2 n.1.4
       In November 2012, Mr. Bourche became infected with strep pneumonia. In
response, Dr. Mooney sent him to the hospital for treatment with vancomycin.
Exhibit 4 at 86; Tr. 123-26.5 The Secretary argued that the infection was
“presumably” related to Mr. Bourche’s fistula. Resp’t’s Posth’g Br. at 2.
However, the Secretary failed to cite any opinions of treating physicians to justify
this presumption. See Pet’r’s Reply at 2.
      In this period, Mr. Bourche periodically complained about pain in his
abdomen. See Tr. 29, 364. Some of these complaints are reflected in his medical
records. E.g., exhibit 10 at 355.
       C.      Heart History before Vaccination

      As alluded to earlier, Mr. Bourche had heart trouble for many years before
the vaccination. For example, x-rays from 2011 showed that his heart was
abnormally enlarged. Exhibit 7 at 148 (“cardiomegaly”), 270; see also Tr. 416
(discussing enlarged heart in the context of endocarditis). His cardiologist was Dr.
Holland, who wrote a report for this case. Tr. 81; exhibit 52.



       3
         In 2015, Mr. Bourche told a doctor that he developed a viral illness on a cruise in 2009,
before the kidney removal. Exhibit 72 at 96.
       4
         After the hepatitis B vaccination, Mr. Bourche may have had another instance of
prurigo nodularis. See exhibit 6 at 11-13; Tr. 331.
       5
       During the critical hospitalization in May 2014, Mr. Bourche again received
vancomycin. Additional information about that drug is provided in that context below.

                                                    6
      By September 2013, Mr. Bourche was not functioning well. Exhibit 8 at 77;
Tr. 16; see also Tr. 408-09, 466-68. His heart’s ejection fraction was 33 percent.
Exhibit 8 at 162-63. “Ejection fraction” refers to “the proportion of the volume of
blood in the ventricles at the end of diastole that is ejected during systole. . . . It is
normally 65 ± 8 per cent; lower values indicate ventricular dysfunction.”
Dorland’s at 740. To assist him, doctors installed a pacemaker on October 4, 2013.
Exhibit 8 at 141-44. This equipment includes two wires that are inserted into the
patient’s heart and an impulse through the wires synchronizes the heart’s beating.
Tr. 410, 466.
       After installation of the pacemaker, Mr. Bourche functioned much better.
Tr. 17. After evaluating Mr. Bourche, Dr. Holland determined that Mr. Bourche’s
“cardiac condition has improved significantly and that [he is] now ready for
transplant from a cardiovascular standpoint.” Exhibit 8 at 56 (Jan. 9, 2014);
accord Tr. 432, 468-70.
        The doctors responsible for coordinating Mr. Bourche’s care in advance of a
potential kidney transplant evaluated him on April 7, 2014. They found that “he
has improved quite a lot, specifically his heart.” Exhibit 10 at 403. His status on
the transplant list indicates relatively good health because good health is required
for a transplant. Tr. 64, 114-15.
      D.     Other Medical Records from early 2014, before Vaccination

      Following the installation of a pacemaker, Mr. Bourche followed up with his
cardiologist, Dr. Holland, on January 9, 2014. His ejection fraction was 35-38
percent. Exhibit 8 at 158. This measurement was better than the ejection fraction
before the pacemaker, which had been 33 percent.
       Dr. Mooney saw Mr. Bourche on February 7, 2014, and recorded that Mr.
Bourche looked well and had no complaints. Exhibit 10 at 1527. While Mr.
Bourche’s brief points out that this medical record does not reflect any skin
problems, Pet’r’s Posthear’g Br. at 4, Dr. Mooney usually did not examine the skin
of his dialysis patients. Tr. 111. Mr. Bourche continued to report abdominal pain.
Exhibit 10 at 1525 (Feb. 3, 2014), 1538 (Mar. 17, 2014).
       In March 2014, a comprehensive care plan was updated for Mr. Bourche.
Here, Mr. Bourche reported that his goals were: (1) to focus his energy on building
his automotive business, (2) to enjoy his family, (3) to pursue a transplant, and (4)
to travel. Exhibit 10 at 317; see also Tr. 48, 112.


                                               7
      Based upon this information, Dr. Mooney was asked during the hearing to
rate Mr. Bourche’s health on a scale of 1-10 with 10 being perfect health. Dr.
Mooney scored Mr. Bourche as an eight, when compared to other dialysis patients.
But, when compared to other men in their 50s, Dr. Mooney gave him a three or
four because he was chronically ill. Tr. 114-15.
        Through lab testing, doctors learned that Mr. Bourche did not have sufficient
antibodies against the hepatitis B virus. Exhibit 7-1 at 6 (Apr. 7, 2014); Tr. 224,
372. Because the Center for Disease Control recommends the hepatitis B vaccine
for all dialysis patients, Tr. 84, Dr. Mooney ordered a vaccination.
       E.      Hepatitis B Vaccine, Vaccination
               on April 23, 2014, and Remainder of April 2014

       The date of vaccination was April 23, 2014, and on that date, one of Dr.
Mooney’s partners was supervising the dialysis center. Tr. 88; exhibit 10 at 126.
Mr. Bourche was itchy. At 17:40, Mr. Bourche was given Benadryl for his
itchiness. Exhibit 10 at 1359. This itchiness is not surprising as Mr. Bourche had
been itchy previously. See, e.g., exhibit 10 at 1267 (Nov. 8, 2013); Tr. 62, 161,
278, 330. The itchiness relates to the dialysis and is not a manifestation of
vasculitis, a condition that later affected Mr. Bourche. Tr. 63, 160, 330.
      The dialysis process removed the waste products normally. See exhibit 10 at
1358. Mr. Bourche received the hepatitis B vaccine at 19:30. Exhibit 2 at 1;
exhibit 10 at 1359.6
       The hepatitis B vaccine is manufactured using recombinant DNA
technology. This process re-creates the outside structure of the hepatitis B virus
without the genetic material of the virus. Thus, unlike an infection with an actual
virus or a vaccine containing a live but attenuated virus, the hepatitis B vaccine
does not replicate once inside a person’s body. Tr. 246; see also Doe 71 v. Sec’y
of Health & Human Servs., 95 Fed. Cl. 598, 601 n.3 (2010).
      A standard dose of the hepatitis B vaccine contains 20 µg of hepatitis B
surface antigen. However, because people receiving dialysis do not create a



       6
          The nursing notes created on this date show that Mr. Bourche first received Benadryl at
17:40, and then received the hepatitis B vaccination at 19:30. These records show that Mr.
Bourche and Ms. Bourche inaccurately recollected that the hepatitis B vaccination preceded the
onset of itchiness. See exhibit 1, ¶ 9; exhibit 63, ¶ 5; Tr. 18.

                                                    8
sufficiently robust response to the vaccination, the dose is doubled, meaning Mr.
Bourche actually received 40 µg. Tr. 251, 308.
       The hepatitis B vaccine is injected into a muscle. In the muscle, a part of the
immune system known as macrophages pick up the antigen and bring the antigen
to the draining lymph nodes. This process stimulates B cells to produce antibodies,
which would, in the case of infection, attack the hepatitis B virus. Tr. 246-47. The
type of antibody to which the hepatitis B vaccine leads is IgG. Tr. 262, citing
exhibit A-30 (Siegrist) at 3. The production of IgG takes a few days.
      At Mr. Bourche’s next dialysis appointment, which took place on April 25,
2014, no complaints were noted. Exhibit 10 at 1360-61; Tr. 85, 202. For example,
the medical records do not describe Mr. Bourche having a blister in his mouth. Tr.
203.
       F.      Health and Hospitalization in May 2014

       On May 2, 2014, nine days after the vaccination, Mr. Bourche reported
mouth blisters. Exhibit 10 at 127.7 A blister is a rounded projecting structure. See
Dorland’s at 226 (referring to bulla and vesicle), 259 (bulla), 2052 (vesicle);
exhibit J at 9; Tr. 263. Based on his observations of the blister (or blisters), Dr.
Mooney determined Mr. Bourche was reacting adversely to the vaccination.
Accordingly, Dr. Mooney entered an allergy to the hepatitis B vaccine in Mr.
Bourche’s medical chart. Tr. 67, 88, 120. Both Dr. Zizic and Dr. Matloubian
recognized this determination, Tr. 162, 336-37, with Dr. Matloubian emphasizing
that the treating doctor assumed a causal relationship.
      Mr. Bourche’s immunity to the hepatitis B virus was retested via laboratory
studies reported on May 7, 2014. The results of this testing showed that he
produced antibodies to the hepatitis B surface antigen. However, the antigen itself
was no longer present in his body. Exhibit 10 at 239; Tr. 210, 226, 308, 333, 373.
       Later in May 2014, Mr. Bourche began to become very sick. Tr. 16. While
Mr. Bourche was hospitalized, doctors determined that he was infected with
bacteria known as staphylococcus aureus. Exhibit 9 at 295 (discharge report), 461
(lab report, dated May 26, 2014). Staphylococcus aureus “causes serious
suppurative infections and systemic disease, including impetigo bullosa,

       7
         Mr. Bourche and Ms. Bourche testified a mouth blister (or blisters) had formed within
two days of the vaccination. Exhibit 1, ¶ 10; exhibit 63, ¶ 6; Tr. 32; see also Tr. 334. Whether
the onset of a blister (or blisters) was two days or nine days does not affect the petitioner’s case
according to Dr. Zizic. Tr. 164.

                                                      9
staphylococcal pneumonia, and staphylococcal scalded skin syndrome, and has
developed resistance to nearly all classes of antibiotics.” Dorland’s at 1765.
Staphylococcus aureus is common on the skin. Tr. 90.
      Mr. Bourche’s condition during his May 2014 hospitalization is controverted
by the parties and their experts. The dispute rests on medical records that are in
some respect inconsistent and, in some respect, vague. This inconsistency and
vagueness, in turn, allow the parties and their experts to draw different inferences
from the same material.8
       Mr. Bourche arrived at the emergency department of the Boulder
Community Hospital by 3:00 in the afternoon on May 23, 2014. Exhibit 9 at 302
(noting he was seen by a provider at 15:01). He reported a one-day history of fever
and chills. In his review of symptoms, he had no rash. The physician in the
emergency room, Deborah S. Lund, conducted a physical exam and recorded that
Mr. Bourche’s skin was “warm and dry, no rash.” Id. at 303. Dr. Lund’s notes
also record that he has a hepatitis B vaccine allergy. Id.
        After laboratory studies determined that Mr. Bourche had an elevated level
of potassium, a condition known as hyperkalemia (see Dorland’s at 890), Dr. Lund
initiated the standard treatment including “IV fluids, calcium, insulin, glucose and
Kayexalate.” Dr. Lund talked to one of Dr. Mooney’s partners, Dr. Bozeman,
“who will arrange for emergent dialysis.” Dr. Lund also stated: “The etiology of
his fever is unclear. There is no evidence of sepsis at this point. There is no
evidence of pneumonia or fistula infection.” Id. at 304.
       Dr. Lund also gave Mr. Bourche vancomycin. Vancomycin is an antibiotic
for severe staphylococcal infections. Dorland’s at 2023.
       Although the records from the emergency department say “no rash,” this
notation may be erroneous as three other medical records from this hospitalization
mention skin problems. Krystie M. Karageorge, an attending doctor, seems to
have seen Mr. Bourche at the end of May 23, 2014, as her report is dictated at 0006
on May 24, 2014. Exhibit 9 at 314. When Dr. Karageorge conducted a physical
exam, she described Mr. Bourche’s skin as “warm, dry, [and] intact.” She also
wrote: “There are 2 macular areas present on the right forearm with overlying
scabs. No fluctuance is noted. No streaking redness, erythema or increased
warmth. Similar areas present over bilateral ankles.” Id. at 313. She diagnosed

       8
         Although Ms. Bourche witnessed some of these events, her testimony was not very
useful due to the lapse of time. Tr. 37-38.

                                                10
Mr. Bourche as suffering from sepsis. Her plan mentioned, among other points,
that Dr. Bozeman was continuing to follow Mr. Bourche.
        Dr. Bozeman saw Mr. Bourche on May 24, 2014 and dictated his report at
1448 on that day. The history of present illness that Dr. Bozeman obtained
indicates that: “Lately he has had problems with elevated phosphorus levels and
sores on his arms and legs. Also, he had an adverse reaction to a hepatitis B
booster vaccine 6 weeks ago where he had blisters in his mouth and nose. These
have healed but he has been picking at and noticing persistence of the sores on his
arms and legs.” Exhibit 9 at 321. Dr. Bozeman’s history also mentions that a
preliminary report of his blood cultures “have grown gram-positive cocci.” Id. Dr.
Bozeman’s physical exam of Mr. Bourche’s skin showed that Mr. Bourche “has
several papular lesions on his arms and legs, some of which are healed with keloid
like scars, some that have more open excoriations and none that appear infected.”
Id. at 322. The impression and plan from Dr. Bozeman included the following: “It
is possible he seeded his bloodstream from the sores that he has had for several
months. His fistula appears fine and is not infected. I am concerned given his
pacemaker that he could have seeded this.” Id.
       Annie Meditz, an infectious disease specialist, saw Mr. Bourche on May 24,
2014, and dictated her report at 1549. The history of present illness from Dr.
Meditz indicates that Mr. Bourche had been “feeling poorly for a 3 to 4 week
period with chronic abdominal pain, . . . [his] symptoms dramatically worsen[ed]
on the day of admission with severe fevers, chills and right rigors. He reports that
he has had a few skin lesions but otherwise has not noticed any abnormalities of
his skin.” Exhibit 9 at 315. Dr. Meditz also noted that his blood culture was
positive for gram-positive cocci. Like Dr. Bozeman, Dr. Meditz indicated that Mr.
Bourche had an allergy to his hepatitis B booster vaccine six weeks ago. Id. at 316
(noting intranasal and oral ulcerations). Dr. Meditz recorded that Mr. Bourche’s
skin showed that “He has some very small scabbed wounds, 1 on the left forehead,
1 on his ankle. No problems with his graft on his left forearm.” Id. The
assessment and plan from Dr. Meditz were that Mr. Bourche has “sepsis and is
found to have bacteremia with gram-positive cocci. Unclear source. Portal of
entry could be related to accessing his graft although his graft does not appear
infected. He also has some minor skin lesions that could be portal of entry. Other
considerations include pneumonia.” Id. Dr. Meditz also recommended that Mr.
Bourche have a “more prolonged course of IV antibiotics, i.e. 6 weeks.” Id. at 317.
Dr. Meditz prescribed vancomycin for him. See exhibit 10 at 131 (June 10, 2014),
exhibit 9 at 295 (discharge report).


                                            11
       The main dispute between the parties and their experts is whether the skin
lesions were vasculitic. Ms. Bourche contends the lesions were vasculitic (and
caused by an adverse reaction to the hepatitis B vaccine).9 The Secretary counters
that the skin problems were not vasculitic. For reasons explained in section III. C
below, this position is more persuasive.
       Regardless of whether the lesions were vasculitic, the doctors treating Mr.
Bourche attempted to determine the portal of entry for the staph bacteria. See Tr.
379 (distinguishing sources of bacteria from portal of entry). Conceivably, as Dr.
Meditz explained, the portal of entry could have been either a skin lesion or Mr.
Bourche’s fistula. Exhibit 9 at 316. Dr. Meditz and Dr. Bozeman each observed
the fistula and stated that the fistula did not appear infected. Exhibit 9 at 316, 322.
The doctor who discharged Mr. Bourche from the hospital wrote: “Ultimately, the
source was unclear . . . .” Id. at 295. The discharging doctor also directed Mr.
Bourche to continue to take vancomycin for six more weeks. Id.
        Before Mr. Bourche was discharged, his heart was tested via a transthoracic
echocardiogram. This echocardiogram did not show any evidence of endocarditis.
Exhibit 9 at 451, 295 (discharge report). The ejection fraction was 15-20 percent.
Id. at 451.
       Mr. Bourche’s last visit in May 2014 was an appointment in Dr. Meditz’s
office on May 28, 2014. Mr. Bourche returned for a follow-up on his methicillin-
susceptible Staphylococcus aureus (“MSSA”) bacteremia, the source of which was
unknown. As part of her record of Mr. Bourche’s history of present illness, Dr.
Meditz referenced her report from May 23, 2014. Mr. Bourche was following up
because his current symptoms had worsened. Worsened symptoms included
severe abdominal pain that was associated with sweats, anorexia, and loose bowel
movements. Mr. Bourche specifically denied a skin rash. He was still taking
vancomycin and was anticipated to continue taking vancomycin until July 6, 2014.
Exhibit 3 at 33.
       When Dr. Meditz conducted a physical exam on his skin and subcutaneous
tissue, she found that Mr. Bourche had “no rashes present [and] no lesions
present.” His skin was also “warm and dry to touch.” Id. Dr. Meditz’s findings,
       9
         Dr. Bozeman wrote that the bacteria could have entered Mr. Bourche’s bloodstream
“from the sores that he has had for several months.” Exhibit 9 at 322. If Dr. Bozeman’s May 24,
2014 report of “several months” meant more than 31 days, then Mr. Bourche had sores before
the April 23, 2014 vaccination. Under this sequence, the vaccination could not have caused the
sores. Tr. 342. However, the more persuasive evidence indicates that Mr. Bourche did not have
sores before the vaccination. Tr. 69, 127.

                                                 12
as presented in this May 28, 2014 report, carry significance in the analysis about
when Mr. Bourche developed vasculitis. See section III.B, below.
       Dr. Meditz diagnosed Mr. Bourche as suffering from bacteremia, among
other problems. Her plan included a continued prescription for vancomycin.
Exhibit 3 at 34.
      G.     Health in June – August 2014

        While Mr. Bourche saw many doctors in these three months, for purposes of
this litigation, the most important appointment was with Dr. Meditz on June 24,
2014. Another important doctor was Steven R. Hong, a dermatologist, who saw
Mr. Bourche at least six times.
       Before Mr. Bourche saw Dr. Hong, Mr. Bourche went to a different
dermatologist, John Fueston, on June 26, 2014. (Mr. Bourche had seen Dr.
Fueston as far back as 2012). Mr. Bourche saw Dr. Fueston because he had a rash
on his four extremities and his nose. Dr. Fueston recorded that Mr. Bourche is a
dialysis patient, who says “his skin does not heal well. He is very itchy, but does
not use moisturizes or anti-itch creams.” Exhibit 6 at 11. Mr. Bourche also
informed Dr. Fueston that he “had a bad reaction a few weeks ago to a hepatitis
booster shot resulting in facial swelling, especially his nose. The swelling has
resolved, but a circular, raised spot remains.” Id.
       After obtaining this history, Dr. Fueston conducted “a full skin exam, except
for the groin.” Id. at 12. Dr. Fueston identified, as lesion B, a 6 mm keratotic
papule on the tip of Mr. Bourche’s nose. Dr. Fueston also recorded that Mr.
Bourche “has a few brown macules and papules on the face, trunk, and 4
extremities. There are many excoriated papules with bruising on the lower
extremities and fewer on the upper extremities, shoulders, and back.” Id.
       Dr. Fueston considered Mr. Bourche as suffering from several possible skin
conditions, including prurigo nodularis because Mr. Bourche “admits to scratching
his skin.” Id. Dr. Fueston also performed a biopsy on skin from the tip of Mr.
Bourche’s nose. This biopsy revealed that Mr. Bourche had “squamous papilloma
with features of lichenification.” Id. at 14. Dr. Matloubian explained this was, in
layperson’s term, a wart. Exhibit A at 4; Tr. 331.
       The critical appointment with Dr. Meditz occurred on June 24, 2014. The
history of present illness is like Dr. Meditz’s report from May 28, 2014, noting that
Mr. Bourche suffers from MSSA bacteremia. For “antibiotic therapy,” Dr. Meditz
recorded that Mr. Bourche’s “current antibiotics include: vancomycin. The end

                                            13
date of antibiotics is anticipated to be 07/06/2014. Side effects of the therapy
include: pruritus.” Exhibit 3 at 22. Mr. Bourche’s current complaints included:
“Painful skin lesions on his LE, concerned because they are not healing and have
been there for weeks.” After Dr. Meditz examined Mr. Bourche’s skin and
subcutaneous tissue, she found “painful purpuric papules/ulceration[s] on shins
bilaterally.” Id. at 23.
       Dr. Meditz assessed Mr. Bourche as suffering from seven conditions of
which the most important was the last listed. Dr. Meditz stated that Mr. Bourche
suffered from a rash. She added: “Clinically appears vasculitic, recommended
Derm eval – patient already has dermatologist and will make appointment.” Id.
      After the follow-up appointment with Dr. Meditz on June 24, 2014, Mr.
Bourche returned to her on July 2, 2014. While Mr. Bourche’s current symptoms
had improved, he was complaining of “ongoing abdominal pain (has appointment
with GI) and rash on bilateral LE.” Id. at 16. Dr. Meditz’s inspection of Mr.
Bourche’s skin and subcutaneous tissue revealed “scattered painful ulcers ½ cm
each, primarily on shins – bilaterally.” Id. at 17; accord Tr. 293.
       The assessment from Dr. Meditz included three items. For the skin rash, Dr.
Meditz “took culture today; saw dermatology who felt it was not vasculitis. Took
[biopsy] of nose.” Exhibit 3 at 17. For the MSSA bacteremia, Dr. Meditz
recorded that: “Some of symptoms of fatigue, nausea could be related to
vancomycin, which will be [discontinued] within the week. Will discuss with Dr.
Holland repeating [transthoracic echocardiogram] in the near future to confirm
lack of vegetation in this high risk patient with pacer in place.” Id. For the
abdominal pain, Dr. Meditz recorded that Mr. Bourche has “appointment with GI.
Talked to Dr. Dolan after last visit and reviewed labs including transient increase
in [liver function tests].” Id.
       The appointment with a gastroenterologist to which Dr. Meditz referred
occurred on July 9, 2014. Dr. Robert Dolan performed an upper gastrointestinal
endoscopy and colonoscopy. Id. at 5-10. The colonoscopy revealed “[d]iffuse
mild inflammation . . . in the entire examined colon.” Id. at 10. Dr. Dolan
consulted a doctor at Johns Hopkins Medicine, who concurred with Dr. Dolan’s
finding. With reference to the inflammation, this consultant stated “some of the
acute inflammation is within small vessel walls (margination) yet with minimal to
absent fibrin and without vascular destruction. Early leukocytoclastic vasculitis,
which can be in the colon and be associated with various chronic medical disease
or allergic reaction, cannot be excluded . . . .” Id. at 12. Dr. Zizic and Dr.
Matloubian explained that margination means the white blood cells are near the

                                           14
blood vessels, but they have not broken the blood vessel wall. Thus, the
colonoscopy did not show vasculitis. Tr. 294, 346, 376.10
                                          Vasculitis
       The term “vasculitis” means inflammation in the blood vessels. Dorland’s at
2026. A leukocytoclastic vasculitis is a hypersensitivity vasculitis. A
hypersensitivity vasculitis, in turn, is “a group of systemic necrotizing vasculitides
thought to represent hypersensitivity to an antigenic stimulus, such as a drug,
infectious agent, or exogenous or endogenous protein; all disorders in this group
involve the small vessels. Types include varieties of Henoch-Schönlein purpura
and serum sickness.” Id. Dr. Zizic provided more information about
leukocytoclastic vasculitis. Tr. 150-54.
       Doctors divide vasculitis into various types. Some vasculitides affect the
skin, some affect the skin plus other organs, and some do not affect the skin at all.
Tr. 254. Dr. Matloubian explained a diagnosis of vasculitis requires a biopsy and
biopsies will inform the specific type of vasculitis. Tr. 254-55. As Mr. Bourche
later had two skin biopsies, details about those results will be discussed in that
context.
       After the biopsy from the colonoscopy, but before the findings were
reported, Mr. Bourche returned to his cardiologist’s office as Dr. Meditz had
recommended. The physician’s assistant for Dr. Holland, Hilary Clark, recorded
the following history: “Pt states he was fine until got hepatitis booster right before
hospitalization in May. He is very upset about this because had been so much
better after BiV-AICD [pacemaker] placed. Broke out in intra and peri-oral ulcers
– roof of mouth sloughed off. Then bacteremic -> hospitalized.” Exhibit 8 at 50
(July 10, 2014). The history via Ms. Clark continues: “Sent home on IV
[antibiotics], started developing leg ulcerations primarily lower extremities but one
on back. . . . Finished [antibiotics] 1 week ago.” Id.
       For more recent problems, Mr. Bourche reported: “Feels overall terribly.”
Id. His abdominal pain and shortness of breath and leg ulcers “are his main
complaint.” Id. Ms. Clark’s physical exam of Mr. Bourche’s extremities showed
“Bilat LE [with] mild edema, multiple ulcerations [with] black scab 1-2 mm to 2
cm in size, surrounding eryth[ema] and tenderness. One on upper back. No
oozing or discharge.” Id. at 52.

       10
         Dr. Zizic linked findings of inflammation on the colonoscopy to findings following the
autopsy. Tr. 188-94. But, Dr. Matloubian disagreed. Tr. 306-07.

                                                  15
        The report, which was signed by Ms. Clark and generated by Dr. Holland,
assesses Mr. Bourche with a rash and other nonspecific skin irruption. “Referral to
Derm here Dr. Hong for further eval. Was not happy [with] first Dermatology
opinion in Longmont . . . These skin lesions are his most bothersome complaint . . .
. Unsure if this is venous stasis only (doubt), inflammatory reaction of some kind
dermal layer or even vasculitis or new secondary [infection].” Id. at 53. The term
“venous stasis” probably refers to “stasis dermatitis,” which is a “chronic,
eczematous dermatitis caused by venous insufficiency in the lower limb, usually
first involving the skin medially near the ankle and sometimes spreading over the
entire lower limb; characteristics include edema, pigmentations, and often
ulceration.” Dorland’s at 496.
        The report about bothersome skin problems seems consistent with his
dialysis record. On July 14, 2014, the dialysis nurse noted: “Pt. has sores to LE
bilat[erally]. Pt going to see dermatologist tomorrow.” Exhibit 10 at 1432. This
note appears to be the first time that vasculitic skin problems were mentioned in
the dialysis records after the vaccination. A similar record from a physician at the
dialysis center comes from July 16, 2014. This record states Mr. Bourche “has
resolving vasculitic rash on LE’s, likely sequela of reaction to hep B vaccine when
he developed oral ulcers as well . . . No new lesions.” Id. at 133. Five days later,
the doctor entered a similar report: “LE rash resolving. This [and] GI findings
consistent with limited leukocytoclastic vasculitis related to Energex [hepatitis B
vaccine reaction].” Id. at 135. Another dialysis center physician on July 30, 2014,
wrote: “Looks like skin lesions are a leukocytoclastic type vasculitis, possible from
hep B vaccine. He thinks lesions are improving, albeit slowly with topical Rx.”
Id. at 136.
      The first of multiple appointments with dermatologist Steven Hong occurred
on July 15, 2014. Because Dr. Hong is a dermatologist, his evaluations of Mr.
Bourche’s skin condition are very informative.
       When Mr. Bourche presented to Dr. Hong, Dr. Hong reported the history of
present illness in two parts. For ulcers, Dr. Hong recorded: “legs and arms.
Dialysis patient. Got a hepatitis booster, blistered nose, mouth and arms.” Exhibit
8 at 47. For the biopsy of Mr. Bourche’s nose, Dr. Hong stated “benign.” Id. The
subjective narrative elaborates that Mr. Bourche had “Hepatitis booster 2 mo ago,
broke out mult mouth ulcers. Hosp. for bacteremia and received vancomycin,
stopped approximately 7/3/14. Had EGD and colonoscopy 7/9: diffuse
gastropathy, mult ulceration colon. I do not have the biopsy results.” Id. at 48.
This section continues: “Legs inflamed and swollen for about 2 weeks with the

                                            16
development of mult sores: painful. Saw a Derm in Longmont and told it was
stasis derm.” Id.11
      For objective findings, Dr. Hong recorded: “Erythematosus/pitting
edematous LE worse on R. Mult sharply marginated hemorrhagic superficial
ulcerations, punctuate to approximately 2.5 cm on LE. Few small papules
forearms.” Id. Based upon this information, Dr. Hong’s first assessment was
“Probable vasculitis, ? Drug-induced (?vancomycin). I assume this is related to the
same process in his colon.” Id.
       Dr. Hong’s plan states that Mr. Bourche “thinks he is getting new ones on
his legs so we will biopsy one. A 4 mm crusted papule r shin was excised.” Id. at
49. This right shin skin was examined in a biopsy.
       Mr. Bourche returned to Dr. Hong’s office two days later for a recheck.
Under objective, Dr. Hong recorded: “Erythema, edema lower legs much
improved, all crusted hemorrhagic ulcers superficial and healing. Path: final
pending, sent to Loren Golitz Denver for 2nd opinion. I looked at it and it showed
epidermal necrosis with assoc. inflammation but no active vasculitis.” Id. at 45
(July 17, 2014). Dr. Hong’s assessment was “Still consistent with probable drug-
induced cause. Most likely the inflammatory response is all subsiding and in the
healing phase.” Id.
       Dr. Golitz, a dermatopathologist, responded to Dr. Hong on July 18, 2014.
His report begins that the clinical impression is “drug induced vasculitis,” and
notes that Dr. Golitz’s reviewed a single glass slide containing multiple skin
sections. After reviewing his microscopic observations, Dr. Golitz’s impression
was: “Leukocytoclastic vasculitis with ulceration, skin, right shin.” Id. at 122. Dr.
Golitz’s commented “the combination of vasculitis with colon involvement raises
the possibility of Henoch-Schonlein purpura. A biopsy for direct
immunofluorescence microscopy is recommended.” Id. Dr. Zizic explained that
Dr. Golitz could diagnose vasculitis because he could see “neutrophils in the walls
of the vessel.” Tr. 172.



       11
           Dr. Hong's reference to a painful rash for two weeks is consistent with (a) an onset
after the May 27, 2014 discharge for his staph infection, and (b) an onset around the time of Mr.
Bourche's follow-up appointment with Dr. Meditz on June 24, 2014. This sequence fits a
timeline supporting vancomycin as the cause of the skin problem. However, as Ms. Bourche
argues, if Mr. Bourche arrived at the hospital with vasculitis, then the vancomycin did not cause
the vasculitis. See Pet’r’s Reply at 3.

                                                   17
      After Dr. Golitz communicated his impression of the biopsy to Dr. Hong,
Dr. Hong reported the possible HSP. Dr. Hong also continued to say that the
vasculitis was probably drug-induced. Exhibit 8 at 43 (July 29, 2014), 41 (Aug. 1,
2014), 38 (Aug. 14, 2014). During these visits, the status of Mr. Bourche’s skin
lesions changed from “resolving” and “healing” to “worse.” Because of this
decline, Dr. Hong referred Mr. Bourche to a rheumatologist and ordered a second
biopsy. Dr. Hong further responded to the decline by prescribing prednisone on
August 14, 2014. Id. at 35-38.
       These three appointments with Dr. Hong overlap with notes from two other
doctors. First, unfortunately, Mr. Bourche’s transplant status changed. Exhibit 10
at 246; see also Tr. 129. Second, Mr. Bourche returned to his gastroenterologist,
Dr. Dolan. Dr. Dolan recorded that Mr. Bourche “has new skin lesions which may
represent leukocytoclastic vasculitis. Earlier he had staph bacteremia, which in
retrospect probably was related to his cutaneous lesions. . . . Colonoscopy revealed
aphthous-type lesions throughout the entire colon but no active bleeding. Biopsies
were possibly consistent with early leukocytoclastic vasculitis.” Exhibit 5 at 5
(Aug. 5, 2014); accord Tr. 350. In Dr. Zizic’s review of this record, Dr. Zizic
emphasizes that the vasculitis was active in the sense of causing new skin lesions.
Tr. 176-77.
       The skin for Mr. Bourche’s second biopsy came from his right foot. The
dermatopathologist who interpreted this study, James E. Fitzpatrick, reported the
results on August 19, 2014. Exhibit 8 at 121. The skin tissues were subject to
direct immunofluorescence. Tr. 172. Direct immunofluorescence help specify the
type of vasculitis. Tr. 254. But, the process of interpreting the results of depends,
in part, on the subjective interpretation of the person looking at images. Tr. 174-
75, 297-98, 348.
      Here, Dr. Fitzpatrick reported the following results:
      IgG: negative                           C3:   Negative
      IgA: 1+ granular vessels                Fibrin: 3+ granular vessels
      IgM: 2+ granular vessels                C1q: Not done
Exhibit 8 at 121.
      After this second skin biopsy, Dr. Hong wrote his next report on Mr.
Bourche. In the context of an August 22, 2014 recheck of Mr. Bourche’s legs, Dr.
Hong presented the following objective observations: “hemorrhagic crusted ulcers
legs much less erythema, no new ulcerations.” Exhibit 8 at 32. Dr. Hong’s
                                           18
assessment was “hypersensitivity vasculitis, ?HSP exacerbated by drug eruption.”
Id.
       Before that visit with Dr. Hong, and while results of the second skin biopsy
were pending, Mr. Bourche saw a rheumatologist, Stuart Weisman, on August 18,
2014. Dr. Weisman’s report begins by saying that Dr. Mooney had referred Mr.
Bourche for systemic vasculitis. Although Dr. Weisman’s history of present
illness is relatively sketchy, it, nevertheless, recapitulates the important events
helpfully. “Has seen Dr. Hong recently – spontaneous ulcers. Started after
hepatitis vaccine (developed facial swelling, blisters in nose and mouth).
Vancomycin given for sepsis. Developed skin reaction from vancomycin. Much
improved. Gastroenterology – multiple ulcers – seen at colonoscopy . . . He was
given prednisone last Friday.” Exhibit 12 at 15. Under assessment/plan, Dr.
Weisman wrote: “I agree that hypersensitivity vasculitis is the most likely
diagnosis. Testing for HSP is pending (skin biopsy for IgA deposits). Has
improved somewhat with recent prednisone trial, will discuss further with
dermatology.” Id. at 19.
                     Henoch-Schönlein Purpura / IgA Vasculitis12
       Henoch-Schönlein purpura is “sometimes a type of hypersensitivity
vasculitis and sometimes of unknown cause, usually seen in children and
associated with symptoms including urticaria, erythema, arthropathy, arthritis,
gastrointestinal symptoms, and renal involvement.” Dorland’s at 1557. As Dr.
Weisman suggested, “the finding of IgA vascular deposits is the sine qua non of
HSP and adult IgA vasculitis.” Exhibit A-4 (Carlson) at 9. According to this
article, on direct immunofluorescence, HSP is an appropriate diagnosis when IgA
vascular deposits are “isolated or predominate.” Id. at 17 (table 3). However,
other sources state that IgA deposits are “dominant.” Exhibit A-6 (Audemard-
Verger) at 580. “Bacteria, virus or parasitic agents were suspected to trigger the
disease in genetically prone individuals, but causative agents and factors remain to
be identified.” Id.
       IgA vasculitis can involve different organs. Tr. 151, 266, citing exhibit A-3
(Fett) at pdf 3. When the IgA vasculitis impairs the kidneys, the results on biopsy
of the kidney resembles the biopsies found in IgA nephropathy. Tr. 151.

       12
           The term “Henoch-Schönlein purpura” is older. The current term is IgA vasculitis.
Exhibit A-6 (Audemard-Verger) at 580; see also Tr. 98. In treating Mr. Bourche, some doctors
used the term Henoch-Schönlein purpura (or its abbreviation, HSP), and other doctors said IgA
vasculitis.

                                                 19
       For Mr. Bourche, after the biopsy of his right foot, he continued to
participate in dialysis. Physicians at the dialysis center continued to make notes
about his skin condition. On August 20, 2014, a doctor wrote: “Legs / ankles
wrapped. [Illegible] [with] ulcers slow to heal.” Exhibit 10 at 140. Another
doctor, who may have been Dr. Mooney, examined Mr. Bourche’s legs on August
25, 2014. Although difficult to read, it appears that the doctor concluded that Mr.
Bourche “likely” had “Stevens Johnson [syndrome]” from reaction “[secondary to]
hepatitis vaccine.” Id.
        In the following weeks, the doctors at the dialysis center observed some
improvement. His legs had “less edema” on September 3, 2014. Id. at 141. On
September 12, 2014, a doctor wrote: “Seen by university [transplant team] on hold
until vasculitis resolves. Remains on pred & wounds / ulcers are slowly healing.”
Id. at 142; exhibit 78 at 70 (duplicate). A doctor, whose handwriting appears to be
from Dr. Mooney, wrote on September 22, 2014: “No new skin lesions. Will track
down skin [biopsy] results. Would favor tapering of prednisone and avoid further
immunization reactions.” Exhibit 10 at 143.13
       Also, by August 2014, Mr. Bourche had consulted attorneys about his claim
in the Vaccine Program. See Pet’r’s Mot. Interim Fees, filed Jan. 31, 2017, exhibit
A (timesheets) at 1.
       H.     Cardiac Problems – October and November 201414

      In October and November 2014, Mr. Bourche suffered significant heart
trouble. However, the first medical record in this time came from Dr. Hong on
October 6, 2014. The subjective portion begins that Mr. Bourche was following up
for IgA vasculitis. Under the objective portion, Dr. Hong memorializes that Mr.
Bourche had “mult eschars lower legs, inflammation is mild. Few ulcerations to
deep dermis/subcu.” Dr. Hong’s relevant assessment was “hypersens vasculitis,
improved.” Exhibit 12 at 45.
      During dialysis on October 24, 2014, Mr. Bourche had a rapid heart rate and
was sent to the hospital. Tr. 21. A transesophageal echocardiogram detected
vegetation on one of his heart valves (a mitral valve), a condition called

       13
        As mentioned earlier, Dr. Fitzpatrick reported the skin biopsy results on August 19,
2014. Testing showed, in part, IgG; negative; IgA: 1+; and IgM 2+. Exhibit 8 at 121.
       14
          Because Mr. Bourche’s history after his August 19, 2014 biopsy contributes less to the
outcome of this case, these events are described more cursorily. Nevertheless, the underlying
records have been reviewed.

                                                  20
endocarditis. Exhibit 9 at 728-29, 731; Dorland’s at 616-17. The ejection fraction
had declined to 15-20 percent from the previous measurement in August 2014,
which was 30 percent. Exhibit 9 at 811-12; exhibit 8 at 153.
       Mr. Bourche remained in the hospital until he could have an operation to
repair his mitral valve. During this interim two records are significant. First, Dr.
Mooney saw him in the hospital. Dr. Mooney, who was consulted due to his
experience in treating Mr. Bourche’s end stage renal disease, reported Mr.
Bourche’s history. With respect to the vaccination, Dr. Mooney provided that Mr.
Bourche “had been admitted to Boulder Community Hospital in May. He had
hyperkalemia and chest pain. He had reported onset of mouth ulcerations along
with upper and lower extremity skin lesions that had started in April. Initially it
was felt that the trigger was hepatitis vaccine. During this time, he may have also
had a reaction to vancomycin.” Exhibit 9 at 738. Dr. Mooney also provided his
understanding of Mr. Bourche’s skin condition. Dr. Mooney stated that Mr.
Bourche’s “lesions continued in spite of the mouth ulcerations healing. . . . He was
seen by Dr. Hong for evaluation of his dermatologic condition. Skin biopsy
revealed a leukocytoclastic vasculitis. In August, he was seen and evaluated by
Dr. Weisman. He has been on high-dose prednisone therapy during this time. It is
not clear whether the patient has been having new skin lesions or not.” Id. at 739.
For allergies, Dr. Mooney listed vancomycin, but did not list the hepatitis B
vaccine. Id.
       Dr. Mooney’s assessment begins with a plan for dialysis. Dr. Mooney then
discusses Mr. Bourche’s other health problems. “He has leukocytoclastic
vasculitis on skin biopsy. It is not clear exactly what the trigger was, but originally
it was felt to be due to his hepatitis B vaccine. He previously received that without
a problem. This is not a finding that I would typically see with IgA nephropathy.
He has been on steroid therapy with slow to heal skin ulcerations. . . . It is
interesting to note that it is hard to tell whether his vasculitis is still active or not in
spite of the slow healing that is going on in his lower extremities.” Id. at 740;
accord Tr. 351.
      The second relevant medical record from the October 2014 hospitalization
was created by Myles S. Gruber on October 28, 2014. Dr. Matloubian identified
Dr. Gruber as the cardiac surgeon. Tr. 353. Dr. Gruber stated that Mr. Bourche
has “numerous vasculitic type ulcers that are chronically infected in both legs.”
Exhibit 9 at 737.




                                                21
       Also, during this hospitalization, Ms. Bourche took pictures of Mr. Bourche
in his hospital bed. One picture shows lesions on his legs, wrapped in plastic.
Exhibit 66; Tr. 24, 43.
       Mr. Bourche underwent mitral valve surgery on November 5, 2014. Exhibit
9 at 741. After this operation, he functioned much better. Tr. 24, 42, 417, 495.
       Following his November 13, 2014 discharge for the mitral valve repair (see
exhibit 9 at 741), Mr. Bourche had an episode of atrial fibrillation for which he was
treated at a hospital. See exhibit 9 at 918-23. During this hospitalization, Richard
K. Halterman consulted on Mr. Bourche’s case. Dr. Halterman recorded that Mr.
Bourche “did have Staph bacteremia. He was placed on vancomycin. Shortly after
that time, he developed a leukocytoclastic vasculitis, with severe skin lesions over
his lower extremities.” Id. at 928.
       I.      Health in 2015 – 2016

       Mr. Bourche’s heart was checked again on January 5, 2015, by a
transthoracic echocardiogram. Exhibit 76 at 230; see also exhibit 76 at 180 (Dr.
Holland’s report of this test). The ejection fraction was 31 percent. Id.
       On January 12, 2015, Mr. Bourche saw Dr. Weisman, the rheumatologist
whom he had seen in August 2014. Dr. Weisman started his history of present
illness by mentioning that Mr. Bourche had a mitral valve repair and feels better in
general. Dr. Weisman stated: “His skin ulcers have improved with routine wound
care, but lesions persist. No new ulcers have developed. Few small erythematous
areas have developed on the arms, legs.” Exhibit 12 at 60. Dr. Zizic interpreted
this report as showing the development of new lesions. Tr. 219. But, Dr.
Matloubian stated this record showed that Mr. Bourche was not developing new
lesions. Tr. 303.
       Another check of Mr. Bourche’s heart happened on March 22, 2015. His
ejection fraction was 23 percent. Exhibit 76 at 225.
      In spring 2015, Mr. Bourche explored whether other hospitals would place
him on a transplant list. Accordingly, he traveled to Cedars-Sinai Medical Center
in Los Angeles California to be examined by doctors there.15

       15
           Although a record from Mr. Bourche’s cardiologist, Dr. Holland, references Cedars-
Sinai (exhibit 13-2 at 286 [pdf 135]), Ms. Bourche did not file records from Cedars-Sinai until
after the hearing. Therefore, the experts did not comment upon records from Cedars-Sinai in
their testimony.

                                                   22
       Consistent with medical records from other providers, the medical records
from Cedars-Sinai are ambiguous about some aspects of Mr. Bourche’s health. A
cardiothoracic surgeon, Fardad Esmailian, evaluated Mr. Bourche on March 21,
2015. Dr. Esmailian’s history noted that Mr. Bourche suffered from vasculitis and
had allergies to hepatitis B vaccine and vancomycin. Exhibit 72 at 10-11. The
physical exam of Mr. Bourche’s skin showed that Mr. Bourche “has an open
wound in the right leg which is still healing from August of 2014 secondary to his
vasculitis.” Id. at 11.
        Due to Mr. Bourche’s history of anemia, a hematologist / oncologist (Kevin
S. Scher) evaluated him on March 25, 2015. Dr. Scher noted that he did not have
complete records available to him, but obtained a history from Mr. Bourche. Mr.
Bourche recounted: “In April of 2014, he had a hepatitis B vaccine, and after the
vaccine suffered with facial swelling, skin breakdown and was diagnosed with a
vasculitis. He then developed a staph infection which presumably led to his
endocarditis in November.” Id. at 69. In accord with this history, Dr. Scher listed
“IgA vasculitis” as one of the conditions afflicting Mr. Bourche. Id. Dr. Scher
listed the hepatitis B vaccine and vancomycin as allergies. Id. at 70. The physical
examination of Mr. Bourche’s extremities showed “[m]ultiple lower extremity skin
ulcerations, 1+ edema bilaterally.” Id.
       An infectious disease doctor, Phillip Zakowski, saw Mr. Bourche on March
26, 2015. Mr. Bourche told Dr. Zakowski about his experience with the hepatitis
B vaccine. “The patient has a history of receiving hepatitis B vaccine on April 24,
2014 [sic, actually April 23, 2014]. The patient states his face blew up that night,
and he developed subsequent skin lesions. He attributes all this to a reaction to the
hepatitis B vaccine.” Exhibit 72 at 139. Mr. Bourche also spoke to Dr. Zakowski
about his skin problems. Mr. Bourche said that he “subsequently had a biopsy of
the skin lesion by a dermatologist in Boulder, Dr. Hong. This was diagnosed as
vasculitis. He has subsequently been on prednisone.” Id. The report from Dr.
Zakowski continues to discuss Mr. Bourche’s skin problem. “The patient
developed multiple skin lesions on his lower extremity. He apparently had
bacteremia from this. I spoke with his Infectious Disease physician listed below
[Dr. Meditz]. She states that he had MSSA [methicillin-susceptible
Staphylococcus aureus] bacteremia 05/23, not MRSA [methicillin-resistant
Staphylococcus aureus]. … Because of a [penicillin] allergy he got 6 weeks of IV
antibiotics of vancomycin . . . After this, he felt the skin lesions were worse, and
that he was concerned that the vancomycin may have triggered a further
inflammatory reaction in his lower extremities.” Id. Dr. Zakowski added: “He
was felt to have an IgA vasculitis of his skin.” Id. at 140.

                                            23
       For the physical examination, Dr. Zakowski was relatively detailed about
Mr. Bourche’s skin. Dr. Zakowski stated that his examination revealed: “healed
old skin lesions, bilateral lower extremity, with the right anterior tibial area, non
healed ulcer approximately 1.5 x 1.5 cm with a clean granulating base, and a right
dorsum forefoot lesion approximately 1 x 1 without active purulence; skin
appearance on bilateral lower extremities suggestive of bilateral vascular changes
or vasculitis.” Id. at 141. In Dr. Zakowski’s discussion, he stated: “A concern of
mine would be the lower extremity lesions, whether he has ongoing vasculitis, and
his lack of ability to heal, particularly the right anterior tibial one. I will discuss
this further with the team.” Id.
        A nephrologist evaluated Mr. Bourche for a possible kidney transplant on
March 25, 2015. Dr. Alice Peng obtained a history that began with Mr. Bourche’s
IgA nephropathy in 2006. As relevant for this litigation, Mr. Bourche told Dr.
Peng that in 2014, he developed vasculitis after a hepatitis B booster. “He
developed skin lesions involving all 4 extremities. He then developed a
superimposed MRSA infection which was complicated by MRSA endocarditis.”
Id. at 96. Dr. Peng listed the hepatitis B vaccine has an allergy that caused
vasculitis. She did not list vancomycin as an allergy.
       As part of her physical examination, Dr. Peng reviewed Mr. Bourche’s skin
and found that it was “[w]arm to touch with multiple healing shallow ulcers
involving the distal extremities.” Id. at 99. Based upon all the information
available to her, Dr. Peng came to the following recommendation: “Overall the
patient does appear to be an appropriate candidate for dual heart and kidney
transplant if cleared by the heart transplant team. He would certainly not be a
candidate for kidney transplant alone. We will make a final determination of
candidacy in recipient selection committee.” Id. at 100.
      Ultimately, according to notes made by Dr. Holland from a conversation
with a Cedars-Sinai doctor, the transplant committee determined that Mr. Bourche
was “too high a risk candidate for combined orthotopic heart transplant and current
commitment renal transplant. Biggest factors included some degree of fixed
pulmonary hypertension, unhealing lower extremity wounds, previous infections,
unknown liver status.” Exhibit 13-2 at 285 [pdf 135] (Apr. 3, 2015).
       By October 2015, Mr. Bourche’s heart function had declined so much that
hospice was contemplated. Exhibit 43 at 7; see also exhibit 13-2 at 286 [pdf 136];
Tr. 52.
      In January 2016, Mr. Bourche was in heart failure. Tr. 189, 358. He died on
January 16, 2016, and an autopsy was performed the next day. Exhibit 47 at 19.
                                          24
The death certificate states severe chronic heart failure caused cardiogenic shock,
which led to mesenteric ischemia / necrosis. Exhibit 45; see also Tr. 446 (Dr.
Stark’s opinion about the death certificate). Following Mr. Bourche’s death, Ms.
Bourche became the representative of his estate and, in that capacity, became the
petitioner. She has continued the litigation, claiming that the hepatitis B vaccine
substantially contributed to the development of vasculitic skin lesions that
substantially contributed to Mr. Bourche’s death.
II.   Standards for Adjudication

      A petitioner is required to establish her case by a preponderance of the
evidence. 42 U.S.C. § 300aa–13(1)(a). The preponderance of the evidence
standard requires a “trier of fact to believe that the existence of a fact is more
probable than its nonexistence before [he] may find in favor of the party who has
the burden to persuade the judge of the fact's existence.” Moberly v. Sec'y of
Health & Human Servs., 592 F.3d 1315, 1322 n.2 (Fed. Cir. 2010) (citations
omitted). Proof of medical certainty is not required. Bunting v. Sec'y of Health &
Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991).
       Distinguishing between “preponderant evidence” and “medical certainty” is
important because a special master should not impose an evidentiary burden that is
too high. Andreu v. Sec'y of Health & Human Servs., 569 F.3d 1367, 1379-80
(Fed. Cir. 2009) (reversing special master's decision that petitioners were not
entitled to compensation); see also Lampe v. Sec'y of Health & Human Servs., 219
F.3d 1357 (Fed. Cir. 2000); Hodges v. Sec'y of Health & Human Servs., 9 F.3d
958, 961 (Fed. Cir. 1993) (disagreeing with dissenting judge's contention that the
special master confused preponderance of the evidence with medical certainty).
      Petitioners bear a burden “to show by preponderant evidence that the
vaccination brought about [the vaccinee’s] 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 a proximate temporal relationship between vaccination and injury.”
Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005).
       In weighing evidence, special masters are expected to consider the views of
treating doctors. Cappizano v. Sec’y of Health & Human Servs., 440 F.3d 1317,
1326 (Fed. Cir. 2006). The views of treating doctors about the appropriate
diagnosis are often persuasive because the doctors have direct experience with the
patient whom they are diagnosing. See McCulloch v. Sec’y of Health & Human
Servs., No. 09-293V, 2015 WL 3640610, at *20 (Fed. Cl. Spec. Mstr. May 22,
2015). However, the views of a treating doctor are not absolute, Snyder v. Sec’y
                                            25
of Health & Human Servs., 88 Fed. Cl. 706, 745 n.67 (2009), even on the question
of diagnosis, R.V. v. Sec’y of Health & Human Servs., 127 Fed. Cl. 136, 141
(2016), appeal dismissed, No. 16-2400 (Fed. Cir. Oct. 26. 2016).
       The views of treating physicians should also be weighed against other,
contrary evidence present in the record—including conflicting opinions among
such individuals. Hibbard v. Sec’y of Health & Human Servs., 100 Fed. Cl. 742,
749 (2011) (finding that it is not arbitrary or capricious for special masters to
weigh competing treating physicians’ conclusions against each other), aff’d, 698
F.3d 1355 (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, 356-57 (2011), aff’d without op., 475 Fed. App’x
765 (Fed. Cir. 2012).
        This principle comes into play in Mr. Bourche’s case because treating
doctors reached opposite conclusions about Mr. Bourche. For example, as
previously described in section I. A, in October 2009, Dr. Walker, the reviewing
pathologist, stated that Mr. B was having a recurrence of his IgA nephropathy.
Exhibit 9 at 628. Yet, Dr. Mooney testified that Mr. Bourche did not. Tr. 84. In
this situation, deferring to all treating doctors is impossible. Thus, as explained
below, the analysis sometimes credits and sometimes rejects statements of treating
doctors, but only after considering all the evidence.
III.   Analysis

       Ms. Bourche has not established her case for four reasons. First, testing in
connection with the vasculitis demonstrated that Mr. Bourche did not respond in a
way that Dr. Zizic’s theory had predicted. Second, although Dr. Zizic had asserted
that Mr. Bourche developed vasculitis in early May 2014, relatively close in time
to the April 23, 2014 hepatitis B vaccination, a careful analysis of the evidence
shows that the vasculitis became manifest near the end of June or beginning of July
2014. These two reasons are the primary reasons for finding that Ms. Bourche is
not entitled to compensation and they are independent of each other. The third
reason weighs less heavily and depends upon the finding that the vasculitis began
near the end of June. This sequence of events makes Mr. Bourche’s course more
consistent, although not perfectly consistent, with a finding that his vasculitis was a
consequence of his staph infection or the vancomycin given for the staph infection.
Finally, Ms. Bourche has not established that the endocarditis, regardless of the
cause of the endocarditis, hastened Mr. Bourche’s death. These reasons are
explained in detail below.


                                             26
      A.     Mr. Bourche did not respond to the vaccination in a way
             petitioner’s theory or theories predicted

       Petitioners should establish, by preponderant evidence, that the vaccinee
responded to the allegedly causal vaccines in the way consistent with the theory
articulated by their experts. See Hibbard v. Sec'y of Health & Human Servs., 698
F.3d 1355, 1364 (Fed. Cir. 2012); Dodd v. Sec'y of Health & Human Servs., 114
Fed. Cl. 43, 52-57 (2013); La Londe v. Sec'y of Health & Human Servs., 110 Fed.
Cl. 184, 205 (2013), aff’d, 746 F.3d 1334 (Fed. Cir. 2014).
      Dr. Zizic’s theory for how hepatitis B vaccine can lead to vasculitis changed
during the litigation. Dr. Zizic’s first report presented the theory that the hepatitis
B vaccine, which contains hepatitis B surface antigens, combines with antibodies
against those antigens to form immune complexes. The antigen-antibody immune
complex lodges in the blood vessels, clogging them, and leading to vasculitis.
Exhibit 15 at 21. This theory can hold persuasive value. See Fields v. Sec’y of
Health & Human Servs., No. 02-311V, 2008 WL 2222141, at *9-10 (Fed. Cl.
Spec. Mstr. May 14, 2008) (finding the hepatitis B vaccine can cause a different
type of vasculitis through immune complexes). This decision will refer to the
theory involving the vaccine-derived hepatitis B surface antigen and hepatitis B
antibody immune complex as the “primary” immune complex theory.
        Dr. Zizic’s second report clarifies his theory, again referencing immune
complexes. He wrote: “With the right amount of antigen and antibody, they form
complexes that are soluble and circulate in the blood and get deposited in the very
small arteries and capillaries that comprise the vascular beds. This is what is seen
in vasculitis or l[eu]kocytoclastic vasculitis.” Exhibit 44 at 1. Neither Dr. Zizic’s
first report nor his second report mention the term “molecular mimicry.”
      Dr. Zizic’s third report does use the term “molecular mimicry,” but in a
strange context. Dr. Zizic uses molecular mimicry to explain how a different
vaccine (the flu vaccine) can cause a different disease (rheumatoid arthritis).
Exhibit 48 (report dated June 9, 2016) at 5. This passage appears to be copied and
pasted from a report intended for a different case. Despite the apparent poor fit in
Mr. Bourche’s case, Dr. Zizic later included molecular mimicry as one causal
theory. He stated: “In summary, the vaccine triggered activation of B and/or T
lymphocytes through molecular mimicry, cross-priming, immune complex
formation or a combination of these, which because of [Mr. Bourche’s] genetic
susceptibility, resulted in autoimmunity and the development of vasculitis.” Id. at
9.


                                             27
       In the final report before the hearing, Dr. Zizic quoted his third report to
explain his theory. He stated: “‘Subsequent to the breaking of immunologic
tolerance, self-antigens replace the initial inciting foreign antigen (E. G. infectious
agent or vaccine) and autoimmune disease develops. Although the infectious agent
may be cleared, or a vaccine eventually degraded, since the self-antigens are
present all the time, the disease is perpetuated for prolonged periods, and
sometimes for life.’” Exhibit 53 at 2, quoting exhibit 48 at 5. Dr. Zizic’s fourth
report did not use the term “mimicry.”
       During the hearing, when Dr. Zizic explained his theory, he returned to the
primary theory of immune complex formation. See Tr. 153-57. In this context,
Dr. Zizic discussed how an infection with hepatitis B virus can lead to problems
outside of the kidneys. Dr. Zizic testified: “the hepatitis B virus with its antibody
that forms these complexes . . . that end up causing an inflammatory process.” Tr.
156. Dr. Zizic further maintained that if the hepatitis B virus could provoke a
reaction, then the hepatitis B vaccine could do the same. Notably, during Dr.
Zizic’s direct testimony he did not discuss “molecular mimicry” at all. See Tr.
221.
       Despite the lack of direct testimony, the undersigned asked Dr. Zizic about
molecular mimicry. Dr. Zizic clarified that molecular mimicry was not between
the hepatitis B surface antigen and the walls of the blood vessels, which is a more
typical autoimmune reaction. “It can be any antigen in any cell that has the same
amino acid sequence, and once the antibody to that antigen combine and circulate
in the blood, they get deposited in the vessels.” Tr. 222. Thus, molecular mimicry
involving an unidentified cell is a step to producing the immune complexes that
lead to vasculitis. This decision will use the term “secondary immune complex
theory” to refer to the process in which molecular mimicry precedes the
development of immune complexes.
       When Dr. Matloubian addressed the primary immune complex theory, he
demonstrated that this theory could not explain what happened with Mr. Bourche.
The critical fact was that Mr. Bourche’s immunity to the hepatitis B virus was
retested approximately two weeks after vaccination.16 This test showed that Mr.
Bourche produced, as expected, antibodies to the hepatitis B surface antigen.
However, the hepatitis B surface antigen, which came from the vaccine, was no
longer present. Exhibit 10 at 239 (May 7, 2014).



      16
           This retesting does not typically happen.

                                                       28
       In both reports and testimony, Dr. Matloubian persuasively explained that
without the continued presence of the hepatitis B surface antigen, Mr. Bourche
could not continue to produce the immune complexes that clog the blood vessels.
Exhibit A at 13-14; Tr. 307-10. Dr. Matloubian’s insight appears to have forced
the presentation of the secondary immune complex theory in Dr. Zizic’s later
reports.17
      The secondary immune complex theory fares no better. First, under Althen
prong one, a petitioner bears the burden of presenting a persuasive medical theory.
Boatmon v. Sec'y of Health & Human Servs., 941 F.3d 1351, 1359 (Fed. Cir.
2019) (citing Moberly, 592 F.3d at 1322). The theory that the hepatitis B surface
antigen contained in the hepatitis B vaccine resemble some unidentified and
unspecified portion of the body and this similarity sparks a cross-reaction was not
adequately developed. It is far from persuasive. Caves v. Sec’y of Health &
Human Servs., 100 Fed. Cl. 119, 135 (noting that the special master “properly”
looked for evidence supporting molecular mimicry in the context of the vaccine
and the injury), aff'd without op., 463 Fed. App’x 932 (Fed. Cir. 2012).
       Second, even if the secondary immune complex theory worked on its face,
the theory leads to the production of immune complexes. Immune complexes, in
turn, contain IgG antibodies. Tr. 310-11. But see Tr. 399-401 (Dr. Zizic pointing
out that IgG is not present in some situations). Dr. Zizic stated that “[i]n the
normal leukocytoclastic vasculitis, they’re generally IgG antibodies against the
antigen. . . .” Tr. 152. However, when Mr. Bourche’s skin biopsy from his right
foot was subject to direct immunofluorescence, the vasculitic tissues did not
contain IgG. Exhibit 8 at 121. Dr. Matloubian was persuasive when he explained:
“So if this [vasculitis in Mr. Bourche] was due to antibodies against the hepatitis B
surface antigen forming immune complexes through molecular mimicry or
whatever mechanism, I would have expected to have IgG in the skin biopsy, and
there is none.” Tr. 297-98.



       17
           Ms. Bourche argues that “Dr. Zizic’s theory is that the Hepatitis B vaccination can
induce an autoimmune reaction through the mechanism of molecular mimicry. Unfortunately, at
trial, both Dr. Matloubian and Respondent’s Counsel devoted much time to a fundamental
misunderstanding of Dr. Zizic’s theory.” Pet’r’s Posth’g Br. at 25. To the extent that anyone
misunderstood Dr. Zizic’s theory, some of the responsibility for the lack of clarify must fall to
Dr. Zizic and Ms. Bourche’s attorneys. It seems telling that of the two cites to the transcript that
Ms. Bourche’s brief identifies as places where Dr. Zizic explained his theory, one comes at page
395, the very end of a two-day hearing.

                                                    29
        The lack of IgG in Mr. Bourche’s skin biopsy undermines the theory that an
adverse reaction to the hepatitis B vaccine caused his vasculitis. This reason, by
itself, is sufficient to find that Ms. Bourche has not established, by preponderant
evidence, that she is entitled to compensation. However, additional reasons
support the denial of compensation.
      B.    Mr. Bourche’s Vasculitis Did Not Arise in May 2014 as Dr. Zizic
            Assumed

       The timing prong of Althen actually contains two parts. A petitioner must
show the “timeframe for which it is medically acceptable to infer causation” and
the onset of the disease occurred in this period. Shapiro v. Secʼy of Health &
Human Servs., 101 Fed. Cl. 532, 542-43 (2011), recons. denied after remand on
other grounds, 105 Fed. Cl. 353 (2012), aff’d without op., 503 F. App’x 952 (Fed.
Cir. 2013).
       As to the “medically acceptable” timeframe, the parties seem to have
relatively little dispute. Dr. Zizic explained that the formation of immune
complexes may take 7 to 14 days. Exhibit 44 at 2. Dr. Matloubian appeared not to
challenge this estimate.
       Rather, the parties dispute the status of Mr. Bourche’s skin generally, and
more particularly when he first manifested signs of his vasculitis. According to
Ms. Bourche, Mr. Bourche was displaying vasculitis before he entered the hospital
for the staph infection on May 23, 2014. Tr. 163-65; Pet’r’s Posth’g Br. at 43-44.
In contrast, the Secretary maintains that Mr. Bourche did not develop vasculitis
until approximately one month later.
       Resolution of this issue requires a detailed examination of Mr. Bourche’s
skin at different times. The evidence, as reviewed below, preponderates in favor of
a finding that the vasculitis began near the end of June or beginning of July 2014.
            1.     Before and During the May 2014 Hospitalization

      When Mr. Bourche arrived at the hospital on May 23, 2014, he had some
lesions on his skin. Records from three doctors support this finding.
       Dr. Karageorge stated that “[t]here are 2 macular areas present on the right
forearm with overlying scabs. No fluctuance is noted. No streaking redness,
erythema or increased warmth. Similar areas present over bilateral ankles.”
Exhibit 9 at 313. The term “macular” means the color has changed. Dorland’s at
1094. The lack of “fluctuance” suggests that the skin lesion did not contain any
liquid content. See Dorland’s at 719. Dr. Matloubian interpreted Dr. Karageorge’s
                                             30
report as suggesting that Mr. Bourche was not suffering inflammation or infection.
Tr. 283-84.
        Dr. Bozeman reported that Mr. Bourche “has several papular lesions on his
arms and legs, some of which are healed with keloid like scars, some that have
some more open excoriations and none that appear infected.” Exhibit 9 at 322.
The term “papular” refers to small circumcised superficial solid elevations of the
skin. Dorland’s at 1373. In contrast to macular, a papular lesion is raised. Exhibit
J at 9; Tr. 284. The term “keloid” is a “sharply elevated, irregularly shaped,
progressively enlarging scar due to formation of excessive amounts of collagen and
in the dermis during connective tissue repair.” Dorland’s at 978.18 The term
“excoriations” refers to scratches. Dorland’s at 657.
      The presence of excoriations or scratches on Mr. Bourche’s arms and legs is
not surprising as the dialysis process often causes dry and itchy skin. In other
medical records, Mr. Bourche stated that he scratched his skin. See exhibit 6 at 11
(Dr. Fueston on June 26, 2014, stating Mr. Bourche “is very itchy, but does not use
moisturizers or anti-itch creams”).
        The third doctor who described skin problems during Mr. Bourche’s May
2014 hospitalization was Dr. Meditz. She wrote that Mr. Bourche “reports that he
has had a few skin lesions but otherwise has not noticed any abnormalities of his
skin . . . .” Exhibit 9 at 315. Her description of Mr. Bourche skin was: “he has
some very small scabbed wounds. 1 on the left forehead, 1 on his ankle.” Id. at
316.
       These three reports stand in conflict with the report from the emergency
room doctor, Dr. Lund. She stated that Mr. Bourche skin had “no rash.” Id. at
303. Dr. Lund’s report carries less weight. Dr. Lund created her report in an
emergent setting, in which careful reporting of Mr. Bourche’s skin condition may
not have been at a premium, considering that Mr. Bourche had come to the hospital
for fever and chills. Id. at 302. Although not specified in Dr. Lund’s report, she
may have been looking for new skin problems, different from the skin problem to
which Mr. Bourche had become accustomed as a dialysis patient. In addition, the
findings of three different doctors corroborate each other and carry, collectively,



       18
          Dr. Bozeman’s description of Mr. Bourche’s rash as "keloid" appears to be the only
instance in which the rash was described as keloid.


                                                  31
persuasive value. Also, Dr. Meditz’s training as an infectious disease specialist
makes her more attuned to skin problems.
       Thus, the evidence supports a finding that Mr. Bourche entered the hospital
with some skin problems, but these skin problems appear to be typical for a
dialysis patient.19
               2.     Skin Condition on May 28, 2014

       Mr. Bourche was discharged from the hospital on May 27, 2014. In the
relatively short discharge report, the discharging doctor did not mention any
problems with Mr. Bourche’s skin. Exhibit 9 at 295-96.
      The next day, Mr. Bourche had a follow-up appointment with Dr. Meditz.
When she reviewed Mr. Bourche’s symptoms, he specifically denied any skin rash.
Similarly, when Dr. Meditz examined Mr. Bourche, she found “no rashes present
[and] no lesions present.” Exhibit 3 at 34.
       The contrast between Dr. Meditz’s May 23, 2014 report to which she
referred in her May 28, 2014 report and Dr. Meditz’s May 28, 2014 report strongly
suggest that Mr. Bourche was not having skin trouble at the end of May 2014. On
May 23, 2014, Dr. Meditz recognized and described “some very small scabbed
wounds.” Exhibit 9 at 316. This documentation demonstrates that Dr. Meditz was
attentive to the skin condition of her patient. Thus, it would seem that if Mr.
Bourche presented to her with similar skin problems on May 28, 2014, she would
have followed this practice and noted them in her report. Instead, she made an
affirmative notation that Mr. Bourche had “no rashes.” Exhibit 3 at 34.




       19
           The mouth blisters (or ulcers) which formed within nine days of the vaccination lasted
for a relatively short amount of time. Although Dr. Mooney documented a blister on May 2,
2014, exhibit 10 at 127, there appear to be no other references to a mouth lesion. For example,
the doctors who examined Mr. Bourche during his hospitalization for the staph infection did not
document any mouth lesions. By June 26, 2014, Dr. Fueston reported that the facial swelling
that Mr. Bourche associated with the hepatitis B vaccination had resolved. Exhibit 6 at 11; see
also Tr. 282 (Dr. Matloubian acknowledging that the mouth lesion healed on its own).
        Dr. Mooney explained that a typical reaction to a medication might be 5-10 days. Dr.
Mooney further opined that Mr. Bourche’s reaction lasted longer than 10 days because it led to
vasculitis. Tr. 119-20. However, for the reasons explained in the text, the hepatitis B
vaccination did not cause Mr. Bourche’s vasculitis.

                                                   32
              3.      June – August 2014

       Mr. Bourche again saw Dr. Meditz on June 24, 2014. Mr. Bourche
complained to her that he was suffering “[p]ainful skin lesions on his LE.” Exhibit
3 at 22. He was “concerned because they are not healing and have been there for
weeks.” Id. After examining Mr. Bourche’s skin, Dr. Meditz reported “painful
purpuric papules/ulcerations on shins bilaterally.” Id. at 23. The term “purpuric”
refers to “1. any of a group of conditions characterized by … small hemorrhages
in the skin . . . 2. any of several conditions similar to the traditional purpuric
group, which may be caused by . . . reactions to drugs.” Dorland’s at 1557. In Dr.
Meditz’s assessment of Mr. Bourche’s rash, she stated that it “[c]linically appears
vasculitic.” Exhibit 3 at 23.
        Dr. Meditz’s description of skin ulcerations as “purpuric” appears to be the
first time that a doctor used that adjective. Similarly, Dr. Meditz’s tentative
diagnosis of vasculitis appears to be the first time a doctor proposed that illness.
This fact is a strong reason for finding that the vasculitis started after May 28,
2014, and before June 24, 2014.20
       Other medical records also support a finding that Mr. Bourche’s skin
condition worsened in July 2014. For example, in his July 10, 2014 appointment at
his cardiologist’s office, Mr. Bourche told the physician’s assistant, Hilary Clark,
that his leg ulcers are one of “his main complaint[s].” Exhibit 8 at 50. Based upon
Mr. Bourche’s complaint, his unhappiness with his previous dermatologist, and the
findings on physical examination, Ms. Clark and Dr. Holland referred Mr. Bourche
to a new dermatologist, Dr. Hong. Id. at 53.
       The dialysis records also point to an onset of new skin problems in July
2014. The dialysis nurse noted that Mr. Bourche “has sores to LE bilat.” Exhibit
10 at 1432. Given that the nursing notes contain complaints about other problems,
it seems likely that the first time Mr. Bourche was complaining about significant
skin problems during dialysis was on July 14, 2014.21 Within a few days, doctors

       20
         Because Dr. Meditz saw Mr. Bourche multiple times during this critical period, the
undersigned directed the parties to seek further information from her. Order, issued April 25,
2018. Unfortunately, however, Dr. Meditz was unable to supply more information about Mr.
Bourche. Exhibit 77 (letter from Dr. Meditz’s employer representing that she did not have any
independent recollection of Mr. Bourche).
       21
         For examples of complaints recorded in the nursing notes around this time, see exhibit
10 at 1382 (May 16 – abdominal pain), 1386 (May 21 – shortness of breath on exertion), 1392
(May 28 – abdominal pain, fatigue), 1402 (June 11 – shortness of breath, generalized pain), 1410

                                                  33
at the dialysis center were also noting the skin problems. See exhibit 10 at 133
(July 16, 2014: “resolving vasculitic rash on LE’s, likely sequela of reaction to hep
B vaccine”), 135 (July 21, 2014: “LE rash resolving . . . consistent with limited
leukocytoclastic vasculitis related to” reaction to hepatitis B vaccination).
       The non-contemporaneous histories also report that Mr. Bourche developed
significant skin problems or vasculitis after he started taking vancomycin. On
August 18, 2014, Dr. Weisman recorded: “Vancomycin given for sepsis.
Developed skin reaction from vancomycin.” Exhibit 12 at 15. On November 13,
2014, Dr. Halterman wrote that Mr. Bourche “was placed on vancomycin. Shortly
after that time, he developed a leukocytoclastic vasculitis, with severe skin lesions
over his lower extremities.” Exhibit 9 at 928. On March 26, 2015, Dr. Zakowski
recorded that after taking vancomycin for six weeks, Mr. Bourche “felt the skin
lesions were worse, and that he was concerned that the vancomycin may have
triggered a further inflammatory reaction in his lower extremities.” Exhibit 72 at
139.
       The microscopic examinations are also consistent with a finding that the
vasculitis developed in either June or early July 2014. Dr. Dolan’s colonoscopy
from July 9, 2014 did not detect vasculitis because the white blood cells were only
at the outside (margin) of the walls of the blood vessels. Exhibit 3 at 12. But, the
July 18, 2014 skin biopsy suggested that Mr. Bourche was suffering from “drug
induced vasculitis.” Exhibit 8 at 122. The August 19, 2014 biopsy, which was
subject to direct immunofluorescence, confirmed the vasculitis. Id. at 121.
              4.      Duration of Active Vasculitis

      Regardless of when Mr. Bourche started to manifest symptoms of vasculitis,
the parties dispute if or when Mr. Bourche stopped suffering from active vasculitis.
“Active” vasculitis refers to a stage in which Mr. Bourche was creating new skin
lesions, as opposed to the continuation (or healing) of old skin lesions. For the
reasons explained below, the evidence supports a finding that Mr. Bourche did not
produce new skin lesions after August 14, 2014, the date when he was prescribed
prednisone.
      At Mr. Bourche’s first appointment with Dr. Hong on July 15, 2014, Mr.
Bourche told Dr. Hong that he was getting new lesions. Exhibit 8 at 49. This
evidence is slightly more persuasive than the report on July 16, 2014 that,

(June 23 – lethargy), 1424 (July 4 – abdominal pain), 1450 (July 30 – stomach pain), 1454
(August 4 – abdominal pain, shortness of breath).

                                                  34
according to Mr. Bourche’s dialysis doctor, he was not experiencing new lesions.
Exhibit 10 at 133-34.
       However, it appears that the development of new lesions appeared to pause
around this time. On July 17, 2014, Dr. Hong reported that Mr. Bourche’s ulcers
are “superficial and healing.” Exhibit 8 at 45. Based upon Dr. Hong’s preliminary
review of the skin biopsy, Dr. Hong specifically concluded that Mr. Bourche had
“no active vasculitis.” Id. The trend that Mr. Bourche’s skin lesions were
improving (and not developing new ones) continued in the next two appointments
with Dr. Hong. Dr. Hong described them as “much improved” (July 29, 2014) and
“healing” (August 1, 2014). Id. at 41, 43.
      At this point, Mr. Bourche’s lesions began to worsen. His
gastroenterologist, Dr. Dolan, reported on August 5, 2014, that Mr. Bourche has
“new skin lesions.” Exhibit 5 at 5. While the report of a gastroenterologist’s
assessment of skin lesions might be questioned, Dr. Hong, a dermatologist, found
that Mr. Bourche’s legs were “worse and more painful” on August 14, 2014, with
“new small crusted papules.” Exhibit 8 at 38. This worsening appears to have
prompted Dr. Hong to prescribe prednisone for Mr. Bourche.
       After Dr. Hong started Mr. Bourche on prednisone, no treating doctor
asserted that Mr. Bourche developed new skin lesions. Instead, Dr. Hong, on
August 22, 2014, affirmatively stated “no new ulcerations.” Id. at 32. On October
6, 2014, Dr. Hong described some lesions and found that Mr. Bourche’s vasculitis
was “improved.” Exhibit 12 at 45. Dr. Hong did not say whether the lesions were
new, nor did he say, “no new lesions.”
       During the hospitalization for the mitral valve repair, Dr. Mooney had an
opportunity to examine Mr. Bourche. Dr. Mooney wrote: “It is not clear whether
the patient has been having new skin lesions or not.” Exhibit 9 at 739. Dr.
Mooney added that Mr. Bourche has been “slow to heal.” Id. at 740.
      On January 12, 2015, Dr. Weisman, a rheumatologist, stated that Mr.
Bourche’s “skin ulcers have improved with routine wound care, but lesions persist.
No new ulcers have developed. Few small erythematous areas have developed on
the arms, legs.” Exhibit 12 at 60. Although Dr. Zizic maintained that Dr.
Weisman reported that Dr. Weisman discovered new lesions, Tr. 219, Dr.
Matloubian’s interpretation that Mr. Bourche is not developing new lesions is more
persuasive. Tr. 303.
     Dr. Matloubian’s opinion finds support in a March 6, 2015 evaluation by Dr.
Meditz. She found “Multiple LEE wounds initially related to IgA vasculitis but
                                           35
component of slow healing likely related to low output heart failure.” Exhibit 13-2
at 213 [pdf 63]. Dr. Meditz mentioned that Mr. Bourche was going to seek a heart
and kidney transplant at Cedars-Sinai.
       Two doctors from Cedars-Sinai commented on healing (but not new)
lesions. First, a cardiothoracic surgeon stated that Mr. Bourche “has an open
wound in the right leg which is still healing from August of 2014 secondary to his
vasculitis.” Exhibit 72 at 11 (Mar. 21, 2015). Next, an infectious disease specialist
reported a “non healed ulcer” on Mr. Bourche’s lower right leg. Id. at 141. This
problem was significant because the doctor indicated Mr. Bourche’s “lack of
ability to heal” was a concern in evaluating Mr. Bourche for a transplant. Id.
      Finally, on May 19, 2015, Dr. Holland wrote that he had spoken to Dr.
Meditz “regarding wound healing. This appears to be progressing but is a slow
process.” Exhibit 76 at 9.
      This evidence collectively supports a finding that Mr. Bourche developed
new lesions until approximately July 15, 2014. Then, there was approximately two
weeks in which Mr. Bourche did not develop new lesions. Then, from
approximately August 1 through August 14, Mr. Bourche developed new and
worsening lesions. After August 14, 2014, Mr. Bourche did not develop any new
vasculitic lesions.
      While the progression of skin lesions carries some consequence for the
theory that vancomycin caused Mr. Bourche’s vasculitis, the more important
finding for evaluating Dr. Zizic’s theory that the hepatitis B vaccine caused the
vasculitis is that the vasculitis did not begin in early May 2014. As noted above,
Dr. Zizic asserted that the vasculitis started with the mouth blister(s) that Dr.
Mooney described on May 9, 2014. While Dr. Zizic’s estimate of the amount of
time for creation of immune complexes appears reasonable, he did not opine that
the onset of vasculitis approximately two months after vaccination was also
reasonable. Thus, Ms. Bourche has not met the burden of establishing that the
vasculitis arose in an appropriate temporal interval.
      C.     An Onset of Vasculitis in June-July 2014 Makes Explanations,
             other than the Hepatitis B Vaccination, More Persuasive

       In determining whether a vaccine caused an illness, it is “commonsense”
that “evidence of other possible sources of injury can be relevant not only to the
‘factors unrelated’ defense, but also to whether a prima facie showing has been
made that the vaccine was a substantial factor in causing the injury in question.”
Stone v. Sec’y of Health & Human Servs., 676 F.3d 1373, 1379 (Fed. Cir. 2012).
                                            36
Here, the Secretary, through Dr. Matloubian, has proposed an infection,
particularly the staph infection, and vancomycin as alternative explanations. See
exhibit A at 9-10.
       These proposed alternative explanations rest upon the proposition that the
vasculitis Mr. Bourche developed was IgA vasculitis. Because the soundness of
this diagnosis is a critical step, see Broekelschen v. Sec'y of Health and Human
Servs., 618 F.3d 1339, 1346 (Fed. Cir. 2010), the analysis begins with the question
of how to classify Mr. Bourche’s vasculitis. Then, the next section discusses the
causes for Mr. Bourche’s IgA vasculitis.
             1.    Diagnosis of IgA Vasculitis

      The vasculitis that Mr. Bourche developed around June-July 2014 was IgA
vasculitis. The basis for this finding is the series of two skin biopsies.
       Dr. Golitz interpreted the first skin biopsy, which came from Mr. Bourche’s
shin, on July 18, 2014. Dr. Golitz commented: “The combination of vasculitis
with colon involvement raises the possibility of Henoch-Scholein purpura. A
biopsy for direct immunofluorescence microscopy is recommended.” Exhibit 8 at
122.
      One purpose of the direct immunofluorescence was to look for IgA deposits.
Exhibit 12 (Dr. Weisman) at 19. When the direct immunofluorescence was done
on the second skin biopsy, which came from Mr. Bourche’s right foot, IgA was
found. Exhibit 8 at 121. The interpretation of the dermatopathologist was the
diagnosis of “vascular IgA, IgM and fibrin.” Id.
       The finding of IgA on direct immunofluorescence leaves two choices for
types of vasculitis – either IgA/HSP or cutaneous small vessel vasculitis. Exhibit
A-3 (Fett) at 8 (table 8); Tr. 257. No doctor has proposed that cutaneous small
vessel vasculitis fits Mr. Bourche’s condition.
      Instead, the written reports from the treating doctors point to IgA vasculitis
also known as HSP. For example, after receiving the report on direct
immunofluorescence, Dr. Hong’s assessment was “hypersensitivity vasculitis,
?HSP exacerbated by drug eruption.” Exhibit 8 at 32.
      Later doctors incorporated “IgA vasculitis” into the histories that they
obtained. See, e.g., exhibit 9 at 921 (Josh Emdur on Nov. 24, 2014); exhibit 76 at
32 (Laura Fries for Dr. Holland on Feb. 12, 2015); exhibit 72 at 69 (Dr. Scher on
Mar. 25, 2015), 140 (Dr. Zakowski on Mar. 26, 2015).

                                             37
       However, in the course of this litigation, Ms. Bourche presented two
witnesses who opined that Mr. Bourche did not suffer from IgA vasculitis. These
were Dr. Mooney and Dr. Zizic. Dr. Mooney testified that Mr. Bourche did not
suffer from IgA vasculitis. Tr. 62, 128, cited in, among other places, Pet’r’s Reply
at 8. However, Dr. Mooney’s testimony at this point was very conclusory and he
was, unfortunately, not asked to address the direct immunofluorescence. Thus,
crediting Dr. Mooney’s opinion about Mr. Bourche’s (lack of) IgA vasculitis is
difficult notwithstanding Dr. Mooney’s status as a treating doctor.
       Dr. Zizic’s opinion about IgA vasculitis is not straightforward. In his initial
report, Dr. Zizic stated that Mr. Bourche suffered from IgA vasculitis. Exhibit 15
at 5, 20 (postulating HSP as a unifying disorder). But, based upon literature that
Dr. Matloubian supplied, Dr. Zizic revised his opinion. Tr. 174.
       Dr. Zizic explained that in IgA vasculitis, the amount of IgA found on direct
immunofluorescence should be dominant, and Dr. Matloubian agreed with this
point. Tr. 173, 348. In Mr. Bourche’s case, the person interpreting the direct
immunofluorescence rated IgA as 1+ and IgM as 2+. Exhibit 8 at 121. Thus, Dr.
Zizic has a fair point that Mr. Bourche did not suffer from IgA vasculitis.
       However, Dr. Zizic and Dr. Matloubian also agreed that the process for
interpreting direct immunofluorescence is subjective. Tr. 175, 298. Thus, the
distinction between 1+ and 2+ is more qualitative than quantitative. Presumably,
Dr. Hong, a dermatologist, was aware of how skin biopsies are tested with direct
immunofluorescence when he concluded that Mr. Bourche suffered from
“hypersensitivity vasculitis, ?HSP exacerbated by drug eruption.” Exhibit 8 at
32.22
       The duration of Mr. Bourche’s skin problem is consistent with the expected
duration of HSP. As discussed above, Mr. Bourche first manifested skin lesions
that could be associated with vasculitis in June 2014, and he continued, with one
interruption, to make new skin lesions until being placed on prednisone in mid-
August 2014. These slow-healing lesions then persisted until at least March 2015,
when he was at Cedars-Sinai.
      HSP lesions can last six months or more. Tr. 305 (Dr. Matloubian). Dr.
Matloubian’s opinion about the duration of HSP lesions was not contested and was
supported by some articles. Exhibit A-4 (Carlson) at 5/pdf 3 (bottom right);

       22
          No treating doctor appears to have diagnosed Mr. Bourche with IgM vasculitis, the
condition that Dr. Zizic proposed in his oral testimony.

                                                  38
exhibit A-6 (Audemard-Verger) at 583 (indicating that the doctors should evaluate
an HSP patient with renal problems after three and six months). Thus, the course
of Mr. Bourche’s health provides some confirmation that he suffered IgA
vasculitis.
       Mr. Bourche’s IgA vasculitis appears linked to his long-standing IgA
nephritis. The results of the skin biopsy on his right foot resembled the results of
the biopsy of his kidney in October 2009. Both showed the presence of IgA and
IgM, but not IgG. Exhibit 9 at 629 (Oct. 6, 2009 - kidney); exhibit 8 at 121 (Aug.
19, 2014 - skin).
       People with IgA nephritis, which, strictly speaking, is a disease limited to
the kidneys may develop symptoms outside the kidneys and become diagnosed
with IgA vasculitis. The underlying pathogenesis of both diseases are the same—
the body makes a defective IgA molecule. See Tr. 98-99, 150-52, 271-72.
             2.     Causes for IgA Vasculitis

       Whether the evolution from IgA nephritis to IgA vasculitis is part of the
natural course of the disease or whether the evolution requires a distinct trigger is
not clear. For Mr. Bourche, Dr. Matloubian proposed two different causes.
      The first was Mr. Bourche’s staph infection in May 2015. See exhibit A at
9. This aspect of Dr. Matloubian’s overall opinion was touched upon only briefly
during the hearing. See Tr. 312.
       Much more attention during the hearing was directed toward Dr.
Matloubian’s other possibility, the vancomycin. Dr. Matloubian opined that
vancomycin can cause IgA vasculitis. Tr. 312, 365. Dr. Zizic agreed vancomycin
can cause IgA vasculitis. Tr. 227. Dr. Mooney agreed, too. Tr. 127-28. Further,
although the parties disputed when Mr. Bourche first manifested signs and
symptoms of vasculitis, the parties did not controvert Dr. Matloubian’s opinion
that an onset of vasculitis in late June or early July 2014, when Mr. Bourche was
taking the vancomycin, was within the appropriate temporal window to infer that
the vancomycin caused the vasculitis. See Tr. 278; Pet’r’s Posth’g Br. at 36-37
(asserting that lesions pre-dated vancomycin but not addressing how long it would
take lesions to appear after vancomycin).
       Treating doctors also suggested that vancomycin caused an adverse reaction
in the form of vasculitis. The most prominent example is Dr. Hong. In the report
of Mr. Bourche’s first visit with Dr. Hong, Dr. Hong first assessment was
“[p]robable vasculitis, ? Drug-induced (?vancomycin).” Exhibit 8 at 48. While the

                                             39
presence of two question marks suggests that Dr. Hong was uncertain about this
etiology initially, Dr. Hong became firmer. After Dr. Golitz interpreted the skin
biopsy from Mr. Bourche’s shin, Dr. Hong stated that the results were “[s]till
consistent with probable drug-induced cause.” Id. at 45 (July 17, 2014). Dr. Hong
carried forward his opinion that the vasculitis was probably drug-induced in
successive appointments. Exhibit 8 at 43 (July 29, 2014), 41 (Aug. 1, 2014), 38
(Aug. 14, 2014).
       Dr. Hong’s assessment appears to underlie the history that Mr. Bourche
provided to his rheumatologist, Dr. Weisman, on August 18, 2014. This history
that Dr. Weisman obtained includes the passage: “Vancomycin given for sepsis.
Developed skin reaction from vancomycin.” Exhibit 12 at 15. However, this
evidence does not carry much weight because Dr. Weisman seems not to have
expressed his own opinion about the origins of the vasculitis. While Dr. Weisman
stated he agreed with the diagnosis of “hypersensitivity vasculitis,” he did not
specify the antigen to which Mr. Bourche was hypersensitive. See id. at 19.
      Finally, when Dr. Mooney was treating Mr. Bourche, Dr. Mooney, too,
considered the possibility that vancomycin caused the vasculitis. When Dr.
Mooney saw Mr. Bourche in the context of being hospitalized for endocarditis, Dr.
Mooney prepared a report about Mr. Bourche. Dr. Mooney wrote: “He had
reported onset of mouth ulcerations along with upper and lower extremity skin
lesions that started in April. Initially it was felt that the trigger was hepatitis
vaccine. During this time, he may have also had a reaction to vancomycin.”
Exhibit 9 at 738 (Oct. 25, 2014).
      While Dr. Hong pointed to vancomycin as the probable cause for a drug-
induced vasculitis, other treating doctors identified the hepatitis B vaccine as the
source of an adverse reaction. This series of doctors begins with Dr. Mooney nine
days after vaccination. On May 9, 2014, Dr. Mooney indicated that Mr. Bourche’s
mouth blisters were due to a reaction to the hepatitis B vaccine. Exhibit 10 at 127.
Similarly, during the hospitalization for the staph infection, Dr. Bozeman and Dr.
Meditz linked the hepatitis B vaccine to oral ulcers. Exhibit 9 at 321, 316. These
opinions may or may not be accurate. But, whether the hepatitis B vaccine caused
mouth blisters is not relevant to the outcome of the litigation because Ms. Bourche
does not seek compensation for this condition.23


       23
           Ms. Bourche and Dr. Zizic use the mouth blisters as an initial manifestation of
vasculitis. Exhibit 44 at 2. But, for the reasons discussed at length in section III.B above, Mr.
Bourche did not begin to suffer vasculitis until June 2014 at the earliest.

                                                    40
      The more significant opinions from treating doctors about the adverse
consequences of the hepatitis B vaccine arose when Mr. Bourche was having more
serious skin problems. In dialysis treatment in July 2014, one physician
commented: Mr. Bourche’s vasculitic rash was “likely sequela of reaction to hep
B vaccine when he developed oral ulcers as well.” Exhibit 10 at 133. Another
doctor wrote that Mr. Bourche’s “limited leukocytoclastic vasculitis [was] related
to Energex [hepatitis B vaccine reaction].” Id. at 135. These are the strongest
statements supporting vaccine-causation from a treating doctor in the course of
treatment.
       Other doctors memorialized a sequence of events in which the hepatitis B
vaccine preceded the development of vasculitis. See, e.g., exhibit 8 at 47 (Dr.
Hong); exhibit 12 at 15 (Dr. Weisman); exhibit 13-1 at 106 (Dr. Ryan’s January
28, 2015 note listing hepatitis vaccine as an allergy); exhibit 72 at 69 (Dr. Scher),
139 (Dr. Zakowski), 96 (Dr. Peng listing hepatitis B vaccine as an allergy).
However, these carry relatively little (if any) weight because the recitation of a
chronological sequence of events is not the same as an opinion regarding
causation. Cedillo v. Sec'y of Health & Human Servs., 617 F.3d 1328, 1347-48
(Fed. Cir. 2010); La Londe v. Sec'y of Health & Human Servs., 110 Fed. Cl. 184,
206 (2013), aff’d on other ground, 746 F.3d 1334 (Fed. Cir. 2014); Langland v.
Sec'y of Health & Human Servs., 109 Fed. Cl. 421, 439 (2013) (stating that the
special master was not arbitrary in finding that the records from treating doctors
“reflect no more than intake histories or temporal associations”); Caves, 100 Fed.
Cl. at 139-40 (2010).
      In the final analysis, the evidence regarding vancomycin is stronger than the
evidence regarding hepatitis B vaccine. The primary reason is that the vasculitis
developed in late June or early July 2014, which is in the time in which an
inference of causation is appropriate for vancomycin, which Mr. Bourche started
taking on May 23, 2014. In contrast, an onset of vasculitis near the end of June or
beginning July 2014 is approximately two months after the April 23, 2014
vaccination. Dr. Zizic did not present any persuasive testimony to explain why
two months would be an appropriate temporal interval. See Tr. 310, 313-14 (Dr.
Matloubian explaining that an onset of vasculitis two months after vaccination
would be coincidental). Another strong reason for downplaying the hepatitis B
vaccine is the pathological similarity between IgA nephritis and IgA vasculitis.
      To be sure, the proposition that Mr. Bourche suffered from IgA vasculitis
has problems itself. The diagnosis is not perfect as the direct immunofluorescence
did not show a dominance of IgA. Further, Mr. Bourche’s fluctuating course in
which his skin lesions appeared, improved, then worsened may not be entirely
                                             41
compatible with vancomycin as the cause. But, the Secretary does not bear the
burden of presenting a perfect case identifying an alternative cause because Ms.
Bourche has not met her initial burden regarding causation. La Londe v. Sec’y of
Health & Human Servs., 746 F.3d 1334, 1340 (Fed. Cir. 2014).
        D.    Ms. Bourche did not persuasively show that the endocarditis
              contributed to Mr. Bourche’s death

       The previous three sections explain why Ms. Bourche is not entitled to
compensation for the vasculitis that Mr. Bourche suffered. But, Ms. Bourche’s
petition also includes the theory that the hepatitis B vaccination was a substantial
factor in causing Mr. Bourche’s death. This theory suffers from the additional flaw
that Ms. Bourche has not presented preponderant evidence that the endocarditis
further weakened Mr. Bourche’s impaired heart such that Mr. Bourche died earlier
than expected.
       Two metrics to evaluate Mr. Bourche’s cardiac function are his ejection
fraction and his cardiologist’s classification of his functioning. A normal ejection
fraction is 65 ± 8 per cent. Dorland’s at 740. This chart summarizes results of Mr.
Bourche’s ejection fractions:
 Date                Event                                Citation
 1/9/2013            TTE: ejection fraction 35-38%        Exhibit 8 at 158
 9/3/2013            TTE: ejection fraction 33%           Exhibit 8 at 162-63
 10/4/2013           TTE: ejection fraction 10-15%        Exhibit 9 at 260-61
 10/4/2013           Pacemaker installed
 11/7/2013           TTE: ejection fraction 35%           Exhibit 8 at 160
 4/23/2014           Hepatitis B vaccination
 5/24/2014           TTE: ejection fraction 15-20%        Exhibit 9 at 451
 8/14/2014           TTE: ejection fraction 20-30%        Exhibit 8 at 153;
                                                          Exhibit 76 at 185
 10/27/2014          TEE: ejection fraction 15-20%        Exhibit 9 at 811-12
 11/5/2014           Mitral valve repair


                                            42
 11/7/2014              TTE: ejection fraction 15-20%                Exhibit 9 at 808-10
 1/5/2015               TTE: ejection fraction 31%                   Exhibit 76 at 180, 230
 1/28/2015              Hospitalized from Jan. 28, 2015 to           Exhibit 13-1 at 99-100
                        Feb. 7, 2015                                 (discharge summary)
 1/29/2015              TTE: ejection fraction 5-10%                 Exhibit 13-1 at 120-21;
                                                                     exhibit 76 at 23 (15%)
 2/12/2015              Ejection fraction 31%. Probably              Exhibit 76 at 32; exhibit
                        incorrect.                                   13-2 at 165 [pdf 15]
 3/2/2015               Ejection fraction 23%                        Exhibit 76 at 225-26;
                                                                     but see exhibit 76 at 22
                                                                     (stating today’s ejection
                                                                     fraction is 31%)
 4/29/2015              TTE: ejection fraction 10%                   Exhibit 13-2 at 264 [pdf
                                                                     114]
 5/19/2015              Ejection fraction approximately              Exhibit 76 at 8, 223
                        20%


       Isolating these test results allows for a focused analysis. After Mr.
Bourche’s pacemaker was installed but before the hepatitis B vaccine, his injection
fraction was approximately 35 percent. This number is higher than the ejection
fraction about on August 14, 2014, which was about four months after the hepatitis
B vaccination. On that date, the ejection fraction was 20-30 percent. Exhibit 8 at
153.24
       Before Mr. Bourche’s November 5, 2014 mitral valve repair, the ejection
fraction had declined to 15-20 percent. Exhibit 9 at 811-12 (Oct. 27, 2014). The
mitral valve repair did not improve Mr. Bourche’s ejection fraction immediately as
echocardiograms from November 2014 showed that the ejection fraction ranged



       24
          In between, Mr. Bourche had one transthoracic echocardiogram when he was
hospitalized for the staph infection. At this time, his ejection fraction was 15-20 percent.
Exhibit 9 at 451.

                                                    43
from 5 percent to 20 percent. For an explanation of why the mitral valve surgery
does not produce higher ejection fractions, see Tr. 511-14.
        However, after more weeks passed, Mr. Bourche’s ejection fraction
improved. On January 5, 2015, it was 31 percent. Dr. Holland stated: “His
ejection fraction is improving. Preoperatively [it] was 5-10[.] Now it is 25-30%.”
Id. at 180. Of course, it is correct that an ejection fraction of 31 percent is lower
than an ejection fraction of 35 percent. Tr. 498 (Dr. LaRue: “[I]t’s been testified to
that he never got back to that prior level, and I think that’s a true statement.”).25
       During the hearing, Ms. Bourche’s expert cardiologist, Dr. Stark argued a
report of an ejection fraction of 31 percent was anomalous. Tr. 418, 433-34. This
argument had some facial plausibility because, then, the record included only a
doctor’s reference to the ejection fraction, not the actual test result. See exhibit 13-
2 at 165 [pdf 15]; Tr. 466, 497-98. However, after the hearing concluded, Ms.
Bourche was instructed to obtain additional medical records. These more recently
filed records from Dr. Holland include the underlying January 5, 2015
echocardiogram. Exhibit 76 at 230.26
       Mr. Bourche’s ejection fractions roughly correspond to changes in his
classification. The New York Heart Association developed a system to classify
congestive heart failures based upon how the person feels. Tr. 411-12. In class I,
the person feels fine. Tr. 411. In class II, the person has some decrease in function
with physical exertion. Tr. 411, 418. In class III, the person has shortness of
breath in doing ordinary tasks like walking or getting dressed but can usually
breathe easily at rest. Tr. 411, 428-29. In class IV, the person can hardly breathe.
Tr. 411.
     At various times, Dr. Holland (or Dr. Holland’s associate) ascribed a class to
Mr. Bourche.



       25
          Dr. LaRue’s assessment was made without the benefit of the more recent records filed
as exhibit 76.
       26
          In narrative reports dated February 12, 2015 and March 2, 2015, Dr. Holland states that
Mr. Bourche has an ejection fraction “today of 31%.” Exhibit 76 at 22, 32. Both reports seem to
carry forward information from Mr. Bourche’s January 5, 2015 echocardiogram. When Mr.
Bourche had a repeat echocardiogram on March 2, 2015, the ejection fraction was 23 percent.
Exhibit 76 at 225-26. Consequently, the undersigned gives little weight to the February 12, 2015
and March 2, 2015 reports that the ejection fraction was 31 percent.

                                                  44
Date         Classification / Note                 Citation
8/24/2010    Class II                              Exhibit 8 at 117
8/26/2011    Class II-III                          Exhibit 8 at 104
8/1/2012     Class III                             Exhibit 8 at 100
9/4/2012     Class II-III, improving               Exhibit 8 at 96
2/28/2013    Class III, definitely worse           Exhibit 8 at 90
7/17/2013    Class III                             Exhibit 8 at 84
9/3/2013     Class III                             Exhibit 8 at 77-78
10/4/2013    Class III                             Exhibit 8 at 141
10/4/2013    Pacemaker installed
10/10/2013   Class III                             Exhibit 8 at 68
1/9/2014     Class III                             Exhibit 8 at 55
4/23/2014    Hepatitis B vaccination
7/10/2014    Class III                             Exhibit 8 at 53; Exhibit
                                                   76 at 1999
8/6/2014     Class III-IV, Class III               Exhibit 76 at 191, 193
8/14/2014    Class III                             Exhibit 76 at 186
11/5/2014    Mitral valve repair
1/6/2015     Class II-III                          Exhibit 76 at 180
3/3/2015     Class III-IV, Class III, Class III+   Exhibit 76 at 23
4/3/2015     Class III                             Exhibit 76 at 14
5/19/2015    Class III, Class IV, Class IV         Exhibit 76 at 8-9




                                           45
       In this chart, the critical entry is for January 6, 2015. Dr. Holland classified
Mr. Bourche as “class II-III.” The indication that he was borderline “class II” for
the first time since 2011 undermines the argument that endocarditis started a
continual decline, leading to his death.
       Moreover, after the November 5, 2014 mitral valve repair, Mr. Bourche
lived for more than a year until he died on January 16, 2016. This also contributes
to a finding that the endocarditis was not a significant factor in Mr. Bourche’s
death. Tr. 498, 518-19. Instead, Mr. Bourche suffered from other illnesses,
including heart problems, which were alleviated by the pacemaker, and his kidney
problems for which he still required dialysis. See Tr. 437 (Dr. Stark’s
acknowledging that people with chronic heart failure and end-stage liver failure
have a “shortened life span”), 462 (Dr. LaRue’s describing heart failure as
following a stair-step—as opposed to linear—pattern). The event that seems to
have most closely preceded a substantial decline in Mr. Bourche’s heart function
was his hospitalization, beginning January 28, 2015. See exhibit 13-1 at 99-100
(discharge summary).
       In short, Dr. LaRue’s opinion on a more-likely-than-not basis that the
endocarditis was not a significant factor in Mr. Bourche’s death (Tr. 497, 508, 515)
is persuasive. Mr. Bourche’s death occurred too remote in time and in the
presence of multiple confounding factors to find that the endocarditis was a
proximate cause of his death.
IV.   Conclusion

       In the last two years of Mr. Bourche’s life, his medical history was very
complicated. He saw many doctors and the reports from these doctors do not agree
with each other entirely. However, the evidence preponderates in favor of a
finding that Mr. Bourche first manifested vasculitic lesions after he was prescribed
vancomycin. This determination, in turn, makes the April 23, 2014 hepatitis B
vaccination an unlikely causal contributor to the vasculitis. In addition, the lack of
IgG in the biopsy reinforces the conclusion that the hepatitis B vaccination was not
to blame for the vasculitis. Finally, regardless of whether the vasculitis contributed
to the endocarditis, the endocarditis seems not to have contributed to Mr.
Bourche’s death.
       For these reasons, Ms. Bourche cannot be awarded compensation.
Certainly, Mr. Bourche suffered vasculitis. Ms. Bourche, as his devoted wife,
suffered along with him. But, special masters cannot compensate cases based upon
the emotional appeal.

                                              46
       In the absence of a motion for review filed pursuant to RCFC Appendix B,
the clerk of the court is directed to enter judgment herewith.
      IT IS SO ORDERED.
                                                 s/Christian J. Moran
                                                 Christian J. Moran
                                                 Special Master




                                          47
                                             Appendix27


      Anna Ankudowicz, Do Patients With End-Stage Chronic Renal Failure
Treated With the Use of Hemodialysis Have Health Skin?, 48 Transpl. Proc., 1435
(2016), filed as exhibit A-1.
      Alexandra Audemard-Verger, et al., IgA vasculitis (Henoch-Shönlein
purpura) in adults: Diagnostic and therapeutic aspects, 14 Autoimmun. Rev. 579
(2015), filed as exhibit A-6.
      J. Andrew Carlson, The histological assessment of cutaneous vasculitis, 56
Histopath. 3 (2010), filed as exhibit A-4.
      Nicole Fett, et al., Evaluation of adults with cutaneous lesions of Vasculitis,
UpToDate (literature review current through Oct. 2016, last updated Apr. 12,
2016), https://www.uptodate.com, filed as exhibit A-3.
      Barbara Knoppova, et al., The Origin and Activities of IgA1-Containing
Immune Complexes in IgA Nephropathy, 7(117) Front. Immun. 1 (2016), filed as
exhibit A-9.
       Claire-Anne Siegrist, Vaccine immunology in Vaccines, (Stanley Plotkin et
al. eds., 6th ed. 2013), filed as exhibit A-30.
      Robert J. Wyatt, et al., IgA nephropathy, 368(25) N. Engl. J. Med. 2402
(2013), filed as exhibit A-8.




       27
        This appendix provides bibliographical information for articles this decision cites.
However, all articles have been reviewed even if they are not cited.

                                                   48
