Jessie Contreras v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

*************************

JESSIE CONTRERAS, *

*

Petitioner, * No. 05-626V

* Special Master Christian J. Moran

v. *

* Filed: November 19, 2013

SECRETARY OF HEALTH *

AND HUMAN SERVICES, * hepatitis B vaccine; tetanus-diphtheria

* vaccine; transverse myelitis (TM);

Respondent. * Guillain-Barré syndrome (GBS);

* one-day onset; decision on remand

*************************

Jeffrey S. Pop, Jeffrey S. Pop, Attorney at Law, Beverly Hills, CA, for petitioner;

Linda S. Renzi, United States Dep’t of Justice, Washington, DC, for respondent.

PUBLISHED DECISION ON REMAND DENYING ENTITLEMENT1

I. Introduction

Jessie Contreras alleges that either a hepatitis B vaccination and/or a tetanus-diphtheria

(Td) vaccination caused him to develop a neurological problem that began one day after his

vaccinations. His case is proceeding in the National Childhood Vaccine Injury Compensation

Program. 42 U.S.C. § 300aa-10 et seq. (2006). The statute authorizes recovery when the

petitioners establish that vaccines caused a new illness or significantly aggravated a preexisting

one.

An April 5, 2012 decision found that Mr. Contreras failed to establish that either the

hepatitis B or Td vaccine caused his illness based on a failure to establish one of the factors set

forth in Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274 (Fed. Cir. 2005), namely, that

one day between vaccination and onset of symptoms constitutes a medically appropriate

temporal relationship from which causation can be inferred. Contreras v. Sec’y of Health &

Human Servs., No. 05-626V, 2012 WL 1441315, at *1 (Fed. Cl. Spec. Mstr. Apr. 5. 2012)

1

The E-Government Act of 2002, Pub. L. No. 107-347, 116 Stat. 2899, 2913 (Dec. 17,

2002), requires that the Court post this decision on its 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.

(Entitlement Decision). The Entitlement Decision did not address the two other Althen prongs

because Mr. Contreras’s failure on the timing aspect was a sufficient basis to deny compensation.

Mr. Contreras filed a motion for review with the Court of Federal Claims (the Court). On

September 28, 2012, the Court granted petitioner’s motion, vacated the Entitlement Decision,

and “remand[ed] for proceedings in accordance with the principles of law and the instructions set

forth in [its] opinion.” Contreras v. Sec’y of Health & Human Servs., 107 Fed. Cl. 280, 283

(2012) (Opinion and Order).

The parties filed briefs on remand that addressed the record and the Court’s Opinion and

Order, but no new evidence. Hence, the previously submitted evidence is reviewed in light of

the Court’s instructions on remand.

After additional consideration, the undersigned finds that Mr. Contreras has failed to

establish by a preponderance of the evidence that he is entitled to compensation. First, he has

not provided preponderant evidence to demonstrate that the hepatitis B vaccine can cause

transverse myelitis2 via his expert’s proposed mechanism of causation, molecular mimicry.

Second, a preponderance of the evidence demonstrates that transverse myelitis cannot manifest

via molecular mimicry within one day.

II. Facts

The record includes much testimony, presented either in writing or orally, from doctors.

Some doctors treated Mr. Contreras and some doctors were retained particularly for this

litigation. A synopsis of their qualifications is presented first as a matter of background in

section II.A.

Collectively, the doctors’ testimony helped explain what happened to Mr. Contreras and,

thus, their comments are interspersed in the discussion about Mr. Contreras’s medical history.

Relevant information for this decision includes Mr. Contreras’s health before and after he was

vaccinated. His history is summarized in section II.C, below, which is preceded in section II.B

by a general discussion about two conditions that arguably afflicted Mr. Contreras, transverse

myelitis and Guillain-Barré syndrome (GBS). This background information about transverse

myelitis and GBS provides a context for understanding the significance of events in Mr.

Contreras’s health history.

2

Mr. Contreras alleged that he developed both transverse myelitis and Guillain-Barré

Syndrome (GBS). As discussed in detail below, a preponderance of the evidence indicates that

he suffered from transverse myelitis only. Accordingly, this decision focuses on whether the

hepatitis B vaccine and/or the Td vaccine can (and did) cause transverse myelitis in

approximately one day.

2

A. Mr. Contreras’s Treating Physicians and the Parties’ Specially

Retained Experts

Mr. Contreras offered the testimony of three of his treating physicians, Dr. Fred Kyazze,

Dr. Jeremy Garrett, and Dr. Mark Wagner. Mr. Contreras also offered the testimony of Dr.

Lawrence Steinman and Dr. Charles Poser, whom he retained as experts in support of his claim.

The Secretary offered testimony from Dr. John Sladky and Dr. Lindsay Whitton, whom she

retained in this litigation.

1. Dr. Kyazze

Mr. Contreras submitted a short affidavit from Dr. Kyazze (exhibit 11), who testified at

the April 19, 2010 hearing. Tr. 41. Dr. Kyazze administered Mr. Contreras’s subject

vaccinations on June 16, 2003, and also examined Mr. Contreras.

Dr. Kyazze received an undergraduate degree in biology from Occidental College in Los

Angeles, California, and attended medical school at Makerere University in Uganda. He

completed a residency in family medicine and later became board-certified in that specialty. Tr.

42.

2. Dr. Wagner

Dr. Wagner treated Mr. Contreras for approximately five hours of his first emergency

room admission on June 17, 2003. Exhibit 12 at 2, ¶ 13; exhibit 6 at 9; Tr. 66-69. Dr. Wagner

submitted an affidavit (exhibit 12) and testified at the April 19, 2010 hearing on Mr. Contreras’s

behalf. Tr. 63.

Dr. Wagner received undergraduate degrees in biology and chemistry from the University

of California at Irvine, and a medical degree from the University of California at Los Angeles.

Tr. 63. He then completed a residency in emergency medicine and later became board-certified

in that specialty. Tr. 63. He has been practicing medicine for more than 30 years. Tr. 64.

3. Dr. Garrett

Dr. Garrett was Mr. Contreras’s attending physician during his lengthy hospitalization

immediately following the onset of his neurological problems. Exhibit 7 at 157. Dr. Garrett, as

discussed below, consulted with other doctors to care for Mr. Contreras.

Dr. Garrett submitted an affidavit (exhibit 13) on Mr. Contreras’s behalf, but was unable

to testify in person. Tr. 101. He received his bachelor’s degree from Northwestern University

and his medical degree from the University of Nebraska. Exhibit 127 at 1. He then completed a

residency in pediatrics and a fellowship in pediatric critical care. Id. He has held numerous

professorships in the fields of pediatrics. Id.

3

At the time he submitted his affidavit, Dr. Garrett was board-certified in general

pediatrics and pediatric critical care medicine, and was a professor of pediatrics at the Saint

Louis University School of Medicine. Exhibit 13 at 1-2. He also had an active clinical practice.

Id. at 2; exhibit 147 at 2.

4. Dr. Poser

Mr. Contreras retained Dr. Poser to testify on his behalf. Dr. Poser submitted two

affidavits (exhibits 22 and 23), but was unable to testify. Tr. 102; see also Opinion and Order,

107 Fed. Cl. at 283 n.5.

Dr. Poser received his bachelor’s degree from the College of the City of New York and

his medical degree from Columbia University. Exhibit 126 at 1. He then completed a residency

in neurology. Id. Dr. Poser held numerous professorships and professional positions in the field

of neurology. Id. at 1-2. At the time he submitted his affidavits, he was board-certified in

neurology and child neurology. Dr. Poser was also retired (exhibit 22 at 1, ¶ 12), with

approximately 50 years of clinical experience. Exhibit 23 at 6, ¶ 13.

5. Dr. Steinman

Dr. Steinman testified for Mr. Contreras as an expert in neurology. Dr. Steinman

prepared four reports with numerous pieces of literature to support his opinions. See exhibits 55,

105, 124, and 152. He also testified at the hearings on April 19-20, 2010, and July 24, 2011.

Dr. Steinman is a professor in Stanford University's Departments of Neurology and

Neurological Sciences, Pediatrics and Genetics. He chairs that institution’s program in

immunology. He has substantial research experience and has published extensively in the fields

of neurology and immunology. He has received national and international honors for his work in

researching multiple sclerosis. Exhibit 56 (curriculum vitae).

6. Dr. Sladky

Dr. Sladky testified for the Secretary as an expert in neurology. He received his

bachelor’s degree and medical degree from Yale University. Exhibit J (Dr. Sladky’s curriculum

vitae) at 1. He completed a residency in pediatrics at Yale-New Haven Hospital and then

completed a fellowship in neurology at the Children’s Hospital of Philadelphia. Id. He is board-

certified in pediatrics, psychiatry, and neurology with special competence in child neurology and

electric diagnostic medicine. Id.; Tr. 276. His CV, which appeared to have been created in 1999

and was filed in 2005, indicated that he was licensed in Pennsylvania and Georgia. Exhibit J at

2.

Dr. Sladky has been a part of the faculty at Emory University School of Medicine since

1995. He has been the chief of the Division of Pediatric Neurology, as well as a professor in the

departments of pediatrics and neurology. Exhibit J at 2, 3.

4

At the hearing, Dr. Sladky explained what his duties at Emory were. He stated that he

spends half of his time teaching and the other half performing clinical work. He “see[s] patients

every week, usually five half days a week, probably [an] average [of] 40-50 patients a week.”

Tr. 275. His teaching duties involve giving clinical lectures to medical students, residents, and

fellows. Tr. 276. At the hearing, Mr. Contreras did not challenge Dr. Sladky’s qualifications,

Tr. 278, and he was accepted as an expert in pediatric neurology. Tr. 278.

During the pendency of this decision on remand, the Secretary filed a status report

to disclose to the court . . . [that the Secretary] ha[d] become aware

that Dr. Sladky agreed not to practice medicine in the [S]tate of

Georgia from August 19, 2008 to March 18, 2009, and agreed to

the indefinite suspension of his license to practice medicine on

June 17, 2009, and that on March 4, 2010, the suspension of his

license was lifted and his license to practice restored on a

probationary basis. The probation was terminated on July 5, 2011.

Resp’t’s Status Rep’t, filed May 1, 2013, at 1. Dr. Sladky’s license had been suspended and he

had been placed on probation due to alcohol abuse problems. See id. at 4. The Secretary

attached supporting documentation to her status report to verify the dates during which Dr.

Sladky’s license had been suspended and he had been on probation. Neither the parties nor their

counsel were aware that Dr. Sladky’s license had been suspended or that he had been on

probation when he had provided expert witness services during the course of this proceeding.

After the Secretary disclosed these facts about Dr. Sladky’s licensing, Mr. Contreras filed

a status report, arguing that Dr. Sladky’s testimony should “carry little, if any weight, due to the

circumstances under which he was providing testimony.” Pet’r’s Status Rep’t, filed May 10,

2013, at 9. Mr. Contreras also indicated that Dr. Sladky’s CV inaccurately stated that he was

licensed in Pennsylvania, although that license had expired in 1996. See id. at 4, 15.

The thrust of Mr. Contreras’s argument is that Dr. Sladky’s testimony is unreliable

because he had an alcohol problem3 at all relevant times, he misled the court in describing his

clinical research and job responsibilities at Emory University when he testified at the hearing,

and he violated the terms of his probation by testifying. Id. at 3, 7. Mr. Contreras asserted that

Dr. Sladky’s substance abuse problems implicated “his physical condition as well as intellectual

processing ability” and his license suspension and probation led him to testify on behalf of the

Secretary for financial reasons. Id. at 9-10.

Pursuant to the parties’ agreement reached at a status conference held on May 20, 2013,

the Secretary filed a response to Mr. Contreras’s arguments regarding Dr. Sladky. See Order,

3

Mr. Contreras stated that Dr. Sladky suffered from an additional problem. However,

there is nothing in the record to support this assertion.

5

filed May 20, 2013; Resp’t’s Br. on Remand, filed June 12, 2013. The Secretary argued that Dr.

Sladky’s licensure issues did not affect the validity or value of his opinions.

First, the Secretary asserted Dr. Sladky did not misrepresent the nature of his professional

responsibilities at Emory University when he testified at the hearing. Resp’t’s Br. on Remand at

37. The Secretary noted that Dr. Sladky’s license suspension had been removed prior to the

hearing and asserted that Mr. Contreras has no evidence to demonstrate that Dr. Sladky’s

testimony regarding his professional responsibilities at Emory University was untrue or

misleading. Id. Second, the Secretary suggested that Mr. Contreras’s argument that Dr.

Sladky’s testimony was financially motivated should be stricken from the record because it is

“disingenuous.” Id. at 37-38. The Secretary pointed out that Dr. Sladky’s opinion in this matter

had been consistent since 2005, years before he had any licensure issues, and Mr. Contreras has

no basis to argue Dr. Sladky’s income had been affected by his licensure issues. Id. Finally, the

Secretary asserted that Mr. Contreras has no evidence to demonstrate that Dr. Sladky’s testifying

in this matter violated the terms of his probation. Id. at 38. For these reasons, the Secretary

argued that Dr. Sladky’s undisclosed licensure issues should not affect the evidentiary weight of

his opinions. Id. at 39.

Mr. Contreras responded to the Secretary’s arguments in his reply brief on remand. See

Pet’r’s Reply Br. on Remand, filed Aug. 13, 2013, at 31-34. Mr. Contreras indicated that the

Secretary did not respond to four issues regarding Dr. Sladky that he mentioned in his May 10,

2013 status report. Id. at 31-32. Mr. Contreras pointed out that the Secretary did not explain

why Dr. Sladky: (1) failed to disclose his licensure issues; (2) did not indicate in his CV that his

Pennsylvania license had been inactive since 1996; (3) worked on his March 4, 2010 report,

when his license was suspended; and (4) worked on other cases within the Program when his

license was suspended and when he was on probation. Id. Mr. Contreras argued that “Dr.

Sladky’s lack of transparency and untruthfulness . . . bear on his bias and character critically

undermining his credibility as an expert.” Id. at 34. Mr. Contreras concluded that these issues

with Dr. Sladky’s licensure should “result in [Dr. Sladky’s] testimony being scrutinized and

given diminished importance.” Id.

As the Secretary correctly pointed out, Dr. Sladky’s opinion has been consistent since his

initial report, filed on October 27, 2005, which predates any licensure issue by almost three

years. See Exhibit I. In that report, Dr. Sladky opined that Mr. Contreras’s injury “was, almost

certainly, transverse myelitis.” Id. at 2. He opined that the onset of Mr. Contreras’s transverse

myelitis within 24 hours after his vaccinations was “purely coincidental” because it would be

“virtually impossible” for a vaccine to trigger “an immunological attack on the nervous system…

within a 24 hour interval.” Id. at 3. He claimed that such a process would take at least five days.

Id. Further, he disputed whether the hepatitis B vaccine can cause transverse myelitis. Id. at 4.

As to the dates when Dr. Sladky was working as an expert, Mr. Contreras has not

established that a suspension of a license to practice medicine means that the person may not

provide opinions based upon the person’s training and experience. Dr. Sladky’s writing of a

report in this case did not entail him seeing Mr. Contreras as a patient.

6

With regard to his Pennsylvania licensure, Dr. Sladky’s CV, which was prepared in 1999,

contained an error because his license expired in 1996. See exhibit J at 1. Whether this error

occurred due to forgetfulness or due to intent is difficult to say. At the hearing, Dr. Sladky did

not state that he was licensed to practice medicine in Pennsylvania. In fact, he was not asked

where he was licensed at the time.

The Secretary does not dispute that Dr. Sladky should have disclosed the information

concerning his health issues and the effect they had on his ability to practice medicine. The

failure to disclose this important information bears on his credibility and reliability as an expert

witness. See Mousseau v. Schwartz, 756 N.W.2d 345, 360 (S. D. 2008); George L. Blum,

Annotation, Propriety of questioning expert witness regarding specific incidents or allegations of

expert's unprofessional conduct or professional negligence, 11 A.L.R.5th 1 (1993).

However, the lack of disclosure and (implicit) misrepresentation about qualifications

does not entirely negate Dr. Sladky’s opinion. Dr. Sladky established his opinion almost three

years before his license was suspended and it has not changed throughout the course of these

proceedings. As the Secretary asserted, it does not appear that Dr. Sladky’s personal health

issues or his licensure problems affected his opinions in any way. In addition, Dr. Sladky’s

opinions are consistent with the opinions of other witnesses. This corroboration shows that Dr.

Sladky’s opinions retain some value.4

7. Dr. Whitton

Dr. Whitton testified for the Secretary as an expert in immunology. Dr. Whitton

submitted four expert reports (exhibits L, N, U, and BB) and testified at the April 20, 2010 and

July 28, 2011 hearings. Tr. 405, 621. Dr. Whitton received his bachelor’s degree in molecular

biology, his medical degree, and his Ph.D. from the University of Glasgow, Scotland. Exhibit M

at 1. He does not treat patients in the United States and is not licensed to practice medicine in

the United States. See Opinion and Order, 107 Fed. Cl. at 286 n.14. He has held a number of

professorships and professional positions in the field of immunology. He has substantial

research experience and has published extensively in the fields of immunology and virology.

Exhibit M at 1-12. Since 2008, he has been a professor at Scripps Research Institute in the

Department of Immunology and Microbial Science. Id. at 1.

B. Overview of Transverse Myelitis and Guillain-Barré Syndrome

As explained below, there is universal consensus that Mr. Contreras suffered from

transverse myelitis. All of the doctors who treated Mr. Contreras diagnosed him with transverse

myelitis. The doctors whom Mr. Contreras retained for this litigation diagnosed him with

4

As discussed more extensively below, one of the issues is diagnosis. On this topic, Dr.

Sladky’s opinion matches the diagnosis of Mr. Contreras’s treating neurologist. Another issue

concerns the effect, if any, of the vaccinations. On this topic, Dr. Sladky’s opinion is similar to

Dr. Whitton’s opinion.

7

transverse myelitis. The doctors whom the Secretary retained for this litigation also diagnosed

him with transverse myelitis.

The complicating factor is that some treating doctors initially considered the possibility

that Mr. Contreras suffered from another disease, GBS. Mr. Contreras’s specially retained

doctors advanced the position that Mr. Contreras suffered from both transverse myelitis and

GBS. However, one of the doctors retained by the Secretary disagreed and opined that Mr.

Contreras never suffered from GBS and suffered from transverse myelitis only.

Because there is no dispute that Mr. Contreras suffers from transverse myelitis, transverse

myelitis is described first in section 1. The following section discusses GBS. Finally, section 3

presents some information about how these two diseases are caused. The section on etiology is

relatively brief because the analysis of whether vaccines can cause these conditions is discussed

in greater detail in section V.B.

1. Transverse Myelitis

Transverse myelitis is an autoimmune condition in which inflammation causes damage to

the spinal cord. See Tr. 125, 315, 414. The clinical presentation often develops suddenly and is

usually marked by bladder and bowel problems, a loss of movements in the legs, and numbness.

See exhibit N, tab 2 (Douglas A. Kerr & Harold Ayetey, Immunopathogenesis of Acute

Transverse Myelitis, 15(3) Current Opinion in Neurology 339 (2002)) at 339-40. “Back and

sometimes radicular pain are often the first symptoms.” Exhibit 29 (L. Reik, Jr., Neurological

complications of immunization, 2 Neurological Infections & Epidemiology 69 (1997)) at 75.

“Although all functions of spinal cord may be disturbed, different degrees of disability occur. It

has been observed that functional recovery depends much on the clinical presentation; an abrupt

and severe onset usually pointing to a poorer prognosis.” Exhibit 16 (Luiz Fernando Fonseca et

al., Early-Onset Acute Transverse Myelitis Following Hepatitis B Vaccination and Respiratory

Infection, 61 Arq Neuropsiquiatr 265 (2003)) at 1-2. Magnetic resonance imaging (MRI) of the

spine is used to diagnose transverse myelitis and will show evidence of acute inflammation.

Exhibit N, tab 2 (Kerr & Ayetey) at 340.

What causes transverse myelitis is generally not known. Exhibit N, tab 2 at 339 (stating

that for acute transverse myelitis “[i]t is unclear what are the triggers and effector mechanisms”).

One article suggest that transverse myelitis can be caused by “a direct infection, a systemic

disease or an autoimmune (post-infectious or post-vaccinal) process.” Exhibit 16 at 3.

Patients with transverse myelitis are usually prescribed steroids. Exhibit 29 at 76. They

are also often treated with intravenous immunoglobulin (IVIG). See Tr. 185.

2. Guillain-Barré Syndrome

Guillain-Barré Syndrome is “an immune-mediated peripheral nervous system . . . disease

that results in a direct destruction of the myelin sheath or the axon itself.” Exhibit L, tab 12

(Ami Schattner, Consequence of coincidence? The occurrence, pathogenesis and significance of

autoimmune manifestations after viral vaccines, 23 Vaccine 3876 (2005)) at 3879. It is a disease

8

that is “usually manifested by a rapidly evolving symmetric and ascending motor paralysis, with

loss of tendon reflexes.” Exhibit L, tab 22 (M. Khamaisi et al., Guillain-Barré syndrome

following hepatitis B vaccination, 22 Clinical & Experimental Rheumatology 767 (2004)) at 767.

Individuals afflicted with GBS present

with paresthesias of the feet, followed by flaccid paralysis of the entire lower limbs,

ascending to the trunk, upper limbs, and face; other characteristics include slight fever,

bulbar palsy, absent or lessened tendon reflexes, and increased protein in the

cerebrospinal fluid without a corresponding increase in cells.

Dorland’s Illustrated Medical Dictionary (32d ed. 2012) (Dorland’s) at 1832. GBS “is diagnosed

by clinical symptoms, such as progressive muscle weakness and loss or decreased level of deep

tendon reflex.” Exhibit L, tab 10 (Tetsuo Nakayama & Kazumasa Onoda, Vaccine adverse

events reported in post-marketing study of the Kitasato Institute from 1994 to 2004, 25 Vaccine

570 (2007)) at 572. The disease “progresses for up to 4 weeks and then reaches a plateau.”

Exhibit N, tab 7 (Richard A.C. Hughes & Jeremy H. Rees, Clinical and Epidemiologic Features

of Guillain-Barré Syndrome, 176 J. Infectious Diseases S92, S92 (1997)). Patients with GBS are

often treated with, among other things, IVIG. See exhibit 111 (R.A.C. Hughes et al., Practice

parameter: Immunotherapy for Guillain-Barré syndrome, 61 Neurology 736 (2003)) at 737-39;

see also Tr. 184.

3. Etiologies for Autoimmune Diseases

As mentioned, both transverse myelitis and GBS are categorized as autoimmune diseases.

The basis for an autoimmune disease is a malfunction in the immune system.

A healthy immune system protects the body. Cells in the immune system circulate

throughout the body, examining molecules to determine whether the molecule is part of the body

(self) or is foreign to the body (an antigen). This determination is made by examining specific

sequences of a few amino acids, known as a peptide. When a patrolling cell of the immune

system identifies a foreign peptide, this cell recruits other parts of the immune system to destroy

the foreign antigen. Tr. 127-30; exhibit 63 (Lawrence Steinman, Autoimmune Disease:

Misguided Assaults on the Self Produce Multiple Sclerosis, Juvenile Diabetes and Other Chronic

Illnesses. Promising Therapies Are Emerging, Scientific Amer. 107 (1993)) and exhibit 143

(extract from exhibit 63). The destructive part of the adaptive immune system is divided into

two types of cells: B cells (also known as antibodies) and T cells.

However, the B cells and T cells can deviate from their normal function by attacking their

host. This produces autoimmune diseases, such as transverse myelitis. Tr. 124-25.

Molecular mimicry is an attempt to explain why the immune system goes awry. It posits

that an antigen contains a sequence of amino acids that resembles (or mimics) a sequence of

amino acids that is similar to a sequence of amino acids normally present in the host. When the

immune system responds to the antigen, the destructive T cells mistakenly are directed against

the body’s own tissue.

9

To this basic outline about molecular mimicry, Dr. Whitton provided additional details.

Dr. Whitton explained that multiple steps comprise molecular mimicry. Dr. Whitton stated:

If the vaccine-induced T cells are to have caused disease, the

following must have happened. (i) The vaccine was injected at a

peripheral site (arm/leg). (ii) The vaccine antigens were carried to

a lymph node; (iii) in the node, the memory T cells (induced by the

previous vaccinations . . .) must have (iv) recognized the antigen,

(v) divided and (vi) moved to the sites where disease occurred, in

this case the cervical spinal cord (to cause transverse myelitis), and

some peripheral nerves (to cause GBS-like disease). . . . Once they

reached the sites the T cells would (vii) have to recognize the

putative (but unidentified) cross-reactive antigen, and (viii)

activate their so-called ‘effector functions’ to cause harm to the

nerve cells. And (ix) it seems reasonable to propose that a fairly

large number of T cells would need to accumulate in the spinal

cord / peripheral nerves, in order to cause the serious signs and

symptoms Jessie showed less than 24 hours after vaccination.

Exhibit L at 9. In reference to this sequence of steps, Dr. Steinman testified that “Dr. Whitton is

entirely right.” Tr. 240.5

The antigens that trigger transverse myelitis or GBS are not known. Frequently, viruses

or bacteria, which cause infections, are postulated as a cause for transverse myelitis or GBS.

However, these potential causative agents have not been established. Consequently, the

testifying experts agreed that the cause (or causes) of transverse myelitis is not known in many

cases. Tr. 264, 267, 300, 414.

In this particular case, Dr. Steinman identifies the hepatitis B vaccine as the triggering

antigen and a portion of Mr. Contreras’s spinal cord, known as myelin, as the tissue that is

attacked. Tr. 123-24. The basis and evaluation of Dr. Steinman’s opinion is discussed

throughout section V.

C. Mr. Contreras’s Medical History

The parties do not dispute the accuracy of medical records created contemporaneously

with the events being described in those records. These records are the basis for the following

facts.

Mr. Contreras was born in 1990. For his first 13 years, Mr. Contreras was generally

healthy, see exhibit 3 and exhibit 4, and respondent has not suggested that any early illness

5

In this portion of Dr. Steinman’s testimony, he was also addressing his analogy to the

tuberculin skin test.

10

contributed to his development of the neurological disorder. See Resp’t’s Post-Hearing Br., filed

Nov. 24, 2010. In this time, Mr. Contreras received doses of the diphtheria-tetanus-pertussis

vaccine on May 12, 1990, September 5, 1990, February 12, 1991, January 20, 1993, and

September 2, 1994. Exhibit 4 at 5, 7-9; petition, filed June 15, 2005, at ¶¶ 5-9. He did not

experience any adverse reaction to these five doses. Similarly, Mr. Contreras received two doses

of the hepatitis B vaccine (the first on January 23, 2001, and the second on August 23, 2001)

without any adverse reaction.

On June 16, 2003, Mr. Contreras saw his pediatrician, Dr. Fred Kyazze, for a routine

examination during which he was given a hepatitis B vaccination and a tetanus-diphtheria

vaccination. Exhibit 4 at 5, 44. This was the sixth time that Mr. Contreras had encountered

some form of the tetanus-diphtheria vaccine and the third dose of the hepatitis B vaccine. Dr.

Kyazze administered the vaccinations at approximately 10:30 A.M.

Shortly before noon on June 17, 2003, Mr. Contreras started crying and told his mother

that he felt bad. He complained that his hands were numb and that he had “a strong pain in his

back.” Tr. 15-16. After Mr. Contreras’s mother reported these problems to his pediatrician, she

was instructed to take her son to the nearest emergency room, which was Memorial Hospital of

Gardena in Gardena, California. Exhibit 8 (affidavit of Rosa Contreras) ¶ 26.

When Mr. Contreras left his home for the emergency room with his parents, he walked to

his family’s car without assistance. During the car trip, he could not maintain his balance and his

mother moved from the front seat to the rear seat to help him. When the family arrived at the

emergency room, Mr. Contreras vomited in the parking lot twice. His mother and father carried

him to the emergency room because he could not walk. Tr. 17.

In the emergency room, Mr. Contreras was seen by Mark Wagner, who testified at the

hearing in this case. Dr. Wagner is board-certified in emergency medicine. Dr. Wagner noted

that Mr. Contreras had weakness in his arms and legs, was retaining urine, and had priapism.

Exhibit 6 at 5-10; see also Tr. 82. A computed tomography (CT) scan of his head and cervical

spine was normal. A MRI of his cervical spine was also normal. Exhibit 6 at 15-18. An MRI of

his chest was negative. Exhibit 6 at 14. Dr. Wagner’s physical examination showed that Mr.

Contreras’s sense of light touching was altered. Id. at 10. Dr. Wagner also testified that Mr.

Contreras’s foot turned downward in response to a Babinski test he performed on Mr. Contreras

on June 17, 2003. Tr. 78 (citing exhibit 6 at 10).6

6

Dr. Steinman explained that one part of a neurologic examination, a Babinski test,

involves running a sharp metal object along the lateral side of the patient’s foot to observe how

their big toe responds. Tr. 121; see also Dorland’s at 1611.

The experts disagreed about the significance of the results of the Babinski test. Dr.

Steinman stated that Mr. Contreras’s turning his toes downward meant that he had GBS. Tr.

121. But, Dr. Sladky disagreed with Dr. Steinman’s opinion that the results of Mr. Contreras’s

Babinski reflex test were indicative of GBS. Tr. 283.

11

Dr. Wagner stated at the time of treatment that Mr. Contreras could have atypical GBS,

transverse myelitis, and priapism. Exhibit 6 at 5, 10; Tr. 84. When Dr. Wagner treated Mr.

Contreras on June 17, 2003, Dr. Wagner did not offer any opinion as to the cause of Mr.

Contreras’s problems. See exhibit 6. Later, Dr. Wagner offered the opinion in this litigation that

the hepatitis B vaccine caused Mr. Contreras’s neurological problem. Tr. 89-92.

After remaining in Gardena Memorial Hospital for approximately two-and-a-half hours,

Mr. Contreras was transferred by ambulance to a higher care facility, Long Beach Memorial

Hospital, which is also known as Miller Children’s Hospital. Exhibit 6 at 5. Mr. Contreras

remained in this facility until he was discharged on September 11, 2003. Exhibit 13 at 3, ¶ 5.

The history at Miller Children’s Hospital taken at admission, exhibit 7 at 6, is consistent with the

facts set forth above.

When Mr. Contreras arrived at Miller Children’s Hospital, the admitting doctor was

Christopher Babbitt.7 Among the first orders given by Dr. Babbitt was a request that Dr. Jean

Lake, a neurologist, see a 13-year-old with “weakness and ? Guillain Barre.” Exhibit 7 at 1377.8

Dr. Lake saw him approximately two hours later, which was 8:00 P.M.

Dr. Lake’s handwritten notes are generally consistent with the history described above.

Dr. Lake recorded that Mr. Contreras “denies any recent infections or fever. He did have dt and

hepatitis B vaccine yesterday.” Dr. Lake also conducted a neurologic and physical examination.

As part of this examination, Dr. Lake recorded that Mr. Contreras’s “plantar reflexes [were]

↓↓.”9 Dr. Lake noted that Mr. Contreras’s CT scans and MRI at Gardena were negative. See

exhibit 7 at 1735. Her impression was “probable atypical Gullain-Barré.” Exhibit 7 at 1735.

The differential diagnoses included “ADEM [and] transverse myelitis (though there are no

sensory abnormalities). MS is also a possibility, though unlikely [with] this clinical

presentation.” Dr. Lake ordered a lumbar puncture as well as MRIs of the brain and complete

spine. Dr. Lake also ordered “IVIG tonight [and] tomorrow [with] total dose 2 gm/kg. Though I

would prefer plasmapheresis,[10] I spoke tonight [with] Dr. Brachenburg from the Blood Bank

who stated this could not be arranged before tomorrow as we use an outside service. I prefer not

to wait until tomorrow to begin treatment given the rapid progression of his neurologic deficit.”

Exhibit 7 at 1727-28, 1734-35.

7

It appears that Dr. Babbitt was the resident initially in charge of Mr. Contreras’s care.

Dr. Garrett was the attending physician. Exhibit 7 at 157.

8

Entries from Miller Children’s Hospital are typically made in all capital letters. In this

decision, the capitalization is eliminated without further notation.

9

Plantar reflexes are “contraction of the toes when the sole of the foot is irritated; cf.

Babinski r.” Dorland’s at 1614.

10

Plasmapharesis is “the removal of plasma from withdrawn blood, with retransfusion of

the formed elements of the donor . . . The procedure may be done for purposes of collecting

plasma components or for therapeutic reasons.” Dorland’s at 1456.

12

Before the results from the MRIs were obtained, Dr. Garrett indicated that both GBS and

transverse myelitis were possible diagnoses. He stated that the critical care team was working

with Dr. Lake, the neurologist, and was implementing her orders. Id. at 136.

A series of MRIs was performed the following morning. The MRI for the brain was

unremarkable. Exhibit 7 at 176. MRIs of Mr. Contreras’s cervical, thoracic, and lumbar spine

revealed an “extensive abnormal signal intensity noted in the cervical spinal cord. . . . The

abnormality extends from the C2-3 interspace down to about C7. . . . Following gadolinium,

there is no significant enhancement.” The radiologist interpreting the image, Scott Lipson, stated

that “[t]his appearance is not suggestive of Guillain-Barre syndrome and more likely represents

an entity such as transverse myelitis.” The results were discussed with Dr. Lake. Exhibit 7 at

167-71, 177-78.

Dr. Lake recorded information about the MRI when she saw Mr. Contreras at 1:45 PM on

June 18, 2003. Dr. Lake stated that a “high signal [in the] cervical cord [was] [consistent with]

transverse myelitis.” Her impression was “? Transverse myelitis of cervical cord.” She

recommended completing the IVIG and starting solumedrol and prednisone.11 Exhibit 7 at 1723.

In the afternoon of June 18, 2003, Dr. Babbitt dictated a progress note about Mr.

Contreras’s history of approximately 24 hours in the hospital. Dr. Babbitt reported that Mr.

Contreras received a second dose of IVIG today and the neurology service started him on “solu-

medrol / prednisone.” Dr. Babbitt also stated that it was “unclear . . . whether he has transverse

myelitis versus a [GBS] . . . type syndrome or even multiple sclerosis.” Id. at 131.

Mr. Contreras was seen by Dr. Kimberly Bedell, who led his pediatric rehabilitation team

throughout his lengthy hospitalization, on June 18, 2003. Exhibit 7 at 139-41. Her report is

similar to Dr. Babbitt’s report. Dr. Bedell recounted that the MRI of Mr. Contreras’s cervical

spine was “consistent with transverse myelitis. The patient will be completing IVIG treatments

and will be started on intravenous steroids.” Exhibit 7 at 139. In Dr. Bedell’s review of

symptoms, she recorded “Downgoing Babinski bilaterally.” Id. at 140.

On June 19, 2003, Mr. Contreras had difficulty breathing and required “emergent

intubation.” Dr. Babbitt’s report from this date also indicated that Mr. Contreras’s disease “is

now thought to be transverse myelitis.” Id. at 129.

During the early portion of Mr. Contreras’s hospitalization, his doctors referred to the

shift in diagnosis. For example, on June 22, 2003, Dr. Babbitt stated Mr. Contreras “receive[d]

two doses of IV IG when we were entertaining the diagnosis of atypical Guillain-Barre. Based

on his markedly abnormal MRI, his diagnosis seems much more consistent with transverse

myelitis.” Id. at 123. Earlier, an infectious disease specialist, Dr. Michele Cheung, stated Mr.

11

Prednisone is “derived from cortisone [and is] administered orally as an anti-

inflammatory and immunosuppressant in a wide variety of disorders.” Dorland’s at 1509.

13

Contreras “received intravenous immunoglobulin for presumed Guillain-Barre syndrome, but

then a repeat MRI scan at our facility showed abnormal signal in the cervical spine from about

C2 through C7 and he was then given solu-medrol for a possible transverse myelitis.” Id. at 145-

47.

In the course of recording Mr. Contreras’s history, Dr. Cheung noted that he had received

his “third hepatitis-B vaccination and his tetanus booster on June 16, 2003.” Mr. Contreras’s

parents were “very concerned that a vaccine may have caused this illness.” Id. at 145. Dr.

Cheung accepted that transverse myelitis was the appropriate diagnosis for Mr. Contreras and

she noted “[i]t is often very difficult to find the exact cause of transverse myelitis, although many

cases are preceded by upper respiratory or gastrointestinal symptoms.” Dr. Cheung listed many

possible antecedent infections but added that Mr. Contreras “has no other real exposures for any

other types of infections.” Id. at 147.

Dr. Cheung intended to address the parental concern about vaccinations. She reviewed

the literature. She found no causal association. She explained:

although there have been case reports associating hepatitis-B

vaccine in particular (and also some with tetanus) with central

nervous system problems and demyelinating diseases, there is no

proof of causation and several cohort studies have suggested that

there is no increased incidence following vaccination. In addition,

the onset of [Mr. Contreras’s] symptoms was quite rapid following

the vaccination and other case reports have suggested a slightly

longer latency prior to the actual onset of neurological symptoms.

Exhibit 7 at 147. Dr. Cheung concluded that she had “arranged an appointment with [Mr.

Contreras’s] parents . . . to discuss the infectious etiologies of transverse myelitis and the lack of

evidence supporting a causal link with the hepatitis-B vaccine.” Id.

Two days later, Dr. Babbitt commented upon the potential causative role of the vaccines.

Dr. Babbitt stated that “[t]he family has been distraught over his underlying condition and the

association of his problem with vaccines. We have tried to put them at ease, unfortunately we

cannot tell them whether or not this was in fact caused by his hepatitis vaccine. There is no clear

medical literature to support anything other than association. I have told the family this as has

Dr. Lake and Dr. Ch[e]ung.” Exhibit 7 at 126. The next day, Dr. Garrett stated “we will also

make sure that the infectious disease service reports to the hepatitis B vaccination distributor the

fact that the patient probably contracted or potentially contracted the transverse myelitis

secondary to the hepatitis B vaccine.” Id. at 106. After this point, although some doctors

accurately stated that the vaccinations occurred before the onset of Mr. Contreras’s neurological

problems, see, e.g., exhibit 7 at 142, the doctors did not opine that the vaccinations caused the

neurologic problem.

Following June 19, 2003, the doctors consistently identified Mr. Contreras’s neurologic

problem as transverse myelitis. Dr. Lake continued to see Mr. Contreras on an almost daily basis

during his hospitalization and consistently considered him to be suffering from transverse

14

myelitis only. See, e.g., exhibit 7 at 16, 1554, 1612, 1627, 1633, 1676, 1698, 1711, 1712, 1714.

Another neurologist, whose signature is illegible, considered Mr. Contreras to be suffering from

transverse myelitis only. See exhibit 7 at 1694-95.

Dr. Garrett frequently stated Mr. Contreras suffered from transverse myelitis. See, e.g.,

exhibit 7 at 99, 101, 103, 107, 121. Furthermore, Mr. Contreras had numerous treating

physicians during and after his hospitalization, many of whom saw him on an almost daily basis,

who consistently opined—for months—that he suffered from transverse myelitis only. See, e.g.,

exhibit 7 at 177-78 (Dr. Scott Lipson, radiologist, on June 18, 2003), 123-24 (Dr. Babbitt on June

22, 2003), 142-44 (Dr. Sarah Sela-Herman, pediatric gastroenterologist, on June 30, 2003), 149

(Dr. Ayal Willner, otolaryngologist, on July 2, 2003), 219 (Dr. Nina Yoshpe, surgeon, July 3,

2003), 147 (Dr. Michele Cheung, infectious disease specialist, on July 7, 2003), 87-88 (Dr.

Maria Elena Imperial on July 13, 2003), 115-16 (Dr. Graham Tse on July 16, 2003), 65-66 (Dr.

Stephen Treiman on July 24, 2003), 61 (“team conference” on July 30, 2003 with, among others,

Dr. Kimberly Bedell and Dr. Jennifer Davidson), 51 (“team conference” on August 20, 2003

with, among others, Dr. Bedell and Dr. Davidson), 154-56 (Dr. Richard Mathis, pediatric

gastroenterologist, on August 25, 2003), 47-50 (“team conference” on September 3, 2003 with,

among others, Dr. Kimberly Bedell and Dr. Jennifer Davidson).

Despite the apparent universal acceptance of the transverse myelitis diagnosis, the

doctors at Miller Children’s Hospital did not ever identify a cause of the transverse myelitis.

They ordered many laboratory tests looking for evidence of an infectious agent. “[A]ll testing

and evaluation for these specific causes,” as Dr. Garrett later averred in his affidavit, “was

unrevealing.” Exhibit 13 at 7.

Mr. Contreras’s condition worsened for approximately five days following his admission

to Miller Children’s Hospital. Among the problems he experienced were quadriplegia, acute

respiratory failure, neurogenic bladder, acute cystitis, and priapism. Exhibit 13 ¶ 10; see also

exhibit 7, passim, especially pages 6-8 (discharge summary).

Fortunately, Mr. Contreras improved. In early July 2003, he started to make some small

movements with his hands and feet. He began to eat orally on July 17, 2003. He was transferred

to a rehabilitation facility on July 30, 2003. He was discharged on September 11, 2003, and by

that date, Mr. Contreras could feed himself finger foods, dress himself with some assistance, and

walk 150 feet with a platform walker.

At Mr. Contreras’s follow-up appointment in October 2003, Dr. Luis Montes recounted

the change in diagnosis. Exhibit 80 at 31 (“initially the patient was felt to have [GBS] . . . [but]

[a]s the symptoms progressed, the diagnosis was later changed to transverse myelitis.”). He was

hospitalized again for two weeks in November 2003 for inpatient rehabilitation. Again, his

admission and discharge diagnoses were transverse myelitis. Exhibit 79 at 204-06.

Dr. Lake also examined Mr. Contreras during follow-up visits on November 2, 2004,

February 1, 2005, and June 7, 2005. See exhibit 82 at 1-5. Her opinion from all three

examinations was that Mr. Contreras suffered from transverse myelitis only. See id. at 1, 3, 5.

15

Mr. Contreras’s treating physicians who cared for him well after his hospitalization also

stated he suffered from transverse myelitis only. See, e.g., exhibit 80 at 10 (Dr. Luis Montes on

Mar. 22, 2005), exhibit 95 at 47 (Dr. Jane Donat, neurologist, on August 17, 2006).

At the time of the hearing in Los Angeles, California, in 2010, Mr. Contreras described

himself as having average health. He reported that he could walk, but not for long periods of

time. Tr. 39; see also Opinion and Order, 107 Fed. Cl. at 285 (describing Mr. Contreras’s

condition at time of hearing).

III. Procedural History

There are two broad periods for the procedural history, separated by the April 5, 2012

Entitlement Decision. The more remote history is set forth to provide a context for the Court’s

September 28, 2012 Opinion and Order.

A. Events before the Court’s Opinion and Order

There are four phases here: first, the early development of the case, second, the parties’

submissions before the hearing and the hearing itself, third, the parties’ post-hearing briefs, and

fourth, the April 5, 2012 Entitlement Decision. Since many of these events were detailed in the

April 5, 2012 Entitlement Decision and the Opinion and Order, 107 Fed. Cl. at 285-90, they are

presented more summarily in the following sections.

1. Early Development

Mr. Contreras filed a petition12 on June 15, 2005, in which he alleged that the hepatitis B

and Td vaccines he received on June 16, 2003, caused him to develop transverse myelitis and

GBS by June 17, 2003, approximately 24 hours after his vaccinations. Early submissions from

Mr. Contreras included medical records, affidavits from Dr. Kyazze (exhibit 11), Dr. Wagner

(exhibit 12), and Dr. Garrett (exhibit 13). Mr. Contreras also submitted two reports from Dr.

Poser. Exhibits 22 and 23.

The Secretary filed her Rule 4 report on October 7, 2005, in which she indicated that Mr.

Contreras was not entitled to compensation. The Secretary asserted that the evidence did not

support a finding that either the Td or the hepatitis B vaccine can cause a demyelination

condition, such as transverse myelitis or GBS. Resp’t’s Rep’t at 9. The Secretary also asserted

that, even if a vaccine could cause a demyelinating condition, it could not have done so within 24

hours of vaccination, as Mr. Contreras alleges occurred. Rather, the Secretary maintained that “a

plausible interval between vaccination and the onset of symptoms is 5-45 days.” Resp’t’s Rep’t

12

At the time the petition was filed, Mr. Contreras’s parents represented him because he

was a minor. The case caption was amended to designate Mr. Contreras as the sole petitioner

because he had reached the age of majority. See Order, filed June 26, 2008. For ease of

reference, this decision refers to Mr. Contreras as the petitioner.

16

at 9. The Secretary supported her position with the report of Dr. Sladky, a neurologist whom she

had retained. Exhibit A.

The presiding special master appears to have sought evidence from Mr. Contreras

showing that the timing in this case was medically appropriate. See Order, filed Nov. 18, 2005,

at 2. In response to the special master’s concern, Mr. Contreras obtained a report from another

neurologist, Dr. Lawrence Steinman. Exhibit 55.13 The parties explored settlement but did not

succeed.

Because the parties’ settlement discussions, including alternative dispute resolution with

another special master, were unsuccessful, the Secretary filed expert reports in support of her

position. The Secretary filed three expert reports from Dr. J. Lindsay Whitton, exhibits N, U,

and BB, and a supplemental report from Dr. Sladky, exhibit O. Mr. Contreras also filed a

supplemental report from Dr. Steinman. Exhibit 152.

2. Pre-Hearing Briefs and Hearing

Mr. Contreras submitted a pre-trial brief on March 8, 2010. Mr. Contreras alleged that he

suffered from both transverse myelitis and GBS. Pet’r’s Pre-trial Br., filed Mar. 8, 2010, at 6.

Mr. Contreras indicated that Dr. Poser, Dr. Steinman, and the Secretary’s expert, Dr. Whitton, all

agreed with this dual diagnosis, but noted that the Secretary’s other expert witness, Dr. Sladky,

opined that the correct diagnosis was transverse myelitis. Id. at 6 n.7. Mr. Contreras did not

anticipate the Secretary challenging his assertion that he suffered from both transverse myelitis

and GBS despite Dr. Sladky’s disagreement. Id. at 6.

Mr. Contreras asserted that both the hepatitis B and Td vaccines can cause demyelinating

injuries, including transverse myelitis and GBS. Id. at 7. In support of this proposition, he noted

that two of his treating physicians—Dr. Wagner and Dr. Garrett—opined that his condition was

vaccine-related.14 He also asserted that his two experts, Dr. Poser and Dr. Steinman, provided a

reliable theory of causation. Id. at 8-10.15 According to Dr. Poser and Dr. Steinman, the

approximately 24-hour onset of Mr. Contreras’s symptoms after vaccination is an acceptable

time-frame due, in part, to Mr. Contreras’s genetic makeup and his medical history, namely, his

prior vaccinations. Id. at 12-13.

In her pre-trial brief, the Secretary asserted that Mr. Contreras had failed to present a

reliable theory of causation. Specifically, the Secretary maintained that, regardless of which

13

Mr. Contreras could not rely exclusively upon Dr. Poser because Dr. Poser’s health

prevented him from continuing in the litigation.

14

As discussed in more detail below, Dr. Garrett diagnosed Mr. Contreras with only

transverse myelitis, whereas Dr. Wagner diagnosed Mr. Contreras with atypical GBS and

potential transverse myelitis.

15

The opinions of Dr. Poser and Dr. Steinman are discussed in detail below.

17

disease afflicted Mr. Contreras, neither transverse myelitis nor GBS could have manifested

within 24 hours after vaccination. The Secretary further questioned whether the hepatitis and/or

the Td vaccines could cause demyelinating diseases, including transverse myelitis and GBS.

The parties filed an extensive amount of medical literature. Mr. Contreras attached an

appendix to his pre-hearing brief that provided “short summaries of medical articles referenced

by Dr. Steinman.” Pet’r’s Pre-hearing Br., App’x A, at 1.

At the hearing held on April 19-20, 2010, Dr. Kyazze, Dr. Wagner, and Dr. Steinman

testified on behalf of petitioner. Dr. Garrett and Dr. Poser were unable to testify. Dr. Whitton

and Dr. Sladky testified on behalf of respondent. At the hearing held by videoconference on July

28, 2011, Dr. Steinman testified on behalf of petitioner and Dr. Whitton testified on behalf of

respondent.

3. Post-Hearing Briefs

The parties each submitted two post-hearing briefs. The parties disputed whether Mr.

Contreras suffered from just transverse myelitis or both transverse myelitis and GBS. Mr.

Contreras asserted that he suffered from both transverse myelitis and GBS. The Secretary

maintained that the correct diagnosis was only transverse myelitis. However, the parties agreed,

albeit for different reasons, that a determination of what afflicted Mr. Contreras was irrelevant to

the outcome of this matter.

Mr. Contreras asserted that whether he suffered from transverse myelits or GBS or both

“should not [a]ffect the outcome of the case since the testimony is that the cause of each disease

was the vaccines administered.” Pet’r’s Post-Hearing Br., filed Aug. 23, 2010, at 15. The

Secretary argued that “[w]hether [Mr. Contreras’s] neurodemyelinating condition is TM or GBS

does not change the fact that petitioner has failed to present a reliable medical theory that Hep B

vaccine can cause either condition within 24 hours of administration.” Resp’t’s Post-Hearing

Br., at 5. Thus, according to Mr. Contreras, he asserted that he had satisfied all three Althen

prongs regardless of what disease (or diseases) a preponderance of the evidence indicated

afflicted him. Likewise, the Secretary argued that Mr. Contreras did not satisfy any of the

Althen prongs even if he suffered from transverse myelitis and GBS.

Mr. Contreras also attached an appendix to his post-hearing brief that summarized the

medical literature on which Dr. Garrett, Dr. Poser, and Dr. Steinman relied. Pet’r’s Post-hearing

Br., App’x A, at 1. Mr. Contreras indicated that these summaries were “written by lay

individuals.” Pet’r’s Pre-hearing Br., App’x , at 57-80. (Although Mr. Contreras did not

indicate that the summaries contained in the appendix to his post-hearing brief were written by

lay individuals, the undersigned assumes that they were.) The undersigned agrees with Mr.

Contreras that the summaries are “not a substitute for review of the article itself and expert

opinion as to its content,” id. at 1 n.1, and has reviewed the entirety of the record, but this

decision focuses on the articles discussed most extensively by the experts in their testimony and

the parties in their briefs.

18

4. Entitlement Decision

The Entitlement Decision found that a preponderance of the evidence supported a

diagnosis of transverse myelitis, but not one of GBS. Before the Entitlement Decision, the

parties did not consider a determination of which disease (or diseases) afflicted Mr. Contreras to

be important. Mr. Contreras asserted that he had established entitlement to compensation either

way, and the Secretary argued that neither GBS nor transverse myelitis could manifest in

approximately 24 hours, as Mr. Contreras alleged.

The more important (and decisive) issue was whether Mr. Contreras had established that

a vaccine can cause a demyelinating disease within one day. The Entitlement Decision found

that Mr. Contreras did not meet his burden of proof on this issue. The Entitlement Decision

found Dr. Steinman’s tuberculin test analogy unpersuasive because it was “most importantly”

based on a finding that “the tuberculin reaction occurs in an area not protected by the blood brain

barrier” and a breach of the blood brain barrier would require much more than 24 hours. 2012

WL 1441315, at *19.16 See Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352

(Fed. Cir. 2008) (discussing the need for a medically acceptable temporal relationship between

vaccine and alleged injury). For that reason, Mr. Contreras’s claim failed on Althen prong three

and, consequently, he was not entitled to compensation. Entitlement Decision, at *1, *23-24.

B. Events after the April 5, 2012 Entitlement Decision

Following the April 5, 2012 Entitlement Decision, activities happened in three phases.

The first phase was the motion for review. The second phase was the Court’s Opinion and

Order. The third phase consisted of the events taking place after the remand.

1. Mr. Contreras’s Motion for Review and Associated Briefing

Mr. Contreras filed a motion for review of the Entitlement Decision with the Court on

April 25, 2012. After a timely initial submission, Mr. Contreras submitted a lengthier motion

that developed and expanded his arguments.

Mr. Contreras’s amended motion, although organized differently, presented essentially

three themes. First, Mr. Contreras challenged the finding that he suffered from transverse

myelitis only and not transverse myelitis and GBS. Mr. Contreras argued that determining

16

Although the Court found no error in that analysis, Opinion and Order, 107 Fed. Cl. at

305-06, it directed a reexamination of that finding, id. at 306 n.40, because the experts’

testimony “regarding the blood brain barrier and the central nervous system . . . gains much

greater importance if the diagnosis of GBS, a disease of the peripheral nervous system, is not

applicable to [Mr. Contreras].” Id. at n.21. As discussed in section V.A below, a preponderance

of the evidence indicates that Mr. Contreras suffered from transverse myelitis, not GBS.

Accordingly, Dr. Steinman’s tuberculin test analogy is not persuasive for the reasons discussed

in the Entitlement Decision. 2012 WL 1441315, at *19.

19

whether he suffered from transverse myelitis and GBS was a significant issue because “the dual

diagnosis . . . demonstrates the uniqueness of [Mr. Contreras].” Pet’r’s Mot. for Review, filed

May 4, 2012, at 20. Mr. Contreras pointed to aspects of his medical history that, in his view,

support a finding that he suffered from GBS in addition to transverse myelitis. He noted that one

of his treating physicians, Dr. Lake, diagnosed him with atypical GBS. Mot. for Rev., at 23

(citing exhibit 7 at 1735). Dr. Steinman interpreted the results of Mr. Contreras’s Babinski reflex

test to indicate the correct diagnosis was GBS. Dr. Steinman opined that the results of Mr.

Contreras’s spinal fluid examination were indicative of GBS. Mot. for Rev., at 21-22.

The second theme concerned the third prong of Althen, which Mr. Contreras recognized

as “[t]he most contentious issue.” Id. at 31. Mr. Contreras argued the undersigned failed to

consider (or improperly assessed) evidence in the record pertaining to the issue of timing. Mr.

Contreras cited to other decisions where special masters found the petitioner was entitled to

compensation for demyelinating injuries that, according to Mr. Contreras, manifested within 72

hours after vaccination. Id. at 32-34. Mr. Contreras asserted these cases demonstrate that “in

certain ‘unique’ individuals, demyelinating disease (involving the central nervous system) can

occur . . . within twenty four (24) hours.” Id. at 34. Mr. Contreras argued it was a mistake of

law for the undersigned to consider legal authorities outside of the Vaccine Program that hold

case reports hold little probative value for establishing causation. Id. at 36. Mr. Contreras also

argued that the undersigned improperly assessed the value of the evidence concerning Dr.

Steinman’s tuberculin skin test analogy.

Further, Mr. Contreras also asserted the Entitlement Decision applied an unduly high

burden of proof with regard to Althen prong three. Mr. Contreras argued this occurred, in part,

due to the findings regarding the reliability of animal studies and the undersigned’s interpretation

of and reliance on other Program cases. Id. at 45-49. Mr. Contreras argued the Entitlement

Decision applied an incorrect standard by “look[ing] for conclusive or persuasive proof in the

medical literature” that would support Mr. Contreras’s argument that transverse myelitis and

GBS can manifest within 24 hours after vaccination. Id. at 41.

Additionally, Mr. Contreras asserted that his unique genetic makeup and immune system

caused his body to respond to the vaccines differently than the general public might. Id. at 20.

Mr. Contreras claimed that Hispanics, such as himself, respond differently to vaccines than do

individuals from other ethnic backgrounds. Id. at 21. Mr. Contreras asserted that his Hispanic

heritage, as well as his receiving multiple prior hepatitis B vaccines, affected (i.e., accelerated)

the onset of his condition after his subject vaccination. Id. at 20, 24.

The third theme concerned the remaining two Althen prongs. Mr. Contreras asserted it

was legal error to find an analysis of Althen prongs one and two unnecessary on the ground that

he had failed to provide preponderant evidence with regard to Althen prong three. Id. at 39-40.

Mr. Contreras also reiterated his assertion that he had satisfied these Althen prongs. He

maintained that Dr. Steinman’s proposed theory of molecular mimicry satisfied Althen prong

one. Id. at 23-24. Likewise, Mr. Contreras asserted that he met his burden under Althen prong

two through the testimony of his experts and treating physicians. Id. at 30.

20

The Secretary filed a response to Mr. Contreras’s motion on June 4, 2012. The Secretary

argued that the Entitlement Decision applied the correct standard with regard to all three Althen

prongs. Resp’t’s Resp. at 6. The Secretary emphasized that evidence established that 24 hours

after vaccination was an inappropriately short temporal interval for both transverse myelitis and

GBS to manifest according to Mr. Contreras’s proposed theory of molecular mimicry. Id. at 10

The Secretary noted that in his Motion for Review, Mr. Contreras “re-argued the same

evidence that was considered in detail, and ultimately found unpersuasive.” Id. at 2. Thus, the

Secretary asserted that Mr. Contreras “has failed to demonstrate that the special master

committed error[,] . . . rehashes interpretations of the evidence . . . and argues for a legal standard

that is inconsistent with binding Federal Circuit precedent.” Id. at 10. Simply stated, the

Secretary argued that the Entitlement Decision properly weighed all relevant evidence and, in

doing so, committed no legal error. Id. at 14.

Mr. Contreras filed a reply to the Secretary’s response on June 25, 2012. In his reply,

Mr. Contreras addressed the arguments made in the Secretary’s response. He made a number of

discrete objections to the Secretary’s interpretations of the evidence, and criticized the

Secretary’s failing to discuss some of his arguments and evidence.

2. The Court’s Opinion and Order

In its Opinion and Order, the Court discerned five “principal questions” that it had to

resolve in its review of the Entitlement Decision. These questions are whether the undersigned

was permitted to: (1) diagnose petitioner’s illness before proceeding to an analysis of

causation; (2) deny the petition without making findings on all three Althen prongs; (3)

deny the petition without making a finding as to whether petitioner had ruled out

alternative causes of his illness; (4) assign little weight to the opinions of treating

physicians as to Althen prong three; and, (5) require a heightened level of proof as to a

proximate temporal relationship between the vaccinations received and petitioner’s

illness.

107 Fed. Cl. at 282.

The Court held that “all but one of these questions must be answered in the negative.” Id.

The only question on which the Court gave a qualified positive response was the second, which

asked whether Mr. Contreras’s petition was properly denied based on a finding on one Althen

prong. The Court held that it was permissible to deny compensation based on a finding that Mr.

Contreras failed to establish one of the three Althen prongs. Id. at 295. Nevertheless, the Court

stated it was “difficult” to determine if the undersigned had considered all evidence relevant to

that prong. Id. Further, in the interest of judicial economy, the Court ordered the undersigned to

make a finding on all three Althen prongs because the Court considers the case “to be a much

closer call if evidence pertinent to all three Althen prongs is considered.” Id. at 296.

The Court provided a “succinct outline of the legal framework [of the Court’s opinion]

for utilization by the [undersigned]” on remand. Opinion and Order, 107 Fed. Cl. at 308. This

21

outline contains six discrete directives with which the undersigned must comply on remand. See

42 U.S.C. § 300aa–12(e)(2)(c) (empowering the Court of Federal Claims to remand “to the

special master for further action in accordance with the court’s direction”); Hanlon v. Sec’y of

Health & Human Servs., 40 Fed. Cl. 625, 630 (1998) (a decision from the Court of Federal

Claims is binding on a special master in the same case on remand), aff’d on other grounds, 191

F.3d 1344 (Fed. Cir. 1999). On remand, the undersigned:

1. “may not diagnose [Mr. Contreras’s] illness, but shall examine whether petitioner has

established a prima facie case that he suffered a vaccine-related combination of TM and

GBS”; 2. “shall make findings on all three Althen prongs”; 3. “shall make a finding as to

whether petitioner has ruled out alternative causes for his illness”; 4. “shall accord the

proper weight to the opinions of [Mr. Contreras’s] treating physicians, as to all three

Althen prongs”; 5. “shall employ the correct standard for Althen prong three”; and 6.

“must consider Dr. Poser’s arguments and evidence” concerning Althen prong three.

Opinion and Order, 107 Fed. Cl. at 308. The Court cautioned, however, that “[r]eference to this

outline… is not a substitute for a thorough consideration and application of the legal analyses

presented in [its] opinion.” Id.

3. Activities on Remand

After the Court issued its Opinion and Order, a status conference was held on October 12,

2012. During the status conference, the parties requested additional time to discuss how to

proceed with the case. See Order, filed October 15, 2012. On October 23, 2012, the parties filed

a joint status report with a proposed briefing schedule. After being granted an extension of time

to file his brief, Mr. Contreras filed his brief on remand on December 4, 2012. Pet’r’s Br. on

Remand, filed Dec. 4, 2012. The Secretary did not file her response to petitioner’s brief on

remand until June 12, 2013, after being granted multiple extensions of time to do so. Resp’t’s

Br. on Remand. Mr. Contreras filed a reply brief on remand on August 13, 2013, after being

granted an extension of time to do so.17

Mr. Contreras argued that he “erroneously agreed in [his] Post Trial Brief that whether

[he] suffered from GBS or TM or a combination of the two diseases should not affect the

outcome of the case.” Pet’r’s Br. on Remand at 7. Thus, his “focus on causation for GBS/TM

without highlighting the difference in timing between GBS and TM was in retrospect an

oversight.” Id. Because his “experts and treating physicians have consistently maintained that

Jessie suffered from both atypical GBS and TM,” petitioner now urges a finding that he suffers

from both GBS and transverse myelitis. Id.

The Secretary maintained her position that the diagnosis of Mr. Contreras’s condition

“does not change the fact that [Mr. Contreras] has failed to present a reliable medical theory that

17

Although the Court expected the case to resolve quickly, Opinion and Order, 107 Fed.

Cl. at 283, the parties sought enlargements of time to comply with the briefing schedule and to

attempt (again) to resolve the case informally.

22

the Hep B or Td vaccine can cause either [TM or GBS] within 24 hours”18 after vaccination.

Resp’t’s Br. on Remand, at 10.

The remainder of the parties’ arguments in their briefs on remand thoroughly explained

their respective positions regarding the Court’s five other directives. Simply stated, Mr.

Contreras asserted that he has provided preponderant evidence to satisfy all three Althen prongs

while the Secretary maintained that the record does not support a finding in his favor on any of

the Althen prongs.

IV. Standards for Adjudication19

To receive compensation under the Program, Mr. Contreras must prove either: (1) that

he suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding

to a vaccine that he received, or (2) that he suffered an injury that was actually caused by his

hepatitis B or Td vaccination. See 42 U.S.C. §§ 300aa-13(a)(1)(A) and 11(c)(1); Capizzano v.

Sec’y of Health & Human Servs., 440 F.3d 1317, 1319-20 (Fed. Cir. 2006). Here, Mr.

Contreras is not claiming an injury listed on the Vaccine Table. Therefore, he must prove

causation-in-fact.

When a petitioner proceeds on a causation-in-fact theory, a petitioner must establish

three elements. The petitioner’s

burden is to show by preponderant evidence that the vaccination brought about

[the] 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, 418 F.3d at 1278.

In this passage, Althen indicates that petitioner’s burden of proof is a preponderance of

the evidence. Accord 42 U.S.C. § 300aaB13(a)(1). In this regard, “close calls regarding

causation are resolved in favor of injured claimants.” Althen, 418 F.3d at 1280.

The preponderance of the evidence standard, in turn, has been interpreted to mean that a

fact is more likely than not. Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1322

18

As discussed in section V.C.2 below, the parties have a minimal (and unimportant)

difference about the exact number of hours that elapsed between vaccination and the onset of

neurological problems.

19

The Court also discussed how a petitioner may establish a causation-in-fact claim.

Opinion and Order, 107 Fed. Cl. at 291-92.

23

n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y of Health &

Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991).

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 judgment

that petitioners were not entitled to compensation); see also Lampe v. Sec’y of Health & Human

Servs., 219 F.3d 1357 (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).

The obligation in determining whether the evidence weighs in petitioner’s favor rests

with special masters in the first instance. 42 U.S.C. § 300aa−12(d)(3)(A). “Congress

envisioned that the special masters would become specialists in vaccine-related injuries and

would use ‘their accumulated expertise in the field [to] judg[e] the merits of the individual

claims.’” Simanski v. Sec’y of Health & Human Servs., 671 F.3d 1368, 1371 (Fed. Cir. 2012)

(quoting Lampe, 219 F.3d at 1362 (citations omitted)).20

Mr. Contreras argues he has provided preponderant evidence to meet his burden under

Althen to prove his TM and GBS were caused in fact by the hepatitis B and/or Td vaccine.21

An evaluation of each prong follows.

V. Analysis

Four aspects of this case are determined. The preliminary question (section V.A.) is

whether Mr. Contreras suffered from either transverse myelitis alone or transverse myelitis and

GBS. The next three sections correspond to the three prongs of Althen. Section V.B. discusses

Mr. Contreras’s submission of a medical theory that causally connects the hepatitis B

vaccination to his neurological injury. Section V.C. explains whether Mr. Contreras has

presented preponderant evidence that this theory explains how a vaccine can cause a neurologic

20

After a motion for review, if the Court finds that the special master’s findings of facts

were “arbitrary, capricious, an abuse of discretion, or otherwise not in accordance of law,” the

Court may “issue its own findings of fact.” 42 U.S.C. § 300aa−12(e)(2)(B); accord Porter v.

Sec’y of Health & Human Servs., 663 F.3d 1242, 1249 (Fed. Cir. 2011). In its Opinion and

Order, the Court did not make any findings of fact. Opinion and Order, 107 Fed. Cl. at 292.

Instead, the Court remanded the case “for further action in accordance with the court’s

direction.” See 42 U.S.C. § 300aa−12(e)(2)(C).

21

Dr. Steinman opined that Mr. Contreras’s hepatitis B vaccination caused his condition,

but also suggested that his Td vaccination could have contributed to it. He explained at the

hearing, however, that “without the hepatitis B vaccine, we would not be in court today.” Tr.

118.

24

injury within a medically acceptable amount of time. The final section discusses whether Mr.

Contreras has presented a logical sequence of cause and effect connecting his vaccination and

his injury.

A. Mr. Contreras’s Injury

Mr. Contreras contends his vaccines caused him to develop both transverse myelitis and

GBS. The Secretary’s position regarding what injury (or injuries) afflicts Mr. Contreras is not

entirely clear or consistent. The Secretary has, however, clearly and consistently maintained her

position that the exact diagnosis of Mr. Contreras’s condition is unimportant because he could

not have developed either transverse myelitis or GBS within approximately 24 hours after

vaccination.

The evidence concerning Mr. Contreras’s diagnosis comes from three sources. The first

and most important source is the material coming from Mr. Contreras’s treating doctors. The

next source is the set of opinions from doctors whom Mr. Contreras has retained. The final

source is the set of opinions from doctors whom the Secretary retained. After the summaries of

this material, there is a determination about how the evidence preponderates.

By weighing the evidence, the undersigned has attempted to comply with the Court’s

instruction not to diagnose Mr. Contreras’s illness. 107 Fed. Cl. at 308. As discussed in more

detail below, the doctors have diagnosed him.

1. Position of Doctors who Treated Mr. Contreras

A chronological presentation of the treating doctors’ diagnoses begins with Dr. Wagner.

Dr. Wagner treated Mr. Contreras on his admission to the emergency room on June 17, 2003.

Upon Mr. Contreras’s admission, Dr. Wagner diagnosed him with atypical GBS. Exhibit 6 at 5;

Tr. 73. Dr. Wagner also considered a diagnosis of transverse myelitis. Tr. 82-83. When Dr.

Wagner transferred Mr. Contreras to Miller’s Children Hospital, Dr. Wagner’s diagnosis was

atypical GBS. Exhibit 6 at 5.

Although Mr. Contreras did not see Dr. Wagner after Dr. Wagner transferred Mr.

Contreras, Tr. 91, Mr. Contreras, acting through his attorney, consulted Dr. Wagner. Dr.

Wagner’s affidavit stated that his “clinical impression [of Mr. Contreras] was atypical [GBS]”

and that his “differential diagnosis was Early Transverse Myelitis.” Exhibit 12, ¶ 5. At the

hearing, Dr. Wagner testified that Mr. Contreras suffered from both transverse myelitis and

GBS. The basis for Dr. Wagner’s opinion concerning a dual diagnosis was primarily his

extensive clinical experience. Tr. 94-95.

The next doctor to reach an opinion regarding Mr. Contreras’s diagnoses was Dr. Lake.

Dr. Lake saw Mr. Contreras within hours of his admission to Miller’s Children Hospital.

Although Dr. Lake initially considered a diagnosis of atypical GBS upon Mr. Contreras’s

admission, exhibit 7 at 1735, she changed her diagnosis to transverse myelitis due to the results

of his June 18, 2003 MRI. Dr. Lake (and Mr. Contreras’s radiologist, Dr. Lipson) considered

the results to suggest transverse myelitis, not GBS. Exhibit 7 at 177, 1723. Dr. Lake was Mr.

25

Contreras’s primary neurologist and, after the June 18, 2003 MRI, she consistently opined that

Mr. Contreras had only transverse myelitis during his three-month hospitalization. Her opinion

was the same in three consecutive follow-up examinations on November 2, 2004, February 1,

2005, and June 7, 2005. See exhibit 82 at 1-5.

The next important doctor to comment upon Mr. Contreras’s diagnosis was Dr. Garrett.

Dr. Garrett’s initial differential diagnosis included atypical GBS, transverse myelitis, acute

disseminated encephalomyelitis, and multiple sclerosis. Exhibit 7 at 136; see also exhibit 13 at

6. However, Dr. Garrett conferred with Dr. Lake and seemingly deferred to Dr. Lake’s opinion

that Mr. Contreras had transverse myelitis. See exhibit 7 at 136. After Dr. Lake stated that Mr.

Contreras had transverse myelitis, Dr. Garrett’s reports consistently mention only transverse

myelitis. None of his reports after June 18, 2003 mentions GBS.

The affidavit that Mr. Contreras procured from Dr. Garrett is consistent with this

characterization. Dr. Garrett averred that Mr. Contreras’s initial workup included treatment for

GBS. But, his final diagnosis was transverse myelitis. Exhibit 13 at 7.

The final doctor who treated Mr. Contreras and presented an opinion for this litigation

was Dr. Kyazze. Dr. Kyazze performed a physical checkup on Mr. Contreras the day before his

vaccinations. Tr. 12. Dr. Kyazze learned from personnel at Miller Children’s Hospital that Mr.

Contreras was hospitalized for transverse myelitis. Exhibit 11 at 2, ¶ 7; Tr. 60. On June 23,

2003, Dr. Kyazze completed a VAERS report in which he indicated that Mr. Contreras had been

“hospitalized in ICU for transverse myelitis on 6/17/03.” Exhibit 4 at 44; Tr. 55-56. When he

testified, Dr. Kyazze did not comment on whether transverse myelitis or GBS was the correct

diagnosis for Mr. Contreras’s condition. See Tr. 59-60.

Additionally, many other doctors saw Mr. Contreras during his hospitalization. Although

they did not testify, their reports are part of the record. These doctors consistently indicated that

he suffered from only transverse myelitis. Whether these doctors determined this diagnosis

independently or whether they deferred to the opinion of Mr. Contreras’s treating neurologist,

Dr. Lake, is not clear. Regardless, none of them suggested GBS.

2. Position of Mr. Contreras

a) Dr. Poser

Dr. Poser opined that Mr. Contreras suffered from both transverse myelitis and GBS.

See exhibit 23 at 7, ¶ 15. In his view, the signs and symptoms of transverse myelitis “masked”

those of GBS. Exhibit 22 at 3, ¶ 4. Dr. Poser acknowledged that “[t]he original diagnosis of

[GBS] . . . was then changed to cervical transverse myelitis as a result of a second MRI . . . on

June 18, 2003,” exhibit 22 at 2, ¶ 3, but he opined that “[f]rom the clinical examination and the

MRI, it is clear that [Mr. Contreras] suffered from a combination of [GBS] . . . and . . .

transverse myelitis.” Exhibit 22 at 3, ¶ 4. Although Dr. Poser recounted his understanding of

Mr. Contreras’s clinical presentation and the results of his June 18, 2003 MRI, see exhibit 22 at

2, ¶ 3, Dr. Poser did not explain how the June 18, 2003 MRI is consistent with GBS. Dr. Poser

26

also did not explain why the results of the June 18, 2003 MRI did not explain the basis for Mr.

Contreras’s clinical symptoms.

b) Dr. Steinman

In his report, Dr. Steinman stated Mr. Contreras “developed transverse myelitis and an

inflammatory peripheral neuropathy, commonly known as Guillain Barre syndrome.” Exhibit 55

at 1. Dr. Steinman agreed with the opinions of Mr. Contreras’s treating physicians, who

diagnosed him with transverse myelitis. In Dr. Steinman’s opinion, “a secondary diagnosis of

inflammatory polyradiculopathy/polyneuropathy [Guillain-Barré Syndrome] could also be

made.” Exhibit 55 at 2 (bracketed material in original).

In his testimony, Dr. Steinman opined that Mr. Contreras exhibited “elements of both

transverse myelitis and [GBS].” Tr. 118. For that reason, he did not consider it “possible to say

[Mr. Contreras] had only one or only the other” of the two diagnoses, Tr. 119, because his

clinical history “doesn’t fit perfectly into either [diagnosis].” Tr. 186.

Dr. Steinman explained that transverse myelitis and GBS can have both similar and

dissimilar initial presentations. Tr. 182. Dr. Steinman considered a diagnosis of GBS due to Mr.

Contreras’s Babinski reflexes, the absence of lymphocytes in his cerebrospinal fluid, and the

diagnoses of his treating physicians. Tr. 121-22, 183-87. Dr. Steinman considered that a dual

diagnosis was a possibility because Mr. Contreras received effective treatment for his GBS

during his hospitalization and the GBS had apparently subsided. See Tr. 185, 213.

Dr. Steinman acknowledged that when Dr. Garrett discharged Mr. Contreras on

September 11, 2003, Dr. Garrett diagnosed him with transverse myelitis, not GBS. Tr. 186. In

developing his opinion on Mr. Contreras’s diagnosis, this specificity did not “concern [Dr.

Steinman] as much as it might concern others” because Dr. Steinman did not attribute much

weight to Dr. Garrett’s discharge diagnosis. Tr. 186; exhibit 7 at 6. Dr. Steinman appeared to

suggest that the discharge diagnosis did not include GBS because hospital personnel, presumably

including Dr. Lake and Dr. Garrett, “may have lost sight of the early nuances in the case.” Tr.

186.

c) Counsel’s Arguments

Mr. Contreras has consistently maintained that he suffered from both transverse myelitis

and GBS. In support, Mr. Contreras pointed to Dr. Wagner’s, Dr. Garrett’s, and Dr. Poser’s

diagnoses, as well as that of the Secretary’s expert, Dr. Whitton. See, e.g., Pet’r’s Br. on

Remand at 8-12; Pet’r’s Post-Hearing Br. at 13.

3. Position of the Secretary

a) Dr. Sladky

Dr. Sladky opined that Mr. Contreras had transverse myelitis only. He explained that he

“found nothing in the medical records . . . to suggest or substantiate a dual diagnosis [of

27

transverse myelitis and GBS].” Exhibit I at 3. He stated that approximately 2-5% of patients

suffer from both transverse myelitis and GBS concurrently. Tr. 293.

Dr. Sladky indicated that the results of the Babinski test did not mean that Mr. Contreras

had GBS. Dr. Sladky also considered Mr. Contreras’s back pain, arm weakness, and

diminished reflexes to be consistent with transverse myelitis. Tr. 283-84. He attributed Mr.

Contreras’s complications in his hands and legs, which may indicate GBS, to be due to

inflammation in the cervical cord. Tr. 287-88.

b) Dr. Whitton

Dr. Whitton testified that when the Secretary retained him in this litigation, he

understood that his role “was to evaluate the immunology and the timing of the immunology . . .

rather than the neurology.” Tr. 438. As such, Dr. Whitton did not consider it important to

determine the correct diagnosis for Mr. Contreras’s condition.

In Dr. Whitton’s first report, he opined that Mr. Contreras suffered from both GBS and

TM. Exhibit L at 3. He testified that “[f]rankly, my opinions expressed in my first report

[regarding Mr. Contreras’s diagnosis] were based largely on reading the expert reports of Dr.

Poser and Dr. Steinman.” Tr. 438.

On further review, Dr. Whitton opined that Mr. Contreras’s medical records “may

indicate that the treating physicians considered his clinical picture more typical of transverse

myelitis than of GBS.” Exhibit N at 5. Specifically, Dr. Whitton stated that Mr. Contreras’s

“discharge diagnosis and the treatment he received (and did not receive)” were more suggestive

of transverse myelitis than GBS. Exhibit N at 5 (citing exhibit 7 at 35 (documenting

intravenous steroid and IVIG treatment)), 113 (documenting that Mr. Contreras did not receive

plasmapheresis22 treatment)).

At the hearing, when pressed to opine about whether Mr. Contreras suffered from GBS,

Dr. Whitton testified that whether Mr. Contreras suffered from transverse myelitis or GBS did

not affect his opinion because neither could manifest within 24 hours after his vaccinations. See

Tr. 438. He also considered the question of diagnosis to be outside of his expertise. See Tr.

438, 454-55.

c) Counsel’s Arguments

The Secretary’s pre-hearing brief is not a model of clarity regarding the appropriate

diagnosis for Mr. Contreras. See Opinion and Order, 107 Fed. Cl. at 287 n. 18. Initially, she

framed the issue of this case as “whether the administration of a Hepatitis B . . . vaccine and

tetanus-diphtheria booster . . . on June 16, 2003, caused in fact Jessie Contreras’s Transverse

Myelitis” within 24 hours. Resp’t’s Prehearing Br. at 1. The reference to transverse myelitis

22

See supra page 12 n.10.

28

implies that the Secretary viewed transverse myelitis as the only diagnosis for Mr. Contreras.

But, under a later section outlining Mr. Contreras’s purported burden of proof, the Secretary

points out that “[n]either GBS or TM are injuries listed in [the] Vaccine Table . . . for the Hep B

and Td vaccine.” Id. at 5. In discussing her stance on the reliability of Mr. Contreras’s experts’

medical theories of causation, the Secretary first concedes that a vaccine “might cause a

neurodemyelinating disease such as TM or GBS.” Id. at 23. These references to transverse

myelitis and GBS suggest that GBS is an appropriate diagnosis for Mr. Contreras. The

Secretary also stated that Dr. Kyazze, Dr. Wagner, and Dr. Garrett all opined that Mr. Contreras

had transverse myelitis; the Secretary did not address whether they believed he also suffered

from GBS. See id. at 26.

In the Secretary’s post-hearing brief, she acknowledged Mr. Contreras’s position that his

vaccines caused him to develop both transverse myelitis and GBS. Resp’t’s Post Hearing Br., at

1. Dr. Whitton initially agreed with Mr. Contreras’s experts that he had both TM and GBS.

The Secretary notes that Dr. Sladky questioned whether Mr. Contreras had GBS, but ultimately

concluded that whether he had transverse myelitis or GBS, or both, did not change his opinion

that Mr. Contreras’s condition was not vaccine-related. Id. at 4. Even though the Secretary’s

experts arguably disagreed on Mr. Contreras’s exact diagnosis, they both unequivocally agreed

that “there was no biologically plausible mechanism by which [the] Hep B vaccine could cause

a neurodemyelinating process within 24 hours of administration.” Id. at 5.

On remand, the Secretary’s position has not changed. In her brief on remand, the

Secretary maintains her position that determining whether Mr. Contreras developed transverse

myelitis or GBS, or both, “does not change the fact that petitioner has failed to present a reliable

medical theory that the Hep B or Td vaccine can cause either condition within 24 hours” after

vaccination. Resp’t’s Br. on Remand, at 10. The Secretary therefore does not necessarily

disagree with Mr. Contreras’s position that he suffered from both transverse myelitis and GBS.

Rather, the Secretary considers the resolution of that issue unimportant because Mr. Contreras’s

claim will fail on other grounds regardless of whether the undersigned finds that he suffered

from transverse myelitis alone or both transverse myelitis and GBS.

4. Determination

Everyone agrees that Mr. Contreras had transverse myelitis. The only dispute is whether

he also had GBS. The evidence about whether Mr. Contreras had GBS is in conflict. Dr.

Steinman, Dr. Poser, and Dr. Wagner opined that Mr. Contreras had both transverse myelitis and

GBS. Dr. Whitton’s opinion on Mr. Contreras’s diagnosis was equivocal. In contrast, Dr.

Garrett, Dr. Sladky, and a number of Mr. Contreras’s treating physicians, including his primary

neurologist, Dr. Lake, opined that he had only transverse myelitis. When evidence is in conflict,

a special master’s role is to weigh the evidence. See Moberly, 592 F.3d at 1325 (special masters

have the responsibility to “assess the reliability of testimony, including expert testimony”).

The opinions of treating physicians are entitled to substantial weight. Capizzano, 440

F.3d at 1326; Opinion and Order, 107 Fed. Cl. at 299 n.31. Dr. Garrett consulted with Dr. Lake

to assess Mr. Contreras’s neurological condition. Although at intake Dr. Lake stated that he had

“atypical GBS,” she changed her diagnosis to transverse myelitis due to the results of Mr.

29

Contreras’s June 18, 2003 MRI. Dr. Lake saw Mr. Contreras on an almost daily basis during his

three-month hospitalization. She saw him multiple times in follow-up examinations in the

months afterward. After all of these visits, Dr. Lake’s diagnosis was transverse myelitis.23 As

Mr. Contreras’s primary neurologist for months, her opinion on the issue of Mr. Contreras’s

diagnosis is highly persuasive.

As discussed, Dr. Garrett was involved with Mr. Contreras’s treatment during his

hospitalization from June 17, 2003 through September 11, 2003. Exhibit 13 at 2-4. Dr. Garrett

“was involved in the acute management and diagnostic workup of [Mr. Contreras’s] presenting

illness.” Id. at 3. Dr. Garrett’s initial differential diagnosis on Mr. Contreras’s presentation

“included . . . Transverse Myelitis, atypical Guillain-Barre syndrome, ADEM . . . or possibly

new onset multiple sclerosis.” Id. at 6. On July 20, 2013, Dr. Garrett stated that Mr. Contreras

“probably . . . or potentially contracted the transverse myelitis secondary to the Hepatitis B

vaccine.” Id. at 6. Mr. Contreras’s discharge diagnosis was cervical transverse myelitis. Id. at

4. Dr. Garrett’s ultimate opinion was that it was “more likely than not that the vaccine was a

substantial factor in causing or significantly contributing to [Mr. Contreras’s] development of

cervical transverse myelitis.” Id. at 13 (emphasis in original).

Dr. Garrett is the only doctor to testify who was substantially involved in Mr. Contreras’s

care. He observed and treated Mr. Contreras during the entirety of his approximately three-

month hospitalization, and stated Mr. Contreras suffered from only transverse myelitis on many

occasions. See, e.g., exhibit 7 at 99, 101, 103, 107, 121. As a treating physician who was

heavily involved in Mr. Contreras’s treatment during the critical time of Mr. Contreras’s

hospitalization, his diagnosis of transverse myelitis is the most persuasive of the testifying

witnesses.

To counter Dr. Garrett’s diagnosis (as well as the diagnoses of numerous other treating

physicians, including Dr. Lake), Mr. Contreras relies upon two doctors who never treated him,

Dr. Steinman and Dr. Poser. Their opinions, although respectfully offered, are not persuasive.

Accordingly, a preponderance of the evidence supports a finding that transverse myelitis is the

sole diagnosis.24

23

Mr. Contreras contended that Dr. Lake diagnosed him with GBS. See Pet’r’s Br. on

Remand at 9 (citing exhibit 7 at 1735, Dr. Lake’s June 17, 2003 diagnosis). Dr. Lake made this

report on the first day of Mr. Contreras’s hospitalization when the only information about the

cervical MRI was negative. See exhibit 7 at 1735. Dr. Lake indicated Mr. Contreras’s condition

was “probable atypical [GBS].” Exhibit 7 at 1728, 1735.

By June 20, 2003, Dr. Lake changed the diagnosis from atypical GBS to transverse

myelitis because of the MRI results from the second day of his hospitalization. See id. at 1714,

1723. Thus, although Mr. Contreras’s argument regarding Dr. Lake has minimal support, the

balance of Dr. Lake’s treatment notes are inconsistent with Mr. Contreras’s argument. See 42

U.S.C. § 300aa-13(a)(1) (a special master is charged with considering the “record as a whole”).

24

The Court indicated that the undersigned special master “may not diagnose Jessie’s

illness.” Opinion and Order, 107 Fed. Cl. at 308. The finding that Mr. Contreras did not suffer

(... continued)

30

It bears repeating that there is no dispute that Mr. Contreras suffered from transverse

myelitis. Even Mr. Contreras’s experts agreed with Dr. Lake’s diagnosis of transverse myelitis.

Exhibit 22 at 2, ¶ 3; exhibit 23 at 7, ¶ 15 (Dr. Poser); exhibit 55 at 2 (Dr. Steinman). The

diagnosis of transverse myelitis is practically inescapable because the June 18, 2003 MRI

showed “extensive abnormal signal intensity . . . in the cervical spinal cord, . . . extend[ing] from

the C2-3 interspace to about C7.” Exhibit 7 at 167. This damage was to the central nervous

system, which is usually protected by the blood brain-barrier. Tr. 226, 305-06, 418.

The April 5, 2012 Entitlement Decision emphasized that the blood brain barrier would

make an autoimmune-mediated injury very unlikely to happen in one day. 2012 WL 1441315, at

*14, *19. The Court expressed concern about the emphasis on the injury within the central

nervous system. Opinion and Order, 107 Fed. Cl. at 289 n. 22. The reason for the emphasis on

transverse myelitis (and the blood-brain barrier, which protects against transverse myelitis) is

that Mr. Contreras unquestionably suffered from transverse myelitis. His theory of causation

must necessarily take into account the lesion in his cervical spine that extended across four

vertebrae. See Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1345 (Fed. Cir.

2010) (“[A] petitioner must provide a reputable medical or scientific explanation that pertains

specifically to the petitioner's case.”).

According to Mr. Contreras, a determination that he also suffered from GBS “drastically

undercuts” the Secretary’s position with regard to Althen prong three because the Secretary’s

“principal argument” is that “the blood brain barrier can not be breached within 24 hours… [in]

central nervous system diseases, not to peripheral nervous system diseases such as GBS where

the blood brain barrier is not applicable.” Pet’r’s Br. on Remand at 49. This argument misses its

mark. Mr. Contreras’s argument might have more appeal if this were a case in which the debate

was over whether the injury was either to the central nervous system or to the peripheral nervous

system. If a person suffered an injury that was exclusively to the peripheral nervous system, then

it seems an autoimmune process could occur more quickly simply because the strong defense

offered by the blood brain barrier would not be an impediment. But, that is not the case with Mr.

Contreras. He claims to have suffered both a disease of the central nervous system (transverse

myelitis) and a disease of the peripheral nervous system (GBS). Thus, even if preponderant

evidence established that Mr. Contreras suffered from both a peripheral and a central nervous

system disease, he would be required to establish, on a more likely than not basis, that a

GBS appears to be in accord with this instruction because Dr. Lake (not the undersigned)

diagnosed Mr. Contreras’s illness. Rather than diagnosing the illness, the undersigned has

weighed all the evidence of record, including Dr. Steinman’s and Dr. Poser’s opinions, and

determined that the stronger and more persuasive evidence supports a finding that Mr. Contreras

suffered from transverse myelitis only. See Whitecotton v. Sec’y of Health & Human Servs., 81

F.3d 1099, 1108 (Fed. Cir. 1996) (“Congress desired the special masters to have very wide

discretion with respect to the evidence they would consider and the weight to be assigned that

evidence.”).

31

vaccination caused both. And part of Mr. Contreras’s case would include a showing that his

injuries (GBS and transverse myelitis) arose in “a medically-acceptable time-frame.” Opinion

and Order, 107 Fed. Cl. at 309. Therefore, the medically-acceptable time-frame for the onset of

transverse myelitis after vaccination would remain an issue even if Mr. Contreras were found to

suffer from GBS in addition to transverse myelitis.25

This discussion about the significance of a finding that Mr. Contreras also suffered from

GBS is purely hypothetical. His treating neurologist (Dr. Lake) and his treating pediatric

intensivist (Dr. Garrett) concluded that Mr. Contreras suffered only from transverse myelitis. As

treating doctors, their identification of the disease afflicting their patient is entitled to “significant

weight.” See Opinion and Order, 107 Fed. Cl. at 300.

Therefore, the remainder of this opinion discusses transverse myelitis. Mr. Contreras

initially asserted that both his hepatitis B and Td vaccines caused his injuries. His experts,

however, consistently attributed his injuries to only the hepatitis B vaccine, not the Td vaccine.

Thus, the following Althen analysis is limited to the issue of whether the hepatitis B vaccine can

cause transverse myelitis.26

B. Prong One from Althen – Medical Theory

After a determination of what disease afflicts a petitioner, the next step is analyzing the

theory proposed by the expert that “causally connect[s] the vaccination and the injury.” Althen,

418 F.3d at 1278. This element of petitioner’s case is sometimes referred to as answering the

“can it” question. Pafford v. Sec’y of Health & Human Servs., No. 01-165V, 2004 WL

1717359, at *4, 9 (Fed. Cl. Spec. Mstr. July 16, 2004), mot. for rev. denied, 64 Fed. Cl. 19

(2005), aff’d, 451 F.3d 1352 (Fed. Cir. 2006).

25

In light of the undisputed results from the MRI showing demyelination in Mr.

Contreras’s cervical spine, exhibit 7 at 177, Mr. Contreras’s attempt to add GBS to his case

actually makes his claim more complicated. Under his theory, he would be required to show that

his immune system directed itself against two different parts of his body, the central nervous

system (cervical spine) and a portion of the peripheral nervous system. This autoimmune attack

would also have to been initiated and to have caused some neurologic symptoms attributable to

both central nervous system and peripheral nervous system in approximately one day.

26

In spite of the fact that preponderant evidence supports a finding that Mr. Contreras

suffered from only transverse myelitis, the undersigned has reviewed the entirety of the record to

ensure that all relevant evidence has been considered. This review included the parties’ medical

literature that pertains to GBS and the Td vaccine. Although all the evidence has been

considered, not all of it will be discussed in this decision. See Paterek v. Sec’y of Health &

Human Servs., ___ F.3d ___, No. 2012-5078, 2013 WL 3028726, at *8 (Fed. Cir. June 19, 2013)

(stating that “[f]inding certain information not relevant does not lead to—and likely

undermines—the conclusion that it was not considered”).

32

In the Vaccine Program, an expert’s opinion may be evaluated according to the factors

identified by the United States Supreme Court in Daubert v. Merrell Dow Pharmaceuticals, Inc.,

509 U.S. 579 (1993). Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir.

1999). After Terran, decisions from judges of the Court of Federal Claims have consistently

cited to Daubert. E.g., Caves v. Sec’y of Health & Human Servs., 100 Fed. Cl. 119, 133 (2011),

aff’d, 463 Fed. App’x 932 (Fed. Cir. 2012) (per curiam). Although supporting medical literature

is not necessary for an expert’s testimony to be reliable, Althen, 418 F.3d at 1279-80, Andreu,

569 F.3d at 1378, it may be considered in assessing the reliability of an expert’s testimony.

The April 5, 2012 Entitlement Decision did not address Mr. Contreras’s medical theory

because his failure to present preponderant evidence on prong three meant that he was not

entitled to compensation. 2012 WL 1441315, at *1. Although the Court held that the omission

of prong one did not constitute an error of law, Opinion and Order, 107 Fed. Cl. at 295, the

Court also instructed that the decision on remand discuss each of the Althen prongs. Id. at 296.

In accord with the Court’s direction, the evidence related to this prong is reviewed, starting with

Mr. Contreras’s evidence.

1. Synopsis of Mr. Contreras’s Evidence

Mr. Contreras elicited testimony from five doctors regarding the cause of his disease.

This group includes three doctors who treated him (Dr. Kyaaze, Dr. Wagner, Dr. Garrett) and

two doctors who did not treat him (Dr. Poser and Dr. Steinman). Of this group, the doctor on

whom Mr. Contreras relied most heavily was Dr. Steinman. See, e.g., Pet’r’s Pre-Hearing Br. at

12; Pet’r’s Post-Hearing Br. at 19, 21-22, 26; Pet’r’s Mot. for Rev. at 9, 27-28, 29-30.

a) Dr. Kyazze

Mr. Contreras offered the affidavit of Dr. Kyazze to demonstrate that he was “a healthy

individual with no infectious disease process taking place” prior to his vaccinations. Pet’r’s Br.

on Remand, at 13. Dr. Kyazze examined Mr. Contreras on June 16, 2003, prior to his subject

vaccines. Exhibit 11 at 2; Tr. 54-55. He did not treat Mr. Contreras any time after June 17,

2013. Tr. 59. He has not reviewed any of Mr. Contreras’s medical records since he

administered Mr. Contreras’s June 16, 2003 vaccinations. Tr. 59. As Mr. Contreras asserted,

Dr. Kyazze considered Mr. Contreras to be entirely healthy prior to his vaccinations. Exhibit 11

at 2, ¶ 4.

On Mr. Contreras’s emergency room admission, Dr. Kyazze was informed that Mr.

Contreras had transverse myelitis. Tr. 59; see also exhibit 4 at 22. After learning that Mr.

Contreras was in the intensive care unit for his transverse myelitis, Dr. Kyazze filed a Vaccine

Adverse Event Report concerning Mr. Contreras. Exhibit 11 at 2, ¶ 7; Tr. 55, 60. He believed

he was required by law to file a VAERS report because Mr. Contreras “developed serious

symptoms within one day of receiving the vaccinations.” Exhibit 11 at 2, ¶ 7; Tr. 56-57, 60.

When asked whether he believed Mr. Contreras’s vaccines caused his transverse myelitis, Dr.

Kyazze stated he “wouldn’t know that.” Tr. 60. Beyond filing a VAERS report, Dr. Kyazze has

not suggested that Mr. Contreras’s transverse myelitis is vaccine-related.

33

b) Dr. Wagner

Dr. Wagner treated Mr. Contreras for approximately five hours of his first emergency

room admission on June 17, 2008. Exhibit 12 at 2; exhibit 6 at 9; Tr. 66-69.

Dr. Wagner’s clinical impression of Mr. Contreras upon his admission was atypical GBS.

Exhibit 6 at 5, 10; Tr. 73, 84. Dr. Wagner’s differential diagnosis of Mr. Contreras included

transverse myelitis. Exhibit 12 at 2, ¶ 5; see also exhibit 6 at 18 (Dr. Wagner ordered an MRI

due to “[c]onsideration of transverse myelitis”). Because Mr. Contreras developed his transverse

myelitis shortly after his immunizations, Dr. Wagner considered them “a suspected cause.”

Exhibit 12 at 2, ¶ 6. Further, he “was not able to find any other reason or condition based on the

medical history and upon my examination of [Mr. Contreras] which could have caused his

reaction.” Id.

In his affidavit, Dr. Wagner did not provide a theory of causation, nor did he expand on

his opinion that Mr. Contreras’s transverse myelitis is vaccine-related. At the hearing, Dr.

Wagner offered additional information. He stated that “[a]fter discussing with Dr. Babbitt . . .

[he] was of the understanding that the most likely possibility at the time was the hepatitis B

[vaccine].” Tr. 89. In Dr. Wagner’s view, “science has shown, and on [his] subsequent readings

after the fact, that there are proteins in [the] hepatitis B vaccine that mimic myelin proteins

around the nerves of human beings. And therefore, you can get an immune reaction,” which can

occur in 24 hours. Tr. 95-96. The readings to which Dr. Wagner referred are Dr. Steinman’s

report and references. Tr. 98.

Dr. Wagner based his testimony upon a review of his treatment records, Dr. Garrett’s

report, and Dr. Steinman’s report and references. Tr. 92, 97-98. Dr. Wagner did not review the

reports of Dr. Sladky or Dr. Whitton. Tr. 97-98.27

c) Dr. Garrett

Dr. Garrett treated Mr. Contreras during his hospitalization in 2003. During this time,

Dr. Garrett did not say what caused Mr. Contreras’s neurological problem, although Dr. Garrett

did recommend the submission of a VAERS report. See exhibit 7 at 106. He did not testify at

the hearing.

Dr. Garrett attributed Mr. Contreras’s transverse myelitis to his vaccines. Exhibit 13 at 6.

Based on his review of the relevant literature, Dr. Garrett asserted that a

multitude of studies including: case reports, case-series, statistical epidemiological

assessments, positive re-challenge or significant exacerbation of symptoms, [and]

27

The Court appears to have criticized the April 5, 2012 Entitlement Decision for noting

that Dr. Wagner’s review of material was selective. Opinion and Order, 107 Fed. Cl. at 302.

34

review articles all report[ed] a connection between the hepatitis B/DT vaccination and

serious neurological reactions.

Exhibit 13 at 12, ¶ 16.

In support of his opinion that the hepatitis B vaccine can cause transverse myelitis, Dr.

Garrett referenced five case reports that document the alleged causal relationship. Exhibit 13 at

8-10. He also referenced a CDC report that found “it is biologically plausible for hepatitis

B/DT vaccines to cause central nervous system disorders and peripheral nervous system

disorders.” Exhibit 13 at 12-13. Although paragraph 16 mentioned “statistical epidemiological

assessments” as one source that supported a causal connection between the vaccination and a

neurological reaction, none of the articles actually submitted to accompany Dr. Garrett’s work

appears to be an epidemiological assessment. See exhibits 14-21.

Dr. Garrett explained that “[t]he proximity in time to the immunization made the

Hepatitis B vaccine and to a lesser extent, the DT vaccine, a suspected cause.” Exhibit 13 at 6.

Based on his treatment of Mr. Contreras and “extensive review of available medical literature

and discussions with colleagues and multiple consultants,” Dr. Garrett concluded Mr.

Contreras’s transverse myelitis was either idiopathic or vaccine-related. Exhibit 13 at 7. Dr.

Garrett explained that all the testing and evaluations done on Mr. Contreras to determine a

specific cause of his transverse myelitis were “unrevealing,” which left him and his colleagues

“with etiologies for [Mr. Contreras’s] transverse myelitis as either idiopathic or potentially

secondary to the recent Hepatitis B vaccination.” Exhibit 13 at 7. He could not “find any other

reason or condition based on [Mr. Contreras’s] medical history and upon [his] examination of

[Mr. Contreras] which could have caused [his] condition and illness.” Exhibit 13 at 7-8.

d) Dr. Poser

Dr. Poser submitted two reports in support of Mr. Contreras’s claim that the hepatitis B

vaccine caused him to develop transverse myelitis and GBS. Exhibit 22 at 3, ¶ 4; exhibit 23 at

7, ¶ 15. He did not testify at either hearing. Mr. Contreras asserted that Dr. Poser’s opinion

provides persuasive evidence for all three Althen prongs. Pet’r’s Br. on Remand at 23-30.

Dr. Poser opined that “all vaccines may potentially cause . . . transverse myelitis, or its

peripheral equivalent such as GBS in vulnerable individuals.” Exhibit 22 at 7, ¶ 10. He

explained that the “immune system’s response to a viral antigen, be it an infection or vaccine,

varies enormously in its manifestations,” and includes transverse myelitis and GBS. Exhibit 22

at 8, ¶ 12. Dr. Poser explained that the immune system’s “original response” to an antigen,

including vaccinations, causes an “inflammation of the vessel wall of cerebral venules and

capillaries causing an alteration of the blood brain barrier and permitting water, lymphocytes

and other substances, including complement and antibodies, to invade the parenchyma of the

nervous system.” Exhibit 22 at 8, ¶ 12. This invasion leads to demyelination, which, in turn,

leads to neurological complications. Exhibit 22 at 8, ¶ 12. Dr. Poser appears to have suggested

that this occurs via molecular mimicry. Exhibit 23 at 3-4 (discussing animal models of

experimental allergic encephalitis).

35

Dr. Poser cited a number of medical literature articles that he claims report on

individuals whose neurological complications, including transverse myelitis and GBS, were

induced by the hepatitis B vaccine. Exhibit 22 at 4-6; exhibit 23 at appendix. Almost all the

articles cited by Dr. Poser are case reports indicating that a neurological disease (such as

transverse myelitis or GBS) arose after a vaccination. Many of these articles are listed in a table

that appears in section V.C.3.b)(9), below. Almost all of Dr. Poser’s second report concerns his

view that epidemiological studies cannot establish or disprove the causal relationship between

Mr. Contreras’s hepatitis B vaccine and his alleged transverse myelitis and GBS because of his

“genetic endowment and immunologic history.” Exhibit 23 at 6, ¶ 14.

Dr. Poser asserted that “[n]europathologic, radiological and experimental evidence

strongly support the causal association between the hep B vaccine and the myelitis-GBS in [Mr.

Contreras].” Exhibit 23 at 7, ¶ 14. Dr. Poser did not discuss in any detail the alleged

“neuropathologic, radiological and experimental evidence” that, according to him, suggested

Mr. Contreras’s hepatitis B vaccine caused his neurological complications.

e) Dr. Steinman

Mr. Contreras relied primarily on Dr. Steinman to satisfy Althen prong one. In Mr.

Contreras’s briefs, he cites to Dr. Steinman frequently. See, e.g., Pet’r’s Pre-Trial Br. at 8-12;

Pet’r’s Post-Hearing Br. at 17-21; Pet’r’s Post-Hearing Reply Br., filed Feb. 3, 2011, at 5-9, 14-

15, 21; Pet’r’s Mot. for Rev. at 24-30; 37-39.

Dr. Steinman opined that the hepatitis B vaccination can cause transverse myelitis via a

process known as molecular mimicry and this process can occur within one day. Exhibit 124 at

3. As described in section II.B.3 above, molecular mimicry is a process comprised of several

discrete steps.

Dr. Steinman proposed that a molecular mimicry reaction can take place in one day. Dr.

Steinman primarily relied upon an analogy to the tuberculin skin test, and a theory based on

sensitization. Dr. Steinman cited to many case reports, including the Sinsawaiwong article

(exhibit 71 (Suwanna Sinsawaiwong & Pornpen Thampanitchawong, Guillain- Barré Syndome

Following Recombinant Hepatitis B Vaccine and Literature Review, 83 J. Med. Assoc’n Thai

1124 (2000))), the Kakar article (exhibit 72 (A. Kakar & P.K. Sethi, Guillain Barre Syndrome

Associated with Hepatitis B Vaccination, 64 Indian J. Pediatr. 710 (1997))), and the Tabor article

(exhibit 73 (Edward Tabor, Guillain-Barré Syndrome and Other Neurologic Syndromes in

Hepatitis A, B, and Non-A, Non-B, 21 J. Med. Virology 207, 209 (1987))).

2. Synopsis of the Secretary’s Evidence

a) Dr. Sladky

Respondent’s expert, Dr. Sladky, opined that the hepatitis B vaccine does not cause

transverse myelitis. Further, Dr. Sladky asserted that an autoimmune process, such as Dr.

Steinman’s proposed theory of molecular mimicry, could not occur in approximately 24 hours,

as Mr. Contreras maintained occurred in his case. Further, Dr. Sladky opined that Dr.

36

Steinman’s proposed theory of molecular mimicry would take at least five days to occur. Thus,

Dr. Sladky asserted that Mr. Contreras’s hepatitis B vaccine did not cause his transverse myelitis.

Dr. Sladky acknowledged that many illnesses often occur prior to an onset of transverse

myelitis, which has led some to suggest a causal relationship. Tr. 300. The most common

illness that predates transverse myelitis is an upper respiratory tract infection. Tr. 300. Dr.

Sladky opined, however, that whether there is a causal relationship between this (and other

illnesses) and transverse myelitis is unknown.

Dr. Sladky opined that a causal relationship between the hepatitis B vaccine and

subsequent central nervous system demyelination has not been established. In support of this

proposition, Dr. Sladky relied primarily on three epidemiological studies that concluded there

was no such causal relationship between the hepatitis B vaccine. See exhibit E (E. Merelli & F.

Casoni, Prognostic factors in multiple sclerosis: role of intercurrent infections and vaccinations

against influenza and hepatitis B, 21 Neurological Science S852 (2000)); exhibit G (Emmanuel

Touze et al., Hepatitis B Vaccination and First Central Nervous System Demyelinating Event: A

Case-Control Study, 21 Neuroepidemiology 180 (2002)); and exhibit H (Frauke Zipp et al., No

increase in demyelinating diseases after hepatitis B vaccination, 5 Nature Medicine 964

(1999)).28

The authors of the Merelli article assessed a number of studies (including the Zipp study

(exhibit H) and the Tourbah study (exhibit 34)) that investigated the relationship between the

influenza and hepatitis B vaccines and multiple sclerosis. Exhibit E at S853-55. Based on the

authors’ review of the available literature, they concluded “that there is no scientific evidence

suggesting a causal link between [hepatitis B] . . . vaccination and [multiple sclerosis].” Id. at

S855. Although none of the experts discussed the Merelli article in their testimony at hearing,

Merelli provides some small support that vaccinations do not cause demyelinating diseases in the

central nervous system.

The authors of the Touze study assessed the possible association between the hepatitis B

vaccine and demyelinating diseases of the central nervous system. Exhibit G at 181.

Id. The study was performed on “236 cases and 355 matched controls (117 pairs and 119

triplets)” limited to “patients with a first isolated well-defined neurological event consistent with

demyelination involving the optic nerve, spinal cord, the brainstem, the cerebellum or the brain.”

Id. at 181-82. The patients all had symptoms that lasted more than one day that lacked any

explanation. Id. at 181. The authors “postulated that the demyelinating events might be causally

linked to [hepatitis B] . . . vaccine if the delay between vaccine injection and onset of the

neurological symptoms did not exceed 60 days.” Id. at 182. The authors later expanded the

range of symptom onset studied to one year after hepatitis B vaccination. Id.

28

Dr. Steinman also referenced the Touze and Zipp studies in his initial report. See

exhibits 75 (Touze) and 76 (Zipp).

37

The results of the study led the authors to conclude that their study “was sufficiently

powerful to rule out a strong association between [hepatitis B] vaccine exposure and a

subsequent demyelinating event.” Id. The authors cautioned, however, that the study “could not

provide a clear indication of a moderately increased risk of a [central nervous system]

demyelinating event shortly after [hepatitis B] vaccination in adults.” Id. at 181.

The authors of the Zipp study likewise found no causal relationship between the hepatitis

B vaccine and demyelinating diseases. Exhibit H at 964. The authors compared the incidence of

demyelinating diseases between 27,229 individuals who received the hepatitis B vaccine with

107,469 non-vaccinated individuals. Id. “The rate of central nervous system demyelinating

episodes in individuals vaccinated against hepatitis B was compared with that in age- and sex-

matched non-vaccinated individuals in the 3 years after vaccination.” Id. Based on their

findings, the authors concluded that their “results do not support the assumption that hepatitis B

vaccination induces demyelination.” Id.

Dr. Sladky found these epidemiological studies more informative than case reports. He

interpreted the Touze study to conclude that “there is no connection between hepatitis B

immunization and multiple sclerosis.” Tr. 311. He also found the Zipp study to be “germane,”

though he acknowledged Caucasians were overrepresented. Tr. 312.

Dr. Sladky discounted the value of case reports due to their bias. Tr. 295-96. According

to Dr. Sladky, case reports have at least three different levels of bias. Tr. 295. The first level is

the bias of the individual who reports the case. Tr. 295. He considers case report authors to have

inherent bias because they look for particular findings and then report them when found. Tr.

295. The second level of bias is due to the publication itself. Tr. 295. As Dr. Sladky explained,

“[i]f I report 100 kids who got [a] hepatitis B vaccine and had no side effects, it’s not news. It’s

not going to be reported.” Tr. 296. The third level of bias is due to how a case report’s findings

are subsequently interpreted. Tr. 296. Dr. Sladky considers case reports to be merely

phenomenological observations and stated that individuals often incorrectly utilize them to

establish causation “when the causality was never established.” Tr. 299.

b) Dr. Whitton

Dr. Whitton did not have a firm opinion on which disease (or diseases) afflicted Mr.

Contreras because he asserted the hepatitis B vaccine cannot cause transverse myelitis or GBS.

See Tr. 438-39. Further, he opined that Dr. Steinman’s proposed theory of molecular mimicry

could not explain causation of transverse myelitis or GBS occurring in approximately one day, as

Mr. Contreras asserts occurred in his case. Tr. 447.

Dr. Whitton rejected the proposition that the hepatitis B vaccine can cause a

demyelinating disease. Dr. Whitton based his opinion on multiple studies that investigated

whether vaccinations have caused either an increased incidence in a demyelinating disease or a

38

pre-existing demyelinating disease to worsen. 29 These studies were the foundation for Dr.

Whitton’s conclusion that “there is no scientifically-acceptable evidence that childhood

vaccination causes autoimmune disease.” Exhibit L at 5.

Dr. Whitton criticized Dr. Steinman’s reliance on case reports. Id. Dr. Whitton opined

that “a single case report is of very questionable significance” because the temporal relationship

it may document between a vaccination and the onset of an injury is necessary, but not sufficient,

to establish causation because “a temporal relationship carries very little weight.” Id. at 6.

29

The articles Dr. Whitton cited primarily studied two particular demyelinating diseases,

multiple sclerosis and GBS. Multiple sclerosis, typically, is a relapsing-remitting disease in

which the person suffers demyelination within the central nervous system. See W.C. v. Sec’y of

Health & Human Servs., No. 07-456V, 2011 WL 4537877, at *6 (Fed. Cl. Spec. Mstr. Feb. 22,

2011), mot. for rev. denied, 100 Fed. Cl. 440 (2011), aff’d, 704 F.3d 1352 (Fed. Cir. 2013). For

articles that found no causal link between hepatitis B vaccination and multiple sclerosis, see

exhibit L, tab 5 (Frank DeStefano et al., Vaccinations and risk of central nervous system

demyelinating diseases in adults, 60 Arch. Neurol. 504 (2003)) at 504 (analyzing more than 400

subjects and nearly 1,000 controls to determine when the first symptoms of multiple sclerosis or

optic neuritis began and finding that “[v]accination against hepatitis B [and four other vaccines]

is not associated with an increased risk of multiple sclerosis or optic neuritis”); exhibit L, tab 8

(Alberto Ascherio et al., Hepatitis B vaccination and the risk of multiple sclerosis, 344 N. Eng. J.

Med. 327, 327 (2001)) at 337 (a multivariate relative risk exposure analyzing 192 women with

multiple sclerosis and 645 matched controls showed “no association between hepatitis B

vaccination and the development of multiple sclerosis”); exhibit L, tab 9 (Christian Confavreux

et al., Vaccinations and the risk of relapse in multiple sclerosis. Vaccines in Multiple Sclerosis

Study Group, 344 N. Eng. J. Med. 319, 319 (2001) at 319 (using European Database for Multiple

Sclerosis to determine whether people with multiple sclerosis experienced a relapse within two

months of a hepatitis B vaccination and concluding that “[v]accination does not appear to

increase the short-term risk of relapse in multiple sclerosis”)).

Other studies investigated GBS. See exhibit L, tab 10 (Nakayama & Onoda) at 570

(analyzing registry containing information on more than 67 million vaccinations and looking for

incidence of, among other diseases, GBS and acute disseminated encephalomyelitis)); exhibit L,

tab 11 (Richard A. Hughes et al., No association between immunization and Guillain-Barré

syndrome in the United Kingdom, 1992 to 2000, 166 Arch. Intern. Med. 1301 (2006)) at 1301

(after searching a database with 1.8 million patients, the authors identified cases of GBS within

42 days of various vaccinations (including hepatitis B) and concluded “[t]here is either minimal

or no risk of GBS associated with routine immunization practice in the United Kingdom”)).

In turn, other articles relied upon some of these studies. These review articles also

supported Dr. Whitton’s opinion that the hepatitis B vaccine does not cause transverse myelitis.

See exhibit L, tab 6 (Ethan Rubinstein, Vaccination and autoimmune diseases: the argument

against, 6 Isr. Med. Assoc. J 433 (2004)) at 434 (stating “no risk for autoimmune disease is

associated with vaccines against infectious diseases, particularly with childhood vaccines”));

exhibit L, tab 7 (David C. Wraith et al., Vaccination and autoimmune disease: what is the

evidence?, 362 Lancet 1659 (2003)) at 1665 (an identified mimicry is of little pathogenic

importance).

39

According to Dr. Whitton, establishing causation would at least require “determining

whether or not the frequency of [an injury] following any given event (e.g., vaccination) is

greater than that which would be expected to occur by chance.” Id. Dr. Whitton asserted that

several large-scale epidemiological studies have investigated exactly this. In his view, these

studies demonstrate that there is no causal relationship between the hepatitis B vaccine and

demyelinating diseases. Id. at 5-6, 8.

3. Assessment of Evidence

For purposes of organization, it is helpful to categorize the evidence into two groups.

The first group consists of the opinions presented by doctors who treated Mr. Contreras. The

second group consists of the opinions presented by doctors whom the parties retained for this

litigation. Although this organization is intended to simplify the analysis, the organization is

somewhat artificial in that the record is being considered as a “whole.” 42 U.S.C. § 300aa-

13(a)(1); accord Capizzano, 440 F.3d at 1326.

a) Treating Doctors

Mr. Contreras cited the opinion of two of his treating doctors, Dr. Garrett and Dr.

Wagner. 30 See, e.g., Pet’r’s Br. on Remand at 3-6. These two doctors, as noted above, did opine

that the hepatitis B vaccine caused his neurologic injury. See exhibit 12 at 2, ¶ 6 (Dr. Wagner’s

affidavit); Tr. 89 (Dr. Wagner); exhibit 13 at 7-8 (Dr. Garrett’s affidavit).

In light of these supporting statements, how should they be considered? One potential

answer is that the opinions of Dr. Garrett and Dr. Wagner—as treating doctors—should be

entitled to so much deference that they are virtually binding as a matter of law. However, this

result would be improper for legal and practical reasons.

A suggestion that a special master must always accept the views of a treating doctor is

contrary to the statute. Congress stated “[a]ny diagnosis . . . shall not be binding on the special

master.” 42 U.S.C. § 300aa-13(b)(1). For an example of a pre-Capizzano opinion that found the

special master was not arbitrary in weighing the testimony of treating doctors, see Hopkins v.

Sec’y of Health & Human Servs., 62 Fed. Cl. 333, 335 (2004). Although the Federal Circuit has

instructed special masters to that the views of treating doctors are “quite probative,” Capizzano,

440 F.3d at 1326, the Federal Circuit’s instruction must be read in accord with the clear words of

the statute.

30

Dr. Kyazze did not opine that Mr. Contreras’s transverse myelitis was vaccine-related.

Mr. Contreras offers Dr. Kyazze’s opinion primarily as evidence that there is no alternative cause

for his injuries, which he asserts “provides a firm foundation supporting the opinions of other

treating physicians . . . stating that the vaccinations were the cause of the injury to [Mr.

Contreras].” Pet’r’s Br. on Remand at 14.

40

Congress’s decision to grant special masters relative freedom in evaluating the reports of

treating doctors makes sense for practical reasons. In some cases, the treating doctors disagree

about aspects of their patient’s care, such as diagnosis or etiology. Logically, two divergent

views cannot both be binding on special masters. In such cases, special masters weigh the

different opinions to determine which is more persuasive. E.g., Broekelshen v. Sec’y of Health

& Human Servs., No. 07-137V, 2009 WL 440624 (Fed. Cl. Spec. Mstr. Aug. 18, 2009), mot. for

rev. denied, 89 Fed. Cl. 336 (2009), aff’d, 618 F.3d 1339 (Fed. Cir. 2010); Doe 60 v. Sec’y of

Health & Human Servs., No. XX-XXXV, 2010 WL 1506010 (Fed. Cl. Spec. Mstr. Mar. 26,

2010), mot. for rev. denied sub nom., Doe v. Sec’y of Health & Human Servs., 94 Fed. Cl. 597

(2010), aff’d, Lombardi v. Sec’y of Health & Human Servs., 656 F.3d 1343 (Fed. Cir. 2011).

Mr. Contreras’s case is one in which the treating doctors had different opinions regarding

causation. As Mr. Contreras argued, Dr. Wagner and Dr. Garrett stated that the hepatitis B

vaccine caused the transverse myelitis. On the other hand, his pediatrician, Dr. Kyazze, was

quite forthright in stating that he did not know what caused Mr. Contreras’s transverse myelitis.

Tr. 60; see supra V.B.1(a). But, Mr. Contreras’s infectious disease doctor, Dr. Cheung, stated

there was no causal relationship between the hepatitis B vaccine and transverse myelitis. Exhibit

7 at 147. Dr. Cheung came to this conclusion after reviewing literature and considering the

amount of time between the vaccination and the onset of neurologic problems. Exhibit 7 at 147.

According to a record Dr. Babbitt wrote, Dr. Lake (Mr. Contreras’s treating neurologist) and he

agreed with Dr. Cheung’s opinion that the vaccinations were not causative. Exhibit 7 at 126.

Although Mr. Contreras did not cite the statements of Dr. Cheung, Dr. Lake and Dr. Babbitt,

these statements are part of the record in this case and must be considered. 42 U.S.C. § 300aa-

13(a)(1).

If it is correct that the opinion of a treating doctor is not binding on a special master, then

it appears that the special master must necessarily weigh any opinions offered by treating doctors

to determine the relative value of divergent opinions. If so, the ensuing question is what factors

should the special master use in evaluating those opinions. Although the Federal Circuit stated

that the opinions of treating doctors “are favored . . . as treating physicians are likely to be in the

best position to determine whether ‘a logical sequence of cause and effect show[s] that the

vaccination was the reason for the injury,’” Capizzano, 440 F.3d at 1326 (quoting Althen, 418

F.3d at 1280), the Federal Circuit has offered no guidance regarding the weight to give the

opinions of treating doctors when their opinions are inconsistent. Similarly, while the Court

stated that the April 5, 2012 Entitlement Decision applied the wrong standard “as a matter of

law” in evaluating Dr. Garrett, the Court did not identify what factors should be used when

comparing the conflicting opinions from treating doctors. See Opinion and Order, 107 Fed. Cl.

at 300-01.

Generally, the Federal Circuit has stated that an expert’s opinion is only as reliable (or

persuasive) as the reasons for the opinion. See Libas, Ltd. v. United States, 193 F.3d 1361, 1366

(“[I]f a trial court relies upon expert testimony, it should determine that the expert testimony is

reliable.”) (citing Perreira v. Sec’y of Health & Human Servs., 33 F.3d 1375, 1377 n.6, for the

proposition that “[a]n expert opinion is no better than the soundness of the reasons supporting

it”). Another special master has commented that “[o]bjective factors, including the

qualifications, training, and experience of the expert witnesses; the extent to which their

41

proffered opinions are supported by reliable medical research and other testimony; and the

factual basis for their opinions are all significant factors in determining what testimony to credit

and what to reject.” Tompkins v. Sec’y of Health & Human Servs., No. 10-261V, 2013 WL

3498652, at *4 (Fed. Cl. Spec. Mstr. June 21, 2013), mot. for rev. filed (July 22, 2013); see also

Franklin v. Sec’y of Health & Human Servs., No. 99-85, 2013 WL 3755954, at *15 (Fed. Cl.

Spec. Mstr. May 16, 2013) (finding written opinion of treating doctor who did not explain the

basis for her views less persuasive than the opinions of doctors retained in the litigation).

Here, these factors generally weigh against finding Dr. Garrett’s and Dr. Wagner’s

opinions persuasive on prong one. Although both doctors said that the vaccine did cause Mr.

Contreras’s injury, and such a statement necessarily implies that the vaccine can cause the injury,

see Caves, 100 Fed. Cl. at 145, the doctors did not explain how they reached the conclusion that

the vaccine can cause transverse myelitis.

Furthermore, Dr. Garrett’s and Dr. Wagner’s areas of expertise do not fit very well with

the topic of vaccines causing neurologic injuries. Dr. Wagner specializes in emergency

medicine, Tr. 64, 91, and Dr. Garrett specializes in pediatrics and pediatric critical care. Exhibit

13 at 1.

In contrast, Mr. Contreras’s treating neurologist, Dr. Lake, apparently informed Mr.

Contreras’s parents that the vaccinations did not cause his transverse myelitis. See exhibit 7 at

126. Her background in neurology makes her more qualified to render an opinion about the

cause of a neurologic disease. In addition, Dr. Cheung reached her opinion (that the vaccines

were not causative) after reviewing medical articles and studies.

For these reasons, Mr. Contreras does not prevail upon Althen prong one based solely

upon the statements of his treating doctors. Consequently, the opinions of the doctors retained

for this litigation will be considered next.

b) Dr. Poser and Dr. Steinman

To review, Dr. Poser and Dr. Steinman present the theory that the hepatitis B vaccine can

cause transverse myelitis via molecular mimicry. See exhibit 23 at 3, ¶ 5; exhibit 124 at 3.

Molecular mimicry is a theory commonly advanced by petitioners to explain how a

vaccine can cause an injury, particularly a demyelinating injury. Molecular mimicry appears in

articles published in highly regarded medical journals and Dr. Steinman has written some of

these articles. See Tr. 126-128 (discussing exhibits 63, 143-44).31 Dr. Steinman has testified

31

Dr. Steinman’s experiments have primarily focused on injecting an animal with a

substance to see if the animal develops a disease. See, e.g., exhibit 112 (Lawrence Steinman,

Blocking Adhesion Molecules as Therapy for Multiple Sclerosis: Natalizumab, 4 Nature Rev.

510 (2005)); see also Tr. 243 (Dr. Steinman stating that he is “a person who has published a lot

about mice”). A premise for these studies is that if animals develop diseases, then humans will,

too.

42

about molecular mimicry and he has explained the basic concepts as well as, if not better than,

any expert appearing in the Vaccine Program.

c) Daubert Analysis of Molecular Mimicry Theory

Whether the theory of molecular mimicry is a reliable explanation for hepatitis B

vaccine causing transverse myelitis is analyzed under Daubert. Terran, 195 F.3d at 1316 n.2

(citing Daubert, 509 U.S. at 592-95). As recognized in Terran, the Daubert factors for

analyzing the reliability of testimony are:

(1) whether a theory or technique can be (and has been) tested; (2)

whether the theory or technique has been subjected to peer review and

publication; (3) whether there is a known or potential rate of error and

whether there are standards for controlling the error; and, (4) whether the

theory or technique enjoys general acceptance within a relevant scientific

community.

Terran, 195 F.3d at 1316 n.2.

(1) Whether the theory of molecular mimicry can be

(and has been) tested

The Federal Circuit has alluded to the testability of a theory as a factor that special

masters may consider in evaluating a petitioner’s expert’s theory of causation. See Perreira, 33

F.3d at 1377 (“When the special master asked the expert to support his theory that a vaccine can

aggravate a preexisting condition 14 days after the vaccine, the expert acknowledged that it was

not supported in the literature and that ‘. . . it hasn’t been studied.’ Therefore, we reject the

argument that there is support for the expert's opinion.”); Moberly, 592 F.3d at 1324

(petitioners’ “expert witness testified that the proposed mechanism had never been tested in any

peer-reviewed study. Although a Vaccine Act claimant is not required to present proof of

causation to the level of scientific certainty, the special master is entitled to require some indicia

of reliability to support the assertion of the expert witness.”).

The evidence in the record concerning whether the theory of molecular mimicry can be

tested to show hepatitis B vaccine can cause transverse myelitis is scant. Dr. Steinman only

discussed it briefly at the hearing, see Tr. 544, and Dr. Whitton briefly addressed it in one of his

reports. See Resp’t’s Ex. L at 10. None of the other experts addressed it.

Dr. Steinman explained that his theory is testable and that “it could be done.” Tr. 544.

Dr. Whitton agreed. Resp’t’s Ex. L at 10. Dr. Steinman was unaware of any research that

specifically sought to determine if the hepatitis B vaccine can cause demyelinating diseases in

humans. Tr. 544-45.

Although the parties agreed that Dr. Steinman’s theory of molecular mimicry is testable,

it has not been tested. This factor does not preponderate in Mr. Contreras’s favor.

43

(2) Whether the theory or technique has been

subjected to peer review and publication

According to Dr. Steinman, his proposed mechanism of molecular mimicry is “a theory

that is based on a lot of articles by prominent people in the peer reviewed literature.” Tr. 123.

Dr. Steinman explained that “there’s a large number of papers that have been published over the

years in support of molecular mimicry.” Tr. 124. The “seminal” paper was the 1985 Oldstone

& Fujinami paper (exhibit 62), Tr. 124, which Dr. Steinman stated put molecular mimicry “on

the map.” Tr. 124. Dr. Steinman averred there are now “hundreds if not thousands of . . .

exemplifications” of molecular mimicry, and he has written “some of the primary papers”

concerning the theory. Tr. 124.

The general theory of molecular mimicry has been explored in numerous peer-reviewed

publications in a variety of contexts. But as Dr. Steinman acknowledged, because his more

specific theory of hepatitis B vaccine causing transverse myelitis via molecular mimicry has not

been tested, it has necessarily not been subject to peer review or publication. As Dr. Steinman

testified, none of the articles on which he relied in his reports addressed whether the hepatitis B

can cause transverse myelitis. Tr. 191.

In the absence of a peer-reviewed article showing the hepatitis B vaccine causes

transverse myelitis, Dr. Steinman relied upon other articles, which, according to Dr. Steinman,

support the theory. As a matter of law, Dr. Steinman may rely upon circumstantial evidence to

support his opinion. See Capizzano, 440 F.3d at 1325.

Relying on the Bogdanos study,32 Dr. Steinman opined that the hepatitis B vaccine has

been shown to cause an increased production of antibodies that react with myelin. Tr. 152.33

Dr. Steinman explained that the authors of the Bogdanos article studied the antibody levels in

adults before and after receiving the hepatitis B vaccine, and “about 60 percent . . . developed

antibodies to hepatitis B that cross reacted with one of the myelin proteins.” Tr. 152. Dr.

Steinman stated that whether children would have a similar reaction is unknown. Tr. 153.

Dr. Steinman interpreted this study to provide an example of molecular mimicry. Tr.

153. According to Dr. Steinman, an antibody to a myelin protein is significant because it

“could be something that leads to an autoimmune demyelinating disease.” Tr. 153. However,

as Dr. Steinman acknowledged, none of the fifty people in the Bogdanos study actually

developed a demyelinating disease. Dr. Steinman distinguished between the production of

autoantibodies and the onset of disease. Bogdanos established only that the former happened,

32

Exhibit 117 (Dimitrios–Petrou Bogdanos et al., A study of molecular mimicry and

immunological cross-reactivity between hepatitis B surface antigen and myelin mimics, 12(3)

Clinical & Developmental Immunology 217 (2005)).

33

Dr. Steinman relied upon Bogdanos even though the subjects were not Hispanic. Tr.

256-57.

44

not the latter. Tr. 235. Dr. Steinman predicted that if another study were done, then a study

involving many more people would identify someone who developed a demyelinating disease

after vaccination. Tr. 153-55.

Dr. Whitton was asked about the Bogdanos article. Like Dr. Steinman, Dr. Whitton

distinguished between the creation of autoantibodies and the onset of disease. He did not find

any evidence that the patients in the Bogdanos study developed autoimmune disease.

Furthermore, Dr. Whitton disagreed with the suggestion that a larger study would have found

people with an autoimmune disease. Tr. 424.

The undisputed distinction between self-antigens and disease was discussed in an article

by David C. Wraith and others. Exhibit L, tab 7. These authors asserted that “an identified

mimicry is of little pathogenic importance.” They explained “[m]olecular mimicry in itself is not

sufficient to trigger autoimmune pathology, and other factors intrinsic to infections, such as

tissue damage and long-lasting inflammatory reaction, might be required as well.” Id. at 1665.

The Oldstone and Fujinami article, which was written in 1985, provides a foundation for

the theory of molecular mimicry. The Bogdanos article moves the theory forward a bit by

showing that the hepatitis B vaccine can prompt the production of antibodies that may react with

a component of the nervous system. This material makes the theory that the hepatitis B vaccine

can cause demyelination possible, and perhaps even plausible.

However, as discussed by Dr. Steinman, Dr. Whitton, and the Wraith article, the onset of

disease requires more than just a similar sequence of proteins and the production of auto-

antibodies. As Dr. Whitton explained, the lack of disease among the Bogdanos participants is

telling. The article demonstrates that the production of autoantibodies does not always cause a

disease. In this study, none of the fifty people developed a demyelinating disease after the

hepatitis B vaccination. Consequently, the peer-reviewed articles do not support a finding that it

is probably correct that hepatitis B vaccine can cause demyelination.

(3) Whether there is a known potential error rate and

whether there are methods for controlling the error

This factor is inapplicable to Dr. Steinman’s theory of molecular mimicry. Thus, it does

not preponderate for or against Mr. Contreras.

45

(4) Whether the theory or technique enjoys general

acceptance within a relevant scientific community34

As discussed, the general theory of molecular mimicry is well known and has been the

subject of a significant amount of academic research. Doctors generally accept that molecular

mimicry explains why some people with rheumatic fever develop Sydenham’s chorea. See

W.C., 704 F.3d at 1360. But, as Dr. Steinman conceded, his theory that the hepatitis B vaccine

can cause transverse myelitis via molecular mimicry has not been studied. Even in the absence

of testing, Dr. Sladky opined that a majority of neurologists would accept the proposition that

the hepatitis B vaccine can cause transverse myelitis. Tr. 386.35 He stated, however, that none

of them would agree with Mr. Contreras that the hepatitis B vaccine could cause a

demyelinating disease within 26 hours. Tr. 386.

Moreover, epidemiological studies “might be needed for a theory to achieve ‘general

acceptance in the scientific or medical communities.’” W.C., 704 F.3d at 1356. As discussed

below, pertinent epidemiological studies have found no evidence that the hepatitis B vaccine can

cause demyelinating diseases.

(5) Epidemiological studies

Although petitioners are not required to produce epidemiological studies, they may be

considered. Andreu, 569 F.3d at 1379 (citing Daubert, 509 U.S. at 593-97). As discussed, Dr.

Sladky and Dr. Whitton relied on epidemiological studies that demonstrated that there is no

causal relationship between the hepatitis B vaccine and transverse myelitis. The most on-point

and persuasive are the Touze study (exhibit G), the Zipp study (exhibit H), and the Mikaeloff

study (exhibit L, tab 29).

The authors of the Touze study assessed the possible association between the hepatitis B

vaccine and demyelinating diseases of the central nervous system. Exhibit G at 181.

Id. The study was performed on “236 cases and 355 matched controls (117 pairs and 119

triplets)” Id. at 181-82. The authors found that their study “was sufficiently powerful to rule out

34

A “general acceptance” in the medical community requires a burden of proof that is

significantly higher than that required under the Act because “[i]n medical research, ‘attribution

of causation is typically not made until a level of very near certainty—perhaps 95%

probability—is achieved.” Andreu, 569 F.3d at 1379-80 (quoting Liable v. Sec’y of Health &

Human Servs., No. 98-120V, 2000 WL 1517672, at *18 (Fed. Cl. Spec. Mstr. Sept. 7, 2000)).

Nonetheless, the Federal Circuit before and after Andreu has endorsed a special master’s use of

the Daubert factors, which include “general acceptance.”

35

Dr. Sladky did not explain the basis for his opinion. Neither party submitted additional

evidence that speaks to whether the medical community generally accepts that the hepatitis B

vaccine can cause transverse myelitis.

46

a strong association between [hepatitis B] vaccine exposure and a subsequent demyelinating

event.” Id. at 182.

The authors of the Zipp study found no causal relationship between the hepatitis B

vaccine and, among other things, demyelinating diseases of the central nervous system, such as

transverse myelitis. See exhibit H at 964. The authors compared the incidence of central

nervous system diseases in 27,229 individuals who had received the hepatitis B vaccine with

107,469 individuals who had not received the hepatitis B vaccine. Id. The authors found that

there was “[n]o significant difference between vaccinated and non-vaccinated individuals . . . for

demyelinating episodes at any time point analyzed.” Id. (citing id. at Table 1). In fact, the

authors found “no evidence of demyelination induced by hepatitis B immunization.” Id. at 964

(emphasis added).

Another informative study was conducted by a group of French researchers. They

identified a group of 356 children who had developed their first episode of demyelination within

the central nervous system before they were age 16. The researchers followed these subjects, for

an average of 5.8 years, to see whether they developed a second episode of neurological

symptoms lasting for more than 24 hours. Exhibit L, tab 29 (Yann Mikaeloff et al., Hepatitis B

vaccine and the risk of relapse after a first childhood episode of CNS inflammatory

demylination, 130 Brain 1105 (2007)) at 1106-07. The authors concluded that the hepatitis B

vaccine “was not associated with a significant increase in the risk of relapse.” Id. at 1108.

The type of study Mikaeloff conducted has been recognized as valuable by the Federal

Circuit. Mikaeloff evaluated people who already suffered from some type of demyelinating

incident within their central nervous system. As such, if the theory that a vaccine could cause

demyelination were correct, then this group of participants would be particularly vulnerable to

the adverse effects of the vaccination. See exhibit L (Dr. Whitton’s report) at 4-8 (describing the

value of epidemiologic studies); Tr. 445.36 The results in Mikaeloff—that people with a previous

disorder did not relapse after vaccination—undermine the theory that the hepatitis B vaccination

can cause demyelination within the central nervous system. See W.C., 704 F.3d at 1361 (finding

that the special master’s assessment of epidemiological studies including those looking for

relapses of multiple sclerosis after hepatitis B vaccination was not arbitrary or capricious).

When Dr. Steinman was asked about the Mikaeloff study, he described it as a “group of

competent people,” who found data showing that “there’s no risk that hepatitis B [vaccine]

would push you to have another relapse.” Tr. 544.

Epidemiological studies like Touze, Zipp, and Mikaeloff are powerful evidence that the

hepatitis B vaccine does not cause demyelinating illnesses. Zipp is a large study involving more

than 100,000 people. Mikaeloff investigated people who should, according to the hypothesis that

vaccinations lead to demyelination, be especially vulnerable to an adverse consequence. These

studies make a finding that the hepatitis B vaccination can cause a demyelinating illness

unlikely, although scientific investigations could never establish, with scientific certainty, that

36

The transcript, unfortunately, does not spell Mikaeloff correctly.

47

the hepatitis B vaccine absolutely does not cause demyelination. See Tr. 460 (“Science cannot

prove all negatives.”).

(6) Case Reports

While epidemiological studies are very probative, case reports are not worth much

weight. The primary value of case reports is to present a signal that two events (such as

vaccination and a disease) have occurred in temporal proximity. This signal may prompt a more

vigorous investigation that may or may not support a causal relationship. See Tr. 295-99 (Dr.

Sladky), cf. 429-30 (Dr. Whitton stating that he gives “isolated case reports[] very little weight”).

According to an article Dr. Garrett cited, “case reports alone are inadequate in answering

questions of causation with [autoimmune diseases].” Exhibit 15 (Robert T. Chen et al.,

Epidemiology of Autoimmune Reactions Induced by Vaccination, 16 Journal of Autoimmunity

309, 310 (2001)).

Some doctors, particularly Dr. Poser, appeared to value case reports more than

epidemiological studies. Dr. Steinman also questioned the value of epidemiology in general. He

opined that it “doesn’t tell you why something happens. It just tells you whether there are

numerical differences. Then you can speculate whether it could be due to diet or other factors.”

Tr. 198-99. For this reason, Dr. Steinman considers case reports to be more persuasive because

“the absence of evidence is nowhere near as compelling as the presence of evidence in certain

cases.” Tr. 195. This view is in conflict with the way scientific studies are usually interpreted.

“In the hierarchy of weight of scientific evidence, data from well-designed randomized clinical

trials clearly outweighs that from well-controlled observational studies, which in turn, is

hierarchically better than uncontrolled observational studies, case series, and then finally, case

reports.” Exhibit 15 (Chen) at 312. Dr. Sladky and Dr. Whitton shared this approach to

weighing evidence.

The predominant view among legal authorities is in accord. The Federal Judicial Center

has published a series of guides designed “to assist judges . . . in reaching an informed and

reasoned assessment concerning the basis of expert evidence.” Jerome P. Kassirer and Gladys

Kessler, Preface, in Reference Manual on Scientific Evidence (3d ed. 2011). A pertinent guide

states “[a]necdotal evidence usually amounts to reports that events of one kind are followed by

events of another kind. Typically, the reports are not even sufficient to show association,

because there is no comparison group.” David H. Kaye and David A. Freedman, “Reference

Guide on Statistics” in Reference Manual on Scientific Evidence at 218. These authors also state

“some courts have suggested that attempts to infer causation from anecdotal reports are

inadmissible as unsound methodology under Daubert.” Id. at 217 n. 14 (citing cases). Reliance

upon the Reference Manual from the Federal Judicial Center is appropriate because the burden of

proof in an off-Table case, like Mr. Contreras’s case, is “the traditional tort standard.” Moberly,

592 F.3d at 1322.

The undersigned’s view is similar to the position advance in the Reference Manual.

Because the parties have included case reports in the record, the undersigned has reviewed those

case reports. 42 U.S.C. § 300aa—13(a). The case reports provide little, if any, value in

assessing causation.

48

4. Finding on Althen Prong One

As the party with the burden of proof and as the proponent of the molecular mimicry

theory, Mr. Contreras bears the burden of demonstrating that the evidence is persuasive. Althen,

418 F.3d at 1278. It is not enough for Mr. Contreras merely to submit an opinion. The opinion

must be reliable. Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir.

1994); see also Caves, 100 Fed. Cl. at 134-35.

Here, Mr. Contreras has not provided preponderant evidence that demonstrates the

reliability of the proposition that the hepatitis B vaccine can cause transverse myelitis (or GBS)

via molecular mimicry with respect to the Daubert factors. At best, Mr. Contreras can cite to

Dr. Sladky’s opinion that most neurologists would accept the proposition that the hepatitis B

vaccine can cause transverse myelitis. However, two other Daubert factors—whether it has

been tested and whether it has been subject to peer review—do not preponderate in his favor.

Further, the epidemiological studies Dr. Sladky and Dr. Whitton referenced found no causal

relationship between the hepatitis B vaccine and the incidence of demyelinating diseases. The

findings of the epidemiological studies suggest that, contrary to Dr. Sladky’s testimony, the

theory is not generally accepted. See W.C., 704 F.3d at 1356. Finally, the case reports on

which Dr. Steinman, Dr. Poser, and Dr. Garrett rely have minimal value. Accordingly, Mr.

Contreras’s claim fails on Althen prong one.

C. Prong Three from Althen - Timing

Although the lack of preponderant evidence on Althen prong one means that Mr.

Contreras is not entitled to compensation, the Court has directed a review of each Althen prong.

Opinion and Order, 107 Fed. Cl. at 296. It is easier to address the third prong, regarding timing,

before addressing the second prong.

1. Standards for Adjudicating Althen Prong Three

In Althen, the Federal Circuit stated that a petitioner must provide preponderant evidence

of “a showing of a proximate temporal relationship between vaccination and injury.” 418 F.3d at

1278. The Federal Circuit elaborated on this aspect of Althen in Bazan, a case in which the

petitioner claimed that a booster dose of a Td vaccine caused her to suffer an injury within her

central nervous system, known as ADEM, approximately eleven hours after her vaccination.

The Federal Circuit stated that this “temporal relationship [was] . . . not such that it is medically

acceptable to conclude that the vaccination and the injury [were] . . . causally linked.” 539 F.3d

at 1352.

The April 5, 2012 Entitlement Decision referenced Althen and Bazan in determining that

Mr. Contreras bore the burden of presenting preponderant evidence that his injury occurred

within a time-frame that “the medical community would accept . . . for inferring that [his] . . .

hepatitis B vaccine caused [his] . . . transverse myelitis.” 2012 WL 1441315, at *23. However,

the Court held this recitation was erroneous. In its Opinion and Order, the Court stated that the

49

correct standard is whether the petitioner has shown “that the alleged vaccine injury occurred

within a medically-acceptable time-frame.” 107 Fed. Cl. at 302.

Pursuant to the Court’s instruction, Mr. Contreras must demonstrate by a preponderance

of the evidence “that the alleged vaccine injury occurred within a medically-acceptable time-

frame” such that it is “medically acceptable to infer causation-in-fact.” Opinion and Order, 107

Fed. Cl. at 302 (citing Pafford, 451 F.3d at 1358; Bazan, 539 F.3d at 1352).

2. Onset of Mr. Contreras’s Condition: 24-26 Hours after

Vaccination

The parties agreed that Mr. Contreras began to experience neurologic problems

approximately 24-26 hours after he received his vaccinations. The parties have slightly different

arguments about when, in this range, the symptoms actually began. See Resp’t’s Post-Hearing

Br. at 3 n. 5 (acknowledging that the parties disputed when, exactly, Mr. Contreras’s symptoms

began). The Secretary proposed a relatively earlier onset, see Resp’t’s Rule 4 Rep’t at 9

(approximately 24 hours), and Mr. Contreras proposed a relatively later onset. See Pet’r’s Br. on

Remand at 42 (26 hours). As discussed in more detail below, whether Mr. Contreras’s

symptoms occurred in 26 hours or fewer does not affect the outcome of this matter because

preponderant evidence establishes that transverse myelitis takes at least a few days to manifest.37

3. Medically Acceptable Time-Frame

a) Previous Adjudications

Throughout this litigation, timing was a critical issue. See Opinion and Order, 107 Fed.

Cl. at 285. After the initial efforts to resolve the case informally did no

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