SUPREME COURT

STATE OF LOUISIANA

STATE OF LOUISIANA, No. 2014-KA-2153

Appeal from Conviction and Death Sentence Imposed In the First Judicial District, the Parish of Caddo, No. 304,048,Hon. Joseph Bleich, Presiding.

Plaintiff-Appellee

v.

RODRICUS CRAWFORD,

Defendant-Appellant.

BRIEF OF THE INNOCENCE NETWORK AS

AMICUS CURIAE IN SUPPORT OF APPELLANT

ANDREW R. LEE (#21196) JONES WALKER LLP 201 St. Charles Avenue New Orleans, Louisiana 70170 (504) 582-8000

MARC WOLINSKY Counsel of Record Pro Hac Vice Application Pending WACHTELL, LIPTON, ROSEN & KATZ New York, New York 10171 (212) 403-1226

Attorneys for Amicus Curiae Innocence Network, Inc.

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TABLE OF CONTENTS

Page

Statement of Interest of Amicus ..................................................................................................... vii 

Preliminary Statement ...................................................................................................................... 1 

ARGUMENT ................................................................................................................................... 3 

I.  MEDICAL SCIENCE ESTABLISHES THAT THE PROSECUTION DID NOT PROVE RODRICUS CRAWFORD’S GUILT BEYOND A REASONABLE DOUBT. ................................................................................................................................. 3 

A.  Medical science establishes that Roderius Lott died of septic shock resulting from pneumonia. ......................................................................................................... 4 

1.  Septic shock resulting from pneumonia is a leading cause of death in children. ....................................................................................................... 4 

2.  Roderius Lott’s medical history and autopsy establish that he died of sepsis. .......................................................................................................... 5 

B.  The prosecution’s medical evidence was biased, consciously and unconsciously, resulting in Dr. Traylor offering justifications for his conclusions that are not based in medical science. ..................................................... 7 

1.  The record establishes that Dr. Traylor’s testimony was marred by bias. .................................................................................................................. 8 

2.  The reasons that Dr. Traylor and Dr. Thoma gave for their conclusion that Roderius did not die of sepsis have no basis in medical science. ............................................................................................. 10 

  The presence of strep pneumoniae bacteria ...................................... 10 a.

  Contamination of the blood sample .................................................. 11 b.

  One dose of Prevnar vaccine ............................................................ 12 c.

  Bronchial vs. lobar pneumonia ......................................................... 13 d.

  The incidence of sepsis in one-year-old children ............................. 13 e.

  The severity of Roderius’ symptoms ................................................ 14 f.

ii

C.  Dr. Traylor’s testimony regarding the injuries to Roderius’ inner lips is contradicted by medical science, and his failure to preserve a tissue sample violated accepted protocol. ........................................................................................ 15 

1.  Dr. Traylor was wrong in claiming that the time of the injuries to Roderius’ inner lips could not be established through microscopic examination. ................................................................................................... 16 

2.  Dr. Traylor failed to follow basic protocol and thereby deprived the defense of the ability to prove scientifically that Roderius’ inner lip injuries were caused by his bathroom fall. ...................................... 17 

II.  THIS CASE IS A PARADIGMATIC EXAMPLE OF THE RISK OF WRONGFUL CONVICTIONS BASED UPON FAULTY SCIENCE. ...................................................... 18 

CONCLUSION .............................................................................................................................. 20 

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TABLE OF AUTHORITIES

Page

Cases 

Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579 (1993) .................................................................................................................. 19

Edmonds v. State, 955 So.2d 787 (Miss. 2007) ...................................................................................................... 19

State v. Bright, 98-0398 (La. 4/11/00), 776 So.2d 1134 ...................................................................................... 3

State v. Chism, 436 So.2d 464 (La. 1983) ............................................................................................................ 3

State v. Martin, 458 So.2d 454 (La. 1984) ............................................................................................................ 3

State v. Quatrevingt, 93-1644 (La. 2/28/96), 670 So.2d 197 ...................................................................................... 19

State v. Seals, 95-0305 (La. 11/25/96), 684 So.2d 368, cert. denied, 520 U.S. 1199 (1997) ............................. 3

United States v. Addison, 498 F.2d 741 (D.C. Cir. 1974) ................................................................................................... 19

Watts v. Radiator Specialty Co., 990 So.2d 143 (Miss. 2008) ...................................................................................................... 19

Other Authorities 

A. Martinot, et al., Sepsis in Neonates and Children: Definitions, Epidemiology, and Outcome, 13 Ped. Emergency 277 (1997) .................................................................................. 14

Adrienne G. Randolph & Russell J. McCulloh, Pediatric sepsis: Important considerations for diagnosing and managing severe infections in infants, children, and adolescents, 5 Virulence 179 (2014) .................................................................................... 5

Benito Morentin, et al., Clinicopathological Features of Sudden Unexpected Infectious Death: Population-based Study in Children and Young Adults, 220 Forensic Sci. Int’l 80 (2012) ..........................................................................................13, 15

iv

Brandon L. Garrett & Peter J. Neufeld, Invalid Forensic Science Testimony and Wrongful Convictions, 95 Va. L. Rev. 1, 2 (2009) ................................................................................... viii

C. Myers & Alain Gervaix, Streptococcus pneumoniae Bacteremia in Children, 30S Int’l J. Antimicrobial Agents S24 (2007) ....................................................................... 5, 15

Center for Disease Control, Identification and Characterization of Streptococcus pneumoniae (2015) ..................................................................................................................... 11

Center for Disease Control, Streptococcus pneumoniae guidelines (2015) .............................12, 13

Christian Torgersen, et al., Macroscopic Postmortem Findings in 235 Surgical Intensive Care Patients with Sepsis, 108 Critical Care & Trauma 1841 (2009) ....................................... 16

Christopher D. Doern & Carey-Ann D. Burnham, It’s Not Easy Being Green: the Viridans Group Streptococci, with a Focus on Pediatric Clinical Manifestations, 48 J. Clin. Microbiol. 3829 (2010) ............................................................................................. 11

Committee on Identifying the Needs of the Forensic Sciences Community, National Research Council, Strengthening Forensic Science in the United States: A Path Forward (2009) ........ vii

Donald Janner, Clinical Guide to Pediatric Infectious Disease (2004) ........................................ 10

Edwin S. Van Amersfoort, et al., Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock, 16 Clin. Microbiol. Rev. 379 (2003) ................................... 4

Elizabeth C. Burton & Nicole A. Singer, “Pediatric Natural Deaths,” in Forensic Pathology of Infancy and Childhood (Kim A. Collins& Roger W. Byard eds., 2014) ........... 5, 6

Henry F. Krous, et al., Sudden Unexpected Death in Childhood: A Report of 50 Cases, 8 Ped. & Dev. Pathol. 307 (2005) ............................................................................................. 15

Innocence Project, Unvalidated or Improper Forensic Science (as of May 29, 2015) ................. vii

Innocence Project, Wrongful Convictions Involving Unvalidated or Improper Forensic Science that Were Later Overturned through DNA Testing (as of May 29, 2015) ................... vii

Itiel E. Dror, et al., New Application of Psychology to Law: Improving Forensic Evidence and Expert Witness Contributions, 2 J. Applied Res. Memory & Cognition 78 (2013) ............. 7

J.A. Morris, et al., Postmortem bacteriology: a re-evaluation, 59 J. Clin. Pathol. 1 (2006) ........................................................................................................ 12

James A. Kellogg, et al., Identification of Streptococcus pneumonia Revisited, 39 J. Clin. Microbiol. 3373 (2001) ............................................................................................ 11

v

Janice J. Ophoven, “Pediatric Forensic Pathology,” in Potter’s Pathology of the Fetus, Infant and Child (Enid Gilbert-Barness, et al. eds., 2d ed. 2007) ............................................. 18

Janice J. Ophoven, “The Forensic Post Mortem,” in Pediatric and Perinatal Autopsy Manual (Marta C. Cohen & Irene Scheimberg eds., 2014) .......................................... 8, 9, 10, 17

Jean W. Keeling, “Post Mortem Examination in Babies and Children,” in Paediatric Forensic Medicine and Pathology (Anthony Busuttil & Jean W. Keeling eds., 2d ed. 2008) ............12, 18

Jesse M. Pines, Profiles in Patient Safety: Confirmation Bias in Emergency Medicine, 13 Acad. Emerg. Med. 90 (2006) ................................................................................................ 7

John T. Cacioppo, et al., Central and Peripheral Routes to Persuasion: An Individual Difference Perspective, 51 J. of Personality and Social Psychol. 1032 (1986) ......................... 19

Joshua A. Perper, “Microscopic Forensic Pathology,” in Spitz and Fisher’s Medicolegal Investigation of Death: Guidelines for the Application of Pathology to Crime Investigation (Werner Spitz & Daniel Spitz eds., 4th ed. 2006) ..........................................17, 18

Jyrki Raekallio, Determination of the Age of Wounds by Histochemical and Biochemical Methods, 1 Forensic Sci. 3 (1972) ............................................................................................. 17

Katherine L. O’Brien et al., Burden of Disease caused by Streptococcus pneumoniae in children younger than 5 years, 374 Lancet 893 (2009) .............................................................. 5

Keith A. Findley, Innocents at Risk: Adversary Imbalance, Forensic Science, and the Search for Truth, 38 Seton Hall L. Rev. 893 (2008). ................................................................ 19

Kent P. Hymel, Distinguishing Sudden Infant Death Syndrome from Child Abuse Fatalities, 118 Pediatrics 421 (2006) ...................................................................................................... 8, 14

Lance D. Reich, Cognitive Biases Make Judges & Juries Believe Weird Things, 10 No. 1 ABA SciTech Law. 4 (2013). ..................................................................................... 19

M. Barnham & C. Henderson, Group b streptococcal infection presenting as sudden death in infancy, 62 Archives Disease Childhood 419 (1987) .................................................. 15

M.A. Weber, et al., Infection and Sudden Unexpected Death in Infancy: A Systematic Retrospective Case Review, 371 Lancet 1848 (2008) ............................................................... 14

M.A. Weber, et al., The Role of Post Mortem Investigations in Determining the Cause of Sudden Unexpected Death in Infancy, 93 Archives Disease Childhood 1048 (2008) ................ 8

N. Sharief, et al., Overwhelming Sepsis Presenting as Sudden Unexpected Death, 69 Archives Disease Childhood 381 (1993) .............................................................................. 15

vi

Nakia N. Gaines, et al., Etiologies of septic shock in a pediatric emergency department population, 31 Ped. Infectious Dis. J. 1203 (2012) ................................................................... 11

National Association of Medical Examiners, Forensic Autopsy Performance Standards (2014) ................................................................................................................................. passim

National Center for Injury Prevention and Control, CDC, 10 Leading Causes of Death, United States, 2013, All Races, Both Sexes ................................................................................. 5

Neil E.I. Langlois, “Dating of Other Injuries in Children” in Forensic Pathology of Infancy and Childhood (Kim A. Collins & Roger W. Byard eds., 2014) ................................. 17

Nils Molander, Sudden Natural Death in Later Childhood and Adolescence, 57 Archives Disease Childhood 572 (1982) .............................................................................. 15

Paolo J.C. Marostica & Renato T. Stein, “Community-Acquired Bacterial Pneumonia,” in Disorders of the Respiratory Tract in Children (Robert W. Wilmott, et al. eds. 2012) .............. 5

Peter M. Cummings, et al., Atlas of Forensic Histopathology (2011) .......................................... 17

Pfizer, Prevnar 13 package insert (2015). ..................................................................................... 13

Reade A. Quinton, Investigation of Sudden Unexpected Infant Deaths, 4 Acad. Forensic Pathol. 316 (2014) ..................................................................................... 8, 18

Reinhard B. Dettmeyer, Forensic Histopathology: Fundamentals and Perspectives (2011) ...... 17

Roger W. Byard, Sudden Infant Death in Infancy, Childhood and Adolescence (2d ed. 2004) .........................................................................................................................14, 19

Saul M. Kassin, et al., The Forensic Confirmation Bias: Problems, Perspectives, and Proposed Solutions, 2 J. Applied Res. Memory & Cognition 42 (2013) .................................... 7

Saul Solomon & Menascu Kalkstein, Pneumonia Due to the Streptococcus Viridans, 205 Am. J. Med. Sci. 765 (1943) .........................................................................................10, 11

Stephanie M. Rangel, et al., The Role of ExoS in Dissemination of Pseudomonas aeruginosa during Pneumonia, PLOS Pathog., (2015). ................................................................................. 4

Tracey S. Corey & Kim A. Collins, “Pediatric Forensic Pathology,” in Pediatric Pathology (Thomas J. Stocker & Louis P. Dehner eds., 2d ed. 2001) ...................................................17, 18

Vinay Kumar, et al., Robbins Basic Pathology (9th ed. 2012) .............................................. passim

vii

STATEMENT OF INTEREST OF AMICUS

The Innocence Network is an association of more than sixty-nine organizations dedicated

to providing pro bono legal and investigative services to convicted individuals seeking to prove

their innocence. The members of the Network represent hundreds of prisoners with innocence

claims in all 50 states and the District of Columbia, as well as in countries around the world. The

work of Innocence Network member organizations led to the exoneration of 330 people who

served a combined 4,620 years behind bars for crimes they did not commit.

Based on its experience exonerating innocent individuals and examining the causes of

wrongful convictions, the Innocence Network has become keenly aware of the role that unreliable

or improper scientific evidence has played in producing miscarriages of justice. In 2009, the Na-

tional Academy of Sciences — the nation’s preeminent authority on scientific matters — pub-

lished its groundbreaking study revealing that many of the traditional forensic sciences are inade-

quately researched and validated, and in short, lack a significant scientific basis.1

Consistent with that conclusion, unvalidated or improper forensic science is the second

greatest contributor to wrongful convictions that were later overturned with DNA testing.2 Exam-

ination of post-conviction, DNA-based exonerations has demonstrated that flawed or inaccurate

forensic science testimony has contributed to more than 50% of those wrongful convictions. 3

An analysis of the first 200 DNA exoneration cases, which included examining the scientific tes-

timony in every one of the 137 cases in which trial testimony of forensic analysts could be locat-

ed, revealed that in 60% of the cases that had had forensic testimony, “forensic analysts called by

the prosecution provided invalid testimony at trial — that is, testimony with conclusions misstat-

ing empirical data or wholly unsupported by empirical data.”4

1 See Committee on Identifying the Needs of the Forensic Sciences Community, National Research

Council, Strengthening Forensic Science in the United States: A Path Forward (2009). 2 See Innocence Project, Wrongful Convictions Involving Unvalidated or Improper Forensic Sci-

ence that Were Later Overturned through DNA Testing (as of May 29, 2015). 3 See Innocence Project, Unvalidated or Improper Forensic Science (as of May 29, 2015). 4 Brandon L. Garrett & Peter J. Neufeld, Invalid Forensic Science Testimony and Wrongful Convic-

tions, 95 Va. L. Rev. 1, 2 (2009).

viii

As a leading national advocate for the wrongly convicted, the Innocence Network has a

compelling interest in ensuring scientific expert testimony is accurate and reliable throughout the

criminal justice system. This interest is implicated by the prosecution’s impermissible reliance on

unsupported and unreliable scientific evidence to convict Rodricus Crawford of killing his son.

1

PRELIMINARY STATEMENT

The death of one-year-old Roderius Lott was a tragedy. But that tragedy would be com-

pounded beyond measure if his father, Rodricus Crawford, were executed for a death that resulted

not from suffocation, as the prosecution’s medical witnesses claimed, but from a fatal illness.

The medical literature assembled for this amicus brief establishes that Roderius’ death

was caused by sepsis, a sometimes fatal condition resulting from the pneumonia that infected all

five lobes of Roderius’ lungs.5 That literature establishes that sepsis is a tragic and too common

cause of death in infants. It establishes that, untreated, death from sepsis can occur in a matter of

hours, often without warning. And the objective medical evidence from Roderius’ autopsy found

the signs that a pathologist would expect to find in an infant who succumbed to this disease.

Employing reasoning that lacks any foundation in medical science, the prosecution’s wit-

nesses, Dr. Traylor and Dr. Thoma, rejected this obvious explanation of the cause of Roderius’

death. Dr. Traylor claimed that Roderius was protected from pneumonia because Roderius had

received one dose out of the three dose regimen of pneumonia vaccine. But that claim has no

basis in accepted medical science— simply put, there is a reason why three doses are required.

Dr. Traylor claimed that Roderius could not have died from sepsis because Roderius did not dis-

play labored breathing or a serious fever. But the medical literature establishes that death from

sepsis can result quickly, with few if any symptoms or warning. Dr. Traylor claimed that Roderi-

us did not die of sepsis because one virulent form of bacteria, streptococcus pneumoniae, could

not be identified in Roderius’ blood sample. But the medical literature establishes that four tests

are required to identify streptococcus pneumoniae; the lab ran only one. And both Dr. Traylor

and Dr. Thoma claimed that Roderius did not die of sepsis because he did not display severe

symptoms before he went to bed the night he died. But the medical literature establishes that sep-

sis can kill infants quickly and without warning.

5 The medical literature cited in this brief can be accessed at https://goo.gl/RQ73sX.

2

The medical literature also establishes that Dr. Traylor violated standard medical proto-

col: he failed to examine slides of the bruised and abraded tissue on the inner part of Roderius’

lips under a microscope. This most basic of tests would have established the timing of the inju-

ries and whether they were the result of the bathroom fall that Roderius suffered the day before he

died. In short, if Dr. Traylor had simply examined the bruised tissue under a microscope, or for

that matter, preserved the tissue so that the defense expert could have done so, medical science

would have established with objective evidence that the inner lip injuries were caused by a prior

fall, instead of a crime.

How could Dr. Traylor and Dr. Thoma be so wrong? The scientific literature explains

that as well. Forensic testimony is prone to error because medical experts are susceptible to con-

firmation bias, a condition where experts begin an investigation with preconceived expectations

and theories, and, as a result, focus only on evidence that supports those theories, ignoring or ex-

plaining away evidence to the contrary. That is what happened here. Dr. Traylor reached his er-

roneous conclusion before he viewed the tissue slides showing that Roderius was suffering from

pneumonia and before he received the lab results establishing the presence of a blood infection.

The result was that both doctors’ opinions were tainted by the sort of bias that has result-

ed in the conviction and even the execution of innocent defendants. But in this case, the prosecu-

tion’s medical witnesses were not merely prone to bias, they admitted to it. Dr. Traylor went into

the autopsy “thinking” that the death was a homicide and concluded that Roderius’ tragic death

was a homicide before he had all the facts. Dr. Thoma started with that presumption and never

re-examined it when evidence to the contrary came in.

The defense medical expert, Dr. Daniel Spitz, provided the jury with accurate medical

science. But he was not cross-examined on the science. He was cross-examined on his compen-

sation, on whether he made a mistake in a single case, whether he performed more autopsies than

recommended in a given year, on whether he was riding on the reputational coattails of his father,

an equally renowned forensic expert. As a result, a search for the truth devolved into a grand-

standing sideshow and the jury accepted demonstrably erroneous claims that came from the

3

mouths of misguided witnesses — one of whom, Dr. Traylor, self-righteously claimed to be the

“voice of the victim.”

Louisiana courts require that every reasonable hypothesis of innocence be excluded.6

Every reasonable hypothesis cannot be excluded here. For the reasons discussed below, it is in-

cumbent upon this Court to exercise its obligation to review the sufficiency of the scientific evi-

dence that lies at the heart of this case with particular care and, upon that review, vacate the con-

viction and assure that Rodricus Crawford is not put to death on the basis of testimony that has no

basis in medical science.

ARGUMENT

I. MEDICAL SCIENCE ESTABLISHES THAT THE PROSECUTION DID NOT PROVE RODRICUS CRAWFORD’S GUILT BEYOND A REASONABLE DOUBT.

The core factual issue in this case was the cause of Roderius Lott’s death. The defense

asserted that Roderius died of “sepsis” or “septicemia,” in lay terms, an extreme reaction of the

immune system caused by his underlying pneumonia infection. There was no dispute that Ro-

derius had pneumonia. He did, in all five lobes of his lungs. And there was no dispute that strep-

tococcus bacteria was found in Roderius’ blood, or that streptococcus bacteria can cause sepsis

and death in infants. The dispute, rather, was on the significance of the pneumonia, the signifi-

cance of the bacteria in Roderius’ blood sample and the significance and extent of Roderius’ pre-

existing illness.

By contrast, the prosecution claimed that Roderius died of intentional smothering at the

hands of his father, pointing to bruising and abrasion on the upper and lower inner lips of Roderi-

us’ mouth.7 There was no dispute as to the presence of the injuries. The dispute was over wheth-

6 State v. Bright, 98-0398, p. 11 (La. 4/11/00), 776 So.2d 1134, 1141; State v. Seals, 95-0305, p. 7 (La. 11/25/96), 684 So.2d 368, 374, cert. denied, 520 U.S. 1199 (1997); State v. Martin, 458 So.2d 454, 462 (La. 1984); State v. Chism, 436 So.2d 464, 470 (La. 1983).

7 “Q: Other than the bilateral bruising what makes you think it was a suffocation? A: That is the reason why.” R2105.

4

er they were caused by manual pressure or by the fall that Roderius suffered one to two days be-

fore in the bathroom of his father’s home and, in the words of his mother, “busted” his lip and

bruised his forehead. R2359-60.8

These factual issues, at bottom, do not turn on questions of judgment or credibility. They

turn on principles of medical science. Thus, as to the defense theory: Objectively, how signifi-

cant was Roderius’ pneumonia? Can this level of pneumonia cause sepsis? Was there objective

evidence of sepsis? Could the type of bacteria found in Roderius’ blood cause sepsis? Did Ro-

derius display extremely serious symptoms in the hours before he died and, if he did not, does

that mean that he did not die of sepsis? And as to the prosecution theory: Could the time of the

injury to Roderius’ inner lips be established by microscopic examination?

The medical literature answers these questions and, in every single respect, answers the

questions in favor of the defense.

A. Medical science establishes that Roderius Lott died of septic shock resulting from pneumonia.

1. Septic shock resulting from pneumonia is a leading cause of death in children.

“Septic shock” or “septicemia” occurs when the body’s immune system, in its effort to

fight off a bacterial infection, attacks not only the bacteria, but also disrupts the normal function-

ing of vital organs, leading to death.9 Septic shock is evidenced by the presence of bacteria in the

blood and by examination of the vital organs themselves, which will display internal bleeding

(“hemorrhaging”) and “fibrin,” proteins associated with blood clotting, particularly in the lungs.10

8 See also R76 (police report); R1016-17 (Prelim. Exam.). 9 Vinay Kumar, et al., Robbins Basic Pathology, 94-95 (9th ed. 2012); Edwin S. Van Amersfoort, et

al., Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock, 16 Clin. Micro-biol. Rev. 379, 380-81 (2003); Stephanie M. Rangel, et al., The Role of ExoS in Dissemination of Pseudo-monas aeruginosa during Pneumonia, PLOS Pathog., 1 (2015).

10 See Elizabeth C. Burton & Nicole A. Singer, “Pediatric Natural Deaths,” in Forensic Pathology of Infancy and Childhood, 860-62 (Kim A. Collins& Roger W. Byard eds., 2014).

5

Bacterial pneumonia is the most common cause of pediatric sepsis11 and the single lead-

ing cause of death in children under five years of age worldwide.12 Streptococcus pneumonia,

i.e., pneumonia caused by the one of the 90-plus known “serotypes,” i.e., variations within a spe-

cies, of the bacteria “streptococcus pneumoniae,” is a leading cause of bacterial pneumonia and

sepsis in children worldwide, and is the number one killer of children under two years old.13 It is

estimated that in 2000, there were approximately 14.5 million cases of serious pneumococcal dis-

ease worldwide, that pneumococcal disease caused about 826,000 deaths in children aged 1–59

months, and that streptococcal pneumoniae caused approximately 11% of all deaths in children

aged 1–59 months.14

According to the National Vital Statistics System maintained by the Centers for Disease

Control (“CDC”), in 2013, bacterial septicemia was the seventh leading cause of death in children

under one year of age. For the next age grouping for which data is published, the 1 to 4 year age

group, septicemia was the eighth leading cause of death.15

2. Roderius Lott’s medical history and autopsy estab-lish that he died of sepsis.

Roderius was not a healthy child. He had a history of respiratory infection with a persis-

tent runny nose and noticeable wheezing. R1940-41. When he was seven months old, his mother

took him to the pediatric clinic because he had been coughing and congested for one month.

R2204-05. One month later, Roderius still had not improved and was continuing to cough,

sneeze, and display a runny nose. R2207. This means that Roderius was consistently sick for at

11 Burton & Singer, “Pediatric Natural Deaths” at 869. See also Adrienne G. Randolph & Russell J.

McCulloh, Pediatric sepsis: Important considerations for diagnosing and managing severe infections in infants, children, and adolescents, 5 Virulence 179, 179 (2014).

12 See Paolo J.C. Marostica & Renato T. Stein, “Community-Acquired Bacterial Pneumonia,” in Disorders of the Respiratory Tract in Children, 461 (Robert W. Wilmott, et al. eds. 2012).

13 C. Myers & Alain Gervaix, Streptococcus pneumoniae Bacteremia in Children, 30S Int’l J. Anti-microbial Agents S24, S24 (2007).

14 See Katherine L. O’Brien et al., Burden of Disease caused by Streptococcus pneumoniae in chil-dren younger than 5 years, 374 Lancet 893, 899 (2009).

15 National Center for Injury Prevention and Control, CDC, 10 Leading Causes of Death, United States, 2013, All Races, Both Sexes.

6

least a two-month period. His great aunt, Latasha Crawford, described Roderius as looking “sick-

ly” two days before he died. R2357-58. The night of his death, Roderius’ mother took a nasal

pump to Rodricus’ house so that Rodricus could use it to clear his son’s stuffed nose. R2340.

Rodricus told police in his voluntary interview the day of Roderius’ death that Roderius “was

breathing heavy” when he went to bed. R41.

The autopsy documented both the extent of his illness and clear signs of sepsis. A lab

culture confirmed the presence of streptococcus bacteria in Roderius’ blood. R68. Dr. Traylor

testified that any bacteria in the blood can cause sepsis. R2221.16 The autopsy found hemorrhag-

ing and abscesses in the lungs and burst capillaries (“petechiae”) in the lungs and thymus, all

signs of death from sepsis. R61.17

Although no chest x-ray or CT scan was done, microscopic examination of tissue slides

showed that Roderius had bronchial pneumonia in all five lobes of his lungs. R2165-66; State

Exs. 22-45. The tissue slides from Roderius’ lungs showed that the pneumonia had dense pockets

of a type of white blood cell (“neutrophils”) and indicia of blood clotting (“fibrin”). R2164,

2169. This means that the pneumonia was “acute” or “full blown,” which is characterized by

“red hepatization,” i.e., the presence of red blood cells, neutrophils and fibrin.18 Additionally, the

presence of excess watery fluid (“edema”), hemorrhaging and microabscesses — all noted by Dr.

Traylor — are indicative of a later stage infection.19

16 See generally Kumar, .et al., Robbins Basic Pathology at 312, Table 8-3 (listing thirteen species of

bacteria that cause sepsis). 17 Burton & Singer, “Pediatric Natural Deaths” at 860-62. 18 See Kumar, et al., Robbins Basic Pathology at 488, 489 (diagramming “acute pneumonia” in the

stage of red hepatization, characterized by neutrophils). 19 R2169 (discussing microabscesses), R2177 (discussing edema), R2181-82 (discussing hemorrhag-

es). See Kumar, et al., Robbins Basic Pathology at 488.

7

B. The prosecution’s medical evidence was biased, consciously and unconsciously, resulting in Dr. Traylor offering justifications for his conclusions that are not based in medical science.

In the face of all of this, Dr. Traylor and Dr. Thoma nonetheless concluded that Roderius

was intentionally smothered to death. The record establishes that they reached this conclusion

because they were biased, both subtly and overtly.

The subtle, unintentional bias that undermined the validity of both doctors’ conclusions is

well-understood and documented in the scientific literature. It is known as “confirmation bias,”

which occurs when an expert begins an investigation with preconceived expectations and theo-

ries, and, as a result, focuses only on evidence that supports those theories, ignoring or explaining

away evidence to the contrary.20 Forensic confirmation bias is particularly dangerous because it

can occur without the individual’s awareness or intention.21 In order to avoid this bias, accepted

standards in the field of forensic medicine demand that a forensic scientist approach his or her

task with no preconceived ideas, reserving judgment until all of the evidence has been gathered.22

Forensic investigation of a childhood fatality typically has three steps: 1) collection and

preservation of evidence; followed by 2) identification and analysis of the key findings, including

the investigation, case documents and post mortem followed by the development of a differential

diagnosis; and finally 3) diagnosis, final opinions, and interpretation.23 These stages ensure that

both evidence and analysis are as reliable as possible. Experts agree that when it is “difficult or

impossible to differentiate between a natural unexplained infant death, an unintentional or acci-

dental infant death, and an unnatural (intentional) infant death,” protocols play a critical role in

20 Saul M. Kassin, et al., The Forensic Confirmation Bias: Problems, Perspectives, and Proposed

Solutions, 2 J. Applied Res. Memory & Cognition 42, 45 (2013); Jesse M. Pines, Profiles in Patient Safety: Confirmation Bias in Emergency Medicine, 13 Acad. Emerg. Med. 90, 92 (2006).

21 Itiel E. Dror, et al., New Application of Psychology to Law: Improving Forensic Evidence and Ex-pert Witness Contributions, 2 J. Applied Res. Memory & Cognition 78, 79 (2013).

22 National Association of Medical Examiners, Forensic Autopsy Performance Standards, 10, Stand-ard B5 (2014) (“Interpretations and opinions must be formulated only after consideration of available in-formation and only after all necessary information has been obtained.”).

23 Janice J. Ophoven, “The Forensic Post Mortem,” in Pediatric and Perinatal Autopsy Manual, 392 (Marta C. Cohen & Irene Scheimberg eds., 2014). See also Forensic Autopsy Performance Standards at 10, Standard B5.

8

diminishing forensic cognitive bias, which in turn reduces the likelihood of erroneous criminal

convictions.24 Particularly in cases of sudden infant death, standards of the profession strongly

advise medical examiners to diagnose the “cause and circumstance (or manner of death) . . .

through the use of scientific methods, principles, and procedures following a complete and thor-

ough investigation.”25

1. The record establishes that Dr. Traylor’s testimony was marred by bias.

The record demonstrates that forensic confirmation bias pervaded the prosecution’s entire

medical case. Thus, even before the autopsy was done, Dr. Thoma assumed that the bruises to

Roderius’ forehead were caused by abuse, unaware that Roderius’ mother had told the authorities

that she had seen the bruises on his forehead the day before he died and understood that the bruis-

es had been caused by a bathroom fall. R2087-88. At the time he ruled Roderius’ death a homi-

cide, Dr. Traylor was unaware of Roderius’ months-long history of respiratory infection; he did

not recall being told that Roderius was wheezing the night he died as reported both by Rodricus

and Roderius’ grandmother, Abigail Crawford, and apparently ignored Rodricus’ statement to the

police that Roderius’ breathing was “heavy” when he went to sleep.26 Dr. Traylor was unaware

that Roderius had pneumonia in all five lobes of his lungs. And he was unaware that Roderius

had streptococcus bacteria in his blood.27

24 Kent P. Hymel, Distinguishing Sudden Infant Death Syndrome from Child Abuse Fatalities, 118

Pediatrics 421, 422 (2006). 25 Ophoven, “The Forensic Post Mortem,” at 376. See also Reade A. Quinton, Investigation of Sud-

den Unexpected Infant Deaths, 4 Acad. Forensic Pathol. 316 (2014) ; M.A. Weber, et al., The Role of Post Mortem Investigations in Determining the Cause of Sudden Unexpected Death in Infancy, 93 Archives Dis-ease Childhood 1048, 1052 (2008) (finding that autopsies conducted by pediatric pathologists using a set methodology significantly improved the ability to ascertain a cause of death).

26 R86 (affidavit in support of search warrant); R41 (police report); R1940-41 (Abigail Crawford tes-timony).

27 Dr. Traylor testified that he reached his preliminary conclusion of the cause of death “[i]mmediately” following the autopsy, which was conducted on February 16, 2012. R2211. The lung tissue samples were first obtained at that time, and were not examined until later. R61, 64 (autopsy report); R2211. And the blood lab results were not reported until February 22, 2012. R68 (blood culture report). As for being unaware of Roderius’ wheezing, see R2221.

9

When faced with evidence that conflicted with his initial conclusion, Dr. Traylor did not

conduct the additional tests that could have proven or disproven homicide as the cause of death.

Indeed, he did not even preserve tissue samples of Roderius’ inner lips so that his conclusions

could be subjected to an independent review, something that standard practice requires.28 And at

trial, he crossed the line from being an expert into being an advocate, claiming that he was testify-

ing as “the voice of the victim,” R2418, and testifying in rebuttal to question not the scientific

underpinnings of Dr. Spitz’s testimony, but on irrelevancies, such as whether Dr. Spitz had con-

ducted more autopsies than deemed advisable by the National Association of Medical Examiners.

R2405-18.

Dr. Traylor not only succumbed to confirmation bias, he admitted to actual bias, conduct-

ing the autopsy not with an open mind, but with the idea that he needed to exclude homicide as

the cause of death. Starting from that premise, he concluded that Roderius’ death was a homicide

before he had all the facts. R2197. Dr. Thoma did the same, testifying that “every case that hap-

pens in a situation where you have an unexpected death in an infant . . . has to be treated as a

homicide until proven otherwise.” R2087. The result was that both doctors fell into a number of

the well-understood “common traps” that have been identified as leading to faulty conclusions in

pediatric autopsies.

Thus, as shown below: (1) he failed “to identify evidence of significant vital reaction in

tissues damaged from what appears to be acute injury”; (2) he failed “to identify, document, and

consider signs and symptoms of illness that identify possible disease conditions”; (3) he failed “to

properly evaluate and collect key biomechanical elements in cases of possible falls”; (4) he failed

“to identify and consider medical records that identify a significant change that may indicate the

28 Ophoven, “The Forensic Post Mortem” at 394, 397 (“Routine histopathology (microscopic) exam-

ination of normal appearing organs and abnormal tissues is a necessary part of a pediatric forensic autop-sy.”), 405 (recommending “[h]istologic sampling of pertinent injuries” in any investigation of “possible asphyxia deaths”); Forensic Autopsy Performance Standards at 22.

10

time of prior injury or serious illness”; and (5) he failed “to adequately document and sample in-

juries that might facilitate timing of injury, such as fractures, bruises, and dura.”29

2. The reasons that Dr. Traylor and Dr. Thoma gave for their conclusion that Roderius did not die of sep-sis have no basis in medical science.

In the face of the objective medical evidence establishing that Roderius had pneumonia,

bacteria in his blood, and hemorrhaging in his vital organs, Dr. Traylor and Dr. Thoma nonethe-

less concluded that Roderius did not die of sepsis. Dr. Traylor offered essentially six reasons for

his conclusion, Dr. Thoma only one. None of their reasoning is supported by medical science.

The presence of strep pneumoniae bacteria. Dr. Traylor claimed that Roderius a.

did not die of sepsis because the laboratory did not isolate the most virulent form of streptococcus

bacteria, “streptococcus pneumoniae,” in Roderius’ blood sample. That conclusion is not found-

ed in medical science.

As noted, the laboratory report on the culture of Roderius’ lung states that Roderius’

blood was infected with “alpha hemolytic streptococcus” and goes on to state that specific type

could not be identified. There are two types of alpha hemolytic streptococci: streptococcus

pneumoniae (“S. pneumoniae” or “strep pneumoniae”) and viridans group streptococci (“viridans

group streptococci” or “VSG”).30

In hearsay testimony, Dr. Traylor claimed that the lab technician had told him that he

could not identify the strain of bacteria found in Roderius’ blood as streptococcus pneumonia.

R2189. But the lab report itself establishes that the lab did not run the tests necessary to reach

this conclusion. It states that only one test was run, a “gram stain.” R68. The CDC Lab Manual

establishes that three tests must be run simultaneously to identify strep pneumonia: a gram stain,

a catalase test and an optochin test, with a fourth test, bile solubility, run as a fourth, confirmatory

29 Ophoven, “The Forensic Post Mortem” at 392-93. 30 See Donald Janner, Clinical Guide to Pediatric Infectious Disease, 5-6 (2004); Saul Solomon &

Menascu Kalkstein, Pneumonia Due to the Streptococcus Viridans, 205 Am. J. Med. Sci. 765 (1943).

11

test.31 In the absence of these tests, there was no basis for concluding that Roderius was not in-

fected with streptococcus pneumonia.32

In any event, the medical literature establishes that the second form of alphahemolytic

streptococcus, the “viridans” group, can cause death, especially in children with compromised

immune systems.33 It also establishes that infections localized to a specific tissue can trigger sep-

sis even without detectable spread to the bloodstream.34

Contamination of the blood sample. In an attempt to explain away the signifi-b.

cance of bacteria in Roderius’ blood sample, Dr. Traylor also speculated that the bacteria may

have come from the surface of Roderius’ skin and been introduced into the sample when he drew

the blood. R2189. The medical literature establishes, however, that the chances of the blood test-

ing positive for alpha hemolytic streptococci as a result of contamination are exceptionally

small.35

Of course, if there was any question in this regard, all Dr. Traylor had to do was follow

the simple protocol recommended by the National Association of Medical Examiners and the

leading practitioners in the field: order a lab culture of the infected tissue in Roderius’ lungs and

31 CDC, Identification and Characterization of Streptococcus pneumoniae, 1 (2015). See also James

A. Kellogg, et al., Identification of Streptococcus pneumonia Revisited, 39 J. Clin. Microbiol. 3373, 3373-3375 (2001) (“The final identification of an isolate either as S. pneumoniae or as a viridans streptococcus should involve, as a minimum, all of the following: colony morphology, hemolysis, and Gram stain mor-phology; either deoxycholate solubility, optochin susceptibility, or Phadebact coagglutination; and a knowledge of the specimen source.”).

32 Moreover, a study of 428 children who presented at emergency rooms with sepsis found that in 76% of the cases, no underlying cause was identified. Nakia N. Gaines, et al., Etiologies of septic shock in a pediatric emergency department population, 31 Ped. Infectious Dis. J. 1203, 1203-05 (2012).

33 See Solomon & Kalkstein, Pneumonia Due to the Streptococcus Viridans, 205 Am. J. Med. Sci. at 765, 769-70 (1943) (finding that viridans was the second most common agent isolated as cause of commu-nity-acquired pneumonia among children less than five years of age); Christopher D. Doern & Carey-Ann D. Burnham, It’s Not Easy Being Green: the Viridans Group Streptococci, with a Focus on Pediatric Clin-ical Manifestations, 48 J. Clin. Microbiol. 3829, 3829 (2010).

34 Kumar, et al., Robbins Basic Pathology at 94. 35 See J.A. Morris, et al., Postmortem bacteriology: a re-evaluation, 59 J. Clin. Pathol. 1, 8 (2006)

(contamination is only “a minor problem if samples are obtained within 24 hours of death”; contamination “can be reduced to levels similar to those taken for samples obtained in life if stringent precautions are taken”).

12

sputum.36 The fact that Dr. Traylor did not do so and that he, instead, offered unscientific specu-

lation to explain away critical evidence that contradicted his initial conclusion demonstrates the

confirmation bias that pervaded his testimony.

One dose of Prevnar vaccine. Dr. Traylor also offered that Roderius could not c.

have died of sepsis resulting from his pneumonia because he had been vaccinated against pneu-

mococcal bacteria. R2230. He continued that “the vaccine would have had to have been bad” for

Roderius to succumb to complications from pneumonia. R2230. These statements are not sup-

ported by medical science.

Roderius’ medical records show that he had only one dose of the pneumonia vaccine

Prevnar, which was administered when he was seven months old. R465, 466. The CDC guide-

lines provide that children who are first vaccinated with Prevnar at seven months of age should

receive a total of three doses, two doses of the vaccine at least four weeks apart and a booster

dose at age 12 through 15 months.37 The only studies that measure the efficacy of the vaccine

measure the immune response after the full course of vaccination has been completed. Nothing in

the medical literature establishes that an infant who receives only a single dose of the vaccine at

age seven months will be immunized against pneumoniae.38

Moreover, the two available types of the Prevnar vaccine — Prevnar 7 and Prevnar 13 —

do not protect against all serotypes of pneumococcal bacteria.39 As its name suggests, the broader

spectrum of the two — Prevnar 13 — protects against only thirteen pneumococcal bacteria sero-

types.40 The vaccine does not immunize against the remaining seventy-nine strains, which ac-

36 Forensic Autopsy Performance Standards at 22. See also Jean W. Keeling, “Post Mortem Exami-

nation in Babies and Children,” in Paediatric Forensic Medicine and Pathology, 148 (Anthony Busuttil & Jean W. Keeling eds., 2d ed. 2008) (“Microbiological investigations are an important part of the investiga-tion of sudden deaths in children.”) (recommending that samples be taken of nose/throat, bronchia and lungs).

37 CDC, Streptococcus pneumoniae at 287-88 (2015). 38 Pfizer, Prevnar 13 package insert, 35 at Table 20 (2015). 39 There are currently ninety-two identified strains of pneumococcus bacteria. See CDC, Streptococ-

cus pneumoniae at 279. 40 Id. at 284.

13

counted for approximately 39% of pneumococcal cases in 2008 among children younger than five

years of age.41 In short, the medical literature does not support Dr. Traylor’s claim that Roderius

was immunized against pneumonia.

Bronchial vs. lobar pneumonia. As noted, a microscopic examination of Ro-d.

derius’ lung tissue establishes that Roderius had “acute” or severe” pneumonia. Dr. Traylor dis-

counted the significance of this fact, claiming that Roderius’ pneumonia was “early” because the

pneumonia was located in the Roderius’ bronchial tubes, and had not “consolidated” in the lobes

of the lungs, i.e., the alveoli of the lungs had not filled up with pus. R2160.42 But bronchial

pneumonia, by definition, does not involve the entire lobe of the lung, and the lack of consolida-

tion in the lobes of Roderius’ lungs does not mean that the bronchial pneumonia was not severe.43

Bronchial pneumonia is more common in the very young than lobar pneumonia and can

cause sudden unexpected death in infants. It can also cause sepsis in infants.44 Moreover, as one

leading treatise notes, “[a]lthough it was for a time thought that infections had to be disseminated

to cause septic shock, infections localized to a specific tissue can trigger sepsis . . . .”45 Thus,

there is no medical basis for Dr. Traylor’s claim that if Roderius had died of sepsis, “[y]ou’d have

a lobar-type pneumonia involving the entire lobe of lung.” R2399.

The incidence of sepsis in one-year-old children. Dr. Traylor testified that he e.

did not believe that Roderius died from sepsis because sepsis typically affects infants in the three

to six month group. R2399. Dr. Traylor’s reasoning was not based on medical science. Pub-

lished data, in fact, establishes that the incidence of sepsis shows a bimodal distribution with a

41 Id. 42 Dr. Thoma repeated that Roderius’ pneumonia was “early,” but did so only on the basis of the

pathologist’s report, not his own investigation. R2097 (Trial Tr. 126:8-22, 11/10/2013). 43 Kumar, .et al., Robbins Basic Pathology at 486. 44 See Benito Morentin, .et al., Clinicopathological Features of Sudden Unexpected Infectious

Death: Population-based Study in Children and Young Adults, 220 Forensic Sci. Int’l 80, 81, 82 (2012) (study of sudden deaths in Biscay, Spain finding that two-thirds of the deaths were caused by myocarditis and bronchopneumonia).

45 Kumar, et al., Robbins Basic Pathology at 94.

14

first peak in the one day-to-one month age group, and a second peak around two years of age.46

And one of the major causes of sudden natural death in children over one year of age is infec-

tion.47 Infectious disorders that are most commonly associated with sudden pediatric death in-

clude bronchopneumonia and septic shock.48

In any event, probabilities are irrelevant in this case. Pneumonia was found in Roderius’

lungs and and streptococcus bacteria in his blood. Indeed, if probabilities were to decide the

question, death from smothering would have been dismissed, as the forensic literature establishes

that death from smothering is an exceedingly rare cause of sudden unexpected death in infants.49

The severity of Roderius’ symptoms. Dr. Traylor and Dr. Thoma both based f.

their conclusion that Roderius did not die of sepsis on the fact that Roderius was not reported to

have passed out or to have a fever, labored breathing or a rapid heart rate when he went to sleep

sometime before 9:00 p.m. the night before he died. R1945; R2190, 2225-26. Dr. Thoma gave

similar testimony, asserting that Roderius would have appeared “very very sick” if he had died

from sepsis. R2096.

But this claim ignores Roderius’ medical history and well-established principles of medi-

cal science. Rodricus reported that Roderius was “breathing heavy” the night he died. R41. And

the medical literature establishes that deaths from sepsis resulting from pneumonia can be sudden

and unexpected.50 There are numerous documented cases of sudden death caused by pneumonia

46 A. Martinot, et al., Sepsis in Neonates and Children: Definitions, Epidemiology, and Outcome, 13

Ped. Emergency 277, 278 (1997). 47 Roger W. Byard, Sudden Infant Death in Infancy, Childhood and Adolescence, 5 (2d ed. 2004). 48 Id. In a study of 507 infant deaths, 56 were explained by bacterial infection. Infants who died of

bacterial infection were significantly older than were infants whose deaths were unexplained. M.A. Weber, .et al., Infection and Sudden Unexpected Death in Infancy: A Systematic Retrospective Case Review, 371 Lancet 1848, 1850 (2008).

49 See Hymel, Distinguishing Sudden Infant Death Syndrome From Child Abuse Fatalities, 118 Pe-diatrics at 422 (“Estimates of the incidence of infanticide among cases designated as SIDS range from less than 1% to 5%.”).

50 See Morentin, et al., Clinicopathological Features of Sudden Unexpected Infection Death, 220 Fo-rensic Sci. Int’l at 81 (“Occasionally, the course of the infectious diseases is atypical, especially aggressive, and death occurs unexpectedly without a diagnosis in life.”) (sudden death defined as “that which occurs

15

after only displaying slight symptoms of illness.51 Indeed, there are documented cases in which

children who died of sepsis in their sleep and did not display any symptoms at all, or only ordi-

nary cold symptoms prior to their death.52 And even Dr. Traylor had to admit that there was a

“possibility” that a child can go to sleep and develop a fever during the course of the night.

R2214.

C. Dr. Traylor’s testimony regarding the injuries to Roderius’ inner lips is contradicted by medical science, and his failure to pre-serve a tissue sample violated accepted protocol.

The final, and ultimately most serious flaw in Dr. Traylor’s testimony and, indeed, his

handling of this case overall, concerned the bruising and abrasion of Roderius’ inner lips. Dr.

Traylor and Dr. Thoma both rested their conclusion that Roderius was smothered on the presence

and pattern of this injury.53

naturally (non-violent), unexpectedly and within a period of few hours from the beginning of the warning symptoms in a person in an apparently good state of health”).

51 See Nils Molander, Sudden Natural Death in Later Childhood and Adolescence, 57 Archives Dis-ease Childhood 572, 573 (1982) (documenting several cases of children who died from bronchopneumonia after displaying only slight symptoms); Myers & Gervaix, Streptococcus pneumoniae Bacteremia in Chil-dren, 30S Int’l J. Antimicrobial Agents at S27 (strep pneumoniae “bacteraemia is still a feared disease in young children because the clinical signs and symptoms are often indistinguishable from a banal viral dis-ease”).

52 N. Sharief, et al., Overwhelming Sepsis Presenting as Sudden Unexpected Death, 69 Archives Disease Childhood 381 (1993) (documenting cases of child deaths by sepsis without significant symptoms); Henry F. Krous, et al., Sudden Unexpected Death in Childhood: A Report of 50 Cases, 8 Ped. & Dev. Pathol. 307, 311 (2005) (bronchopneumonia and sepsis present in a 1 year, 5-month-old male who died suddenly and unexpectedly); M. Barnham & C. Henderson, Group b streptococcal infection presenting as sudden death in infancy, 62 Archives Disease Childhood 419, 419-20 (1987) (documenting death of “healthy 8 month old girl” who “developed a slightly hoarse voice” and was found dead the next morning; “A similar rapidly fatal course was noted in 50% of infants who died in a recent survey of group B strepto-coccal disease in Britain”).

53 Dr. Traylor acknowledged that none of his other findings — “petechiae” (burst capillaries) on the thymus and surface of the lungs, “cerebral edema without herniation” (mild swelling of the brain), and the bruising to Roderius’ buttocks and face and scratches to his skin — were in themselves indicia of smother-ing. R2133-34, 2136-37, 2139, 2149, 2215. Dr. Thoma was more direct: “Q: Other than the bilateral bruising what makes you think it was a suffocation? A: That is the reason why.” R2105. See generally Christian Torgersen, et al., Macroscopic Postmortem Findings in 235 Surgical Intensive Care Patients with Sepsis, 108 Critical Care & Trauma 1841, 1846 (2009) (cerebral edema found in 15% of studied popula-tion)

16

As noted, Roderius’ mother, Lakendra, testified that Roderius had a “busted” lip and

bruises on the side of his head on the morning of Wednesday, September 15, the day before he

died. She stated that Roderius sustained the injuries when he fell on hard surfaces in Rodricus’

bathroom, and that the fall had occurred either on the night of September 14th, or early in the

morning of September 15th. 54 Thus, if the injury to Roderius’ inner lips was caused by a fall, it

would have happened approximately eighteen to thirty-six hours before Roderius died.55 Dr.

Traylor claimed that dating the bruises could not have been done with any accuracy and failed to

even make a slide of the tissue.56 His testimony is refuted by the medical literature and his failure

to preserve a slide of the tissue is an egregious violation of accepted protocol.

1. Dr. Traylor was wrong in claiming that the time of the injuries to Roderius’ inner lips could not be es-tablished through microscopic examination.

Dr. Traylor testified that “[t]here’s really no accurate way to date a bruise” by microscop-

ic examination. R2228. This testimony was wrong and, indeed, flatly contradicted by generally

accepted forensic science. While the time of an injury that caused a bruise or abrasion by micro-

scopic examination cannot be pinpointed to the minute, it can be established in the frame of refer-

ence relevant here: eighteen to thirty-six hours.

Basic forensic treatises and a variety of scientific studies establish that microscopic ex-

amination of damaged skin samples can be used to establish the time a skin injury was sustained.

The underlying science is basic, well-understood and well-documented in the literature.57 Dam-

aged skin responds to injury in a standard pattern as the skin undertakes the healing process. A

54 See footnote 8, supra. 55 Based on the condition of Roderius’ remains when they were brought to the hospital, Dr. Thoma

estimated that Roderius died between 1:30 and 3:30 a.m. on Wednesday, September 16. R2093-94. 56 Dr. Thoma offered no opinion on the subject. 57 E.g,. Reinhard B. Dettmeyer, Forensic Histopathology: Fundamentals and Perspectives, 191-192

(2011); Tracey S. Corey & Kim A. Collins, “Pediatric Forensic Pathology,” in Pediatric Pathology, 251, 266 (Thomas J. Stocker & Louis P. Dehner eds., 2d ed. 2001); Jyrki Raekallio, Determination of the Age of Wounds by Histochemical and Biochemical Methods, 1 Forensic Sci. 3 (1972); Joshua A. Perper, “Micro-scopic Forensic Pathology,” in Spitz and Fisher’s Medicolegal Investigation of Death: Guidelines for the Application of Pathology to Crime Investigation, 1114 (W. Spitz & D. Spitz eds., 4th ed. 2006).

17

type of white blood cell, neutrophils, become readily observable four hours after injury. The

presence of neutrophils at the site of the injury increases over time, peaking at one to two or three

days post-injury. A second type of white blood cell, macrophages, may first appear as early as

eight hours after the injury is suffered and peak at one to two days post-injury.58

By taking sections of Roderius’ inner lips and staining them to fix the samples, a forensic

pathologist could have established when the injuries were sustained based on whether white

blood cells (and which types of them) were present. Dr. Traylor did not perform this most basic

test.

2. Dr. Traylor failed to follow basic protocol and there-by deprived the defense of the ability to prove scien-tifically that Roderius’ inner lip injuries were caused by his bathroom fall.

But not only did Dr. Traylor fail to perform this basic test, he failed to preserve tissue

samples so that the defense could conduct the test itself. This was a fundamental violation of the

standard protocol in post-mortem examinations generally,59 and in pediatric post-mortems in par-

ticular.60 The guidelines, textbooks, and articles all stress the importance of preserving tissue so

that this critical evidence can be examined. Had this protocol been followed, a scientific answer

58 Neil E.I. Langlois, “Dating of Other Injuries in Children” in Forensic Pathology of Infancy and

Childhood, 376 (Kim A. Collins & Roger W. Byard eds., 2014); Peter M. Cummings, et al., Atlas of Fo-rensic Histopathology, 3, Table 1.1 (2011). See generally Ophoven, “The Forensic Post Mortem,” at 394, 397 (“Timing of injury in skin, soft tissue, traumatized organs, and especially dura matter can be aided by special stains such as iron and trichrome.”).

59 E.g,, Forensic Autopsy Performance Standards, 22, Standard G26 (“Specimens must be routinely collected, labelled, and preserved to be available for needed laboratory tests”); Joshua A. Perper, “Micro-scopic Forensic Pathology,” at 1092, 1109 (“the failure to perform a satisfactory microscopic examination may lead to important diagnostic failures”) (in examining a case of alleged child abuse “multiple samplings of injuries, including an adjacent wedge of normal tissue, are required”).

60 See, e.g., Janice J. Ophoven, “Pediatric Forensic Pathology,” in Potter’s Pathology of the Fetus, Infant and Child, 752, 761, 763 (Enid Gilbert-Barness, et al. eds., 2d ed. 2007) (“At postmortem examina-tion all, or appropriately representative, bruises should be carefully incised and microscopic sections tak-en”); Corey & Collins, “Pediatric Forensic Pathology” at 266, (sampling for microscopic examination should always be done if possible); Quinton, Investigation of Sudden Unexpected Infant Deaths, 4 Acad. Forensic Pathol. at 326 (“Areas of trauma should be sectioned to include samples of skin and subcutaneous tissue from areas of contusion”); ; Keeling, “Post Mortem Examination in Babies and Children,” at 162 (“Thorough sampling for histological examination is an essential part of perinatal, infant and childhood post-mortem examination.”).

18

on whether Roderius’ inner lips were bruised hours before, or at the time of, his death could have

been obtained.61

The prejudice to the defense of this breach cannot be overstated. Whether out of care-

lessness, bias or incompetence, evidence that could have proven Dr. Traylor wrong and exonerat-

ed Rodricus was destroyed.

II. THIS CASE IS A PARADIGMATIC EXAMPLE OF THE RISK OF WRONGFUL CONVICTIONS BASED UPON FAULTY SCIENCE.

This Court and others have recognized the power of scientific evidence to mislead the ju-

ry. State v. Quatrevingt, 93-1644, p. 11 (La. 2/28/96), 670 So.2d 197, 204.62 That potential is all

too common in cases involving infant deaths.63

All of the factors that lead to jurors erroneously crediting fallacious scientific evidence

were present here. Because juries are usually comprised of lay persons, decisions about science

tend to be made based on assessments of the perceived credibility of the experts, more than on the

validity of the science underlying their conclusions.64 This phenomenon is well understood in the

scientific literature, which establishes that in cases involving complex scientific concepts, jurors

61 Dr. Traylor also failed to take tissue samples of the buttock bruising in order to microscopically

date the bruising or preserve samples for future tests. If he had followed standard autopsy procedures and taken or preserved tissue samples, a pathologist could have determined the bruising was inflicted while the child was in Rodricus’ care. To the extent he offered any excuse for this failure to follow accepted proto-col, Dr. Traylor offered only that “we don’t commonly dissect the face, it’s just bad form. It doesn’t allow the family to have a good open casket.” R1064. But in a death penalty prosecution, with no indication that anyone asked him to cut a corner that would have exonerated a grieving father, that excuse reveals the ex-tent to which he abandoned his role as a scientist.

62 See Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579, 595 (1993) (“Expert evidence can be both powerful and quite misleading because of the difficulty in evaluating it.”); United States v. Addison, 498 F.2d 741, 744 (D.C. Cir. 1974) (“scientific proof may in some instances assume a posture of mystic infallibility in the eyes of a jury of laymen”); Watts v. Radiator Specialty Co., 990 So.2d 143, 146-47 (Miss. 2008) (unreliable expert testimony has a profound effect on the decision making process of a juror because “[j]uries are often in awe of expert witnesses because, when the expert witness is qualified by the court, they hear impressive lists of honors, education and experience”).

63 See Byard, Sudden Infant Death in Infancy, Childhood and Adolescence at 491. 64 See Keith A. Findley, Innocents at Risk: Adversary Imbalance, Forensic Science, and the Search

for Truth, 38 Seton Hall L. Rev. 893, 948-49 (2008).

19

will readily absorb familiar information, and filter out information that is new and complex.65

That problem is compounded in criminal cases, where the defense of necessity has to retain a paid

medical expert to prove its case, leaving the prosecution with the ability to take a cheap shot at

the defense’s expert as a “hired gun.”

The defense expert, Dr. Spitz, was not cross-examined on the scientific basis for his opin-

ions; he was cross-examined on irrelevancies. Forty-four pages of transcript were devoted to

whether Dr. Spitz was overworked, whether he had made a single mistake in the course of his

career, how much he was getting paid, whether his bills were outstanding, whether he had a web-

site and the like. R2269-2313.

The prosecutor drove home his attack on Dr. Spitz in summation, arguing “Why else

should you . . . not believe Dr. Spitz? Dr. Thoma and Dr. Traylor have a legal obligation that Dr.

Spitz does not have when it comes to deciding how this baby died. Dr. Spitz can fly on back to

Michigan; he’s gone. Here for one afternoon, one and done.” R2437. Thus, in the prosecution’s

words, medical science was reduced to punditry.

65 See Lance D. Reich, Cognitive Biases Make Judges & Juries Believe Weird Things, 10 No. 1 ABA

SciTech Law. 4, at *7 (2013). See also John T. Cacioppo, et al., Central and Peripheral Routes to Persua-sion: An Individual Difference Perspective, 51 J. of Personality and Social Psychol. 1032 (1986) (explain-ing the differences in the way the brain processes direct arguments versus complex and peripheral infor-mation).

20

CONCLUSION

The medical evidence that lies at the heart of Rodricus Crawford’s conviction was deeply

flawed. The Innocence Network therefore urges this Court to reverse the conviction, and to use

this case as a vehicle for reinforcing the principle that appellate courts have a role, indeed, an ob-

ligation, to review scientific evidence critically so as to assure that innocent people are not exe-

cuted.

Dated: August ___, 2015

Respectfully submitted,

ANDREW R. LEE (#21196) BY:______________________ JONES WALKER LLP 201 St. Charles Avenue New Orleans, Louisiana 70170 (504) 582-8000

MARC WOLINSKY Counsel of Record Pro Hac Vice Application Pending BY:______________________ WACHTELL, LIPTON, ROSEN & KATZ New York, New York 10171 (212) 403-1226

Attorneys for Amicus Curiae Innocence Network, Inc.

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Certificate of Service

I certify that a copy of the foregoing Brief of Amicus Curiae has been forwarded on

August 24, 2015, by U.S. Mail to:

The Honorable Joseph Bleich First Judicial District Court 501 Texas Street Shreveport, LA 71101 Suzanne Morelock Williams Caddo Parish District Attorney 525 Marshall St. Shreveport, LA 71101 smwilliams@caddoda.com Cecelia Trenticosta Kappel Capital Appeals Project 636 Baronne St. New Orleans, LA 70113 ctkappel@thejusticecenter.org ____________________________________ Andrew R. Lee