In Reply.

Abstract

In Reply.—We thank the Centers for Disease Control and Prevention's (CDC's) Infectious Diseases Pathology Branch laboratory for performing these tests and for sharing the full extent of its workup.The investigating forensic pathologist is in the best position to integrate all of the autopsy, laboratory, and clinical information to determine the cause of death. The CDC unfortunately overstepped its role with patient B by diagnosing the death as “attributable directly” to clostridial sepsis “based on the composite histological, immunohistochemical, and molecular findings.” It misinterpreted common postmortem findings, including bacterial overgrowth. This is what causes bodies to putrefy after death as the intestinal flora spread throughout the body, and this is why there was no associated inflammation. The autopsy on patient B was done 2 days after his death. Practicing forensic pathologists routinely see this type of postmortem bacterial overgrowth at autopsy. In fact, studies have used the postmortem growth of clostridium to attempt to determine the postmortem interval.1,2 This bacterial invasion is not the cause of death but a consequence of death.3 The adrenal glands undergo early autolysis and it is common to see some “hemorrhage” after death. Clostridium septicum is a very small component of the human colon flora and rarely causes infection.4,5 It has been described to cause sepsis with colonic malignancies that offer a portal of entry into the circulation.6 Both forensic pathologists who certified these deaths spoke directly with the parents to confirm the clinical histories and did not rely upon tertiary accounts.The clinical history and cardiac findings simply do not support a diagnosis of clostridial sepsis. The clostridial “diagnosis” was not included in the report because it was a postmortem artifact; it was not an “important finding” or an “alternate cause of death.”For patient A, we agree that for completeness the parvovirus B (PVB) results should have been included in our report. We note that the CDC also did not diagnose this death as caused by PVB19 myocarditis. It noted in its report that “the significance of this finding is unclear as parvovirus-19 likely has long-term persistence in heart tissues, and is frequently detected in heart tissues from autopsies with no clinical or histopathologic evidence of myocarditis.1,2”4,7,8 In a study4 using 84 persons who died by suicide as a control group, PVB genomes were detected by polymerase chain reaction in 44% of the hearts. The authors concluded “that a positive PVB polymerase chain reaction test in cardiac autopsy specimens most likely represents a persistent infection with no or limited association to myocarditis. Hence, caution should be taken when interpreting the results for establishing the cause of death.”4 The histologic features in patient A were not those of viral myocarditis, nor would the ischemic injury be explained by such an infection. Thus, we conclude that the detection of the PVB genome is an incidental finding.