Epidemiological and pathobiological profiles of Clostridium perfringens infections: review of consecutive series of 33 cases over a 13-year period

Abstract

Background: Although Clostridium perfringens (C. perfringens) is well known as the causative agent of several forms of enteric disease, precise epidemiological and pathobiological aspects are still unknown.

Methods: We retrospectively reviewed the culture results of samples collected in our hospital from 2001 through 2013. In addition, for the detection and toxinogenic typing of C. perfringens, polymerase-chain-reaction amplification (PCR)-based rapid analysis was performed in 6 cases using DNA extracted from paraffin-embedded tissues.

Results: A total of 35 samples from 33 cases were positive for C. perfringens, representing an incidence of 0.017% (35/205, 114). Among 33 patients, 21 patients manifested sepsis and 7 patients had bacteremia. One of the septic cases was complicated by fatal intravascular hemolysis and thus, the prevalence was estimated at 3.0% among C. perfringens infections (1/33). The direct causative disease or state for C. perfringens infection was identified in 18 patients: surgery or intervention for cancers, 8 patients; chemotherapy for cancer, 2 patients; surgery or intervention for non-neoplastic disease, 6 patients; liver cirrhosis, 3 patients, etc. PCR-based toxinogenic typing of C. perfringens detected the alpha-toxin gene only in tissue from a patient who died of massive hemolysis; none of the toxin genes could be amplified in the other 5 cases examined.

Conclusions: The prevalence of overt C. perfringens infection is low, but upon detection, infected patients should be carefully monitored for fatal acute hemolysis caused by type A C. perfringens. Furthermore, PCR-based rapid detection of C. perfringens and toxinogenic typing by archival pathological material is applicable as a diagnostic tool.

Keywords: Clostridium perfringens; alpha-toxin; fatal acute hemolysis; polymerase-chain-reaction amplification.

Figure 1

Radiographical imaging of the liver showing gas-containing (pseudo)cystic lesion in the liver found in Case 12.

Figure 2

A. Gross appearance of the liver obtained from the autopsy in Case 12. Cut surface revealed pseudocystic and partially necrotic lesion of 8 cm in the maximum dimension (arrow heads). B. Histological features of pseudocyst wall of the liver in Case 12. Lumen was filled with blood clot and fibrin (*). Inner surface was covered by inflammatory exudate and necrotic material (arrow heads), and surrounded by viable hepatic tissue (arrows). C. Around the inner necrotic area, colonies of gram-positive bacillus were observed (arrows).

Figure 3

Agarose gel electrophoresis of PCR amplicons obtained using formalin-fixed paraffin-embedded colon tissues from 6 cases (lanes 2-7, Case 5, 10-12, 23, and 25, respectively). Clostridium perfringens type A (NCTC8798) carrying alpha- and entero-toxin gene (lane 8), and type B (GTC15078) carrying alpha-, beta-, and epsilon-toxin gene (lane 9), type E (GTC15081) carrying alpha- and iota-toxin gene (lane 10), negative control (lane 11), and molecular size marker (lanes 1 and 12). Lane 5 (Case 12) showed amplified product of Clostridium perfringens type A-specific alpha-toxin gene.