Clostridium cadaveris explained

Clostridium cadaveris is an enteric, gas-forming, motile, strictly anaerobic gram-positive bacterium of the genus Clostridium. First described by Klein in 1899, it was noted to be the most prominent bacteria during human decomposition; historically it was described as "putrefying flora".

Clostridium cadaveris is usually considered non-pathogenic; unlike other species of Clostridium, it does not produce toxins.[1] Clostridium cadaveris is found in soil, water, and is a normal component of the human intestinal tract.

The genus Clostridium is large and phylogenetically diverse, comprising over 150 species.[2] Clostridia are found extensively in nature predominantly as benign soil saprophytes. A number of Clostridium species are pathogenic to humans. Members including C.botulinium, C. perfringens, and C.septicum are spore forming and the cause of botulism and gas gangrene respectively. Clostridium cadaveris is closely related phylogenetically to Clostridium fallax and Clostridium intestinale.[3]

Infections in humans due to C. cadaveris are rare and the organism is seldom found is clinical specimens. Most cases reported in medical literature document infections in immunocompromised patients, but isolated cases in immunocompetent hosts have been reported.[4] [5]

Colony characteristics

Primary isolation media is blood agar incubated anaerobically at 35-37 degrees Celsius for 40–48 hours. Microscopic appearance shows gram positive rods with both smooth and rough colony types and further spore staining technique may be utilized to determine spore shape and position.[6] Currently the standard to identify clostridial species such as C. cadaveris is via molecular techniques utilizing ribosomal RNA gene sequencing.[7]

Infections

Infections due to C. cadaveris are rare and present predominantly as bacteremia of gastro-intestinal origin and may occur endogenously.[8] Associated risk factors for bacteremia due to C. cadaveris include a compromised immune system, trauma, recent surgical procedures, diabetes, and perforated bowel.[9] Bacteremia and sepsis caused by Clostridium cadaveris have been implicated following orthopedic procedures, in patients undergoing oncological treatment, and in cases of necrotic decubitus.[10] Due to the rare clinical manifestation of bacteremia attributed to C. cadaveris, the organism's susceptibility to antibiotic treatment is not well documented. Case reports indicate a susceptibility to most antibiotics including metronidazole and penicillin as well as resistance to clindamycin and possibly beta-lactams.[11] Infections may be persistent due to the organisms ability to sporulate.[12]

In the human gut

Clostridium cadaveris normally colonizes in the gastrointestinal tract. Microbiota (gut flora) contain between 400 and 800 bacterial species and are usually classified in two divisions: Bacteroidota and Bacillota; Clostridium cadaveris are Bacillota.[13] Species diversity of human microbiota is unique and microbiota display unequal distribution in the digestive tract. Smaller populations are found in the small intestines, whereas populations one hundredfold are found in the ileum, colon, and rectum.[14] Imbalance of the ratio between Bacillota and Bacteroidota levels are connected to obesity, Crohn's disease, and other health complications.[15] Antibiotic treatment can also alter the balance of microbiota causing pathogenic bacterial growth.

In human decomposition

In humans, one of the first signs of decomposition is a yellow-green discolorization of the abdomen in the area of the cecum due to the build up of gases from bacteria and autolysis of cells.[16] Clostridium cadaveris, C. welchii, E. coli, and B. aerogenes are found in large numbers after death due to nutrient supply for anaerobic bacteria allowing for optimal organismal growth.[17] In initial stages of decomposition bacteria feed on both intestinal contents and intestinal tissues, prolific colonization occurs allowing digestive enzymes and anaerobic bacteria such as C. cadaveris to breach the intestinal tract invading other tissues and organs.[18] Translocation and proliferation of gut flora such as C. cadaveris allow for these organisms to serve as bacterial indicators for time of death in individuals.[19]

External links

Notes and References

  1. Clostridium cadaveris bacteremia: Two cases and review. Scandinavian Journal of Infectious Diseases. 28 September 2006. 38. 1. 59–78. 10.1080/00365540500388792. 16338840 . 38559710 . Schade . Rogier P. . Van Rijn . Michiel . Timmers . Henri J. L. M. . Dofferhoff . Anton S. M. . Klaassen . Corne H. W. . Meis . Jacques F. G. M. .
  2. Identification of Clostridium Species and DNA fingerprinting of Clostridium perfringens. Journal of Clinical Microbiology. September 2006. 44. 11. 4057–65. 10.1128/jcm.01275-06. 16971642. 1698353. Keto-Timonen . R. . Heikinheimo . A. . Eerola . E. . Korkeala . H. .
  3. Bacteremia Caused by Clostridium Intestinale. Journal of Clinical Microbiology. April 2005. 43. 4. 2018–2020. 10.1128/JCM.43.4.2018-2020.2005. 15815049. 1081394 . Elsayed . Sameer . Zhang . Kunyan .
  4. Clostridium cadaveris bacteremia in the immunocompromised host. Medical and Pediatric Oncology. 1993. 21. 1. 70–2. 8426578. 10.1002/mpo.2950210114. Gucalp. Rasim. Motyl. Mary. Carlisle. Penny. Dutcher. Janice. Fuks. Joachim. Wiernik. Peter H..
  5. Poduval. Rajiv . Rajesh Mohandas . Dilip Unnikrishnan . Marilou Corpuz . Clostridium cadaveris in an Immunocompetent Host. Clinical Infectious Diseases. November 1999. 29. 5. 1354–1355. 10525006. 10.1086/313491. free.
  6. Applied Microbiology . Comparison of Schaedler Agar and Trypticase Soy-Yeast Extract Agar for the Cultivation of Anaerobic Bacteria . 4943275 . October 1971. 22 . 4. 655–658 . 10.1128/AEM.22.4.655-658.1971. 376381 . Starr . S. E. . Killgore . G. E. . Dowell . V. R. .
  7. Clostridium bacteramia characterized by 16S ribosomal RNA gene sequencing. Journal of Clinical Pathology. 2005. 58. 3. 301–307. 10.1136/jcp.2004.022830. 15735165. 1770585 . Woo . P C Y. . Lau . S K P. . Chan . K-m . Fung . A M Y. . Tang . B S F. . Yuen . K-y .
  8. Clostridium cadaveris: an unusual cause of spontaneous bacterial peritonitis.. American Journal of Gastroenterology. January 1992. 87. 1. 140–142. 1728112 . Herman . R. . Goldman . I. S. . Bronzo . R. . McKinley . M. J. .
  9. Bacteremia caused by Clostridium intestinale.. Journal of Clinical Microbiology. April 2005. 43. 4. 10.1128/jcm.43.4.2018-2020.2005. 2018–2020. 15815049. 1081394 . Elsayed . Sameer . Zhang . Kunyan .
  10. Clostriduim cadaveris septic arthritis in a metastatic breast cancer patient.. J. Athroplasty. February 2007. 22. 2. 289–292. 17275650. 10.1016/j.arth.2006.02.158 . Morshed . S. . Malek . F. . Silverstein . R. M. . O'Donnell . R. J. .
  11. Book: Willis, A. T.. Anaerobic bacteriology: clinical and laboratory practice.. 1977. Butterworth. Boston. 111–166.
  12. Pleural empyema due to Clostridium difficile and Clostridium cadaveris. Clinical Infectious Diseases. July 1997. 160. 10.1086/516893. 9243057. 25. 1. free . Stolk-Engelaar . Virginia . Verwiel . Jeroen . Bongaerts . Ger . Linsen . Vic . Lacquet . Leon . Cox . Anton .
  13. The active gut microbiota differs from the total microbiota. PLOS ONE. 2011. 6. 7. 21829462 . 10.1371/journal.pone.0022448. 3145646. e22448. free . Peris-Bondia . F. . Latorre . A. . Artacho . A. . Moya . A. . d'Auria . G. .
  14. Human gut microbiota and bifido bacteria from composition to functionality. June 2008. 94. 1. 18338233. 10.1007/s10482-008-9232-4. 35–50 . Antonie van Leeuwenhoek. 6592189 . 11381/1721297. free . Turroni . Francesca . Ribbera . Angela . Foroni . Elena . Van Sinderen . Douwe . Ventura . Marco .
  15. Bercik. P.. Gastroenterology. August 2011. 141. 2. 599–609. 10.1053/j.gastro.2011.04.052. The Intestinal Microbiota Affect Central Levels of Brain-Derived Neurotropic Factor and Behavior in Mice. 21683077. free.
  16. Book: Ritz, Karl Ritz . Dawson . Lorna . Miller . David . Criminal and Environmental Soil Forensics. 23 December 2008. Springer Science. 978-1-4020-9203-9.
  17. Book: Sherman, Henry C. . Chemistry of Food . 1946 . 7th . MacMillan and Company . New York . 567049.
  18. Vass. Arpab. Beyond the grave - understanding human decomposition. Microbiology Today. November 2001. 28. 190–192. 6 February 2016. https://web.archive.org/web/20160207095442/http://www.microbiologysociety.org/download.cfm/docid/84D1BD42-1963-4CE2-8D67CC5561EB1B08. 7 February 2016. dead.
  19. Bacterial Transmigration as an indicator of time of death.. Journal of Forensic Sciences . April 1984 . 29 . 2 . 412–417 . 10.1520/JFS11687J . 6726153 . Melvin . JR . Cronholm . LS . Simson . LR . Isaacs . AM .

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