Clostridium cadaveris

Clostridium cadaveris
Scientific classification
Domain: Bacteria
Phylum: Bacillota
Class: Clostridia
Order: Clostridiales
Family: Clostridiaceae
Genus: Clostridium
Species:
C. cadaveris
Binomial name
Clostridium cadaveris
(Klein 1899) McClung and McCoy 1957
Synonyms
  • Bacillus cadaveris[1]
    Klein 1899
  • Plectridium cadaveris[1]
    (Klein 1899) Prevot 1938

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.[2] 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.[3] 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.[4]

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.[5][6]

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.[7] Currently the standard to identify clostridial species such as C. cadaveris is via molecular techniques utilizing ribosomal RNA gene sequencing.[8]

Infections

Infections due to C. cadaveris are rare and present predominantly as bacteremia of gastro-intestinal origin and may occur endogenously.[9] Associated risk factors for bacteremia due to C. cadaveris include a compromised immune system, trauma, recent surgical procedures, diabetes, and perforated bowel.[10] Bacteremia and sepsis caused by Clostridium cadaveris have been implicated following orthopedic procedures, in patients undergoing oncological treatment, and in cases of necrotic decubitus.[11] 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.[12] Infections may be persistent due to the organisms ability to sporulate.[13]

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.[14] 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.[15] Imbalance of the ratio between Bacillota and Bacteroidota levels are connected to obesity, Crohn's disease, and other health complications.[16] 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.[17] 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.[18] 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.[19] 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.[20]

References

  1. 1 2 "Clostridium cadaveris: (Klein 1899) McClung and McCoy 1957". National Center for Biotechnology Information (NCBI).
  2. ↑ Schade, Rogier; Michiel Van Rijna; Henri J. L. M. Timmersb; Anton S. M. Dofferhoffab; Corne H. W. Klaassena; Jacques F. G. M. Meis (28 September 2006). "Clostridium cadaveris bacteremia: Two cases and review". Scandinavian Journal of Infectious Diseases. 38 (1): 59–78. doi:10.1080/00365540500388792. PMID 16338840. S2CID 38559710.
  3. ↑ Keto-Timonen; Heinkinheiomo,Eerola,Korkeala (September 2006). "Identification of Clostridium Species and DNA fingerprinting of Clostridium perfringens" (PDF). Journal of Clinical Microbiology. 44 (11): 4057–65. doi:10.1128/jcm.01275-06. PMC 1698353. PMID 16971642.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ↑ Elsayed, S.; Zhang (April 2005). "Bacteremia Caused by Clostridium Intestinale". Journal of Clinical Microbiology. 43 (4): 2018–2020. doi:10.1128/JCM.43.4.2018-2020.2005. PMC 1081394. PMID 15815049.
  5. ↑ Gucalp, R.; Carlisle,Dutcher,Fuks,Wiernik (1993). "Clostridium cadaveris bacteremia in the immunocompromised host". Med. Perdiatric Oncology. 21 (1): 70–2. doi:10.1002/mpo.2950210114. PMID 8426578.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ↑ Poduval, Rajiv; Rajesh Mohandas; Dilip Unnikrishnan; Marilou Corpuz (November 1999). "Clostridium cadaveris in an Immunocompetent Host". Clinical Infectious Diseases. 29 (5): 1354–1355. doi:10.1086/313491. PMID 10525006.
  7. ↑ Starr, S..E.; Killgore, Dowell (October 1971). "Comparison of Schaedler Agar and Trypticase Soy-Yeast Extract Agar for the Cultivation of Anaerobic Bacteria". Applied Microbiology. 22 (4): 655–658. doi:10.1128/AEM.22.4.655-658.1971. PMC 376381. PMID 4943275.
  8. ↑ Woo, P.C.; Lau,Chan,Fung,Tang,Yuen (2005). "Clostridium bacteramia characterized by 16S ribosomal RNA gene sequencing". Journal of Clinical Pathology. 58 (3): 301–307. doi:10.1136/jcp.2004.022830. PMC 1770585. PMID 15735165.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ↑ Goldman, Herman; Bronzo,McKinley (January 1992). "Clostridium cadaveris: an unusual cause of spontaneous bacterial peritonitis". American Journal of Gastroenterology. 87 (1): 140–142. PMID 1728112.
  10. ↑ Elsayed, S.; Zhang (April 2005). "Bacteremia caused by Clostridium intestinale". Journal of Clinical Microbiology. 43 (4): 2018–2020. doi:10.1128/jcm.43.4.2018-2020.2005. PMC 1081394. PMID 15815049.
  11. ↑ Morshed, S.; Malek (February 2007). "Clostriduim cadaveris septic arthritis in a metastatic breast cancer patient". J. Athroplasty. 22 (2): 289–292. doi:10.1016/j.arth.2006.02.158. PMID 17275650.
  12. ↑ Willis, A.T. (1977). Anaerobic bacteriology: clinical and laboratory practice. Boston: Butterworth. pp. 111–166.
  13. ↑ Stolk-Engelaar, Virginia; Verweil,Bongaerts,Linsen,Lacquet,Cox (July 1997). "Pleural empyema due to Clostridium difficile and Clostridium cadaveris". Clinical Infectious Diseases. 25 (1): 160. doi:10.1086/516893. PMID 9243057.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ↑ Bondia, F.; Latorre,Artach0,Moya (2011). "The active gut microbiota differs from the total microbiota". PLOS ONE. 6 (7): e22448. doi:10.1371/journal.pone.0022448. PMC 3145646. PMID 21829462.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ↑ Turroni, F.; Angela Ribbera; Elena Foroni; Douwe van Sinderen; Marco Ventura (June 2008). "Human gut microbiota and bifido bacteria from composition to functionality". Antonie van Leeuwenhoek. 94 (1): 35–50. doi:10.1007/s10482-008-9232-4. hdl:11381/1721297. PMID 18338233. S2CID 6592189.
  16. ↑ Bercik, P. (August 2011). "The Intestinal Microbiota Affect Central Levels of Brain-Derived Neurotropic Factor and Behavior in Mice". Gastroenterology. 141 (2): 599–609. doi:10.1053/j.gastro.2011.04.052. PMID 21683077.
  17. ↑ Ritz (23 December 2008). Criminal and Environmental Soil Forensics. Springer Science. ISBN 978-1-4020-9203-9.
  18. ↑ Sherman, Henry C. (1946). Chemistry of Food (7th ed.). New York: MacMillan and Company. OCLC 567049.
  19. ↑ Vass, Arpab (November 2001). "Beyond the grave - understanding human decomposition". Microbiology Today. 28: 190–192. Archived from the original on 7 February 2016. Retrieved 6 February 2016.
  20. ↑ Melvin, J. R.; Cronholm, Simson (April 1984). "Bacterial Transmigration as an indicator of time of death". Journal of Forensic Sciences. 29 (2): 412–417. doi:10.1520/JFS11687J. PMID 6726153.
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