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Clostridium cadaveris

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Clostridium cadaveris
Scientific classification
Kingdom:
Bacteria
Division:
Firmicutes
Class:
Clostridia
Family:
Clostridiaceae
Genus:
Clostridium
Species:
Cl. 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] Clostrida are extensively found in nature predominately 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 clostrida species such as C. cadaveris is via molecular techniques utilizing ribosomal RNA gene sequencing.[8]

Role in infection

Infections due to C. cadaveris are rare and present predominately as bacteremias of gastro-intestinal origin and may occur endogenously.[9] Associated risk factors for bactremias of C. cadaveris origin 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 bactremias 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]

Role as human gut flora

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: Bacteroidetes and Firmicutes; Clostridium cadaveris are Firmicutes.[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 Firmicutes and Bacteroidetes 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.

Role 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. ^ a b
  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 bactremia: Two cases and review". Scandinavian Journal of Infectious Diseases. 38 (1): 59–78. doi:10.1080/00365540500388792.
  3. ^ Keto-Timonen; Heinkinheiomo,Eerola,Korkeala (September 2006). "Identification of Clostridium Species and DNA fingerprinting of Clostridium perfringens". Journal of Clinical Microbiology. 44 (11): 4057. doi:10.1128/JCM.0125-06.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ^ Elsayed, S.; Zhang (April 2005). "Bactremia Caused by Clostridium Intestinale". Journal of Clinical Microbiology. 43 (4): 2018–2020. doi:10.1128/JCM.43.4.2018-2020.2005.
  5. ^ Gucalp, R.; Carlisle,Dutcher,Fuks,Wiernik (1993). "Clostridium cadaveris bactremia 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 Disease. 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. 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: 301–307. doi:10.1136/jcp.2004.022830.{{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 Gastrenterology. 87 (1): 140–142. PMID 1728112.
  10. ^ Elsayed, S.; Zhang (April 2005). "Bactremia caused by Clostridium intestinale". Journal of Clinical Microbiology. 43 (4): 2018–2020. doi:10.1128/jcm.43.4.2018-2020.2005.
  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 laborartory 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 Disease. 25: 160. doi:10.1086/516893. Retrieved 2012-02-14.{{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) CS1 maint: numeric names: authors list (link) CS1 maint: unflagged free DOI (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. PMID 18338233.
  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.
  17. ^ Ritz. 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. 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. PMID 6726153.
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