Clostridial necrotizing enteritis: Difference between revisions
Jump to navigation
Jump to search
m (Bot: Automated text replacement (-{{SIB}} + & -{{EH}} + & -{{EJ}} + & -{{Editor Help}} + & -{{Editor Join}} +)) |
m (Changes made per Mahshid's request) |
||
| (3 intermediate revisions by 3 users not shown) | |||
| Line 1: | Line 1: | ||
__NOTOC__ | |||
{{SI}} | {{SI}} | ||
{{CMG}} | |||
{{SK}} Enteritis necroticans; pigbel | |||
'''Clostridial necrotizing enteritis''' (CNE) | ==Overview== | ||
'''Clostridial necrotizing enteritis''' (CNE) is an often fatal type of [[food poisoning]] caused by a [[β-toxin]] of ''[[Clostridium perfringens]]'', Type C. It occurs in some [[developing countries]], but was also documented in [[Germany]] following [[World War II]]. The toxin is normally inactivated by certain [[proteolytic enzyme]]s and by normal cooking, but when these protections are impeded, the disease emerges. | |||
== | ==Pathophysiology== | ||
CNE is a necrotizing inflammation the small bowel (especially the jejunum but also the ileum). Clinical results may vary from mild diarrhea to a life-threatening sequence of severe abdominal pain, vomiting, bloody stool, ulceration of the small intestine with leakage (perforation) into the [[peritoneal cavity]] and possible death within a single day due to [[peritonitis]]. | |||
= | ===Other Clostridial Toxemias=== | ||
==Other Clostridial | |||
*[[Leukemia]] patients, cancer [[chemotherapy]] recipients and others suffering from suppressed [[white blood cells]] ([[neutropenia]]) can be afflicted by a similar syndrome, [[neutropenic enterocolitis]], in which the [[cecum]] is targeted by ''[[Clostridium septicum]]'' in much the same way. | *[[Leukemia]] patients, cancer [[chemotherapy]] recipients and others suffering from suppressed [[white blood cells]] ([[neutropenia]]) can be afflicted by a similar syndrome, [[neutropenic enterocolitis]], in which the [[cecum]] is targeted by ''[[Clostridium septicum]]'' in much the same way. | ||
*In neonatal [[intensive care units]], the syndrome of [[neonatal necrotizing enterocolitis]] may be caused in a similar way by ''[[Clostridium perfringens|C. perfringens]]'', ''[[Clostridium butyricum|C. butyricum]]'', and ''[[Clostridium difficile|C. difficile]]'', but this has not been proved<ref>Cooke RA. "Pig Bel." ''Perspectives in Pediatric Pathology''. 1979;5:137-52. PMID: 575409</ref>. | |||
==Epidemiology and Demographics== | |||
All the factors collectively causing CNE are generally only present in the hinterlands of [[New Guinea]] and parts of [[Africa]], [[Latin America]], and [[Asia]]. These factors include [[protein deprivation]] (causing inadequate synthesis of trypsin protease (an enzyme), to which the toxin is very sensitive), poor food hygiene, episodic meat feasting, staple diets containing [[trypsin]] inhibitors ([[sweet potatoes]]), and infection by ''[[Ascaris]]'' parasites which secrete a trypsin inhibitor. In New Guinea (origin of the term “pigbel”), the disease is usually spread through contaminated meat (especially pork) and perhaps by peanuts. (CNE was also diagnosed in post WWII Germany, where it was known as ''Darmbrand'' or "fire bowels")<ref>Murrell TG, Egerton JR, Rampling A, Samels J, Walker PD. "The ecology and epidemiology of the pig-bel syndrome in man in New Guinea." ''Journal of Hygiene, London''. 1966 Sep;64(3):375-96. PMID: 4288244</ref>. | |||
==Treatment== | |||
===Medical Therapy=== | |||
Treatment involves suppressing the toxin-producing organisms with antibiotics such as [[penicillin G]] or [[metronidazole]]. About half of seriously ill patients require surgery for perforation, persistent intestinal obstruction, or failure to respond to the antibiotics. An investigational toxoid vaccine has been used successfully in some developing countries but is not available outside of research<ref>Murrell TG, Roth L, Egerton J, Samels J, Walker PD. "Pig-bel: enteritis necroticans. A study in diagnosis and management." ''Lancet''. 1966 Jan 29;1(7431):217-22. PMID: 4159182</ref>. | |||
== References == | == References == | ||
{{reflist|2}} | |||
[[Category:Food safety]] | [[Category:Food safety]] | ||
[[Category:Foodborne illnesses]] | [[Category:Foodborne illnesses]] | ||
[[Category:Nutrition]] | [[Category:Nutrition]] | ||
[[Category:Disease]] | |||
[[Category:Bacterial diseases]] | |||
{{WikiDoc Help Menu}} | {{WikiDoc Help Menu}} | ||
{{WS}} | {{WS}} | ||
Latest revision as of 17:25, 18 September 2017
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Synonyms and keywords: Enteritis necroticans; pigbel
Overview
Clostridial necrotizing enteritis (CNE) is an often fatal type of food poisoning caused by a β-toxin of Clostridium perfringens, Type C. It occurs in some developing countries, but was also documented in Germany following World War II. The toxin is normally inactivated by certain proteolytic enzymes and by normal cooking, but when these protections are impeded, the disease emerges.
Pathophysiology
CNE is a necrotizing inflammation the small bowel (especially the jejunum but also the ileum). Clinical results may vary from mild diarrhea to a life-threatening sequence of severe abdominal pain, vomiting, bloody stool, ulceration of the small intestine with leakage (perforation) into the peritoneal cavity and possible death within a single day due to peritonitis.
Other Clostridial Toxemias
- Leukemia patients, cancer chemotherapy recipients and others suffering from suppressed white blood cells (neutropenia) can be afflicted by a similar syndrome, neutropenic enterocolitis, in which the cecum is targeted by Clostridium septicum in much the same way.
- In neonatal intensive care units, the syndrome of neonatal necrotizing enterocolitis may be caused in a similar way by C. perfringens, C. butyricum, and C. difficile, but this has not been proved[1].
Epidemiology and Demographics
All the factors collectively causing CNE are generally only present in the hinterlands of New Guinea and parts of Africa, Latin America, and Asia. These factors include protein deprivation (causing inadequate synthesis of trypsin protease (an enzyme), to which the toxin is very sensitive), poor food hygiene, episodic meat feasting, staple diets containing trypsin inhibitors (sweet potatoes), and infection by Ascaris parasites which secrete a trypsin inhibitor. In New Guinea (origin of the term “pigbel”), the disease is usually spread through contaminated meat (especially pork) and perhaps by peanuts. (CNE was also diagnosed in post WWII Germany, where it was known as Darmbrand or "fire bowels")[2].
Treatment
Medical Therapy
Treatment involves suppressing the toxin-producing organisms with antibiotics such as penicillin G or metronidazole. About half of seriously ill patients require surgery for perforation, persistent intestinal obstruction, or failure to respond to the antibiotics. An investigational toxoid vaccine has been used successfully in some developing countries but is not available outside of research[3].
References
- ↑ Cooke RA. "Pig Bel." Perspectives in Pediatric Pathology. 1979;5:137-52. PMID: 575409
- ↑ Murrell TG, Egerton JR, Rampling A, Samels J, Walker PD. "The ecology and epidemiology of the pig-bel syndrome in man in New Guinea." Journal of Hygiene, London. 1966 Sep;64(3):375-96. PMID: 4288244
- ↑ Murrell TG, Roth L, Egerton J, Samels J, Walker PD. "Pig-bel: enteritis necroticans. A study in diagnosis and management." Lancet. 1966 Jan 29;1(7431):217-22. PMID: 4159182