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At least 1,081 records · Page 60Linked to original sources
PubMed1978

The effects of Clostridium perfringens enterotoxin on rat and rabbit ileum: an electron microscopic study.

Intestinal epithelial damage caused by Clostridium perfringens enterotoxin in rats and rabbits was identified by light microscopy and compared at the surface (scanning electron microscopy), and the ultrastructural (transmission electron microscopy) levels. Under the light microscope damage to the epithelial layer of villus tips was clearly evident in cross-sections. Whole tissue viewed under the scanning electron microscope showed comparable tip localization of morpholigic damage in the form of collapsed tips and a dense covering of rounded blebs on the tips. Ulstructuctural observations included partial and sometimes complete disappearance of microvilli structures, budding of the terminal web region into the lumen, and even complete destruction of epithelial cells. These data suggest that C. perfringens enterotoxin attacks the epithelial cells with a preference for cells at the villus tips and causes damage at least in part by altering the cells' apical membranes. This then leads to cellular sloughing, death, and lysing.

Animals↗
PubMed1978

Enterotoxemia in rabbits.

The presence of Clostridium perfringens Type E iota toxin was confirmed from the cecal contents of 23 of 46 rabbits which died of enteritis complex. The most consistent lesions observed were hemorrhage and edema in the cecum. Rabbit toxicity tests showed the toxic cecal contents were lethal for young rabbits unless incubated with Clostridium perfringens Type E antiserum.

Animals↗
PubMed1978

[Necrotizing enteritis in suckling pigs (Clostridium perfringens type C enterotoxemia). II. Toxin formation, heat and drug resistance of Clostridium perfringens strains isolated from suckling pigs and broilers with necrotizing enteritis].

Nineteen Clostridium perfringens Type C strains and ten foreign control strains of subtypes C1, C3, and C4 were tested for their toxin formation and spore resistance to heat. The 19 Type C strains had been isolated from unweaned piglets in the context of necrotising enteritis outbreaks in the GDR. The Clostridium perfringens Type C strains formed beta-toxin, but they failed to form epsilon-toxin or gamma-toxin, alpha-toxin was successfully recorded from 15 of the 19 strains tested from unweaned piglets. The minor-lethal toxin fractions were also tested, with delta-toxin being recorded from all strains, non-alpha-delta-theta-toxin from six, theta-toxin from five, and K-toxin from one. Tests for delta-toxin, lambda-toxin, and mu-toxin were negative. The Clostridium perfringens Type C strains isolated in the GDR from unweaned piglets with necrotising enteritis were, basically, identical with those described in Denmark by von Hogh (1967) with regard to toxin formation. Clostridium perfringens strains cultured in broilers with necrotising enteritis were characterised by regular toxin production in the context of alpha, theta, delta as well as non-alpha-delta-theta. They failed to form beta, epsilon, gamma and lambda, while mu-toxin was formed by them quite irregularly. They, consequently, are Type A strains. Resistance to chloramphenicol and/or oxytetracycline was exhibited by 78.5 per cent of 237 tested Clostridium perfringens strains which had been isolated from unweaned piglets and broilers with necrotosing enteritis. Multiple resistance was recorded from 33.9 per cent. All strains were susceptible to penicillin, nitrofurantoin, and erythromycin.

Animals↗
PubMed1990

Clostridium perfringens type C in bloody and watery diarrhea in Bangladesh.

A two-week age-matched case-control survey to detect Clostridium perfringens type C-associated illness was conducted among diarrheal patients hospitalized following the consumption of high protein meals on the occasion of an annual religious festival. From the stool of 33 patients screened, C. perfringens type C was isolated from one patient with bloody diarrhea and from two patients with watery diarrhea. In Bangladesh, C. perfringens type C has been isolated in both bloody and watery diarrhoeal illness and is not necessarily associated with necrotizing enteritis (pigbel).

Bangladesh↗
PubMed1990

Testing strains of Clostridium perfringens type A isolated from diarrhoeic piglets for the presence of the enterotoxin gene.

A diarrhoeic syndrome in piglets has been linked to Clostridium perfringens type A because this organism has been isolated in large numbers from all cases. The strains isolated from these cases and strains isolated from healthy piglets were screened for the enterotoxin gene of C perfringens by DNA-hybridisation. Using two different synthetic DNA-probes, none of the strains isolated from diseased pigs was positive in this reaction, indicating that the enterotoxin of C perfringens is not involved in the syndrome.

Animals↗
PubMedDate not supplied

The prevention of experimentally induced necrotic enteritis in chickens by avoparcin.

Four groups of about seventy 2-week-old broiler chickens were challenged with a Clostridium perfringens Type A isolate. Inclusion of avoparcin at 20 ppm in feed prevented necrotic enteritis in one group, but 10 ppm was only marginally effective. Bacitracin at 110 ppm also prevented the disease. Necrotic enteritis was successfully reproduced in untreated control birds.

Animals↗
PubMed1979

[Studies of necrotizing enteritis of suckling piglets (Clostridium perfringens type C enterotoxemia) in industrialized sow breeding units. 4. Epizootiology].

Necrotising enteritis had been the cause of death of 4.9 per cent in 5,177 nursed piglets, which was established by pathological examination. The number of piglets, in that context, which had come from industrialised sow breeding units was equivalent to 92 per cent. The nursed piglet held the third position, next to smaller ruminants (19.4 per cent) and fowl (6.0 per cent), with regard to the occurrence of Clostridium perfringens enterotoxemia or necrotising enteritis in 112,218 animals which were pathologically examined after death. Necrotising enteritis so far has been rare in the GDR. No regional accumulation has been observed. Several outbreaks on industrialised sow breeding units actually remained stationary. The occurrence of the disease may be favoured by a number of factors which are conducive to accumulation of Clostridium perfringens Type C in a given stock. Group keeping of pregnant sows, simultaneous farrowing of larger groups of sows, group treatment of nursed piglets, using neomycin, chloramphenicol, oxytetracycline, and other antibiotics to which Clostridium perfringens is primarily resistant or has acquired resistance in the course of time are some of those contributive factors. Transmission of Clostridium perfringens Type C through feedstuff is possible, though it would lead to a real outbreak only by high intensity of the contamination, and it played a minor role in proliferation of the disease. 3479 Clostridium perfringens strains were isolated from 9,481 animals, both clinically intact and after death, with 30 species being included. Type classification revealed 2454 strains of Type A (70 per cent), 204 of Type D (5.88 per cent), 164 of Type C (four per cent), and 48 of Type B (1.34 per cent). There were 688 atoxic strains (17 per cent). Swine is the major carrier of Clostridium perfringens Type C, with 87 per cent of all Clostridium perfringens Type C strains having been isolated from swine. Swine was followed by fowl (four per cent), sheep (four per cent), cattle, rabbit, and dog (1.27 per cent each). Clostridium perfringens Type C was obtained from the faeces of clinically intact sows in seven instances, including two cases with sows (0.46 per cent) from farms with no previous record of necrotising enteritis.

Animals↗