The Clostridium perfringensα-toxin

Titball, Richard W.; Naylor, C.E.; Basak, A.K.

doi:10.1006/anae.1999.0191

Cited by 172 publications

(115 citation statements)

References 76 publications

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“…The occurrence and intensity of color changes observed in infected guinea pigs are related to the intensity of vascular lesions and/or activity toxins produced by these clostridia NAYLOR;BASAK, 1999). Especially in guinea pigs inoculated with C. perfringens type A, the change in the color of muscle and subcutaneous tissue was similar to pseudomelanosis and easily confused with postmortem changes.…”

Section: Discussionmentioning

confidence: 99%

Comparative analysis of lesions caused by histotoxic clostridia in experimentally induced myonecrosis

et al. 2012

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The comparative anatomical and histopathological lesions caused by different histotoxic clostridia are considered an important step in the diagnosis of epidemiological mionecrosis. In the present study, guinea pigs (Cavia porcellus) were used to reproduce gas gangrene caused by Clostridium septicum, C. chauvoei, C. novyi type A, C. perfringens type A and C. sordellii. The clinical signs, gross and histopathological lesions were compared between inoculated groups and an immunohistochemistry (IHC) was standardized for detection of agents in tissues. On clinical evaluation, animals showed swelling at the injection point, discomfort and limited mobility. The intensity and extent of gross and microscopic lesions varied with the inoculated agent. IHC was able to identify each agents inoculated without cross reactions. All observed results demonstrate that the evaluation of lesions could be usefull in the presumptive etiologic diagnosis. Key words: Blackleg, gas gangrene, myonecrosis, histopathology, immunohistochemistry ResumoO estudo comparativo das lesões anatomo-histopatológicas causadas pelos diferentes clostrídios histotóxicos é considerado uma etapa importante no diagnóstico epidemiológico das mionecroses. Para reproduzir experimentalmente a gangrena gasosa causada por Clostridium septicum, C. chauvoei, C. novyi tipo A, C. perfringens tipo A e C. Sordellii foram utilizados cobaios (Cavia porcellus). Os sinais clínicos, lesões macroscópicas e histopatológicas foram comparadas entre os grupos inoculados e uma imuno-istoquímica (IHQ) foi padronizada para detecção dos agentes nos tecidos das cobaias experimentalmente infectadas. Na avaliação clínica os animais apresentaram aumento de volume no ponto de inoculação, desconforto e dificuldade de locomoção. A intensidade e extensão das lesões macroscópicas e microscópicas variaram com o agente inoculado. Na IHQ foi possível identificar cada um dos agentes inoculados, sem a detecção de reações cruzadas. Todos os resultados observados demonstram que este tipo de avaliação das lesões é de extrema importância para o diagnóstico etiológico conclusivo, possibilitando assim a adoção de medidas preventivas acertivas.

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Section: Discussionmentioning

confidence: 99%

Comparative analysis of lesions caused by histotoxic clostridia in experimentally induced myonecrosis

et al. 2012

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“…The N-terminal domain is related (29% identity) to the non-toxic Bacillus cereus PC-PLC (phosphatidylcholine PLC), which does not possess the C-terminal domain. Both proteins show similar folding patterns (Naylor et al, 1998;Titball et al, 1999;Justin et al, 2002).…”

Section: Plc (Phospholipase C) Activitymentioning

confidence: 96%

Bacterial protein toxins and lipids: role in toxin targeting and activity

Geny

Popoff

2006

Biology of the Cell

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All bacterial toxins, which globally are hydrophilic proteins, interact first with their target cells by recognizing a surface receptor, which is either a lipid or a lipid derivative, or another compound but in a lipid environment. Intracellular active toxins follow various trafficking pathways, the sorting of which is greatly dependent on the nature of the receptor, notably lipidic receptor or receptor embedded into a distinct environment such as lipid microdomains. Numerous other toxins act locally on cell membrane. Indeed, phospholipase activity is a common mechanism shared by several membrane‐damaging toxins. In addition, many toxins active intracellularly or on cell membrane modulate host cell phospholipid pathways. Unusually, a few bacterial toxins require a lipid post‐translational modification to be active. Thereby, lipids are obligate partners of bacterial toxins.

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“…Η αύξηση της περιεκτικότητας του σιτηρεσίου σε πρωτεΐνες ή σε συγκεκριμένα αμινοξέα πιθανώς να αποτελείτο έναυ σμα για την υπέρμετρη ανάπτυξη του C. perfrìngens στο γαστρεντερικό σωλήνα των πτηνών, επειδή τόσο η ανάπτυξη του όσο και η παραγωγή της τοξίνης -α επηρεάζεται άμεσα από την παρουσία ορισμένων αμινοξέων (Titball et al 1999). …”

Section: σιτηρέσια υψηλής περιεκτικότητας πρωτεϊ νών ζωικής προέλευσηςunclassified

Update on the emergence and pathogenesis of necrotic enteritis in broiler chickens

Tsiouris

Georgopoulou

Petridou

2018

J Hellenic Vet Med Soc

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Necrotic enteritis (NE) is a disease of broiler chickens, which is caused by Clostridiumperfringens type A or C and is characterized by high mortality and severe intestinal lesions. NE is described as a disease of high economical importance which affects health and welfare of broilers and also may pose a threat to public health. Although NE was known as a disease since 1930, it did not cause serious problems to the poultry industry. The emergence of the disease occurred after 1986 in Scandinavia and 2000 in the European Union and was related with the ban of in-feed antimicrobial growth promoter. Furthermore, the ban of meat meal and bone meal from the feed of broiler chickens and their replacement by fishmeal increased further the occurrence of NE. NE breaks the Koch's postulate, which supports that "a disease-causing organism should not be present in healthy individuals", because C perfringens may be detected in high populations in the gut of birds with no visible signs of NE. Moreover, challenge of birds with C perfringens does not \eadperse to the development of the disease. It is very well accepted that NE is a multi-factorialdisease in which a number of co-factors are usually required for the proliferation and toxinogenesis of C. perfringens and manifestation of the disease. Toxin -a, since 2006, has been proposed to be the main virulence factor for NE in poultry. The origin of this assumption seems to lie to observation that crude supernatant from C perfringens type A cultures induced necrotic lesions in broilers. Moreover, the development of NE lesions prevented partially by antibodies against C. perfringens toxin -a. The interpretation of these early studies is not clear, because they used crude supernatant and the assumption was made that the effects were caused by the dominant protein present (i.e. toxin -a). However, many other proteins are also present in the supernatant ofC perfringens cultures. The most convincing evidence, that toxin -a is not essential virulence factor for the pathogenesis of NE, comes from studies using a toxin -a negative mutant (epa mutant) of a C perfringens strain from NE outbreak, which was able to produce characteristic NE lesions. Recently, netB, a novel toxin that is associated with broiler NE, has been described. A netB mutant of C perfringens was unable to cause necrotic lesions in the gut of experimentally infected broilers, but a complemented netB mutant was virulent, like the wild-type strain. However, netB per se, might not be an essential component of virulence factor for the pathogenesis of NE, because not all strains isolated from diseased birds carry the netB gene. The presence of the toxin -β2, although it has been linked with increased incidence of bovine enterotoxaemia, intestinal disorders in human, horses and diarrhea in piglets, does not seem to be involved in the pathogenesis of NE in broiler. Most C. perfringens strains isolated from cases of NE do not carry the gene (cpb2) which is responsible for the production of toxin -β2. The efficacy of antitoxin -a toxoid vaccines, the high concentration of toxin-a at the supernatant of C. perfringens culture and feces of diseased birds, as well as the high titer of antibodies against toxin-a in birds with NE, indicate that toxin -a definitely play a role, major or minor, on the pathogenesis of NE in broilers.

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The Clostridium perfringensα-toxin

Cited by 172 publications

References 76 publications

Comparative analysis of lesions caused by histotoxic clostridia in experimentally induced myonecrosis

Comparative analysis of lesions caused by histotoxic clostridia in experimentally induced myonecrosis

Bacterial protein toxins and lipids: role in toxin targeting and activity

Update on the emergence and pathogenesis of necrotic enteritis in broiler chickens

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