Abstract:Staphylococcus chromogenes strains were isolated in pure culture from six to eight adult pigs affected with exudative epidermitis (EE), while those were isolated from healthy adult pigs, piglets affected with EE and healthy piglets at low rate. The culture filtrates (CFs) of the above isolates caused rounding effect on cultured cells and exfoliation in 1-day-old chickens. The exfoliative toxin was isolated from CF of a strain (PC-16) possessed strong toxic activity and designated S. chromogenes exfoliative tox… Show more
“…Sato et al [40] isolated S. aureus ETC from a horse with phlegmon. In addition, two S. hyicus ETs, SHETA and SHETB, and two S. chromogenes ETs were obtained from pigs with exudative epidermitis [29,[41][42][43], and the S. intermedius ET SIETwas isolated from dogs with pyoderma [44]. DNA encoding ETC, SHETA, SHETB, SIET, and an S. chromogenes ET were cloned, and the nucleotide sequences deposited in GenBank [5,31,[43][44][45].…”
“…Sato et al [40] isolated S. aureus ETC from a horse with phlegmon. In addition, two S. hyicus ETs, SHETA and SHETB, and two S. chromogenes ETs were obtained from pigs with exudative epidermitis [29,[41][42][43], and the S. intermedius ET SIETwas isolated from dogs with pyoderma [44]. DNA encoding ETC, SHETA, SHETB, SIET, and an S. chromogenes ET were cloned, and the nucleotide sequences deposited in GenBank [5,31,[43][44][45].…”
“…Exudative epidermitis (EE) is a severe skin disease that affects principally suckling and weaned piglets 42 . It is now known to be due to exfoliatin toxin‐producing strains of several Staphylococcus species that include – mostly – Staphylococcus hyicus , 42,43 but also Staphylococcus chromogenes 44,45 and Staphylococcus sciuri. 46 Affected piglets usually develop an acute or peracute dermatitis that originates on the face and extends rapidly to the characteristic generalized erythema, brown exudation and crusting overlying shallow erosions (Figure 6a,b).…”
Section: Bacterial Proteolytic Acantholytic Dermatoses In Animalsmentioning
Failure of desmosomal adhesion with ensuing keratinocyte separation - a phenomenon called acantholysis - can result from genetic, autoimmune or infectious proteolytic causes. Rare hereditary disorders of desmosomal formation have been identified in animals. Familial acantholysis of Angus calves and hereditary suprabasal acantholytic mechanobullous dermatosis of buffaloes appear to be similar to acantholytic epidermolysis bullosa of human beings. A genetic acantholytic dermatosis resembling human Darier disease has been rarely recognized in dogs. In autoimmune blistering dermatoses, circulating autoantibodies bind to the extracellular segments of desmosomal proteins and induce acantholysis. Autoantibodies against desmoglein-3 are found in canine pemphigus vulgaris and paraneoplastic pemphigus. Autoantibodies against desmoglein-1 have been rarely detected in dogs with pemphigus foliaceus. When circulating autoantibodies target desmogleins-1 and -3, mucocutaneous pemphigus vulgaris develops in dogs. Finally, several infectious agents can release proteases that cleave desmosomal bonds. In superficial pustular dermatophytosis of dogs and horses, Trichophyton hyphae colonize the stratum corneum, and acantholysis presumably develops because of proteases secreted by the dermatophytes. In exudative epidermitis of piglets, Staphylococcus bacteria - usually Staphylococcus hyicus- release exfoliatin toxins that bind to and specifically cleave desmoglein-1. Any of the above mechanisms can result in impairment of desmosomal function with subsequent acantholysis. The end point of adhesion failure is identical among these diseases: there is cleft formation where desmosomes are affected. The similarity of mechanisms explains why clinical and microscopic skin lesions overlap between entities, thus leaving clinicians and dermatopathologists with the conundrum of determining whether the acantholysis is of genetic, autoimmune or infectious origin.
“…hyicus wurde bei Infektionskrankheiten verschiedener Tiere isoliert, insbesondere gilt er als Erreger der Exsudativen Epidermitis des Schweines (Sompolinsky, 1953). Einiges deutet darauf hin, daß diese Erkrankung, die auf als Exfoliatine bezeichnete Toxine zurückgeführt wird (Andresen et al, 1997), aber auch durch S. chromogenes hervorgerufen werden kann (Sato et al, 2004;Andresen et al, 2005). Infektionen mit S. hyicus beim Menschen scheinen selten zu sein.…”
Zusammenfassung: Staphylococcus aureus kann sich unter geeigneten Bedingungen in Lebensmitteln vermehren und dabei Enterotoxine bilden, die beim Konsumenten Erbrechen und Durchfall auslösen. Im Gegensatz zu dem Erreger selbst sind diese Toxine sehr widerstandsfähig insbesondere gegenüber hohen Temperaturen und können durch eine küchenmäßige Bearbeitung des sie enthaltenden Lebensmittels im allgemeinen nicht mehr inaktiviert werden. Da demnach die Anwesenheit der Staphylokokken zur Auslösung der Erkrankung nicht mehr erforderlich ist, handelt es sich bei dieser um eine typische Lebensmittelintoxikation. Die Abschätzung einer potentiellen Gesundheitsgefährdung über den Erregernachweis ist daher nur bei rohen Lebensmitteln sinnvoll. Bei Produkten, die im Verlauf ihrer Herstellung einem für die Keime abträglichen Verfahren, z. B. einer Wärmebehandlung, unterzogen wurden, kann der Thermonukleasetest (indirekter Nachweis einer Kontamination mit hoher Anzahl an Staphylokokken, unabhängig davon, ob die Erreger zum Zeitpunkt der Untersuchung noch präsent sind) oder der direkte Enterotoxinnachweis durchgeführt werden. Der Nachweis der Toxingene mit molekularbiologischen Verfahren hat in diesem Zusammenhang nur unterstützende Funktion, da im Fall eines positiven Ergebnisses aus diesem nicht geschlossen werden kann, daß die Gene auch exprimiert wurden, also Toxine im Lebensmittel vorhanden sind. In der vorliegenden Übersichtsarbeit werden der Erreger und seine Enterotoxine sowie die verschiedenen Nachweisverfahren unter besonderer Berücksichtigung der molekularbiologischen Methoden besprochen.Abstract: Under appropriate conditions, Staphylococcus aureus can grow in food and produce enterotoxins which cause vomiting and diarrhoea when ingested. In contrast to the staphylococci these toxins are resistant especially to high temperatures and are not inactivated by usual kitchen practice. As the presence of staphylococci is not essential to cause illness, this condition is a typical food poisoning. The estimation of a potential health risk by targeting the organism is therefore only appropriate to raw food. For products which underwent a procedure detrimental to the bacteria, e. g. heat treatment, testing for thermonuclease (indirect detection of a contamination with high numbers of staphylococci, irrespective of the presence of living bacteria at the time of testing) or the detection of enterotoxins can be applied. In this context, the detection of enterotoxin genes using molecular biological tests provides only supplemental information, as positive results are not evidentiary for gene expression and thus for the presence of toxins in the food. In this review, the causative organism and its toxins as well as methods of detection are discussed with special emphasis on molecular biological methods.
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