Effect immunization with highly purified alpha- and beta-toxins on staphylococcal mastitis in rabbits

Adlam, C.; Ward, P.D.; McCartney, A. Christine; Arbuthnott, J. P.; Thorley, C. M.

doi:10.1128/iai.17.2.250-256.1977

Cited by 71 publications

(20 citation statements)

References 13 publications

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“…The clinical features of this condition strongly suggested a toxin-mediated pathology. This was confirmed when it was shown (Adlam et al 1977) that rabbits immunized with a-toxoid were protected from the symptoms of gangrenous spreading tissue destruction. By contrast animals immunized with p-toxoid showed no such protection.…”

Section: Role Of A-toxin In Pathogenesismentioning

confidence: 71%

Staphylococcal toxins in human disease

Arbuthnott

Coleman

Azavedo

1990

Journal of Applied Bacteriology

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Section: Role Of A-toxin In Pathogenesismentioning

confidence: 71%

Staphylococcal toxins in human disease

Arbuthnott

Coleman

Azavedo

1990

Journal of Applied Bacteriology

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“…1988;Bhakdi and Tranum-Jensen. 1987), Alpha-toxin is an important virulence factor in the pathogenesis of mastitis in rabbits (Adlam et a'., 1977). Immunization with d-toxoid prevented the gross tissue necrosis and fatal outcome of the gangrenous form of the disease, but did not prevent the formation of intramammary abscesses.…”

Section: Introductionmentioning

confidence: 99%

Cryptic α‐toxin gene in toxic shock syndrome and septicaemia strains of Staphylococcus aureus

O’Reilly

Kreiswirth²,

Foster

1990

Molecular Microbiology

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The majority of clinical isolates of Staphylococcus aureus that produce toxic shock syndrome toxin-1 (TSST-1) fail to express alpha-toxin, despite having a copy of the hla gene in the chromosome. The hla gene was cloned from an Hla- TSST-1+ strain, Todd 555, which had been isolated from a case of toxic shock syndrome in the USA. Of the 630 bases of the Todd 555 gene sequenced, 46 differed from the hla gene sequence of strain Wood 46. The defect in alpha-toxin expression was shown to be due to a nonsense mutation which converted a CAG glutamine codon in the equivalent position in the functional Wood 46 sequence to a TAG stop codon. The same mutation was present in the hla gene cloned from a human septicaemia strain (V37) isolated in Dublin. The nonsense mutation of Todd 555 was suppressed by the supE44 mutation in Escherichia coli resulting in haemolytic activity in cell lysates. Hybrid hla genes were formed by splicing fragments of hla from Todd 555 and Wood 46. Expression of one such chimaeric hla gene in S. aureus demonstrated that the Todd 555 hla gene has a functional agr-regulated promoter. The silent hla gene may be a cryptic gene in S. aureus.

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“…K-Toxin exhibits cytolysis in many mammalian cells [1,34^36] and causes dermonecrosis [1], keratitis [31], and mastitis [37]. L-Toxin [1,37] and N-toxin, which have a broad range of target cells [38,39], have cytolytic activity. Despite all those known in vitro and in vivo characteristics of staphylococcal toxins, the actual virulent properties of S. aureus in sepsis remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Possible virulence factors of Staphylococcus aureus in a mouse septic model

Tao

1999

FEMS Immunology and Medical Microbiology

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Twenty clinical isolates of Staphylococcus aureus were examined to elucidate the virulence factors which are directly related to lethality in a mouse septic model. Heat or formalin treatment of the organism abolished the lethal activity of the live organism during challenge intravenously administered via the tail vein. Nevertheless, injection of ten times concentrated culture supernatant fluid (SUP) showed lethal activity in the mouse. However, there was no lethality when SUP was heated at 60 degrees C for 15 min. To examine variations of SUP lethality among strains, we collected 20 strains of S. aureus from four different hospitals. Then, we compared several factors for SUP lethality, which were the extracellular toxins and enzymes, such as toxic shock syndrome toxin 1, enterotoxin A, B, D, and hemolysins (alpha,beta,gamma), and also cytotoxic activity to human polymorphonuclear leukocytes and Vero cells. No difference was found among these factors except cytotoxic activity to Vero cells. Furthermore, we compared two strains in a mouse septic model according to the grade of bacteremia and lethal events. We found that mortality was higher with challenge by the strain whose SUP was lethal in comparison to the strain whose SUP was not lethal, even though the viable bacteria counts in the septic blood in both strains were not significantly different. This strongly supports the possibility that extracellular products, not the cell wall components, of S. aureus play the key role in the lethal event in this mouse septic model. In addition, among the extracellular products, those which have cytotoxic activity to Vero cells may contribute to the lethality in sepsis caused by S. aureus in this murine model.

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Effect immunization with highly purified alpha- and beta-toxins on staphylococcal mastitis in rabbits

Cited by 71 publications

References 13 publications

Staphylococcal toxins in human disease

Staphylococcal toxins in human disease

Cryptic α‐toxin gene in toxic shock syndrome and septicaemia strains of Staphylococcus aureus

Possible virulence factors of Staphylococcus aureus in a mouse septic model

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