Experimental gas gangrene with food-poisoning Clostridium perfringens type A

1968 ◽  
Vol 14 (6) ◽  
pp. 705-709 ◽  
Author(s):  
A. H. W. Hauschild ◽  
F. S. Thatcher
Keyword(s):  
Clostridium Perfringens ◽  
Food Poisoning ◽  
Type A ◽  
Gas Gangrene ◽  
Sheep Blood Agar ◽  
Alpha Toxin ◽  
Cell Numbers ◽  
Fatal Infection ◽  
Virulent Strains ◽  
Resistant Strains

Classical and food-poisoning strains of Clostridium perfringens type A were tested for their capacity to produce gas gangrene in guinea pigs.The virulence of food-poisoning strains producing heat-sensitive spores and showing beta hemolysis on sheep-blood agar was comparable to that of the classical strains. The most virulent strains of both groups produced fatal infection with only three to five vegetative cells. Of 13 food-poisoning, heat-sensitive strains showing no beta hemolysis, only three were lethal when a minimum of 4 × 104 to 4 × 108 cells was injected. None of the food-poisoning, heat-resistant strains produced fatal infection with cell numbers up to 4 × 108. The groups of strains showed a correlation between virulence and formation of alpha toxin in liquid culture.It is concluded that a number of heat-sensitive, beta-hemolytic strains of C. perfringens may cause gas gangrene as well as food poisoning, and that the current subdivision of C. perfringens type A strains into classical and food-poisoning groups is no longer tenable.

scholarly journals Use of Genetically Manipulated Strains of Clostridium perfringens Reveals that Both Alpha-Toxin and Theta-Toxin Are Required for Vascular Leukostasis To Occur in Experimental Gas Gangrene

1999 ◽  
Vol 67 (9) ◽  
pp. 4902-4907 ◽  
Author(s):  
Darren M. Ellemor ◽  
Rebecca N. Baird ◽  
Milena M. Awad ◽  
Richard L. Boyd ◽  
Julian I. Rood ◽  
...  
Keyword(s):  
Clostridium Perfringens ◽  
Type A ◽  
Toxin Production ◽  
Gas Gangrene ◽  
Necrotic Tissue ◽  
Alpha Toxin ◽  
Tissue Necrosis ◽  
Clostridial Myonecrosis ◽  
Leukocyte Aggregation ◽  
Genetically Manipulated

ABSTRACT A hallmark of gas gangrene (clostridial myonecrosis) pathology is a paucity of leukocytes infiltrating the necrotic tissue. The cause of this paucity most likely relates to the observation of leukocyte aggregates at the border of the area of tissue necrosis, often within the microvasculature itself. Infecting mice with genetically manipulated strains of Clostridium perfringens type A (deficient in either alpha-toxin or theta-toxin production) resulted in significantly reduced leukocyte aggregation when alpha-toxin was absent and complete abrogation of leukocyte aggregation when theta-toxin was absent. Thus, both alpha-toxin and theta-toxin are necessary for the characteristic vascular leukostasis observed in clostridial myonecrosis.

scholarly journals Clostridium Perfringens Bacteremia with Acute Hemolytic Anemia in the Setting of Endometrial Malignancy

2019 ◽  
Vol 9 (1-2) ◽  
pp. 127-133
Author(s):  
Luke R. Cypher ◽  
Christopher Sullivan ◽  
Ryan Jones ◽  
Angelina Phillips
Keyword(s):  
Phospholipase C ◽  
Hemolytic Anemia ◽  
Clostridium Perfringens ◽  
Rare Case ◽  
Food Poisoning ◽  
Gas Gangrene ◽  
High Grade ◽  
Alpha Toxin ◽  
Intravascular Hemolysis ◽  
Poorly Differentiated

Acute intravascular hemolysis is a rare and often lethal complication of Clostridium perfringens septicemia.Clostridium perfringens is an anaerobic, gram-positive spore-forming rod which is commonly implicated in cases of food poisoning, gas gangrene, and severe hemolytic anemia in humans via the alpha-toxin (phospholipase C). We report an interesting and rare case of a 72-year-old woman who developed massive intravascular hemolysis secondary to C perfringens bacteremia in the setting of poorly differentiated high-grade endometrial malignancy.

scholarly journals Perfringolysin O Expression in Clostridium perfringens Is Independent of the Upstream pfoR Gene

2002 ◽  
Vol 184 (7) ◽  
pp. 2034-2038 ◽  
Author(s):  
Milena M. Awad ◽  
Julian I. Rood
Keyword(s):  
Escherichia Coli ◽  
Homologous Recombination ◽  
Gene Product ◽  
Structural Gene ◽  
Clostridium Perfringens ◽  
Deletion Mutant ◽  
Gas Gangrene ◽  
Alpha Toxin ◽  
Clostridial Myonecrosis ◽  
Perfringolysin O

ABSTRACT The pathogenesis of Clostridium perfringens-mediated gas gangrene or clostridial myonecrosis involves the extracellular toxins alpha-toxin and perfringolysin O. Previous studies (T. Shimizu, A. Okabe, J. Minami, and H. Hayashi, Infect. Immun. 59:137-142, 1991) carried out with Escherichia coli suggested that the perfringolysin O structural gene, pfoA, was positively regulated by the product of the upstream pfoR gene. In an attempt to confirm this hypothesis in C. perfringens, a pfoR-pfoA deletion mutant was complemented with isogenic pfoA+ shuttle plasmids that varied only in their ability to encode an intact pfoR gene. No difference in the ability to produce perfringolysin O was observed for C. perfringens strains carrying these plasmids. In addition, chromosomal pfoR mutants were constructed by homologous recombination in C. perfringens. Again no difference in perfringolysin O activity was observed. Since it was not possible to alter perfringolysin O expression by mutation of pfoR, it was concluded that the pfoR gene product is unlikely to have a role in the regulation of pfoA expression in C. perfringens.

scholarly journals Amentoflavone Attenuates Clostridium perfringens Gas Gangrene by Targeting Alpha-Toxin and Perfringolysin O

2020 ◽  
Vol 11 ◽  
Author(s):  
Shui Liu ◽  
Xiaofeng Yang ◽  
Hong Zhang ◽  
Jian Zhang ◽  
Yonglin Zhou ◽  
...  
Keyword(s):  
Clostridium Perfringens ◽  
Gas Gangrene ◽  
Alpha Toxin ◽  
Perfringolysin O

scholarly journals Organization of the Plasmid cpe Locus in Clostridium perfringens Type A Isolates

2002 ◽  
Vol 70 (8) ◽  
pp. 4261-4272 ◽  
Author(s):  
Kazuaki Miyamoto ◽  
Ganes Chakrabarti ◽  
Yosiharu Morino ◽  
Bruce A. McClane
Keyword(s):  
Clostridium Perfringens ◽  
Horizontal Transfer ◽  
Food Poisoning ◽  
Type A ◽  
Gastrointestinal Diseases ◽  
Open Reading Frame ◽  
Enterotoxin Gene ◽  
Genetic Element ◽  
Reading Frame ◽  
Food Borne

ABSTRACT Clostridium perfringens type A isolates causing food poisoning have a chromosomal enterotoxin gene (cpe), while C. perfringens type A isolates responsible for non-food-borne human gastrointestinal diseases carry a plasmid cpe gene. In the present study, the plasmid cpe locus of the type A non-food-borne-disease isolate F4969 was sequenced to design primers and probes for comparative PCR and Southern blot studies of the cpe locus in other type A isolates. Those analyses determined that the region upstream of the plasmid cpe gene is highly conserved among type A isolates carrying a cpe plasmid. The organization of the type A plasmid cpe locus was also found to be unique, as it contains IS1469 sequences located similarly to those in the chromosomal cpe locus but lacks the IS1470 sequences found upstream of IS1469 in the chromosomal cpe locus. Instead of those upstream IS1470 sequences, a partial open reading frame potentially encoding cytosine methylase (dcm) was identified upstream of IS1469 in the plasmid cpe locus of all type A isolates tested. Similar dcm sequences were also detected in several cpe-negative C. perfringens isolates carrying plasmids but not in type A isolates carrying a chromosomal cpe gene. Contrary to previous reports, sequences homologous to IS1470, rather than IS1151, were found downstream of the plasmid cpe gene in most type A isolates tested. Those IS1470-like sequences reside in about the same position but are oppositely oriented and defective relative to the IS1470 sequences found downstream of the chromosomal cpe gene. Collectively, these and previous results suggest that the cpe plasmid of many type A isolates originated from integration of a cpe-containing genetic element near the dcm sequences of a C. perfringens plasmid. The similarity of the plasmid cpe locus in many type A isolates is consistent with horizontal transfer of a common cpe plasmid among C. perfringens type A strains.

scholarly journals Synergistic Effects of Alpha-Toxin and Perfringolysin O in Clostridium perfringens-Mediated Gas Gangrene

2001 ◽  
Vol 69 (12) ◽  
pp. 7904-7910 ◽  
Author(s):  
Milena M. Awad ◽  
Darren M. Ellemor ◽  
Richard L. Boyd ◽  
John J. Emmins ◽  
Julian I. Rood
Keyword(s):  
Structural Gene ◽  
Clostridium Perfringens ◽  
Synergistic Effects ◽  
Gas Gangrene ◽  
Alpha Toxin ◽  
Coagulative Necrosis ◽  
Clostridial Myonecrosis ◽  
Perfringolysin O ◽  
Vascular Disruption ◽  
Rapid Spread

ABSTRACT To examine the synergistic effects of alpha-toxin and perfringolysin O in clostridial myonecrosis, homologous recombination was used to construct an alpha-toxin deficient derivative of a perfringolysin O mutant of Clostridium perfringens. The subsequent strain was complemented with separate plasmids that carried the alpha-toxin structural gene (plc), the perfringolysin O gene (pfoA), or both toxin genes, and the resultant isogenic strains were examined in a mouse myonecrosis model. Synergistic effects were clearly observed in these experiments. Infection with the control strain, which did not produce either toxin, resulted in very minimal gross pathological changes, whereas the isogenic strain that was reconstituted for both toxins produced a pathology that was clearly more severe than when alpha-toxin alone was reconstituted. These changes were most apparent in the rapid spread of the disease, the gross pathology of the footpad and in the rate at which the mice had to be euthanatized for ethical reasons. Elimination of both alpha-toxin and perfringolysin O production removed most of the histopathological features typical of clostridial myonecrosis. These effects were restored when the mutant was complemented with the alpha-toxin structural gene, but reconstituting only perfringolysin O activity produced vastly different results, with regions of coagulative necrosis, apparently enhanced by vascular disruption, being observed. Reconstitution of both alpha-toxin and perfringolysin O activity produced histopathology most similar to that observed with the alpha-toxin reconstituted strain. The spreading of myonecrosis was very rapid in these tissues, and coagulative necrosis appeared to be restricted to the lumen of the blood vessels. The results of these virulence experiments clearly support the hypothesis that alpha-toxin and perfringolysin O have a synergistic effect in the pathology of gas gangrene.

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