scholarly journals A retrospective study on the diagnosis of clostridial myonecrosis in ruminants in Brazil

2017 ◽  
Vol 47 (1) ◽  
Author(s):  
Prhiscylla Sadanã Pires ◽  
Roselene Ecco ◽  
Rodrigo Otávio Silveira Silva ◽  
Marina Rios de Araújo ◽  
Felipe Masiero Salvarani ◽  
...  
Keyword(s):  
Retrospective Study ◽  
Clostridium Perfringens ◽  
Type A ◽  
Gas Gangrene ◽  
The Other ◽  
Post Mortem ◽  
Tissue Samples ◽  
Clostridial Myonecrosis ◽  
Endemic Areas ◽  
Clostridium Chauvoei

ABSTRACT: A standardized immunochemistry method for the diagnosis of clostridial myonecrosis was applied to 38 formalized tissue samples from ruminants with clinical and post mortem history suggestive of blackleg or gas gangrene. The diagnosis of clostridial myonecrosis was confirmed in 37 out of 38 (97.4%) samples tested. Clostridium chauvoei and Clostridium perfringens type A were the most common agents found alone, being detected in ten (26.3%) and six (15.8%) samples, respectively. The other cases showed an association of two or three clostridia, with C. perfringens type A detected in 11 (29%) cases. Based on the findings of the present study, polyvalent vaccines against clostridial infections of animals incorporating C. perfringens would be more adequate for preventative purposes in the endemic areas.

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 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 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.

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 Stress proteins of Clostridium perfringens type A immunoreact with antiserum from rabbits infected with gas gangrene

2003 ◽  
Vol 6 (4) ◽  
pp. 259-261
Author(s):  
Norma Heredia ◽  
Elva Ar�chiga ◽  
Ronald Labb� ◽  
Santos Garc�a
Keyword(s):  
Clostridium Perfringens ◽  
Stress Proteins ◽  
Type A ◽  
Gas Gangrene

A comparative study on the conditions of growth and sporulation of three strains of Clostridium petfringens type A

1996 ◽  
Vol 42 (3) ◽  
pp. 298-304 ◽  
Author(s):  
Mathilde Decaudin ◽  
Jean-Luc Tholozan
Keyword(s):  
Clostridium Perfringens ◽  
Slow Growth ◽  
Type A ◽  
High Volume ◽  
The Other ◽  
Additional Information ◽  
Mutant Strains ◽  
Dependent Strain ◽  
Kinetics Of

Different conditions of growth and sporulation of a strain of Clostridium perfringens type A (NCTC 8798) and two derived mutant strains, the lysozyme-germination dependent strain 8-6 and the revertant strain R3, have been determined. No sporulation was detected for the three strains in the Duncan and Strong (DS) medium; 100% sporulation was routinely obtained for the two mutant strains in the defined (D) medium. Factors promoting in vitro sporulation of C. perfringens type A were assayed: the volume of the culture, the type of preculture, and the addition of lysozyme in precultures. The paper also provides additional information on growth and sporulation of the mutant strains 8-6 and R3. Glucose concentrations up to 11 mM produced high percentages of sporulation. However, strain R3 still sporulated at 20% with 56 mM of glucose. A high volume of D medium led to slow growth kinetics and favoured sporulation. Faster kinetics of growth and the best percentage of sporulation were obtained with a young inoculum of the two mutant strains. On the other hand, the type of medium in the preculture (fluid thioglycollate (FTG) or basal carbonate yeast trypticase (BCYT)) did not influence the percentage of sporulation. However, while strain R3 was not affected by the addition of lysozyme in D medium, kinetics of growth were strongly influenced by this addition in strain 8-6, and the percentage of sporulation increased with a preculture in FTG medium and decreased when BCYT medium was used.Key words: Clostridium perfringens, medium, growth, sporulation.

scholarly journals Mode of action of plectasin-derived peptides against gas gangrene-associated Clostridium perfringens type A

PLoS ONE ◽  
2017 ◽  
Vol 12 (9) ◽  
pp. e0185215 ◽  
Author(s):  
Xueling Zheng ◽  
Xiumin Wang ◽  
Da Teng ◽  
Ruoyu Mao ◽  
Ya Hao ◽  
...  
Keyword(s):  
Clostridium Perfringens ◽  
Mode Of Action ◽  
Type A ◽  
Gas Gangrene

scholarly journals Deficient Skeletal Muscle Regeneration after Injury Induced by a Clostridium perfringens Strain Associated with Gas Gangrene

2019 ◽  
Vol 87 (8) ◽  
Author(s):  
Ana Mariel Zúñiga-Pereira ◽  
Carlos Santamaría ◽  
José María Gutierrez ◽  
Alberto Alape-Girón ◽  
Marietta Flores-Díaz
Keyword(s):  
Clostridium Perfringens ◽  
Muscle Regeneration ◽  
Transforming Growth Factor ◽  
Multiorgan Failure ◽  
Inflammatory Cells ◽  
Gas Gangrene ◽  
Skeletal Muscle Regeneration ◽  
Regeneration Process ◽  
Content Type ◽  
Clostridial Myonecrosis

ABSTRACT Gas gangrene, or clostridial myonecrosis, is usually caused by Clostridium perfringens and may occur spontaneously in association with diabetes mellitus, peripheral vascular disease, or some malignancies but more often after contamination of a deep surgical or traumatic lesion. If not controlled, clostridial myonecrosis results in multiorgan failure, shock, and death, but very little is known about the muscle regeneration process that follows myonecrosis when the infection is controlled. In this study, we characterized the muscle regeneration process after myonecrosis caused in a murine experimental infection with a sublethal inoculum of C. perfringens vegetative cells. The results show that myonecrosis occurs concomitantly with significant vascular injury, which limits the migration of inflammatory cells. A significant increase in cytokines that promote inflammation explains the presence of an inflammatory infiltrate; however, impaired interferon gamma (IFN-γ) expression, a reduced number of M1 macrophages, deficient phagocytic activity, and a prolongation of the permanence of inflammatory cells lead to deficient muscle regeneration. The expression of transforming growth factor β1 (TGF-β1) agrees with the consequent accumulation of collagen in the muscle, i.e., fibrosis observed 30 days after infection. These results provide new information on the pathogenesis of gas gangrene caused by C. perfringens, shed light on the basis of the deficient muscle regenerative activity, and may open new perspectives for the development of novel therapies for patients suffering from this disease.

scholarly journals The Agr-Like Quorum-Sensing System Is Important for Clostridium perfringens Type A Strain ATCC 3624 To Cause Gas Gangrene in a Mouse Model

mSphere ◽  
2020 ◽  
Vol 5 (3) ◽  
Author(s):  
Mauricio A. Navarro ◽  
Jihong Li ◽  
Juliann Beingesser ◽  
Bruce A. McClane ◽  
Francisco A. Uzal
Keyword(s):  
Quorum Sensing ◽  
Mouse Model ◽  
Clostridium Perfringens ◽  
Regulatory System ◽  
Type A ◽  
Gas Gangrene ◽  
Null Mutant ◽  
Wild Type ◽  
Content Type

ABSTRACT Clostridium perfringens type A is involved in gas gangrene in humans and animals. Following a traumatic injury, rapid bacterial proliferation and exotoxin production result in severe myonecrosis. C. perfringens alpha toxin (CPA) and perfringolysin (PFO) are the main virulence factors responsible for the disease. Recent in vitro studies have identified an Agr-like quorum-sensing (QS) system in C. perfringens that regulates the production of both toxins. The system is composed of an AgrB membrane transporter and an AgrD peptide that interacts with a two-component regulatory system in response to fluctuations in the cell population density. In addition, a synthetic peptide named 6-R has been shown to interfere with this signaling mechanism, affecting the function of the Agr-like QS system in vitro. In the present study, C. perfringens type A strain ATCC 3624 and an isogenic agrB-null mutant were tested in a mouse model of gas gangrene. When mice were intramuscularly challenged with 106 CFU of wild-type ATCC 3624, severe myonecrosis and leukocyte aggregation occurred by 4 h. Similar numbers of an agrB-null mutant strain produced significantly less severe changes in the skeletal muscle of challenged mice. Complementation of the mutant to regain agrB expression restored virulence to wild-type levels. The burdens of all three C. perfringens strains in infected muscle were similar. In addition, animals injected intramuscularly with wild-type ATCC 3624 coincubated with the 6-R peptide developed less severe microscopic changes. This study provides the first in vivo evidence that the Agr-like QS system is important for C. perfringens type A-mediated gas gangrene. IMPORTANCE Clostridium perfringens type A strains produce toxins that are responsible for clostridial myonecrosis, also known as gas gangrene. Toxin production is regulated by an Agr-like quorum-sensing (QS) system that responds to changes in cell population density. In this study, we investigated the importance of this QS system in a mouse model of gas gangrene. Mice challenged with a C. perfringens strain with a nonfunctional regulatory system developed less severe changes in the injected skeletal muscle compared to animals receiving the wild-type strain. In addition, a synthetic peptide was able to decrease the effects of the QS in this disease model. These studies provide new understanding of the pathogenesis of gas gangrene and identified a potential therapeutic target to prevent the disease.

Sign in / Sign up

Export Citation Format

Share Document