Rational attenuation of Corynebacterium pseudotuberculosis: potential cheesy gland vaccine and live delivery vehicle

Hodgson, A. L. M.; Krywult, Jolanta; Corner, L. A.; Rothel, J.S.; Radford, Anthony J.

doi:10.1128/iai.60.7.2900-2905.1992

Cited by 78 publications

(61 citation statements)

References 22 publications

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“…PLD assists the spread of Corynaebacteria from the site of infection by causing hydrolysis of vascular and lymphatic endothelial walls. Moreover, PLD contributes to the in vivo survival of C. pseudotuberculosis in the host for at least 18 weeks, thus leading to strong stimulation of the immune system (Hodgson et al, 1992). The production of PLD of C. pseudotuberculosis in tissues of infected animals has been shown to impair neutrophil chemotaxis toward the site of infection thus allowing the escape from neutrophils in addition to its killing ability of the phagocytic neutrophil.…”

Section: Selimmentioning

confidence: 99%

“…This may have lead several authors to attempt the development of living attenuated corynebacterial vaccines against CLA in sheep. With the help of genetic engineering methods, Hodgson et al (1992) could delete the gene responsible for PLD production from the wild strain of C. pseudotuberculosis, obtaining a new non-PLD-producing strain called`Toxminus strain' of Corynebacteria.…”

Section: Immunological Aspectsmentioning

confidence: 99%

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Oedematous Skin Disease of Buffalo in Egypt

Selim

2001

Journal of Veterinary Medicine, Series B

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This review covers a historical view and etiology of oedematous skin disease which affects buffalo in Egypt, the microbiology of Corynebacterium pseudotuberculosis causing the disease: its virulence; clinical signs; mechanism of pathogenesis; histopathology; mode of transmission; immunological aspects; treatment and control. It is concluded that C. pseudotuberculosis serotype II is the main cause of OSD and exotoxin phospholipase D and its lipid contents of the cell wall are the major causes of pathogenesis. After declaring the role of Hippobosca equina in transmission of the causative agent among buffaloes, control of OSD is now available.

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Section: Selimmentioning

confidence: 99%

Section: Immunological Aspectsmentioning

confidence: 99%

Oedematous Skin Disease of Buffalo in Egypt

Selim

2001

Journal of Veterinary Medicine, Series B

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“…11 The PLDs from C. pseudotuberculosis, C. ulcerans and A. haemolyticum have been shown to have similar biological effects to Loxosceles venom 11,12,14,15 with C. pseudotuberculosis PLD playing a vital role in the pathogenesis of caseous lymphadenitis in sheep and goats. 16,17 We have previously shown that the lysis of erythrocytes induced by Loxosceles sphingomyelinases is dependent on activation of complement (C) via the alternative pathway, 9,10 which was caused by induction of cleavage of cellsurface glycophorins. 18 The sialic acid on glycophorins increases the binding of factor H (f H; the co-factor for factor I in the degradation of C3b) to surface-bound C3b, 19,20 which can limit activation of the alternative pathway.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of induction of complement susceptibility of erythrocytes by spider and bacterial sphingomyelinases

et al. 2002

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SUMMARYWe have recently shown that the sphingomyelinase toxins P1 and P2 from the venom of the spider Loxosceles intermedia induce complement (C)-dependent lysis of autologous erythrocytes by induction of the cleavage of cell surface glycophorins through activation of an endogenous metalloproteinase facilitating the activation of the alternative pathway of C. Phospholipase D (PLD) from Corynebacterium pseudotuberculosis shows some degree of homology with the spider sphingomyelinases and can induce similar clinical symptoms to those observed after spider envenomation. The aim of this study was to investigate if the bacterial PLD-induced haemolysis of human erythrocytes was C dependent and if cleavage of glycophorins occurred. We show here that haemolysis of both PLD-and P1-treated human erythrocytes was C dependent, but while PLD-mediated haemolysis was dependent on activation of the classical pathway of C, P1 induced lysis via both the classical and alternative pathways. P1, but not PLD, induced cleavage of glycophorins and no change in expression of complement regulators was induced by either of the toxins. In both cases, annexin V binding sites were exposed, suggesting that the membrane asymmetry had been disturbed causing exposure of phosphatidylserine to the cell surface. Our results suggest that C susceptibility induced by L. intermedia and C. pseudotuberculosis PLD is a result of exposure of phosphatidylserine, and the higher potency of P1 toxin can be explained by its additional effect of cleavage of glycophorins.

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“…It is well known that phospholipase D (PLD) of C. pseudotuberculosis was identified as the major virulence factor of 31 KDa and it was suggested that PLD exotoxin facilitate the dissemination and infiltration of the bacteria in host tissues (Hodgson et al, 1992). The duration of lethality depends upon the number of exotoxins contained in the same isolate.…”

Section: Mediamentioning

confidence: 99%

Some studies on Corynebacterium pseudotuberculosis causing Oedematous Skin Disease in Egyptian buffaloes

Essa¹

2010

Journal of Veterinary Medical Research

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Out of 63 bacteriologically examined sanguineous fluids samples which were collected from Oedematous Skin Disease (O.S.D.) lesions, 37 isolates of C. pseudotuberculosis (C.p.) were recovered. The sensitivity tests revealed that isolates were highly sensitive to trimethoprim + sulphamethoxazole, amoxycillin, gentamicin and enrofloxacin. Diphtheria toxin (DT) produced by C. pseudotuberculosis of buffalo was determined by using the double immunodiffusion technique, it was applied on concentrated exotoxins which was prepared from C.p. isolates against Diphtheria toxin antiserum, its results were 15 (40.54%) positive and 22 (59.46) %) negative to presence of DT.

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Rational attenuation of Corynebacterium pseudotuberculosis: potential cheesy gland vaccine and live delivery vehicle

Cited by 78 publications

References 22 publications

Oedematous Skin Disease of Buffalo in Egypt

Oedematous Skin Disease of Buffalo in Egypt

Mechanism of induction of complement susceptibility of erythrocytes by spider and bacterial sphingomyelinases

Some studies on Corynebacterium pseudotuberculosis causing Oedematous Skin Disease in Egyptian buffaloes

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