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J Mainil

Publications and source records attributed to J Mainil.

43 records · Page 3Linked to original sources
PubMed1989

Detection and identification of pathotypes of verocytotoxigenic Escherichia coli isolated from weaned piglets using gene probes for seven E. coli toxins.

Seventy verocytotoxigenic (VTEC) and sixty-three non VTEC haemolytic Escherichia coli isolated from recently weaned piglets were examined by the colony hybridization assay using gene probes for three verocytotoxins: Edema disease principle (EDP) and Shiga-like toxins I and II (SLTI and SLTII). The results with the EDP and SLTII probes were identical. All VTEC hybridized with these two probes, while non VTEC did not. All 133 E. coli were negative for the SLTI probe. Hybridization of the plasmid content of 14 VTEC did not show any evidence for plasmid localization of the genes coding for the EDP. The 70 VTEC were also assayed with gene probes for heat-stable (STaP, STb) and heat-labile (LT, LTIIa) enterotoxins. Only the STb probe was hybridized by 36 of them. Most STb-positive isolates belonged to serotype O141: K85 biotypes 9 and 13 PC.

Animals↗
PubMed1988

Phenotypic and genotypic characterization of enterotoxigenic Escherichia coli serotype O8:KX105 and O8:K"2829" strains isolated from piglets with diarrhea.

Twelve pathogenic and seven nonpathogenic enterotoxigenic Escherichia coli strains which were previously identified as belonging to serogroup O8:KX105 (A. Broes, J. M. Fairbrother, S. Larivière, M. Jacques, and W. M. Johnson, Infect. Immun. 56:241-246, 1988) were further examined for their phenotypic and genotypic properties. Only the 12 pathogenic strains were confirmed to possess the capsular antigen KX105. The seven nonpathogenic strains did not possess this antigen and thus were incorrectly assigned to have capsular antigen KX105. All seven nonpathogenic strains apparently possessed a previously unrecognized capsular antigen which has been designated K"2829". Studies with antisera prepared against F1 (type 1) fimbriae from three E. coli strains suggested that at least three antigenic subtypes of F1 fimbriae were represented among the O8:KX105 strains examined. By using serotyping, biotyping, and outer membrane protein profile analyses, the O8:KX105 strains were divided into at least two distinct clusters, whereas the O8:K"2829" strains were grouped into a single unique cluster. Most of the strains of the same cluster were further differentiated by testing for antibiotic resistance and colicin production and resistance and by analysis of plasmid content. With the exception of one strain which lost its enterotoxicity during storage, all of the O8:KX105 strains hybridized with the gene probes for the heat-labile (LT) and heat-stable (STb) enterotoxins. For each O8:KX105 strain, a single plasmid ranging in size from 61 to 77 megadaltons carried the LT and STb genes. All of the enterotoxigenic O8: KX105 strains fermented sorbose, whereas the nonenterotoxigenic strain did not. All of the O8:K "2829" strains hybridized with the STb probe only. For each O8:K "2829" strain, the STb genes were located on a single plasmid of 61 or 22 megadaltons. None of the strains demonstrated homology with the genes encoding the F4 (K88), F5 (K99), F6 (987P), and F41 fimbrial antigens and STaP and STaH.

Animals↗
PubMed1985

Hybridization on bovine enterotoxigenic Escherichia coli with two heat-stable enterotoxin gene probes.

Hybridizations were done on bovine enterotoxigenic Escherichia coli with 2 heat-stable (ST) enterotoxin gene probes from porcine and human origin (STp and STh). Of the baby mouse-positive isolates, 56 (53%) hybridized the STp probe and 50 (47%) did not. There was no isolate that hybridized the STh probe. Hybridization with the Stp probe was more frequent (P less than 0.005) for E coli isolated from calves that died before 2 weeks of age (49 STp-positive isolates of 77 [64%] isolates) than for E coli isolated from calves that died after 2 weeks of age (2 STp-positive of 21 [10%] isolates).

Animals↗
PubMedDate not supplied

Study of the virulence of five strains of amyxomatous myxoma virus in crossbred New Zealand White/Californian conventional rabbits, with evidence of long-term testicular infection in recovered animals.

The virulence of five amyxomatous myxoma virus (MV) strains, the clinical and pathogenetic effects of which had been studied previously in specific pathogen-free (SPF) rabbits, was determined by inoculation of five groups of 10 crossbred New Zealand White/Californian conventional rabbits. A much more acute myxomatosis syndrome was produced in conventional rabbits than that reproduced previously in SPF animals. However, the main clinical signs were of the respiratory type. The MV strains MYX 254/95 and 801 appeared very virulent, killing all the inoculated animals. The strains MYX 217/95, MYX 555/94 and Saint Benoist were somewhat attenuated, killing only seven, six and six rabbits, respectively. Extensive lung lesions due to supervening bacterial infections were observed in 36 of the 39 rabbits that died. Lethality was found to be a better estimate of virulence than mean survival time. By 98 days after viral inoculation, all the surviving animals had completely recovered. At that time, they were immunosuppressed by treatment with adrenocorticotrophic hormone (ACTH) for 10 days to determine whether they still harboured the virus. After the ACTH treatment, eight of the 11 surviving rabbits showed clinical signs that resembled amyxomatous myxomatosis. All the virological examinations performed on naso-conjunctival exudate, on mononuclear cells, on eyelids and on ovaries remained negative but infectious virus was isolated from the testes of three of six surviving male rabbits.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

The efficacy of two vaccination schemes against experimental infection with a virulent amyxomatous or a virulent nodular myxoma virus strain.

Two types of myxomatosis vaccine are available commercially, namely, vaccine prepared from the Shope fibroma virus (SFV) and that prepared from an attenuated myxoma virus (MV) strain, e.gSG33. An experiment was designed to compare two vaccination schemes for their ability to protect rabbits against challenge with either a virulent amyxomatous MV strain or a virulent nodular MV strain. Apart from a difference in the cutaneous expression of the disease, the two challenge strains resembled each other in respect of mortality rate, naso-conjunctival shedding of virus, and tissue infection. Vaccination with SFV alone failed to prevent clinical signs, naso-conjunctival shedding or tissue infection. Vaccination with SFV followed by a booster inoculation with SG33 protected rabbits against the development of clinical signs and significantly reduced both viral shedding in naso-conjunctival exudates and viral infection of eyelids, lungs and testes; virus was, however, isolated from testes of some surviving animals.

Animals↗
PubMedDate not supplied

Shiga/verocytotoxins and Shiga/verotoxigenic Escherichia coli in animals.

Vero/Shiga toxins (VT/Stx) have an A-B structure: the A subunit carries the enzymatic activity and the B subunit binds the toxin to the membrane receptor (Gb3 or Gb4). The VT/Stx inhibit protein synthesis in the target eucaryotic cells, mainly the endothelial cells of blood vessels. The VT/Stx are subdivided into two families. VT1/Stx1 is a homogeneous family of toxins identical to the Stx of Shigella dysenteriae. VT2/Stx2 is a more heterogeneous family of toxins more distantly related to this Stx toxin. The VT2/Stx2 variants can be distinguished by the polymerase chain reaction (PCR) and/or the reaction with monoclonal antibodies. The VT/Stx-producing Escherichia coli are also subdivided into two main groups on the basis of the presence or absence of additional properties: the enterohaemorrhagic E. coli (EHEC) induce the formation of attaching/effacing lesions and carry a 60 MD plasmid encoding a specific haemolysin (the enterohaemolysin); the vero/shiga-toxigenic E. coli (VTEC/STEC) do not show these properties. The EHEC are isolated from humans and ruminants, especially young calves. They are associated with haemorrhagic enterocolitis and its sequelae in humans, the haemolytic-uraemic syndrome (HUS). The VT/Stx play a role in the occurrence of blood in the faeces and in the HUS by their action on the endothelial cells of blood vessels in the intestinal submucosa and in the renal glomeruli, after resorption through the intestinal walls. The VTEC/STEC are isolated from piglets, calves and humans. In recently weaned piglets, they cause the oedema disease, an enterotoxaemia characterized by subcutaneous, mesenteric and cerebral oedemas, with nervous disorders as main clinical signs. The oedema disease is the consequence of the action of the VT/Stx on the endothelial cells of blood vessels in various organs. In calves and humans, the role in disease of VTEC/STEC is controversial, but they could be associated with some cases of diarrhoea and HUS. The case of the O157:H7 EHEC which are present in healthy cattle of various ages, but are highly virulent for humans is of special interest. The potential zoonotic aspect of VT/Stx-producing E. coli infections in animals is detailed chapter by chapter. Prophylaxis of these infections by vaccination is the subject of the discussion on the future of the research studies on these pathogenic bacteria.

Animals↗