- Volume 43, Issue 5, 1995

Staphylococcal scalded skin syndrome (SSSS) is a recognised clinical entity that affects primarily the very young and, in rare cases, the very old or the immunocompromised. Koch’s postulates have been fulfilled in that: (i) Staphylococcus aureus is isolated from every case; (ii) S. aureus can reproduce the syndrome in an experimental animal model; (iii) a specific extracellular toxin can reproduce the syndrome; and (iv) antibody to the toxin can protect experimental animals. Although exfoliative toxin (ET) is responsible for the skin loosening seen in SSSS, it does not account for all the symptoms of the disease. Purified ET does not cause erythema in either neonatal mice or man, and the lesions are not painful unless the loosened epidermis is removed. This suggests that other factors, e.g., δ-haemoiysin, are involved in the pathogenesis of this condition. Although much has been learned about the pathogenesis of the syndrome, we are still largely ignorant of the factors which govern host resistance to SSSS (i.e., intoxication by ET-producing strains of S. aureus). It is fortunate from the patient’s point of view that the aetiological agent can be destroyed readily by the use of appropriate antibiotic therapy.

The relative effectiveness of a poly(L-lactic acid) ciprofloxacin hydrochloride (CIP) microsphere formulation (250–425 μm) against peritoneal implanted biofilm of Pseudomonas aeruginosa was investigated in a rabbit model. Correlations between in-vivo CIP pharmacokinetics in peritoneal dialysate and serum after intraperitoneal administration, in-vivo cell counts and rabbit survival rate were obtained. Dialysate and serum concentrations after 12 h (C12h) were greater than those obtained with free drug whereas maximum serum concentrations (Cmax) were lower and the time to reach Cmax (tmax) was longer. A silastic implant device pre-colonised with P. aeruginosa for 2 days was implanted in the rabbit peritoneum, and dialysate with or without drug or microspheres was administered via a catheter. Rabbits receiving no antibiotic and those receiving free drug (10 mg in dialysate) died of peritonitis and septicaemia, whereas all rabbits given CIP microspheres recovered completely from infection. The viable count of P. aeruginosa was markedly reduced or eliminated from the catheter, the device and the peritoneal wall in CIP microsphere-treated rabbits but not in rabbits treated with free drug, as determined from histological and scanning electronmicroscopic evidence. These results demonstrate that sustained release of antibiotics at biofilm eradication concentrations (BEC) is required to treat biofilm infections associated with peritoneal implanted devices.

The subtype of verotoxin 2 (VT2) found in 22 VT2-positive stool samples from severely diseased Italian and German children with haemorrhagic colitis or haemolytic uraemic syndrome, or both, and that produced by the corresponding VT-producing Escherichia coli (VTEC) strains isolated from the stools were studied by cytotoxicity sero-neutralisation assays and by polymerase chain reaction (PCR) amplification of the VT2 B-subunit gene, followed by restriction fragment length polymorphism (RFLP) analysis. The free faecal toxin was serotyped as the classical VT2 in 21 stool samples, and as the VT2 variant VT2c in one. For all but one of the VTEC isolates, the toxin phenotype was consistent with the type of VT produced in vivo and found in the corresponding stool samples. Genotyping was in agreement with phenotyping for those strains harbouring a single type of VT2 gene. Three O157: H7 isolates carrying both VT2 and VT2c genes had the VT2 phenotype, instead of the expected VT2c phenotype. Direct PCR analysis of stools detected VT genes in only 11 of 20 VT-positive stool samples suggesting that the Vero cell cytotoxicity assay is more sensitive in diagnosing VTEC infection. Immunological and genetic subtyping of VT2 performed directly on stool samples from patients with haemolytic uraemic syndrome could be a useful complementary approach to understanding the role of the different types of VT in this syndrome.

An ELISA was developed for the detection of IgG antibodies to Staphylococcus aureus collagen binding protein (CnBP) in 95 patients with S. aureus endocarditis, complicated septicaemia with bone and joint involvement or uncomplicated septicaemia and in 95 control patients. Sixty percent of S. aureus-infected patients showed a positive peak anti-CnBP antibody level or a significant rise in titre, or both, during infection, but patients with S. aureus endocarditis or complicated septicaemia could not be differentiated from those with uncomplicated S. aureus septicaemia. The collagen binding capacity of S. aureus strains from 82 of the 95 patients was investigated in a particle agglutination assay and a 125 I-labelled assay. All strains bound collagen in the particle agglutination assay as did 68 % in the 125 I-labelled assay, but there was no correlation between collagen binding of the patient strain and endocarditis, joint or skeletal involvement. An anti-CnBP antibody response was seen in 16 patients infected with a S. aureus strain negative for collagen binding in vitro, indicating in-vivo expression of CnBP.

The present study was undertaken to investigate whether less pathogenic Candida species (C. tropicalis, C. stellatoidea, C. krusei and C. glabratd) express a fibronectin receptor (FNr) antigenically related to α5βl integrin, which mediates their binding to fibronectin (FN). By flow cytometric analysis, a monoclonal antibody (MAb) directed against human α5 integrin subunit (clone SAM-1) and two different antisera to FNr positively stained C. tropicalis, C. stellatoidea and C. glabrata, with the greatest expression observed for C. tropicalis. No or only marginal immunoreactivity was found on C. krusei. C. tropicalis, C. stellatoidea, C. glabrata, but not C. krusei yeasts specifically adhered to FN; higher levels of adhesion were found for C. tropicalis and C. stellatoidea with respect to C. glabrata. Less pathogenic Candida spp. bound to the Arg-Gly-Asp (RGD) containing 120-kDa fragment of FN and adhesion to intact FN was markedly inhibited by Gly-Arg-Gly-Asp-Ser-Pro (GRGDSP), but not by Gly-Arg-Gly-Glu-Ser-Pro (GRGESP) peptides. In addition, anti-α5 SAM-1 MAb and both anti-FNr antisera strongly blocked binding of less pathogenic Candida spp. to FN. Overall, these results indicate that less pathogenic Candida spp., including C. tropicalis, C. stellatoidea and C. glabrata, express a receptor antigenically related to α5βl integrin which mediates their adhesion to FN.