Conjugative transfer, in the apparent absence of plasmid DNA, of high-level vancomycin resistance from Enterococcus faecalis NCTC 12201 to Staphylococcus aureus B111 has been demonstrated in vivo and in vitro. Selection of transconjugants on media containing erythromycin or chloramphenicol may result in the transfer of resistance to erythromycin, chloramphenicol, gentamicin, streptomycin and vancomycin though these are capable of separate transfer. Vancomycin resistance has not been transmitted from staphylococcus to staphylococcus though transfer of erythromycin and of chloramphenicol resistance has been achieved.
Erythromycin-resistant staphylococci can be divided into two phenotypic classes based on their pattern of cross-resistance to other macrolides, lincosamides and type B streptogramins. Strains inducibly or constitutively resistant to all MLS antibiotics possess erythromycin ribosomal methylase (erm) genes, whereas strains inducibly resistant to only 14 and 15-membered ring macrolides and type B streptogramins harbour msrA, which encodes an ATP-dependent efflux pump. Dot-blot hybridization was used to study the distribution of ermA, ermB, ermC and msrA in five epidemiologically distinct groups of staphylococci. The most widely-distributed resistance determinant was ermC, which was detected in 112 (50.6%) of 221 isolates, alone in 106 isolates and in combination with a second erythromycin resistance determinant in six strains. MsrA was detected in 73 (33%) of isolates, alone in 65 and in combination with a methylase gene in eight strains. This determinant was responsible for erythromycin resistance in over one-third (36.4%) of clinical isolates of coagulase-negative staphylococci. ErmA and ermB were present in only a minority of isolates (5.9 and 7.2% of strains, respectively). The resistance determinants present in ten strains did not hybridize to any of the four probes although, in all cases, their resistance phenotype was consistent with the possession of a methylase gene. Interestingly, ermB was found exclusively in animal isolates of Staphylococcus intermedius, Staphylococcus xylosus and Staphylococcus hyicus, but not in coagulase-negative staphylococci of human origin. This determinant has previously only been found in a small number of epidemiologically related strains of Staphylococcus aureus.
Although the deleterious effect of Staphylococcus aureus on atopic eczema is well recognized, the mechanism of this effect may be more complex than pyogenic infection alone. We have shown that the majority of S. aureus cultures isolated from atopic eczema produced exotoxins with superantigenic properties, although this was no more frequent than in a control group, and was not restricted to one particular superantigen. However, the widespread nature of staphylococcal infections in atopic eczema indicates that sufficient superantigen may be released to cause T-lymphocyte activation, cytokine release, and mast cell degranulation. These mechanisms could, in part, explain the exacerbations of atopic eczema associated with S. aureus infection.
Two rapid spectroscopic approaches for whole-organism fingerprinting of pyrolysis-mass spectrometry (PyMS) and Fourier transform-infrared spectroscopy (FT-IR) were used to analyze a group of 29 clinical and reference Candida isolates. These strains had been identified by conventional means as belonging to one of the three species Candida albicans, C. dubliniensis(previously reported as atypical C. albicans), and C. stellatoidea (which is also closely related to C. albicans). To observe the relationships of the 29 isolates as judged by PyMS and FT-IR, the spectral data were clustered by discriminant analysis. On visual inspection of the cluster analyses from both methods, three distinct clusters, which were discrete for each of the Candida species, could be seen. Moreover, these phenetic classifications were found to be very similar to those obtained by genotypic studies which examined the HinfI restriction enzyme digestion patterns of genomic DNA and by use of the 27A C. albicans-specific probe. Both spectroscopic techniques are rapid (typically, 2 min for PyMS and 10 s for FT-IR) and were shown to be capable of successfully discriminating between closely related isolates of C. albicans, C. dubliniensis, and C. stellatoidea. We believe that these whole-organism fingerprinting methods could provide opportunities for automation in clinical microbial laboratories, improving turnaround times and the use of resources.
Nose, throat and finger carriage of Staphylococcus aureus was investigated in a series of random samples from a normal European population.No evidence for a seasonal trend in carriage was found but the intersample variation between successive random samples was obtained. The mean nasal carrier rate was 29 % with a standard deviation of 7 %.No association was found between nasal or throat carriage of staphylococci and stay in hospital or antibiotic therapy but respondents with penicillin-resistant staphylococci in the nose had skin infections more frequently than those with penicillin-sensitive strains.Evidence was obtained for a family, perhaps genetic, ‘predisposition’ to carry staphylococci in the nose.
Aspects of bacterial resistance to the major classes of antimicrobials used in veterinary dermatology are presented in this review. Resistance of gram-positive and gram-negative bacteria to tetracyclines, macrolide-lincosamide-streptogramin antibiotics, chloramphenicol, mupirocin, sulphonamides, trimethoprim, aminoglycosides,¯uoroquinolones and b-lactam antibiotics are depicted with respect to the dierent mechanisms of acquired and intrinsic resistance. Examples are given for the three major resistance mechanisms, enzymatic inactivation, decreased intracellular drug accumulation and target modi®cation. In addition, basic information about mobile genetic elements which carry resistance genes, such as plasmids, transposons and gene cassettes, and their modes of spreading via transduction, conjugation, mobilization and transformation is provided.
The ability of a particle to remain airborne, its ability to pass through filters, the site at which it may be deposited in the respiratory tract and the rate at which it will be removed from the air by sedimentation are all dependent on the size and density of the particle. In the course of a variety of investigations we have determined the size distribution of particles carrying various species of bacteria and fungi, using the size-grading slit-sampler described by Lidwell (1959). A few of the results obtained have already been quoted in part, but the majority have not been published previously.The air sampler used separates the airborne particles into four size ranges, each of which is deposited on the surface of the agar medium contained in one of four 6 in. Petri dishes. This apparatus is constructed so that the air sample, entering through a slit 7 mm. wide, impinges on to the surface of the first Petri dish at such a velocity that only the larger particles, i.e. those having an equivalent particle diametert greater than about 18,t, are deposited. The air stream carrying the smaller particles is then caused to impinge in turn on to the surface of the three remaining Petri dishes, each time at an increased velocity and through a narrower slit, so that the minimum particle size for 50 % deposition is about 10jt for the second dish, 4,t for the third and less than 1,u for the fourth and last. When the plates have been incubated the colonies found will be derived from organisms which entered the sampler carried on airborne particles corresponding approximately to the four size ranges, greater than 18,t, between 18 and 10Q, between 10 and 4,u and less than 4,t. These size limits correspond to the value of equivalent particle diameter for 50 % deposition so that there is, in fact, a considerable size overlap between the fractions. In spite of this, however, reasonably good estimations of the particle size distribution within the sample and hence of the median equivalent particle diameter and of the dispersion, expressed either as an interquartile range or, if appropriate, as a standard deviation, can be made by plotting on probability paper the cumulative fraction oversize against the 50 % collection limits, namely 18-2, 9-6 and 4 2,t. As there are internal losses in the instrument it is necessary to correct the numbers of colonies counted in the later stages in order to arrive at a good estimate of the size distribution in the original sample. The numbers found on * Now at The Wright-Fleming Institute, St Mary's Hospital, London, W. 2. t rhe equivalent particle diameter is the diameter of a sphere of unit density which has a settling rate in air equal to that of the particle in question. 24 Hyg. 61, 4
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