European Journal of Clinical Microbiology最新文献

To evaluate a non-marketed research prototype of a solid-phase enzyme immunoassay for detection of herpes simplex virus in genital lesions, 154 clinical specimens were collected from 127 men and 27 women with symptoms suggestive of herpes simplex virus infection (erythema, vesicles, ulcers and crustae). The samples were tested using the assay and cultures on four monolayers of human embryonic lung fibroblasts and Vero cells. When the culture was used as reference method, sensitivity was 76.9% and specificity 100% (prevalence 42.4%). Comparison of results by patient group showed that sensitivity was highest in material from patients with vesicles and ulcers. The highest sensitivity was obtained in specimens which developed a cytopathological effect within 48 h and in specimens with three or four positive cell cultures. These findings suggest that the assay is more successful in specimens with high virus titres. The enzyme immunoassay was found to be a rapid, moderately sensitive, highly specific test for detection of herpes simplex virus from genital lesions, but the usefulness of the assay is limited and culture methods should be preferred.

A 36 year old man with Down's syndrome developed group B streptococcal (subtype Ia) mitral endocarditis, which was complicated by widespread abscess formation. He was given antibiotics for one year, and no surgery was performed. Despite the underlying condition, the IgM response and the production of specific antibodies against the bacteria were normal.

The pathogens most often isolated from lesions in skin and soft tissues were Staphylococcus aureus and Streptococcus pyogenes. Cultures from venous leg ulcers, decubitus ulcers and infectious gangrene often yielded also Pseudomonas spp., enterobacteria and enterococci. Obligate anaerobes were frequently isolated especially from abscesses and decubitus ulcers. One third of the abscesses and half of the decubitus ulcers yielded obligate anaerobes.

Antibiotic-resistant pneumococci, especially penicillin-resistant strains, are being increasingly isolated. Pneumococci with intermediate penicillin-resistance (MIC 0.1-1.0 micrograms/ml) have been reported from many parts of the world over the past two decades, and highly resistant strains (penicillin MICs greater than or equal to 2 micrograms/ml) have also appeared. Infection may be acquired in the hospital or community, and nosocomial outbreaks may occur which require control measures to limit organism spread. Most infections occur in children with diminished host responses. Disease caused by pneumococci with intermediate penicillin-resistance may be treated with high doses of penicillin, but disease caused by highly resistant strains, especially meningitis, may require alternative therapy. Pneumococci resistant to sulfonamides, tetracyclines, erythromycin, lincomycin, clindamycin, chloramphenicol, aminoglycosides and rifampin have also appeared. Strains resistant to all the above-mentioned agents, including all beta-lactam antibiotics tested, have been reported from South Africa and Spain. Alternative therapy for resistant strains may include vancomycin, cefotaxime, cefoperazone, ceftriaxone and imipenem. Pneumococci isolated from sites suggestive of infection, especially blood and cerebrospinal fluid, should be routinely tested for penicillin-susceptibility.

The beta-lactamase inducing properties of various new beta-lactam antibiotics in two isogenic strains of Enterobacter cloacae were investigated. Beta-lactamase activity was measured two hours after addition of inducer to cells in the late logarithmic growth-phase. Beta-lactamase expression was highly dependent on the growth medium used, highest levels being obtained after induction with cefoxitin in Tryptic Soy broth, Mueller-Hinton broth and Nutrient broth. Upon induction the mutant 908 Ssi produced tenfold higher beta-lactamase levels than its parent wild type 908 Swi. Among the new antibiotics investigated, sulfoxides of several oxyimino-cephalosporins, HR 810, cefetamet, cefteram, carumonam and BRL 36650 were moderate or poor inducers. The penem FCE 22101 resembled imipenem in its strong inducing properties.

Roxithromycin protected mice against a lethal infection with the extremely virulent RH strain and the C56 strain of Toxoplasma gondii. Therapy initiated 2 h after infection with 2 X 10(3) or 2 X 10(4) RH or C56 tachyzoites protected more than 80% of the mice, compared with 0% of untreated controls (p less than 0.001). Paradoxically, Toxoplasma gondii was isolated more frequently (greater than 80%) in treated mice surviving infection with the less virulent strain (C56) than those surviving infection with the more virulent RH strain (less than 25%). Furthermore, in vitro studies revealed that roxithromycin at dosages up to 250 micrograms/ml had no effect on the proliferation of Toxoplasma gondii in murine peritoneal macrophage cultures.

Protein G is a cell wall protein of group C and G streptococci which binds human IgG antibodies of all four subclasses with high affinity. This property of the molecule was utilized to develop a sensitive Western blot assay to detect antibodies against HIV proteins in patient sera.

The in vitro susceptibilities to gentamicin, tobramycin, amikacin and netilmicin were determined by a standardized microdilution method in unsupplemented Mueller-Hinton broth using blood and urine isolates from hospitalized patients in 29 laboratories in 12 European countries. The distribution of bacteria was similar in each laboratory, Escherichia coli and staphylococci predominating. While resistance rates varied between laboratories (e.g., rates of 1.1-34% were reported for gentamicin), they were consistently higher in southern Europe for all four antibiotics. Production of aminoglycoside-modifying enzymes was observed among resistant strains, ANT(2''), AAC(3)-V and AAC(6')-II predominating in gram-negative bacilli and APH(2)'' + AAC(6')-I in staphylococci.

Eighteen patients are described in whom initially sensitive microorganisms were replaced by resistant isolates during administration of ceftriaxone (n = 8), cefoperazone (n = 5), moxalactam (n = 4), cefotaxime (n = 2) or ceftazidime (n = 1), despite combination with aminoglycosides. All patients had documented gram-negative infections; in 12 patients underlying haematological diseases were present. Resistant strains of Enterobacter cloacae (14), Serratia marcescens (4), Klebsiella oxytoca (3), Pseudomonas aeruginosa (2) and Citrobacter freundii (2) emerged within 2 to 19 (mean 9) days after the beginning of treatment. In 12 patients relapse or secondary infections occurred. Seven of the patients with haematological disorders died. Resistance development was seen in 8 of 29 patients on ceftriaxone and 4 of 10 patients on moxalactam during prospective evaluations; the other drugs were used sporadically. Thus, selection of resistant bacteria is relatively frequent and may have serious clinical consequences in patients with impaired host-defense mechanisms.