Role of Stenotrophomonas maltophilia in hospital-acquired infection.

Stenotrophomonas maltophilia (previously Pseudomonas maltophilia, Xanthomonas maltophilia) is highly resistant to antibiotics. It causes infections that result in increased morbidity, but not usually mortality, in patients with weakened host defences. The increase in S. maltophilia nosocomial infections is due to the changing nature of the hospital patient population and to changes in antibiotic usage. Detection, identification and susceptibility testing methods require improvement, and this complicates the comparison of published data. Susceptibility testing should be reserved for those isolates that are clearly associated with disease. Treatment can be difficult and may be complicated by biofilm formation. S. maltophilia can both acquire and transfer resistance to antibiotics. Future therapeutic development may be directed against biofilms and efflux mechanisms, in order to render the organism more susceptible to available antimicrobial agents.

Small-colony variants of Staphylococcus aureus.

Staphylococcus aureus remains a versatile and dangerous pathogen. Small-colony variants (SCVs) of S. aureus are a naturally occurring sub-population, first described nearly 100 years ago. These variants, of which there are different classes, grow slowly and have many atypical characteristics thought to be due to defective electron transport, and include minute colony forms. SCVs have been isolated from sites of infection, particularly persistent recurrent ones (e.g. in chronic osteomyelitis and cystic fibrosis), and also may arise following exposure to certain antibiotics. During infection the intraendothelial-cell milieu stimulates the formation of SCVs, which can better survive the assault of cell-mediated immunity. SCV phenotypes produce less tissue damage than normal staphylococci. Although microscopic morphology and Gram's staining of SCVs are normal, clinical microbiology laboratories may fail to detect them because of their very slow growth. The full extent of the role of S. aureus SCVs in clinical disease, and the most appropriate means of identifying such strains or testing to predict the clinical usefulness of therapeutic regimens, remains unknown. Failure to recover SCVs results in a major susceptibility reporting error, as the more resistant component of the infection will not have been reported. No controlled trials of therapy have been conducted, and, thus, optimal therapy has yet to be defined. However, SCVs are resistant to aminoglycoside antibiotics, and may be resistant to trimethoprim-sulphmethoxazole. The effectiveness of cell-wall-active antibiotics is reduced. SCVs are transmissible, and current infection control recommendations for normal S. aureus infections are appropriate.

Pneumocystis carinii infection in human immunodeficiency virus-positive patients.

Pneumocystis carinii is a ubiquitous, atypical unicellular fungus. P. carinii pneumonia (PCP) is responsible for considerable morbidity and mortality in acquired immune deficiency syndrome (AIDS) patients, and is the leading complication in advanced human immunodeficiency virus (HIV) infection. Many different host (mammal)-specific species of Pneumocystis exist, but the life-cycle is not understood fully. Human strains are designated as P. carinii f. sp. (special form) hominis (at least 59 different types). P. carinii is spread via the airborne route. Disease is most frequently caused by fresh exposure to a source of P. carinii, rather than by reactivation of latent infection. Asymptomatic carriage among healthy persons may occur. PCP occurs in HIV-infected patients when the CD4+ count falls below a certain threshold; organisms multiply and gradually fill the alveoli. Symptoms, which include a mildly productive cough, progressive dyspnoea and fever, may persist for months prior to diagnosis. Without treatment, progressive respiratory insufficiency invariably ends in death. Pulmonary specimens may be obtained by procedures of varying sensitivity and risk. Diagnosis is usually confirmed by detection of stained organisms; however, staining procedures vary in sensitivity and ease of use. Robust polymerase chain reaction (PCR) protocols with good predictive results may be useful in the future. Therapy falls into two categories: for acute primary infections and for prophylaxis. A confirmed diagnosis ensures that patients do not receive potentially toxic medication (adverse drug reactions can occur). Prophylaxis can dramatically reduce the frequency of PCP in HIV patients, and its more widespread use should lead to a decline in the incidence of PCP in the future.

Cyclospora species as a cause of diarrhoea in humans.

Within the past 10 years, the coccidian parasite Cyclospora cayetanensis has been clearly recognised as a cause of protracted diarrhoea in humans. Heavy infection results in inflammation and epithelial injury in the duodenum and jejunum. Of the multiple symptoms, diarrhoea may neither be the presenting nor predominant one. Following an incubation period of 12 hours to 11 days, the abrupt onset of watery diarrhoea occurring in a relapsing cyclic pattern is characteristic, lasting from six to eight weeks in immunocompetent patients, but three months in the immunocompromised. Of worldwide distribution, it is endemic in certain regions where it can be associated with rainy seasons. Outbreaks or isolated cases may also occur in developed countries. Contaminated water can transmit the oocysts, and usual control procedures for potable water supplies fail to detect the parasite, which resists chlorination. Diagnosis depends upon laboratory investigations, usually faecal microscopy. For reliable detection of characteristic oocysts in the faeces, special procedures may be necessary. Trimethoprim-sulphamethoxazole is established as the treatment of choice and leads to rapid relief of symptoms, although relapse in immunocompromised patients may require secondary prophylaxis.

Evaluation of the ATB 32 A system for identification of anaerobic bacteria isolated from clinical specimens.

A new miniaturized 4-h method for the identification of anaerobic bacteria, ATB 32 A (API System SA, Montalieu Vercieu, France), was evaluated against conventional methods of identification. The evaluation was done by using 260 recent clinical isolates and 21 reference strains of anaerobic bacteria. All reference strains were correctly identified and did not figure in the detailed analysis. Of the 140 gram-negative bacilli, 90.6% of Bacteroides spp. and 95.5% of Fusobacterium spp. were correctly identified to the species level, with an additional 8.4% of the Bacteroides spp. being identified to the genus level. Clostridia were correctly identified in 85.9% of cases, with an additional 9.9% being identified to the genus level. Peptostreptococci were correctly identified in 91.6% of cases. The 4 strains of Actinomyces spp. were all identified correctly, as were 10 of the 11 strains of Propionibacterium spp. A total of 3.1% of strains were not identified by ATB 32 A, while for 1.9% of strains, completely false identifications were obtained. Estimation of the individual preformed enzyme results may pose problems, although these decrease with familiarity with the system. With certain enzyme profiles, additional testing was necessary to arrive at an identification; however, there was no requirement for gas-liquid chromatography. If certain additions are made to the data base and the difficulties of determination of organisms to the species level among the non-Bacteroides fragilis (sensu stricto) members of the B. fragilis group can be reduced, this system holds promise as a reliable standardized alternative for the identification of anaerobic bacteria in clinical laboratories.