The prevalence, aetiological agents and therapy of onychomycosis in patients with psoriasis: a prospective controlled trial.

BACKGROUND: Nail involvement morphologically resembling onychomycosis frequently accompanies psoriatic lesions. The role of psoriasis as a predisposing factor for onychomycosis and the possible influence of psoriasis on responsiveness of onychomycosis to treatment are controversial. AIM: To investigate the frequency of onychomycosis, the aetiological agents responsible for it, and the efficacy of terbinafine 250 mg/day in patients with psoriasis compared with controls in order to reveal the role of psoriatic process on fungal growth. METHODS: Over a 1-year period, 168 patients with psoriasis and 164 nonpsoriatic controls were recruited. In the case of clinically suspected of fungal infection, further mycological investigations were performed. Systemic terbinafine therapy 250 mg daily for 12 weeks was administered to the patients with onychomycosis. Patients were followed up clinically and mycologically for 24 weeks. RESULTS: Onychomycosis was diagnosed in 22 patients with psoriasis (13.1% of the psoriasis group, which constituted 28.6% of patients with suspicion of onychomycosis) and 13 controls (7.9% of control group; 40.6% of controls with suspicion of onychomycosis). The prevalence rates of onychomycosis were similar in both groups. The most commonly isolated fungi were dermatophytes in the psoriasis group and nondermatophytic moulds in controls. Dermatophytes were more common in psoriatic than control nails (P = 0.02). All patients in each group were cured at the end of the therapy. CONCLUSION: It seems that nail psoriasis constitutes a risk factor not for onychomycosis, but specifically for dermatophytic nail infections. Because of the similar therapeutic results in each group, different antifungal treatment protocols may not be needed in psoriasis. However, to confirm this, new comprehensive studies are necessary.

Successful treatment of multidrug resistant Acinetobacter baumannii meningitis.

BACKGROUND: Acinetobacter baumannii is a major cause of nosocomial infections in many hospitals and appears to have a propensity for developing multiple antimicrobial resistance rapidly. CASES: We report two cases with post-surgical meningitis due to multidrug resistant A. baumannii which were successfully treated with high-dose intravenous meropenem therapy. CONCLUSIONS: Multidrug resistant Acinetobacter spp. in intensive care units are a growing concern. High-dose meropenem is used in the treatment of these infections.

An experience from an outbreak of tinea capitis gladiatorum due to Trichophyton tonsurans.

'Tinea corporis gladiatorum' describes a dermatophytosis transmitted mainly from close skin contact among wrestlers. Although tinea corporis is well recognized, no data are available for tinea capitis infections in wrestlers. After finding tinea capitis infection in a student wrestler, we aimed to search for possible ringworm infections among wrestlers in a wrestling boarding-school. Of the 32 wrestlers, 29, aged 12-18 years, were affected, of whom 22 had scalp involvement. Trichophyton tonsurans was isolated from 20 of the patients, and T. mentagrophytes from the remaining two. Isolated strains of dermatophytes were susceptible to terbinafine and itraconazole. The patients with tinea capitis received oral terbinafine for 4 weeks, and patients with more than two lesions but without scalp involvement received oral terbinafine for 2 weeks. Overall clinical and mycological cure rate was 72.4% and 70%, respectively, at assessment at week 6. The asymptomatic dermatophyte carrier rate was negative 1 year after control of the epidemic. Terbinafine seems to be an alternative drug for the treatment of tinea capitis caused by T. tonsurans; however, control of an outbreak may be very difficult and effective preventive measures should be considered.

Antithrombin III Prevents Early Bacterial Translocation in Burn Injury.

We experimentally studied the effects of antithrombin III (AT III) on bacterial translocation (BT) and intestinal morphology in the early period of burn injury. For this aim, 30 male albino rats were used. A sham burn group (group 1, no. 10) was exposed to 21 °C water. A burn group (group 2, no. 10) and a burn + AT III group (group 3, no. 10) were exposed to 95 °C water for 10 sec, producing full-thickness burn in 30% of the total body surface area. In group 3 the rats received 250 U/kg AT III via the right jugular vein, 15 min before burn injury. One ml 0.9% NaCl was given as a placebo in group 1 and in two rats by the same route. All group 3 rats were sacrificed on day 2 post-burn using an overdose anaesthetic. Cultures of the mesenteric lymph nodes, liver, spleen, blood, and caecal contents were performed. Histopathological examinations, including polymorph nuclear leukocyte (PNL) infiltration and villus morphologies, were qualitatively evaluated on the resected distal ileal segment. The incidence of BT was 1/10 (10%) in group 1, 7/10 (70%) in group 2, and 1/10 (10%) in group 3. A significant increase in BT incidence was observed in group 2 compared with groups 1 and 3 (p = 0.02), while a significant decrease in BT incidence was found in group 3 rats with AT III treatment. Although the PNL infiltration rate was reduced by AT III treatment, a significant decrease was not found compared with group 2 (50% and 90%, respectively). On the other hand, the villus degeneration rate was significantly reduced by AT III treatment compared with group 2 (30% and 90%, respectively). These results suggest that the incidence of BT was enhanced by the burn injury. AT III decreased the incidence of BT in the early period of burn injury. We conclude that AT III can be effectively used to protect from intestinal mucosal injury and to prevent bacterial translocation, especially in early post-burn period.

Does rigid bronchoscopy induce bacterial translocation? An experimental study in rats.

BACKGROUND: Although some reports suggest that bronchoscopy induces bacterial translocation (BT), the mechanisms of BT remain unclear. OBJECTIVE: We aimed to assess whether bronchoscopy or hypoxemia during bronchoscopy is responsible for BT. METHODS: We evaluated 24 rats divided into three subgroups: the control group (group 1, n = 8); the rigid bronchoscopy group (group 2, n = 8), and the group receiving bronchoscopy + mechanical ventilation (group 3, n = 8). Oxygen saturation (SaO(2)) was measured during the bronchoscopic procedure. Blood and tissue cultures from mesenteric lymph nodes (MLNs), liver, spleen and cecal contents were obtained 24 h following bronchoscopy. RESULTS: In group 2, SaO(2) was significantly lower than in groups 1 and 3 (p < 0.01). In group 2, BT significantly increased (6/8, 75%; p < 0.01 vs. group 1, and p < 0.05 vs. group 3). The main site of translocation was MLNs (6/8, 75%) in group 2, while BT was detected in only 1 rat in group 3 (1/8, 12.5%). CONCLUSION: Hypoxemia during rigid bronchoscopy resulted in intestinal mucosal damage in a rat model. Hypoxemia may have been the trigger for BT from the intestine following bronchoscopy.

Production by Escherichia coli isolates of siderophore and other virulence factors and their pathogenic role in a cutaneous infection model.

Escherichia coli isolates from urinary tract infections (UTIs) (n = 124), extra-urinary sites (n = 37) and normal faecal samples (n = 51) were examined for the presence of virulence factors, including siderophores (aerobactin and enterobactin). The proportion of aerobactin producers was significantly higher in UTI (69.4%; p 0.001) and extra-urinary samples (70.3%; p 0.007) than in controls (41.2%), while the proportion of enterobactin producers was significantly lower in the UTI samples than in the controls (p 0.027). In a cutaneous infection model, aerobactin-positive E. coli showed more growth than non-aerobactin and non-enterobactin isolates, even when other virulence factors were identical.

Somatostatin: possible cause of bacterial translocation in obstructive jaundiced rats.

The purpose of this study was to examine the effect of endogenous somatostatin hormone on bacterial translocation in obstructive jaundiced rats. Five groups of rats were studied: group I (n = 10), non-operated group (control); group II (n = 10), sham-operated group which underwent laparotomy and dissection of portal elements, while the common bile duct was not ligated and somatostatin was not injected; group III (n = 10), same as group II, plus injection of somatostatin; group IV (n = 10), common bile duct was ligated with laparotomy but somatostatin was not injected; group V (n = 10), same as group IV, plus somatostatin injection. The blood was analyzed for somatostatin, alkaline phosphatase, and bilirubin levels on the third and tenth days in all animals. At study termination (tenth day), peritoneal swab and blood cultures were taken, and liver, spleen, lung, and mesenteric lymph nodes were harvested for microbiological studies. Bacterial translocation levels were higher in groups III, IV, and V when compared with levels in groups I and II. Similar translocation levels were obtained when blood somatostatin levels were comparable. However, the highest translocation rate was found in groups IV and V in which the blood somatostatin level was also higher when compared with that in other groups. This finding shows that blood somatostatin level is increased in obstructive jaundice. This may explain the bacterial translocation and related sepsis found in obstructive jaundice.

Antiphospholipid antibodies in eclamptic women.

Our purpose was to determine the prevalence of antiphospholipid antibodies (APA) in eclamptic women as well as the rates of intrauterine growth retardation (IUGR) and fetal death in APA-positive and -negative eclamptic women. Thirty-six eclamptic and 30 healthy pregnant women were enrolled in this study. APA in those groups were determined. The prevalences of IUGR and fetal death were determined in APA-positive and -negative eclamptic women. In the eclamptic group, APA were positive in 9 out of 36 patients (25%), where as only 2 out of 30 controls (6.7%) were positive (p < 0.05). Fetal death was encountered in 4 out of 9 (44.4%) APA-positive eclamptic women; this was a significantly larger proportion than that for APA-negative eclamptic women (1/27; p < 0.01). The rates of IUGR in APA-positive and -negative eclamptic women were not significantly different (p > 0.05). Similar conclusions about our results could also be made, when weakly positive anticardiolipin antibodies were regarded as negative in our study group and controls. Our study suggests that positive levels of APA in eclamptic women increase the risk for intrauterine fetal death.