Urinary catheterization in medical wards.

AIMS: THE STUDY AIMS TO DETERMINE THE: 1. frequency of inappropriate catheterization in medical wards and the reasons for doing it. 2. various risk factors associated with inappropriate catheterization, catheter associated urinary tract infections (CAUTI) and bacterial colonization on Foley's catheters (BCFC). SETTINGS AND DESIGN: Hospital-based prospective study. MATERIALS AND METHODS: One hundred and twenty five patients admitted consecutively in the medical wards of a tertiary care hospital, who underwent catheterization with a Foley's catheter, at admission, have been included in the study. Patient profiles were evaluated using the following parameters: age, sex, diagnosis, functional status, mental status, indication, duration and place of catheterization, development of BCFC and CAUTI. STATISTICAL TESTS USED: Chi-square test. RESULTS: Thirty-six out of 125 (28.8%) patients included were inappropriately catheterized. BCFC developed in 52.8% and 22.4% were diagnosed with a CAUTI. The most frequent indication for inappropriate catheterization was urinary incontinence without significant skin breakdown (27.8%). The risk factors for inappropriate catheterization were female sex (RR=1.29, 95% CI=0.99, 1.69, P<0.05) and catheterization in the emergency (RR=0.74, 95% CI=0.61, 0.90, P<0.05). The risk factors for developing a BCFC were age>60 years (RR=0.65, 95% CI=0.48, 0.89, P<0.05), non-ambulatory functional status (RR=0.57, 95% CI=0.39, 0.84, P<0.01), catheterization in the emergency (RR=2.01, 95% CI=1.17, 3.46, P<0.01) and duration of catheterization>3 days (RR=0.62, 95% CI=0.43, 0.89, P<0.01). The risk factors for acquiring a CAUTI were age>60 years (RR=0.47, 95% CI=0.25, 0.90, P<0.05), impaired mental status (RR=0.37, 95% CI=0.18, 0.77, P<0.01) and duration of catheterization>3 days (RR=0.24, 95% CI=0.10, 0.58, P<0.01). CONCLUSIONS: Inappropriate catheterization is highly prevalent in medical wards, especially in patients with urinary incontinence. The patients catheterized in the medical emergency and female patients in particular are at high risk. Careful attention to these factors can reduce the frequency of inappropriate catheterization and unnecessary morbidity.

Tooth enamel defects in mice with a deletion at the Arhgap 6/Amel X locus.

The amelogenin proteins regulate enamel mineral formation in the developing tooth. The human AMELX gene, which encodes the amelogenin proteins, is located within an intron of the Arhgap 6 gene. ARHGAP 6 encodes a Rho GAP, which regulates activity of Rho A, a small G protein involved in intracellular signal transduction. Mice were generated in which the entire ARHGAP 6 gene was deleted by Cre-mediated recombination, which also removed the nested Amel X gene. Enamel from these mice appeared chalky white, and the molars showed excessive wear. The enamel layer was hypoplastic and non-prismatic, whereas other dental tissues had normal morphology. This phenotype is similar to that reported for Amel X null mice, which have a short deletion that removed the region surrounding the translation initiation site, and resembles some forms of X-linked amelogenesis imperfecta in humans. Analysis of the enamel from the Arhgap 6/Amel X-deleted mice verifies that the Amel X gene is nested within the murine Arhgap 6 gene and shows that removal of the entire Amel X gene leads to a phenotype similar to the earlier Amel X null mouse results, in which no amelogenin protein was detected. However, an unusual layer of aprismatic enamel covers the enamel surface, which may be related to the 1.1-Mb deletion, which included Arhgap 6 in these mice.

Microbial pattern of acute infective exacerbation of chronic obstructive airway disease in a hospital based study.

Chronic bronchitis is associated with acute exacerbation, most often infective in origin. In order to study the bacteriological profile in such cases a total of 58 patients were enrolled in this study from the chest clinic of our hospital. The male to female ratio was 2 to 1. Mean age of study group was 47 years. All patients had increased cough and sputum production. Barlett count, gram stain and sputum cultures were done for all patients. IgM and IgG antibodies for M. pneumoniae by ELISA were estimated in all cases. The etiological diagnosis could be established in 72% cases. S. pneumoniae (25.8%), P. aeruginosa (12%), Klebsiella sp (10.3%), B. catarrhalis (3.4%), S. aureus (1.7%) were isolated. Although M. pneumoniae was not cultured it was demonstrated serologically in 20% of cases. H. influenzae was not isolated in any case. The frequency of isolating an etiological agent increased with severity of dysponea.

Functional analysis of ARHGAP6, a novel GTPase-activating protein for RhoA.

Microphthalmia with linear skin defects (MLS) is an X-linked dominant, male-lethal syndrome characterized by microphthalmia, aplastic skin and agenesis of the corpus callosum, and is caused by the deletion of a 500 kb critical region in Xp22.3. Our laboratory isolated a novel rho GTPase-activating protein (rhoGAP) gene named ARHGAP6 from the MLS region. ARHGAP6 contains 14 exons encoding a 974 amino acid protein with three putative SH3-binding domains. Because exons 2-14 are deleted in all MLS patients, we hypothesized that ARHGAP6 may be responsible for some of the phenotypic features of MLS. We pursued two approaches to study the function of ARHGAP6 and its role in the pathogenesis of MLS: gene targeting of the rhoGAP domain in mouse embryonic stem cells and in vitro expression studies. Surprisingly, loss of the rhoGAP function of Arhgap6 does not cause any detectable phenotypic or behavioral abnormalities in the mutant mice. Transfected mammalian cells expressing ARHGAP6 lose their actin stress fibers, retract from the growth surface and extend thin, branching processes resembling filopodia. The ARHGAP6 protein co-localizes with actin filaments through an N-terminal domain and recruits F-actin into the growing processes. Mutation of a conserved arginine residue in the rhoGAP domain prevents the loss of stress fibers but has little effect on process outgrowth. These results suggest that ARHGAP6 has two independent functions: one as a GAP with specificity for RhoA and the other as a cytoskeletal protein that promotes actin remodeling.

Pleuro pulmonary infection with Salmonella group E.

A patient was admitted with a history of cough, shortness of breath and fever. After investigations, he was found to have a left-sided pneumonia with pleural effusion. Culture of the patient's sputum, pleural fluid and blood revealed Salmonella senftenberg. The patient was started on antibiotics according to the sensitivity report and responded to therapy. The past history revealed attempt at suicide by the intake of corrosive acid, which caused an esophageal stricture. The leak of gastric contents into the mediastinum lead to the infection of the pleural cavity and pneumonia.

Characterization of a novel chromo domain gene in xp22.3 with homology to Drosophila msl-3.

The Drosophila male-specific lethal (MSL) genes regulate transcription from the male X chromosome in a dosage compensation pathway that equalizes X-linked gene expression in males and females. The members of this gene family, including msl-1, msl-2, msl-3, mle, and mof, encode proteins with no sequence homology. However, mutations in each of these genes produce a similar phenotype: sex-specific lethality of male embryos caused by the failure of mutants to increase transcription from the single male X chromosome. The MSL gene products assemble into a multiprotein transcriptional activation complex at hundreds of sites along the chromatin of the X chromosome. Here we report the isolation and characterization of a human gene, named MSL3L1, that encodes a protein with significant homology to Drosophila MSL-3 in three distinct regions, including two putative chromo domains. MSL3L1 was identified by database queries with genomic sequence from BAC GS-590J6 (GenBank AC0004554) in Xp22.3 and was evaluated as a candidate gene for several developmental disorders mapping to this region, including OFD1 and SED tarda, as well as Aicardi syndrome and Goltz syndrome.

Community acquired methicillin resistant Staphylococcsus aureus: a new threat for hospital outbreaks?

Methicillin resistant Staphylococcus aureus (MRSA) is a major nosocomial pathogen. Recently, there have been reports of increasing prevalence of MRSA in the community. We here report an outbreak of post operative wound sepsis by MRSA in the surgical ward of LN hospital. A surveillance study for MRSA was undertaken in the corresponding surgical ward, operation theater and OPD and the source of this outbreak was traced to an outdoor patient with community acquired MRSA infection. A total of 320 clinical and environmental samples were screened for MRSA. Seventy (21.8%) S. aureus were obtained, of which 12.8% were resistant to methicillin. 14% of the MRSA infections were from the community. Nasal carriage rates of MRSA in the screened hospital staff and admitted patients were 5.8% and 4.3% respectively. None of the environmental sites sampled yielded MRSA. A study of antibiogram revealed that all the MRSA were uniformly resistant to penicillin, erythromycin, gentamicin, tobramycin and tetracycline and sensitive to vancomycin. All isolates belonged to the same biotype and were nontypable by the standard set of phages.

Salmonella senftenberg: a new pathogen in the burns ward.

This is the first report of Salmonella senftenberg serovar outbreak in a burns unit. This unit admits about 2000 patients with major burn injuries annually. Routine sampling from wound swabs in December 1995 revealed S. senftenberg in a few samples following which a study was instituted from January to March 1996. Of 446 burn admissions during this period 80 patients were culture positive for S. senftenberg in wound swabs. The protocol for investigation included wound swabs on admission and then at biweekly interval, blood culture studies on clinically toxic patients, anti-microbial sensitivity studies, environmental sampling and hand swabs and stool cultures from about 50 staff members of the burns ward. No wound swab at the time of admission was positive for S. senftenberg. Environmental study and the study of staff members did not reveal any obvious source of the infection. S. senftenberg strains were sensitive to more than seven of the 11 anti-microbials tested at the beginning of the study but later 96.3% of the strains showed multidrug (more than three drugs) resistance. By April 1996 the isolates became negligible and later disappeared completely. The organism resurfaced again in March 1997 and the same study was instituted again on 413 admissions between March and May 1997. Fifty patients were culture positive for S. senftenberg. This time stool sample from one burn dresser tested positive for S. senftenberg. Interestingly, again at the beginning of the second outbreak the Salmonella strains were sensitive to 9 out of 11 anti-microbials tested, but later 96.11% strains became multidrug resistant. S. senftenberg strains showed maximum resistance to amoxycillin (97.5%) and minimum to chloramphenicol, tetracycline and cotrimoxazole (12%). It was noticed that Salmonella strains surfaced in wound swabs after 3-4 weeks of hospital stay. Forty-five out of 130 patients studied, in both the episodes, died due to septicemia. The majority of the patients who died had sustained > 60% TBSA burns. Blood cultures were done in 34/130 patients and eight yielded growth (2 S. senftenberg, 4 Klebsiella spp., and two Pseudomonas spp.)

Cell-mediated and humoral immunity in leprosy in children.

Cell-mediated and humoral immunity were studied in 25 children between 0 and 14 years with leprosy. Cell-mediated immunity was studied in vivo by lepromin and epicutaneous sensitization with dinitrochlorobenzene (DNCB) and T-lymphocytes and their subpopulations (T4 and T8) in the peripheral blood. Humoral immunity was evaluated by B-lymphocyte count and immunoglobulins (IgG, IgM and IgA). Along with complement, component C3 was also measured in the serum. Lepromin (Mitsuda) and DNCB responses were significantly poor in mid-borderline (BB) leprosy. The hematological profile, including T-lymphocytes, their subpopulations, B-lymphocytes, serum immunoglobulins, and C3, were found to be normal in all forms of leprosy. The relatively short duration of disease and the low bacterial load may explain these findings.