Sharps injuries; Hospital versus community

Sharps injuries; Hospital versus community

MICROBIOLOGY CRITICAL ISSUES IN THE STUDY OF EPIDEMIOLOGICAL PATTERN Of HEPATITIS C VIRUS INFECTION: MALA YSIAN EXPERIENCE. SHARPS INJURIES; HOSPITAL...

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MICROBIOLOGY CRITICAL ISSUES IN THE STUDY OF EPIDEMIOLOGICAL PATTERN Of HEPATITIS C VIRUS INFECTION: MALA YSIAN EXPERIENCE.

SHARPS INJURIES; HOSPITAL VERSUS COMMUNITY

P.K.Das.* K.K.Phua S.Oeorge 1 and N.Hilmi Departments of Pathology and Immunology, School of Medical Sciences, Universiti Sains Malaysia, 1599( Kubang Kerian, Kelantan, and Abbott Laboratories. Inc. Petaling Jaya, Selangor Malaysia1

Gordon Rich and Janice Vickery The Mount Hospital and Western Diagnostic Pathology Australian Medical Enterprises, Perth

Objectives:- 1. To detennine the epidemiological pattern of hepatitis C virus(HCV: infection in specific groups of Malaysian population viz. children below 10 years oJ age, voluntary blood donors, pregnant women, female drug addicts, recipients 01 multiple transfusion and chronic liver disease patients in a semi urban population. 2. To identify the risk factors in the transmission of the infection anc reliability of el'.isting laboratory tests. Methodology: Sera from the above subjects were tested for markers of HCV , HBV, HIV and syphilis using Abbott and other diagnostic kits. Repeated reactives for HC, were confinned by Abbott Matrix system and further screened for surrogate markers Detailed drug, sexual and transfusion related history was obtained and subsequentl) corroborated with physical examination. Results: We observed that sera from 64.7% and 73.3% of female drugs addict~ were positive for HCV and HBV markers respectively while HCV seropositivity ir other groups was variable viz. multiple transfused subjects(35.5%), blood donors(l7%), children
CEFTRIAXONE-RESISTANT KLEBSIELLA IN SINGAPORE: PREVALENCE, ASSOCIATED RESISTANCE AND RECOMMENDATIONS FOR TESTING RVTPLin Diagnostic Bacteriology, Department of Pathology, Singapore General Hospital, Outram Road 0316, Singapore Ceftriaxone-resistant Klebsiella associated with multiple antimicrobial resistance is an increasing problem worldwide, particularly in tertiary referral hospitals. Appropriate laboratory procedures are required to detect extendedspectrum beta-lactamases. In this paper, the susceptibility testing criteria given in the NCCLS disc diffusion method is examined. The associated antimicrobial resistance of strains isolated in our laboratory is described. The distribution and prevalence of resistant strains in our hospital is presented. Selected Klebsiella isolates in our laboratory were tested by the NCCLS disc diffusion method (modified Bauer-Kirby) and by the Augmentin disc approximation test to screen for extended-spectrum beta-Jactamases. The distribution of zone sizes were plotted. Representative MICs were determined by the E test. Records of Klebsiella isolations from 1 to 15 March 1994 were traced from the laboratory information system. 59/60 ·resistant", 23/23 "intermediate" and 5156 "sensitive" strains identified by the NCCLS method were positive by the Augmentin disc approximation test_ Intermediate strains formed a microbial population distinct from sensitive strains and had MICs lQ-lOOx higher than sensitive strains. It is recommended that strains identified as ·intermediate" on testing by the NCCLS method be regarded as resistant. 40 % of Klebsiella isolates were ceftriaxone-resistant. Gentamicin resistance was strongly associated with ceftriaxone resistance, being found in 4/112 (3.6 %) of ceftriaxone-sensitivestrains and in S2n4 (70.3 %) of ceftriaxoneresistant strains. Trimethoprim-sulfa(25% vs. 59%) and tetracycline (13.8% vs. 51.8 %) resistance were also associated with ceftriaxone resistance. Ceftriaxone resistant strains were widely distributed throughout the hospital in all clinical disciplines, and predominated over sensitive strains in neurosurgical, haematology and intensive care units.

'l he "sharps injury" is a Health Care Worker (HCW) problem. W ·.~stern Diagnostic Pathology has investigated 1,297 injured pt\l."sons in the last three years. Only 3% were not Health Cli\re Workers. Most hospitals have good programmes in place, with at least a reasonable degree of compliance from staff members. 120 (28%) of hospital staff involved in 425 sharps injuries were found to be non immune to Hepatitis B. In 39 (9%) there was insufficient investigation to ensure In contrast, in 609 incidents adequate managemen:t. involving community HCWs 359 (60%) were non immune and there was insufficient investigation for management. The sharps protocol should arrange for the donor and recipient to have blood tests done 80 that if there is a high risk situation then prophylaxis against Hepatitis Band/or Human Immunodeficiency Virus can be started soon enough to be effective. Outside of the hospital environment this is rarely achieved. It is apparent that there is an urgent requirement for an education programme in clinics and medical practices. Institution of a protocol in these non-hospital locations would reduce the risk to the injured HCW and secondly the awareness created might lead to a reduction in injuries.

PATHOGENESIS OF DISEASE CAUSED BY SHIGELLA DYSENTERlAE AND ESCHERICHIA COil Paul N. Goldwater Microbiology and Infectious Disease Services, Women's and Children's Hospital, Adelaide 5006. A number of virulence factors are known to be important in disease causation by these enteric bacteria. Proteins expressed by these bacteria regulate invasiveness and allow penetration of the bacterium into the enterocyte and into the adventitia (enteroinvasiveness) with production of typical symptoms and signs of disease. Sh. dyenteriae is internalized via bacterium-directed phagocytosis; polymerization of host cell actin filaments is also bacterially encoded. Other genes (invasion plasmid antigens: IpaA, JpaB , IpaC, IpaD , etc.) encode invasins through plasmid DNA . Virulence genes (VirB, VirG, VirF), are encoded also by a large plasmid. The gene products are produced in defined amounts at critical times in the infection cycle in response to environmental signals such as temperature, osmolality, etc. Cell wall lipopolysaccharide (O-antigen) is needed for intercellular spread and protection against epithelial cell defenses . Enteroinvasive E. coli (EJEC) use shigella-like mechanisms to invade enterocytes. Shiga toxin produced by Sh. dysenteriae I is a ribosome poison. Enterohaemorrhagic E. coli (EHEC) utilise Shiga-like toxins I, 11, and variants of these toxins to induce disease. Not only are these toxins a major mechanism for production of bloody diarrhoea, but they are responsible for severe forms of toxaemic systemic disease including haemolytic uraemic syndrome (HUS) (mainly SLT-I! mediated) , and thrombotic thrombocytopenic purpura (TTP) through perturbation of endothelial cell and platelet function . SLT-I and SLT-lI are encoded in DNA of bacteriophages and become incorporated into the genome of a restricted number of E. coli OH serotypes. E. coli 0157:H7 is responsible for ",50% of cases of BUS in the Northern Hemisphere but is stilI uncommon in Australia where a wide variety of serotypes are associated with HUS, but E. coli 0111 :H- seems to be common . Glycosphingolipid (ceramide) receptors for B subunits of SLTs (Gb3 and Ga2 on endothelial cells, and erythrocyte P1 antigen) probably play a role in pathogenesis of HUS and TTP. Enterotoxigenic E.coli (ETEC), cause disease through production of either or both heat stable toxin(s) (ST) or beat labile toxin(s) (LT). Enteropathogenic (EPEC) cause diarrhoea via non-toxigenic mechanisms.