Care of patient with MRSA:

when selecting an empirical regimen is to choose an agent that has adequate activity against the infecting organisms. Empirical antibiotic choices should be individualized based on institutional antibiograms, which tend to be quite different from hospital to hospital, from city to city, and from country to country. Pitout J.D., et al. 2008 The next issue surrounding the therapy of ESBL-producing infections is that even if an agent is selected that has activity against the bacteria in vitro, clinical efficacy in patients is not always guaranteed. Although in vitro tests ESBLs are inhibited by ß-lactamase inhibitors such as clavulanic acid, other study has shown the activity of ß-lactamß- lactamase inhibitor combination agent e.g. piperacillin-tazobactam is influenced by the bacterial inoculums, dose administration regimen and specific type of ESBL present. The other consideration treatment of ESBL-producing bacteria are cephamycins e.g. cefoxitin, cefotetan and Cefepime. This is widely believe to occur as a result of the so-called inoculums effect that occurs when the minimum inhibitory concentration of the antibiotic rises i.e. the antibiotic looses activity with the increasing size of the inoculums or number of bacteria tested. This effect has been described for cephalosporins, β-lactam-β lactamase inhibitor combinations piperacillin, tazobactam and to a lesser extent with the quinolones. Tigecycline is also one of the drugs in the pipeline which can be considered for treatment. Pitout J.D., et al. 2008; Perez et al. 2007 The carbapenems imipenem, meropenem, ertapenem, doripenem are still the first choice of treatment for serious infections with ESBL-producing E coli and K pneumonia. It has been reported that 98 of the ESBL-producing E coli, K pneumonia and P. mirabilis are still susceptible to these drugs. This agents are highly stable to hydrolysis by ESBLs, are distributed into body tissues in high concentration and there is no inoculums effect. Perez et al, 2007; Pitout J.D., et al. 2008. But with the emergence of the carbapenem – resistant Enterobateriaceae, the “magic bullet” is actually difficult to find. There are some older drugs which can be used to treat the ESBL-producing E. coli or K. pneumonia infections. Fosfomycin was reported of having admirable in vitro activity against the ESBL- producing E. coli or K. pneumonia. In HongKong, most of the ESBL-producing E coli isolates were reported to be sensitive to fosfomycin. Ho et al., 2010. Colistin is another choice which we can consider for the treatment of these organisms. Although once considered as quite a toxic antibiotic, it is a last resort that we can consider at the present moment as there is no new anti gram negative antibiotics available for the treatment of these multidrug resistant organisms. Perz et al. 2007 To reduced the problem of antimicrobial resistance, action should be taken along to tracks; promotion of prudent use of antibiotics and prevention of the spread of resistant bacteria. Improving antibiotic use can be achieved by changing the prescribing behavior of doctors, education, guideline and clinical pathway, antimicrobial cycling, antimicrobial order form, combination therapy streamlining or de-escalation, dose optimization, intravenous or oral therapy. REFERENCES Alekshun,MN., Levy, SB., 2007. Molecular mechanisms of antibacterial multidrug resistance. Cell 128. 1027-1050 Chong Y, Yakushiji H, Ito Y, Kamimura T. Clinical and molecular epidemiology of Extended-spectrum ß-lactamase-producingg Escherechia coli and Klebsiella pneumonia in a long-term study from Japan. Eur J Clin Microbiol Infect Dis 2011;30 :83-7 Falagas ME, Karageorgopoulos DE. Extended-spectrum ß-lactamase-producing organisms. Journal of Hospital Infection 2009;73:345-354 Gayatri Y, Merati TP. 2013. Clinical Features and Antibiotics Resistant Pattern of MRSA Infection in Sanglah Hospital. Free oral presentation in Petri XIX Aceh Ho, P.L., Yip, K.S., Chow,K.H., Lo, J.Y., Que, T.L., Yuen, K.Y., 2010. Antimicrobial resistance among uropathogens that cause acute uncomplicated cystitis in womaen in HongKong: a prospective multicenter study in 2006 to 2008. Diagn. Microbiol. Infect, Dis. 66, 87-93 Johnson, J.R., Menard, M. Johnston, B., Kuskowski, M.A., Castanheira, M. 2008. Escherichia coli sequence type ST 131 as the major cause of serious multidrug-resisntant E.coli infections in the United States. Clin Infect Dis;51:286-294 Kelly S., Collins J., David M., Gowing C., Murphy PG. 2006. Linezolid resistance in coagulase negative staphylococci. J Antimicrob Chemother 58: 898-899 Moran GJ., Krishnadasan A., Gorwithz RJ et al. 2006. EMERGEncy ID Net Study Group. Methicillin-resistant S aureus Infection among patients in the emergency department; 355: 666-674 Paterson DL., Bonomo RA. Extended-spectrum ß-lactamase: a clinical update. Clin Microbiol Rev 2005, 18: 657-86 Perez, F., Endimiani, A., Hujer, K.M., Bonomo, R.A., 2007. The continuing challenge of ESBLs. Curr. OPin. Pharmacol. 7, 459-469 Pitout JD, Loupland KB. 2008. Extended-Spectrum ß-lactamase-producing Enterobacteriaceae :an emerging public-health concern.Lancet Infect Dis ;8:159-66 Rybak MJ., LaPlente KL. 2005. Community acquired methicillin resistant Staphylococcus aureus: a review. Pharmacotherapy; 25: 74-85 Sievert,D.M., Riks, P., Edwards,J.R., et al. 2013. Antimicrobial-resistant pathogens associated with healthcare- associated infections: summary of data reported to the National Healthcare Safety Network at the Centers of Disease Control and Prevention, 2009-2010. Infect Control Hosp Epidemiol.; 34:1-14 Diagnosis and Treatment of Dengue Infection Dewi Dian Sukmawati Division of Tropical and Infectious Disease Department of Internal Medicine Udayana University School of Medicine-Sanglah Hospital Denpasar Dengue infection, a mosquito – borne flavivirus, is caused by dengue virus transmitted mainly by vector Aedes aegypti and Aedes albopictus, other species Aedes polynesiensis and Aedes scutellaris play the role of less common vector. There are five serotypes, DEN-1, 2, 3, 4 and 5. Each episode of infection induces a life-long protective immunity to the homologous serotype which confers partial and transient protection against subsequent infection by the other serotypes. Secondary infection by another serotype is a major risk factor for DHF, mainly due to antibody induced enhancement. Epidemiologic studies have identified young age, female sex, high body-mass index, virus strain or virulence and genetics of the human host e.g. major histocompatibility complex class I related sequence B and phospholipase C epsilon 1 genes as risk factors for severe dengue. All five serotypes may be circulating in the population at any one time but from the experience in the south-east Asia it appears that the predominant circulating dengue virus will show a sinusoidal pattern – with a peak to peak interval of 7 – 9 years. It is likely that this interval allows a buildup of immune – naïve population of children. 1,2,3,4 1. Course of Dengue Infection Infection by Dengue viruses may cause symptomatic infections or asymptomatic seroconversion. Symptomatic dengue infection manifests as a systemic and dynamic disease with wide clinical spectrum. The spectrum ranges from non severe to severe clinical manifestations. Following the incubation period, the illness begins abruptly and evolving in three phases: febrile, critical and recovery Figure 1. Due to its dynamic nature, the severity of the disease will usually only be apparent around defervescence period during the transition of the febrile to the afebrile phase and often overlapping with the onset of the critical phase. 5,6