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"Tujuan: Untuk memahami mekanisme terjadinya resistensi terhadap obat antituberkulosis dengan mempergunakan pendekatan epidemiologik genetik. Bahan dan metode penelitian:Disain penelitian : kasus - kontrol.Tempat: Rumah Sakit Persahabatan, Jakarta, Rumah Sakit Umum dr. M. Jamil, Sumatera Barat dan Rumah Sakit Umum dr. Wahidin Sudirohusodo, Makasar. Laboratorium Mikrobiologi FKUI, Jakarta, Lembaga Biologi Molekuler Eijkman, Jakarta dan Laboratorium Bioteknologi Universitas Padjajaran, Bandung. Lama penelitian: 8 bulan ( Januari 2002 - Agustus 2002 ). Subjek penelitian: Masing-masing 279 sampel dahak yang sensitif dan resisten INH serta 36 sampel dahak yang sensitif dan resisten rifampisin. Bahan: sampel dahak yang dikirim dari ketiga rumah sakit tersebut, diperiksa silang di laboratorium mikrobiologi FKUI, Jakarta, lalu diadakan pemeriksaan PCR dan sequencing di Lembaga Eijkman dan laboratorium BioteknoIogi Universitas Padjajaran, Bandung. Disamping itu dilakukan wawancara untuk mendapatkan keterangan mengenai kepatuhan berobat dan pengobatan yang tidak optimal. Data yang terkumpul dianalisis dengan menggunakan analisis uji statistik. Hasil: Prevalensi resistensi terhadap INH dari ketiga propinsi berkisar dari 11,9 % sampai 15,6 %, prevalensi resistensi terhadap rifampisin berkisar dari 1,3 % sampai 1,6 % dan prevalensi resistensi ganda berkisar dari 0,6 % sampai 1,3 %, M. tuberculosis yang mengalami mutasi padagen katG dari ketiga propinsi didapatkan sebesar 60,2 % dan mempunyai kemungkinan risiko resisten terhadap INH sebesar 32,6 kali bila dibandingkan dengan M. tuberculosis yang tidak mengalami mutasi pada gen katG. M. tuberculosis yang resisten terhadap rifampisin dari ketiga propinsi menunjukkan bahwa semua M tuberculosis tersebut mengalami mutasi padagen rpoB, dimana mutasi gen rpoB pada kodon 516 (16,6 %), kodon 526 (63,8 %), kodon 529 dan kodon 531 masing-masing sebesar 5,5 %. Hal ini dapat dikatakan bahwa M. tuberculosis dari ketiga propinsi yang resisten terhadap INH dan rifampisin mengalami beraneka ragam jenis mutasi (diversity). Di ketiga propinsi, ketidakpatuhan penderita tuberkulosis berobat didapatkan sebesar 56,3 % pada M. tuberculosis resisten terhadap INH dan 75 % M. tuberculosis yang resisten terhadap rifampisin. 65,9 % penderita tuberkulosis yang mendapatkan pengobatan monotherapy mengalami resisten terhadap INH dan 75 % penderita tuberkulosis yang mendapatkan pengobatan tidak optimal mengalami resisten terhadap rifampisin. Mutasi baru gen rpoB pada kodon 529 ditemukan 2 buah yang berasal dari propinsi Jakarta dan propinsi Sumatera Barat. Mutasi baru ini tidak mempunyai dampak klinik dan biologis karena kedua kodon tersebut menyandi asam amino yang lama yaitu arginin.

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Genetic Epidemiological and Risk Factor Of M. Tuberculosis For Being Resistant To INH And Or RifampicinObjective of the Study: To understand the mechanisms of resistance to antituberculosis drugs by genetic epidemiological study.

Methods and materials of the study:

Study design: Case - control study.

Location: Persahabatan Hospital (Jakarta), M. Jamil General Hospital (West Sumatra), Wahidin Sudirohusodo General Hospital (South Sulawesi), Microbiology Laboratory FKUI (Jakarta), Eijkman Institute for biology molekuler (Jakarta) and Padjadjaran University Biotechnology Laboratory (West Java).

Duration of study: 8 months ( January 2002 - August 2002 ).

Subject: 279 samples sputum each that were sensitive and resistant to NH, 36 sample sputum each that were sensitive and resistant to rifampiscin.

Material of study: - Sputum sample from three hospitals were sent to Microbiology Laboratory FKUI for crosschecking. Subsequently PCR examination and sequencing were performed in Eijkman Institute and Padjadjaran University Biotechnology Laboratory. In addition interviews were conducted to obtain information about patient compliance and optimal treatment. All data were subjected to statistical analysis.

Results: Resistance prevalence to INH from three provinces range from 11.9 % to 15.6 %; resistance prevalence to rifampicin 1.3 % to 1.6 % and multidrug resistant prevalence: 0.6 % to 1.3 %. Mutation on gene katG M. tuberculosis from three provinces were 60.2 % and have a probability resistance risk to INH 32.6 times compared to M. tuberculosis that didn't have mutation on gene katG. All M. tuberculosis resistant to rifampicin isolated from three provinces have a mutation on gene rpoB, on codon 516 (16.66 %), codon 526 (63.8%), codon 529 and codon 531 respectively 5.5 %. This situation showed that M. tuberculosis from three provinces resistant to INH and rifampicin have a diversity mutant, In the three provinces, non compliance from tuberculosis patient - were 56.3 % of M. tuberculosis resistant to INH and 75 % of M. tuberculosis resistant to rifampicin. INH monotherapy result in 65.9 % resistance and sub optimal treatment result in 75 % resistance to rifampicin. Two new mutations have been found in gene rpoB codon 529 from Jakarta and West Sumatra. And this new mutant has no clinical and biology impact because the two codons encode amino acid was same, is arginine.

Conclusions: Resistance prevalence to NH and or rifampicin in three provinces is significantly high despite a good health infrastructure. If this problem occurs in other provinces with difference geographic characteristic, demographic, socioeconomic and health infrastructure, most probably the resistance prevalence to INH and or rifampicin will be much be more pronounced. The development of resistance of M. tuberculosis to INH and or rifampicin is influenced by mutation on gene encoding enzyme catalase peroxidase (katG) and RNA Polymerise ( rpoB ). Non-compliance and sub optimal treatment are selection factors for katG and rpoB mutant.

Recommendations: It is recommended to continue a similar study in the other provinces with difference geographic, demographic, socio economic, health infrastructure and also other study with mutant. For the Department of Health it is recommended to accelerate methods of early detection of tuberculosis cases that are sensitive or resistant to antituberculosis drugs and monitoring system to record and to report tuberculosis cases from other public health services e.g. Private practices, non government clinics, hospitals and institution to ensure continuous availability and quality of controlled drugs."

"This is the first report of HIV drug resistance in RSUPN Dr. Cipto Mangunkusumo. We tested We reviewed eleven new cases of HIV patients who had virologic failure after 6 months first-line antiretroviral therapy. With the sequencing method, analysis of gene mutations encoded HIV drug resistance. Genotypic resistance results and HIV-1 subtype were interpreted by Stanford DR database. Of ten plasma samples that were successfully amplified and sequenced, all samples were resistant to at least one antiretroviral drug. Genotypic resistance towards the antiretroviral drugs being used was observed in lamivudine (90%), tenofovir (83%), nevirapine (100%) dan efavirenz (100%). It is interesting that no zidovudine resistance were found, including in four patients receiving zidovudine in their HAART. The common NRTI mutations were M184VI and K65R, while NNRTI mutations were Y181CFGVY, K103N, A98AG, E138GQ and G190AGS. No mayor PI mutations were found. Based on these findings, we supports the need for appropriate virology monitoring and HIV drug resistance survey in clinical practice and access to drug options in case of virology failure."

"Objective: There are many factors that govern growth and resistant of Salmonella typhi. A study had reported that the use of sodium benzoate caused antibiotic resistant. However, no study has directly evaluated the effect of sodium benzoate exposure on S. typhi sensitivity to chloramphenicol. The aim of this study was to evaluate the resistance or sensitivity of S. typhi to chloramphenicol after sodium benzoate exposure. Methods: The study was conducted in seven groups: three treatment groups (sodium benzoate insensitive S. typhi+8 μg/mL, 16 μg/mL, and 32 μg/mL of chloramphenicol), three positive control groups (sodium benzoate sensitive S. typhi+8 μg/mL, 16 μg/mL, and 32 μg/mL of chloramphenicol), and one negative control groups (sodium benzoate sensitive S. typhi+0 μg/mL of chloramphenicol). The effect of sodium benzoate exposure to S. typhi sensitivity to chloramphenicol was measured after 24 hours. Spearman test was used to analyzed this association. Results: In this study, we found that the average S. typhi growth in the treatment groups (A, B, C) was 445 CFU/mL, 385 CFU/mL, and 171 CFU/mL, respectively. While in the positive control group (D, E, F) was not obtained any S. typhi growth. Average S. typhi growth in the negative control group was 430 CFU/mL. We found that sodium benzoate exposure inhibited S. typhi growth and affected S. typhi sensitivity to chloramphenicol (p<0.05). In addition, we found that 32 μg/mL chloramphenicol had the highest mean difference value, so this showed that the dose 32 μg/mL of chloramphenicol had the best effectiveness of various treatment groups (p<0.05). Conclusions: Sodium benzoate exposure can inhibit S. typhi growth and cause S. typhi resistant to chloramphenicol.;"

"ABSTRAKLatar Belakang. Anak epilepsi dengan usia awitan di atas lima tahun merupakan kelompok dengan karakteristik epidemiologis dan klinis khas yang mungkin memiliki faktor risiko resistensi terhadap obat anti epilepsi OAE spesifik. Penelitian mengenai resistensi obat pada kelompok usia ini masih sedikit. Tujuan. Mengidentifikasi faktor risiko resistensi OAE pada anak epilepsi dengan usia awitan di atas lima tahun. Metode. Dilakukan penelitian kasus kontrol terhadap anak epilepsi dengan usia awitan di atas lima tahun yang berobat di poliklinik RS Cipto Mangunkusumo dan Mohammad Hoesin bulan Agustus-September 2016. Kelompok kasus adalah anak yang resisten OAE sedangkan kelompok kontrol adalah anak responsif OAE berdasarkan klasifikasi ILAE 2010. Faktor risiko yang diteliti yaitu awitan, jumlah kejang dan lama sakit sebelum berobat, etiologi, jenis kejang, status epileptikus, gambaran EEG awal, evolusi EEG, pencitraan otak dan respon awal terapi. Hasil. Sebanyak 32 pasang anak ikut dalam penelitian. Setelah analisis regresi logistik, faktor yang ditemukan berhubungan dengan resistensi OAE adalah etiologi simtomatik adjusted OR 84,71; IK 95 5,18-1359,15 dan respon awal pengobatan tidak baik adjusted OR 72,55; IK 95 7,08-743,85 . Simpulan. Etiologi simtomatik dan respon awal pengobatan tidak baik merupakan faktor risiko resistensi terhadap OAE pada anak epilepsi dengan usia awitan di atas lima tahun yang bersifat independen.

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Background. Epileptic children with onset above five years encompass distinct epidemiological and clinical characteristics that may have specific risk factors for resistance to anti epileptic drugs AED . Studies on this age group are limited. Objective. To identify risk factors for drug resistance in epileptic children with age of onset above five years. Methods. A case control study was conducted on epileptic children with onset above five years visiting Pediatric Neurology clinic of Cipto Mangunkusumo and Mohammad Hoesin Hospital between August and September 2016. Cases consisted of drug resistant children while control consisted of drug responsive children according to 2010 ILAE classification. Risk factors studied include onset, number of seizures and illness duration before treatment, cause, seizure type, status epilepticus, initial EEG and evolution of EEG, brain imaging, and initial treatment response. Results. Thirty two pairs of children were included in the study. After logistic regression analysis, symptomatic etiology and failure to achieve early response to treatment were found to be associated with drug resistance with adjusted OR 84.71 95 CI 5.18 1359.15 and 72.55 95 CI 7.08 743.85 respectively. Conclusion. Poor initial response to AED and symptomatic etiology are independent risk factors for drug resistance in epileptic children with age of onset above five years. "

"This book, which is the translated version of a Swedish book, combines a general introduction of a variety of antibiotics with a more in-depth discussion of resistance. The focus on resistance in learning about antibiotics will help future scientists recognize the problem antibiotics resistance poses for medicinal and drug-related fields, and perhaps trigger more research and discoveries to fight antibiotic resistant strains. Current overviews of the topic are included, along with specific discussions on the individual mechanisms (betalactams, glycopeptides, aminoglycosides, etc) used in various antibacterial agents and explanations of how resistances to those develop. Methods for counteracting resistance development in bacteria are discussed as well."

"ABSTRACTBackground: human immunodeficiency virus (HIV) infection and acquired immune deficiency syndrome (AIDS) cause serious health problems and affect the Indonesian economy. Papua province has the highest prevalence of HIV infection in the country; however, epidemiological data are limited. Therefore, in order to reveal the current situation of HIV/AIDS in Papua province, sero and molecular epidemiological studies of HIV were conducted. Methods: serological tests were conducted on 157 healthy individuals from the general population residing in Paniai, Papua. In addition, a molecular epidemiological study was then conducted on HIV type 1 (HIV 1) genes derived from infected individuals. Peripheral blood samples from HIV 1 positive individuals and 15 additionally enrolled, previously confirmed HIV 1 positive individuals were subjected to a genotypic analysis. Results: serological tests revealed that 2 out of 157 (1.27%) healthy individuals were HIV positive. In addition, HIV 1 subtyping revealed that subtype B and CRF01_AE were the major subtype and circulating recombinant form (CRF) of HIV 1 prevalent in the region, while subtype A1 and a recombinant form including viral gene fragments of CRF01_AE and subtype B was also detected. In addition, HIV drug resistance-associated major mutations were detected in the reverse transcriptase gene derived from infected individual on antiretroviral therapy. Conclusion: these results provide important information for clearer understanding on the current situation of HIV/AIDS in Papua province in Indonesia."

"ABSTRACTBackground: the global scale-p of antiretroviral therapy (ART) is the primary factor contributing to the decline in deaths from acquired immune deficiency syndrome (AIDS)-related illnesses. However, the emergence of transmitted drug resistance (TDR) compromises the effects of ART in treatment-naive individuals, which may hinder treatment success. The present study aimed to identify the presence of TDR among treatment-naive individuals in Buleleng, Bali, which is currently ranked sixth among Indonesian provinces with the highest cumulative human immunodeficiency virus type 1 (HIV-1) infection cases. Methods: thirty-nine ART-naive individuals in Buleleng Regency General Hospital were enrolled in the present study. Blood samples from participants were subjected to a genotypic analysis. Results: 28 protease (PR) and 30 reverse transcriptase (RT) genes were successfully amplified and sequenced from 37 samples. HIV-1 subtyping revealed CRF01_AE as the dominant circulating recombinant form in the region. No TDR for PR inhibitors was detected; however, TDR for RT inhibitors was identified in five out of 30 samples (16.7%). Conclusion: these results indicate the emergence of TDR among ART-naive individuals in Buleleng, Bali. This issue warrants serious consideration because TDR may hamper treatment success and reduce ART efficacy among newly diagnosed individuals. Continuous surveillance with a larger sample size is necessary to monitor TDR among ART-naive individuals."

"Latar Belakang: Kusta atau Morbus Hansen (MH) merupakan penyakit kronik yang disebabkan oleh infeksi Mycobacterium leprae dan masih menjadi masalah kesehatan di dunia. Penelitian ini mengkaji beberapa faktor risiko yang berkontribusi pada kekambuhan kusta pada pasien di RS dr. Sitanala periode Juni-Desember 2020, disertai dengan analisis kepekaan M. leprae terhadap obat anti kusta rifampisin, dapson dan ofloksasin. Tujuan: Mengetahui kepekaan M.leprae terhadap rifampisin, dapson dan ofloksasin menggunakan metode molekular dan faktor risiko yang berkonstribusi yaitu putus obat, indeks bakteri yang tinggi, riwayat penggunaan kortikosteroid dan kontak erat pada pasien kusta kambuh. Metode: Seratus delapan puluh pasien dengan lesi multibasiler dan terapi kurang dari 2 bulan diikutkan dalam penelitian ini. Pemeriksaan PCR konvensional dilakukan untuk identifikasi M. leprae dan amplifikasi gen rpoB, folP dan gyrA terhadap 50 sampel kerokan kulit yang menunjukkan indeks bakteri >2+ melalui pemeriksaan mikroskopik BTA dengan pewarnaan Zeihl Neelsen. Perunutan gen resistansi dilakukan dengan metode sekuensing dan dilanjutkan dengan analisis sekuen menggunakan software sequence scanner v1.0 software Applied Biosystems dan BioEdit Sequence Alignment. Data faktor risiko pasien diperoleh dari hasil wawancara. Hasil: Faktor risiko pada 180 pasien lepra yang berhubungan dengan kekambuhannya adalah lepra tipe LL, pengunaan kortikosteroid, kontak erat, riwayat putus obat dan indeks bakteri yang tinggi. Lima puluh sampel teridentifikasi sebagai M.leprae dengan metode PCR. Analisis sekuensing gen rpoB, folP dan gyrA dari 24 sampel tidak menunjukkan adanya mutasi, yang mengindikasikan M. leprae masih peka terhadap rifampisin, dapson, dan ofloksasin. Kesimpulan: Dengan profil M. leprae yang peka berdasarkan analisis molekuler, kekambuhan leprae pada pasien lebih berkorelasi dengan faktor risiko.

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Background: Leprosy or Morbus Hansen (MH) is a chronic disease caused by Mycobacterium leprae infection and is still a health problem in the world. This study examines several risk factors that contribute to the recurrence of leprosy in patients at dr. Sitanala for the period June-December 2020, accompanied by an analysis the susceptibility of M. leprae to anti-leprosy drugs rifampin, dapsone and ofloxacin.

Objective: To determine the susceptibility of M. leprae to rifampin, dapsone and ofloxacin using molecular methods and the risk factors that contribute to, default, high bacterial index, history of corticosteroid use and close contacts in relapsed leprosy patients.

Methods: One hundred and eighty patients with multibacillary lesions and less than 2 months of therapy were included in this study. Conventional PCR was performed for the identification of M. leprae and amplification of the rpoB, folP and gyrA genes on 50 skin scraping samples showing a bacterial index >2+ by microscopic examination of AFB with Zeihl Neelsen staining. Sequencing of resistance genes was carried out using the sequencing method and continued with sequence analysis using the software sequence scanner v1.0 software Applied Biosystems and BioEdit Sequence Alignment. Patient risk factor data obtained from interviews.

Results: The risk factors in 180 leprosy patients associated with recurrence were type LL leprosy, use of corticosteroids, close contacts, default and high bacterial index. Fifty samples were identified as M. leprae by PCR method. Sequencing analysis of the rpoB, folP and gyrA genes from 24 samples showed no mutations, which indicated that M. leprae was still sensitive to rifampin, dapsone, and ofloxacin.

Conclusion: Recurrence in leprosy patients is associated with several risk factors and does not occur due to mutations in the rpoB, folP, gyrA genes."

"This book describes antibiotic resistance amongst pathogenic bacteria. It starts with an overview of the erosion of the efficacy of antibiotics by resistance and the decrease in the rate of replacement of redundant compounds. The origins of antibiotic resistance are then described. It is proposed that there is a large bacterial resistome which is a collection of all resistance genes and their precursors in both pathogenic and non-pathogenic bacteria. Ongoing resistance surveillance programs are also discussed, together with the perspective of a clinical microbiologist. The book then turns to specific themes such as the most serious area of resistance in pathogens, namely in Gram-negative organisms. The role of combinations of antibiotics in combating resistance emergence is discussed, particularly in the tuberculosis field, and then the importance of non-multiplying and persistent bacteria which are phenotypically resistant to antibiotics and prolong the duration of therapy of antibiotics which leads to poor compliance and resistance emergence. The role of anti-microbial compounds in textiles is covered, with its potential to exacerbate the spread of resistance. Then, efflux pumps are discussed. The final chapter describes the compounds which are in late stage clinical development, illustrating the paucity of the antibiotic pipeline, especially for Gram-negative bacteria."

"The first book was on "Theory and practice" of antibiotic stewardship in its broadest sense -the how to do it and the do's and don’ts. The second, on "Controlling resistance" was very much on the relationships between use and resistance and beginning to home in on the hospital as the main generator of resistance, but mainly looking at it from a disease/clinical perspective. The last 3 chapters on MRSA, ended where the 3rd book will take off. "Controlling HAI " will concentrate on specific MDR organisms highlighting their roles in the current pandemic of HAI and emphasizing that the big issue is not so much infection control but antibiotic control, in the same way that antibiotic over-reliance/ over-use has caused the problem in the first place. Up 'till now the emphasis for controlling MRSA, C diff and all the other MDROs has very much been on IC, which clearly isn't working. This book will gather all the evidence for the increasingly popular view that much more must be done in the area of antibiotic policies/ stewardship, especially when we are in danger of a "post antibiotic" era, due to a real shortage of new agents in the pipeline."