Dengue has affected Indonesia for the last five decades and become a major health problem in many cities in the country. Jakarta, the capital of Indonesia, reports dengue cases annually, with several outbreaks documented. To gain information on the dynamic and evolutionary history of dengue virus (DENV) in Jakarta, we conducted phylogenetic and evolutionary analyses of DENV isolated in 2009. Three hundred thirty-three dengue-suspected patients were recruited. Our data revealed that dengue predominantly affected young adults, and the majority of cases were due to secondary infection. A total of 171 virus isolates were successfully serotyped. All four DENV serotypes were circulating in the city, and DENV-1 was the predominant serotype. The DENV genotyping of 17 isolates revealed the presence of Genotypes I and IV in DENV-1, while DENV-2 isolates were grouped into the Cosmopolitan genotype. The grouping of isolates into Genotype I and II was seen for DENV-3 and DENV-4, respectively. Evolutionary analysis revealed the relatedness of Jakarta isolates with other isolates from other cities in Indonesia and isolates from imported cases in other countries. We revealed the endemicity of DENV and the role of Jakarta as the potential source of imported dengue cases in other countries. Our study provides genetic information regarding DENV from Jakarta, which will be useful for upstream applications, such as the study of DENV epidemiology and evolution and transmission dynamics.

Background: The World Health Organization reported Indonesia as one of the countries with the most prevalent cases of diphtheria worldwide. The microbiological aspects of diphtheria-inducing bacteria are of great significance in tracing disease transmission and case management. However, clinical aspects are critical for updating clinical features and case management in the field, which may sometimes differ from theoretical foundations. Objectives: This study aimed to identify the microbiological and clinical aspects, including molecular typing and case fatality rates, in diphtheria-confirmed cases from the capital city of Indonesia, Jakarta, and surrounding areas in 2017. Methods: The microbiological aspect of 40 diphtheria-confirmed cases were obtained by re-identify diphtheria-inducing bacteria isolated from the samples, while the clinical aspects of the cases were obtained from the medical records and epidemiological data. The chi-square test was used to examine the correlation between fatal cases and myocarditis and diphtheria antitoxin administration delay. In this study, P ≤ 0.05 was set as the significance level. Results: All 40 diphtheria confirmed cases were induced by toxigenic Corynebacterium diphtheriae with two biotypes, namely intermedius (60.0%) and mitis (40.0%). There are six sequence types of bacteria with two main sequence types, ie, ST534 (46.4%) and ST377 (35.7%). The proportions of cases that had a fever and sore throat were 72.5% and 77.5%, respectively; however, the prevalence rates of the cases with pseudomembrane and bull neck were 100% and 47%, respectively. Most cases were administered a combination of penicillin or erythromycin with other antibiotics (40%), and 22.5% of the cases only received penicillin. Myocarditis was noticed in three fatal cases, and their relationship was statistically significant (P = 0.000). All five fatal cases (12.5% of cases) received diphtheria antitoxin (DAT) lately or had not received it yet. Conclusions: Toxigenic C. diphtheriae with two biotypes (namely mitis and intermedius) and two main sequence types (ie, ST534 and ST377) was the causative agent of diphtheria-confirmed cases from Jakarta and surrounding areas in 2017. It was also concluded that those fatal cases were correlated with myocarditis complications.

The work performed by Ito et al was much appreciated since the authors addressed a novel and important issue in antibiotic rational uses, particularly the resistance of Cefmetazole in ESBL-producing E. coli and the involved gene regulations. Cefmetazole have been used as an alternative to carbapenems in addition to the use of quinolone and trimethoprim or sulfamethoxazole in infection cases caused by ESBL-producing E. coli. 1,2 In their study, 14 ESBLproducing and 12 ESBL-non-producing E. coli from 63 E. coli strains in total were isolated clinically. 3 The ESBLproducing ability of those E. coli isolates did not determine their behavior against Cefmetazole treatment in this study, since the MIC of either ESBL-non producing or ESBL-producing E. coli isolates vary (still relatively low at 1-4 μg/mL) in the first culture. Eleven strains of total 25 isolate gained resistance after being cultured with Cefmetazole at a low dose. Interestingly, after passage culture with the antibacterial-free medium, only 4 strains from these 11 isolates remain resistant to Cefmetazole, while the others gained susceptibility. The purpose of the authors was to unravel the mechanisms involved in the resistance acquisition against Cefmetazole in ESBL-producing E. coli clinical isolates, with the use of ESBL-non-producing isolates as the controls.The previous study, reported more than thirty years ago, addressed the potential mechanism of action of Cefmetazole in methicillin and cephem-resistant (MR) strains of Staphylococcus aureus. 4 However, the progression in this particular issue is relatively slower than the mechanism study of other type of antibiotic, especially in ESBL-producing E. coli. In this study, authors tried to explore the mechanism of how Cefmetazole resistance acquisition occurred in ESBLproducing E. coli isolates. Therefore, the transcription (mRNA) levels of porin encoding genes (ompF, ompC, phoE), chromosomal β-lactamase AmpC encoding genes (acrA, yhiV, mdfA), and drug efflux pump were detected in this particular study. However, as also discussed well in their discussion section, these mechanisms were not the novel part.Moreover, the authors also combined the use of Relebactam (the β-lactamase inhibitor) in observing the effects obtained in Cefmetazole use in E. coli isolates, which resulted in alteration in Cefmetazole susceptilbity. The addition of Relebactam suppressed the resistance toward Cefmetazole. However, the remaining question is, while β-lactamase was inhibited, what mechanism was underlying the suppression of Cefmetazole resistance acquisition? Is the effect caused by inhibiting β-lactamase alone enough to suppress antibiotic resistance? Should the upstream regulators be checked for details of their mechanisms, since the authors themselves mentioned that the Relebactam probably caused the porin deficiency. Novel regulation and details of the mechanisms involved probably could be unraveled if any transcription factors or specific motifs in DNA level were to be predicted and proven. 5,6 If there are any pred...

Abstrak Latar belakang: Lepra masih menjadi masalah kesehatan di Papua terutama di Kota Jayapura.Banyaknya kasus relaps dan default juga menjadi tantangan dalam eliminasi lepra di Jayapura. Kasusrelaps dan riwayat default pada beberapa penelitian berkaitan dengan resistensi terhadap multi drugtreatment (MDT). Tujuan penelitian ini adalah mendeteksi keberadaan mutasi gen rpoB M. leprae padapasien relaps, default dan pasein yang kurang peka terhadap terapi MDT di Kota Jayapura. Metode: Sampel diperoleh dari pasien yang terdiagnosis lepra dengan kriteria pasien relaps, default danpasien yang terus bergejala setelah terapi MDT sebanyak 34 sampel. Sampel diambil dalam bentuk insisikulit (skin silt) daun telinga. DNA diekstraksi dengan menggunakan kit Qiagen. Gen rpoB diamplifikasimelalui teknik PCR dan analisis nukleotida dilakukan melalui sekuensing. Analisis mutasi dilakukanmelalui BLAST dengan basis data GenBank. Hasil: Sebanyak 34 sampel yang diperiksa, 9 diantaranya positif BTA sedangkan 25 yang lainnya negatifBTA. Pada hasil PCR, sampel yang berhasil teramplifikasi sebanyak 31 sampel, dan 3 sampel tidakteramplifikasi. Hasil BLAST menunjukkan bahwa tidak ditemukan adanya mutasi pada gen rpoB yangdapat menyebabkan resistensi terhadap rifampisin. Kesimpulan: Kesimpulan dari penelitian ini adalah gen rpoB Mycobacterium leprae asal Jayapuratidak mengandung mutasi yang dapat menyebabkan terjadinya resistensi terhadap rifampisin. Dengandemikian rifampisin masih sensitif untuk pengobatan lepra di Kota Jayapura. Kata kunci: Lepra, gen rpoB, rifampisin, Mycobacterium leprae. AbstractBackground: Leprosy remains a prominent health problem in Papua especially in Jayapura City. Numerouscases of relapse and default are also challenges in leprosy elimination in Jayapura. Studies in Relapsecases and history of defaults revealed some resistance related to multi-drug treatment (MDT). The purposeof this study was to detect the presence of mutation in rpoB M. leprae gene in patient relapse, default andpatients who are less sensitive to MDT therapy in Jayapura City. Method: Samples were obtained from patients diagnosed with leprosy with criteria of relapse, defaultand symptomatic patients after receiving MDT therapy. A total of 34 samples were taken in the form ofskin incision (skin silt) of the earlobe. DNA was extracted using Qiagen kit. rpoB gene from extractedDNA was amplified through PCR method followed by nucleotide sequences. Analysis of mutation waselaborated using BLAST according to GenBank database. Result: 34 samples were examined, and 9 were positive for Ziehl-Neelsen (ZN)staining, while the 25 werenegative. In the PCR results, the samples that successfully amplified were 31 samples, and 3 samples werenot amplified. The results of BLAST indicated that no mutations in the rpoB gene found in which able toinitiate resistance to rifampicin. Conclusion: The conclusion of this study is the rpoB Mycobacterium leprae gene from Jayapura did notcontain any mutations that could trigger resistance to rifampicin. Thus rifampicin is still sensitive forleprosy treatment in Jayapura City. Keywords: Leprosy, rpoB gene, rifampicin, Mycobacterium leprae

One of the challenges in TB control of Papua is increasing number of multidrug-resistance tuberculosis (MDR-TB). The aim of the study is to imply the WGS tools for predicting TB drugs resistance even MDR as well XDR in clinical samples as an initiation model of laboratory improvement for accurate treatment in MDR TB. Twenty Lowenstein Jansen M. tuberculosis cultures from sputum clinical samples were taken as a DNA source for WGS. Samples preparation was perform using Nextera XT Kit by Illumina and read by Mi-Seq whole genome sequencing. Sequencing result was analyze using TB profiler and visualize by UGENE. We found mutations that direct to drugs resistance in 19 samples consist of 14 samples are MDR and 5 samples are non MDR mutation. Among the 4 samples of non MDR, 2 of them previously show mutation of rifampicin resistance in gene expert but non mutation resistance in WGS. Whole Genome Sequencing technology is the advance technology that may apply to predict the resistance of TB drugs even MDR or XDR and distinguish the accurate drugs for patients individually.