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Background and PurposeNo suitable scale was identified in literature that comprehensively measure self-efficacy of Pakistani breast cancer patients. The study aimed to develop a self-efficacy scale in Urdu language and determine its dimensions.MethodsThe scale was developed with input from experts and literature. It was administered, in crosssectional phase of two pilot studies, on breast cancer patients receiving chemotherapy. Post hoc internal consistency reliability was computed and principal component analysis (PCA) was performed.ResultsSES-U comprised 17 questions. PCA revealed a total of five factors explaining cumulative variance of 68.7%. These factors were self-confidence, faith, coping, optimism, and decision making. Post hoc internal consistency (Cronbach's alpha) value was high (∞ = 0.87).ConclusionsThe self-efficacy scale has acceptable validity and reliability and has potential to obtain information related to self-efficacy of cancer patients receiving chemotherapy.

Purpose This study aimed to determine the effect of individualized patient education along with emotional support on the quality of life (QoL) of breast cancer patients undergoing chemotherapy. It also aimed to determine the intervention's feasibility in the Pakistani context. Methods A quasi-experimental design, with pre- and post-test, in two groups, via time block, was used. The study was conducted at a public hospital in Karachi with a sample of 50 patients; 25 patients each in the intervention and control group. The intervention was delivered over a period of six weeks. It comprised verbal and written patient education, availability of a nurse during patients' chemotherapy administration and over the telephone, and a telephone follow-up of the patients by the nurse. patients' QoL was assessed at baseline and at the sixth week of receiving chemotherapy. Results Tests indicated a significant improvement in the overall QoL, breast cancer subscale scores, and the physical and emotional well-being of the intervention group, as compared to the control group. The intervention effect size was moderate (0.655) for the QoL. Conclusion The intervention was found to be effective in improving patients' QoL. However, a larger study, in a multi-center setting, is recommended to ascertain the findings of this pilot study.

Non-typhoid Salmonella (NTS) infects 250 to 3200 per 100,000 individuals from all over the world. NTS infection is relatively high in Jeddah (ranges between 44-132/100,000 population) as compared to other cities of Saudi Arabia. NTS isolates have also shown increasing resistance to conventional antibiotics. Therefore, fluoroquinolone (FQ) is considered drug of choice for the treatment of invasive NTS infections. A rapid detection of FQ resistance may greatly assist in appropriate therapy and containment of resistant NTS strains. Thus, molecular detection of mutations in FQ resistance genes (gyrA and parC) may play a promising role. Since limited data were available about FQ resistance among NTS isolates, therefore, this study primarily explored the occurrence of phenotypic and genotypic FQ resistance among NTS isolates from Jeddah, Saudi Arabia. Study also explored any correlation between phenotypic and genotypic FQ resistance. Fifty NTS isolates were collected from a public sector hospital of Jeddah from January to December, 2014. FQ susceptibility was determined for 48 NTS isolates using Kirby-bauer disk diffusion method and results were interpreted according to Clinical and Laboratory Standards Institute (CLSI) methodology. Genotypic resistance to FQ was determined by exploring mutations in gyrA and parC genes using PCR- based gene-sequencing method. Results were statistically analyzed using Social Package of Statistical Science (SPSS) version 22. Phenotypic antibiogram revealed that 38% (18/48) NTS isolates were FQ resistant, that 23% (11/48) were intermediately susceptible and that 39% (19/48) were susceptible. Genotypic resistance revealed mutations in only four codons of gyrA and parC genes among 39% (7/18) of FQ resistant isolates. 43% (3/7) of FQ resistant isolates showed mutations at two codons 83 (S83F, S83Y) and 87, (D87G, D87Y, D87W) of gyrA gene. Two resistant isolates showed triple mutations i.e. at codons 83 and 87 of gyrA and codon 80 (S80I and S80W) of parC gene, while one resistant isolate revealed mutation at codon 87 of gyrA and 57 (S57T) of parC gene. Moreover, 55% (6/11) intermediately susceptible isolates for FQ also revealed mutation at codon 83 of gyrA gene whereas; one intermediately susceptible isolate (1/6) also revealed additional mutation at codon 57 of parC gene. None of the FQ susceptible NTS isolates showed any mutations in gyrA or parC genes. Occurrence of mutations at only four codons in gyrA and parC genes among FQ resistant isolates may assist in development of rapid molecular method for FQ resistance detection. Presence of mutations among more than fifty percent of intermediately susceptible FQ isolates is alarming and may serve as a predictor for pre-resistant isolates for FQ. Moreover, absence of mutation in about sixty percent of phenotypically FQ resistant NTS isolates shows existence of an alternate resistance mechanism requiring further investigations.

It is challenging to understand mechanisms of drug resistance in Mycobacterium tuberculosis (MTB) due to the large variability in resistance associated genes. Efflux pump genes contribute to drug resistance and thus add to this complexity. Efflux pump gene protein superfamilies have been characterized by genome analysis of drug resistant strains and through in vitro transcriptional studies. However, there is limited information regarding efflux pump genes in extensively drug resistant (XDR) tuberculosis (TB) isolates. Whole genome sequencing (WGS) based analysis of 37 extensively drug resistant (XDR) and five drug sensitive (DS) MTB clinical isolates was performed. Single nucleotide polymorphisms (SNPs) in efflux pump genes Rv0194, Rv1217, Rv1218, drrA, drrB, Rv1258, Rv1634, Rv2688, Rv1273, Rv1819, Rv1458, Rv1877 and Rv1250 were determined in the clinical isolates as compared with the H37Rv reference strain. Allele frequencies of SNPs identified in XDR strains were compared with DS strains. Gene expression of Rv0194, Rv2688, Rv1634, drrA and drrB was determined in XDR -TB isolates (n = 9), DS-TB strains (n = 4) and H37Rv. We identified SNPs in XDR-TB isolates which were either unique or present at very low frequencies in DS strains; Rv0194 G170V; Rv1217 L151R; Rv1258 P369T and G391R; Rv1273 S118G and I175T; Rv1877 I534T; Rv1250 V318X/A and S333A, and Rv2688 P156T. The expression of Rv2688 and drrB was found to be raised in XDR-TB as compared with DS-TB strains. We identified unique SNPs in efflux pump genes which may be associated with increased drug resistance in the isolates. Increased levels of Rv2688 and drrB efflux pump gene expression observed in XDR strains even in the absence of antibiotics suggests that these clinical isolates may be more refractory to treatment. Further studies are required to directly associate these mutations with increased resistance in MTB.

Improved molecular diagnostic methods for detection drug resistance in Mycobacterium tuberculosis (MTB) strains are required. Resistance to first- and second- line anti-tuberculous drugs has been associated with single nucleotide polymorphisms (SNPs) in particular genes. However, these SNPs can vary between MTB lineages therefore local data is required to describe different strain populations. We used whole genome sequencing (WGS) to characterize 37 extensively drug-resistant (XDR) MTB isolates from Pakistan and investigated 40 genes associated with drug resistance. Rifampicin resistance was attributable to SNPs in the rpoB hot-spot region. Isoniazid resistance was most commonly associated with the katG codon 315 (92%) mutation followed by inhA S94A (8%) however, one strain did not have SNPs in katG, inhA or oxyR-ahpC. All strains were pyrazimamide resistant but only 43% had pncA SNPs. Ethambutol resistant strains predominantly had embB codon 306 (62%) mutations, but additional SNPs at embB codons 406, 378 and 328 were also present. Fluoroquinolone resistance was associated with gyrA 91-94 codons in 81% of strains; four strains had only gyrB mutations, while others did not have SNPs in either gyrA or gyrB. Streptomycin resistant strains had mutations in ribosomal RNA genes; rpsL codon 43 (42%); rrs 500 region (16%), and gidB (34%) while six strains did not have mutations in any of these genes. Amikacin/kanamycin/capreomycin resistance was associated with SNPs in rrs at nt1401 (78%) and nt1484 (3%), except in seven (19%) strains. We estimate that if only the common hot-spot region targets of current commercial assays were used, the concordance between phenotypic and genotypic testing for these XDR strains would vary between rifampicin (100%), isoniazid (92%), flouroquinolones (81%), aminoglycoside (78%) and ethambutol (62%); while pncA sequencing would provide genotypic resistance in less than half the isolates. This work highlights the importance of expanded targets for drug resistance detection in MTB isolates.

Objectives The global increase in drug resistance in Mycobacterium tuberculosis (MTB) strains increases the focus on improved molecular diagnostics for MTB. Extensively drug-resistant (XDR) – TB is caused by MTB strains resistant to rifampicin, isoniazid, fluoroquinolone and aminoglycoside antibiotics. Resistance to anti-tuberculous drugs has been associated with single nucleotide polymorphisms (SNPs), in particular MTB genes. However, there is regional variation between MTB lineages and the SNPs associated with resistance. Therefore, there is a need to identify common resistance conferring SNPs so that effective molecular-based diagnostic tests for MTB can be developed. This study investigated used whole genome sequencing (WGS) to characterize 37 XDR MTB isolates from Pakistan and investigated SNPs related to drug resistance. Methods XDR-TB strains were selected. DNA was extracted from MTB strains, and samples underwent WGS with 76-base-paired end fragment sizes using Illumina paired end HiSeq2000 technology. Raw sequence data were mapped uniquely to H37Rv reference genome. The mappings allowed SNPs and small indels to be called using SAMtools/BCFtools. Results This study found that in all XDR strains, rifampicin resistance was attributable to SNPs in the rpo B RDR region. Isoniazid resistance-associated mutations were primarily related to kat G codon 315 followed by inh A S94A. Fluoroquinolone resistance was attributable to gyr A 91–94 codons in most strains, while one did not have SNPs in either gyr A or gyr B. Aminoglycoside resistance was mostly associated with SNPs in rrs , except in 6 strains. Ethambutol resistant strains had emb B codon 306 mutations, but many strains did not have this present. The SNPs were compared with those present in commercial assays such as LiPA Hain MDRTBsl, and the sensitivity of the assays for these strains was evaluated. Conclusions If common drug resistance associated with SNPs evaluated the concordance between phenotypic and genotypic testing, the results would be rifampicin (100%), isoniazid (89%), fluoroquinolones (95%), aminoglycoside (81%) and ethambutol (61%). This work highlights the importance of expanded targets for drug resistance detection in MTB isolates.