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An epidemiological study of syphilis and predictors of treatment failure in University Malaya Medical Centre

Mohamed AK, Raja IA, Rukumani DV

Med J Malaysia, 2020 05;75(3):199-203.
PMID: 32467532

INTRODUCTION: There are limited studies on the epidemiology of syphilis in Malaysia. In this study we describe the clinical features and treatment outcomes of patients with syphilis attending a tertiary referral university hospital.
METHODS: We retrospectively reviewed the case records of patients with positive serology findings for syphilis in University Malaya Medical Center (UMMC) from January 2010 to December 2015. Serological positivity was defined as having a positive rapid plasma reagin (RPR) or Venereal Disease Research Laboratory (VDRL) with a confirmatory positive Treponema pallidum particle agglutination assay (TPPA). Treatment outcomes were divided into two, success or failure. Demographic and clinical characteristics associated with predictors of treatment failure were assessed using statistical package for the social science (SPSS). This study also included a neurosyphilis descriptive sub-study.
RESULTS: There were 637 patients identified with positive syphilis serology, but 258 patients were excluded as they did not meet the inclusion criteria. 379 patients were then taken for the demographic study; 14 patients (3.7%) were treated for neurosyphilis; 170 patients with complete data were included. In all 42/170 (24.7%) failed treatment, 12/170 (7.1%) had reinfection and 116/170 (68.2%) had treatment success. A final number of 158 patients were then taken and analyzed for predictors of treatment failure after excluding the 12 reinfection patients. Only low baseline RPR (<1:16) was found to be significant on multivariate logistic regression analysis (p value: 0.007, 95% CI: 1.42, 9.21).
CONCLUSION: Most of the patients were HIV positive and from the MSM (Men who have sex with Men) population. Low baseline RPR titre is a predictor of treatment failure.
Fulltext Identification of Mycobacterium species following growth detection with the BACTEC MGIT 960 system by DNA line probe assay

Ng KP, Rukumani DV, Chong J, Kaur H

Int J Mycobacteriol, 2014 Jun;3(2):82-7.
PMID: 26786328 DOI: 10.1016/j.ijmyco.2014.03.005

The tuberculosis and infections caused by nontuberculous mycobacterial (NTM) species are increasing in patients presented with respiratory illness, and it is crucial to document the epidemiology of these infections.
Fulltext Short report: Predictors of severe disease in melioidosis patients in Kuala Lumpur, Malaysia

Mohd Roslani AD, Tay ST, Puthucheary SD, Rukumani DV, Sam IC

Am J Trop Med Hyg, 2014 Dec;91(6):1176-8.
PMID: 25246695 DOI: 10.4269/ajtmh.14-0354

The predictors of severe disease or death were determined for 85 melioidosis patients in Kuala Lumpur, Malaysia. Most of the patients were male, > 40 years old, and diabetic. Severe disease or death occurred in 28 (32.9%) cases. Lower lymphocyte counts and positive blood cultures were significant independent predictors of severe disease, but age, presentations with pneumonia, inappropriate empirical antibiotics, or flagellin types of the infecting isolates were not. Knowledge of local predictors of severe disease is useful for clinical management.
Fulltext Recent advances targeting innate immunity-mediated therapies against HIV-1 infection

Shankar EM, Velu V, Vignesh R, Vijayaraghavalu S, Rukumani DV, Sabet NS

Microbiol. Immunol., 2012 Aug;56(8):497-505.
PMID: 22900503 DOI: 10.1111/j.1348-0421.2012.00485.x

Early defence mechanisms of innate immunity respond rapidly to infection against HIV-1 in the genital mucosa. Additionally, innate immunity optimises effective adaptive immune responses against persistent HIV infection. Recent research has highlighted the intrinsic roles of apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3G, tripartite motif-containing protein 5, tetherin, sterile α-motif and histidine/aspartic acid domain-containing protein 1 in restricting HIV-1 replication. Likewise, certain endogenously secreted antimicrobial peptides, namely α/β/θ-defensins, lactoferrins, secretory leukocyte protease inhibitor, trappin-2/elafin and macrophage inflammatory protein-3α are reportedly protective. Whilst certain factors directly inhibit HIV, others can be permissive. Interferon-λ3 exerts an anti-HIV function by activating Janus kinase-signal transducer and activator of transcription-mediated innate responses. Morphine has been found to impair intracellular innate immunity, contributing to HIV establishment in macrophages. Interestingly, protegrin-1 could be used therapeutically to inhibit early HIV-1 establishment. Moreover, chloroquine inhibits plasmacytoid dendritic cell activation and improves effective T-cell responses. This minireview summarizes the recently identified targets for innate immunity-mediated therapies and outlines the challenges that lie ahead in improving treatment of HIV infection.
Fulltext HIV-Mycobacterium tuberculosis co-infection: a 'danger-couple model' of disease pathogenesis

Shankar EM, Vignesh R, Ellegård R, Barathan M, Chong YK, Bador MK, et al.

Pathog Dis, 2014 Mar;70(2):110-8.
PMID: 24214523 DOI: 10.1111/2049-632X.12108

Tuberculosis (TB) and human immunodeficiency virus (HIV) infection interfere and impact the pathogenesis phenomena of each other. Owing to atypical clinical presentations and diagnostic complications, HIV/TB co-infection continues to be a menace for healthcare providers. Although the increased access to highly active antiretroviral therapy (HAART) has led to a reduction in HIV-associated opportunistic infections and mortality, the concurrent management of HIV/TB co-infection remains a challenge owing to adverse effects, complex drug interactions, overlapping toxicities and tuberculosis -associated immune reconstitution inflammatory syndrome. Several hypotheses have been put forward for the exacerbation of tuberculosis by HIV and vice versa supported by immunological studies. Discussion on the mechanisms produced by infectious cofactors with impact on disease pathology could shed light on how to design potential interventions that could decelerate disease progression. With no vaccine for HIV and lack of an effective vaccine for tuberculosis, it is essential to design strategies against HIV-TB co-infection.
Fulltext Attrition of TCR Vα7.2+ CD161++ MAIT cells in HIV-tuberculosis co-infection is associated with elevated levels of PD-1 expression

Saeidi A, Tien Tien VL, Al-Batran R, Al-Darraji HA, Tan HY, Yong YK, et al.

PLoS One, 2015;10(4):e0124659.
PMID: 25894562 DOI: 10.1371/journal.pone.0124659

Mucosal-associated invariant T (MAIT) cells are evolutionarily conserved antimicrobial MR1-restricted CD8(+) T cells co-expressing the semi-invariant TCR Vα7.2, and are numerous in the blood and mucosal tissues of humans. MAIT cells appear to undergo exhaustion in chronic viral infections. However, their role in human immunodeficiency virus type 1 (HIV-1) mono-infection and HIV/tuberculosis (TB) co-infection have seldom been elaborately investigated. We conducted a cross-sectional study to investigate the frequencies and phenotypes of CD161(++)CD8(+) T cells among anti-retroviral therapy (ART)/anti-TB therapy (ATT) treatment-naïve HIV/TB co-infected, ART/TB treated HIV/TB co-infected, ART naïve HIV-infected, ART-treated HIV-infected patients, and HIV negative healthy controls (HCs) by flow cytometry. Our data revealed that the frequency of MAIT cells was severely depleted in HIV mono- and HIV/TB co-infections. Further, PD-1 expression on MAIT cells was significantly increased in HIV mono- and HIV-TB co-infected patients. The frequency of MAIT cells did not show any significant increase despite the initiation of ART and/or ATT. Majority of the MAIT cells in HCs showed a significant increase in CCR6 expression as compared to HIV/TB co-infections. No marked difference was seen with expressions of chemokine co-receptor CCR5 and CD103 among the study groups. Decrease of CCR6 expression appears to explain why HIV-infected patients display weakened mucosal immune responses.