ABSTRACT
@#Introduction: S. haemolyticus is known to be commensals residing on human skin. However, their ability to develop as pathogens among the healthy community has becoming increasingly vital. Methods: In this study, a total of 49 non-duplicated samples of S. haemolyticus was isolated from the skin of healthy adults and confirmed via sodA gene sequencing method. Cefoxitin (30μg) disc diffusion test was performed to determine methicillin resistance among the S. haemolyticus isolates. The isolates were then subjected to mecA amplification and Staphylococcus Cassette Chromosome (SCCmec) typing of I, II, III, IV and V. Results: Interestingly, 59.2% of the S. haemolyticus commensal isolates were found to be methicillin-resistant (MRSH) while the remaining 40.8% was methicillin-sensitive (MSSH). Amplification of mecA gene showed that 43 isolates (87.8%) were positive while only six isolates were negative for the gene. A majority of the positive mecA isolates (90.7%) were discovered to harbour SCCmec Type II while the remaining 44.2% were Type V followed by 23.3% of Type I and 18.6% of Type IV. Only one of the isolates was found to be SCCmec Type III while another isolate, T187 was non-typeable. Conclusion: The data indicates the acquisition of SCCmec typing circulated among the commensal strains which could be a potential route of pathogenicity among the isolates.
ABSTRACT
Background: Hand, foot and mouth disease (HFMD) is caused by enteroviruses such as Coxsackie virus A16 (CVA16) and Enterovirus 71 (EV71). The diagnostic hallmarks are oral ulcers and maculo-papular or vesicular rash on the hands and feet. Severe form of this disease can lead to death due to neurological and cardiopulmonary complications. This case report aims to describe a fatal case of HFMD with minimal oral and skin manifestations. Case report: A four-year-old girl was brought to a hospital after suddenly becoming unresponsive at home. She had a history of fever and lethargy for three days prior to her demise. The patient, and five other children in her neighbourhood had been diagnosed to have HFMD at a local health clinic; the other children had recovered without complications. Results: Autopsy revealed a few punctate, sub-epidermal vesicles measuring 1 to 2 mm on the palm of her right hand and sole of the right foot, visible only with a magnifying glass. Internal examination revealed prominent nodularity at the oro- and hypopharynxes. The lungs were markedly congested and oedematous. Histopathology of the lung showed marked oedema and haemorrhage with mild pneumonic changes. Oedema with increase in macroglia and astrocytic proliferation were seen in the cerebral tissue, but no lymphocytic infiltration was evident. Enterovirus EV71 was detected by polymerase chain reaction in samples from the lung, cerebrospinal fluid and serum. The cause of death was given as HFMD complicated by pneumonia. Conclusion: Fatal HFMD may have minimal signs. A complete history, careful physical examination and relevant investigations lead to a diagnosis at post mortem examination. Awareness of the subtle signs and rapid deterioration associated with a fatal case of HFMD is a challenge to clinicians who encounter these cases.
ABSTRACT
Background: HIV-infected patients pose a high risk of contracting skin and soft tissue infections caused by Staphylococcus aureus. Those who are colonized with methicillin-resistant S. aureus (MRSA) that carry Panton-Valentine leukocidin (PVL) are predisposed to severe infections that could lead to necrotic skin infections. However the association of S. aureus specifically methicillin sensitive S. aureus carrying PVL gene in HIV patients has not been widely reported. Here, we study the prevalence and the molecular epidemiology of PVL-producing S. aureus in HIV-infected patients. Methods: Swabs from four body sites of 129 HIV-infected patients were cultured for S. aureus and identified by standard microbiological procedures. The isolates were subjected to antimicrobial susceptibility testing by disk diffusion against penicillin, erythromycin, clindamycin, and cotrimoxazole. PCR was used to detect the PVL gene and genetic relationship between the isolates was determined by using pulse field gel electrophoresis. Results: A total of 51 isolates of S. aureus were obtained from 40 (31%) of the patients. The majority (43.1%) of the isolates were obtained from the anterior nares. Thirteen (25.5%) of all the isolates were resistant to more than one category of antibiotics, with one isolate identified as MRSA. Thirty-eight (74.5%) isolates (including the MRSA isolate) carried PVL gene where the majority (44.7%) of these isolates were from the anterior nares. A dendogram revealed that the isolates were genetically diverse with 37 distinct pulsotypes clustered in 11 groups. Conclusion: S. aureus obtained from multiple sites of the HIV patients were genetically diverse without any clonality observed.