Hepatitis B virus (HBV) is endemic in Africa, where it may occur as an HIV coinfection. Data remain limited on HIV-HBV epidemiology in Africa, particularly in children. Using programmatic data from pediatric HIV clinics in Lusaka, Zambia during 2011-2014, we analyzed the prevalence of chronic HBV coinfection (defined as a single positive hepatitis B surface antigen [HBsAg] test) and its impact on immune recovery and liver enzyme elevation (LEE) during the first year of antiretroviral therapy. Among 411 children and adolescents, 10.4% (95% confidence interval, 7.6-14.1) had HIV-HBV. Coinfected patients were more likely to have World Health Organization stage 3/4, LEE and CD4 <14% at care entry (all p < 0.05). During treatment, CD4 increases and LEE incidence were similar by HBsAg status. HBsAg positivity decreased (11.8% vs. 6.6%; p = 0.24) following HBV vaccine introduction. These findings support screening pediatric HIV patients in Africa for HBV coinfection. Dedicated cohorts are needed to assess long-term outcomes of coinfection.

Congenital Pulmonary Airway Malformation (CPAM) is a rare abnormality of pulmonary airway malformation and may remain undiagnosed until it is discovered as an incidental finding later in life. Reported here are two cases of CPAM, a seven-month-old infant and a two-year-old toddler. A seven-month-old ex-premature male infant presented with recurrent pneumonia and failure to thrive. He had an unresolving consolidation on chest radiograph and was eventually treated as pulmonary tuberculosis with no response. Computerised tomography scan (CT-scan) chest revealed bilateral CPAM of lungs. A 2-year-old female toddler presented to the University Teaching Hospital, Department of Paediatrics & Child Health, as a referral from a second level hospital with a long-standing history of recurrent symptoms and signs of pneumonia with failure to thrive. She was commenced on antituberculous treatment with no improvement. A CT-scan of the chest revealed bilateral CPAM of lungs. These two cases highlight clinical, diagnostic and treatment challenges in children with CPAM in a resource limited setting like Zambia.

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Abstract Hunter syndrome is one of the Mucopolysaccharidosis (MPS), type II. It is a rare genetic disorder due to a deficiency in the enzyme Iduronate 2-sulphatase. This deficiency leads to the accumulation of glycosaminoglycans (GAGs) dermatan sulphate and heparan sulphate. The GAGs accumulate both intracellularly and extracellularly, leading to abnormalities in different organ systems in the body. The definitive diagnosis of Hunter syndrome requires biochemical methods which can be a challenge in resource-limited settings, Zambia included.  Presented here is a case of Hunter Syndrome in a 12-year-old male child and highlight clinical acumen as the main ingredient in making the diagnosis and distinguishing different types.