Prevalence of Attention-Deficit/Hyperactivity Disorder Among Primary School Children in Oforikrom, Ghana Based on the Disruptive Behavior Disorders Rating Scale.

OBJECTIVE: To determine the prevalence of attention-deficit/hyperactivity disorder (ADHD) among primary school children in Oforikrom, Kumasi, Ghana. METHODS: 10 of 35 primary schools in Oforikrom were readily available. Of 2000 children aged 5 to 13 years selected, 1540 (77%) of their parents/guardians consented to participate. Their parents/guardians and six teachers from each school were asked to complete the Disruptive Behavior Disorders Rating Scale to screen children for the presence of ADHD, oppositional defiant disorder, or conduct disorder. Children who displayed symptoms (pretty much or very much) in most related items as determined by parents and/or teachers were considered positive cases. RESULTS: The mean age of 1540 pupils was 9 ± 2.16 years. Most (31%) were primary 4 pupils. 5% of pupils displayed ADHD symptoms (attention deficit disorder subtype in 36%, hyperactivity disorder subtype in 27%, and combined subtype in 37%). Of them, 51% were male. Most (19%) of those who displayed the symptoms were in primary 5. CONCLUSION: The prevalence of ADHD among primary school children in Oforikrom was 5%. 51% of those with ADHD symptoms were male. Most (19%) of those with ADHD symptoms were in primary 5.

T594M mutation of the beta-subunit of the epithelial sodium channel in Ghanaian populations from Kumasi and London and a possible association with hypertension.

We have tested 186 individuals from Ghana, 95 indigenous and 91 who have settled in the United Kingdom, for the presence of the T594M mutation in the beta-subunit of the epithelial sodium channel, which is associated with hypertension in black populations. The group living in Ghana had a mean age of 27 years and were normotensive, but had an increased frequency of the T allele compared to the London-based population. If this is reflected in larger studies, and the link with hypertension is maintained in the Ghanaian population, this mutation could be a significant cause of hypertension in Ghana.

Resistance to Mycoplasma pulmonis mediated by activated natural killer cells.

Infection of C57BL/6J mice with Mycoplasma pulmonis (MP) enhanced NK cell function 3-7 days later, as detected by in vitro and in vivo assays. Moreover, spleen and lung cells of acutely infected C57BL/6J mice inhibited MP growth in vitro. The effectors were eliminated by treatment with anti-NK antibody in vivo and anti-asialo GM1 serum or anti-3A4 antibody plus complement in vitro. Clearance of viable and radiolabeled MP from the lungs was also enhanced in acutely infected mice. Acutely infected mice with severe combined immunodeficiency (SCID) eliminated viable MP faster than did uninfected mice. Antibodies to interferon-gamma (IFN-gamma) impaired clearance of MP from the lungs of SCID mice and decreased their survival times. Activated NK cells can function in resistance to early stages of infection with MP. NK cells directly inhibit MP with secrete IFN-gamma, which may activate macrophages or inhibit the growth of MP or both.

Mycoplasma pulmonis depresses humoral and cell-mediated responses in mice.

Humoral and cell-mediated immune responses to sheep red blood cells (SRBC) were studied in mice infected experimentally with Mycoplasma pulmonis. The hemagglutinating (HA) antibody against SRBC was evaluated at 0, 3, 5, 7, 14, 21 and 28 days postinfection (PI). Antibody tiers during all days PI were depressed significantly (p less than 0.05) in infected mice as compared to noninfected controls. The HA antibody, which is of the IgM class, peaks at day 5 PI. There is no shift in the kinetics of the humoral response in M. pulmonis infected mice. Cellular immune responses were evaluated by a delayed-type hypersensitivity (DTH) reaction and the lymphocyte transformation technique. Mice were sensitized at 0,3,5,7,14, 21 and 28 days PI with SRBC and challenged by footpad injection of SRBC 7 days later. The DTH reaction measured at 24 hours after challenge was depressed significantly (p less than 0.05) in all infected animals. After a transient enhancement on day 3 PI, the DTH responses remained depressed through day 28 PI. The lymphocyte transformation test showed a significantly (p less than 0.05) depressed response except on days 5 and 7 PI. These results indicate that M. pulmonis infection in mice suppresses the humoral antibody and cell-mediated immune responses.