Background: Prisons are known to be high-risk environments for the spread of bloodborne and sexually transmitted infections. Prison officers are considered to have an intermittent exposure potential to bloodborne infectious diseases on the job, however there has been no studies on the prevalence of these infections in prison officers in Ghana.

Although the high prevalence of blood-borne viral infections and syphilis in correctional facilities has been well documented globally, such data are sparse from Africa, and there has been no such data from Ghana. This study sought to estimate the prevalence of human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV) and syphilis among prison inmates and officers at prisons in Nsawan and Accra, Ghana. Prisoners and officers in 3 of the 46 prisons in Ghana were surveyed from May 2004 to May 2005. Subjects voluntarily completed a risk-factor questionnaire and provided blood specimens for unlinked anonymous testing for the presence of antibodies to HIV, HCV and Treponema pallidum, the causative agent of syphilis, and the surface antigen of hepatitis B virus (HBsAg). Almost 16 % (3770) of the total of 23 980 prison inmates in Ghana were eligible, and 281 (7?5 %) of those eligible took part, whilst almost 23 % (1120) of the total of 4910 prison officers were eligible, and 82 (7?3 %) of those eligible took part. For the 281 inmates tested, HIV seroprevalence was 19?2 %, 17?4 % had HBsAg, HCV seroprevalence was 19?2 % and reactive syphilis serology was noted in 11 %. For the 82 officers tested, HIV seroprevalence was 8?5 %, 3?7 % had HBsAg, HCV seroprevalence was 23?2 % and reactive syphilis serology was noted in 4?9 %. The data indicate a higher prevalence of HIV and HCV in correctional facilities (both prison inmates and officers) than in the general population in Ghana, suggesting their probable transmission in prisons in Ghana through intravenous drug use, unsafe sexual behaviour and tattooing as pertains to prisons worldwide. INTRODUCTIONThe relation between incarceration and the high transmission of blood-borne viruses, such as human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV) and syphilis, in prisons has been known for several years (Catalan-Soares et al., 2000;Haber et al., 1999;Heimberger et al., 1993;Mutter et al., 1994;Stark et al., 1997), and injecting drug use is the most commonly reported risk factor (Alizadeh et al., 2005;Massad et al., 1999; Taylor et al., 2000; Wield et al., 2000). The other risk factors identified for the higher prevalence of these infections in prisoners are previous imprisonment, tattooing and high-risk sexual behaviours (Haber et al., 1999;Massad et al., 1999;Skoretz et al., 2004;Veeken, 2000). There is growing evidence that HIV, HBV and HCV infections have actually been transmitted to individuals while they were in prison (Haber et al., 1999; Hutchinson et al., 1998;Mutter et al., 1994;Skoretz et al., 2004;Stark et al., 1997;Taylor et al., 1995 Taylor et al., , 2000, although there is also evidence that some had the infection before they were sent to prison. Data on the prevalence of HIV, HBV, HCV and syphilis in prisons are scanty in Africa, and no such information exists on prisoners in Ghana. Outside the prison setting in Ghana, the prevalence of HIV infection is between 1?5 and 3?8 % among blood donors (Ampofo et...

A national multicentre cross-sectional study was undertaken on the correlates of hepatitis C virus (HCV) infection in a sample of inmates from eight Ghanaian prisons. A total of 1366 inmates from eight of the ten regional central prisons in Ghana were enrolled between May 2004 and December 2005. Subjects voluntarily completed a risk-factor questionnaire and provided blood specimens for unlinked anonymous testing for the presence of antibodies to HCV. These data were analysed using both univariate and multivariate techniques. The median age of participants was 36.5 years (range 16-84 years). Of the 1366 inmates tested, HCV seroprevalence was 18.7 %. On multivariate analysis, the independent determinants of HCV infection were being incarcerated for longer than the median time served of 36 months [odds ratio (OR) 5.8; 95 % confidence interval (95 % CI) 5.0-6.9], history of intravenous drug use (OR 4.5;) and homosexuality (OR 3.1;. Consistent with similar studies worldwide, the prevalence of HCV in prison inmates was higher than the general population in Ghana, suggesting probable transmission in prisons in Ghana through intravenous drug use and unsafe sexual behaviour.

1 A study was undertaken in the anaesthetized rabbit to classify the a-adrenoceptor subtypes responsible for increasing renal tubular sodium reabsorption and renin secretion. Intrarenal administration of noradrenaline, at doses which did not change renal blood flow or glomerular filtration rate, significantly decreased urine flow, absolute and fractional sodium excretion by between 26% and 29%. These renal responses to noradrenaline were abolished by the selective a,-adrenoceptor antagonist, prazosin, but not by the selective M2-adrenoceptor antagonist, idazoxan. 2 Noradrenaline, given intrarenally, increased renin secretion between two and three fold and this response was not modified by either prazosin or idazoxan. 3 Intrarenal administration of the selective a-adrenoceptor agonists, phenylephrine and methoxamine, at dose rates which did not change renal haemodynamics, significantly reduced urine flow, absolute and fractional sodium excretion by 15% to 33%, but at doses which reduced blood flow and filtration rate, by between 11% and 26%, urine flow, absolute and fractional sodium excretion decreased between 42% and 49%. 4 Infusion of guanabenz (selective M2-adrenoceptor agonist), at doses with no renal haemodynamic action, increased urine flow, absolute and fractional sodium excretion by 11 % to 15%, while at doses which decreased blood flow by 7%, these other variables did not change. 5 Administration of UK 14304 (selective o2-adrenoceptor agonist) reduced blood flow and filtration rate by 3% and 9% respectively but had no other measurable action. At higher doses, which decreased blood flow by 14% and filtration rate by 24%, urine flow, absolute and fractional sodium excretion fell by between 27% and 50%. 6 Renin secretion was significantly increased by the high doses of phenylephrine and UK 14304 but not by the low doses of these drugs. 7 These studies show that adrenergic stimulation of renal tubular sodium reabsorption involves the activation of al-but not M2-adrenoceptors. Further, adrenergic activation of the juxtaglomerular cells to release renin does not appear to involve either al-or M2-adrenoceptors.

SUMMARY1. A study was undertaken in pentobarbitone anaesthetized rabbits, undergoing a saline diuresis, to determine the subtype of a-adrenoceptor mediating renal tubular sodium reabsorption.2. Stimulation of the renal nerves at low rates, to cause an 11 % fall in renal blood flow, did not change glomerular filtration rate but significantly reduced urine flow rate, and absolute and fractional sodium excretions by approximately 40 %. These responses were reproducible in different groups of animals and with time.3. Renal nerve stimulation during an intra-renal arterial infusion of prazosin, to block a1-adrenoceptors, had no effect on the renal haemodynamic response but completely abolished the reductions in urine flow rate, and absolute and fractional sodium excretion.4. During intra-renal. arterial infusion of yohimbine, to block renal a2-adrenoceptors, stimulation of the renal nerves to cause similar renal haemodynamic changes resulted in significantly larger reductions in urine flow rate, and absolute and fractional sodium excretion of about 52-58 %.5. These results indicate that in the rabbit a1-adrenoceptors are present on the renal tubules, which mediate the increase in sodium reabsorption caused by renal nerve stimulation. They further suggest the presence of presynaptic a2-adrenoceptors on those nerves innervating the renal tubules.

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An attempt has been made to classify the subtypes of alpha-adrenoreceptors mediating renal vasoconstriction in vivo using renal nerve stimulation and alpha-adrenoreceptor agonists and antagonists of varying selectivity in anesthetised rabbits. In the first series of experiments prazosin more potently inhibited the phenylephrine than the nerve induced renal vasoconstriction while phentolamine inhibited the response to phenylephrine and nerve stimulation nearly equally. In the second series of experiments low to moderate doses of yohimbine potently inhibited the renal vasoconstriction of clonidine, was less potent on that induced by noradrenaline and did not significantly affect that of phenylephrine. Prazosin was a potent antagonist of phenylephrine induced vasoconstriction but was less potent on nerve stimulation and noradrenaline, and was without effect on clonidine. In the third series of experiments, prazosin partially inhibited the renal vasoconstriction produced by all frequencies of nerve stimulation and that produced by high doses of noradrenaline. The prazosin resistant component of nerve stimulation and exogenous noradrenaline was significantly reduced by the addition of yohimbine. These results have been taken to suggest the presence of both alpha 1- and alpha 2-adrenoreceptors in the renal vasculature of the rabbit which mediate the renal vasoconstriction of exogenous and endogenous noradrenaline. They further show that in the rabbit the alpha 2-adrenoreceptors mediate a much greater proportion of the total renal vasoconstriction compared with the dog, cat or rat in which the alpha 1-adrenoreceptor population appears to be the predominant receptor.