C.J. Uneke, O. Ogbu, P.U. Inyama & G.I. Anyanwu

Directory of Open Access Journals

J Vect Borne Dis 42, December 2005, pp 151–154Malaria infection in HIV-seropositive and HIV-seronegativeindividuals in Jos-NigeriaC.J. Unekea, O. Ogbua, P.U. Inyamab & G.I. AnyanwubaDepartment of Medical Microbiology/Parasitology, Faculty of Clinical Medicine, College of Health Sciences (EBSUTH),Ebonyi State University, Abakaliki, Nigeria; bApplied Parasitology Unit, Department of Zoology, University of Jos, NigeriaKey words Acquired  immunodeficiency syndrome – co-infection –  Jos-Nigeria – malaria – P. falciparumShort NotesInfections by malaria parasite and human immunodefi-ciency virus (HIV) represent major public healthproblems in many parts of the world. Both infectionskill millions of people each year and both infectionsare scourges of developing nations in Africa, India,southeast Asia and South America1. In recent years, ithas been hypothesised that a possible deleterious in-teraction between both infections exists. The pre-sented hypothesis suggested that chronic latent malariainfection prepares the niche where otherwise feebleHIV infection can thrive and cause acquired immuno-deficiency syndrome (AIDS)2. However, an earliercritical review from numerous available reports on thissubject showed that there were hardly evidences tosupport this hypothesis3. Depending on the perspec-tive it is viewed, malaria has either a lot or very little incommon with HIV. With shared geography and de-mographics especially in sub-Saharan Africa, co-in-fection is common, yet surprisingly few obvious clini-cal associations between HIV and malaria are re-ported in this region1.Till date there is a dearth of information on the preva-lence of malaria and HIV co-infection in Nigeria. Thelife expectancy in Nigeria was estimated to havedropped from 53 years in 1990 to 51 years in 2002,largely due to the AIDS epidemic. The epidemic inNigeria has extended beyond the commonly classifiedhigh-risk groups and is now common in the generalpopulation with the adult prevalence rate at 5.8% in20014. Our objective in this study was to determinethe prevalence of malaria infection in HIV-seronega-tive individuals as part of the preliminary investigationleading to a more advanced research on malaria andHIV co-infection in Nigeria.The study was conducted from April 2002 throughNovember 2003 in Jos-Plateau located in an areacovering about 9,400 km2 of the crystalline complexin Central Nigeria. The area has two seasons, the dryseason (November–March) and the rainy season(April–October). Malaria transmission is usually hightowards the end of the rainy season. The Central Ni-geria is known to record the highest prevalence ofHIV infection in the country4.Patients who visited Jos University Teaching Hospital(JUTH) and the Plateau Specialist Hospital (PSH),who presented themselves for retroviral screening,were enrolled in the study. Informed consent was ob-tained from each patient with the assistance of theirphysicians. Thereafter, 5 ml of blood sample was ob-J  VECT  BORNE  DIS  42,  DECEMBER  2005 152tained by vene puncture from each of these patientsfor HIV and malaria parasite screening to identify theappropriate study group. The HIV serostatus of 490of them (age range 17–60 yr) was confirmed byimmunoblot analysis (Bio-Rad, Novapath DiagnosticGroup, U.S.A.) at the International Centre for Scien-tific Culture (ICSC) Retroviral Laboratory, PSH, Jos.This was after an initial HIV screening using theVironostica® HIV-1 microelisa system (OrganonTeknika, Durham, U.S.A.) at the AIDS/LeishmaniasisResearch Laboratory, University of Jos. These 490individuals constituted the HIV-seropositive popula-tion. Thick and thin blood films were made 2–3 h ofcollection, stained with Giemsa according to standardprotocol for the identification of malaria parasite5.The HIV-seronegative population comprised of 578individuals (10–59 yr age) who were HIV-seronega-tive by the Vironostica® HIV-1 microelisa system andwere participants of the community targeted voluntarycounseling test (VCT) for HIV-infection conducted invarious areas of Jos-Plateau. These individuals willing-ly offered to be screened for HIV during these pro-grammes. All the study participants were informedverbally and their consent duly obtained. Thick andthin blood films for malaria parasite diagnosis wereperformed as described earlier5, after the HIV-se-rostatus was established for each individual. Differ-ences between proportions were evaluated by the chi-square test. Statistical significance was achieved if p <0.05.Of the 490 HIV-seropositive individuals studied 103(21%, 95% CI 17.41–24.63) had malaria infection,while 67 (11.6%, 95% CI 8.98–14.2) of the 578HIV-seronegative individuals also had malaria infec-tion. Plasmodium falciparum was identified in all thecases.  Mixed infections of P. falciparum and  P. ma-lariae occurred in 2.6% of all the infected cases.Amongst the HIV-seropositive individuals, the maleswere significantly more infected than the females(27.4%, 95% CI 21.2–33.52 vs 16.6%, 95% CI12.32–20.9);  (c2 = 8.198, p < 0.05, df =1 ) (Table 1)The prevalence of malaria infection increased with ageamongst the HIV-seropositive individuals with thehighest rate of 32% (95% CI 13.71–50.29) at the 51–60 yr age group, although there exist no significant dif-ference in the trend (c2 =5.697, p < 0.05, df = 4). Theprevalence of malaria infection was slightly higheramongst the males (12.7%, 95% CI 8.76–16.58) thanthe females (10.4%, 95% CI 6.84 –14.02) in the HIV-seronegative population (Table 1). There was no signifi-cant difference statistically (c2 = 0.693, p < 0.05, df  =1). Amongst the HIV-seronegative individuals, the high-est prevalence of malaria infection of 14.8% (95% CI8.68–21) was observed at the 31–40 yr age category(Table 1). There was also no sigificant difference statis-tically (c2=4.987, p < 0.05, df = 4).Table 1. Malaria infection amongst HIV-seropositive andseronegative individuals in Jos-NigeriaParameter No. No. with 95% examined malaria confidenceinfection intervalHIV-seropositiveSexMale 201 55 (27.4) 21.2–33.52Female 289 48 (16.6) 12.32–20.9Total 490 103 (21) 17.41–24.63Age (yr)< 20 15 2 (13.3) 3.87–30.5321–30 184 27 (14.7) 9.56–19.7831–40 188 44 (23.4) 17.35–29.4541–50 78 21 (26.9) 17.08–36.7651–60 25  8 (32) 13.71–50.29Total 490 103 (21) 17.41–24.63HIV-seronegativeSexMale 300 38 (12.7) 8.76–16.58Female 278 29 (10.4) 6.84–14.02Total 578 67 (11.6) 8.98–14.2Age (yr)< 20 215 20 (9.3) 5.42–13.1821–30 195 26 (13.3) 8.56–18.131–40 128 19 (14.8) 8.68–2141–50 35 2 (5.7) 1.98–13.451–60 5  0 (0) –Total 578 67 (11.6) 8.98–14.2Figures in parentheses are percentages.UNEKE et al : MALARIA IN HIV-SEROPOSITIVE/-SERONEGATIVE INDIVIDUALS 153This investigation demonstrated that HIV-seropositiveindividuals had a higher prevalence of malaria infectionthan the HIV-seronegative individuals in the studyarea. Jos-Plateau is considered as an area of stable P.falciparum malaria transmission although consider-able urbanisation processes are going on. Neverthe-less, the inhabitants have developed a high degree ofimmunity to the parasite through repeated exposures,and thus are not generally susceptible to the effects ofsevere clinical malaria. This may have accounted forthe lower prevalence of malaria infection amongst theHIV-seronegative population.The humoral and cell-mediated immunity to malariaparasite are reported to be developed in such an areaof stable transmission6. This immunity can be alteredin HIV-infected persons and could influence the fre-quency and course of malaria infection7, 8. This mayexplain the higher prevalence of malaria infection in theHIV-seropositive population. This submission may notbe conclusive as HIV-disease progression co-factorssuch as : presence of opportunistic infections, nutri-tional status, age, viral load and genotype9, could alsohave influenced the malaria infection in the HIV-in-fected population. Our inability to record the parasitedensity is a major drawback to this research. Futurestudies integrating the parasite density are advocated.Present result showed that males were more infectedwith the malaria parasite than the females in both ofthe study population. This was not unexpected be-cause analysis of sociobehavioural factors revealedthat males expose themselves more to the risk factorsof malaria acquisition. It is a common habit of males inJos-Plateau to stay long hours into the night outsidethe houses or sleep outdoors without appropriatecoverings. There is also high level of indifference tothe use of insecticide-treated bednets by the males.Malaria infection prevalence increased with ageamongst the HIV-seropositive individuals, although asomewhat similar pattern was observed amongst theHIV-seronegative population but it was less obviousin the latter. A review of a number of studies in differ-ent transmission groups confirmed that age is a co-factor for disease progression9. The immunity to ma-laria and HIV-1 infection has been shown to be agedependent10. It is possible that the older HIV-infectedindividuals may be more likely to develop infectionsincluding malaria than the younger HIV-infectedindividuals.In conclusion it is imperative to state that people whohave grown up in malaria endemic regions especiallyin the sub-Saharan Africa often retain partial immunityto malaria, and there is no solid evidence that this im-munity is lost, as HIV disease progresses1. However,it is suggested that the roots of the HIV outbreak andAIDS pandemic lay in the urbanisation processes inmany developing countries of the sub-Saharan Africaincluding Nigeria, which have resulted in the eradica-tion of the Anopheles vector from previously endemicareas, with consequent loss of natural immunitythereby enhancing vulnerability to opportunistic infec-tions, HIV among them2. Our findings have providedadditional baseline information on the burden of ma-laria and HIV coinfection in Nigeria. Further researchis advocated on this subject especially in the sub-Sa-haran Africa, the region with the highest prevalence ofboth infections.References1. Huff  B. HIV and malaria: two intertwining epidemics. AmFound Aids Res 2000; 6: 1–5.2. Yaffe  I. AIDS possibly caused by HIV and latent malariacoinfection. Hypothesis  2001; 57: 419–22.3. Chandramohan D, Greenwood BM. Is there an interactionbetween human  immunodeficiency virus and Plasmodiumfalciparum? Int  J Epidemiol 1998;  27: 296–301.4. National HIV/AIDS and reproductive health survey.Abuja, Nigeria: Federal Ministry of Health  2003;  p. 1–4.5. Manual of basic techniques for a health laboratory.Geneva : WHO 2003; p. 172–82.6. Dean JA, Cohen S. Immunology of malaria. Ann RevMicrobiol 1983; 37: 161–7.7. Stekette RW, Wirima JJ, Bloland PB, Chilima, B, MerminJH, Chitsulo  L, Breman  JG. Impairment of a pregnantwoman’s acquired ability to limit   Plasmodium falciparumJ  VECT  BORNE  DIS  42,  DECEMBER  2005 154by infection with human immunodeficiency virus type-1.Am  J  Trop  Med  Hyg  1996; 55: 42–9.8. Chaisavaneeyakorn S, Moore JM, Otieno J, Chaiyaroj SC,Perkins DJ, Shi YP,  Nahlen  BL, Lal AA, Udhayakumar V.Immunity to placenta malaria III. Impairment of interleukin(IL)-12, not IL-18, and interferon-inducible protein-10responses in the placental intrevillious blood of humanimmunodeficiency virus/malaria-co-infected-women. JInfect Dis 2002; 185: 127–31.9. Osmond  H. HIV disease progression from infection toCDC defined AIDS.  In: Cohen PT, Sande MA, VolberdingPA editors. The AIDS knowledge base.  New York : Little,Brown & Company 1994; p. 1.7:1–1.7:19.10. Wabwire-Mangen  F, Shiff CJ, Vlahov D, Kline R, Serwad-da D, Sewankambo NK, Mugerwa RD, Quinn TC. Immuno-logical effects of HIV-1 infection on the humoral responseto malaria in an African population.  Am J Trop Med Hyg1989; 41: 504–11.Corresponding author: C.J. Uneke, Department of Medical Microbiology/Parasitology, Faculty of Clinical Medicine, Collegeof Health Sciences (EBSUTH), Ebonyi State University, P.M.B. 053, Abakaliki, Nigeriae-mail: unekecj@yahoo.com

Malaria infection in HIV-seropositive and HIV-seronegative individuals in Jos-Nigeria

Abstract

Similar works

Full text

Available Versions

Directory of Open Access Journals