MALARIA TREATMENT OUTCOME AMONG UNDER-FIVE CHILDREN ATTENDING PRIMARY HEALTH CARE CENTRES IN UMUAHIA NORTH LOCAL GOVERNMENT AREA OF ABIA STATE NIGERIA. BY RY AKHIMIEN OBEIMEN MOSES RA MATRICULATION NUMBER 148635 LI B N IN PARTIAL FULFILLMENT OF THE REQUIREMENT FAOR THE DEGREE OF MASTERS OF PUBLIC HEALTH (FIELD EPIDEMIOLOGY PRACTICE) DEPARTMENT OF EPIDEMIOLOGY, MEDICAL STATISTICS ANDD ENVIRONMENTAL HEALTH, FACULTY OF PUBLIAC HEALTH UNIVERSIT F YI OBF IBADAN O ITY RS DEPARTMENVT OEF EPIDEMIOLOGY, MEDICAL STATISTICS AND ENVIRONMENTALI HEALTH UN OCTOBER 2010 ABSTRACT Malaria remains a major health problem in Africa where one child in 10 dies before the age of five years. Despite the availability of affordable preventive/curative interventions in the Primary Health Centres (PHC) in Nigeria, morbidity and mortality from malaria remains high. This study was carried out to determine factors associated with malaria treatment outcome of under-five children that were treated for malaria at the PHC facilities in Umuahia North Local Governm ent Area (LGA) of Abia State. AR Y An analytical cross sectional study involving caregivers of children less thaBn fiRve years attending PHCs in Umuahia North LGA was carried out. A three stage sampliLng Itechnique was used to select four of 31 PHCs, at Amaogwugwu, Umuawa-Alaocha, ONjike and World Bank Housing Estate, based on site and population of under-five attendees. AKey Informant Interview (KII) was carried out with the PHC coordinator of the LGA and AheaDds of the four selected PHC facilities to assess their knowledge and practices of malari a ItrBeatment. A semi-structured questionnaire was administered on caregivers of 562 coOnsecFutive children presenting with fever to determine factors associated with malaria treatm ent outcome. Outcome was considered good when a sick child recovers within 48hrs IofT coYmmencing treatment. Data were analyzed using descriptive statistics, Chi square test aSnd logistic regression at 5% level of significance. ER From KII, theI fVacility health workers based malaria treatment on presumptive diagnosis. Median age foUr chNildren was 24 months (Range = 2 - 59 months) and mean age of caregivers was 32.5 ± 6.6 years. Two hundred and fifty-five (45.4%) of the children were brought to the health centre early. Among the mothers, 355 (63.2%) had been taught homecare of malaria. At presentation, 48 (8.5%) of the children had anaemia; 248 (44.1%) of them were sleeping under Insecticide Treated Nets (ITN). About 416 (74%) of the children had good treatment outcome. More ii children (77.9%) treated on outpatient basis had a good treatment outcome compared with those who were admitted for observation (22.1%) p < 0.05. Also, a higher proportion of children presenting without anaemia (76.7%) had a significantly good treatment outcome compared with those that presented with anaemia (23.3%). Presence of anaemia [O.R 0.25 (C.I 0.13-0.500)] and being admitted [O.R 3.40 (C.I 2.22-6.49)], were both associated with poor treatment outcome. Providing health education on homecare of malaria to caregiver [O.R 3.85 (C.I 2.31-5.55 )], making a child to sleep under ITN [O.R 2.37 (C.I 1.52-3.71)] and taking a sick child eRarlyY to the health centre [O.R 2.07 (C.I 1.34-3.18)], were all significant predictors of gAood treatment outcome. R LIB Educating caregivers on home management of malaria for their cNhild ren, children sleeping under insecticide treated nets and taking sick children to the hDealAth centre promptly would improve malaria treatment outcome in the health centres. IB A Key words: Malaria, Treatment outcomOe, CFaregiver, Under-five, Primary health care centre Word count: 452 ITY RS VE UN I iii DEDICATION This work is dedicated to the Almighty God, to my aged mother, my darling wife, son and my course mates for their support and understanding. RY BR A LI DA N BA F I O SI TY R VE UN I iv CERTIFICATION This is to certify that this work titled “Malaria treatment outcome among under-five children attending primary health care centres in Umuahia North Local Government Area of Abia State Nigeria”, is the original work of Akhimien Obeimen Moses and is submitted in Ypar tial fulfillment for the requirements for the award of Masters in Public Health Field EpiRdemiology Practice in the department of Epidemiology Medical statistics and EnvironmeRntalA Health of the Faculty of Public Health, University of Ibadan, Nigeria. B LI DA N A F I B O Dr Ikeoluwapo Ajayi ITY Dr Akin Fatiregun MBBS; M.Cl.Sc; MPH; PShD MBBS; M.Sc (Epid.Med.Stat) FWACP; FMCGP FAWCP ER NI V U v ACKNOWLEDGEMENT I am indebted to my lecturers Prof O. Oladepo for his fatherly advice, Dr Ikeoluwapo AjayYi (m y supervisor) for her guidance and support and mentorship, Dr Olufunmilayo Fawole (mRy Head of Department) for her advice, Dr Akin Fatiregun (Co supervisor) and other membRers Aof staff of the Department of Epidemiology Medical statistics and Environmental HealthI fBor their assistance, Dr Nguku Patrick and other staff of the Nigerian Field Epidemiology aLnd Laboratory Training Programme (NFELTP) for their patience, co-operation and unAdersNtanding and all the encouragements I got from them all through the period ofD this programme. I will not forget to mention the Centre for Disease Control and PrevenBtionA for their funds, technical and moral support. My gratitude goes to the lecturers frFom oIther sister departments of the University who made invaluable inputs towards the ac tuOalization of this study. Finally, I thank the data collectors for their diligence without whicTh thYis work would have been impossible. SI VE R I UN vi TABLE OF CONTENT Content Page Title page............................................................................................................................. (i) Abstract................................................................................................................................(ii) Dedication............................................................................................................................. (Yiv) Certification..............................................................................................................A......R.....(v) Acknowledgement........................................................................................B......R.................(vi) Table of content.................................................................................. ...L.....I.........................(vii)List of tables..................................................................................N...................................... (x) List of figures..........................................................................A.............................................(xiii) Operational definitions..............................................A......D...................................................(xiv) Abbreviations................................................... ..I...B.............................................................. (xv)F CHAPTER ONE: - O INTRODUCTION...............I..T......Y................................................................................................1 1.1 Background..............S............................................................................................................. 3 1.2 Statement of tEhe pRroblem..................................................................................................... 6 1.3 Purpose oIfV the study............................................................................................................7 1.4 SiUgnifNicance of the study....................................................................................................... 71.5 Research questions................................................................................................................ 7 1.6 Assumptions........................................................................................................................... 7 1.7 Limitation................................................................................................................................ 8 1.8 Justification of the study........................................................................................................ 8 vii 1.9 Aims and objectives 9 1.9.1 Aims.............................................................................................................................. 9 CHAPTER TWO: - 2.0 Literature review..................................................................................................................10 2.1 Malaria.................................................................................................................................. 11 2.2 Signs and symptoms.................................................................................................R......Y...... 13 2.3 Epidemiology......................................................................................................A...................14 2.3.1 Burden..................................................................................................B......R.........................14 2.3.2 Correlates/risk factors..................................................................L.....I.................................15 2.4 Signs and symptoms................................................................N...... .........................................19 2.5 Clinical types...............................................................D.......A................................................... 202.6 Pathogenesis of complicated disease....................A............................................................... 22 2.7 HIV and malaria......................................... ..I...B..................................................................... 29 2.8 General treatment guideline of maOlariFa.............................................................................. 292.9 Malaria parasite life cycle.....Y...... ......................................................................................... 322.10 Vector............................I...T.................................................................................................... 34 2.10.1 Distribution..........S............................................................................................................. 40 2.10.2 Means of dEispeRrsal............................................................................................................ 40 2.11 MalariaI cVontrol.................................................................................................................... 40 2.12 MUalaNria elimination............................................................................................................ 44 CHAPTER THREE 3.0 Subject and methods/methodology.....................................................................................46 3.1 Background of study area.................................................................................................. 46 viii 3.2 Study design.........................................................................................................................46 3.3 Study period......................................................................................................................... 47 3.4 Selection of the facilities...................................................................................................... 47 3.5 Study population.................................................................................................................. 47 3.6 Sample size determination.................................................................................................. 48 3.7 Sampling technique............................................................................................................. 49 3.8 Data collection tools/instrument..............................................................................R.......Y..... 50 3.9 Data management and analysis.........................................................................A................. 53 3.10 Ethical consideration...........................................................................B......R........................ 54LI CHAPTER FOUR N 4.0 Results...............................................................................A.................................................... 55 4.1 Treatment outcome among under five studied...A.....D.......................................................... 55 4.2 The resources available for the provision oIf Bmalaria treatment services....................... 56 4.2.1 Material resources available for rendFering malaria treatment services at PHCs:.....57 4.3 Factors that affected under fi OYve y ear children malaria treatment outcome in PHCfacilities in Umuahia.......I..T.................................................................................................... 61 4.3.1 Descriptive anaRlysisS........................................................................................................... 614.3.2 Bivariate anEalysis............................................................................................................... 69 4.3.3 MultivaIrViate analysis......................................................................................................... 86N CHAUPTER FIVE 5.0 Discussion............................................................................................................................. 88 5.1 Conclusion............................................................................................................................ 93 6.0 References............................................................................................................................ 95 ix 7.0 Appendix 111 List of Tables RY 1.0 Table 1, Malaria treatment outcome................................................................A.................. 55 2.0 Table 2, Demographic characteristics of the PHC Facility heads/PHBC cRoordinator and trainings relevant to malaria treatment in the last five LyeaIrs ........................... 57 3.0 Table 3, Staff strength/workload at the four facilities........N...... ........................................ 58 4.0 Table 4, Treatments reportedly given to the children bAy the caregivers at home before they are brought to the health facility.A......D.........................................................59 5.0 Table 5, Assessment of the health facilitie s IfrBom inception till date and malaria treatment/control activities..F................................................................................ 60 6.0 Table 6, Socio - demographic ch arOY acteristics of caregivers............................................ 627.0 Table 7, The mean/mediaInT cost of treating an under - five child presumed to have malaria aRt vaSrious locations................................................................................. 638.0 Table 8, SociaEl classification of caregiver’s household using their average monthly iInVcome.................................................................................................................... 63 9.0 TaUbleN 9, Average income earned by the caregiver household in a month...................... 6410.0 Table 10, The effect of social classification of the caregivers on good treatment outcome.................................................................................................................. 64 11.0 Table 11, Demographic information on the sick children...............................................66 12.0 Table 12, Baseline clinical information of the children before treatment was started.67 x 13.0 Table 13, Clinical information of the sick children 48 hrs after treatment was started ..................................................................................................................................68 14.0 Table 14, Number of episodes of fever experienced by the children in the last two months.................................................................................................................... 68 15.0 Table 15, Treatment sought by caregivers before coming the health centre...............69 16.0 Table 16, The time interval between when drugs were administered and when the fever stopped..............................................................................................R......Y...... 70 17.0 Table 17, Activities of the caregivers when a child develop fever at homeA.................. 71 18.0 Table 18, Drugs used by caregivers when they do home treatmentB of mRalaria.......... 72 19.0 Table 19, Frequency of caregivers perceived knowledge of maLlarIia prevention........72 20.0 Table 20, Malaria prevention efforts by the caregivers...N...... ....................................... 73 21.0 Table 21, Antenatal periods malaria prevention activAities when the child was been conceived................................................A......D.......................................................... 73 22.0 Table 22, Postnatal information concern iInBg the sick child from mothers/caregivers .75 23.0 Table 23, What mothers were taughtF during ANC........................................................ 75 24.0 Table 24, Impression about the sOervices rendered at the health facilities................... 76 25.0 Table 25, Suggestions bIyT caYregivers on how government can curtail the menace of malariaR.......S............................................................................................................ 7626.0 Table 26, AsEsociation between who decides when a child is taken to the clinic when IVsick and good treatment outcome.................................................................. 77 27.0 UTabNle 27, Association between the various ANC activities by mothers and goodtreatment outcome among the children........................................................ 78 28.0 Table 28, Demographic information of the sick children and its association with good treatment outcome.......................................................................................... 78 xi 29.0 Table 29, Association between caregiver’s level of education or who accompanied them to the health centre and good treatment outcome.............................. 79 30.0 Table 30, Association between the various signs and symptoms of the sick child at the time of presentation in the clinic and good treatment outcome.................. 80 31.0 Table 31, Association between duration of fever and treatment outcome...................81 32.0 Table 32, Association between number of episodes of fever in the last two months before presentation and treatment outcome.....................................R......Y...... 81 33.0 Table 33, Association between how a caregiver detects fever in her sick chAild and good treatment outcome at the health facilities.......................B......R........................ 81 34.0 Table 34, Association between when treatment was given aft eLr dIetecting fever andtreatment outcome............................................N.............................................. 82A 35.0 Table 35, Association between the type of home trDeatment and good treatment outcome....................................I...B..... A................................................................ 82 36.0 Table 36, Association between the drFugs used by caregivers during home treatment of malaria and good tre aOtment outcome........................................................... 83 37.0 Table 37, Association beTtweYen malaria prevention practices by caregivers andtreatmenSt ouItcome.......................................................................................... 8338.0 Table 38, AssocRiation between good treatment outcome and location of the health VceEntre............................................................................................................... 84 39.0 TabNle 3I9, Association between treatment outcome and how a sick child was treated.84 40.0 UTable 40, Association between a mother taking prophylactic treatment during pregnancy and she treating her child prophylactically for malaria after birth.................................................................................................................. 85 41.0 Table 41, Association between a caregiver sleeping under ITN during ANC and her child using same as malaria preventive method after birth....................... 85 xii 42.0 Table 42, Logistic regression modeling result of those variables that were significant from bivariate analysis of factors associated with good treatment outcome ...........................................................................................................................87 List of Figures RY 1.0 Figure 1, Life cycle of the female Anopheles mosquito..............................R......A..................36 2.0 Figure 2, The sexual and asexual life cycle of Plasmodium specie inI Bma and mosquito 37 3.0 Figure 3, Conceptual model important risk factors affecting m aLlaria prevalence in the tropic points of control efforts........................A.....N..............................................41 4.0 Figure 4, Larvae in stagnant water...........................D......................................................... 42 5.0 Figure 5, Dragonflies are natural predators Bof mAosquitoes.............................................43 6.0 Figure 6, A graph of weather the caregFive rI was accompanied to the clinic and who did ..................................... ...O...................................................................................... 65 7.0 Figure 7, A graph of the nTumYber of under five - years children in each caregiverhouseholdS......I...................................................................................................... 708.0 Figure 8, Time iRnterval between consultation and administration of drugs................ 71 9.0 Figure 9, VTimEe interval between when fever is noticed and drugs are given during home NItreatment of malaria.......................................................................................... 64U xiii Operational definitions AR Y A child with malaria: Was any child below 5 years who presented in anyB of Rthe selected PHCs in Umuahia North LGA with a fever of at least 2-3 days duration with Lor wIithout vomiting, chills and rigors or any other signs of severe malaria in the absence oNf runny nose, measles, abscess, ear ache or signs and symptoms of any other well knownD cauAses of fever (WHO malaria manual for community health workers 1996, Sirima et al., 200A3). Baseline status: The baseline status of the pr eIseBnting children with fever were assessed both from clinical history taken from the careO givFers and physical examination by the researchers. The essence of this is to help us determYine the children’s status before treatment was commenced so as to eliminate those factors thIaTt may confound our results from the study. Treatment outcome: ThisS could either be good or poor. Good outcome: AE goRod outcome was when a child less than 5 years is treated in any of the selected PHCIs Vfor malaria and respond well to the administered anti malaria drugs (fever stops, and thUe cNhild does not require any further treatment/visit to the health centre for the same ailment) at 48 hrs after treatment was started. Poor outcome: A poor outcome was when an <5 years child is treated in any of the selected PHC for malaria and responds poorly to the administered anti malaria drugs (fever persist, xiv convulsion sets in, severe anaemia, readmission in the health facility, requires immediate referral or death) 48 hrs after anti-malaria drugs were given. Key informant interview The PHC coordinator of Umuahia North LGA as well as the head of the four selected PHC facilities participated in the structured Key informant interview that was administered by the researchers. AR Y Abbreviations LIB R ABSEED Abia State economic empowerAmeNnt developmentACT Artemisinin - based combiDnation therapy AIDS Acquired immunodeficAiency syndrome ARDS Acute respirator y IdBistress syndrome CD36 Cluster ofO difFferentiation 36 DDT DichlYoro diphenyltrichloroethane DEET IAT,A-Diethyl-meta-toluamide GPI RSGlycosylphosphatidylinositolHLA E Human leukocyte antigen HIV IV Human immunodeficiency virus ICAMU - N1 Intercellular adhesion molecule 1 IL Interleukin IMCI Integrated management of childhood illnesses iNOS Induction of nitric oxide synthase ITN Insecticide treated net xv MDG Millennium developmental goal NDHS National demographic and health survey PfEM - 1 Plasmodium falciparum erythrocyte membrane protein - 1 TNF Tumor necrotic factor UNICEF United nation children’s fund VAT - genes Visceral adipose tissue - gene V - CAM - 1 Vascular cell adhesion molecule - 1 Y WHO World health organization R RA LI B N AD A F I B O ITY RS VE UN I xvi CHAPTER ONE 1.0 INTRODUCTION Malaria is a major infectious disease in tropical and subtropical countries. It has continued to be a major global health problem, with over 40% of the world’s population - more than 2,400 million people - exposed to varying degrees of malaria risk in some 100 countries (Hay et al., 2004, WHO, 2005). Most countries in Sub Sahara Africa have struggled in recent years to def ine affordable alternatives to the rapidly declining effectiveness of chloroquine and oRtherY social cultural factors that are affecting the treatment outcome of malaria in the HealthA care facilities (Etuk et al., 2008). The treatment and control of malaria pose a serious chaBllenRge in sub-Saharan Africa where each year about 300 - 500 million attacks occur, froLm Iwhich 1.5-2.7 million people die (WHO Bulletin, 2000). These deaths occur mainly aNmon g children under five years old and pregnant women (Shane, 2001, Steketee et al., 2001A, Heggenhougen et al., 2003). The epidemiological, medicinal and entomological aspectsA of Dmalaria are well documented, as are its consequences for the social and economic outl oIoBk of countries in which it is endemic (NDHS, 2003, WHO, 2003, Bryce et al., 2005, BremFan et al., 2004). Strategies for combating malaria in sub Sahara Africa and Asia now Yfoc u Os on reducing morbidity and mortality through prompt diagnosis and treatment (BrucIe-TChwatt, 1984, Hetzel et al., 2007). Eradication attempts in earlier days were largely succesSsful in Europe and North America with Mass Drug Administration (MDA) strategy. AElthoRugh, it failed in Africa, Central America, South America and Asia due to lack of resouIrcVes and poor political will (Von Seidlein et al., 2003, Kaneko et al., 2000). HoweUver Nsome local successes were achieved in South East Asia and this was mainly due to acombination of MDA and Artemisinin Combination Therapy (ACT) treatment campaign (Greenwood et al., 1987, Song et al., 2010). The number of malaria cases worldwide appears to be growing until the advent of the Artemesinin combination therapy (ACT), due to the increasing risk of transmission in areas where malaria control has declined and as a result of increasing prevalence of drug-resistant parasite strains (e.g. chloroquine resistance). In a relatively few 1 cases, because of increasing international travels, with modern rapid means of travel, large numbers of people from non-malarious areas are being exposed to the infection, which may seriously affect them only after they return home (Pasvol, 2005). The reported cases of increasing resistance of chloroquine and even more recently that of the ACTs in some south East Asian countries to malaria has led to a growing concern that in future no effective remedies will be available. The strategy adopted in the 1990s emphasized early diagnosis and prompt a nd efficient treatment. It was to be supplemented by initiatives aimed at prevention, theR conYtrol of epidemics and continued observation of each country’s malaria situation (Global mAalaria control strategy, 1992). There is currently a renewed interest in MDA (White, 200B8, RSong et al., 2010) because of the previous successes in malaria control (Okiro et al., 2007L); Ihighly efficacious anti­ malarial drugs with a transmission reducing potential (ShekalagNhe et al., 2007, Nosten et al., 2000) and new insights in the nature of malaria transmissionA using sensitive parasite detection methods (Babiker et al., 2008). Mathematical modeliAng hDas shown that malaria transmission is, in theory, susceptible to mass treatment pr oIgBrammes if all subjects within an endemic community could be given anti-malarias thaFt clear parasitaemia during a period of absent or very low vector densities in areas wherYe th e O intensity of transmission is already low (Maude et al., 2010). Only time would tell IifT these strategies would work. However, it is worth noting that global targets for malariSa prevention, treatment, and disease reduction are unlikely to be achieved without cEonsRiderable investment in health delivery systems (O’meara et al., 2009). In some areas, tIheV malaria mortality rate remains high for a number of reasons including limited accessU toN healthcare and/or increased drug resistance (Dzeing-Ella et al., 2005). A better understanding of predictive factors that can make an uncomplicated malaria among under-five progress to severe malaria could aid health workers at the primary level of care to avoid delays in the referral of such cases so identified to the next level of care thereby reducing the probability of these children dying from malaria. 2 1.1 Background According to the Carter Center, each year, malaria kills more than 1 million people, mostly children, with 350-500 million cases reported worldwide. Approximately 90% of all cases of malaria (a preventable disease) are in Africa, where one child in 10 dies before the age of five (WHO, 2005, FMOH, 2000). Malaria is a major threat to public health in Africa (Nafo-Traore, 2005) and remains the leading cause of death as well as debilitating fevers, low birth weigh ts, anaemia, epilepsy and death in children under 5 years in this region (Black et al., 2003R). BYryce et al., 2005 reported that 94% of deaths due to malaria worldwide occur in AfrAica where the economic impact is to the tune of $12 billion in lost productivity andB heRalth costs a year. However, national and international malaria control programs LhavIe been implemented, including: Integrated Management of Childhood Illness (IMCI), RNoll Back Malaria initiative, the United States President Malaria Initiatives and the Global FunAd. Major progress in the prevention and treatment of malaria has been reported from sAeveDral countries through the adoption of Artemisinin-based combination therapy (ACT) (IWBHO, 2006), the use of insecticide treated bed nets (ITN), and Intermittent PreventivOe TFreatment (IPT) for pregnant women and children.However, despite the existence oYf th ese effective treatment and protective measures, malariacontinues to be of concern (YIaTmey, 2004). One strategy of the Roll Back Malaria Initiative to halve malaria mortality bSy 2010 is through prompt access to effective anti-malaria treatment, especially among uEndeRr-five years children (Nabarro et al., 1998, WHO, 2003). Primary Health Centres (PHCIsV) are the main channel through which key treatment and preventive interventions for mUalarNia are delivered and for effective treatment of clinical malaria (Noor et al., 2007).However recent findings suggest that despite these affordable preventive and curative interventions in the Primary Health Centres (PHC), morbidity and mortality from malaria still remains high in most African countries and this may be as a result of not having quality paediatric care in both outpatient and inpatient services of health facilities; though this is essential for a credible and efficient primary health care system (Duke et al., 2002). It has been 3 shown from most studies that the poor child, health care delivery in many developing countries are mainly as a result of incorrect diagnosis and assessments, misuse and inappropriate prescription of drugs and long waiting hours (Abubakar, 2006, Rowe et al., 2000 and 2001). This could be a likely reason for the malaria treatment failure normally seen in the PHC facilities leading to severe consequences where referrals are delayed. The need to focus on improving primary health care delivery is essential in all developing countries (Zurovac et al., 2006). T he World Health Organization health Statistics (2009) showed that in 2007, there were anR estYimated 9 million child deaths. This was, significantly fewer than the 12.5 million estimateAd in 1990, and amounts to a 27% decline in the under-5 mortality rate over that period to 6B7 pRer 1000 live births in 2007. Also a UNICEF data shows a 28 percent decline in the undeLr-fiIve mortality rate, from 90 deaths per 1000 live births in 1990, to 65 deaths per 1000 livNe b irths in 2008. According to these estimates, the absolute number of child deaths in 2008 dAeclined to an estimated 8.8 million from 12.5 million in 1990; the base line year for the AMilDlennium Development Goals (MDGs). Reducing child mortality increasingly depends oInB tackling neonatal mortality on one hand and reducing morbidity and mortality from vFaccine preventable diseases as well as malaria, HIV/AIDS and diarrhea diseasesY on Othe other and this would help countries to attain the Millennium Development GoaIlTs 4, 5 and 6 especially in Africa. The Integrated ManagemeSnt of Childhood Illnesses (IMCI) strategy was introduced by the WHO and UNICEF to EimpRrove skills of health workers, the health system itself; and also the knowledge anIdV practices of families in relation to the care of their young children (Oluwole et al., 20U00,N Zurovac et al., 2006). Yet, each year approximately 10 million children less than 5 years of age mainly in developing countries still die mostly from one of the following five conditions: pneumonia, diarrhea, malaria, measles and malnutrition. Surveys performed prior to the IMCI intervention revealed that many sick children were not properly assessed and treated by health care providers and that their parents were poorly advised on importance of home care and 4 how it can be done and as a result effective homecare was lacking in most cases (Duke et al., 2002, Tangpukdee et al., 2007). The major causes of death in under-five children in Nigeria are malaria, vaccine preventable diseases, Acute Respiratory Infection (ARI) particularly pneumonia, diarrhea and malnutrition (FMOH, 2005). Despite initiating an integrated approach by the Federal Government of Nige ria to tackle these diseases by using the IMCI strategy, not much has been achieved largRely Ydue to the low coverage of this intervention. Evidence suggests that universal coveArage of those interventions with evidence of impact on the major causes of death canB siRgnificantly reduce childhood mortality. LI In Nigeria, malaria is endemic throughout the country with moNre th an 90 % of the population living in areas with constant risk of infection. Malaria is respoAnsible for 25 % of infant mortality and 30 % of childhood mortality (FMOH, 2005). ANigDeria accounted for one fourth of all estimated malaria cases in the WHO African R IegBion in 2006. Nigeria like most other African countries is home to the most deadly form oFf the parasite (Plasmodium falciparum) and has the conducive climate for the vector (An opOheles mosquito species), to proliferate. Due to lack of funds, political will and/or infIrTastrYucture the federal government can not single-handedly mount effective anti-malaria camSpaigns, so there are a number of International Organizations rendering their full support toE theR malaria control effort in Nigeria. Abia state, isI Vlocated in the southeastern region of Nigeria and lies within approximately latitudUes N40 40' and 60 14' north, and longitudes 70 10' and 80 east. It covers an area of about5,243.7 sq. km which is approximately 5.8 per cent of the total land area of Nigeria and shares common boundaries to the north with Ebonyi State; the south and southwest with Rivers State; and, to the east and southeast with Cross River and Akwa lbom States, respectively. To the west is Imo State, and to the northwest is Anambra State. It has a total population of 2.8 million people and is divided roughly equally between females and males (1.39million and 1.43million 5 respectively). The population is projected to grow at three per cent per annum meaning that the state will have a population of about 3,379,168 in 2015. Due to the climatic condition of the State which is favourable for the breeding of the Anopheles mosquitoes, malaria remains a scourge affecting the populace especially the vulnerable group (women of child bearing age and under - five children who constitute 25 per cent and 21 percent of the state population respectively). Malaria is the leading cause of ill health and death in Abia; accounting for over 35 per cent of mortality and more than 60 per cent of morbidity (Abia State Health DatRa BuYlletin, 2007 and Abia SSHDP, 2010). The Abia State Economic Empowerment DevelopAment Strategy (ABSEEDS) document, 2005 stated that chloroquine resistant strain of PlaBsmRodium falciparum is responsible for most of the malaria deaths in the State. In UmuahiaL NoIrth LGA of Abia state, of the estimated 49,418 under-five year population, 1,011 cases Nof m alaria were recorded in the health facilities in 2009 and nearly half of them needed DimmAediate referral to secondary or/and tertiary health facilities (Umuahia North LGA AnnuaAl health report, 2010). Meanwhile, there is gross under reporting of these cases from the IhBealth facilities due to poor patronage by the populace, suggesting that this figure may beF an underestimation of the real burden of malaria in Umuahia North LGA. O ITY 1.2 Statement of the proSblem Despite affordableE anRd effective anti-malaria therapy, the disease remains a leading cause of under-five moIrVtality worldwide. A lot of factors are believed to be responsible for this trend. Such UfactNors include late presentation at the health centres; cultural practices of caregivers ofunder - five children, availability of antimalarial drugs have been documented in most documents. So, it is pertinent to identify which of the above factors are responsible for the poor malaria treatment outcome that was found in Umuahia North LGA PHC facilities among under - five children from a pilot study done in two PHC facilities in Umuahia (21%). Identifying probable causes of poor malaria treatment outcome among under - five children is very 6 important considering the fact that it could lead to progression of uncomplicated malaria to the severe form with its accompanying high morbidity and mortality. 1.3 Purpose of the study This study was carried out to identify reasons while despite the huge amount of money government and cooperate bodies are sinking into the prevention and control of malaria at the primary health care level, a lot of under - five children still die every year even after RpresYenting at the health facility. A 1.4 Significance of the study BR This study is to assist the health workers in the local government hLeaIlth facilities, to timely identify factors contributing to poor treatment outcome of under-Nfive children and so, reduce the number of late referrals to the secondary health facilities. WiAth the anticipated drop in <5 years mortality, the society would be geared toward achieviAng Dthe millennium development goal 4; so in the long run individual households, health ca reI wBorker and the society shall benefit immensely from this study. O F 1.5 Research questions ITY What are those factors thaSt if well addressed can improve the treatment outcome of under - five children receivingE treRatment for malaria fever in Umuahia North LGA PHC facilities while drastically redIuVcing the incidence of referral to higher health facilities (secondary/tertiary)?N 1.6 AUssumptions The assumption is that there are certain factors that may be associated with malaria treatment outcome in under - five children. These include (a) Stage of the disease when the patient first presented to the clinic (b) Level of home treatment activities carried out before coming to the clinic 7 (c) Duration of fever before the commencement of treatment (d) Type of treatment given (e) Maternal education (f) Socio-economic status of mother and/or father The variables that appear to be associated with malaria treatment outcome would then be subjected to appropriate statistical test to determine association. RY A 1.7 Limitations BR The results of the study may not be generalisable to the whole State givLen Ithe fact that the study was undertaken in a town in one of the 17 LGAs making up AbiaN Stat e. So it is possible socio­ cultural practices may differ in the various senatorial districts Aor LGAs. It may be necessary therefore to conduct a bigger study to have a compreheAnsiDve picture of the problem but it can however be generalised for Umuahia North LGA I. ABlso it is worth noting that malaria diagnosis was made presumptively and this could OaffecFt the specificity and sensitivity of the diagnosis so made. ITY 1.8 Justification of the stuSdy The major causes Eof mRortality in Nigerian children include malaria (30%), vaccine preventable diseases partiIcVularly measles (22%), diarrhea (19%), acute respiratory infections (16%) with malnuUtritiNon underlying about 60% of these childhood deaths (National Health Management Information System, 1999). This child health situation poses a serious threat to future national productivity and development. From the National Demography and Health survey 2008, the under - five mortality rate was 157 deaths per 1,000 live births in the country an improvement from the figure of 201 in the 2003 NDHS, which is quite high compared to other African countries. However it is still a far cry from the target of the MDG. From the NDHS 2008, 42.4% 8 of under - five who developed fever in the 2 weeks before the survey in the urban areas took anti-malaria drugs as against 30.2% in the rural areas. In the urban areas 19.9% of the children took the treatment within 48 hours while 13.7% did so in the rural area. In 2003 Abia state had a life expectancy of 55 years for women and 54 years for men at birth higher than the national life expectancy at birth of 47.7 years. The high under - five mortality rate of 142 deaths per 1,000 live births contributing a great deal to this life expectancy. According to the Abia State Hospit als Management Board Statistical Data/ Information, 2008, over 75% of the Abia populatRion Yresides in the rural areas where PHC serves as the main source of health care to the popuAlace and only the privilege few patronizes the private clinics. Also about 14% of theB chRildren and 5% of pregnant women in the State would treat malaria fever with any availa bLle Ianti malaria drugs.N 1.9 Aims and objectives A 1.9.1 Aims: AD This study aimed at determining factors that cIonBtribute to malaria treatment outcome among under - five children seen at Primary HeOalthF Centres in Umuahia North LGA of Abia State. 1.9.2 Specific objectives ITY 1. To determine the oSutcomes of malaria treatment in under five children seen at the PHC facilities inE UmRuahia North LGA 2. To deIteVrmine the human and material resources available for the provision of malaria UtreNatment services for under - five children attending Primary Health Care facilities in Umuahia North LGA, of Abia State. 3. To identify factors that could affect under - five malaria treatment outcome in PHC facilities in Umuahia (health facility or household/caregiver) related. 9 CHAPTER TWO 2.0 LITERATURE REVIEW Much work has been done on malaria largely because of the interest it has generated inY rec ent past and the huge funding from the Bill Gates foundation, the “Global fund” as weRll as other international funding agencies. In a study carried out by Biritwum et al., 2000R in Accra Ghana, they reported that malaria was the most common ailment reported by thIe Bcaregivers in the two communities where their study was carried out (an average of two e pLisodes in the nine months periods of their study). They also discovered that the levAel Nof education of the caregivers determine their use of left over drugs and un-prescribed dDrugs to treat their under - five children when they come down with malaria. Children oIfB the A poor and uneducated mothers among the study population were less likely to be takeFn to a clinic for treatment early when they are sick. This fact alone can cause high mortalit yO rate among those children because they will end up been taken to the clinics when the sicTknYess becomes severe (such that severe anaemia, convulsion and dehydration) may have setS in.I Efforts have been made to reduce the incidence of malaria among the vulnerable groups R(pregnant women and under - five children) in most community through a lot of multi-ageVncyE collaborations using various means and techniques such as early diagnosis, prompt treNatmIent of cases, withdrawal of resistant drugs from the malaria treatment protocol and vectorU control (elimination or reduction of contact with man) by using bed nettings. However a lot of factors would influence the way these insecticide treated bed nettings are used by the public. For instance, in a study conducted by Nuwaha in Mbarara, Uganda in 2001, he recommended that in order to increase the use of bed nets among the rural dwellers, it has to be affordable and there should be increase dissemination of health educational messages that stress 10 the benefits and ways of using bed nets in homes. He arrived at this conclusion because he found that owning a television, having mosquito nets in ventilators of houses, being a skilled worker or a professional, or living in a permanent house, believing that bed nets prevent malaria and believing that bed nets are not expensive affected the use of bed nets by the study group (ownership of a television were higher predictors). Salako et al., 2001, carried out a study in Nigeria and found that the commonest form of first-line treatment given to under five child ren when they are sick was drugs gotten from patent medicine vendors or drug hawkers. RTheYy also found a configuration of signs and symptoms associated with chloroquine usAe, to include perception of the child having malaria, high temperature and loss of appetitBe. TRhis is in order just that chloroquine has been abandoned for newer combination therapLy dIrugs for malaria. The ability of the child's caregivers, both parental and professionalN, to make these distinctions in medication use will provide the foundation for health eduDcatiAon in the promotion of appropriate early treatment of childhood fevers. IB A 2.1 Malaria F Malaria, which is a life-threatening diOsease, has been around since ancient times. The early Egyptians wrote about it on paIpTyruYs, and the famous Greek physician Hippocrates described it in detail. It devastated the inSvaders of the Roman Empire (NIAID, 2002). In ancient Rome, as in other temperate EclimRates, malaria lurked in marshes and swamps. People blamed the unhealthinessI iVn these areas on rot and decay that wafted out on the foul air, or, as the Italians were Uto saNy, “Mal aria” or bad air. In 1880, Laveran a French physician working in Algeria, firstidentified the causative agent for human malaria while viewing blood slides under a microscope, to be the one-celled Plasmodium parasite (The Nobel foundation, 2007, Cox, 2010). Eighteen years later, they attributed the transmission of malaria to the bites of infected Anopheles mosquito (NIAID, 2002). Though in rare cases, a person may contract malaria through contaminated blood during transfusions (Kitchen et al., 2005). There are equally documented 11 cases where a fetus may become infected transplacentally by its mother during pregnancy (Uneke, 2007). The plasmodia responsible for malaria are protozoan parasites distinguished by their largely intracellular location in the human host and their dependence upon a vector both for completion of their life cycle and the transmission necessary for their survival. Unlike many of the larger metazoan parasites, plasmodia can multiply within the human host, so that a single infection c an lead to an overwhelming parasitic burden. Malaria is the most important human parasiRtic dYisease in terms of the morbidity and mortality for which it is responsible. Of the four maAjor species of plasmodia that routinely infects humans (P. falciparum, P. vivax, P. malariBae Rand P. ovale), one (P. falciparum) is responsible for nearly all the severe diseases and LmoIrtalities due to malaria (1million to 2.5 million deaths every year) (Obionu, 2007). TNhe other species cause febrile illness, sometimes leading to anaemia but rarely to death. A fAifth species, Plasmodium knowlesi, is a zoonoses that causes malaria in macaques but canA alsDo infect humans (Fong YL et al., 1971, Singh B et al., 2004). Plasmodium vivax, the m oIstB geographically widespread of theplasmodium species and the cause of most malaria cOases Fdiagnosed in the United States, produces less severe symptoms. Relapses, however, canY occ ur for up to 3 years in P. vivax infection, and the resulting chronic disease can be debilitIaTting (Adak et al., 1998). Once common in temperate climate, P. vivax is now found mostSly in the tropics, especially throughout Asia (Mendis et al., 2001). Plasmodium malarEiaeR infections not only produce typical malaria symptoms but they can also persist in the IbVlood for very long periods, possibly decades, without ever producing symptoms (GilleUs, 2N002). A person with asymptomatic (no symptoms) P. malariae, however, can infect others, either through blood donation or mosquito bites. P. malariae has been wiped out from temperate climates, but it persists in Africa. Various stages of the parasite include sporozoites, hepatic-stage parasites, circulating intra­ erythrocytic asexual parasites, gametocytes and hypnozoites (the latter develop in P. vivax and P. 12 ovale only) and they do not cause symptoms. Three processes fundamental to the parasite’s life cycle are believed to result in disease manifestation: (1) The release of merozoites and other red cell contents when mature blood-stage schizont rupture; (2) The accompanying destruction of infected erythrocytes and (3) The adherence of parasitized erythrocytes to vascular endothelia, leading to the sequestrat ion of parasitized erythrocytes in micro vascular beds (this process of cytoadherencYe and sequestration is peculiar to P. falciparum) (Miller et al., 2002, Molyneux et al., 200A8) R BR 2.2 Signs and symptoms LI Symptoms of malaria include fever, shivering, arthralgia (joint pNain) , vomiting, anemia (caused by haemolysis), hemoglobinuria, retinal damage (BearDe etA a.,l 2006) and convulsions. The classic symptom of malaria is cyclical occurrence of sAudden coldness followed by rigor and then fever and sweating lasting four to six hours, o ccIuBrring every two days in P. vivax and P. ovale infections, while every three days in P.O maFlariae infection (Malaria life cycle & pathogenesis, 2006). P. falciparum can have recur rent fever every 36-48 hours or a less pronounced and almost continuous fever. ThiIs TfevYer with its accompanying malaise, anorexia, headache, chills, sweating and rigors (a cytSokine mediated host response) is common to infections by almost all pathogens (MolyneEux Ret al., 2008). Malaria fever is not usually distinguishable clinically from fever due to oItVher agents. A periodicity of fever may develop that becomes highly suggestive of malarUia, Nbut this is usually in prolonged untreated infections. Periodicity results from synchronization of the parasite population, which may be due to the fact that elevated body temperature differentially slows the growth of late-stage parasites, allowing younger parasites to ‘catch up’. Monoclonal antibody to tumour necrosis factor (TNF) has been shown to reduce fever in West African children suffering from severe malaria. What triggers the host cytokine response in 13 malaria is unknown but is likely to be a toxin, or possibly several toxins, released from the rupturing schizont. Glycosylphosphatidylinositol (GPI) of parasite origin is one candidate for the role of a ‘malaria toxin’ (Molyneux et al., 2008). When administered as a vaccine to mice, a P. falciparum GPI conjugated to a suitable carrier prevents complications and death in animals challenged with a subsequent P. falciparum infection. A comparable effect is yet to be demonstrated in human malaria. It is probable that the ‘antitoxic immunity’ that is characteris tic of older children and adults in endemic areas (less fever and illness, for a given RdenYsity of parasitaemia, than in non immune people) may result from immune mechanisms dAirected against some of such parasite ‘toxin’ (Molyneux et al., 2008). BRI 2.3 Epidemiology N L 2.3.1 Burden DA Directly, malaria causes about 250 million cases oBf feAver and approximately one million deaths annually (WHO Malaria report, 2008). The vFast mIajority of cases occur in children under 5 years old (Greenwood et al., 2005); pregnan t Owomen are also especially vulnerable. Despite efforts to reduce transmission and increasTe tYreatment, there has been little change in those areas at risk of this disease since 1992 (SHayI et al., 2004). Indeed, if the prevalence of malaria stays on its present upwards coursRe, the death rate could double in the next twenty years (Brema, 2001). Precise statisticVs arEe unknown because many cases occur in rural areas where people do not have access to NhosIpitals or the means to afford health care. As a consequence, the majority of cases are unUdocumented (Brema, 2001). Malaria is presently endemic in a broad band around the equator, in areas of the Americas, many parts of Asia, and much of Africa; however, it is in sub­ Saharan Africa where 85 - 90% of malaria fatalities occur (Layne, 2007). The geographic distribution of malaria within large regions is complex, and malaria endemic and malaria-free areas are often found close to each other (Greenwood and Mulabingwa, 2002). In drier areas 14 within the malaria endemic belt, outbreaks of malaria can be predicted with reasonable accuracy by mapping rainfall (Crover et al., 2005). Malaria is more common in rural areas than in cities; this is in contrast to dengue fever where urban areas present the greater risk (Van Benthem et al., 2005). For example, the cities of Vietnam, Laos and Cambodia are essentially malaria-free, but the disease is present in many rural regions (Trug et al., 2004). By contrast, in Africa malaria is present in both rural and urban areas, though the risk is lower in the larger cities (Keiser et al., 2004) . The global endemic levels of malaria have not been mapped since the 1960sR. HYowever, the Wellcome Trust, UK, has funded the Malaria Atlas Project (Hay, 2006) tAo rectify this, providing a more contemporary and robust means with which to assesBs cRurrent and future malaria disease burden. LI Indirectly, malaria affects human development by impairing AinteNllectual development and cause developmental abnormalities (especially following AcereDbral malaria). In endemic areas the disease is responsible for most lost school attendIanBce and decrease productivity at work. Malaria also impacts negatively the economies of cFoun tries where the disease is endemic, by retarding the economy (the cost of a single bo uOt of malaria is equivalent to over ten working days in Africa). Also the cost of treaTtingY an episode of malaria is in the range of $0.08 to $5.30 depending on the type ofS druIgs prescribed as required by the local pattern of drug resistance. Meanwhile, it has beeRn estimated in 2001 that 1.1 billion people had consumption levels below one dollar a dayV (AErrow et al., 2004).I 2.3.2 UCorNrelates/risk factorsEpidemics are caused by migration (i.e. Introduction of susceptible hosts), the introduction of new vectors, or changes in the habits of the mosquito vector in the human host (Pates and Curtis, 2005) . Epidemics have occurred in North India, Sri Lanka, South East Asia, Madagascar and Brazil. What determines whether a particular individual infected with P. falciparum would 15 develop negligible, mild, moderate, severe or fatal disease is the result of an inter-play of several parasite, host, vector and circumstantial factors (Brema, 2001, Brema et al., 2007). Parasite factors We know that the different species of plasmodia cause different degrees of illness, with only P. falciparum commonly causing severe and fatal disease. Even within the species P. falciparu m, different parasite ‘strains’ have different capacities to cause disease, a fact well RknoYwn to physicians who administered malaria parasites to generate fever for the treatmeAnt of syphilis early in the last century (Raju, 2006). Virulence in P. falciparum may depBendR on the parasite’s growth (multiplication) rate, its PfEMP-1 expression (affecting its cytLoadIherence characteristics or tissue specificity), its capacity for agglutination or rosette foNrmat ion, and its toxin-releasing and cytokine-inducing potential (Molyneux et al., 2008). ParAasite mutations are known to affect susceptibility to drugs for example, point mutatiAons Din the genes for parasite enzymes dihydrofolate reductase and dihydropteroate s ynItBhetase confer degrees of resistance to drugs, such as pyrimethamine and sulfadoxine rFespectively, that target these enzymes. While not affecting parasite virulence, these mu taOtions may impair responses to initial treatment and thus influence disease severity (KyIaTbayYinze et al., 2003). Host factors RSThe most obvious Ehost determinant of the severity of malaria is the level of acquired specific anti-malarial IimVmunity (Kwiatkowski, 1999). Thus adults in an area of intense P. falciparum transmUissiNon tend to suffer few or mild symptoms while children in the same areas are at risk ofsevere and fatal disease. Immunity is directed against all stages of the parasite’s life cycle in the human host (sporozoites, liver stages, blood stage asexual parasites and gametocytes) and probably also against ‘toxins’. Both antibody and T cell-mediated mechanisms contributes to acquired specific immunity (Miller et al., 2002). Humans are diverse both in their capacity to mount an effective specific immune response and also in components of most or all of the non- 16 specific disease mechanisms (Molyneux et al., 2008). Since P. falciparum can kill large numbers of people before they reach reproductive age, it is likely that the parasite has exerted a selective pressure on many genes in populations in malarious areas. The most readily demonstrable example of such an effect is the gene mutation causing substitution of valine for glutamic acid at position 6 in the beta chain of hemoglobin (Chitins, 2001). An individual inheriting this mutation from both parents suffers from sickle cell disease, with frequent hematological crises and a strong likelihood of dying in childhood. An individual inheriting the mutation fromR onYly one parent has almost no clinical disease from the mutation but is dramatically proAtected against severe and fatal malaria. A balanced polymorphism results in the populBatioRn, accounting for much higher prevalence of the sickle mutation in malarious than other LareIas of the world, and the prevalence of the heterozygous sickle state among children wiNth s evere malaria is about one tenth or less of its prevalence in the population as a whDole A(Kwiatkowski, 1999). Similar, but usually less powerful and less consistent, host geneticA contributions to malaria susceptibility are now being identified through large case-contro l IaBnd parent-child studies with carefully defined severe disease in the index patients. MutFations affecting HLA class I and II antigens, the promoter region of TNF genes, ICAM O-1 expression on vascular endothelium and many other mutations have been reported ItoT beY under or over represented among children with severe or fatal malaria (Molyneux et al., S2008). Some of these effects are seen in some populations but not in others, and some aEre aRssociated with certain malaria complications (e.g. coma or severe anaemia) and not otherIs.V With the completion of sequencing of both human and P. falciparum genomes and wUith Nthe increasing use of multicentre epidemiological studies, it is likely that more will be learned in the near future about parasite and host characteristics that determine disease severity and about particular combinations of host and parasite that may be critical for morbidity or mortality (Warrell and Gilles 2 0 0 2 ). 17 Influence of transmission pattern Even within malarious areas, there are great geographical differences in the frequency and seasonality of infections. There is some evidence to suggest that although children bear the brunt of disease in all such areas, the patterns of disease in children differ. Where transmission of P. falciparum is intense year ‘round, the commonest complication is severe anemia in infants and toddlers, while in areas with restricted seasonal transmission, encephalopathy in toddlers a nd slightly older children is more common (Anumudu et al., 2007, Angyo et al, 1996)R. WYhether and how disease patterns will be affected by the introduction of measures that Aalter infection rates such as impregnated bed nets remains to be seen as these methods arBe inRcreasingly widely introduced. LI N Human host A The behavior of man plays an important role in the epiAdemDiology of malaria. There must be a human reservoir of gametocytes to transmit the inIfBection. In areas of high transmission, infants and young children are more susceptible to mFalaria. Circumstance affecting the impaYct o f Omalaria on a population The impact of malaria in a IpTopulation is partly determined by how quickly the disease is recognized and how well Sit is treated (Meremikwu et al., 2008, Noor et al., 2003). These are dependent upon thEe aRvailability of health services, the quality of diagnostic and therapeutic facilities and IthVe accessibility of these to all sectors of the population (Raso et al., 2005). The efficaUcy oNf drugs used in the first-line treatment of uncomplicated disease is also an important factor: there is epidemiological evidence of increasing malaria mortality associated with decreasing efficacy of chloroquine in parts of Africa over recent decades (Warsame et al., 2002, Sudre et al., 1992). Adequate drugs are an important though they are not a sufficient defence against severe malaria. However, as many fatal illnesses develop over a matter of hours and even 18 the most immediate therapy could not be expected to rescue the patient. Malaria control must therefore advance along all fronts, and the development of a vaccine continues to be a priority. 2.4 Signs and symptoms Initially the symptoms resemble those of a minor viral illness. These include: lack of sense of well being, headache, fatigue, abdominal discomfort, muscle aches followed by fever a nd nausea/vomiting. These may ultimately be followed by typical malaria picture sucRh asY fever spikes (sudden rise and fall in temperature), chills and rigors (Warrell and Gilles, 20A02). Cold stage: As the temperature begins to rise, there is intense heaBdacRhe and muscular discomfort. The patient feels cold, clutches blankets, and cLurlIs up shivering and uncommunicative. Within minutes the limbs begin to shakNe a nd teeth chatter, and the temperature climbs rapidly to a peak (chills and rigor). ThDe riAgor usually lasts 10-30 minutes but can last up to 90 minutes. A Hot stage: By the end of rigor there is periphe rIalB vasodilatation and the skin feels hot and dry and the temperature becomes high. F Sweating: Profuse sweat then breYaks o Out lasting for 2-4 hours. The patient is soaked in sweat and the temp falls. The bloodI Tpressure is relatively low. The patient feels exhausted and may sleep off. Defervescence Susually takes 4-8 hours. Fever is irregular at first with temperature exceeding 39°C anEd mRay rise up to 40°C. Incubation tiImVe: The time interval between mosquito bite and development of malaria is 13-14 days UexceNpt for P. malariae (35 days). If the infection is left untreated, the fever would recurs every third day in P. vivax and in ovale infection establishing a 2-day cycle (tertian). If the spike occurs every three days (Quartan) as in P. malariae infection i.e. fever recurs every fourth day (Obionu, 2007). The pattern of fever in P. falciparum infection is erratic. Paroxysms with rigors are more common in P. vivax & P. ovale than in P. falciparum and P. malariae related malaria. True 19 rigors are unusual in naturally acquired falciparum malaria. As the infection continues the spleen and liver enlarge and anemia develops (Warrell and Gilles, 2002). The patient loses weight. If no treatment is given the natural infection stabilizes for several weeks or months and then gradually resolves. Associated Symptoms: Mild abdominal discomfort, constipation and diarrhea are associated with malaria. Children would be irritable and have less appetite. Malaria in Pregnancy: There is increased risk of severe Falciparum malaria in the sRecoYnd and third trimester of pregnancy. In areas of less transmission, it is an important causeA of fetal death and results in high maternal mortality. In areas of intense transmission, it mBay Rbe associated with low birth weight (Duffy and Fried, 2003). The infected mothers may evLenI be asymptomatic. Malaria in children: The majority of childhood malarial infeNctio ns present with fever and malaise. In addition to the clinical features mentioned for aduAlts, malaria in children may lead to; convulsions, coma, hypoglycaemia, metabolic acidosiAs anDd severe anaemia (Warrell and Gilles, 2 0 0 2 ). IB Diagnosis: Malaria is diagnosed by micOroscFopic examination of the blood where thick and thin blood films are made on clean, grease free glass slides. This diagnosis rests on the demonstration of asexual forms of the paIraTsiteY in peripheral blood smears stained with Giemsa’s stain. Clinically, any patient suSffering from fever with rigors in an endemic area should arouse a suspicion of malariEa. TRhus in endemic areas a doctor or any health worker can make a diagnosis of malaria basIeVd on the signs and symptom (presumptive diagnosis) (FMOH, 2005). 2.5 CUliniNcal typesAccording to severity of illness, malaria can be broadly classified into two types viz Uncomplicated (Benign) and Complicated (Malignant) malaria. Uncomplicated (benign) malaria This form of malaria is a relatively milder disease which is generally caused by P. vivax and is seldom fatal. The chance of involvement of other organs (complications) is much less. 20 Complicated (malignant) malaria This is malaria where the disease has become severe taking a rapid downhill course. It is caused mainly by P. falciparum and rarely by P. vivax. It has a poor prognosis (outcome). Severe malaria Severe malaria is almost exclusively caused by Plasmodium falciparum infection, and usually arises 6-14 days after infection (Trampuz et al., 2003), especially in the non-immune a nd untreated, to cause possibly life-threatening organ or tissue dysfunction. In children iRn enYdemic areas, the common complications are severe anaemia, acidosis, prostration, hypoAglycemia and encephalopathy (convulsions and altered consciousness); these may ocBcur Rsingly or in any combination. For reasons that are poorly understood, but that may be LrelaIted to high intracranial pressure, children with malaria frequently exhibit abnormal posNturin g, a sign indicating severe brain damage (Molyneux et al., 2008). Malaria has been fouAnd to cause cognitive impairments, especially in children. It causes widespread anemiAa. DThis neurologic damage results from cerebral malaria to which children are more v uIlnBerable (Boivin et al 2 0 0 2 and Holding et al 2001). Cerebral malaria is associated with reFtinal whitening (Maude et al 2009), which may be a useful clinical sign in distinguishYing m Oalaria from other causes of severe fever (Beare et al 2006). Non-immune adults mIaTy suffer the same complications but are also liable to develop spleenomegaly (enlarged Sspleen), severe headache, cerebral ischemia, hepatomegaly (enlarged liver), hypoglycemEia, Racute respiratory distress syndrome (ARDS), disseminated intravascular coagulation aInVd intravascular haemolysis giving rise to hemoglobinuria which can cause renal failureU, (rNenal failure may cause black water fever, where hemoglobin from lysed red blood cellsleaks into the urine) (WHO, 2000). Severe malaria can progress extremely rapidly and cause death within hours or days (Trampuz et al., 2003). In the most severe cases of the disease, fatality rates can exceed 20%, even with intensive care and treatment (Kain et al., 1998). In endemic areas, children suffer most of the severe disease, adults being protected by a combination of innate and acquired immunity (Kwiatkowski, 1999). Even in children in endemic 2 1 areas, it is only a minority of infections that progress to severe disease. In endemic areas, treatment is often less satisfactory and the overall fatality rate for all cases of malaria can be as high as one in ten (Mockenhaupt et al., 2004). Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria (Taylor et al., 2004, Carter et al., 2005). Relapsing malaria is seen in both P. vivax and P. ovale, but not in P. falciparum. Here, the disease can relapse months or years after exposure, due to the presence of latent parasRitesY in the liver. Describing a case of malaria as cured by observing the disappearance of paraAsites from the bloodstream can, therefore, be deceptive. The longest relapse period repBortRed for a P. vivax infection is 30 years (Trampuz et al., 2003). Approximately one in fiveL oIf P. vivax malaria cases in temperate areas involve over wintering by hypnozoites (i.e., Nrela pses begin a year after the mosquito bite) (Hulden et al., 2005, Adak et al., 1998). A AD 2.6 Pathogenesis of complicated disease IB Cytoadherence and sequestration F Erythrocytes containing mature stage s Oof P. falciparum adhere to micro-vascular endothelium and thereby accumulate in caIpTillarYies and venules of deep tissues (sequestration). Several lines of evidence suggest that tShe process of sequestration may be important in the pathogenesis of severe disease: (1) EseqRuestration is peculiar to P. falciparum, which is the only plasmodia species causing severIe Vdisease; (2 ) histological samples from various tissues in fatal malaria commonly revealU intNense sequestration of parasitized erythrocytes; (3) sequestration is maximal in thosetissues or organs that are most susceptible to functional impairment in severe falciparum malaria i.e. brain, bone marrow, intestinal mucosa and the lungs (Molyneux et al., 2008). Cytoadherence involves a specific linkage between proteins expressed on the surface of the infected red cell and receptors on host tissues. As the parasite matures in the infected erythrocyte, a family of highly variable parasite genes (‘var’ genes) begin to encode proteins that pass to the surface of the cell, 2 2 where they are collectively known as P. falciparum erythrocyte membrane protein 1 (PfEMP-1) (Beeson and Brown, 2004). Other parasite-derived proteins are similarly expressed on the red cell surface but remain to be characterized. Variability in the PfEMP-1 expressed by a particular population of parasites has been estimated at around 2 % per parasite life cycle, a property that may enable the parasite to evade some of the host’s specific acquired immune responses directed at these proteins. When studied in an in vitro culture, PfEMP-1 expression and spec ific cytoadherence are accelerated and enhanced with elevation of the surrounding temperaturYe from 37° to 40°C, suggesting that fever may have a similar effect in vivo (Molyneux et aAl., 2R008). Host receptors capable of mediating cytoadherence include CD36, ICAM-1, chBondRroitin sulphate A, hyaluronic acid, e-selectin, V-CAM-1 and thrombospondin. ICAML-1 Imay be the principal receptor mediating cytoadherence in the brain, CD36 in mostN oth er tissues and chondroitin sulphate A in the placenta. Cytoadherence of parasitizeDd eArythrocytes resembles that of host leucocytes in that there are rolling and static componAents and it is likely that different receptors mediate each of these processes. Cytokines su cIh Bas TNF-a up-regulate the expression of host endothelial receptors, providing another mecFhanism by which malaria infection enhances its own sequestration. Parasitised erythrocytes cOytoadhere not only to endothelial cells but also to other parasitized erythrocytes, a proIcTessY leading to ‘auto-agglutination’ of infected red cells. In some (not all) instances, plateletSs appear to be a necessary intermediary between adjacent cells. Auto­ agglutination may EaccRount for the appearance of heavily sequestered venules and capillaries, in which parasitIizVed cells towards the centre of the vessel lumen are some distance from the vascuUlar Nendothelium and unlikely to be adherent to it (Wahlgreen et al., 1999). Parasitized erythrocytes may also adhere to uninfected erythrocytes, resulting in the formation in vitro of ‘rosettes’, each consisting of a parasitized red cell surrounded by several uninfected erythrocytes (Chitnis, 2001). Although some studies have shown that parasites with a capacity to form rosettes are more likely than others to be associated with severe disease, this has not been found in all surveys, and rosettes have not been identified in human tissues from patients dying of 23 falciparum malaria, so that the contribution of rosetting to sequestration is uncertain. There is still no incontrovertible evidence that sequestration mediates tissue or organ dysfunction, but the circumstantial evidence is strong. Several mechanisms are plausible and require continued research: ( 1 ) actively metabolizing parasites may ‘rob’ local tissues of ingredients essential to their viability, such as glucose and micronutrients; (2 ) the perfusion of tissues may be impaired by the mass of stationary parasitized red cells; (3) damage can be demonstrated to junctio ns between adjacent endothelial cells, with loss of integrity of the vessel wall (which in theY brain constitutes the ‘blood-brain barrier’) (Taylor et al.,); (4) the eventual rupture of AP. fRalciparum schizont, with the local discharge of merozoites, ‘toxins’ and haemozoin (pBigmRent resulting from the parasite’s digestion of hemoglobin) must provide a large aLddIitional local stimulus. Consequences of this include demonstrable recruitment of leucoNcyt es, deposition of fibrin and platelets, and the induction of nitric oxide synthase (iNOS), wAhich suggests that nitric oxide, may be generated locally (Molyneux et al., 2008). It is AcleaDr that sequestration commonly has no detectable adverse effect on tissue or organ fu ncItBion, because sequestration is also a feature of uncomplicated falciparum malaria (no lOate-sFtage parasites are visible in the peripheral blood). It remains to be determined whethYer i mpaired tissue function results when there is an over whelming mass of sequesteIreTd parasites or from a crucial distribution or quality of the sequestered cells. S Cytokine responseEs R Cytokines meIdViate the characteristic fever of malaria, as of other infections (discussed above). WhethUer cNytokines are essential to the pathogenesis of severe and fatal disease remains a subjectof important inquiry (Molyneux et al., 2008). Several studies have demonstrated an association between circulating cytokine concentrations (TNF, IL-1, IL-6 , IL-8 ) and disease severity, but whether this association is causal and if so in which direction remains to be elucidated. A large randomized controlled trial of recombinant anti-TNF in West African children with malarial coma demonstrated an anti-fever effect but no benefit to survival. This however does not 24 disprove a role for TNF in pathogenesis of fatal disease, as the intervention may have been too late or in other ways ineffectual (Grau et al., 2003). A lot of studies using drugs that ameliorate cytokine responses such as pentoxyfilline, have so far failed to provide evidence that such drugs prevent or reverse severe disease. Several problems make it difficult to study the role of cytokines in the pathogenesis of fatal malaria. There is no readily available animal model of severe falciparum malaria. Malaria in common animal models have different pathology; trials of anti-cytokine treatments in patients with severe malaria may enroll subjects after cruciRal dYamage has already been done and important cytokine effects may occur locally in tissues Anot accessible to study during life (Molyneux et al., 2008). Similar problems surrounBd thRe study of other mediators and downstream effects of cytokine activity. LIN Severe anaemia A A degree of anaemia develops in most malaria infeActioDns, and severe anaemia (packed cell volume 15% or less, hemoglobin concentration 5I gB/dl or less) is a common and important single complication, especially in infants and todFdlers in endemic areas (Orimadegun et al., 2007, Anumudu et al., 2007). Mechanisms t haOt may contribute to the development of anaemia include ( 1 ) the destruction of red ceIllsT byY parasites at schizont rupture; (2 ) reduced life span of un­ parasitized erythrocytes, pSossibly resulting from cross-reacting antibodies developed against the surface of parasitiEzedR cells - increased splenic clearance of un-parasitized red cells can be demonstratedI dVuring malaria; and (3) impaired bone marrow function, as dyserythropoiesis is visiblUe onN light microscopy of bone marrow smears and reticulocytes are absent from the peripheral blood even when anaemia is severe (Molyneux et al., 2008). Sequestration of parasitized erythrocytes in bone marrow sinusoids is a common finding and it seems likely that dyserythropoiesis is mediated by altered local cytokine secretions. Some studies suggest that in severe anaemia there is a relative deficiency of the IL-10 response that normally modulates TNF activity (Miller et al., 2002). It is possible that haemozoin, released with rupture of schizont- 25 infected red cells, is toxic to the macrophages that consume it, with consequent deficient secretion of IL-12, leading to impaired generation of a TH1 host response. This impairment of macrophage function may partially explain the increased occurrence of non-typhoid salmonella infections observed in children with severe malarial anaemia (Graham et al., 2000). Coma and convulsion In an individual with altered consciousness and P. falciparum parasitaemia, several possibilit ies must be considered: ( 1 ) the illness may have another cause, with incidental parasitaemRia, thYis is a strong possibility in populations having a high prevalence of asymptomatic parasitAaemia; (2 ) the patient may be having a seizure, sometimes extraneous movements are notB obvRious, and the true nature of the event is revealed by electro-encephalography: malaria fevLerI is particularly likely to precipitate a febrile convulsion in infants and young children, aNnd more complex seizures are also common in malaria in this circumstance, consciousneAss may be regained within a few minutes or hours after the seizure stops or is treated; (3A) thDe patient may be in the post-ictal phase after a recent convulsion again, recovery of con sIcBiousness may then be imminent; (4) there may be a metabolic complication of malaria, suchF as hypoglycemia; or (5) the disease may have none of the foregoing explanations and be dOirectly due to P. falciparum infection (Molyneux et al., 2008). Mechanisms by which IinTtraY cerebral sequestration may contribute to encephalopathy have been discussed above. ISn considering the likely pathophysiology of malaria coma, two observations must Ebe rRecognized: (1) about 90% of children and 95% of adults who recover from a malaria coImVa do so without detectable neurological sequelae: whatever the principal mechaUnismNs of coma, they do not generally produce irreversible damage to brain tissue; (2 )conversely, 10% of children and 5% of adults who recover consciousness have detectable neurological sequelae, and these are often accompanied by areas of infarction demonstrable by computed tomography of the brain (Grau et al., 2003). It is likely that coma is usually the result of a diffuse impairment of cerebral function related to sequestration and that sequelae result in a minority of cases when a vessel or group of vessels become secondarily obstructed by parasites, 26 pigment and fibrin deposition, leading to localized infarction (Grau et al., 2003). In the majority of children with ‘cerebral malaria’, the opening pressure of the cerebrospinal fluid is high. Papilloedema is occasionally found and is associated with a poor prognosis. At autopsy, brain weights tend to be higher than appropriate for the child’s age and weight, and flattened gyri and filled sulci suggest that the brain has been swollen within the skull. All these features suggest that cerebral oedema is a common component of the pathology of fatal cerebral malaria (Tay lor et al., 2004). Frank herniation of brain between compartments is, however, rarelyR foYund at autopsy in a patient dying of malaria coma. RAB Hypoglycemia LI Children with malaria of vary grade commonly have hypoglycemNia, b ut correction of the plasma glucose concentration with a dextrose infusion rarely rAestores consciousness, suggesting additional causes of coma (Molyneux et al., 2008). HyApogDlycemia in these circumstances may be due to a combination of reduced hepatic glyc oIgBen reserves, inhibition of hepatic glucuronyl transferase (and therefore of gluconeogenesFis) by cytokines and anaerobic glycolysis in hypoxic or under perfused tissues (Maitland et aOl., 2003). Plasma insulin concentrations are appropriately low. Hypoglycemia may alsoI dTevYelop through a different mechanism in individuals especially pregnant women who are Sreceiving treatment with quinine. This drug is a potent stimulus to the secretion of insulinE froRm the pancreatic beta cells, which have increased activity and sensitivity in pregnancy,I aVnd plasma insulin concentrations in this circumstance are higher than appropriate for theU plaNsma glucose concentration. 27 Acidosis Often indicated clinically by the patient’s characteristically deep breathing, acidosis may be largely the result of impaired tissue oxygenation through a combination of anaemia, hypovolaemia and impaired tissue perfusion and metabolism in the presence of sequestered parasites (Maitland et al., 2003). Acute renal failure RY Rarely seen in children in malarious areas, acute renal failure is a grave and qAuite common complication of falciparum malaria in non-immune adults. It developBs iRn the context of hypovolaemia and hypotension that may follow fluid losses th roLugIh anorexia, vomiting, sweating and hyperventilation (Maitland et al., 2003). ClinicalNly and histopathologically, the underlying event is acute tubular necrosis, and recovery is uAsual within a few days or weeks if the patient survives the illness and is appropriately diaAlyzeDd (Molyneux et al., 2008). IB Disseminated intravascular coagulation F An overt bleeding tendency in severe m Oalaria is uncommon (rare in children), but some degree of activation of the coagulation IcTascaYde is usual and some degree of thrombocytopenia is almost invariable. In most patienSts with symptomatic malaria, plasma antithrombin III concentrations are low, in assocEiatioRn with increased plasma levels of thrombin-antithrombin III. Platelet survival is redIuVced and bone marrow appearances suggest dyspoietic thrombogenesis (Miller et al., 2U002N). Intravascular deposition of platelets can be demonstrated in sites of intense sequestration, sometimes in association with micro-thrombi (Warrell and Gilles, 2002). Pulmonary oedema and acute respiratory distress syndrome (ARDS) These two complications may resemble each other clinically and radiologically but have a different pathogenesis. Pulmonary oedema may follow excessive infusion of fluids, especially in 28 the presence of impaired renal function (Maitland et al., 2003). In ARDS, there has not been over-hydration, and pulmonary wedge pressures are low or normal. Histology indicates the presence of both parasitized red cells and leucocytes in pulmonary micro-vessels. This condition is uncommon in children and is often fatal when it occurs in adults (WHO,2000, Molyneux et al., 2008). 2.7 HIV and malaria RY Although co-infection with HIV and malaria does cause increased mortality, thAis is less of a problem than with HIV/tuberculosis co-infection, due to the two diseaBses Rusually attacking different age-ranges, with malaria being most common in the young a nLd aIctive tuberculosis most common in the old (Korenromp et al., 2005). Although HIV/maNlaria co-infection produces less severe symptoms than the interaction between HIV and TB,A HIV and malaria do contribute to each other's spread. This effect comes from malariaA inDcreasing viral load and HIV infection increasing a person's susceptibility to malaria in feIcBtion (Abu-Raddad et al., 2006).F 2.8 General treatment guidelines O When a patient in or from a mIalTarioYus area presents with fever, a blood smear should be prepared and examined to confirmS the diagnosis and identify the species of infecting parasite. The management of maElariRa depends very much on the health facilities available and the endemicity of the diseaseI,V i.e. the likely immune status of the patient. For example, in areas of intense transmissiNon asymptomatic parasitaemia is common in older children and adults, and fever is more Ulikely to be the result of some other infection. On the other hand fever may precede detectable parasitaemia in non immune adults or young children. Patients with severe malaria or those unable to take oral drugs should receive parenteral anti malarial therapy. If there is any doubt about the resistance status of the infecting organism, then quinine, quinidine or artemisinin combination therapy (ACT) should be given. If the temperature is high on admission (greater 29 than 38.5oC) then symptomatic treatment with antipyretics and tepid sponging brings symptomatic relief, and also reduces the likelihood that the patient will vomit the oral anti- malarials. This is particularly important for young children. Several drugs are available for oral treatment, and the choice of drug depends on the likely sensitivity of the infecting parasites. Chloroquine and amodiaquine used to be the treatment of choice for the benign human malarias. This has been abandoned for the newer ACTs like artemether + lumefantrine (co-artem ), Artesunate + Amodiaquine, Artesunate + mefloquine and ArtesRunatYe + sulfadoxine/pyrimethamine due to the development of resistance by the parasite (AFMOH, 2005, Obionu, 2007). BR In uncomplicated malaria: Infections due to P. vivax, P. malariLae,I P. ovale and known sensitive strains of P. falciparum should be treated with oral sulfaNdox ine/pyrimethamine (Ross et al, 2008). A Patients should be monitored for vomiting for 1 hAourD after the administration of any oral antimalarial drug. IB Symptom based treatment with tepid sOpongFing and acetaminophen administration lowers fever and thereby reduces the patient’s Yprop ensity to vomit these drugs (WHO, 2001). Minor central nervous system reactions (naIuTsea, dizziness, and sleep disturbances) are common. Pregnant women, young children, pSatients unable to tolerate oral therapy and non immune subjects (e.g. travelers) with suspEectRed malaria should be hospitalised. If there is anyI Vdoubt as to the identity of the infecting malarial species, treatment for falciparum malarUia sNhould be given. A negative blood smear does not rule out malaria; thick blood films should be checked 1 and 2 days later to exclude the diagnosis. Non immune subjects with malaria should have daily parasite counts performed until negative thick films indicate clearance of the parasite. If the level of parasitaemia does not fall below 25 percent of the admission value at 48 hours or if the parasitaemia has not cleared by 7 days (and 30 compliance is assumed), drug resistance is likely and the regimen should be changed (WHO, 2 0 0 1 ). In severe malaria: Severe falciparum malaria constitutes a medical emergency requiring intensive nursing care and careful management. The patient should be weighed and if comatose, placed on his or her side and given a single parenteral dose of phenobarbital (5 to 20 mg/ kg) to prevent convulsions especially in children. Frequent evaluation of the patient’s condition is essential. The choice of antimalarial drug depends on knowledge of the prevailing senRsitiYvity of P. falciparum to anti-malaria (Ross et al, 2008) and if there is any doubt, quinAine should be given. The optimal therapeutic range for quinine in severe malaria is not kBnoRwn with certainty, but total plasma concentrations between 8 and 2 0 mg/ml are effectiveL anId do not cause serious toxicity. An initial loading dose should be given so that therapeutNic co ncentrations are reached as soon as possible. If the patient remains seriously ill or in acAute renal failure for more than two days, the maintenance dose should be reduced by 30 tAo 50D percent to prevent toxic accumulation of the drugs. The initial doses should never be reIdBuced if chloroquine is given, dose reduction is unnecessary even in renal failure (WhOite, F2005). Provided that it can be performed safely,exchange transfusion is indicatedY for patients with high level parasitaemia (greater than 15percent) and vital organ dysfuInTction. Exchange transfusion should be considered for severely ill patients with a level of parSasitaemia between 5 and 15 percent (Brema et al., 2006). When patient is uEncoRnscious: The blood glucose level should be measured every 4 to 6 hours, and values bIelVow 40mg/dl indicate prompt treatment with intravenous dextrose. All patients treated wNith intravenous quinine should receive a continuous infusion of 5 to 10 percent dextroUse. The parasite count and hematocrit level should be measured every 6 to 12 hours. Anaemia develops rapidly; if the hematocrit falls below 2 0 %, then whole blood (preferably fresh) or packed cells should be transfused slowly, with careful attention to circulatory status and judicious use of a small dose of a diuretic to prevent fluid overload. Exchange transfusion should be strongly considered for patients with a high level of parasitaemia (greater than 1 0 %) and 31 altered mental status. Renal function should be checked daily. Management of fluid balance is difficult in severe malaria because of the thin dividing line between over hydration (leading to pulmonary oedema) and under hydration (contributing to renal impairment). If necessary, pulmonary artery occlusion pressures should be measured and maintained in the low normal range. As soon as the patient can take fluids, oral therapy should be substituted for parenteral treatment (Gilles, 2002). In acute renal failure: If the level of blood urea nitrogen or creatinine rises despiteR adYequate rehydration, fluid administration should be restricted to prevent volume overloaAd. Even with adequate peritoneal dialysis, secondary bacterial infections are common in tBhe tRropics, and hemo­ dialysis and hemo-filtration are preferable. Some patients will passL smI all volumes of urine sufficient to allow control of fluid balance; these cases can be mNana ged conservatively if other indications for dialysis do not arise (Warrell and Gilles, 2002)A. Renal function usually improves within days, but full rAecoDvery may take weeks. In other complications: Patients who develop spIoBntaneous bleeding should be given fresh blood and intravenous vitamin K. ConvulOsionFs should be treated with intravenous or rectal benzodiazepines. Aspiration pneuYmon ia should be suspected in any unconscious patient with convulsions, particularly withI pTersistent hyperventilation. Intravenous antimicrobial agents and oxygen should be adminisStered, and pulmonary toilet should be undertaken. Hypoglycaemia or gram negative seEpticRaemia should be suspected and treated when any patient suddenly deteriorates foIrV no obvious reason while receiving anti-malaria treatment.N 2.9 MUalaria parasite life cycle The life cycle of the parasite in the mosquito take about 12 days to complete, depending on the atmospheric temperature (optimum temperature is 17°C to 80°C). The incubation period in mosquito which is the interval elapsing from the ingesting of infected blood by the mosquito to the appearance of sporozoites in the saliva of the mosquito is known as the extrinsic incubation 32 period. The pre-latent period (intrinsic incubation period) is the time which elapses between the infection of man by the sporozoites and the first appearance of erythrocytic parasites in the blood and this is usually 6 - 9 days except in P. malariae in which it can range from 13 - 16 days. Thereafter symptoms of malaria appear as the parasitaemia builds up (Molyneux et a l, 2008). The life cycle of malaria parasite (plasmodium) takes place partly in the mosquito - sexual phase and partly in man - the asexual phase. Infection is initiated when the female Anopheles mosqu ito inoculates sporozoites into the body during a blood meal. In all the four species of PlaRsmoYdium, the sporozoites after a few hours (usually 30 minutes to one hour) invade the liveAr parenchyma cells to form the primary tissue schizont or pre-erythrocytic or (the primBaryR exo-erythrocytic) liver schizont. When mature, the liver cells rupture liberating thousaLndIs of merozoites which invade the red blood cells. N In P. ovale and vivax, the pre-erythrocytic schizonts produDce, Ain addition to the blood merozoites,other merozoites which invade more liver cells (secAondary exo-erythrocytic phase) to liberate more merozoites into the blood stream. Th eIsBe merozoites resulting from the secondary (persistence) liver phase (the hypnozoites) aFre responsible for relapse at a later stage (Cogswell, 1992). Some of these asexual forms Oof the parasite in the red blood cells differentiate to trophozoites, appearing first IaTs riYng trophozoites and later develop to form mature schizont containing daughter merSozoites (erythrocytic schizont). The red cells rupture releasing merozoites and initEiatiRng clinical attack (Obionu, 2007). Clinical symptoms are thus produced by the rupture oIf Vlarge numbers of erythrocytic schizont. The asexual cycle last approximately 48 hoursU in PN. falciparum, ovale and vivax and 72 hours in P. malariae. Some of the asexual cells inthe red blood cells differentiate into sexual forms called gametocytes. The gametocytes in the infected red blood cells serve as source of infection when they are picked up by mosquitoes during blood meals. In the mosquito, the gametocyte escapes from the containing red blood cells and mature into male and female gametes (micro and macro-gametes). Fertilization takes place giving rise to ookinate, then oocyst. The oocyst undergoes some mitotic division producing large 33 numbers of sporozoites, the infective parasitic forms. These are however found in all parts of the insect body, some eventually reaching the salivary glands from where they are injected with the saliva into the human host (Obionu, 2007). 2.10 Vector The epidemiology of malaria results from the demands of its life cycle, which requires reservo irs of infected and uninfected humans, competent anopheline vectors, and multiple opportRunitYies for contact between the vector and its human host. Vectors are insects, which transmAit infection by biting or by depositing infected material on the skin, food or other objectBs VRectors for malaria are female Anopheles mosquitoes. Vectors differ considerably in LtheIir natural abundance,feeding, and resting behaviours, breeding sites, flight rangesN, choice of blood source and vulnerability to environmental conditions and insecticides MAalaria is often seasonal, coinciding with the rainy season which provides water for mAosqDuito breeding and increased humidity favoring mosquito survival For transmission of mIBalaria, the mosquito must live at least 10 days after an infective blood meal during which itF must bite a susceptible human host. Mosquito from the Spanish meaning l ittOle fly is a common insect in the family Culicidae (from the Latin culex meaning midgIe Tor Ygnat) (Brown, 1993). Mosquitoes resemble crane flies (family Tipulidae) and chironomSid flies (family Chironomidae), with which they are sometimes confused by the caEsualR observer. Mosquitoes go through four stages in their life cycle: egg, larva, pupa, and aduIlVt or imago. Adult females lay their eggs in water, which can be a salt-marsh, a lake, Ua puNddle, a natural reservoir on a plant, or an artificial water container such as a plasticbucket. The first three stages are aquatic and last 5-14 days, depending on the species and the ambient temperature; eggs hatch to become larvae, then pupae. The adult mosquito emerges from the pupa as it floats at the water surface. Adults live for 4-8 weeks (Western County Department of health, 2010). Mosquitoes have mouthparts which are adapted for piercing the skin of plants and animals. While males typically feed on nectar and plant juices, the female 34 needs to obtain nutrients from a "blood meal" before she can produce eggs. There are about 3,500 species of mosquitoes found throughout the world (Leisnham, 2010). In some species of mosquito, the females feed on humans, and are therefore vectors for a number of infectious diseases affecting millions of people per year (Molavin, 2003; American Mosquitoes Control Association, 2008). All forms of human malaria are transmitted in nature by the bites of Anopheles mosquito thou gh other forms of infections seldom occur i.e. transfusion of blood containing erythrocytiRc phYase of the parasite (transfusion malaria) or even from mother to child through the placenAta (congenital malaria). The major vectors of human malaria are Anopheles gambiae, ABnopRheles arabiensis, Anopheles Junestus and Anopheles melas. Anopheles arabiensis arLe Imost dominant in the savannah and cities while Anopheles gambiensis are found mainNly in the forested regions of the tropics. Anopheles Junestus are unevenly distributed while AnAopheles melas are found in coastal areas as it has a high affinity for salty waters. The feAmalDe mosquito get infected when it ingest human blood containing male and female game toIcBytes (Warrell and Gille, 2 0 0 2 ). Mosquitoes of different species lay their eFggs in a variety of water sources that range from small containers to vast expanses Yof m a Orshland. The larval stage is always aquatic and shuttles from the subsurface where itI fTilters feeds on micro-organisms to the surface to obtain oxygen through a snorkel-like breSathing apparatus. The pupa stage does not feed but unlike most Insect pupae is extremelyE actRive. The adult emerges from the pupa case using air pressure and assume a terrestrial eIxiVstence. MosqUuitoN larvae have a well-developed head with mouth brushes used for feeding, a large thorax with no legs and a segmented abdomen. Larvae breathe through spiracles located on the eighth abdominal segment, or through a siphon, and therefore must come to the surface frequently. The larvae spend most of their time feeding on algae, bacteria, and other micro-organisms in the 35 AR Y LIB R N AD A Fig 1: Life cycle of the fe mIaBle Anopheles mosquitoF Y O IT ER S IV UN 36 Y ARR LI B DA N BA I O F SI TY VE R NI FUig 2: The sexual and asexual life cycle of Plasmodium specie in man and mosquito surface micro-layer. They dive below the surface only when disturbed. Larvae swim either through propulsion with the mouth brushes, or by jerky movements of the entire body, giving 37 them the common name of "wigglers" or "wrigglers". Larvae develop through four stages, or instars, after which they metamorphose into pupae. At the end of each instar, the larvae molt, shedding their exoskeleton, or skin, to allow for further growth. The pupa is comma-shaped, as in Anopheles when viewed from the side, and is commonly called a "tumbler". The head and thorax are merged into a cephalothorax with the abdomen curving around underneath. As with the larvae, pupae must come to the surface frequently to bYreat he, which they do through a pair of respiratory trumpets on the cephalothorax. HoweAverR, pupae do not feed during this stage. After a few days, the pupa rises to the water surface,R the dorsal surface of the cephalothorax splits and the adult mosquito emerges. The pupa is leIssB active than larvae.. L Mosquitoes can develop from egg to adult in as little as five days Nbut usually takes 10-14 days in tropical conditions. The duration from egg to adult variDes cAonsiderably among species and is strongly influenced by ambient temperature. The variAation of the body size in adult mosquitoes depends on the density of the larval population aIndB food supply within the breeding water. Adult flying mosquitoes frequently rest in a tunneFl that they build right below the roots of the grass. Adult mosquitoes usually mate wi OYthin a few days after emerging from the pupa stage. In most species, the males form large IsTwarms, usually around dusk, and the females fly into the swarms to mate. Males live foRr aboSut a week, feeding on nectar and other sources of sugar. Females will also feed on sugarE sources for energy but usually require a blood meal for the development of eggs. After oIbtVaining a full blood meal, the female will rest for a few days while the blood is digestUed aNnd eggs are developed. This process depends on the temperature but usually takes 2-3 days in tropical conditions. Once the eggs are fully developed, the female lays them and resumes host seeking. The cycle repeats itself until the female dies. While females can live longer than a month in captivity, most do not live longer than 1 -2 weeks in nature. Their lifespan depends on temperature, humidity, and also their ability to successfully obtain a blood meal while avoiding host defenses. Length of the adult varies but is rarely greater than 16 mm (0.6 in) (Virginia Tech, 38 2007) and weight up to 2.5 mg (0.04 grain). All mosquitoes have slender bodies with three sections: head, thorax and abdomen. The head is specialized for acquiring sensory information and for feeding. The head contains the eyes and a pair of long, many-segmented antennae. The antennae are important for detecting host odors as well as odors of breeding sites where females lay eggs. In all mosquito species, the antennae of the males in comparison to the females are noticeably bushier and contain auditory receptors to detect the characteristic whine of the fema le. The compound eyes are distinctly separated from one another. Their larvae only posRsessY a pit- eye ocellus. The compound eyes of adults develop in a separate region of the heaAd (Harzsch et al., 2006). New ommatidia are added in semicircular rows at the rear of thBe eyRe; during the first phase of growth, this leads to individual ommatidia being square, but LlatIer in development they become hexagonal. The hexagonal pattern will only become viNsible when the carapace of the stage with square eyes is molted (Harzsch et al., 2006). The hAead also has an elongated, forward- projecting "stinger-like" proboscis used for feeding, aAnd tDwo sensory palps. The maxillary palps of the males are longer than their proboscis wIhBereas the females’ maxillary palps are much shorter. (This is typical for representativeFs of subfamilies.) As with many members of the mosquito family, the female is equip pOed with an elongated proboscis that she uses to collect blood to feed her eggs. The thIoTrax Yis specialized for locomotion. Three pairs of legs and a pair of wings are attached to theS thorax. The insect wing is an outgrowth of the exoskeleton. The Anopheles mosquiEto cRan fly for up to four hours continuously at up to 1-2 km/h (Kaufmann et al., 2004), traIvVelling up to 12 km (7.5 miles) in a night. The abdomen is specialized for food digestUion Nand egg development. This segmented body part expands considerably when a female takes a blood meal. The blood is digested over time serving as a source of protein for the production of eggs, which gradually fill the abdomen. 39 2.10.1 Distribution While many species are native to tropical and subtropical regions, some such as Aedes have successfully adapted to cooler regions. In the warm and humid tropical regions, they are active the entire year long; however, in temperate regions they hibernate (over winter). Eggs from strains in the temperate zones are more tolerant to the cold than ones from warmer regions (Hawley et al., 1986; Hanson et al., 1995). They can even tolerate snow and temperaturesY un der freezing conditions. In addition, adults can survive throughout winter in suitable micRrohabitats (Romi et al., 2006). BR A 2.10.2 Means of dispersal LI Over large distances the worldwide distribution is carried oAut pNrimarily through sea routes, in which the eggs, larvae, and pupae in combination with waDter-filled used tires and cut flowers are transported around. As with sea transport, the ItBrans Aport of mosquitoes in personal vehicles, delivery trucks, and trains plays an importanFt ro le. 2.11 Malaria control OY Malaria is entrenched in StheI Ttropical part of the world because of three main factors viz, (environmental factorRs, biological factors and human related factors). We will be able to effectively conVtrolE and possibly eliminate malaria from our world only when we have a good understanNdingI of how these factors interact. The current thinking in tackling malaria is the curatiUve, preventive and vector control approach. Curative approach: This is focused on making early diagnosis treating all infected persons with the right drugs preferably the ACTs and at the right dosage so as to prevent the development of resistance to the drugs by the parasites. 40 Y ARR LI B N AD A IB Fig 3: Conceptual model of important riskF fa ctors affecting malaria prevalence in the tropics and points of control efforts Y O Preventive approach: This IimTplies the use of anti malaria drugs to prevent malaria before infection occurs or beRforeS it becomes obvious. The aim is to prevent the occurrence of the disease by acting oEn the parasites while still confined to the liver (causal or true prophylaxis) or to prevent anIy Vof the disease symptoms by suppressing the number of malaria parasites in the bloodU to sNuch a low level that they will not cause any clinical symptoms (clinical prophylaxis or suppression). In highly endemic areas, the use of chemoprophylaxis is limited to people who are at high risk from severe and complicated malaria (pregnant women, persons with sickle cell disease and non immune visitors or residents). 41 Integrated vector control: Vector control aims at eliminating or reducing the mosquito population through chemical control using insecticides, environmental control, personal protection (barrier) and biological control. Vector control AR Y BR N LI A Fig 4: Larvae in stagnAant Dwater F I B There are many methods used for mOosquito control. Depending on the situation, source reduction, bio-control, larvicideTs toY kill larvae, or specifically the adults may be used to manage mosquito populations. ThSese Itechniques are accomplished using habitat modification, such as removing stagnant wRater and other breeding areas, pesticide like Dichloro-diphenyl- trichloroethanIeV (DD ET), natural predators, (e.g. Dragonflies, larvae-eating fish), and trapping. OrgaUnic Nrepellents With increasing reports of the harmful effects V,V-Diethyl-weta-toluamide, abbreviated (DEET) has on humans, there has been a gradual move to rely on repellents that are devoid of it, specifically to repellents that are organic and otherwise are of the kind that have had traditional 42 household purposes prior to their becoming used now more often as mosquito repellents (Agency for Toxic Substance and Disease Registry, 2004). Natural predators AR Y R IB Fig 5: Dragonflies are natural predators of mNosqu it Loes DA The dragonfly nymph eats mosquitoes at all stIaBges Aof development and is quite effective in controlling populations (Singh et al., 2003). FAlt hough bats and Purple Martins can be prodigious consumers of insects, many of which aOre pests, less than 1 % of their diet typically consists of mosquitoes. Neither bats nor PTurpYle Martins are known to control or even significantly reduce mosquito populations (FrSadinI, 1998). Some cyclopoid copepods are predators on first instars larvae, killing up to 4R0 Aedes or Anopheles larvae per day (Marten et al., 2007). Larval of ToxorhynchiteIsV mo Esquitoes are known as natural predators of other Culicidae. Each larva can eat an averagNe of 10 to 20 mosquito larvae per day. During its entire development, a Toxorhynchites larva Ucan consume an equivalent of 5,000 larvae of the first instar (L1) or 300 fourth instar larvae (L4). However, Toxorhynchites can consume all types of prey, organic debris, or even exhibit cannibalistic behavior. A number of fish are also known to consume mosquito larvae, including bass, bluegill, piranha, catfish, fathead minnows, the western mosquito-fish (Gambusia affinis), 43 goldfish, guppies, and killifish Bacillus thuringiensis israelensis has also been used to control them as a biological agent. 2.12 Malaria elimination Recent data shows that large-scale use of WHO recommended strategies could rapidly reduce malaria, especially in areas of high transmission such as Africa. WHO and Member States ha ve made significant gains in malaria elimination efforts. For example, the Maldives, Tunisia aYnd the United Arab Emirates have eliminated malaria. Country successes are due to inAtensRe national commitments and coordinated efforts with partners. BR Community mobilization and education have been part of efforts aime dL atI achieving the efforts to eliminate malaria. There have equally been global efforts to eliNminate malaria such as the Roll Back Malaria Initiatives. DAA Roll Back Malaria Initiative IB The World Health Organization in 1998 decFlared malaria control one of its priority assignments and announced the introduction of Ya ne w O initiative- the Roll Back Malaria (RBM) initiative. The RBM was a global health sectIorT wide partnership approach to combat malaria worldwide, using available knowledge, skillSs and tools to launch a new concerted effort against the disease. The general objective oEf thRe initiative is to reduce malaria burden by 50% by 2010 and to halve it again in the foIlVlowing five years through interventions adapted to local needs and by reinfoUrcemNent of the health sector.The specific objectives are: - To increase to 60% the use of insecticide treated bed nets (ITN) by pregnant women and children under-five years of age. - To ensure that 60% of children under five receive appropriate treatment within 24 hours of onset of illness. 44 - To ensure that at least 60% of all pregnant women at risk of malaria will have full intermittent preventive treatment. - To develop an effective environmental management strategy for RBM (integrated vector management) Also the six elements of the RBM strategy are; prompt diagnosis and treatment, multiple prevention strategies, well coordinated effort, dynamic global partnership, effective management and evidence based responses and to have focused research on malariaR.. Y RA LIB AN AD F I B O ITY ER S V UN I 45 CHAPTER THREE 3.0 SUBJECT AND METHODS / METHODOLOGY 3.1 Background of study area Abia state is located in the southeastern region of Nigeria. Umuahia North is one of the 17 Local Government Area (LGA) of the state and it has situated in it Umuahia town which Yis the administrative capital of Abia State. The inhabitants are basically Ibos whose main Roccupation includes civil service, petty trading and subsistence farming. It has a total popuRlatiAon of 240,537 and under - five populations of 48,108. The vegetation of this town aInBd the heavy rain fall encourage the breading of mosquitoes. Though malaria is endemic in tLhe area, its transmission is highest at the peak of the rainy seasons (March - July). AN There are 31 PHC facilities, 1 secondary health facilAity, D1 tertiary health facility and about 50 private health facilities in the Local GovernmenIt BArea. Only 17 of the 31 PHC facilities in the LGA render at least the essential three chilFd h ealth services (growth monitoring, immunization and sick child consultations) out of th eO full range of child health services (growth monitoring, immunization, nutrition and brTeasYt feeding support services, oral rehydration and treatment of common childhood illnessSes).I Six of these 17 PHC facilities are in the urban area (metropolis) while the remaining 11R are in the suburb. The PHCs are manned by health workers ranging from community heaVlth Enurses, registered nurses/midwives and health extension workers. Just like in other partNs ofI Africa, the people would prefer to patronize the medicine vendors and would only presenUt at the health centres when the illness becomes very severe. 3.2 Study Design This is an analytical cross sectional study. 46 3.3 Study Period This study was carried out between April 2010 and June 2010. 3.4 Selection of the facilities Umuahia North LGA was chosen out of the 17 LGAs that make up Abia State because of its’ accessibility and patients turn over rate at the health care facilities been the administrative capital of Abia State. Four PHC facilities were selected from the 17 PHC facilities rendering the th ree essential child health services in the LGA using a three stage (multistage) randomR saYmpling method. Stratification was by rural and urban location. Two health facilities were Aselected from the six urban PHCs using a table of random numbers and two PHCs from thBe 11R PHC facilities in the rural PHCs using the same table of random numbers. All the fac ilLitieIs render essentially the same services. AN 3.5 Study Population AD (i) Umuahia North LGA PHC coordina toIr B(1 person). (ii) Caregivers of under-five chilOdrenF presenting at the selected PHCs(iii) Under- five children preYsen ting with febrile illness at the selected PHCs(iv) Heads of the selectIeTd PHC facilities (4 persons).S Inclusion criteria:E AnRy under five child who presented in the selected four health facilities in Umuahia NorIthV LGA, with fever (Children who were found to be febrile, with a temperature > 38.0°CU) oNf at least 2-3 days duration with or without vomiting, chills and rigors in the absence of runny nose, measles, abscess, ear ache or signs and symptoms of any other well known causes of fever and who received medication for malaria in the health facilities or purchase from the chemist shop within 24 hrs of consultation either as an in-patient or out-patient and it is possible to asses the child’s response 48 hrs after treatment through direct observation either in the hospital (in-patients) or at home (out-patients). 47 Exclusion criteria: Any under five child presenting at the selected health facilities in Umuahia North LGA, with fever (Children who were found to be febrile, with a temperature > 38.0°C) of at least 2-3 days duration with or without vomiting, chills and rigors that is associated with runny nose, or other known causes of fever or children meeting our case definition of malaria who could not get their drugs within 24hrs of consultation or where it is not possible to assess the child’s response to treatment after 48 hrs either in the clinic or at home or where there was risk to the child (i.e. a life-threatening illness that required immediate treatment and evacuRatioYn to a specialized hospital). A 3.6 Sample size determination BR The sample size was calculated using the formula (reference) LIz2pq N n = ___________ X 2 DAd2 A Where P = Proportion of < 5 yrs childr enI Bwith good treatment outcome after 48 hrs of commencing treatment. (This was 79%O frFom a pilot study we done in 2 PHC facilities in Umuahia). q = 1 0 0 - p SI TY d = 0.5 z = SEtanRdard normal deviate at 95% confidence interval (1.96) (Where 2 is aI mVultiplication factor for the design effect, in order to increase our precision to get minimUal vNariance since the study is not a prevalence study and we would be doing a lot of comparisms and sub group analysis. 1.962 x 7 9 x 2 1 ___________ X 2 = 510 n = 52 48 The anticipated non response is 10% (Abubakar, 2006) = 10/100 x 510 = 51.0 (510 + 51 = 561) (rounded up to an even number of 562). 562 questionnaires would be administered on care givers and similar number of children would be examined clinically for signs and symptoms of un-complicated as well as complicated malaria (anaemia, jaundice, convulsion, severe vomiting, and dehydration among other). 3.7 Sampling technique RY Stratified sampling technique (using proportionate allocation) based on the averaAge number of children who made use of the child health services in the last two monthBs (FRebruary - March 2010) at the four selected PHCs was used to select the number of childLrenI to be examined as well as the number of care givers to be interviewed in each facility. N The number of children who attended the four selected PHDCs Abetween February and March 2010were; A Ojike street PHC (Urban)-------------------------- --I--B------------------- 780 World Bank Housing Estate PHC (UrbaOn)--F---------------------------330Amaogwugwu PHC (Rural)------------- --------------------------------- 270 Umuawa-Alaocha PHC (RuraIl)T ---Y-------------------------------------- 600 Total-------------------------S----------------------------------------------- 1980 ER = Average patieVnts seen in Ojike street PHC from February - March 2010 ___________I__________________________________________ X 562 TotaUl paNtients seen in all four selected PHC from February - March 2010 (i.e. Ojike Street, Amaogwugwu, Umuawa-Alaocha and World Bank Housing estate PHCs) Doing same for each PHC gave the number of caregivers of under-five children with presumed malaria cases interviewed at each facility as well as the number of children to be examined. 49 (a) For Ojike street PHC; the average monthly attendance was 780 and the total average monthly attendance for the 4 PHC facilities was 1980. So, the number of caregivers interviewed as well as the number of children to be examined were; 780 ________ X 562 = 221 1980 (b) For World Bank Housing Estate PHC; Y 330 ________ X 562 = 94 R 1980 RAB (c) For Umuawa-Alaocha PHC; LI 600 __________ X 562N = 170 1980 DA (d) For Amaogwugwu PHC; IB A 270 ____________ F X 562 = 77 1980 O On the whole 562 children/caregivYers were enrolled at the minimum. Since patient attendance aSt theI P THC facilities are a floating population, all caregivers who brings an under-five child wiRth fever that meet our inclusion criteria at the four selected PHC facilities during the stuVdy Eperiods were recruited consecutively after informed verbal consent was obtained, Ntill tIhe allocated sample to each facility was obtained. 3.8 DUata collection tools/instrument The following tools, (a) interviewer administered structured questionnaires for exit interviews of caregivers. (b) Guided (structured) key informant interviews for health care facility head and the PHC coordinator of Umuahia North LGA. (c) Assessment of the sick child before treatment and 48hrs after treatment were developed and used to collect data after having pretested them at two 50 health facilities in the LGA (Nkata PHC and Nkwuegwu PHC) that were not chosen for the main study. The key informant interviews as well as questionnaires were structured in a way to capture the following variables: Characteristics and knowledge of the mothers - Level of education - Occupation RY - Level of income, monthly expenditure and cost of managing incidenceA of malaria in the < 5 child BR - The number of antenatal visits made during pregnancy LI - If exclusive breastfeeding was done N - Awareness of the causes of malaria and the posDsiblAe preventive strategies - If child was fully immunized A - Knowledge about child’s health Fpro mIo Btion activities and home management of some common childhood conditionOs like ORT preparation for diarrhea, febrile conditions - Who makes the decisionY to take a sick child to the clinic in the house - Was she accompanIieTd to the clinic by the husband? - If she was ReduScated on how to continue with home care for the child each time she brinVgs hEim/her to the health facility- NAtItitude of staff at the health centersU- Acceptability of the services available at the facility - Distance from the facility The health care facility head - Level of training acquired and if any have had some trainings on Integrated Management of Childhood Illness (IMCI) 51 Number of trained staff in the facility - How they diagnose and care for malaria (type of anti-malaria drugs used). - Do these health facilities have a national malaria case management algorithm - Number of hours of services rendered - Availability of basic materials like thermometer, weighing scale, growth monitoring charts - Average number of patients per day RY - Routine immunization records and how many children got compleRtely Aimmunized at the facilities IB - Good record keeping i.e. year the facility became operatio nLal and what year record is available and if they are up to date N - Availability of drugs for malaria DA - The level of community patronage wouBld bAe assessed - If there are supervisory visits I The LGA PHC coordinator OF - Organizational/managerYial structure of the entire PHC in the LGA - Staffing of the faciIliTties - AvailabilityR of Sin-service training especially; on IMCI - TotaVl imEmunization coverage of the LGA - NSuIpply of drugs and materials to the facilitiesU- Monitoring of activities (how often these are done) - If the IMCI strategies is been operated by the LGA - If the LGA have a protocol of systematic supervision of health workers - Cost of treating malaria in the health facilities. 52 Determination of treatment outcome: This was done by looking at the treatment given in the facility retrospectively (clinic record) were consultation had taken place before the team gets there and monitoring the response to treatment of the children prospectively after 48 hrs of commencing treatment (by interviews of the care givers and physical examination of children either in the clinic for those on admission or at home for out-patients. Assessment of the sick child: All the children meeting our inclusion criteria seen at the selec ted health centers were assed for their clinical state when they were brought to the health RcenYters by examining them for signs of fever (with a thermometer), anaemia, drowsiness, sApleenomegaly and sunken eyes. BR The age of the sick: The caregivers were asked how old the sick child LwaIs. Data collection method N Four research assistants were recruited from the DepartmenAt of Nursing Services of the Abia State Ministry of Health and they were given a 4 - daAy inDtensive training on how to collect both qualitative and quantitative data with the abov eI tBools trying as much as possible to reduce the inter and intra observer concordance/difOferenFces. 3.9 Data Management and AInTalyYsis Data obtained from the quSestionnaire were checked for accuracy, completeness and consistency of information. DaEta cRleaning was done before entering them into statistical soft ware (Epi-info version 3.8). IDVescriptive statistics was used to summarize the data obtained. Univariate and bivariUate Nanalysis were done to ascertain the degree of association between various factors that may be responsible for the outcome of malaria treatment in children brought to the health facilities; by comparing both quantitative variables and proportions among more than two groups using Chi-square test at 5% level of significance. Multivariate analysis using logistic regression was done to model those variable that when altered affects the malaria treatment outcome of 53 under-five children that are attended to in Umuahia North Local Government Area of Abia State PHC facilities. 3.10 Ethical considerations Permission and approval was obtained from the Ethical and scientific committee of the Abia State Ministry of Health, Umuahia. Informed verbal consent was obtained from all those that participated in the study (facility hea ds, PHC coordinator and caregivers).In conformity with the ethical requirement, all vital inRforYmation obtained from the respondents were accessed only by the investigators BR A N LI AD A F I B O ITY ER S V UN I 54 CHAPTER FOUR 4.0 RESULTS The result of the study is presented in line with the objective of the study to ascertain the malaria treatment outcome among under five years children managed at the primary health care centres (PHCs) in Umuahia North LGA. The second part present the health resources (human, material and financial) available at these health facilities for the provision of malaria treatment for un der five years children. The next part presents those factors that affected under five malariaR treYatment outcome at the health facilities in Umuahia. A Grouping the four facilities into urban and rural, World bank housing estBate Rhealth centre and Ojike road health centre were classified as urban each hosting 94 (16 .7L%)I and 221(39.3%) of the caregivers interviewed/recruited under five years children reNspectively. While Umuawa - Alaocha health centre and Amaogwugwu health centre wDere Agrouped as rural each also hosting 170 (30.3%) and 77 (13.7%) of the caregivers/recruiteAd under five years children respectively. IB 4.1 Treatment outcome among the under Ffive children studied The prevalence of good treatment o uOtcome among the 562 under five year children that participated in this study was I7T3.5%Y as shown in Table 1. Meanwhile 305 (54.3%) of them were males and 480 (85.4 %R) wSere treated on out patients basics. Table 1: MalIaV E ria treatment outcome UNVariable Frequency %Treatment outcome (N = 562)Good 413 73.5% Poor 149 26.5% 55 4.2.0 The resources available for the provision of malaria treatment services Human: The key informant interviews with the heads of the selected PHC facilities showed that they were all female and their mean age was 44.0±1.4 years. Their minimum qualification was Staff nurse midwife and the maximum was B.Sc from (Table 2). Meanwhile the LGA PHC coordinator was also a female and holds an M.sc degree. Though the LGA operates the Integrated Management of Childhood Illness (IMCI) only 10 of the heads of the 31 PHCs in the LGA were trained on the use of this strategy which waRs aiYmed at improving the child health services rendered at the Primary health care level. Of theA four selected PHC heads, only two including the PHC coordinator had been trained on thBe uRse of IMCI (about 4 years ago) and all of them including the PHC coordinator again hadL alIso received training on malaria treatment protocol by the State ministry of health in the Nlast one year (Table 2). Though there was provision for in-service training, none of the DheaAlth staff had undergone any major training programme or had been re-trained on the Use Aof IMCI in the last one year.B OF I SI TY R IV E UN 56 Table 2: Demographic characteristics of the PHC Facility heads/PHC coordinator and trainings relevant to malaria treatment in the last five years Response by respondents and the facility they head Variable Amaogwugwu WBHE Ojike Umuawa- Umuahia Alaocha North LGA PHC coordinator Rank ACNO ACNO DDNS NO DNS Age (Yrs) 44 45 45 42 48 Highest Bsc NM Bsc NM RMY.scqualification Gender Female Female Female FemaleRA Female IMCI training Yes No Yes INBo Yes How long ago was 4 yrs NA 4 yrs LNA 5 yrs IMCI training? N Malaria training in Yes Yes DYesA Yes Yeslast I year *ACNO Assistance chief nursing officer; DDNS Deputy director of nursing services; NM Nurse midwife and DNS Director nursing services A IB The LGA PHC coordinated reported that theF health department is forced to carry out quarterly supervisory visits to the various PHC f aOcilities instead of the stipulated twice monthly visits due to inadequate staff and funds. IHTowYever these supervisions were done without written protocols.S 4.2.1 Material reEsouRrces available for rendering malaria treatment services at the PHCs: The UmuahiaI VNorth LGA PHC coordinator also stated that the health department has never distribUutedN the IMCI guidelines as well as the National malaria treatment protocol to its PHCfacilities since these guidelines were published. She also reported that, three years ago, the LGA health department gave anti malaria drugs for under-five children to all its health facilities which were used in treating malaria freely without extra charges to the patients. However, no new stock or other drugs have been given in recent times apart from the vaccines used for routine immunization which WHO and UNICEF are coordinating and supporting. It was also noted that 57 the LGA gave free Insecticide treated nets (ITN) to the various PHC facilities for distribution about two years ago to pregnant/nursing mothers as part of her effort to reduce the incidence of malaria in the locality. Part of the challenges facing the health department that was identified were, poor funding, inadequate staff, poor infrastructures and lack of staff training and re-training programs. It was observed that World Bank Housing Estate (WBHE) PHC had the highest number of staff w ith the ability to diagnose malaria although Ojike street PHC sees the highest proportion Rof chYildren with malaria every day. Also of the four PHC facilities visited, it was only OjiAke street PHC facility that does not have the ability to admit patients for observation (TablBe 3)R. It was also observed that prior to presentation at the four PHCs visitLedI all the children would have been given chloroquine anti malaria drugs by their caregiNvers at home apart from Ojike street PHC where some of the children where equally givDen thAe recommended anti malaria drugs Artemisinin based combination therapy (ACT) (Table 4). IB A Table 3: Staff strength/work load at thOe foFur facilitiesVariables AmYaog wugwu WBHE Ojike Umuawa-Alaocha Reported N° of staff with IT 2/3 7/9 4/7 4/5capacity to attend to malar cases (x/n) Sia Reported average NE° oRf 8 1 0 30 2 0children seen IinV the facility per day (N) PropoUrtionN of children 6 (75%) 8 (80%) 10 (33.3%) 5 (25%)treated for malaria daily (X/N) Availability of facility for Yes Yes No Yes admission x = number of staff with the capacity to treat malaria and n = total number of staff in the PHC facility 58 Table 4: Treatments reportedly given to the children by the caregivers at home before they are brought to the health facility Variables Amaogwugwu WBHE Ojike Umuawa- Alaocha Type of treatment given by caregivers before coming to the facilities Concoctions No No No No PCM Yes Yes Yes Yes CQ Yes Yes Yes Yes ACT No No Yes RNYo Nil treatment given before No No No No coming to the facility RA LI B From the assessment of the visited health facilities, it was oAbseNrved that though the oldest and newest facilities were 72 years and 11 years respectivAely Donly three years records were available in each of the four facilities. Apart from WBHIBE health centre, all the others still prescribe chloroquine as part of malaria treatment. It Fwas also observed that when prescribed anti malaria drugs are not available, apart from Um uOawa - Alaocha health centre that would prefer to ask the patients to go and purchase thesTe dYrugs themselves the other three facilities would rather restock these drugs immediately Sto Iensure it is handed over to the patients there and then. All the facilities visited made Rmalaria diagnosis presumptively without using rapid diagnostic test kits or microscopy. UImVua Ewa - Alaocha was the only facility that had at least a supervisory visit from either the NLGA health department or the State ministry of health in the last five months (Table 5).U 59 Table 5: Assessment of the health facilities from inception till date and malaria treatment/control activities Variables Amaogwugwu WBHE Ojike Umuawa- Alaocha Year of establishing PHC 1948 1999 1991 1996 Availability of complete No No No No record from inception at the facilities N° of years with complete 3 yrs 3 yrs 4 yrs 3 yrs records since inception RY Type of drugs used in the treatment of malaria at the facilities PCM Yes Yes Yes YAes CQ Yes No Yes IB RYes SP Yes No No No ACT Yes Yes Yes Yes Blood syrups/tabs Yes Yes Y eLs Yes Antibiotics No No NYes Yes If above drugs are always No Yes A Yes Yes available at the facilities D Receipt of free ACT/ITN No ANo No No for distribution in the last IB one year F Where there occasions when Y eOs Yes No Noprescribed anti-malaria drugs were not available at Y the facility in the last 3 months ITS What facilities wouldR do in situations where anti--malaria drugs are not available?Buy from a chemisEt to Yes Yes Yes Norestock V Prescribe Nfor Ipatients to go No No No Yesand buy ReporUted N° of supervisory 1 1 4 6 visits from the LGA in the last 5 months If malaria diagnosis are Yes Yes Yes Yes presumptively made 60 4.3.0 Factors affecting under - five years children malaria treatment outcome in PHC facilities in Umuahia 4.3.1 Descriptive analysis The mean age of the caregivers was 32.6±6.6 years. Most of the caregivers 478 (85.0%) were married and 130 (23.1%) were civil servants, majority (23.1%) were secondary school leavers and 13 (2.3%) had no formal education. The 25 - 39 years age group was in the majority 423 (75.3%) and Christians {Pentecostal 297 (52.8%) as well as Orthodox 260 (46.3%)} wRere Yalso in the majority. Among the caregivers that brought their sick children to the clinic, maAjority 528 (94.0%) were the mothers (Table 6 ). BR The median cost of treating a child at the chemist was N300 (range = 2L0 - I1,500), if the child was taken to a private clinic, the median cost was N1,300 (range =N 110 - 6,000). Meanwhile the median cost of treating the child at the PHC facility, was ND700A (range = 270 - 1,600). (Table 7) BA F I Y O IT ER S NI V U 61 Table 6: Socio-demographic characteristics of caregivers Variable F requ en cy % Age (Years) < 2 0 4 0.7 20-24 54 9.6 25-29 152 27.0 30-34 141 25.1 35-39 130 23.1 40-44 52 9.3 45 and above 29 5.2 Total 562 100.0 Marital Status Y Single mother 42 7.5 Married 478 85.0 R Divorce 2 2 3.9 A Widow 2 0 3R.6 Total 562 100.0 Occupation LIBHousewife 78 13.9 Farmer 25 4.5 Hairdresser 47 N 8.4 Trader 193 A 34.3 Tailor 2 1 3.7 Student A13D 2.3Teacher 52 9.3 Paramilitary B 3 0.5 Civil servant I 130 23.1 Total 562 100.0 Level of education F Nil O 13 2.3 Primary 55 9.8 Secondary ITY 364 64.8Tertiary 130 23.1 Total S 562 100.0Religion Islam R 4 0.7 OrthVodoEx church 260 46.3PenItecostal church 297 52.8NTraditional 1 0 . 2Total 562 100.0U Relationship with the sick childFather 25 4.4 Mother 528 94.0 Relatives 9 1 . 6 Total 562 100.0 62 Table 7: The mean/median cost of treating an under-five child presumed to have malaria at various locations (N) Characteristics Mean (S.D) Median (Range) Cost of treating a child in a chemist 347.5 192.6 300 20 - 1,500 Cost of treatment in the health centre 729.6 348.0 700 100 - 3,000 Cost of treatment in the private clinic 1,637.0 933.5 1,300 1 1 0 - 6 , 0 0 0 Total cost of present treatment in the facility 734.4 263.9 700 270 - 1,6 00 RY Using the centile poverty scale (Table 8 ) to grade the caregivers and their houRsehAolds, majority 231 (41.1%) of them from their earnings were observed to be on the 60IthB poverty centile scale (middle class) followed by the upper middle class with 176 (31.3%) 8L0th poverty centile (Tables 9). It was also observed that the upper class (from the sociaAl claNssification in Table 8 ), had the most proportion of children with good treatment outcomDe (82.1%) and the lower class had the least (50%). There wasn’t much difference in thBe prAoportion of children with good treatment outcome between the middle and upper mFidd leI social classes both having 72.3% and 72.2% respectively (Table 10). O ITY RS Table 8: SociaVl claEssification of caregiver’s household using their average monthly income NHIousehold income per month Poverty grade (centile) Social classificationU < N5,000 2 0 LowerN5,000 - N10,000 40 Lower middle N11,000 - N30,000 60 Middle N31,000 - N50,000 80 Upper middle > N50,000 1 0 0 Upper 63 Table 9: Average income earned by the caregiver household in a month (N = 562) Amount earned by household in a month Frequency % < N5,000 (Lower class) 2 0.4 N5,000 - N10,000 (Lower middle class) 47 8.4 N11,000 - N30,000 (Middle class) 231 41.1 N31,000 - N50,000 (Upper middle class) 176 R31.3Y> N50,000 (Upper class) 106 A 18.9R Table 10: The effect of social classification of the caregivers on good trIeBatment outcome Social class % of children with good % Lof children with bad treatment outcome N treatment outcomeA Lower (N=2) 50.0 D 50.0 Lower middle (N=47) 6 6 . 0 BA 34.0Middle (N=231) 72.3 I 27.7 Upper middle (N=176) 72.2 27.8 Upper (N=106) O82.1 F 17.9 TY It was observed that more SthanI half of the caregivers 304 (54.1%) came alone with their children for treatment at the heaRlth centres, while the rest were either accompanied by relative 127 (22.6%) or thIeiVr hu Esbands 75 (13.3%) (Fig 6 ). Also abouNt half of the caregivers 287 (51.1%) had two under - five years children in their houseUhold followed by those with one under - five years child in their household 217 (28.6%) (Fig 7). 64 -Chart of who accompanied the caregiver and sick child to the health centre Alone Relative Neighbour AR Y Father BR 0 50 100 150 200 250 300 I 350 400 □ F re q u e n c y □ % N L Fig 6: A graph of weather the caregiver was accompanied Ato the clinic and who did AD A g raph o f the n u m b er o f ch ildren pIeBr ho u se hold o f care g iver OF Y T SI VE R I UN Number of children in house hold 0 50 100 150 200 250 300 350 400 □ F re q u en cy □ % Fig 7: A graph of the number of under five - years children in each caregiver household 65 Also from the descriptive analysis of the data on the 562 under - five children enrolled into the study, it was observed that the median age of the children was 24 months (Range 2 - 59). One fifth 118 (21.0%) of the children were under 12 months old and 305 (54.3%) were male, (Table 1 1 ). Table 11: Demographic information on the sick children (N=562) Y Variables Frequency %AR Age (Months) R < 1 2 118 LIB2 1 . 012 - 17 75 13.3 18 - 23 78 N 13.9 24 - 29 83 A 14.8 30 - 35 36 - 41 A55D 9.857 1 0 . 1 42 - 47 IB 32 5.7 48 - 53 F 42 7.5 54 - 60 O 2 2 3.9 Total Y 562 100 Gender T Male SI 305 54.3 Female R 257 45.7 TotalVE 562 100 UN I 66 It was also observed that majority of the children 480 (85.4%) were treated on outpatient basis and 82 (14.6%) were admitted for observation. From their baseline status before treatment was given, all 562 children had fever (measured with a thermometer > 38°C) at the start of the study and 383 (68.1%) were vomiting. Some had the following signs of severe malaria, convulsion 57 (10.1%), anaemia 48 (8.5%) and jaundice 17 (3.0%) (Table 12). Table 12: Baseline clinical information of the children before treatment was started Y (N=562) R Variables Frequency R%A Signs & symptoms on presentation apart from fever B Vomiting 383 LI 6 8 . 1 Chills & rigor 132 23.5 Convulsion* 57 AN 1 0 . 1 Dull not active 349D 62.1 Anaemia * A48 8.5 Jaundice * IB 17 3.0 Sunken eyes* Drowsy* F 33 5.949 8.7 Spleenomegaly O 1 2 2 . 1 * Associated with severe malIarTia YS It was observed thEat Rafter 48hrs post anti-malaria treatment, 146 (26.0%) still had fever, 16 (2.8%) had jauVndice, 17 (3.0%) were still vomiting and they were all referred while about 413 (73.5.0%)N resIponded well to treatment without requiring further treatment (good outcome). (TableU 13) 67 Table 13: Clinical information of the sick children 48 hrs after treatment was started (n=562) Variables Frequency % Signs & symptoms 48 hrs after treatment Fever 146 26.0 Jaundice 16 2 . 8 Vomiting 17 3.0 Chills & rigor - - Febrile convulsion - - Y Sunken eyes 3 0.A5 RDrowsy 1 2 R2 . 1 Dull & not active 29 B 5.2 Non of the above signs /symptoms 413 LI 73.5 Outcome of treatment after 48 hrs Satisfactory (good) 4N13 73.5 Poor DA149 26.5 Total A 562 100 IB The number of episodes of fever the c hiOldren F had suffered in the two months preceding the study was observed to be 31.0%, 34% aYnd 29% for those that had suffered one episode, two or three episodes of fever respectivSely I(Table 14).R Table 14: NumVberE of episodes of fever experienced by the children in the last two monthsVariablIe Frequency % UNumNber of episodes of fever in the last 2 monthsOnce 174 31.0 Twice 191 34.0 Thrice 162 28.8 Four times 35 6 . 2 Total 562 100 68 Most of the children 394 (70.1%) was observed would have been taken to a chemist shop for treatment before they were eventually brought to the health centre, while 114 (20.3%) were brought straight to the health centres (Table 15). Table 15: Treatment sought by caregivers before coming to the health centre Variables Frequency % Traditional healer 9 1 . 6 Y Church 45 8 . 0 R Chemist 394 70.1A Sort no treatment 114 2R0.3 Total 562 LIB100.0 N One hundred and ninety eight (35.2%) of the caregivers DwereA observed to first notice fever in a child <12hrs as of the time of presentation at the healtAh facilities while 364 (64.8%) first noticed fever after 12hrs. It was again observed that aIboBut 107 (19.0%) of the children had stopped having fever about 2 hrs after anti-maOlariaF drugs were administered and 250 (44.5%) and 56 (10%), stopped having fever <24hYrs and 24-48hrs respectively, after treatment was given and these were the children that wIeTre classified as having good treatment outcome (Table 16). For the remaining 149 (26R.5%S), in which the fever persisted leading to referral, they were the ones referred to as havinEg poor outcome and they are the group of interest i.e. what were those factors that made theI oVther 413 to recover from the fever and they did not. Efforts were made to identify these UfactNors in the analytical section that will soon follow. 69 Table 16: Time interval between when drugs were administered and when the fever stopped Variables Frequency % About 2 hrs after treatment 107 19.0 < 24 hrs 250 44.5 24 - 48 56 1 0 . 0 Fever persisted 149 26.5 Total 562 100.0% Y AR Anti - malaria drugs were administered on about half (49.0%) of the children imRmediately after consultation while 51.0% had their drugs <24hrs after consultation and noInB got beyond 24hrs (Fig. 7). Most of the time 540 (96.1%) a caregivers would notice a ch ilLd to be having fever when the body is hot to touch, while 354 (63.0%) of the time it is wAhen Nthe child is restless. AD Graph of time of administration IoBf anti-malaria drugs after consFult ation 60% O 50% ITY 40% RS 30% VEI 20% UN 10% 0% Immediately after <24hrs after consultation 24-48hrs after consultation consultation Fig 7: Time interval between consultation and administration of drugs 70 When a child is noticed to have fever 45% of the caregivers would give home treatment <24hrs after the fever is first noticed and 55% of them would give treatment after 24hrs (Fig 8 ). Pie chart of time interval between when fever is notice and when drugs are given AR Y <24hrs 45% RIB ■ <24hrs >24hrs L □ >24hrs55% N AD A Fig 8: Time interval between when fever is no tIicBed and drugs are given during home treatment of malaria F Immediately after noticing fever in a c hOild (Table 17), 523 (93.1%) of the caregivers would give PCM, 255 (45.4%) of them wouTld Ytake the sick child to the health centre and 346 (61.6%) would tepid sponge the child to bSringI down the temperature.R Table 17: AcItiVvitie Es of the caregiver when a child develop fever at home (N = 562) Variables Frequency % Wait tUNill it is serious 17 3.0 Give PCM immediately 523 93.1 Give malaria treatment immediately 43 7.7 Take a child to the health centre 255 45.4 Tepid sponge 346 61.6 71 It was observed that when the caregivers do home treatment of malaria (Table 18), nearly all the caregivers 523 (98.9%) would give paracetamol (PCM) while 190 (33.8%) would give chloroquine and 93 (16.5) of them would give left over drugs used in previous treatment irrespective of the type of drugs. Table 18: Drugs used by caregivers when they do home treatment of malaria (N = 562) Variable Frequency % Y PCM 556 98.9 R Chloroquine 190 33.8A Camoquine 43 BR7.7Artesunate 73 I 13,0 ACT 24 L 4.3 Blood syrups/tablets 343 N 61.0 Herbs 3 A 0.5 Left over drugs 93 D 16.5 BA It was observed that a good number of careFgiv erIs know about activities that could prevent them and their children from having malaria.O Majority of them 517 (92.0%) believed sleeping under ITN and 490 (87.2%) cutting bushYes a round the houses would prevent malaria in the household (Table 19). IT Table 19: Frequency Rof cSaregivers perceived knowledge of malaria prevention (N = 562) Variables E Frequency % Clearing bushIeVs 490 87.2 CoverUing Nopen water containers 348 61.9Draining blocked gutters 345 61.4 Sleeping under ITN 517 92.0 Spraying homes with insecticides 402 71.5 Taking prophylactic treatment 386 68.7 72 Also the caregivers carried out the following malaria prevention activities at home 248 (44.1%) of them agreed that their children were sleeping under ITN and 310 (55.2%) sprayed their rooms regularly in the evenings with insecticide (Table 20) Table 20: Malaria prevention efforts by the caregivers Prevention effort Frequency % Child sleeps under ITN 248 4Y4.1 Doors & windows have nettings 398 R70.8 Child usually treated prophylacticaly 352 A 62.6 Rooms are sprayed with insecticides I3B10 R 55.2 Family staying outside in the evenings 381 67.8 Burning mosquito coil while outside in the evenings N L 106 18.9 A Malaria prevention activities during the antenatal peAriodD by mothers while the child was been conceived were reported/observed to be 213 (3 7I.9B%) mothers slept under ITN while pregnant, 508 (90.4%) took Intermittent Preventive TrFeatment (IPT) (Table 21). A high proportion of the caregivers 35 2O (62.6%) agreed that either parents decides when a sick child should be taken to the heIaTlth Ycentre (Fig 9). Table 21: Antenatal pReriSod malaria prevention activities when the child was been conceived Antenatal actiVvitieEs Frequency %Mothers slepIt under ITN Yes UN 213 37.9No 349 62.1 Total 562 100.0 Mothers took IPT Yes 508 90.4 No 54 9.6 Total 562 100.0 73 A graph of who takes the decision to take a child to the health centre RY BR A LI AN □ Frequency □ pAercDentageFig 9: A bar chart of who decides when a childI sBhould be sent to the health facility It was observed from post natal informationF obtained from mothers/caregivers that, 100 (17.8%) of the sick children were small foYr a ge O at birth, 335 (59.6%) were exclusively breastfed, 511 (90.9%) were fully immunizeIdT for age (Table 22). Also it was observed that 355 (63.2%) of mothers were taught homSe treatment of malaria during ANC and 238 (42.3%) were equally taught what to do wEhenR a child develop fever as shown in (Tables 23). IV UN 74 Table 22: Postnatal information concerning the sick child from mothers/caregivers Variables Frequency % Child small for age at birth Yes 1 0 0 17.8 No 462 82.2 Total 562 100.0 Did exclusive breastfeeding Yes 335 59.6 No 227 40.0 Y Total 562 100.0 R Child fully immunized A Yes 511 BRNo 51 I 90.99.1 Total 562 N L 100.0 A Table 23: What mothers were taught during ANC D Variable of interest FrequencyA % Taught home treatment of malaria during AN ICB Yes OF355 63.2No 207 36.8 Total TY 562 100.0 Taught ORS during ANC SIYes 549 97.7 No R 13 2.3 Total E 562 100.0 Taught whatI tVo do when child is febrile Yes UN 238 42.3No 324 57.7 Total 562 100.0 Taught tepid sponging Yes 1 1 0 19.6 No 452 80.4 Total 562 100.0 75 Majority 482 (85.8%) of the caregivers believed the services rendered at the four health facilities used in this study was good (Table 24). Table 24: Impression about the services rendered at the health facility Variables Frequency % Feelings about services in the clinic Good 482 85.8 Not good 80 5 14.2 Total 562 100 AR Y Majority 440 (78.3%) of the caregivers interviewed, live greater than 1 km fromR the health centre while few of them about 122 (21.7%) lives about 1km from the health cenItrBe. Asked how government could curtail the malaria menace in the Lcommunity, most of the caregivers 462 (82.2%) agreed that the provision of free anti-mAalaNria drugs will improve the fight against malaria in the communities. While 480 (85.4%A) ofD them believed free ITN would be vital in curbing malaria menace in their community ( TIaBble 25). Table 25: Suggestions by caregivers oOn hoFw government can curtail the menace of malaria in the community Variable Y Frequency % Provision of free anti-malaria IdTrugs 462 82.2 Provision of free ITN S 480 85.4 Clearing of bushy EenviRronment 45 8 . 0Provision of hIeValth centers in the community 4 0.7EducatingN mothers on the need for ITN 40 7.1AvoidUing stagnant water 15 2.7Provision of free laboratory 13 2.3 76 4.3.2 Bivariate analysis After carrying out an initial univariate analysis, some variables were identified that were considered to be capable of influencing the malaria treatment outcome among the under-five years children observed in this study. So it was decided that a Bivariate/multivariate analysis on them would be carried out. Variables like who decides when a sick child should be sent to the hospital had no association with the treatment outcome of malaria noticed among under - f ive children in Umuahia North LGA of Abia State (Table 26). AR Y Table 26: Association between who decides when a child is taken to theR clinic when sick and good treatment outcome IB Variable of interest Good outcome x(% L) X2 P = value Who decides when to take a child to the clinic? Father alone decides N Yes (n = 65) 44D (67A.7)A 0.953 0.329No (n = 497) 269 (74.2)Mother alone decides Yes (n =145) IB 110 (75.9)F 0.413 0.520No (n = 417) 302 (72.7) Either parent decides Yes (n =352) OY 259 (73.6) 0 . 0 0 1 0.972 No (n = 210) IT 154 (73.3)S However there was aRn association between a mother sleeping under ITN while pregnant and good treatmen EItV outcome among the sick children as it was significant at a p<0.003 (Table 27). The signiNficance at p<000 noticed between mothers been taught home care of malaria during ANC Uand good treatment outcome was also a sign of an association between them (Table 27). 77 Table 27: Association between the various ANC activities by mothers and good treatment outcome among the children Variable of interest Good outcome x(%) X2 P = value Mothers took prophylactic malaria treatment during ANC Yes (n = 508) 375 (73.8) 0.147 0.701 No (n = 54) 38 (70.4) Mothers slept under ITN during ANC Yes (n = 213) 172 (80.8) 8.698 0.003** No (n =349) 241 (69.1) Mothers taught home care of malaria during ANC Y Yes (n = 355) 291 (82.0) R 34.437A 0 .0 0 0 **No (n = 207) 122 (58.9) Mothers taught preparation of ORS during ANC R Yes (n = 549) 404 (73.6) IB0.467 0.973 No (n = 13) 9 (69.2) L Mothers taught what to do when child is febrile Yes (n = 238) 178 A(74.N8) 0.253 0.615 No (n = 324) 2D35 (72.5) ** Significant at p< 0.05 IB A There was neither an association between aF sick child been less than or greater than 1 2 months old and good treatment outcome nYor th Oe gender of the sick child and good treatment outcome (Table 28) SI T Table 28: DemogErapRhic information of the sick children and its association with goodtreatment outcVome Variable of iInterest Good outcome x(%) X2 P = value Age g < 1 2 mUrouNp of the childrenonths (n = 118) 81 (6 8 .6 ) 1.498 0 . 2 2 1 > 12 months (n = 444) 332 (74.8) Gender of the sick child Male (n = 305) 220 (72.1) 0.487 0.485 Female (n = 257) 193 (75.1) 78 An association was observed between a caregiver having formal education and having good treatment outcome i.e. the proportion of the educated caregivers to those without formal education was 407 (74.1%) to 6 (46.8%) at p<0.05. Also obtaining good treatment outcome had no association with who accompanied the caregiver to the clinic (Table 29). Table 29: Association between caregiver’s level of education or who accompanied them to the health centre and good treatment outcome Variable of interest Good outcome x(%) X2 P =Y value Is caregiver educated R Yes (n = 549) 407 (74.1) 3.77A 0.05** No (n = 13) 6 (46.8) R Child’s father accompany caregiver to the H/C B Yes (n = 75) 56 (74.8) LI 0 . 0 1 2 0.913 No (n = 487) 357 (73.3) Neighbors accompany caregiver to the H/C N Yes (n = 56) D39 (A69.6)A 0.278 0.598No (n = 506) 374 (73.9)Relatives accompany caregiver to the H/C Yes (n = 127) IB 1 0 1 (80.2)F 3.282 0.070No (n = 437) 312 (71.6) Caregiver was alone Yes (n = 304) Y O 212 (70.7) 2.327 0.127 No (n = 258) T 201 (76.7) ** Significant at p< 0.05 SIR It was observIedV tha Et among all the baseline signs and symptoms that the children presented with at the heNalth facility (Table 30), a sick child having signs of severe malaria like febrile convuUlsion, anaemia, jaundice, sunken eyes, drowsy and spleenomegaly were all significant predictor of poor treatment outcome as they were significant at p<0 .0 0 , p<0 .0 0 , p<0 .0 0 , p<0 .0 0 , p<0.00 and p<0.00 respectively. A child having chills & rigor where however a predictor of good treatment outcome and was significant at p<0.03. 79 Table 30: Association between the various signs and symptoms of the sick child at the time of presentation in the clinic and good treatment outcome Variable of interest Good outcome x(%) X2 P = value Vomiting Yes (n = 383) 273 (71.3) 2.664 0.103 No (n = 179) 140 (78.2) Chills & rigor Yes (n = 132) 107 (81.1) 4.582 0.032** No (n = 430) 306 (71.2) Febrile convulsion Y Yes (n = 57) 19 (33.3) R 50.227 0.0000** No (n = 505) 394 (78.0) A Child dull & not active R Yes (n = 349) 256 (73.4) IB0.000 0.995 No (n = 213) 157 (73.7) L Anaemia Yes (n = 48) 19 (A39.6N) 29.091 0.0000** No (n = 514) 3D94 (76.7) Jaundiced Yes (n = 17) IB A 4 (23.5)* 0.000 0.0000** No (n = 545) F 409 (75.0)Drowsy Yes (n = 49) O 22 (44.9)Y 20.941 0.0000**No (n = 513) 391 (76.2) Had sunken eyes Yes (n = 33) TSI 12 (36.4) 22.816 0.0000** No (n = 529) 401 (75.0) Spleenomegaly R Yes (n = 12) IV E 3 (25.0)* 0.000 0.0004** No (n = 5N50) 410 (75.5)* FisheUr s exact test ** Significant at p< 0.05 An association was also observed between when the duration of fever was <48hrs or >48hrs before presentation and good treatment outcome as it was significant at p<0.05 (Table 31). 80 Table 31: Association between duration of fever and treatment outcome Variable of interest Good outcome x(%) X2 P = value Fever started <48hrs before presentation (n=462) 348 (75.3) 3. 983 0.046** Fever started >48hrs before presentation (n=100) 65 (63.0) ** Significant p< 0.05 An association was not observed between the number of episodes of fever in the last two mon ths preceding the study and good treatment outcome (Table 32). Y AR Table 32: Association between number of episodes of fever in the last twRo months before presentation and treatment outcome IB Variable of interest Good outcome xL(%) X2 P = value < 3 episodes of fever in the last 2 months (n = 527) 38A4 (7N2.9) 1.208 0.272 > 3 episodes of fever in the last 2 months (n = 35) AD29 (82.9) IB There was no observable association betweFen when a caregiver detects fever in a child through direct touch and good treatment outco mOe while there was an association between good treatment outcome and when fever is eIliTciteYd in a child when he/she is observed to be restless as it was significant at p<0.00 (TablSe 33).R Table 33: AssVociaEtion between how a caregiver detects fever in her sick child and good treatment ouItcome at the health facilities VariaUble Nof interest Good outcome x(%) X2 P = valueDetect fever through touchYes (n = 540) 398 (73.3) 0.108 0.742 No (n = 22) 15 (68.2) Detect fever when child is restless Yes (n = 354) 277 (78.3) 10.478 0.001** No (n = 208) 136 (65.4) ** Significant at p< 0.005 81 Giving treatment to a sick child within or >24hrs of detecting fever and good treatment outcome had no association (Table 34). Table 34: Association between when treatment was given after detecting fever and good treatment outcome______________________________________________________________ Variable of interest Good outcome x(%) X2 P = value Treatment given within 24 hrs of detecting fever 220 (70.7) (n = 311) 2.392 0.122 Treatment given > 24 hrs of detecting fever (n = 193 (76.9) 251)___________________________________________________ RY On comparing the type of home treatment given to a child when he/she is noRticedA to be febrile and good treatment outcome, it was observed that there were significanIt Bdegree of association between good treatment outcome and when a child is taken immed iaLtely to a health centre as soon as fever is noticed and also when tepid sponging is doneA onN a child with fever as they were both significant at a p< 0.00 and p<0.00 respectively D(Table 35). Also giving a sick child chloroquine by caregivers during home treatmenIt Bof Amalaria was significant at p<0.00 showing that it was a predictor of good treatment outcFom e (Tables 36). Table 35: Association between th OYe ty pe of home treatment and good treatment outcomeVariable of interest Good outcome x(%) X2 P = value Give PCM when a child devIelTops fever Yes (n = 523) S 388 (74.2) 1.412 0.235 No (n = 39) R 25 (64.1) Usually give fuVll mEalaria treatmentYes (n = 43) I 35 (81.4) 1.087 0.297 No (nU = 5N19) 378 (72.8)Take a child to the H/C immediatelyYes (n = 255) 205 (80.4) 10.783 0.001** No (n = 307) 208 (67.8) Tepid sponge as soon as fever is detected Yes (n = 346) 277 (80.1) 19.078 0.000** No (n = 216) 136 (63.0) ** Significant at p< 0.05 82 Table 36: Association between the drugs used by caregivers during home treatment of malaria and good treatment outcome Variable of interest Good outcome x(%) X2 P = value Give CQ during home treatment Yes (n = 190) 157 (82.6) 11.620 0.000** No (n = 372) 256 (68.8) Give ACT during home treatment Yes (n = 24) 21 (87.5) 1.831 0.179 No (n = 538) 393 (72.9) Give other left over drugs Y Yes (n = 93) 62 (66.7) 2.258 R0.133 No (n = 469) 251 (74.8) A ** Significant at p< 0.05 BRI It was equally observed that when a child was made to sleep under IT NL was positively associated with good treatment outcome as it was significant at p<0.02, hoNwever having mosquito nets on the doors and window as well as treating a child prophDylacAtically had no association with the treatment outcome (Table 37). A IB Table 37: Association between mala F rOia prevention practices by caregivers and treatment outcome Variable of interest Y Good outcome x(%) X2 P = value Child usually sleep under ITINTYes (n = 248) S 195 (78.6) 5.559 0.018** No (n = 314) ER 218 (69.4)Doors/windows in the house are netted Yes (n = 398)IV 294 (73.9)N 0.046 0.830No (n = 164) 119 (72.6)ChildU is treated prophylacticalyYes (n = 352) 263 (74.7) 0.571 0.450 No (n = 210) 150 (71.4) ** Significant at p< 0.05 Though there was no direct association between treating a sick child in either the urban or rural health centre and treatment outcome however, treating a sick child in Ojike-street PHC as oppose 83 to World Bank housing estate PHC both of which are in the urban area was associated with good treatment outcome as it was significant at p<0.04 (Tables 38). Table 38: Association between good treatment outcome and location of the health centre Variable of interest Good outcome x(%) X2 P = value Child treated in an urban health centre (n = 315) 234 (74,3) 0.150 0.70 Child treated in a rural health centre (n = 247) 179 (72.5) Y Child treated at Ojike road H/C (n = 221) 172 (77.8) R 4R.26A 0.04** Child treated at WBHE H/C (n = 94) 62 (66.0) LIB Child treated at Amaogwugwu H/C (n = 77) 51 (66.2N) 1.75 0.19 Child treated at Umuawa-Alaocha H/C (n = 170) D128 A(75.3) Significant at p, 0.05 BA It was observed that treating a child on out pFati enIt basis, was a good predictor of good treatment outcome at a p<0.00 as opposed to adm iOtting a child for observation (Table 39).Y Table 39: Association betSweeIn T treatment outcome and how a sick child was treated Variable of interest R Good outcome x(%) X2 P = value Child admittedV for Eobservation (n = 82) 39 (47.6)I 31,584 0.0000** Child wasN treated on outpatient basics (n = 374 (77.9) 480) U Significant at p< 0.05 Though there was no association between caregivers taking malaria prophylactic treatment during pregnancy and good treatment outcome, it was however observed that, there was 84 significant degree of association between a mother taking prophylactic malaria treatment during pregnancy and a child been treated prophylacticaly for malaria at p<0.00 (Table 40). Table 40: Association between a mothers taking prophylactic treatment during pregnancy and she treating her child prophylacticaly for malaria after birth Variable of interest Child treated prophylacticaly x(%) X2 P = value If mother took prophylactic malaria treatment during her pregnancy Yes (n = 508) 341 (67.1) Y 43.62 R0.000** No (n = 54) 11 (20.4) RA ** Significant at p< 0.05 LI B In the same vain, there was significant association between a moNther sleeping under ITN during her ante natal (ANC) period and her child using same afteDr birAth at p<0.00 (Table 41).A Table 41: Association between a caregiver sleIeBping under ITN during ANC and her child using same as malaria preventive method Faft er birth Variables O Child using ITN x(%) X2 P = value If mothers used ITN during ATNCY (while pregnant of the sick child)Yes (n = 213) I 147 (69.0)S 84.54 0.0000** No (n = 349) R 101 (28.9) ** Significant at Vp<0.E05 UN I 85 4.3.3 Multivariate analysis The 18 variables that were significantly associated with good treatment outcome were further subjected to multivariate analysis by carrying out logistic regression modeling and the following models came out (Table 42). (1) A child having signs of severe malaria would negatively affect the good treatment outcome i.e. (a) A child having febrile convulsion {OR 0.1562 (C.I = 0.0797 - 0.3064)} p<0Y.000 (b) A child having anaemia {OR 0.3027 (0.1319 - 0.6589)} p<0.003 AR (c) A child having jaundice {OR 0.1801 (0.0490 - 0.6624)} p<0B.01R0 (d) A child been severely dehydrated {OR 0.2806 (0.1184 -L 0.I6651)} p<0.004 (2) When mothers of the children were educated during ANCN (a) On home treatment of malaria {OR 2.5603 (1.A6312 - 4.0185)} p<0.000 (3) Practices by caregivers when a child develop feAverD at home (a) Taking a child to a health centre {I1.B9530 (1.2257 - 3.1117)} p<0.005 (b) Carrying out tepid sponging {F1.5475 (0.9801 - 2.4434)} p<0.061 (c) Giving chloroquine Y{1.9 3 O48 (1.1779 - 3.1780)} p<0.009 (4) Malaria prevention TS actIivities at home by caregivers (a) Caregiver sRleeping under ITN WhiVle pEregnant of the sick child {2.2285 (1.3741 - 3.6139)} p<0.001I UN 86 Table 42: Logistic regression modeling result of those variables that were significant from bivariate analysis of factors associated with good treatment outcome Variable of interest Odds ratio 95% Confidence interval P = value Signs of severe malaria Febrile convulsion 0.1562 (0.0797 - 0.3064) 0.000** Anaemia 0.3027 (0.1391 - 0.6589) 0.003** Jaundice 0.1801 (0.0490 - 0.6624) 0.010** Sunken eyes 0.2806 (0.1184 - 0.6651) 0.004* * What mothers were taught during ANC Y Taught home care of malaria 2.5603 (1.6312 - 4.0185) R0.000** Practices when a child develops fever A Takes a child to a health centre 1.9530 (1.2257 - 3.I1B117 R) 0.005** Tepid sponge 1.5475 (0.9801 -L 2.4434) 0.061** Give chloroquine 1.9348 (1.1779 - 3.1780) 0.009** Malaria prevention activities N Mothers slept under ITN while 2.2285 DA(1.3741 - 3.6139) 0.001**pregnant of the sick child ** Significant at p< 0.05 A F I B O ITYS VE R I UN 87 CHAPTER FIVE 5.0 Discussion In this analysis of the study on “Malaria treatment outcome among under-five children attending primary health care centres in Umuahia North LGA of Abia State Nigeria, a prevalence of good treatment outcome of 73.5% was recorded. This prevalence is lower than 79% that was foYund in a pilot study that had earlier been carried out few weeks preceding this study at twRo primary health centres in Umuahia North LGA that were excluded from this study. TRangApukdee et al., 2007 reported a prevalence of uncomplicated malaria progressing up tIoB severe malaria after admission of 3 - 5% (poor outcome) making a good treatment outcom Le of about 95% which was quite higher than what was observed in this study. At the sAelecNted Primary health care (PHC) centres, the facility heads had the necessary trainings to Dcarry out malaria treatment in children and they uses presumptive diagnosis to arrive IatB the A diagnosis of malaria in under-five years children in line with the WHO IMCI GuideFline for malaria. However, with poor record keeping at the facilities, lack of access to the IM OCI guideline and the National malaria treatment protocol and poor supervision by the LTGAY health department, quality health care/services cannot be guaranteed. This may be oIne of the reasons while some of the facilities still prescribe chloroquine contrary tRo thSe National policy on the treatment of malaria. Krause and Sauerborn had in 2000 obVserEved in their work in rural Burkina Faso that health care services/intervention utilizationN by Imost community is dependent on availability of quality services by the health care providUers among others. It was observed that a child getting treatment at ojike street PHC have a better outcome than if treated at World bank housing estate PHC both of which are in the urban area. The only remarkable thing about Ojike street PHC is that it had the highest number of supervisory visits in the last five months preceding the study as well as been the only PHC studied that does not have the capability to admit patients for observation. Malaria is known to 88 be the major cause of mortality and morbidity in the tropical and subtropical regions in the world. However, mortality can be reduced by effective use of standard treatment procedures such as the National treatment protocol and the IMCI guideline. Patients who require hospitalization and those who need intensive care can be identified promptly and treated before they develop complications. About 10% of cases of falciparum malaria can be classified as severe malaria, among which the mortality is 10% but may rise to as high as 50% (Pasvol, 2005). It is w ell established that the prognosis of acute uncomplicated falciparum malaria patients whoY might progress to severe malaria vary depending on the early diagnosis, prompt managAemeRnt and the presence of any of the complications associated with malaria disease (MarsBh eRt al., 1995, White, 2003 Mishra et al., 2006). LI In this study, 94% of the caregivers bringing children with fevNer t o the health facilities were mothers which is in line with Tarimo et al, 2000 work in TanAzania of 89%, Njama et al., 2003 in Uganda of 95% and Yewhalaw et al., 2010 in EthiopiAa ofD 97.4%. The findings in this study also showed that only 45.4 % of caregivers would gIoB to a health facility as first line of care for a febrile child as opposed to Yewhalaw eOt al.F, 2010 value of 71.5%. Very few caregivers (1.6%) from this study would seek treatmYent from traditional healer whereas Njam et al., 2003 in his study in Uganda reported thatI nTone of the caregivers sort helps from the traditional healers. Most of the children in this studSy were <24 months (48.2%) while the findings by Snow et al., 2005 in Mozambique was EaboRut 50% of the same age group. This study also noted that majority of the caregivers woIuVld seek care at the patent medicine dealers first (70.1%) compared to (20.3%) that wouldU goN straight to the health centre. This is a major challenge to attaining the Roll back malaria strategy of prompt access to health care services by children with fever in Sub Sahara Africa region that need to be addressed urgently and this will also help to protect poor households from double spending accessing the same health care services twice that would impoverished them. Biritwum et al., 2000 in their work in Ghana had reported similar findings where 82% of the care givers would have patronize the patent medicine stores before going to 89 the clinic. Although treating a child at the chemist looks cheaper, when one consider the sub standard treatment that could be given and the associated consequences of delayed access to prompt care as well as the eventual cost of getting retreated on the long run, accessing prompt services at the health facility obviously appeared to be the best thing to do. The observation in this study that the proportion of children with good treatment outcome increases as one goes up the social classes of the caregivers is collaborating the argument by international health c are partners that there should be a strong advocacy at all levels for a pro - poor approachY to the provision of health care services. Gwatkin and Guillot, 2000 in there work hadA obRserved the relationship between poverty and health; poverty leading to ill health, andB illR health leading to increased poverty. Treating the children as outpatient was associaLtedI with good treatment outcome and this could be as a result of the fact that children wNith severe malaria or presumed malaria complication would most likely be admitted for obseArvation during treatment than those with no complications. Those mothers that would disAcovDer that there children have fever when they are restless are more likely to seek hel p IiBmmediately than those who elicits fever by touching as the former would consider OrestFlessness as a sign of severity of the illness while the later would want to observe the chil d in case the fever subsides and this is consistent with Yewhalaw et al., 2010 findingIsT thaYt in Ethiopia caregivers would wait until the child is seriously sick before seeking care aSt the health facility. The use of chloroquine during home management of malaria was assEociaRted with good treatment outcome as compared to the ACT , this also may be as result ofI tVhe fact that majority of the caregivers are familiar with the dosage of chloroquine as comUparNe to the newer drugs which even if they give they are likely to give wrong doses. This is consistent with the findings of Salako et al., 2001, who carried out a study in Nigeria and found that 77.5% of their respondents who had taken chloroquine as self administered first line of treatment were satisfied with the outcome, and this is also an indication that some strains of the falciparum malaria may have retained some form of sensitivity to chloroquine. 90 Majority of the caregivers were knowledgeable about the efficacy of ITN in the prevention of malaria which is similar to the findings by Tarimo et al., 2000 in Tanzania and Nuwaha, 2001 in Ugadan. This study also found that taking a child promptly to the health centre as soon as fever is noticed is a strong predictor of good treatment outcome of children presenting with signs of malaria in the health centres which is in line with the findings of other workers in Africa such as Ibadin et al., 2000 in Benin, Dzeing-Ella et al., 2005 and Mishra et al., 2006. The use of ITN by mothers during pregnancy was a predictor of good treatment outcome and this may havYe been influenced by the strong association that existed between a mother using ITN dAurinRg her ante natal periods and her child using same as was observed in this study. The uBse Rof ITN is believed to reduce the level of parasitaemia in the blood of individuals and this iLs thIought to in turn reduce the level of haemolysis and subsequently the incidence of anaemNia and thus the severity of the illness (Mathanga et al., 2010). Guinovart et al., 2008 had earAlier observed in their study that the level of parasitaemia is significantly associated withA thDe development of anaemia in children with malaria. When caregivers are taught home mIBanagement of malaria or other form of malaria prevention technique, it had significant OimpaFct in predicting positive treatment outcome of under - five children with malaria and thYis is also supported by the work of Ajayi et al., 2008 which showed that when mothers oIr Tcaregivers were taught a new malaria control technique it was largely embraced by the cSommunity and this led to an improvement of the health of children in the community. It EwasR also observed that the presence of signs of severe malaria like anaemia, febrile convuIlsVion etc led to poor treatment outcome and this in effect mean that a child not presenUtingN with them is likely to have a good treatment outcome. This is collaborated by the findings of Mishra et al., 2006 who had earlier documented that the presence of signs of complication of malaria disease can actually lead to the progression of uncomplicated malaria to the severe form. Tangpukdee et al., 2007 while working with adults that had malaria in trying to develop predictive score of uncomplicated falciparum malaria patients turning to severe malaria found dehydration (sunken eyes in children in this study) to be associated with progression of un 91 complicated malaria to the severe form a fact that was also collaborated by Ibadin et al., in their earlier study in 2000. Also (Dzeing et al., 2005) also reported that anaemia, was the frequent features of children patient with severe malaria followed closely by hypoglycaemia and then cerebral malaria (we did not investigate both). However having chills & rigor was a predictor of good outcome in this study with a proportion of 107 (81.1%) to 306 (71.2%) of not having chills & rigor at a statistical significance of P<0.03 and the reason for this might be the fact that whe n a child develops chill and rigors it is mistaken for convulsion and as such help is immediateYly sort at the health facilities. It has already be stated that as part of the findings of thisA stuRdy, it was observed that when a sick child is taken to the clinic <48hrs after fever haBd sRtarted there was a strong associated with good treatment outcome at p<0.046 which is in LessIence supporting one of the Roll back malaria strategies to promptly treat any child with mNalar ia. The observation in this study that when a caregiver uses propAhylactic anti malaria drugs or slept under an ITN while pregnant she is likely to treat herA owDn child prophylacticaly or made him or her sleep under ITN after birth further collabo rIaBted Ajayi et al., 2008 findings in their work. They had observed as earlier stated aboOve tFhat mothers or caregivers could actually during their ANC period be made a useful means of introducing a new malaria control technique into the community as a means of impIrTovinYg the health of children. Though it was observed in this study that when a child sleeps uSnder an ITN and when the mother had earlier used an ITN too during her ANC periods wEereR initially both predictors of good treatment on bivariate analysis. However when both wIeVre subjected to logistic regression modeling, only mother using ITN during pregnUancyN was significant showing that the later was actually a confounding variable. The lessons one can draw from here is that the uptake of those health care interventions that are shared by mothers and their children alike can be enhanced by encouraging/enforcing their practices among mothers. The importance of this finding is further strengthened by the fact that mother taking intermittent preventive treatment (IPT) during her ante natal period was a strong predictor of the child benefiting from same at P<0.00. 92 5.1 Conclusion In conclusion this study has shown that effective management of malaria in children under the ages of five years requires mothers to be knowledgeable about causes and early signs of malaria such as fever that has been proven to be the interactive clinical indicator of malaria infection. They should then seek, obtain, and use medication appropriately as early as possible through timely decision, accessibility and correct use of the drugs and follow-up. When a child prese nts with signs and symptoms of severe malaria at the health centre, there is a high tendency tYhat the illness would deteriorate or the child will not recover within 48hrs (WHO manuAal fRor CHW). Therefore the child would need extra medical care either in a secondaryB facRility or a tertiary facility. If and when the caregiver cannot afford this treatment the lifLe oIf the child would be in danger. It is therefore pertinent that the incidence of mothers wNho sort care elsewhere before coming to the health facility should be reduced as this doeDs noAt only cause unnecessary delays of treatment but also waste the meager resources at Athe disposal of the affected households. Behavioral change communication is an impo rItaBnt method that can be employed so that the incidence of malaria can be reduced drastiFcally in the community. As mothers can be trained during ANC (as was observed in this sOtudy as well as in works done by Ajayi et a l, 2008 and Anumudu et al., 2007) and bIeT mYade to be agents of change and positive influence on other members of the communiSty especially fellow mothers. In this way, the home care practices for the sick child wouEld Rbe strengthened, early presentation of children with fever at the health centres wouldI Vimprove, majority of under - five years children in the community would be sleepiUng uNnder an ITN in line with the Roll back malaria strategy and there would be lower level of parasitaemia in children leading to fewer cases of signs of severe malaria such as anaemia among under - five children in the community. If the government can empower health care workers especially those at the community level, to go into the communities and communicate these various behavioral changes to the mothers, then avoidable mortalities due to malaria among under - five years children would be greatly reduced. This strategy could even be further 93 strengthened to include all the malaria control and prevention measures targeting other members of the community. Finally if we enforce health care service interventions shared by mother and child alike on mothers either during the ante natal or post natal periods, then there are higher chances of the intervention getting to the child. 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Interviewer codIeB 3. Interview date (dd/mm/yyyy)___________________N__ _ L DA SectionB BA F I Demographics of Household/ca rOegivers 4. Marital status: MarrieTd Y Single mother DivorceWidow SI 5. Age in yrs ER 6. OccupatIioVn: 7. LUeveNl of education: Ni I Primary O Secondary Tertiary 8. Relationship with sick child Mother Father Relative Neighbour 9. Who accompanied the care giver and the sick child to the health center? (Check as appropriate) 111 (a) Child’s father (b) Neighbor(s) (C) Relatives (d) Was alone (d) Others specify 10. Residence LGA: Ward: RY Village: A 11. Religion: Pentecosta Orthodox church IslaRm Traditional Others specify______ LIB 12. Number of children < 5 years in the house hold N 13. How much does your household earn in a monthD? A 14. Approximately how much does your housBe hAold spend in a month (housing, feeding, health etc?____________ I OSFection C ASSESSMENT OF THE SICYK CHILD 15. Age of the sick child (SYrIs T)___ 16. Gender of the sick Rchild: Male FemaleE 17. The chiNld isI: V Admitted for observation Outpatient BaselineU information (condition of the child on presentation at the clinic) (History taken from the mother) 18. Which of these symptoms was your child having before bringing him/her for treatment? (Check as appropriate) (a) Fever.............. (b) Vomiting......... (c) Chills & rigor.......... (d) Convulsion............ 112 (e) Child was dull not active (From physical examination of the sick child) 19. These signs were found from examination of the sick child (Check as appropriate) (a) Temperature °C .........(Check with a clinical thermometer) (b) Anaemia............. (c) Jaundice............. (d) Sunken eyes.......... (e) Drowsy.......... (f) Spleenomegaly.......... Y History of the illness R 20. Number of episodes of fever in the last two months? One Two Three Four Others RA 21. When did this current episode of fever start? LIB <12 hrs ago __2 - 48 hrs ago 8 hrs ago Nl~ ~~kact tim e)...... :....... Hrs 22. Where else was this child taken to before bringinDg hAim/her to the health center? Chemist shop Traditional healer BA Church 23. How much does it cost you to treat an < I5 yrs child fever in the (a) Chemist shop ......................... F (b) Using traditional medicine......O............ (c) Health center................. (d) Private hospital..........I..T....Y 24. How much does it coSst you to treat your <5 child with malaria in the health facility? (a) Registration/carRd .........................................(b) Admission pEer day .........................................(c) Anti pyrIeVtic ..............................................(d) Artemisinin combination therapy................................................. (d) ChloNroquine ................................................. (e) HUaematinics .................................................(f) Transportation to the clinic.................................... (g) Others Specify.................................................................................................... Post treatment information/assessment (condition of the child 48hrs later) 25. 48 hours after treatment, child is having (Check as appropriate) (a) Fever............. 113 (b) Jaundice............ (c) Vomiting............ (d) Chills & rigor............ (e) Febrile convulsion.............. (f) Sunken eyes............. (g) Drowsy.............. (h) Child is dull and not playing (i) Non of the above 26. When was anti-malaria drug given to the sick child? RY Immediately after consultation CD 24 hrs after consultation > 24 hrs after consultation | ^act time of administration ... RAHrs LIB 27. When did the fever stop 48 hours after treatment? (a) Immediately after treatment was started..... N (b) < 24 hrs after treatment was started......... A (c) 24 - 48 hrs after treatment was started . . .D (d) Exact time fever stopped.......... :.....B.....AHrs I 28. Classification of treatment 48 hrs aFfter treatment was commenced u □ O Good B SI aTd Y ER Section D Care giver’s aIbVility to carry out home care of a child with fever 29. HowU dNo you recognize fever in your child? (Check as appropriate)(a) When body was hot to touch............. (b) When child became restless ............ 30. When a child is noticed to be febrile, how long does it take before treatment is given? <24 hrs 24 - 48 hrs >48hrs 114 31. Which of these do you normally do when this child develop fever? (Check as appropriate) (a) Wait until it gets serious (b) Give Paracetamol immediately (c) Give full malaria treatment immediately (d) Give treatment the next day (e) Take child to a chemist (f) Take child to health centre (g) Tepid sponge RY 32. Which of these drugs do you give when you do home treatment onR yoAur child with fever. IB (a) Give Paracetamol................. L (b) Give Chloroquine.............. (c) Give camoquine.............. N (d) Give Artesunate.......... A (e) Give Artesunate combination therapy.....D..... (f) Give blood tablet......... A (g) Herbs................ B (h) Other left over drugs from preFvio uIs treatment OSection E Care givers’ general awaIrTenYess about causes of malaria and its prevention 33. Malaria is transmittedS by: Mosquitoes bite Cockroach bite Houseflies bite R others specify__ 34. Which of tIhVese E is/are correct, malaria can be prevented by (Check as appropriate) (a) Clearing the bushes around our homes......... (b) NCovering all open water containers..............U(c) Draining all blocked gutters............(d) Sleeping under IT N .............. (e) Spraying our homes with insecticides............. (f) Taking prophylactic treatment.......... 35. Care givers malaria causing/prevention activities at home (a) Child sleep under mosquitoes net Y N (b) Doors/windows at home has protective nettings Y N 115 (c) Child is usually treated prophylactically for malaria Y N (d) Rooms are sprayed with insecticide Y N (e) Family staying outside in the evenings for fresh air? Y N (f) When you stay outside do you burn mosquitoes coil? Y N Section F Antenatal/postnatal activities 36. Did you sleep under ITN when you were still pregnant of this sick child? Y N Y 37. Did you take prophylactic malaria treatment while pregnant of this sickA chRild?Y N 38. Number of times you were treated for malaria while pregnant ofB thiRI s sick child 39. Was your child small for age at birth? Y N L 40. Did you do exclusive breastfeeding for your baby? AY NN 41. If yes for how long?_____________months AD 42. Is your child fully immunized for age? IYB N 43. If no, how many visits did he/she OmisFses?_____________ 44. Were you ever taught child’s Yhea lth promotion activities in the clinic? Y N IT 45. If yes which of these wSere you taught? (Check as appropriate) (a) Home treatRment of malaria.........(b) How to Eprepare ORS..........(c) What to do when a child has fever at night in the home......... (d) NOthIe Vrs specify_________________ 46. WhUo decides weather to take a sick child to the clinic? (Check as appropriate) (a) Father only............ (b) Mother only............ (c) Either of u s .......... 116 Section G Satisfaction with the services at the health facility 47. What is your opinion about the attitude of the health staff? Good Fair Poor 48. Would you like to come back to this clinic if your child was ever sick? Y N If yes why? _______________________- 49. Did you get all the drugs you need to treat the child in the clinic? Y N If yes which did you get? (Check as appropriate) Y a. Paracetamol............ R b. Chloroquine............. c. Camoquine............. A d. Artesunate............. R e. Artesunate combination therapy.......... IB f. Blood tonic............ LN 50. How far is the clinic from your home? A < 1 km 1 -2 km | 2 -5 km | > 5kmAD 51. What do you think can be done to impro vIeB on the malaria care of <5 yrs in your community? O F ITYS VE R UN I 117 MALARIA TREATMENT OUTCOME AMONG UNDER FIVE CHILDREN AT PRIMARY HEALTH CARE CENTRES IN UMUAHIA NORTH LOCAL GOVERNMENT AREA, ABIA STATE [UMUAHIA NORTH PHC COORDINATOR STRUCTURED KII] Section A Identification RY 1. Questionnaire number______ 2. Interviewer code A 3. Interview date (dd/mm/yyyy)_______________________ BR LI Section B AN Demography/training BA D 4. Rank:— i I DSNO 1— I PNO SNOF NO Others specify____ O ITY 5. Qualification;________S______________ 6. What are the variEouRs units that make up the LGA health dept? IV UN 7. What is the level of training of the various unit head? 118 8. Does the LGA operate the IMCI strategy? Y N 9. Number of staff heading the various PHC facility in the LGA that are trained on IMCI 10. Level of training of the various health facility heads in the LGA? RY RA LIB 11. Is there any arrangement for in service training for the hNeal th staff?Y N A 12. Number of training on IMCI conducted for theA stDaff of the department in the lastone year?_________________________ F I B OSection CMaterial /drugs 13. Did the department distributeY IMCI guidelines/National malaria treatment protocol to the various health faciliStiesI Tin the LGA? Y N 14. Does the LGA havRe enough drugs for the PHC facilities? Y N 15. Which are thVe aEI nti-malaria drugs that are in stock? UN 119 16. How often are these drugs supplied to the various health facilities? weekly monthly yearly 17. Are drugs given freely to the under five been treated for malaria in the health facilities? Y N 18. Are there any extra charges on these drugs by the health facility? Y N if yes, how much?_______ Y 19. On the average what is the cost of treating malaria in the health facility? R (a) Registration/card ......................................... (b) Admission per day ......................................... A (c) Anti pyretic .............................................. R (d) ATC .................................................. IB (d) CQ ................................................. L (e) Haematinics ................................................. (f) Others Specify____________________________A___N_ 20. How often does the LGA health department carryD out supervisory visit to the various health facilities?_______________B__A__ 21. Does the LGA have a protocol of systFem aItic supervision of its health workers at thevarious health facilities? Y O N 22. Does the department have enoYug h staff to carry out its activities?Y IT N 23. Have the department rSeceive any ITN for distribution this year? Y R N 24. What are so EImVe of the malaria control activities carried out by the department? UN 25. Are these activities well funded? Y N 26. What is the immunization coverage of the LGA? 120 27. What are some of the challenges faced by the department? AR Y LIB R AN D IB A O F TY RS I E IV UN 121 MALARIA TREATMENT OUTCOME AMONG UNDER-FIVE CHILDREN AT PRIMARY HEALTH CARE CENTRES IN UMUAHIA NORTH LGA, ABIA STATE [PHC FACILITY HEAD KII] Section A; Identification RY 1. Questionnaire number___ 2. Interviewer codeA 3Interview date (dd/mm/yyyy) IB R Section B; LN Demography and training DAA 4. Age: (Yrs) IB 5. Gender: Male Female O F 6. Rank: Y DSNO PTNO SNO NO CHW Others specifyS_ I 7. Level of trainingE; RV PGD B.Sc Sch of Nurs NI Sch of Health tech Others specify_ 8. WheUre you ever trained on use of IMCI? Y N If yes how long ago_______________ 9. Did you receive any training on the management of malaria in the last one year? Y N 122 10. How many staff in this clinic can attend to patients with malaria? 11. On the average, how many patients come to this clinic in a day? 12. How many of them were treated for malaria? _________ 13. How many other support staff do you have in this clinic?______ Section C: Y Materials R 14. Do you have the IMCI guideline? A Y N If yes sight............. R 15. Do you have the National treatment protocol for malaria?IB Y N If yes s ig h t................ L 16. Does this facility have any provision for patient admNission? Y N If yes, how mDanAy beds? ______ 17. Does this facility have the following maBterAials? (a) Thermometer? Y N If yes sIight......... (b) Weighing scale? Y N If yFes sight......... (c) Water? Y N If yes sighOt tap or water/container.... (d) Mosquitoes nets for patYien ts on admission? Y N If yes s ig h t.(e) Stethoscope? Y IT N If yes sight...........(f) Monitoring chart? SY N If yes s ig h t............R 18. Number of hoEurs the clinic js_open for service <24 hrs n IV 24 hrs UN Section D; Patronage 19. Average Number of patients seen per day (from treatment book record) 123 20. From your observation, what proportion of mothers would have commenced treatment for their sick child before coming to the clinic? < 30% 30 - 50% 50 - 80% >80% 21. What form of treatment do mothers normally give at home before coming to the health centre? (a) Gave concoctions/herbal medicine Y N (b) Gave PCM Y N (c) Gave Chloroquine Y N (d) Gave Artesunate Y N Y (e) Gave nothing Y N R Record keeping RA 22. What year did this facility become fully operational____L__I_B___ 23. Does this facility have complete record of all itsA acNtivities since inception?Y N If yes confirm... D 24. How many years’ records are availablBe?.A......... 25. How many children where immunFize dI in this facility last year? _____Check the immunization reOgister......... Availability of antiI TmaYlarial drugs/ITN 26. What drugs do youS normally use in the treatment of malaria in this facility? VE R NIU Are these drugs available in this clinic? Y N Sight to confirm which are available.................... 27. Have this facility received any ACT from the LGA this year? Y N 124 28. If yes are they still in stock? Y N 29. Have this facility given ITN for distribution this year? Y N 30. If yes, are they still in stock? Y N 31. Have you been out of stock of drugs? Y N If yes how long 32. When out of stock of drugs what do you advice patients to do? Y (a) Buy drugs in a chemist shop? Y N R (b) Refer patients to other clinics? Y N RA 33. Number of times supervisors from the LGA visited this faIcBility in the last two months L N 34. On the average what is the cost of treating malAaria in this health facility? (a) Registration/card .................................D....... (b) Admission per day ............................A............ (c) Anti pyretic ..................... ..I..B....................(d) ATC ..................F.............................(d) CQ ................................................ (e) Haematinics ..........O...................................... (f) Others Specify................Y..... ................................................ .........................IT 35. How do you make dSiagnosis of malaria in the health center? (a) From laboratoRry results? Y N (b) Clinical exEamination? Y N (c) FroNm tIh Ve complaints? Y N U 125 Map of Abia State with the study area marked in green RY RA LI B N AD A IB O F ITY RS VE UN I 126