PREVALENCE OF MALARIA AMONG CHILDREN BETWEEN 0-5 YEARS IN SANGERE COMMUNITY OF GIREI LOCAL GOVERNMENT, ADAMAWA STATE BY AINA SOLOMON DL/HC/17D/0073 1 TABLE OF CONTENTS CHAPTER ONE .................................................................................................................. 4 1.0 INTRODUCTION ......................................................................................................... 4 1.1 Background of the Study ............................................................................................... 4 1.2 Statement of the Problem ............................................................................................... 5 1.3 Aim of the Study ............................................................................................................ 6 1.4 Objective of the Study ................................................................................................... 6 1.6 Significance of the Study .......................................................................................... 6 1.7 Limitations of the Study................................................................................................. 6 CHAPTER TWO ................................................................................................................. 7 LITERATURE REVIEW .................................................................................................... 7 2.1 Epidemiology of Malaria. .............................................................................................. 7 2.2 The Role of Climate on the Spread of Malaria ............................................................ 11 2.3 The Parasite .................................................................................................................. 11 2.3.1. Life Cycle of Malaria Parasite ................................................................................. 12 2.3.1.1. Human Cycle ........................................................................................................ 12 2.3.1.2. Mosquito Cycle ..................................................................................................... 13 2.4 The Vector ................................................................................................................... 16 2.5 The Host Factor............................................................................................................ 16 2.6 Pathology and Clinical Manifestations ........................................................................ 17 2.7 Mode of Transmission ................................................................................................. 17 (a) Vector Transmission/Direct Transmission ............................................................... 17 (c) Congenital Transmission .......................................................................................... 18 2.8 Diagnosis and Treatment of Malaria............................................................................ 19 Treatment and Chemoprophylaxis of Malaria ................................................................... 19 2.9 Control of Malaria...................................................................................................... 21 2 CHAPTER THREE ........................................................................................................... 24 RESEARCH METHODOLOGY....................................................................................... 24 3.1 Research Design........................................................................................................... 24 3.2 Study Area ................................................................................................................... 24 3.3 Study Population .......................................................................................................... 24 3.4 Sampling Technique .................................................................................................... 24 3.5 Instrument of Data Collection ...................................................................................... 25 3.6 Method of Data Analysis ............................................................................................. 25 REFERENCES .................................................................................................................. 26 APPENDIX ........................................................................................................................ 30 3 CHAPTER ONE 1.0 INTRODUCTION 1.1 Background of the Study Malaria is an infectious disease caused by a parasite known as plasmodium which infects red blood cells, is transmitted to human from person to person through the bite of an infected female anopheles’ mosquito (Benson, 1985) The disease is caused by one of’ the four (4) species of protozoa of the genus plasmodium to which humans are susceptible; they are plasmodium falciparum, plasmodium malaria, plasmodium ovale and plasmodium vivax. The disease occurs throughout the tropical and subtropical regions and it can occur also in temperate climate if the condition of’ the temperature is favorable for the plasmodium to complete their life cycle as mosquito. The plasmodium falciparum is the most virulent in all parts of’ Africa, accounting for up to 98% of the cases in Nigeria and is associated with significant morbidity, mortality and also responsible for all features of severe malaria. The other species which include Plasmodium malaria, Plasmodium vivax and Plasmodium ovale are still found sporadically in some temperate regions in the Nigerian context and most levers are not all malaria Fever. The rule of’ thumb is 24 hours before journey to malarious country and continuous 14 days after exist. according to Djo and Briggs (2000) that the parasite can be transmitted through these ways, firstly infected anopheles’ mosquito bite, secondly through transfusion of’ blood that was already infected with malaria parasite and thirdly through the use of’ unsterilized syringe and needles during injection that has been contaminated with the parasite. Furthermore, malaria infection may have diverse catastrophic effect in pregnant women and children under 5years raging from mild to severe which lead to miscarriage or maternal abortion, anemia and maternal death to pregnant woman and also death of’ under five (5) years children in Nigeria and our communities. The disease is characterized clinically by fever, headache, chills, rigour vomiting, and malaise, general weakness of’ the body anorexia (loss of’ appetite) and profuse sweating. The risk of malaria is higher in the rural areas but the disease is also in urban areas where they have poor environmental sanitation. The disease starts when an infected female anopheles mosquito bites and inject parasite into the human blood stream while feeding. These threads make Parasite disappear from the blood about half’ an hour known as “pre-erythrocyte schizoids’ this last for 5 to days, schizoid burst to release Merozoites invade blood cell (RBC) and become trophoziote 4 which mature in the large schizoid. During the second feeding the mosquito inoculates the ingested parasite into a healthy person and this is the commonest mode of infection (Ojo, 1982). The federal ministry of’ health (FMOH), (1990) stated that malaria remains one of’ the leading causes of’ morbidity and mortality among pregnant women and children in the tropical especially in Nigeria communities. The Roll Back Malaria programme (RBM) initiative came as a result of the commitment by the former Director General of World Health Organization, Dr Gro Harlem Brundtland. She, in conjunction with other organizations including, United Nations International Children Education Fund (UNICEF), United Nation Development Programmed (UNDP) and WORLD BANK, initiated this project targeted at reducing the morbidity and mortality of malaria in African region by 50% by year 2010. Nigeria showed a strong commitment by hosting the first Africa malaria summit at Abuja on 25th April 2000. The malaria is a burden worldwide by the year 2000 through multination approach (Bola, 2004). The federal government of’ Nigeria has demonstrated her political commitment to the initiative by hosting the Africa summit on Roll back Malaria (RBM) in Ahuja in April 2000 which resulted in signing of’ the African summit on RBM. OBIONU (2001) defined as the number of people in a population who have the disease, both new and old cases at a given point in time. He further added that prevalence depends on the incident and the duration of that prevalence disease and this relationship is expressed mathematically as thus. Prevalence Rate = incidence rate X average duration. The disease is still a scourge of mankind in Sengere Community, Girei LGA of Adamawa state. Where its’ average still remains uncontrolled, the malaria disease in Sengere community for children from 059months of age. 1.2 Statement of the Problem Malaria is a serious illness that negatively affects the wellbeing of human beings. The disease has no restriction of age status and gender it has been revealed to be more severe among children whose ages range between (O-5years). Records from public and private clinics revealed that malaria and its related cases are still rampant in rural areas of Girei local Government area of Adamawa State which affects Children, adults, old age, especially pregnant mothers and Children between age 0— 59months old. 5 Observations indicate that most parents spend a lot on their children and other dependents over the treatment of malaria, this affects their wellbeing and state of health of the families lining in the area as well as their economic status respectively. 1.3 Aim of the Study The aim of this study is to determine the prevalence of malaria disease among children of 0 to 5 years in Girei LGA Adamawa State. 1.4 Objective of the Study 1. To determine the prevalence of malaria among children between 0-5years of age in both male and female 2. To suggest relevant drugs that are recommended for the management of malaria disease. 3. To promote community sensitization and awareness of malaria control and management at the community level 1.6 Significance of the Study 1. Assist the government to know the level of Malaria infection in that local government among children. 2. Assist in identifying the relevant drugs to treat the disease. 3. Sensitize the inhabitants on health education such as keeping of healthy environment. 1.7 Limitations of the Study This work is limited to the study of prevalence of Malaria among children between the age 0-5years in Girei Local Government Area, Adamawa state. 6 CHAPTER TWO LITERATURE REVIEW 2.1 Epidemiology of Malaria. Malaria, a mosquito-borne Protozoa disease, is older than recorded history; and probably plagued prehistoric man. The first record of a treatment for the disease dates from 1600 AD, in Peru, and utilized the quinine rich bark of the cinchona tree (Garnham, 1966). Scientifically, it is not a newly described disease. Approximately 40% of the world’s population lives in regions where malaria transmission is endemic, mainly tropical and subtropical regions (Aultman et al., 2002). Malaria has been successfully controlled, in fact effectively eliminated, in temperate regions of the world (Sachs and Malaney, 2002). The control strategies employed in temperate regions included changes in agricultural and construction practice reducing the availability of standing water and targeted vector control using insecticides such as DDT (Greenwood and Mutabingwa, 2002). Industrialization and improved housing conditions were instrumental in the elimination of the disease in temperate countries (Budiansky, 2002). The role of mosquito in the life cycle of P. falciparum requires that the parasite be able to maintain an extended infection in order to ensure transmission ability during the following season (Kyes et al., 2001). Now that the sequences of the three participants in the life cycle of human malaria, Plasmodium species, Anopheles species, and Homo sapiens, are all complete and available in endemic areas, perhaps new strategies of disease control will succeed. Malaria is distributed mainly between latitudes 450-670 south (Clyde, 1981). These regions embrace about 102 countries or areas of the world reported with indigenous malaria. These areas are typically in the tropical belt. In studying the malaria situation and distribution, China and India have continued to report downward trends. However, the malaria situation continues to deteriorate in rural area where intensive economic, social, behavioural and technical factors are taking place, particularly in Asia and America, while in the remaining area, it is fluctuating. African countries lying in the tropical belt have been known to be highly endemic for malaria, particularly in the early 1970s when malaria deaths were estimated to be in the order 9, 750,000 annually. The most common type of malaria caused by P. vivax occurs in the temperate regions, whereas P. falciparum is largely confined to the tropics, P. malariae is considerably rarer and has a focal distribution, P. ovale, rather than P. vivax is the benign relapsing fever in 7 West Africa but it is found less frequently in other parts of Africa. This pattern of distribution is because P.vivax (not P. ovale) requires Duffy blood group receptors on erythrocyte membrane and these receptors are lacking in many Africans, particularly west African (Miller et al., 1976). Chloroquine-resistance and P. falciparum malaria has now been confirmed in more than 40 countries, but the situation tends to deteriorate further, especially in Africa, as the drug pressure on the parasites increase in the absence of substantive vector control. Sulfadoxine/pyrimethamine resistance has now been reported from 11 countries and resistance to mefloquine reported in the Philippines, the United Republic of Tanzania and Thailand. P. falciparum continues to be sensitive to these drugs in Middle America, the Caribbean, West Africa and most countries in Asia, west of India. Figure 1 shows global distribution of malaria as shown in the world map. The unshaded region shows areas (which occupies 28% of world population) where malaria either never existed or disappeared without specific anti-malaria measures, while the doted areas correspond to region (16% of the world population), in which the disease has been eliminated during recent decade by the general improvement of health service, changes in the environment and successful anti-malaria activities and the striped regions correspond to region (about 50% of world population), in which anti-malaria measures are carried out because of the prevalence or endemicity of the malaria disease (WHO, 1986). In many of these areas the health infrastructure is not sufficiently developed to ensure that the favorable epidemiological situation is maintained. Their epidemiological situation is precarious as they are under the constant threat of intensification and spread of specific malaria problems, such as resistance of parasites to drugs or vectors to insecticides, thus making control measure less effective and more costly. Although efforts are being made to incorporate appropriate anti-malaria activities into developing primary health care systems, progress appears to be slow, managerial and organizational problems persist (WHO, 1986). In Africa north of Sahara, transmission continued to be limited to a small facet. The total number of cases reported in this area increased from 453 in 1983 to 666 in 1984. An increase of transmission was observed in the northern provinces of Morocco. In Africa south of the Sahara, the malaria situation did not change. In the malarious areas, endemicity varies greatly from place to place although in general, malaria prevalence has remained unchanged. It has been estimated that some 115 million cases occur in mesoendemic zone and 231 in areas where malaria is hyper-endemic to holo-endemic. In most of these countries, vector control operations are not feasible, especially in rural areas, for a 8 variety of technical, operational, administrative and financial reasons. The only action that could be currently attempted in these countries is the prevention and reduction of mortality and morbidity through the rational use of anti-malaria drug. But one of the major constraints hampering the implementation of these anti-malaria actions is the lack or shortage of trained personnel for the planning, organization, monitoring and evaluation of programmes that are carefully designed with clearly stated objectives and targets that can actually be implemented and maintained according to the available resources and local conditions (WHO, 1986). 9 10 2.2 The Role of Climate on the Spread of Malaria Climate can influence all three components of the life cycle of malaria parasites. It is thus a key determinant in the geographic distribution and seasonality of malaria. Rainfall can create collections of water (breeding sites) where Anopheles eggs develop into adulthood, a process that takes place in damp areas. Such breeding sites may dry up prematurely in the absence of rainfall, or conversely, they can be flushed, and destroyed by excessive rains (Mouchet, 1998). Once adult mosquito has emerged, the ambient temperature, humidity and rains determine their chances of survival. To transmit malaria successfully, female Anopheles must survive long enough after they have been infected (through blood meal on an infected human) to allow the parasite they now harbor to complete their growth cycle (extrinsic cycle). The cycle takes 9-12 days at 250C or 770F. Warmer ambient temperatures shorten the duration of the extrinsic cycle /transmission. Conversely, below a minimum ambient temperature (150C or 590F for Plasmodium vivax, 200C or 680F for P. falciparum), the extrinsic cycle may not be completed. This explains in part why malaria transmission is greater in warmer areas of the globe (tropical and semi-tropical areas and low altitudes particularly for P falciparum (Mouchet, 1998). It has been speculated that current trends of global warming may increase the geographic range of malaria and may be responsible for malaria epidemics (Wilson, 1991). Climate also determines human behaviours that may increase contact with Anopheles mosquitoes between dusk and dawn, when the Anopheles are most active. Hot wheather may encourage people to sleep outdoors or may discourage people from using bed nets. During the harvest season, farmers may sleep in the fields or nearby locals, without protection against mosquito bites (Mouchet, 1998). 2.3 The Parasite Human malaria results from infection with Plasmodium falciparum, P. vivax, P. ovale, or P. malariae. Plasmodium falciparum causes a large majority of the clinical cases and mortalities (Bozdech et al., 2003). Plasmodium is a protozoan parasite of the Phylum Apicompleza, Class Sporozoea. Reproduction generally is both sexual and asexual. Locomotion of mature organisms is by body flexon, gliding, or undulation of the longitudines ridges. Flagella is present only in microgametes, pseudopods ordinarily absent (Cheng, 1986). 11 2.3.1. Life Cycle of Malaria Parasite Malaria is transmitted by the bites of infected female anopheline mosquitoes or by inoculation of infected blood (e.g. transfusion malaria, congenital malaria) (Hendrick, 1972). Malaria parasite shows a complex life cycle involving alternating cycles of asexual division (schizogony) occurring in man (intermediate host) and sexual development (sporogony) occurring in female Anopheles mosquito (definitive host). (Arora and Arora, 2005). Therefore, Plasmodium shows alternation of generation and alternation of hosts (Webster, 2000) 2.3.1.1. Human Cycle The infective stage called sporozoites, are injected from the mosquito salivary glands into subcutaneous capillaries and circulate to the liver where they invade parenchyma cells. Arora and Arora (2005) outlined the process of Plasmodium life cycle in man as follows: Within one hour of infection all the sporozoites leave the blood stream and enter into liver parenchyma cells. The sporozoites which are elongated, spindle-shaped bodies become rounded inside the liver cells. They undergo a process of multiple nuclear division, followed by cytoplasmic division and develop into primary exoerythrocytic schizont. This varies in size according to species from 24-60nm in diameter and contains 2,00050,000 merozoites (Bruce-Chwatt, 1985). Primary exoerythrocytic schizogony consists of only one generation. The duration of this cycle varies, for P. falciparum, P. vivax, P. ovale and P. malariae it is 6,8,9 13-16 days respectively (Breman, 2001). When primary exoerythrocytic schizogony is complete, the liver cell ruptures and releases merozoites in the blood stream. The merozoites liberated from primary exorythrocytic schizogony enter the blood stream and invade red blood cells where they multiply at the expense of the host cells. The age of erythrocytes is an important determinant of its susceptibility to invasion by different species of the parasite. Only young erythrocytes are infected by P. vivax and P. ovale, and only old subpopulation of erythrocytes is susceptible to P. malariae, in contrast, P. falciparum can develop in erythrocytes of all ages. Here they pass through the states of trophozoites, schizonts and merozoites. Depending on the species, about 6-32 nuclei are produced followed by cytoplasmic division and the red cell ruptures to release the individual merozoites, which then infect fresh red blood cells (Miller et al., 1976), it is at the time of the escape of merozoites that chill and fever beset the host (Pyrexia) (Cheng, 1986). Erythrocytic schizogony may be continued for a considerable period, but in the course of 12 time the infection tends to die out. P. falciparum differs from the other forms of malaria parasite in that developing erythrocytic schizonts occur in internal organs, so that only ring forms are found in peripheral blood. This process is approximately 72 hours for P. malariae and 48 hours for the other three species. After malaria parasites have undergone erythrocytic schizogony for certain period, some merozoites develop within red cells into male and female gametocytes known as macrogametocytes and micro-gametocytes respectively. They develop in the red blood cells of capillaries of internal organs like spleen and bone marrow. Only mature gametocytes are found in the peripheral blood. They do not cause any febrile condition in human host. These are produced for the propagation and continuance of the species. The micro-gametocytes of all the four species of Plasmodium are small in size. Cytoplasm stains light blue and the nucleus is diffuse and large, on the other hand, the macro-gametocytes are large, the cytoplasm stains deep blue and the nucleus is compact and small (Cheesbrough, 2005). Although the longevity for mature gametocytes may exceed several weeks, their half-life in the blood stream may be only 2 or 3 days, while waiting for the mosquito to take them up (Freyvogel, 1966). In case of P. vivax and P. ovale, some sporozoites on entering into hepatocytes enter into a resting (dormant) stage before undergoing sexual multiplication while others undergo multiplication without delay. The resting stage of the parasite is rounded, 4-6um in diameter, uninucleate and is known as hypnozoite. After a period of weeks, months or years (usually up to 2 years), hypnozoites are reactivated to become secondary exoerythrocytic schizonts and release merozoites, which infect red blood cells producing relapse of malaria. Therefore, it is the situation in which the erythrocytic infection is eliminated and a relapse occurs later because of a new invasion of the RBCs from liver merozoites. Hypnozoites are not formed in case of P. falciparum and P. malariae, therefore relapse does not occur in disease caused by the species (BruceChwatt, 1983). 2.3.1.2. Mosquito Cycle Sexual cycle actually begins in the human host by the formation of gametocytes, which are present in the peripheral blood. Both asexual and sexual forms of the parasite are ingested by female Anopheles mosquito during its blood meals from the patient. In the mosquito, only the mature sexual forms are capable of further development and the rest dies. In order 13 to infect a mosquito, the blood of human carrier must contain at least 12 gametocytes and the number of female gametocytes must be in excess of number of males (Garnham, 1966). Within the gut of the mosquito, the male gametocytes undergo a process of exflagellation which results in the release of up to 8 male gametes. The fertilized macrogamete is known as zygote. This occurs in 20 minutes to 2 hours, in the next 24 hours, the zygote lengthens and matures into ookinete, a motile vermiculate stage (Freyvogel, 1966). It enters the epithelial lining of the stomach of the mosquito and comes to lie between the external border of the epithelial cell and peritrophic membrane. Here it develops into oocyst. It is rounded, 6-12nm in diameter with a single vesicular nucleus. It increases in size to reach a diameter of 40-50 um. Inside this develop sporozoites. The number of sporozoites in each oocyst varies from a few hundreds to a few thousands and number of oocysts in the stomach wall varies from a few to more than a hundred. On about the 10th day, the oocyst is fully mature, rupture and release sporozoites in the body cavity of the mosquito. Through body fluid the sporozoites are distributed to various organs of the body except the ovaries. They have special predilection for salivary glands and ultimately reach in maximum numbers in the salivary ducts. At this stage the mosquito is capable of transmitting infection to man (Garnham et al., 1961; Garnham, 1963, 1966). 14 15 2.4 The Vector Anopheles gambiae, A. arabiensis and A. funestus transmit most of human malaria and are all found in Africa (Besansky et al., 2004). A. gambiae, the most famous and significant of these three, is one of sixty anophline mosquitoes able to transmit malaria to humans (Budiansky, 2002). A. gambiae is the primary malaria vector; this can be attributed, in part, to its relatively long life, strong anthropophily and endophily (the tendency to target humans for blood meal and rest inside of houses, respectively) (Besansky et al., 2004). Adult mosquitoes normally rest during the day inside human habitat and emerge to feed at night (Holt, 2002). Their larvae tend to develop in temporary bodies of water, such as that typically found near agricultural sites or even in flood hoof prints (Vogel, 2002). All these characteristics combine to make A. gambiae a successful vector. The behaviour is remarkable and can be highlighted with comparison of the entomological inoculation rate (EIR) of infectious mosquitoes in Asia or South America and sub-Saharan Africa. The EIR measures how often one person is bitten by an infected mosquito. In Asia and South America a person’s EIR rarely exceeds 5 bites per year. In Sub-Saharan Africa, a person may have an EIR of over 1000 bites per year (Greenwood and Mutabingwa, 2004). Greenwood and Mutabingwa (2004) also reported that during a single night in sub-Saharan Africa, hundreds of mosquitoes typically collect in a room occupied by humans; 1-5% of these are infectious. Some diseased control strategies deal with the Anopheline mosquito rather than the parasite. One strategy for attacking mosquitoes is to develop more effective insecticides. The main obstacles to this line of attack are growing insecticides resistance and environmental concern. The publication of A. gambiae genome (Holt, 2002) should help to identify the genes involved in resistance and to design chemicals for attacking new targets in the mosquito. The failure of the WHO’s malaria eradication program was, to a significant degree, due to increasing resistance to DDT and the fact that people did not want their homes to be sprayed (Greenwood and Mutabingwa, 2002). The current and most widely used technique for vector control is insecticide treated bed-nets. Genomics may prove key in the development of new insecticides and may also improve the longevity of available insecticides (Hemingway et al., 2002) 2.5 The Host Factor Factors in humans that determine the status of malaria are acquired and inborn. An acquired strain-specific immunity has been observed that appears to depend upon the presence of 16 low-level parasitaemia that somehow inhibits new infections or maintains the infection at a non symptomatic level. This so called premunition or concomitant immunity, is soon lost after the parasites disappear from the blood. Exoerythrocytic forms in the liver cannot alone support premunition, and they elicit no host inflammatory response (Mckerrow and Parslow, 2001). Natural genetically determined partial immunity to malaria occurs in some populations, notably in Africa, where sickle cell disease (AS genotype), glucose-6phosphate dehydrogenase deficiency, and thalassemia provide some protection against lethal levels of falciparum infection (Mckerrow and Parslow, 2001). Most blacks in West Africa, where malaria is endemic are not infected by P. vivax because they lack the Duffy antigen (FyFy), which acts as a receptor for P. vivax; in its absence, P. vivax cannot invade erythrocytes. P. ovale frequently replaces P. vivax in this region (Mckerrow and Parslow, 2001; Voller, 1993). 2.6 Pathology and Clinical Manifestations Periodic paroxysms of malaria are closely related to events in the blood stream. An initial chill, which lasts from 15 minutes to 1 hour, begins as synchronously dividing generations of parasites rupture their host red cells and escape into the blood. Nausea, vomiting and headache are common at this time. The succeeding febrile stage lasting for several hours, is characterized by a spiking fever that frequently reaches 400C or more. During this stage, the parasites presumably invade new red cells. The third or sweating stages conclude the episode. The fever subsides and the patient falls asleep and later wakes feeling relatively well. In the early stages of infection, the cycles are frequently asynchronous and the fever irregular, later paroxysms may occur at regular 48-72 hour intervals, although P. falciparum pyrexia may last for 8 hours or longer and may exceed 410C. As the disease progresses, splenomegaly and to a lesser extent, hepatomegaly appears, particularly in P. falciparium infections (Peters and Pasvol, 2002). 2.7 Mode of Transmission (a) Vector Transmission/Direct Transmission The female Anopheles mosquito is the transmitter of malaria parasite, this is facilitated by its blood meal from man and other vertebrate host. The proboscis plays a crucial role in the blood meal. Transmission depends not only upon the presence of gametocytes in the blood, but also upon the infectivity of these for mosquitoes. The growth rate of the larva of mosquito determines transmission rate and is directly proportional to the suitability of the 17 environment to its requirements which vary from species to species. The distribution and frequency of malaria in tropical Africa depend more or less directly on the climate and among the various climatic factors involved, two surpass the others in importance: rainfall and temperature (Mouchet, 1998). The most striking feature of malaria is its high endemicity with hardly any seasonal changes. The climatic condition favours an intense transmission of P. falciparum, the prevailing parasite, through mosquito vector of which the notorious and ubiquitous A. gambiae is the most important because of its wide distribution, breeding habits, large numbers and preference for human blood. In a general way, the transmission of malaria diminishes progressively from the equator as latitude increases (Bruce –Chwatt, 1984). (b) Blood Transmission Malaria can be transmitted by the transfusion of blood from an infected person to healthy persons. In this way the sexual blood forms continue to develop in their own periodicities and the peripheral blood forms producing attacks of fever in the recipient, but preerythrocytic and exo-erythrocyitc stages are not formed in the liver, because these forms originate only from sporozoites inoculated by mosquitoes. Malaria transmitted in this way is easily cured and relapses do not occur. The possibilities of acquiring malaria by heroin intravenous infection has also been established, cases of induced malaria in narcotic abusers due to P. falciparum infection were also reported in Europe (Ring and Jepsen, 1979; Orlando et al., 1982). (c) Congenital Transmission Congenital malaria was reported by Covell (1950) who concluded that intra uterine transmission from mother to child is established. Congenital infection may be achieved without damage to the placenta, infection of the placenta may break down the barrier. This applies to all species of malaria parasite. This results in still birth, abortion and death in new born babies. Madecki and Kretscher, (1966) studied Nigeria women and found that in most cases, the babies are infected during parturition. Malaria in pregnancy is a critical problem, various studies show that parasitaemia increases between the first and second trimester of pregnancy. Trasmammary transmission is also possible. 18 2.8 Diagnosis and Treatment of Malaria Diagnosis of malaria involves identification of malaria parasite or its antigens/products in the blood of patients (WHO, 1997). Early, prompt and accurate diagnosis and treatment of malaria is crucial to the management of the morbidity and mortality caused by the infection. Accurate diagnosis is one of the main interventions used in the global control of malaria (Menakaya, 2000). Malaria is diagnosed by the examination of the blood (WHO, 1993). Immunodiagnosis has limited clinical usefulness but positive indirect hemagglutination (IHA) and indirect fluorescent antibody (IFA) tests are valuable for epidemiological surveys and with the complement fixation test, for screening potential blood donors. The diagnosis of malaria is confirmed by blood test and can be divided into microscopic and non-microscopic (Makler 1998, WHO, 2000). (a) Microscopic Test: For nearly a hundred years, the direct microscopic visualization of the parasite on the thick and/or thin blood smear has been the accepted method for the diagnosis of malaria in most settings, from the clinical laboratory to the field surveys. The careful examination for a well prepared and well stained blood film currently remains the ‘gold standard’ for malaria diagnosis. This includes: i. Peripheral smear study, ii. Quantitative Buffy Coat (OBC) Test, (b) Rapid Diagnostic Test: Several attempts have been made to take malaria diagnosis out of the realm of the microscope and microscopy. These tests involve identification of parasite antigen or the antiplasmodial antibodies or the parasitic metabolic products. Nucleic acid probes and immunofluorescence for detection of plasmodia within the erythrocytes; gel diffusion, counter-immunoelectrophoresis, radio immunoassay, and enzyme immunoassay for malaria antigens in the blood fluid, and hemagglutination test, indirect immunoflourescence, optimal assay, polymerase chain reaction, immunochromatography, and Western blotting for anti plasmodial antibodies in the serus have all been developed. These are (RDTs) (Makler, 1998). Treatment and Chemoprophylaxis of Malaria Treatment for malaria was not available to Europeans until the 1600s, when the Incas in Peru offered the concoction from the bark of a “fever tree” (Cinchona). Modern-day quinine originated from it. Current drug to treat malaria such as doxycyline, proguanil and 19 primaquine attack liver stage, thus preventing the release of parasite into the blood stream. Others, such as chloroquine, quinine sulfadoxine, pyrimethamine (fansider) and mafloquine, kill the parasite within the red blood cells (Russel, 1996). Chemoprophylaxis for malaria is recommended for non-immune persons entering areas endemic for malaria to reduce, but not totally eliminate, the risk of infection. Chemoprophylaxis is also recommended for high-risk group such as infant and young children, pregnant women, recent immigrant from malaria-free area. Prophylaxis for children is debated because of the risk of long-term side effects and selection for resistant parasite strains (Collins and Paskewitz, 1995). Chemoprophylaxis of malaria is directed at prophylaxis and presumptive treatment (Jeffery, 1984). a. Presumptive Treatment: This is the treatment of cases suspected of being malarious on the basis of symptoms by the patient, but not symptoms diagnosed by blood film examination prior to treatment. The drug used should be curative with a single dose, have a minimum side effect and acceptable to population (Jeffery, 1984). The most common single dose for suspected malaria has 600 mg (base) of chloroquine as the adult dose, this is usually administered as 1.5 base over a 3 day period b. Prophylaxis: Since the segments at greatest risk are pregnant women and children up to age 5, there is no doubt as to the benefit of regular prophylaxis in women (reduced mortality and morbidity). The aims of therapy are to destroy the first hepatic schizonts before they liberate their daughter (merozoite cells) which infect red cells, to destroy the erythrocytes blood schizont form before their merozoites are released, to destroy the gametocytes before they are taken up by a mosquito bite Chemotherapeutic drugs used against the attack of malaria are classified into the following depending on the parasite stage of attack: i. Blood Schizonticidal Drugs: These drugs are used in the treatment of acute malaria attack, -4- aminoquinolines e.g. chloroquine are blood schizonticides most effective against the blood form of the parasite. ii. Tissue Schizonticidal Drugs: Destroys the asexual form of the parasite. Some drugs have a pronounced anti-relapse effect and are extensively used for radical treatment of malaria. 20 iii. The Gametocidal Drugs: Destroys the sexual form of the parasite. iv. Sporozoiticidal Drugs: Inhibits the development of oocysts on the stomach wall of the mosquito. The UK malaria reference laboratory recommends that proguanil or chloroquine may be used (as opposed to drugs found locally) as these drugs give protection against P. vivax and susceptible strains of P. falciparum. 2.9 Control of Malaria Control of malaria is undoubtedly the best method of protecting a community against the disease. During the 20th century, human efforts to control malaria and general socioeconomic development including access to health care have markedly reduced the spread of malaria (MacDonald, 1957). Control of this deadly menace would therefore involve three living beings: man (the host), Plasmodium (the agent) and Anopheles mosquito (the vector). Several methods are used to prevent the spread of malaria, to reduce transmission and manage morbidity among the infected. Such methods are broadly divided into transmission control and morbidity control. These controls include: a. Chemotherapy: the treatment for various species is different (Goldsmith, 2004), chloroquine and drugs like it will kill all four species of Plasmodium when they are in the cell (Goldsmith, 2004) and prompt treatment is the best means for the management of all species of malaria. This is because prompt treatment eliminates an essential component of the cycle (the parasite) and thus interrupts the transmission cycle (WHO, 2000). Chemotherapy of malaria is directed at prophylaxis and presumptive treatment. The artemisinin-based combined therapy (ACT) has in recent times been the most effective treatment for malaria. The more recent drug is Coartem, which was developed in 1994, and combines artemisinin (a compound from wormwood plant) with lumefantirine. Designed by Chinese Scientists, Coartem not only kills the parasite, it also stays long in the blood to help prevent any resistance by the malaria parasite (Oyeniyi, 2009) b. Biological Control: This method of control includes natural measures; natural limiting factors are deliberately intensified without any reliance on chemical or mechanical devices. Larvivorous fish are natural enemies of mosquito larva and have been utilized with advantage for malaria control E.g. Gambusia affinis, gold 21 fish (Carasius quratus), Romanomermis jingdeensis, a newly identified mamethid nematode has been found to parasitize larva of A. sinesis. In the semi-arid region of North Somalia, it was shown that malaria can be controlled by introduction of species for larvivorous fish (Oreochromis spilurur spiluru) into mosquito breeding site (Zahar, 1984). Carp (Cyrinus capio) a species of tilapia eat aquatic plants, floating algae and other vegetable shelter for Anopheles; Baccillus shaerious, a larvicidal bacterium is toxic to several species of mosquito. It is capable of recycling even in highly polluted water. Coelomyes, a fungus of the Chytridomycete sub class is obligate parasite of mosquito and most are specifically pathogenic, each to a single species complex of Anopheles mosquito (Ree, 1982). c. Genetic Control: This method reduces the reproductive potential of insect by altering the hereditary material of the vector species. Genetic control may be achieved by the following methods; i. Irradiation – Males are sterilized by ionizing irradiation- the principle is that the sterilized males seek out and mate with the wild female in the natural populations thus preventing the hatching of the eggs and lowering their reproductive potential. ii. Another method of genetic control is based on crossing sibling species of an insect. This leads to hybrid that are released, their competition with fertile male will eventually reduce the size of succeeding generation below the normal threshold where transmission of malaria is possible (Mouchet, 1998). Arora and Arora (2005) outlined various measures in controlling malaria. These include: i. Spraying residual insecticides such as DDT or marathion. ii. Spraying the breeding sites with petroleum oils and paris green (copper acetoarsenite as larvicides.) iii. Using larvivorous fish, Gambusia affinis iv. Flooding and flushing of breeding places. v. Eliminating breeding places such as lagoons and swamps vi. Avoiding exposure to mosquito bites by; a. Wearing long-sleeved clothing and trousers after sunset when the insects are most active 22 b. Using an electric matt to vaporize synthetic pyrethroid or burning mosquito coils. c. Using bed nets impregnated with pyrethroid. d. Application of mosquito repellents containing diethyltoluamide. vii. Chemoprophylaxis viii. Early diagnosis and prompt treatment of patients. 23 CHAPTER THREE RESEARCH METHODOLOGY 3.1 Research Design A cross sectional survey within the observational study design would use to find the prevalence of malaria among children (0-5years) in Sengere community of Girei Local Government Area of Adamawa State. 3.2 Study Area Girei is a town and local government area of Adamawa State, Nigeria. It lies on the Benue River. The dominant tribe in the area are the Fulɓe or Fulani; however, a substantial number of Bwatiye also dwell in villages such as Greng, Ntabo, and Labondo within the Girei local government area. The primary occupation of the people in the area is farming and cattle rearing. Girei is also a home to Radio Gotel. Girei has a latitude of 9°22'2.31"N and a longitude of 12°32'59.58"E or 9.367308 and 12.549882 respectively. Sengere is a ward in Girei Local Government Area of Adamawa State. The study would be carried out in Sengere health facility, which is located in Girei LGA of Adamawa State, Northeastern of Nigeria. Adamawa has two season which include the rain (wet) season ranges from May to October and the dry season that ranges from December to March. The period is characterized by dry, dusty and hazy, Northern Trade wind that blow over the area from Sahara desert. Adamawa has average annual rain fall of 969mm, the temperature ranging from 25.2 – 28.1oC. 3.3 Study Population Clinical based records of children of age 0-5years would be analyzed to the prevalence within that specific age groups. 3.4 Sampling Technique With the assistance of health care workers, Secondary data were collected in respect to the child birth, malaria cases and treatment of malaria in the Primary health Care centres of the different wards and community of the locality. 24 3.5 Instrument of Data Collection Refer to the exsting or secondary information, raw or treated from the facilities in Girei, the total number of persons diagnosed with malaria including children ( 0-5 years) from July 2021 to December 2021. 3.6 Method of Data Analysis Results obtained from this study will be analyzed by using the statistical for social sciences (SPPSS) 25 REFERENCES Abiodun, I.I.R., Olusoga, B.O. and Bolanle, M.E. (2006). Neonatal Malaria in Nigeria A 2 Year Review. Htt/www.Biomedcentral.com/1471-2431/6/19/prepub.p Arora, D.R. and Arora, B. (2005). Medical Parasitology. Second Edition: Satish Kumar Jain for CDC Publishers and Distributors. India. Aultman, K.S., Gottlieb, M., Giovanni, M.Y. and Fauci, A.S. (2002). Anopheles gambiae genome: Completing the Malaria triad. Science. 298:13. Besansky, N.J., Hill, C.A. and Constantini, C. (2004). No Accounting for taste: Host Preference in Malaria Vectors. Trends in Parasitology. 21:115. Bozdech, Z., Llinas,M., Pulliam, B.L., Wong, E.D., Zhu, J. and Derisi, J.I. (2003). The transcription of the intraerythrocytic Developmental Cycle of Plasmodium falciparum. Plos Biology. 1:85-100. Breman, J.G. (2001). The Ears of the Hippopotamus, Manifestations, Determinants, and Estimates of the Malaria Burden. American Journal of Tropical Medicine and Hygiene. 64: (1, 25): 1-11. Brewer, G.T. and Powel, R.D.(1965). The Study of the Relationship between the Content of Adenosine Triphosphate in Human Red Cells and the Cause of - 97 - falciparum Malaria; A New System that may Counter Protection against Malaria Proceeding of National Science. 52:714-715. Bruce-Chwatt, L.J. (1983). Essential Malariology. Heinemann Medical Books Ltd. London. Bruce-Chwatt, L.J. (1984). Essential Malariology. Oxford University Press. London. Bruce-Chwatt, L.J.(1985). Essential Malariology. Second Edition. John Willey and Sons Inc. New York. Budiansky, S. (2002). Mosquitoes and Disease. Science. 298:82-86. Cheesbrough, M. (2005). District Laboratory Practice in Tropical Countries. Part 1. Second Edition. Cambridge University Press. New York. Cheng, T.C. (1986). General Parasitology. Second Edition. Academic Press Inc. India. Clyde, D.F. (1981). Malaria Medical Microbiology and Infectious Disease. International Text book of Medicine. Samiy-Smith Wyngaarden: W.B. Saunders Company. Pp.1478-1486. Collins, F.H. and Paskewitz, S.M. (1995). Malaria: Current and Future. Malaria Journal. 2: 156-157. - 98 26 Covell, G.C. (1950). Congenital Malaria. Tropical Disease. 47:147-167. Freyvogel, F.A.(1966). Shape, Movement in Site and Locomotion of Plasmodial Ookinetes. Annals of Tropical Medicine and Parasitology. 23:201-222. Gardner, M.J. (2002). The Genome of the Malaria Parasite. Current Options in Genetics and Development. 9:704-708. Garnham, P.C.C. (1963). Malaria Parasite and other Haemosporidia. Blackwell Scientific Publication. Oxford. Garnham, P.C.C. (1966). Malaria Parasite and other Haemosporidia. Blackwell Scientific Publication. Oxford. Garnham, P.C.C., Brood, R.G., Baker, J.R. and Bray, R.S (1961). Electronmicroscope Studies of Motile Stage of Malaria Parasite. Transactions of Royal Society of Tropical Medicine and Hygiene. 43:6-8. Goldsmith, R.S. (2004). Infectious Diseases: Protozoal and Helminthic. In: (Pp. 36-38). Tierney, L.M. Jr., McPhee, S.J. and Papadakis, M.A. Current Medical Diagnosis and Treatment. McGraw-Hill. Boston. Good, M.F. (2001). Towards Blood Stage Vaccine for Malaria: are we following the lead? Nature Reviews. 1:117-125. Greenwood, B. and Mutabingwa, T. (2002). Malaria in 2002. Nature. 415:670-672. - 99 – Hemingway, J., Field, L. and Vontas, J. (2002). An Overview of Insecticide Resistance. Science. 298:96-97. Hendrick, P.G. (1972). Quatan Malaria Nephritic Syndrome. Collaborative Clinical Pathological Study in Nigeria Children. Lancet. 1:1143. Holt, R.A. (2002). The Genome Sequence of the Malaria Mosquito. Anophelese gambiae. Science. 298:129-149. Hornby. A.S. (2007). Oxford Advance Learners Dictionary of Current English. Oxford University Press. London. Jeffery, G.M. (1984). The Role of Chemotherapy in Malaria Control through Primary Health Care: Constraints and Future Prospects. Bulletin of World Health Organization. 62: (supp): 49-53. Korenromp, E.L. (2003). Measuring Trends in Childhood Malaria Mortality in Africa: A New Assessment of Progress Towards Targets Based on Verbal Autopsy. Lancet. 58:119-125. Kyes, S., Horrocks, P. and Newbold, C. (2001). Antigenic Variation at the Infected Red Cell Surface in Malaria. Annual Review of Microbiology. 55:673-707. 27 MacDonald, G. (1957). Epidemiology and Control of Malaria. Oxford University Press. London. - 100 – MacLeod, C.L. (1988). Parasitic Infections in Pregnancy and Newborn. Oxford University Press. London. Madecki, C.L. and Kretschner, W. (1966). Human Ecology and Behaviour in Malaria Control in West Africa. Tropical Medicine and Parasitology. 92:419-433. Makler, M.T. (1998). A Review of Practical Techniques for the Diagnosis of Malaria. Annals of Tropical Medicine and Parasitology. 92:419-433. Manakaya, T. (2000). We Cannot Afford to Continue to Pay Malaria Tax. A World Health Organization News Letter. 15 (12):16-17./ Mckerrow, J. and Parslow, T.G. (2001). Parasitic Diseases. Medical Immunology. 10th Edition. McGraw-Hill. Boston. Miller, L.H., Mason, S.T., Clyde, D.F. and McGuiness, M.H. (1976). The Resistance Factor in Plasmodium Vivax in Blacks. American Journal of Tropical Medicine and Hygiene. 25:451-453. Mouchet, J. (1998). Evolution of Malaria in Africa for the Past 40 years: Impact of Climate and Human Factors. Journal of American Mosquito Control Association. 14: (2):121-130. - 101 – Nwanyanwu, O.C. (1997). Malaria and Human Immunodeficiency Virus Infection among Male Employees of Sugar Estate in Malawi: Transactions of Royal Society of Tropical Medicine and Hygiene. 91 (5):567-569. Okeke, T.A., Uzochukwu, B.S.C. and Okafor, H.U. (2006). Patent Medicine Seller’s Perspectives on Rural Malaria in Nigerian Community. Malaria Journal. 5:97. Orlando, A., Marini, U. and Esposito, R. (1982). An Outbreak of P.Malaria Among Drug Adicts. Journal of Medicine and Parasitology. 4:399-405. Peters, W. and Pasvol, G. (2002). Tropical Medicine and Parasitology. 5th Edition. Mosby. Ree, P.H. (1982). Studies on Sampling Techniques of mosquito Larva and other Aquatic Invertebrates in the Rice Field. Korean Journal of Enomology. 12(1): 37-45. Ring, L.H. and Jepson,S. (1979). Accidentally Induced Malaria. ugestkrift for Laeger. 4: 2129-2130. Russel, P.K. (1996). Vaccine Against Malaria. hope in Gathering Storm. National Academy Press. Washington DC. - 102 - 28 Sachs, J.D. and Malaney, P. (2002). The Economic and Social Burden of Malaria. Nature. 415: 680-685. Shell Petroleum Development Company of Nigeria, (2000). Stekettee, R.W. (2001) The Burden of Malaria in Pregnancy in Malaria – Endemic Areas. American Journal of Tropical Medicine and Hygiene. 64 (2,2, 5): 28-35. Toure, Y.T. and Oduola, A. (2004). Malaria. Nature. 2: 276-277. Trape, J.F. (2001). The Public Health Impact of Chloroquine Resistance in Africa. American Journal of Tropical Medicine and Hygiene. 64 (1,25): 29 - 31. Vogel, G. (2002). In Pursuit of a killer. Science. 298: 87-89. Voller, A. (1993). Immunology of Tropical Parasitic Infections. Transactions of Royal Society of Tropical Medicine and Hygiene. 87: 497 Webster, J. (2000). Malaria in Complex Emergencies. African Health. 22:29-31. WHO (1993). A Global Strategy for Malaria Control. The World Health Organization Technical Report Series 92. - 103 - WHO (1986). Malaria in Geographical Distribution of Arthropod- borne Disease and their Principal Vector. World Health Organization Expert Committee on Malaria: 20th Report, Geneva. WHO (1997). Improving Child Health: The Integrated Approach Division of Child Health and Development. The World Health Organization Technical Report. Geneva. WHO (2000). Malaria Diagnosis. New Perspectives. The World Health Organization Technical Report on Malaria. Wilson, M.E. (1991). A World Guide to Infectious Disease Distribution and Diagnosis. Oxford University Press. London. Zahar, A.R. (1984). Vector Control Operation in the African Context. Bulletin of World Health Organization. 62:89-100. Alajaka, W. (2009). The Malaria Palaver. Tell, April 6.P49. Oyeniyi, S. (2009). The Malaria Palaver. Tell. April, 6. P.49. Sofola, Y. (2009). The Malaria Palaver. Tell April 6. P. 49. 29 APPENDIX QUESTIONNAIRE Modibbo Adama University, Yola Centre for Distance Learning, Community Health Programme, P.M.B 2076 Yola Adamawa State. Dear Respondent, I am a student of the Modibbo Adama University of Technology, Yola, undertaking research on Prevalence of malaria among children between 0-5 years in Sangere community of Girei Local Government, Adamawa state. Being part of the requirement for the award of Bachelor of Science degree in Community Health. You are please requested to answer all questions as every information provided will be treated confidentially. No name is required but just fill in or tick () in the appropriate column of your choice and fill in the gap where necessary. 30 Part I: Identification 1. Ward __________________________ 2. Village __________________________ 3. Sub – village __________________________ Part II: Socio – demographic factors 4. Sex: Male { } Female { } 5. Level of education: Primary { } Secondary { } College { } Others { } 6. Employment position: CHO { } CHEW { } 7. Rate of monthly child birth: 5 – 10 { } Clerk { } lab staff { } 10 – 15 { } 15 – 20 { } Others { } 8. Rate of malaria cases among children between 0 – 5 years monthly: 5 – 10 { } 10 – 15 { } 15 – 20 { } Others { } Part III: Knowledge on malaria given to the parent 9. What are the signs of malaria told to the parent _______________________________________ _______________________________________ _______________________________________ 10. What main preventive measures were the parent taught __________________________________________ __________________________________________ __________________________________________ 11. Was ways of keeping personal hygiene to prevent malaria taught: Yes { } No { } Don’t know { } 12. Was parent taught how to use treated mosquito net: Yes { } No { } Don’t know { } 31 13. Was self-medication one of the cures of malaria instructed to the parents? Yes { } No { Don’t know { } } 14. When were the parents instructed to use the treated net for the children ages 0 – 5 years? Seasonally { } Daily { } Don’t know { } Part IV: Treatment and Management of Malaria Among Children Aged 0-5 Years 15. What are the signs to be observed to be sure its malaria ______________________________________________ ______________________________________________ ______________________________________________ 16. What is usually the first medication given to children aged 0 – 5 years suffering from malaria as emergency ____________________________________ 17. What drug is administered to children aged 0 – 5 years suffering from malaria ______________________________________________ 18. Is anti – malaria given to children aged 0 – 5 years suffering from malaria? Yes { } No { } Don’t know { } 19. Is treated mosquito net issued to parents with children aged 0 – 5 years? Yes { } No { } Don’t know { } 20. Do you hold seminars for the community on how to prevent and control malaria? Yes { } No { } Don’t know { } 21. What type of seminars do you conduct? House – House { } Community gathering { } Don’t know { 22. How often do you conduct such seminar? Monthly { } Weekly { } Don’t know { } 23. What is the feedback from the seminars conducted? Encouraging { } Not encouraging { } 32 Don’t know { } }