Commenting on malaria control, through treatments, Foster (1995) while investigating on rural malaria in Gambia, reported that a large proportion of malaria patients in most endemic areas, receive some form of treatment in the home or community without ever making contact with the formal health services, and that home treatment of fever in Africa South of the Sahara can account for up to 75% of all cases. Ezedinachiet al (1997) working on perception of malaria infection by people in two rural communities (Awi and IkotEdemOdo) in Cross River State of Nigeria, also reported that unspecified drugs and traditional medicines were initial treatment responses, while formal health sector was consulted only if home initiated measures failed. Also Uzochukwuet al (2008) while investigating Rural-Urban (AmechiAwkunanaw – Uwani) differences in maternal responses to childhood fever in South East, Nigeria, reported that surveys in Africa revealed that 80-90% of fever presumed to be malaria cases were treated at home, while formal health care is sought only if initial treatment fails. Tore (1995) reported, in WHO 12thProgramme Report, (1995) that in most malaria treatment, 80% in malaria endemic areas like Nigeria is handled at home without microsopic confirmation of the suspected malaria episode. Coker and Adesegun (2006) were also of same opinion by reporting that in Africa almost 70-80% of the population patronise traditional healers for their medical care, and that in rural communities, the herbalists or traditional healer is usually the first port of call in the event of illness. Salakoet al (2001) and Iweze (1987) reported that in Nigeria, patent medicine stores (PMS) are usually the first choice in health care and a recognised primary source of orthodox drugs fro both rural and urban populations, especially the poor.
2.4 TRANSMISSION OF MALARIA
On transmission of this disease, Ernest et al (1974) reported that the transmission of malaria is limited to the tropics and subtropical regions of the world. However, they remarked that in the past, transmission occurred in many temperate regions and that in the zone, malaria was unstable and relatively easy to control or eradicate, while tropical malaria is often more difficult to eradicate. This is very evident in Nigeria. Markellet al (1999) reported that transmission of all species of malaria parasites depends on the presence of both the suitable species of Anopheline mosquitoes and of the (gametocyte-bearing) humans, and that the suitability of a mosquito as a vector of human malaria disease depends not only on the physiologic adaptation to the infection, but also on such factors as feeding preferences, hour of biting and flight, resting and breeding habits. They also reported that favourable breeding places abound in the tropics, such as old cans, coconut shells, wells, old tyres, poor drainage systems, bushes and hedges around dwelling houses etc. These factors, obviously, promote mosquito multiplication.
Apart from transmission through the bites of infected female Anopheles mosquitoes, transmission through blood transfusion and mechanical transmissions through shared syringes by drug users are also known. The World Health Report (2002) remarked that in areas of stable malaria transmission, very young children and pregnant women are the population group at highest risk for malaria morbidity and mortality, and that most children experience their first malaria infection during their first year or two of lives, when they have not yet acquired adequate clinical immunity – which makes these early years particularly dangerous. Commenting also on transmission, Murphy and Breman (2001) reporting on malaria transmission in urban sub-Sahara Africa stated that a review of malaria transmission in sub-Sahara Africa cities shows the strong likelihood of transmission occurring within these sprawling cities, whatever the size or characteristics of their bioecologic environment. However, considerable variation in the level of transmission exists among cities and within different districts in the same city.
2.5 Life Cycles of Malaria Parasites
Plasmodium undergoes three (3) cycles: two (2) asexual cycles, which occur in man and the sexual cycle, which occurs in the mosquito vector
Liver stage: Human infections are initiated when sporozoites are injected with the saliva during the infected female Anopheles mosquito feeding. The sporozoites enter the circulatory system and within 30-60 minutes will invade a liver cell. The speed and selectivity of the process have indicated that sporozoite invasion of heptatocytes involves parasite-encoded surface proteins and host molecule(s). Despite the body of information that is available on the biology of the sporozoite, and the hepatic stages of Plasmodium, the exact route of sporozoites to their target cells is still not entirely clear (MeisansVerhave, 1998; Sinnis and Sim, 1997). After invading the heptocytes, the parasite undergoes an asexual replication. This replicative stage is often called exoerythrocytic (or pre-erythrocytic) schizogony. Schizogony refers to a replicate process in which the parasite (schizonts) undergoes multiple rounds of nuclear division without cytoplasmic division followed by a segmentation, to form a progeny. The progeny, called merozoites are released into the circulatory system following rupture of the host hepatocyte.
In P.vivax and P.ovale, some of the sporozoite do not immediately undergo a sexual replication, but enter a dormant phase known as the hypnozoite. This hypnozoites can reactivate and undergo schizogony at a later time resulting in a relapse. Relapse refers to the reactivation of the infection via hypnozoites. Recrudescence is used to describe the situation in which parasitaemia falls below detectable levels and then later increases to a patent parasitaemia, as it is found in Plasmodium falciparum and P.malariae
Blood Stage:
Sometimes called the erythrocytic stage is initiated with the release of approximately 105 to 106merozoites from the matured and ruptured schizonts in the liver. This is the product of 5 to 100 successful sporozoites. These merozoites liberated into the blood circulation invade passing red blood cells immediately. After entering the erythrocyte the parasite undergoes a trophic period followed by asexual replication. The young trophozoite is often called a ring form due to its morphology in Giemsa-stained blood smears. As the parasite increases in size, this ‘ring’ morphology disappears and it is called a trophozoite.
Nuclear division marks the end of the trophozoite stage and the beginning of the schizont stage. Erythrocyticschizogony consists of 3-5 rounds (depending on species) of nuclear replication followed by a budding process. Late stage schizonts in which the individual merozoites become discernable are called segmenters. The host erythrocyte ruptures and releases the merozoites. These merozoites invade new erythrocytes and initiate another round of schizogony.
The blood stage parasites within a host usually undergo a synchronous schizogony. The simultaneous rupture of the infected erythrocytes and the concomitant release of antigens and waste products accounts for the intermittent fever paroxysms associated with malaria.
Sexual Stage:
As an alternative to schizogony, some of parasites will undergo a sexual cycle and terminally differentiate into either micro- or macro gametocytes. The factors involved in the induction of gametogenesis are not known. However, commitment to the sexual stage occurs during the asexual erythrocytic cycle that immediately precedes gametocyte formations. Daughter merozoites from thisschizonts will develop into either all asexual forms or all sexual forms. Gametocytes do not cause pathology in the human host and will disappear from the circulation if not taken up by a mosquito.
Gametogenesis is inductive when the gametes (micro and macro) are ingested by a mosquito. After ingestion by the mosquito, the microgametocyte undergoes three rounds of nuclear replications. These eight nuclei then become associated with flagella that emerge from the body of the microgametocyte. This process is readily observable by light microscopy due to the thrashing flagella and is called ex- flagellation. The microgametocyte mature into microgametes.
Ex-flagellation occurs spontaneously when infected blood is exposed to air. Critical factors involved in the induction of this gametogenesis include: decrease in temperature, a decrease in dissolved CO2 and the subsequent increase in PH to above 8.0.
The highly mobile microgamete will seek out and fuse with a macrogamete within 12-hours, the resulting zygote develops into an Ookinete. The Ookinete is a motile invasive stage, which will traverse both the peritrophic matrix and the midgut epithelium of the mosquito.
Sporogony:
After reaching the extracellular space between the epithelial cells and the basal lamina, the Ookinete develops into an Oocyst. The Oocysts undergoes an asexual replication called sporogony, this generally takes 10-28 days depending on species and temperature. Upon maturation, the Oocyst, ruptures and release the
