Research Key

PREVALENCE OF MALARIA IN CHILDREN 1-10 YEARS IN UNIVERSITY QUARTER II BUEA

Project Details

Department
NURSING
Project ID
NU196
Price
5000XAF
International: $20
No of pages
52
Instruments/method
QUANTITATIVE
Reference
YES
Analytical tool
DESCRIPTIVE
Format
 MS Word & PDF
Chapters
1-5

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Abstract

 The study sought to determine the prevalence of malaria in children of age 1-10 years in university quarter 2 Buea. To achieve the objectives of this study, the study tested the following hypothesis: null hypothesis (Ho): malaria prevalence rate of children 1-10 years in university quarter 2 is not significant: alternative hypothesis (H1): malaria prevalence of children 1-10 years in university quarter 2 is significant.  The sample size of the study was selected from a target population.

The sample was drawn using stratified random sampling techniques. Data was collected with the use of questionnaire and by children diagnosis in which Blood smears were obtained from 100 children and all were tested microscopically using capillary blood method of collection for identification of plasmodium falciparum only.

Questionnaires were administered to parents of these children only. Furthermore, the result obtain from both the questionnaire and children diagnosis were able to show that there were significant differences on the malaria prevalence rate among children of the giving age range.  age group 7-10years had the least rate of malaria while 4– 6years had a higher rate of malaria prevalence and the age group 1 – 3 had the highest prevalence rate of malaria.

Females were seen to have a higher prevalence rate of malaria than males. The results from the chi square test revealed that malaria is a major public health problem among children aged 1 – 10 years in university quarter 2 Buea.

It was concluded that the high rate of malaria was due to lack of preventive measures like the use of mosquito treated bed nets which were absent. The study further recommend that the government should improve on the sanitation condition of this area and provide some preventive measures like mosquito treated bed nets.

CHAPTER ONE

INTRODUCTION AND LITERATURE REVIEW

  1. Introduction

Malaria is an acute chronic disease caused by an obligate intracellular protozoan of the genus plasmodium. The malaria parasite was discovered by Laveran a military physician working in Constantine Algeria (1880).

Malaria is a parasitic disease of mammals including birds and reptiles. It is the most common disease amongst children and young adults in Africa.

Malaria is a life threatening disease transmitted by the female anopheles mosquito. Malaria is by far the most important insect transmitted disease.

The female mosquito needs blood meal for egg development hence needs to bite. Out of approximately 430 known species of anopheles, only 30 – 50 transmit malaria in nature.

The successful development of the malaria parasite in the mosquito vector (from the ˝gametocyte˝ stage to the ˝sporozoit˝ stage) depends on several factors. The most important is ambient temperature and humidity (higher temperature accelerate the parasite growth in the mosquito) and whether the anopheles survives long enough to allow the parasite to complete it cycle in the mosquito host (˝sporogonic or extrinsic˝ cycle duration is 10 – 18 days). Differently from the human host, the mosquito host does not suffer noticeable from the presence of the parasite.

The vectors of human malaria all belong to the genus anopheles whose adults are recognized by their ˝tail in the air˝ posture, tapped wings in most tropical species and long pair of palps beside the proboscis in the female.

Malaria remains the most important parasite disease in the tropics with over half of the world’s population being at risk. In Africa alone, malaria has been estimated to cause the death of million children annually.

W.H.O estimated that there are 300 – 500 million cases of clinical malaria per year with 1.4 – 2.6 million deaths, mainly among Africa children?

Malaria is therefore a major cause of infant mortality and is the only insect borne parasite disease comparable in impact to the world’s major killer disease like diarrhea, acute respiratory infection, tuberculosis and AIDS.

In Cameroon malaria is the most common cause of outpatient to hospitals and it consistently rank among the three most important cause of death among children.

Four species of malaria parasites can affect humans under natural conditions namely; Plasmodium Falciparum, P. Vivax, P. Ovale and P. Malariae. The first two species cause the most infection worldwide. Plasmodium falciparum is the agent of severe, potentially fatal malaria causing an estimated 700,000 – 2.7 million deaths annually most of them in young children in Africa.

Plasmodium vivax and P. Ovale have higher dormant hirer state parasite (hypriozoites) which can reactive (˝relapse˝) and cause malaria several months or years after the infecting mosquito bites.

Plasmodium malariae produced long lasting infections and if left untreated can persist asymptomatically in the human host for years, even a life time.

Four countries have been certified in recent years as having eliminated malaria, and 19 countries are currently implementing pre elimination or elimination of phase. Despite this progress, millions of people who are exposed to malaria risk still do not access to preventive interventions such as insecticides treated net.

1.2 Literature Review

Information on malaria at local level is scanty and the effects of the disease on the population are not well documented for which reason, this study has been designed to provide baseline pre – control data required for planning.

Plasmodium falciparum is the most virulent in the tropics and is resistant to various antis – malaria drug.

1.2.1 Discovery of the falciparum parasite

A German physician, Johann Friedrich Meckel, have been the first to see P. Falciparum but not knowing what it was. He reported the presence of black pigment granules from the blood and spleen of a patient who died of malaria. (1847)

The French army physician Charles Lovis Alphonse Laveran, while working at Bone hospital (now in Algeria) correctly identified the parasite as a causative pathogen of malaria (18800). He presented his discovery before the French Academy of medicine in Paris, and published it the lancet. He gave the scientific name oscillariamalariae (1881). But his discovery was received with skepticism mainly because by that time leading physicians such as Theoder Albrecht Edwin Klebs and CorradoTommasi – Crudel claimed that they have discovered a bacterium as the pathogen of malaria. Laveran discovery was widely accepted only after five years when Camillo Golgi confirmed the parasite using better microscope and staining technique. Laveran was awarded thenoble prize in medicine for his work (19907). The Italian Zoologist Giovanni Battista Grassi categorized plasmodium species based on the timing of fever in the patient malignant tertian malaria was caused by laveranianmalariae (1900).

The British physician Patrick Manson formulated the mosquito malaria theory (1894). Until that time, malaria parasite was believed to be spread in air as miasma, a Greek word for pollution. His colleague Ronald Ross, a British army surgeon travelled to India to test the theory.

Ross discovered that malaria parasite live in certain mosquitoes (1897). The next year, he demonstrated that a malaria parasite of birds could be transmitted by mosquitoes from one bird to another. Around the same time Grassi demonstrated that P. Falciparum was transmitted in humans only by female anopheles mosquitoes (1898).

The international commission on zoological nomenclature officially approved the binominal plasmodium falciparum (1954). The valid genus plasmodium was created by two Italian physicians EttoreMarchialava and Agelo Celli in (1885). The species name was introduced by an American physician William Henry Welch (1897).

Plasmodium falciparum is a unicellular protozoan parasite of humans and the deadliest species of plasmodium that causes malaria in humans. It is transmitted through the bite of a female anopheles’ mosquito. It is responsible for roughly 50% of all malaria cases. It causes the disease most dangerous form called falciparum malaria. It is there for regarded as the deadliest parasite in humans, causing 435,000deaths in 2017. It is also associated with the development of blood caner and is classified as group ZA carcinogen.

The species originated from the malaria parasite laverania found in gorillas around 10,000 years ago. Alphonse laveran was the first to identify the parasite (1880) and named it oscillariamalariae. Ronald Ross discovered it transmission by mosquito (1897), Giovanni Battista Grassi elucidated the complete transmission from a female anopheline mosquito to humans (1898).William Welch created the name plasmodium falciparum which assumes several different forms during it life cycle (1897). The human infective stages are sporozoite from the salivary gland of a mosquito. The sporozoites grow and multiply in the liver to become merozoites. These merozoites invade the erythrocytes (RBC) to form trophozoites,schizonts and gametocytes during which the symptoms of malaria are produced in the mosquito, the gametocytes undergo sexual reproduction to a zygote, which turns into oocytes from which sporozoites are formed. Almost every malarial dead is caused by p. falciparum and 93% of death occurs in Africa.

Whereas in most other malaria countries other less virulent plasmodia species predominate

  1. falciparum does not have a fixed structure but under goes continuous change during the course of its life cycle.

A sporozoite is spindle shape and 10 – 15mm long. The schizont is 30 – 70mm in diameter, the merozoites is roughly 1.5mm in diameter the trophozoit of p, falciparum feed on hemoglobin and form a granular pigment called haemozoin unlike those of other plasmodium species, the gametocytes of p. falciparum are elongated and crescent – shaped by which they are sometime identified.

Microscopic examination of a blood film will reveal only early (ring form) trophozoites and gametocyte that are in the peripheral blood.

The apical complex which is actually a combination of organelles is an important structure. It contains secret organelles called rhoptries and micro names which are vital for mobility, adhesion, host cell invasion and parasitophorous vacuole formation, as an apicomplexan, it harbors a plastid, an apicoplast, similar to plant chloroplasts, which they probably acquired by engulfing.

The apicoplast is involved in the synthesis of lipid and several other compounds and provide an attractive drug target.

Infections in humans begins with the bite of an infected female anopheles’ mosquito, the infective stage called sporozoites released from salivary glands through the proboscis of the mosquito enter the blood stream during feeding. The mosquito saliva contains anithemostatic and anti-inflammatory enzymes that disrupt blood clothing and inhibit thin pain reaction. Each infected bite contains 20 – 200 sporozoites.

The immune system clears the sporozoites from the circulation within 30 minutes but a few escapes and quickly invades liver cells (hapatocytes). The sporozoites move in the blood stream by gliding which is driven by motor made up of protein act and myosin beneath their plasma membrane.

Entering the hapatocytes, the parasite loses it apical complex and surface coat and transforms in to trophozoite.within the parasite the phorous vacuole of the hapatocyte ,it undergoes 13-14 rounds of mitosis and meiosis which produce a syncytial cell called a schizont .this process is called schizogony. A schizont contains tens of thousands of nuclei from the surface of the schizont; tens of thousands of haploid daughter cells called marozoites emerge. The liver stage can produce up to 90,000 merozoites which are eventually release in to the blood stream in parasite filled vesicles calledmerosomes.

– merozoite.Use the apicomplexan invasion organelles to recognize and enter the host erythrocyte.  The parasites first bind in to erythrocyte and a random orientation. it then reorients such that the apical complex is in proximity to the erythrocyte membrane. The parasite forms a parasitophorous vacuole to allow for its development inside the erythrocyte. This infection cycle occur in a highly synchronous fashion with roughly the entire parasite throughout the blood in the same stage of development. This precise cloting mechanism has been shown to be dependent on the human host own circadian rhythm.

Within the erythrocyte the parasite metabolism depends on the digestion of hemoglobin. The clinical symptoms of malaria such as fever, anemia, neurological disorder are produce during the blood stage.

The parasite can also alter the morphology of the erythrocyte, causing knobs on the erythrocytes membrane. Infected erythrocytes are often sequestered in various human tissues or organs, such as the heart, liver and brain. This is caused by parasite derived cells surface proteins being present on the erythrocyte membrane and it is these proteins that bind to the receptor on human cells.

Sequestration in the brain causes cerebral malaria, a very severe form of the disease, which increases the victim’s likelihood of death.

The time of appearance of the symptoms from infection is shorter for p. falciparum among plasmodium species an average incubation period is 11 days, but may range from 9 to 30 days in isolated causes prolonged incubation period as long as 2,3 or even 8 years have been recorded in pregnancy and co-infection with HIV.

Parasite can be detected from blood smear by the 10th day after infection. Attempts to make synthetic anti-malarial began in 1891; the choice of artemisinin based combination therapies [ACT] is based on the level of resistance to the constituents in the combination. Artemisinin and it derivatives are not appropriate for immunotherapy. As a second line anti-malarial treatment does not work, an alternative ACT known to be effective in the region is recommended, such as artesunate plus tetracycline or doxycline or clindamycin and quinine plus tetracycline. Any of these combinations is to be given for 7 days.

For children especially in malaria endemic areas of Africa,artesunate 4 or IM, quinine and artemether IM are recommended.

1.3 Statement Of The Problem

Children below the age of 5 years, particularly infants the disease tends to be a typical and more severe.

In the first two months of life, children may not contract malaria or the manifestation may be mild with low grade parasitemia, due to the passive immunity offered by the maternal antibiotics. In endemic and hyper endemic areas the parasite rate increases with age from 0 – 10% during first three months of life to 80 – 90% by one year of age and the rate persist at high level during early childhood. In areas of low endemicity were the immunity is low, severe infection occurs in all age groups including adults.

Malaria is intracellular obligate parasite in which man is the definitive host and female anopheles mosquitoes are the definitive host. Malaria has no reservoir host. Except p. malaria in which monkey are reservoir host and the infective stage to man from the insect vector is sporozoitesand from the insect vector to man is gametocytes. Malaria is endemic in 91 countries with about 40 percent of the world population at risk with the infection. p.falciparium is the most prevalence species in the hotter and more humid areas.

1.4 Rationale

Children under 10 years of age are one of most vulnerable groups affected by malaria. In Africa, about 285,000 children died before fifth birthday in 2016.

In high transmission areas partial immunity to the disease is acquired during childhood. In such settings, the majority of malaria disease and particularly severe disease with rapid progression to death occurs in young children without acquired immunity.

Severe anemia, hypoglycemia and cerebral malaria are features of severe malaria more commonly seen in children than in adults.

1.5.Aim

This study is to screen children from one to ten years of malaria species p. falciparum

1.6 General Objectives

The objective is to determine the prevalence of malaria among children between the ages of 1 – 10 years.

1.7 Specific Objectives

  1. -To know the age range at which children are more infected
  2. -To know the malaria prevalence rate on male children compare to female children
  3. -To know if malaria is a major public health problem among children in dirty south

1.8 Research Questions

  1. -Between male children and female children who will have a high prevalence rate of malaria?
  2. -What age group will children have a high prevalence rate of malaria?

1.9 Hypothesis

The hypothesis of this study is generated as follows:

Null Hypothesis (Ho): Malaria prevalence rate in children with age 1 – 10yearsin university quarter 2 is not significant.

Alternative Hypothesis (H1): Malaria prevalence rate in children with age 1-10 years in university quarter 2 is significant.

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