Prevalence of Urinary schistomomiasis in Primary 3 Pupils
Prevalence of Urinary schistomomiasis in primary 3 pupils. The standard test for urinary schistosomiasis is urine filtration and microscopic examination of the urine sample (WHO,1991).
TABLE OF CONTENTS ON
PREVALENCE OF URINARY SCHISTOSOMIASIS IN PRIMARY 3 PUPILS .
Title Page i
Table of Content v
1.0 Introduction 1
1.1 Aim and Objective of the Study 4
2.0 Literature Review 5
2.1 Taxonomy, Structure and Biology 5
2.1.1 Taxonomy 5
2.1.2 Structure 6
2.1.3 Structure of the Genome 6
2.1.4 Live Cycle and Biology of the Worm 6
2.2 Epidemiology of Infection 9
2.2.1 Prevalence and Geographical Distribution 9
2.2.2 Transmission, Risk Factors for Infection 10
2.2.3 Persistency, Latency and Natural History of Infection 11
2.3 Characteristics of Schistosomiasis 12
2.4 Pathogenicity/Toxicity 13
2.4.1 Schistosomiasis Pathology and Patterns of Morbidity 14
2.5 Chronic Urogenital Schistosomiasis 15
2.6 Symptoms 17
2.7 Laboratory Diagnosis 19
2.8 Treatment and Prevention 19
3.0 Materials and Methods 21
3.1 Study Area 21
3.2 Study Population 21
3.3 Ethical Consideration 21
3.4 Sampling Techniques 22
3.5 Laboratory Analysis 22
3.6 Parasitological Diagnosis 23
3.7 Microscopic Examination of the Urine Deposits 23
3.8 Detection of Haematuria by Urinalysis 24
3.9 Identification of Ova and Adult Worm 24
3.10 Statistical Analysis 25
4.0 Results 26
5.0 Discussion and Conclusion 29
5.1 Discussion 29
5.2 Recommendation 30
5.2 Conclusion 30
Human schistosomiasis is a chronic disease caused by the blood flukes belonging to the genus Schistosoma. The main disease causing schistosome species are Schistosomahaematobium (S. haematobium), S. mansoni, S. japonicum, S. mekongi and S. intercalatum (Gryseels et al., 2006). Schistosomiasis is estimated to affect 249 million people worldwide, of which at least 224 million affected people live in sub-Saharan Africa (WHO, 2015). It ranks second only to malaria as the most common parasitic disease, killing an estimated 280,000 people each year in the African region alone (CDC, 2011).
S. haematobium is the aetiologic agent of urinary schistosomiasis and it is most prevalent in Africa (NaTHNac, 2008). In sub-Saharan Africa, S. haematobium infection is estimated to cause 70, 32, 18 and 10 million cases of hematutria, dysuria, bladder-wall pathology and major hydronephrosis, respectively (van der Werf et al., 2003). The infection is also responsible for nutritional deficiencies and growth retardation (Stephenson, 1993), adverse effects on cognitive development (WHO, 2002) as well as for decreasing physical activity, school performance, and work capacity and productivity (Stephenson, 1993)
Transmission of urinary schistosomiasis is dependent on availability of specific snail hosts and human activities with water contacts (WHO, 2010). Therefore, the risk and reemergence of urinary schistosomiasis is attributed to the range of snail habitats promoted by water development schemes such as dam construction (Jamison et al., 2006). On the other hand, school age children were thought to have frequent water contact that would make them more vulnerable to schistosomiasis, and hence this age group would be associated more frequently with schistosomiasis problems (Deribe et al., 2011; Bala et al., 2012).
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Human infection with S. haematobium is acquired through contact with water bodies containing cercariae, the larval form of the parasite. The cercariae are able to penetrate human skin and migrate via blood vessels to the liver, where they mature into male and female forms for reproduction. Typically, they then migrate further to the venous plexus of the urinary bladder, and begin to produce eggs which the infected person excretes in their urine (Gryseels et al.,2006). If these eggs reach water, they hatch into miracidia, infect specific freshwater snails which act as intermediate hosts, before emerging as cercariae that can infect humans (Gray et al.,2011; Ross et al.,2002).
Any illness associated with acute infection is typically mild, but chronic schistosomiasis can cause considerable morbidity with chronic pain, anaemia, fatigue, under nutrition and reduced exercise tolerance (King et al.,2005). A review of 124 observational studies and 11 randomized controlled trials (RCTs) in 2005 estimated that up to 15% of people infected with any form of schistosomiasis suffer disabling long-term complications (King et al.,2005).
The main pathological process occurs when schistosome eggs become trapped in the tissue around the bladder and ureters causing chronic inflammation, which may obstruct the ureters, damage the kidneys, and lead to bladder cancer. Occasionally, eggs can become trapped in other tissues such as the brain and spinal cord (WHO,1985).
Two-thirds of all infected persons are schoolchildren (aged five to 14 years), and the intensity of infection with S. haematobium is highest in children aged ten to 14 years (WHO,1985).
The standard test for urinary schistosomiasis is urine filtration and microscopic examination of the urine sample (WHO,1991). The urine sample is passed through a filter paper and the eggs retained on the filter are counted either with or without staining. Sedimentation and centrifugation is less commonly used for urine concentration (Cook et al.,2003). High urine egg counts are related to high infection intensity.
Parasitologists define cure when eggs can no longer be detected in one or more urine samples using standard methods. Besides parasitological cure, researchers also record the relative reduction in egg output after treatment compared to pre-treatment levels. This outcome, expressed as % egg reduction, is an indirect estimate of a reduction of the worm burden (Cook et al.,2003).
Blood and protein excretion in the urine is usually elevated in urinary schistosomiasis and decreases when the infection resolves. The most commonly used test is a dipstick test. Ultrasound can demonstrate organ involvement of the urinary tract as well as its resolution.
1.1 Objective of the Study
The objective of this study is to determine the prevalence and intensity of urinary schistosomiasis in Izzi Local Government Area of Ebonyi State.
2.0 LITERATURE REVIEW
Schistosomahaematobium is an important digenetictrematode, and is found in Africa and the Middle East. It is a major agent of schistosomiasis; more specifically, it is associated with urinary schistosomiasis.
Adults are found in the venous plexuses around the urinary bladder and the released eggs travels to the wall of the urine bladder causing haematuria and fibrosis of the bladder. The bladder becomes calcified, and there is increased pressure on ureters and kidneys otherwise known as hydronephrosis. Inflammation of the genitals due to S. haematobium may contribute to the propagation of HIV (Lieutscher et al., 2005). Studies have shown the relationship between S. haematobium infection and the development of squamous cell carcinoma of the bladder (Khurana et al., 2005).2.1 Taxonomy, Structure, and Biology
Schistosomes are parasitic blood-dwelling fluke worms belonging to the genus Schistosoma; family, Schistosomatidae; order, Digenea; class, Trematoda; phylum, Plathyhelminths; and kingdom, Animalia. The genus Schistosoma contains six species that are of major pathological importance to man, Schistosomahaematobium (S. haematobium), S. mansoni, S. japonicum, S. mekongi, S. intercalatum, and S. guineensis (Webster et al., 2006). The species differ in their final location in the human host, the species of the intermediate (snail) host they use in their life cycle, the pathology they induce, and the number, size and shape of the eggs they produce.
Unlike all other pathologically important trematodes, schistosomes are not hermaphroditic, but have separate sexes. The adult worms are 1–2 cm long with a cylindrical body that features two terminal suckers, a complex tegument, a blind digestive tract, and reproductive organs. The male’s body forms a groove orgynaecophoric channel, in which it holds the longer and thinner female. As permanently embraced couples, the schistosomes live within the perivesical (S. haematobium) or mesenteric (other species) venous plexus. Schistosomes feed on blood particles through anaerobic glycolysis (Rumnajek, 1987).
2.1.3 Structure of the Genome
The genome of S. mansoniis currently being sequenced and is almost completed; an Expressed Sequence Tag (EST) sequencing project has also started for S. japonicum, and S. haematobium (El-Sayed et al., 2004).
2.1.4 Life Cycle and Biology of the Worm
The female S. haematobiumworm produces hundreds of eggs per day throughout her life. The eggs (144×58 μm, with a characteristic terminal spine) penetrate through the bladder wall where they are excreted with urine. Each ovum contains a ciliated larva (miracidium), which secretes proteolytic enzymes that help the eggs migrate into the lumen of the bladder. About half of the eggs produced do not reach the vesical lumen, and are carried away with the bloodstream, and/or trapped in the tissues. These retained eggs provoke a granulomatous inflammatory response, which is the main cause of pathology in the human host. The excreted eggs hatch if they come into contact with water, and release the miracidium.
These remain viable for up to 48 hours and are able to locate a suitable freshwater snail host (i.e. Bulinus spp. for S. haematobium) using external stimuli such as light and snail-derived chemicals. In the snail, asexual multiplication takes place, and several generations of multiplying larvae (sporocysts) develop. Eventually, these sporocysts produce large numbers of infective larvae with a typical bifurcated tail (cercariae). These leave the snail at a rate of thousands per day after a period of weeks. Shedding of these cercariae can continue for months. The cercariae survive for up to 72 hours and use water turbulence and skin-derived chemicals to locate the human host.
They attach to and penetrate the human skin within 3–5 minutes. They lose their tail, and the young parasites (schistosomulae) migrate with the bloodstream via the lungs to the liver, where they mature into adult worms in the portal vein and mate. The paired worms migrate against the bloodstream to the perivesicular veins, where in a total of 4–7 weeks after infection they start producing eggs throughout their adult life. The lifespan of an adult worm averages 3–5 years, but can be as long as 30 years (Wilkins, 1987). An infected person probably harbours an average of hundreds (range, 10s–1000s) of worms (Gryseelsand De Vlas, 1996).
A: paired adult worms; B: egg; C: miracidium; D: intermediate snail host; E: cercariae
Fig. 1: Life Cycle of Schistosomiasishaematobium (Gryseels, 2006)
2.2 Epidemiology of Infection
2.2.1 Prevalence andGeographic Distribution
Human schistosomiasis is endemic in large areas of the (sub)tropics. It has been estimated that over 700 million people in 74 countries are exposed to the risk of schistosomal infection, and almost 200 million were estimated to be infected in 2003 (Fenwick, 2006), of which 85% in subSaharanAfrica. About 95% of the cases are due to S. mansoniand S. haematobiuminfections. S.haematobiumis endemic in 53 countries, in the Middle East and most of the African continent (Chitsuloet al., 2000).Schistosomiasis is largely an infection found in rural areas, but urban schistosomiasisis an increasing problem in many countries (Mott et al., 1990).
Natural streams, ponds and lakes are typical sources of infection, but over the past few decades, man-made reservoirs and irrigation systems, as well as population growth and migration, have contributed to the spread of schistosomiasis (Gryseelset al., 2006; McManusandLoukas, 2008).
Within countries, regions and villages, thedistribution of schistosomiasis can be very focal, depending on variations in snail populations and human–water contact behaviour (GryseelsandNkulikyinka, 1988). Also, the distribution of schistosomiasis can be highly uneven across individuals.
The majority of the parasites are usually present in a small fraction of the infected individuals. Prevalence and intensities of infectiongenerally show a typical convex-shapedcurve with a peak at the ages of 5–15 years, and a decrease in adults. Sex-related patterns vary in relation to behavioural, professional, cultural, and religious factors (Jordan andWebbe, 1993).
2.2.2 Transmission, and Risk Factors for Infection
All Schistosomainfections follow directcontact with freshwater-harbouringcercariae(see life cycle). Three major factors are responsible for maintaining the transmission of the infection: 1) contamination of fresh water with excreta containing schistosome eggs, 2) the presence of the snail intermediate hosts, and 3) human contact with water-infested with cercariae (Jordan andWebbe, 1993).
Contact with contaminated freshwater is the major risk factor of infection (Jordan andWebbe,1993). The main risk groups are school-age children, specific occupational groups (fishermen, irrigation workers, farmers), and women and other groups using infested water for domestic purposes (WHO Expert Committee, 2002). Many other host-related and environmental risk factors have been identified that may affect the risk of acquiring schistosome infection, and/or influence the distribution, prevalence, intensity of infection, morbidity and mortality of schistosomiasis.
Among these are genetic factors(Quinnell, 2003), behaviour, household clustering (Bethonyet al., 2001), climate, immune response of the host, and concomitant infections (e.g. hepatitis) (IARC, 1994).
2.2.3 Persistence, latency, and natural historyof infection
Schistosome worms do not multiply in the host.The infection status is the result of an accumulation of consecutive infections, where individuals with the most intense infections usually have a higher risk of developing morbidity (Gryseelset al., 2006). In the absence of re-infection, the infection subsides when the schistosome worm dies, which is usually after 3–5 years. However, in endemic areas with continuous exposure, re-infection is the rule rather than the exception. In highly endemic areas, children start to accumulate worms as soon as they are old enough to have contact with water and may, because of the chronic nature of the infection and continued susceptibility to re-infection, remain infected throughout their lives.
The possibility that adults might developimmunity to schistosome infections was initially suggested based on the shape of the age–intensity curve in endemic communities, which characteristically shows a rise in intensity during the first two decades of life, followed by a decline in adults to very low levels (Butterworth, 1998). Indeed, numerous studies have provided epidemiological and clinical evidence that people living in endemic areas acquire some form of protective immunity after years of exposure.
However, age related innate resistance mechanisms may also play an important part in the epidemiology of schistosomiasis (Butterworth, 1993; Gryseelset al., 2006).
b) Latency and Natural History
Not much is known about the latencybetween the onset of infection and the appearance of cancer, nor about the steps that might lead to cancer. Infection with S. haematobiumis not synonymous with clinical disease, and many infections are asymptomatic. Of those infected, a small proportion develops serious chronic disease, after varying durations of exposure and infection (Homeidaet al., 1988; Vennervald and Dunne,2004). Mostafa et al. (1999) noted that the incidence of bilharzial bladder cancer in various
African countries peaks between the ages of40–49 years, while infection with S. haematobiumbegins in childhood (as early as 6 months of age), and peaks usually in the second decade of life (between the ages of 5–15 years). This would imply a latency period of 20–30 years.
2.3 Characteristics of Schistosomiasis
Species of the genus Schistosoma are trematode blood flukes belonging to the Schistosomatidae family (Snyder and Loker, 2009). They are dioecious, have a two host life cycle, and exhibit a high degree of sexual dimorphism (Murray et al., 2003; Snyder and Loker, 2009). Adult worms are 7-28 mm in length and 0.3-0.6 mm in width (Krauss et al., 2003).
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