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istozomijaza

Uzrok nastanka

Uzronik je jedna od nekoliko vrsti parazitnih trematoda (vrsta metilja, u vidu upljihcrva) roda Schistosoma. Najei uzronici su Schistosoma haematobium, Schistosomamansoni, Schistosoma japonicum, a ree su Schistosoma mekongi i Schistosomaintercalatum.istozome prvo inficiraju pojedine vrste vodenih pueva, koji zatim otputaju larve(cercariae) u vodu, gde one u roku ood 48 sati se ili zakae za kou oveka koji dolazi udodir sa kontaminiranom vodom ili umiru. Larve zatim migrigaju do superficijalnih vena au toku nekoliko narednih dana stiu do plune vaskulature. Za to vreme larve menjaju svojizgled i sastav i postaju otporne na imunoloki sistem domaina, nazivaju se istozomule, avezuju se za proteine domaina. Zatim dospevaju iz plunih kapilara u sistemskucirkulaciju i tako dospevaju do portalnih vena gde i sazrevaju. Zatim dalje odlaze u

mezenterine vene gde produkuju jajaca. Jajaca, koja mogu izazvati burnu alergijskugranulomatoznu reakciju, se zatim izbacuju putem fecesa ili urina, dospevaju u vodu i takozatvaraju krug infekcije. Neka jajaca se mogu i zadrati u u portalnoj ili plunojcirkulaciji.

Klinika slikaBolesnici sa akutnom istozomijazom (Katajama groznica), nekoliko nedelja nakoninfestacije, imaju povienu temperaturu, groznicu, glavobolje, malakslaost, bolove umiiima i zglobovima, hepatosplenomegaliju (uveane jetra i slezina), kaalj, krvavestolice, bol u gornjem desnom kvadrantu abdomena, nekada urtikariju, limfadenopatiju.

Kod hroninog oblika prvi simptomi i znaci se mogu javiti mesecima i godinama nakoninfestacije. Javljaju se krvavi prolivi, bol u abdomenu, hepatosplenomegalija, hematemeze(povraanje krvavog sadraja), portna hipertenzija, ascites (nakupljanje tenosti u trbunojduplji), hematurija (krv u mokrai), dizurija (bolno mokrenje), lezije u predelu vulve iliperianalno u vidu ulceracija ili fistula, dispneja (oteano disanje), pulmonarna hipertenzija,kaalj, palpitacije, bol u grudima, epi napadi ili izmene stanja svesti, fokalni neurolokiispadi, paralize.

DijagnozaPostavlja se na osnovu anamneze, klinike slike, pregleda krvi, mokrae i stolice (nalazuzronika u urinu i stolici), serolokih testova, ultrazvuka, biopsije kolona, cistoskopije iendoskopije.

LeenjeOrdiniraju se antihelmintni lekovi, a lek izbora je praziquantel. Bolest ne ostavlja trajan

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imunitet, tako da lako moe doi do reinfekcije, pa je prevencija (higijenski uslovi) veomabitna.

Schistosoma mansoni

Schistosoma mansoniis a significantparasite of humans, a trematode that is one of themajor agents of the diseaseschistosomiasis. The schistosomiasis caused by Schistosomamansoni is intestinal schistosomiasis.

Schistosomes are atypical trematodes in that the adult stages have two sexes (dioecious)and are located in blood vessels of the definitive host. Most other trematodes arehermaphroditic and are found in the intestinal tract or in organs, such as the liver. Thelifecycle of schistosomes includes two hosts: a definitive host (i.e. human) where theparasite undergoes sexual reproduction, and a single intermediate snail host where there area number of asexual reproductive stages. S. mansoni is named afterSir Patrick Manson,who first identified it in Formosa (Taiwan).[2]

Morphology of adult schistosomes

Schistosomes, unlike other trematodes, are long and slim worms. The male S. mansoni isapproximately 1 cm long (0.61.1 cm)[3]and is 0.1 cm wide. It is white, and it has afunnel-shaped oral sucker at its anterior end followed by a second pediculated sucker. Theexternal part of the worm is composed of a double bilayer, which is continually renewed asthe outer layer, known as the membranocalyx, is shed continuously.[4] The tegument bears alarge number of small tubercules. The suckers have small thorns in their inner part as wellas in the buttons around them. The male genital apparatus is composed of 6 to 9 testicularmasses, situated dorsally. There is one deferent canal beginning at each testicle which is

connected to a single deferent that dilates into a reservatory, the seminal vesicle, located atthe beginning of the gynacophoric canal. The copula happens through the coaptation of themale and female genital orifices.[5]

The female has a cylindrical body, longer and thinner than the male (1.2 to 1.6 cm long by0.016 cm wide). The female parasite is darker, and it looks gray. The darker color is due tothe presence of a pigment (hemozoin) in its digestive tube. This pigment is derived fromthe digestion of blood. The ovary is elongated and slightly lobulated and is located on theanterior half of the body. A short oviduct conducts to the ootype which continues with theuterine tube. In this tube it is possible to find 1 to 2 eggs (rarely 3 to 4) but only 1 egg isobserved in the ootype at any one time. The genital pore opens ventrally. The posterior

two-thirds of the body contain the vittelogenic glands and their winding canal, which uniteswith the oviduct a little before it reaches the ootype.

The digestive tube begins at the anterior extremity of the worm, at the bottom of the oralsucker. The digestive tube is composed of anesophagus which divides in two branches(right and left) and that reunite in a single cecum. The intestines end blindly, meaning thatthere is no anus.

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[edit] Epidemiology

Schistosoma mansoni infects about 83.31 million people worldwide,[6] causing the diseaseintestinal schistosomiasis (schistosomiasis caused by all the Schistosoma species infectsover 200 million people.)[7][8]

S. mansoni is the most widespread of the human-infecting schistosomes, and is present in54 countries.[citation needed] These countries are predominantly in South America and theCaribbean, Africa includingMadagascar, and the Middle East.

[edit] Life cycle

After the eggs of the human-dwelling parasite are emitted in the faeces and into the water,the ripemiracidium hatches out of the egg. The hatching happens in response totemperature, light and dilution of faeces with water. The miracidium searches for a suitable

freshwatersnail (Biomphalaria glabrata,Biomphalaria straminea,BiomphalariatenagophilaorBiomphalaria sudanica[9] ) to act as an intermediate host and penetrates it.Following this, the parasite develops via a so-called mother-sporocyst and daughter-sporocyst generation to the cercaria. The purpose of the growth in the snail is the numericalmultiplication of the parasite. From a single miracidium result a few thousand cercaria,every one of which is capable of infecting man.

Libora et al. (2010)[10] have detected in Venezuela, that a land snailAchatina fulica can alsoserve as a host ofSchistosoma mansoni.[10]

The cercaria emerge from the snail during daylight and they propel themselves in water

with the aid of their bifurcated tail, actively seeking out their final host. When theyrecognise human skin, they penetrate it within a very short time. This occurs in threestages, an initial attachment to the skin, followed by the cercaria creeping over the skinsearching for a suitable penetration site, often a hair follicle, and finally penetration of theskin into the epidermis usingproteolytic secretions from the cercarial post-acetabular, thenpre-acetabularglands. On penetration, the head of the cercaria transforms into anendoparasitic larva, the schistosomule. Each schistosomule spends a few days in the skinand then enters the circulation starting at the dermal lymphatics and venules. Here theyfeed on blood, regurgitating the haem as hemozoin.[11] The schistosomule migrates to thelungs (57 days post-penetration) and then moves via circulation through the left side ofthe heart to the hepatoportal circulation (>15 days) where, if it meets a partner of the

opposite sex, it develops into a sexually mature adult and the pair migrate to the mesentericveins.[12] Such pairings are monogamous.[13]

Male schistosomes undergo normal maturation and morphological development in thepresence or absence of a female, although behavioural, physiological and antigenicdifferences between males from single-sex, as opposed to bisex, infections have beenreported. On the other hand, female schistosomes do not mature without a male. Femaleschistosomes from single-sex infections are underdeveloped and exhibit an immature

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reproductive system. Although the maturation of the female worm seems to be dependenton the presence of the mature male, the stimuli for female growth and for reproductivedevelopment seem to be independent from each other.

The adult female worm resides within the adult male worm's gynaecophoric canal, which is

a modification of the ventral surface of the male forming a groove. The paired worms moveagainst the flow of blood to their final niche in the mesenteric circulation where they beginegg production (>32 days). The S. mansoni parasites are found predominantly in the smallinferior mesenteric blood vessels surrounding the large intestine and caecal region of thehost. Each female lays approximately 300 eggs a day (one egg every 4.8 minutes), whichare deposited on theendothelial lining of the venous capillary walls.[14] Most of the bodymass of female schistosomes is devoted to the reproductive system. The female convertsthe equivalent of almost her own body dry weight into eggs each day. The eggs move intothe lumen of the host's intestines and are released into the environment with the faeces.

[edit] Genome

Schistosoma mansoni has 8 pairs ofchromosomes (2n = 16)7 autosomal pairs and 1 sexpair. The female schistosome is heterogametic, or ZW, and the male is homogametic, orZZ. Sex is determined in the zygoteby a chromossomal mechanism. The Schistosomagenomeis approximately 270 MB with a GC content of 34%, 48% highly repetitivesequence, 3236% middle repetitive sequence and 60% single copy sequence. Numeroushighly or moderately repetitive elements have been identified, and their frequency ingenomic sequence data also suggests at least 30% repetitiveDNA. Chromosomes range insize from 18 to 73 MB and can be distinguished by size, shape and C banding. There areestimated to be 1520 thousand expressedgenes. [15]

In 2000, the first BAC library of Schistosome was constructed.[16] In June 2003, a ~5xwhole genome shotgun sequencing project was initiated at the Sanger Institute. Togetherwith the shotgun data being generated by TIGR, an ~8x coverage of the genome will beobtained, assembled and annotated. [17]Also in 2003, 163,000 ESTs (expressed sequencetags) were generated (by a consortium headed by the University of So Paulo) from sixselected developmental stages of this parasite, resulting in 31,000 assembled sequences andan estimated 92% of the 14,000-gene complement. [18]

In 2009 the genomes of both S. mansoni and S. japonicum were published, with eachdescribing 11,809 and 13,469 genes respectively. Analysis of the S. mansoni genomehighlighted expansions in protease families and deficiencies in lipid anabolism; both

observations can be directly related S. mansoni's parasitic lifestyle. The former included theinvadolysin (host penetration) and cathepsin (blood feeding) gene families, while the latterencompassed several enzymes required for the de novo synthesis of fatty acids and sterols(so the worm must rely on its host for these products). The results open the way forresearch on new targeted treatments.[19][20]

In 2012 an improved version of the S. mansoni genome was published, with only 885scaffolds and more than 81% of the bases organised into chromosomes. In the same study

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the authors have also used transcriptome sequencing (RNA-seq) from four time points inthe parasites life cycle to refine 45% gene predictions and profile their expression levels.[21]

[edit] Pathology

A Schistosoma mansoni egg with the characteristic lateral spine

Schistosome eggs, which may become lodged within the hosts tissues, are the major causeof pathology in schistosomiasis. Some of the deposited eggs reach the outside environmentby passing through the wall of the intestine; the rest are swept into the circulation and arefiltered out in the periportal tracts of the liver resulting in periportal fibrosis. Onset of egglaying in humans is sometimes associated with an onset of fever (Katayama fever). This"acute schistosomiasis" is not, however, as important as the chronic forms of the disease.ForS. mansoni and S. japonicumthese are "intestinal" and "hepatic schistosomiasis",associated with formation ofgranulomas around trapped eggs lodged in the intestinal wallor in the liver, respectively. The hepatic form of the disease is the most important,granulomas here giving rise to fibrosisof the liver and hepatosplenomegaly in severe cases.Symptoms and signs depend on the number and location of eggs trapped in the tissues.Initially, the inflammatory reaction is readily reversible. In the latter stages of the disease,the pathology is associated with collagen deposition and fibrosis resulting in organ damagethat may be only partially reversible.

Granuloma formation is initiated by antigens secreted by the miracidium throughmicroscopic pores within the rigid egg shell, and there is strong evidence that the vigorousgranulomatous response, rather than the direct action of parasite egg antigens, isresponsible for the pathologic tissue manifestations in schistosomiasis.[22] The granulomasformed around the eggs impair blood flow in the liver and consequently induceportalhypertension. With time, collateral circulation is formed and the eggs disseminate into thelungs, where they cause more granulomas, pulmonary arteritis and, later, cor pulmonale. A

contributory factor to portal hypertension is Symmers' fibrosis, which develops aroundbranches of the portal veins. This fibrosis occur only many years after the infection andapparently is caused in part by soluble egg antigens and various immune cells which reactto them.

Recent research has shown that granuloma size is consistent with levels of IL-13, whichplays a prominent role in granuloma formation and granuloma size. IL-13 receptor 2 (IL-13R2) binds IL-13 with high affinity and blocks the effects of IL-13. Thus, this receptor is

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essential in preventing the progression of schistosomiasis from the acute to the chronic(and deadly) stage of disease. Synthetic IL-13R2 given to mice has resulted in significantdecreases in granuloma size, implicating IL-13R2 as an important target inschistosomiasis.[23]

[edit] Evasion of host immunity

Adult and larval worms migrate through the host's blood circulation avoiding the host'simmune system. The worms have many tools that help in this evasion, including thetegument, antioxidant proteins, and defenses against host membrane attack complex(MAC).[24]

Tegument

The tegument coats the worm and acts as a physical barrier to host antibodies andcomplement.

Antioxidant proteins

Host immune defenses are capable of producing superoxide, which has a tremendousdetrimental effect on the worm. However, they are able to produce a number of antioxidantproteins that block the effect of superoxide. Schistosomes have four superoxide dismutases,and levels of these proteins increase as the schistosome develops and matures.

Antioxidant pathways were first recognised as a chokepoints for Schistosomes[25] and laterextended to other trematodes and cestodes. Targeting of this pathway with differentinhibitors of the central antioxidant enzyme Thioredoxin Glutathione Reductase (TGR)

results in reduced viability of worms [26]

Defense against host MAC

Schistosomes have evolved ways to block host complement proteins.Immunocytochemistry techniques have found decay accelerating factor (DAF) protein onthe tegument. DAF is found on host cells and protects host cells by blocking formation ofMAC. It has also been found that the schistosome genome consists of human CD59homologs. CD59 inhibits MAC.

[edit] SymptomsMany individuals do not experience symptoms. If symptoms do appear, it usually takesfour to six weeks from the time of infection. The first symptom of the disease may be ageneral ill feeling. Within twelve hours of infection, an individual may complain of atingling sensation or lightrash, commonly referred to as "swimmer's itch", due to irritationat the point of entrance. The rash that may develop can mimic scabies and other types ofrashes. Other symptoms can occur two to ten weeks later and can includefever, aching,

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cough, diarrhea, or gland enlargement. These symptoms can also be related to avianschistosomiasis which does not cause any further symptoms in humans.

[edit] Katayama fever

Another primary condition, called Katayama fever, may also develop from infection withthese worms, and it can be very difficult to recognize. Symptoms include fever, lethargy,the eruption of pale temporary bumps associated with severe itching (urticarial) rash, liverand spleen enlargement, and bronchospasm.

[edit] Intestinal schistosomiasis

In intestinal schistosomiasis, eggs become lodged in the intestinal wall and cause animmune system reaction called a granulomatous reaction. This immune response can leadto obstruction of the colon and blood loss. The infected individual may have what appearsto be a potbelly. Eggs can also become lodged in the liver, leading to high blood pressure

through the liver, enlarged spleen, the buildup of fluid in the abdomen, and potentially life-threatening dilations or swollen areas in the esophagus or gastrointestinal tract that can tearand bleed profusely (esophageal varices). Rarely, the central nervous system is affected.Individuals with chronic active schistosomiasis may not complain of typical symptoms.

[edit] Diagnosis and treatment

Diagnosis of infection is confirmed by the identification of eggs in stools. Eggs ofS.mansoni are approximately 140 by 60 m in size, and have a lateral spine. The diagnosis isimproved by the use of the Kato-Katz technique(a semi-quantitative stool examinationtechnique). Other methods which can be used are enzyme linked immunosorbent assay(ELISA), circumoval precipitation test (COPT) and alkaline phosphatase immunoassay(APIA).[27]

Currently there are two drugs available,praziquantel and oxamniquine, for the treatment of[28] schistosomiasis. They are considered equivalent in relation to efficacy and safety. Dueto its lower cost per treatment, praziquantel is generally considered the first option fortreatment. The recommended dose is: praziquantel, 60 mg/kg of body weight for childrenup to 15 years old, and 50 mg/kg of body weight for adults; oxamniquine, 15 mg/kg foradults, and 20 mg/kg for children up to 15 years old. The treatment objective is to cure thedisease and to prevent the evolution of the acute to the chronic form of the disease. Allconfirmed cases should be treated.

Schistosoma japonicum

Schistosoma japonicum is an importantparasite and one of the major infectious agents ofschistosomiasis.This parasite has a very wide host range, infecting at least 31 species ofwild mammals, including 9 carnivores, 16 rodents, oneprimate (Human), twoinsectivoresand threeartiodactylsand therefore it can be considered a truezoonosis.

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Disease

Schistosoma japonicum is the only human blood fluke that occurs in China. It is the causeof schistosomiasis japonica, a disease that still remains a significant health problemespecially in lake and marshland regions. Schistosomiasis is an infection caused mainly by

three schistosome species; Schistosoma mansoni, Schistosoma japonicum and Schistosomahaematobium. S. japonicum being the most infectious of the three species[1]. Infection byschistosomes is followed by an acute Katayama fever. Historical accounts of Katayamadisease dates back to the discovery ofS. Japonicum in Japan in 1904. The disease wasnamed after an area it was endemic to, Katayama district, Hiroshima, Japan [2]. If leftuntreated, it will develop into a chronic condition characterized by hepatosplenic diseaseand impaired physical and cognitive development. The severity ofS. japonicum arises in60% of all neurological diseases in schistosomes due to the migration of schistosome eggsto the brain[3].

[edit] MorphologyThe S. japonicum worms are yellow or yellow-brown. The males of this species are slightlylarger than the other Schistosomes and they measure ~ 1.2 cm by 0.5 mm. The femalesmeasure 2 cm by 0.4 mm. The adult worms are longer and narrower than the relatedS.mansoni worms.

By electron microscopythere are no bosses or spines on the dorsal surface of the male,which is ridged and presents a spongy appearance. Many spines cover the inner surface ofthe oral sucker and extend to thepharyngeal opening. The oral sucker shows a rim withspines of variable size and sharpness inward and outward from the rim. The ventral sucker

possesses many spines which are smaller than in the oral sucker. The lining of thegynecophoric canal is roughened by minute spines. The integument of the female is ridgedand pitted and possesses fewer spines than in the oral sucker, the ventral sucker, and thegynecophoric canal of the male. Anterior to the acetabulum, the integumental surfaces aredevoid of spines. However, in the other areas, spines are equally distributed except for thevicinity of the excretory pore.

The ova are about 55 - 85 m by 40 - 60 m, oval with a minute lateral spine or knob.

[edit] Life cycle

The life cycles ofSchistosoma japonicum and Schistosoma mansoni are very similar. Inbrief, eggs of the parasite are released in the feces and if they come in contact with waterthey hatch into free-swimming larva, called miracidia. The larva then has to infect a snailof the genusOncomelania such as species ofOncomelania hupensiswithin one or twodays. Inside the snail, the larva undergo asexual reproduction through a series of stagescalled sporocysts. After the asexual reproduction stage cercaria (another free-swimminglarva) are generated in large quantities, which then leave (shed into the environment) thesnail and must infect a suitable vertebrate host. Once the cercaria penetrates the skin of the

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host it loses its tail and becomes a schistosomule. The worms then migrate through thecirculation ending at the mesenteric veins where they mate and start laying eggs. Each pairdesposits around 1500 3500 eggs per day in the vessels of the intestinal wall. The eggsinfiltrate through the tissues and are passed in the feces.

[edit] Pathology

Once the parasite has entered the body and begun to produce eggs, it uses the hostsimmune system (granulomas) for transportation of eggs into the gut. The eggs stimulateformation of granuloma around them. The granulomas, consisting of motile cells, carry theeggs to the intestinal lumen. When in the lumen, granuloma cells disperse leaving the eggsto be excreted within feces. Unfortunately, about two-thirds of eggs are not excreted,instead they build up in the gut. This can lead to fibrosis in chronic cases. S. japonicum isthe most pathogenic of the schistosoma species because it produces up to 3,000 eggs perday, ten times greater than that ofS. mansoni.[3].

As a chronic disease, S. japonicum can lead to Katayama fever, liver fibrosis, livercirrhosis, liver portal hypertension, splenomegaly, and ascites. Some eggs may pass theliver and enter lungs, nervous system and other organs where they can adversely affect thehealth infected individual.[3].

[edit] Diagnosis

Histopathological image of old state of schistosomiasis incidentally found at autopsy. Thedeposition of calcified eggs in the colonic submucosa suggests prior infection ofSchistosoma japonicum.

Microscopic identification of eggs in stool orurine is the most practical method fordiagnosis. Stool examination should be performed when infection with S. mansoni orS.

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japonicum is suspected, and urine examination should be performed if S. haematobium issuspected.

Eggs can be present in the stool in infections with all Schistosoma species. Theexamination can be performed on a simple smear (1 to 2 mg of fecal material). Since eggs

may be passed intermittently or in small amounts, their detection will be enhanced byrepeated examinations and/or concentration procedures (such as the formalin - ethyl acetatetechnique). In addition, for field surveys and investigational purposes, the egg output canbe quantified by using the Kato-Katz technique (20 to 50 mg of fecal material) or theRitchie technique.

Eggs can be found in the urine in infections with S. haematobium (recommended time forcollection: between noon and 3 PM) and with S. japonicum. Detection will be enhanced bycentrifugation and examination of the sediment. Quantification is possible by usingfiltration through aNucleopore membrane of a standard volume of urine followed by eggcounts on the membrane. Tissue biopsy (rectal biopsy for all species and biopsy of the

bladder forS. haematobium) may demonstrate eggs when stool or urine examinations arenegative.

Since the eggs ofS. japonicum are small, concentration techniques may be required.Biopsies are mostly performed to test for chronic schistomiasis with no eggs. An ELISAtest can be performed to test for antibodies specific to schistosomes. A positive resultindicates a present or recent infection (within the past two years). Ultrasonographicexamination can be performed to assess the extent of hepatic and spleen-related morbidity[1]. The problems with immunodiagnostic methods are that 1) It is only positive a certaintime after infection 2) They can cross interact with other helminthes infections.[3].

[edit] Treatment

The chemotherapy of choice ispraziquantel, a quinolone derivative. Praziquantel isgenerally administered in an oral form in one or two doses from 4060 mg/kg body weight.

Combination treatment may prevent morbidity due to schistosomiasis. Praziquantel is mostactive against adult worms. However, it has been found that artemether prevents thedevelopment of adult worms, thus decreasing egg production in the host. If bothpraziquantel and artemether can be used together, the entire lifespan ofS. japonicum wouldbe covered in the vertebrate host[4].

[edit] Prevention

Human waste should be hygienically disposed of. Human waste in water with theOncomelania snail intermediate host is a major cause to the perpetuation ofschistosomiasis. To prevent this from occurring, human waste should never be used fornightsoiling (fertilization of crops with human waste) and unsanitary conditions should beimproved. To avoid infection, individuals should avoid contact with water that is

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contaminated by human or animal waste, especially water sources that are endemic toOncomelania snails.[3].

If necessary to enter potentially infected water, cercarial repellants and cercaricidalointments can be applied to the skin before entering the water. Barrier cream with a

dimethicone base offered high levels of protection for at least 48 hours[5]

.

The search for a practical vaccine continues and could greatly benefit affected areas.[3].

[edit] Control

Control against infection ofS. japonicum requires multiple efforts consisting of education,eliminating the disease from infected individuals, controlling the vector, and providing aprotective vaccine.[3].

Education can be incredibly effective, but difficult with lack of resources. Also, asking

people to change customs, traditions and behaviors can prove a difficult task[3].

Controlling S. japonicum with molluscicide has proved ineffective because Oncomelaniasnails are amphibious and only frequent water to lay their eggs [3].

[edit] Social Impacts

Individuals at risk to infection from S. japonicum are farmers who often wade in theirirrigation water, fisherman that wade in streams and lakes, children that play in water, andpeople who wash clothes in streams [3].

Ablution is a religious requirement in some Moslem countries to achieve cleanliness bywashing of the anal or urethral orifices after urination or defecation. However, this actleads to the transmission of schistosomiasis. The water source typically used for ablution isa contaminated river or canal from previously deposited human waste, thus furthering thecontamination in the population.[3].

Important factors to influence transmission are age, sex of an individual, as well as theeconomic and educational level of a population. Males show the highest rates of infection,as well as the most intense infections. This may be due to occupational risk. As was thecase of Suriname, the highest prevalence occurs in both sexes where both male and females

work in fields.

[3]

.Climate change may have potential impact on the transmission of schistosomiasis in China.The development ofS. japonicum in the intermediate host Oncomelania hupensis occurredat the threshold of 15.4C. Previously, O. hupensis has been restricted to areas where themean January temperature has been over 0C. With rising climate change, it is predictedthat by 2050, O. hupensis will be able to cover 8.1% of the surface area of China, thusleading to greater concern to new populations being at risk to schistosomiasis

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1. 2. (/)3. pKa

( ) , P- (P-gp).

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