Trematodes PDF

# FASCIOLIASIS A disease of the hepatobiliary system caused by a large parasite which belongs to phylum: platyhelminthes, class: Trematoda, genus: Fasciola. It is a parasite of sheep, cattle and related animals worldwide and occasionally man. Fascioliasis belongs to the group of foodborne trematode...

# FASCIOLIASIS A disease of the hepatobiliary system caused by a large parasite which belongs to phylum: platyhelminthes, class: Trematoda, genus: Fasciola. It is a parasite of sheep, cattle and related animals worldwide and occasionally man. Fascioliasis belongs to the group of foodborne trematode infections and is a zoonotic disease; i.e. an animal disease which may be transmitted to man. Fascioliasis is caused by two species namely Fasciola hepatica (F. hepatica) and Fasciola gigantica (F. gigantica). ## OCCURRENCE Fascioliasis is a global disease, and human cases have been reported from more than 75 countries worldwide including Egypt mainly in sheep and cattle-raising areas. Human fascioliasis in Egypt has been found in almost all governorates of the Delta region, in Alexandria city, in some governorates of Upper Egypt, and in the reclaimed desert land. Where it occurs sporadically, fascioliasis affects people from all age groups, and there is no specific risk group. Where the infection is highly endemic, the prevalence and intensity of infection tend to peak in school age children. People living in rural areas are typically more likely to become infected; however, cases may occur anywhere and can follow the trade routes of the carrier plants, which are part of the usual diet in many countries. ## CYCLE OF INFECTION ### Causative agent: Fasciola species ### Habitat The parasite inhabits the bile ducts of sheep, goats and buffaloes. Human infection is rather infrequent. ### Morphology F. hepatica is a leaf-like trematode, pale grey in color, with dark converging lateral margins and a spiny cuticle. It measures 2.5-3 cm in length and about 1 cm in breadth. It has relatively large cephalic cone and prominent anterior shoulders. The oral and ventral suckers are found at the apex and at the base of the cephalic cone respectively. It is hermaphrodite with a highly branched digestive and genital systems (Figures 1 & 2). F. gigantica is similar in morphology to F. hepatica with minor differences. It is larger (7cm in length) with shorter cephalic cone and parallel sides (Figure 1). ## Life cycle and mode of transmission The eggs of F. hepatica are large (150 µm X 80 µm), oval, light-yellow in color and operculated. They are passed with bile to the intestine and then discharged in feces (Figure 3). When freshly evacuated the eggs are immature and must reach fresh water of rivers or canals to mature. After maturity in water for 9-15 days at an optimal temperature of 22°C-25°C, the miracidium escapes from the egg. Within 8 hours, the miracidium invades the appropriate snail. In Egypt, Lymnaea truncatula snail is the intermediate host (Figure 4). In the lymph space of the snail, the miracidia metamorphose into sporocysts. Within three weeks, sporocysts produce several generations of rediae, then cercariae develop. The latter leave the snail late in the evening and within few hours they encyst on water vegetations or grass after shedding their tail and are now called encysted metacercariae (Figure 5). These appear as small spherical white bodies on vegetation or floating on water. Microscopically, they appear round with a cyst wall, rudimentary gut and suckers. The encysted metacercariae are the infective stage of Fasciola. When the herbivorous animals, less frequently man, ingest the encysted metacercariae, they excyst in the duodenum to become juvenile flukes which migrate through the intestinal wall into the body cavity, through Glisson's capsule, traverse the liver parenchyma to the biliary passages, where they settle down and grow to maturity (Figure 6). The incubation period in the definitive host requires 3-4 months. On rare occasions, juvenile flukes may enter the systemic circulation where they are distributed in abnormal sites causing ectopic fascioliasis. In F. gigantica, the eggs are larger in size (180 µm X 80 µm). In Egypt, the snail intermediate host of F. gigantica is Lymnaea natalensis. The development in the snail is slower and the encysted metacercariae are more susceptible to desiccation. ## PATHOLOGY & PATHOGENESIS The excysted metacercariae migrating through the intestinal wall, into the peritoneal cavity, and then into Glisson's capsule hardly produce any damage. However traumatic and necrotic lesions are produced during their migration in the liver parenchyma. These lesions are infiltrated by eosinophils. After arrival in the bile ducts the larvae develop into adults provoking an inflammatory and adenomatous response of the biliary epithelium. ## CLINICAL PRESENTATION ### Acute stage Acute stage occurs about two months following the ingestion of the encysted metacercariae. Acute signs and symptoms may start and can last for weeks. This stage is caused by migration of immature flukes through hepatic parenchyma. - Main symptoms are upper right abdominal pain, cough, dyspepsia, anorexia, vomiting, diarrhea, weight loss, urticaria and headache - Main signs are fever, tender hepatomegaly with or without splenomegaly, and jaundice. This stage is characterized by high eosinophilia up to 80%. ### Chronic stage The chronic stage is due to the presence of adult flukes in the bile ducts reflecting intermittent biliary obstruction and inflammation. - Main symptoms are nausea, vomiting, fatty food intolerance, upper right abdominal pain and pruritus. - Main signs are cholestatic jaundice with hepatomegaly, and fever with cholangitis, calcular or acalcular cholecystitis. - Fascioliasis was also associated with normocytic normochromic anaemia which change to microcytic hypochromic anemia in the advanced chronic period. Chronic blood loss due to the blood-sucking activity of the adult flukes and leakage of blood from the bile duct to the intestine results in iron deficiency anemia and hypoproteinemia. Anemia is caused also by a toxic substance released from the worms. - Hemobilia is a very rare complication associated with chronic fascioliasis due to arterial bleeding associated with ulcer caused by a dead parasite in the common bile duct. It can cause fatigue, hematemesis, melena and anemia. - This stage is characterized by moderate eosinophilia up to 40%. ### Ectopic fascioliasis Ectopic fascioliasis has been reported in several foci as subcutaneous tissues, brain, lungs, inguinal lymph nodes and cecum causing eosinophilic infiltration and inflammation. Ectopic fascioliasis can cause eosinophilic panniculitis, pulmonary infiltrate, pleuropericarditis, meningitis and lymphadenopathy. ## HALZOUN Hazloun is a type of F. hepatica infection in which the worm attaches and settles in the pharynx. This occurs when an individual consumes infected raw liver. The young adult worms then attach themselves to the laryngeal-pharyngeal mucosa, which causes considerable pain, edema, and bleeding that can interfere with respiration. ## DIAGNOSIS ### Clinical diagnosis - Medical history Living in an endemic areas and eating fresh raw vegetables (consumption of green salad). - Clinical presentation Presence of fever, abdominal pain, enlarged liver and moderate to high eosinophilia. ### Laboratory diagnosis - Direct methods Specific diagnosis is based on the recovery of the immature egg (which could be found only in chronic stage after maturation of adult worm) from stool samples or duodenal samples obtained either by aspiration or the entero-test capsule. In cases of suspected spurious infection (i.e false fascioliasis due to ingestion of infected liver containing Fasciola eggs leading to passage of eggs in stools), patients should follow a liver-free diet for several days before repeating follow-up stool examinations. - Immunological methods These are of value in the early invasive stage, as specific antibodies to Fasciola may become detectable 2 to 4 weeks after acquisition of infection, whereas egg production typically does not start until at least 3 to 4 months after exposure. Serologic testing can also be of value for cases of chronic fascioliasis in persons with low-level or sporadic egg production, as well as in persons with ectopic infection. It may also help rule out pseudofascioliasis associated with ingestion of parasite eggs in sheep or beef liver. Loss of detectable antibodies occurs 6-12 months after cure. A variety of techniques are available including ELISA and indirect hemagglutination (IHA) test. Other available techniques are immunofluorescence (IF), counterimmunoelectrophoresis (CIE), gel electrophoresis and metacercariae precipitin test though not commonly used. During the invasive course of infection (as early as two week post infection), antigen can be detected in the sera of fascioliasis patients, then it decreases and becomes undetectable in later phases of infection. Detection of Fasciola antigen in stool (coproantigens) by ELISA is also useful in diagnosis of acute early and chronic phases of infection as it has an ability to detect the infection in subjects, shedding very low number of eggs. - Blood picture Blood picture shows moderate to high eosinophilia. It is the most important laboratory abnormality in fascioliasis (80% in the acute stage and 40% in the chronic stage). This is in addition to leucocytosis and anemia. - Liver function Liver function tests denote cholestasis. ### Radiological diagnosis Radiologic diagnosis includes ultrasound, computerized tomography (CT), and magnetic resonance imaging (MRI). Endoscopic retrograde cholangiopancreatography (ERCP) and percutaneous cholangiography may be also useful. CT frequently shows hypodense lesions in the liver during the acute stage of fascioliasis. CT, MRI, ERCP and cholangiography can detect biliary tract abnormalities in chronic disease. ### Differential diagnosis - Other causes of hepatomegaly as schistosomiasis, hydatid cyst, amoebic hepatitis, amoebic liver abscess, visceral larva migrans, viral hepatitis and other liver flukes. - Other causes of cholangitis and gall stones. ## TREATMENT - Medical treatment Triclabendazole is the recommended regimen in a dose of 10 mg/kg body weight administered as a single dose after a meal in both clinical practice and preventive chemotherapy interventions. In clinical practice, where treatment failure occurs, or in patients who have severe or heavy Fasciola infections, the dose may be increased to 20 mg/kg body weight in two divided doses 12-24 hours apart. - Nitazoxanide is a good alternative to triclabendazole especially for chronic stage of Fasciola infection. Adult dose is 500 mg twice a day for 7 days. - Endoscopic therapy In cases of obstructive jaundice, endoscopic retrograde cholangiopancreatography (ERCP) can be used to relief the obstruction with sphincterotomy and worm extraction followed by fasciolicidal drugs. - Surgical therapy Cholecystectomy is performed with common bile duct exploration in cases of jaundice. ## PREVENTION & CONTROL 1. Proper washing of vegetables that will be eaten raw in either 6% vinegar or potassium permanganate for 5 to 10 minutes, which destroys the encysted metacercariae. 2. Avoid drinking unfiltered water. 3. Veterinary public health measures, including treating domestic animals. 4. Snail elimination by using molluscicides. # HETEROPHYIASIS Heterophyiasis is infection with the intestinal fluke Heterophyes heterophyes which belongs to phylum Platyhelminthes, class: Trematoda, genus: Heterophyes. About 30 million people worldwide are estimated to be infected with this fluke. ## OCCURRENCE Egypt, the Middle East, and Far East. ## CYCLE OF INFECTION ### Causative agent: Heterophyes heterophyes (H. heterophyes) ### Habitat Small intestine of man, cats, dogs and fish-eating birds. These animals serve also as reservoir hosts. ### Morphology - Oral sucker - Ventral sucker - Genital sucker - Uterus - Testes ## Life cycle and mode of transmission Eggs of H. heterophyes is 30 x 15 µm, light brown and when excreted with the stools contain a fully developed miracidium (Figure 2). The eggs must reach brackish water of lakes (mixture of fresh and salty water), where they are eaten by the first intermediate host, Pirenella conica snail, and hatch inside it releasing the miracidia. In about three to four weeks, the miracidia develop into sporocysts, two generations of rediae and finally cercariae. The latter leave the snail and swim for two to three days till they find the second intermediate fish host, Mugil cephalus (Boury) and Tilapia nilotica (Bolty). Cercariae attack these fish, particularly around their tail and under the fins; they lose their tail and encyst. These encysted metacercariae (Figure 3), are spherical in shape, about 250 μ in diameter, and are infective after three weeks. Man gets infected with H. heterophyes through eating imperfectly cooked fish or under-salted fish (sweet fessikh i.e. fish salted for less than seven days), containing the infective encysted metacercariae which are liberated from their cyst wall and attach themselves to villi of the small intestine by their suckers. They grow to adulthood in about two weeks (Figure 4) ## PATHOLOGY & PATHOGENESIS Two principal factors are generally related to the pathogenicity and virulence of intestinal trematodes; they include mechanical and chemical irritations by the flukes. - Mechanical irritation is chiefly caused by the movement of worms which can give harmful effects on the mucosa of the small intestine. - Chemical substances produced by the flukes, which include excretory-secretory proteins (ESP), can also play a role for not only as antigens but as toxins to the host. At the site of worm attachment, the mucous membrane shows a mild catarrhal inflammation, sometimes with superficial ulcers and necrosis. Pathological changes in the mucosa lead to difficulty in nutrient absorption from the intestine and increase in the permeability of the intestinal mucosa. The resulting watery diarrhea seems to be due to poor absorption of intestinal secretions from secretory crypt cells. Decreased enzyme activities were suggested to be associated with malabsorption and diarrhea also. Sometimes the eggs of H. heterophyes can enter the blood and lymphatics and go to ectopic sites in the body, including the brain and spinal cord, where they cause neurological disorders and be found encapsulated in the patients' brains. Eggs may sometimes migrate through the lymphatics to the heart, where they can induce tissue reactions in the valves and myocardium, causing myocarditis and heart failure. Deposition of antigens or immune complexes in the kidneys and brain were thought to play important roles in histopathological changes in the kidneys and brain. ## CLINICAL PICTURE - Most infections are asymptomatic or associated with mild intestinal discomfort, mucous diarrhea, colicky pains, intermittent neurasthenia and lethargy. There may be abdominal pain. - Ectopic heterophiasis may give signs of myocarditis (cardiomegaly, cough, dyspnea, cyanosis, fatigue, edema and ascites, palpitation, loss of reflexes and abnormal heart sounds. In the spinal cord or brain, parasite may cause neurological disease, transverse myelitis and loss of sensory and motor function. ## DIAGNOSIS The diagnosis is based on the microscopic identification of eggs in the stool. ## TREATMENT Praziquantel as a single oral dose of 10 – 20 mg/kg. It is highly effective and is the drug of choice. ## PREVENTION 1. Proper disposal of human excreta. 2. Avoid eating undercooked fish. # SCHISTOSOMIASIS Schistosomiasis is an important parasitic disease caused by the trematode worm Schistosoma, which belongs to the phylum: Platyhelminthes, class: Trematoda. According to the WHO, more than 200 million people are infected with schistosomiasis. The disease is prevalent in tropical and subtropical areas, especially in poor communities without access to safe water supply and adequate sanitation. It is estimated that at least 90% of those requiring treatment for schistosomiasis live in Africa. Adult worms of Schistosoma live in the venous plexus of the host, the location varies according to the species of the parasite. The three most important Schistosoma spp. infecting man are: - Schistosoma haematobium inhabiting the blood vessels of the urogenital system causing urogenital schistosomiasis. - Schistosoma mansoni inhabiting the blood vessels of the large intestine - Schistosoma japonicum inhabiting the blood vessels of the small intestine Both S. mansoni and S. japonicum are the causative agents of intestinal schistosomiasis. ## Diseases Associated With Schistosomiasis Schistosomiasis has been associated with the following infections: - Viral infections: as by HIV and hepatitis viruses - Bacterial Infections: as by Salmonella, Mycobacterium tuberculosis and staphylococcus. In addition to sexually transmitted diseases caused by Neisseria gonorrhea, Chlamydia trachomatis and Mycoplasma genitalium. - Parasitic Infections: Coinfections with Plasmodium species, Leishmania species and Trichomonas vaginalis have been well documented in experimental models as well as humans. ## Chronic Salmonellosis Associated With Schistosomiasis The most established of these, with highest impact on morbidity is salmonellosis. This has been described with intestinal schistosomiasis as well as with urinary schistosomiasis. Acute appendicitis, cholecystitis, pyelonephritis and exudative glom erulonephritis have been documented with this association. ## Pathogenesis The bacteria are found in the tegument or in the intestinal tract of S. mansoni adult worms. The role of schistosomes as a source and vehicle of Salmonella infection has been suggested and sera from patients with hepatosplenic schistosomiasis were found to have reduced antibody activities against Salmonella typhi as compared with normal controls. ## Clinical picture Chronic persistent Salmonella bacteremia has been described in association with S. mansoni infection. The most common characteristics of the clinical syndrome are: - An indolent febrile disease (from several weeks to a few years) - Bacteremia with one of many species of the genus Salmonella - Chronic active schistosomiasis. ## Treatment Effective treatment of schistosomiasis alone deprives the Salmonella of favorable foci for growth and eliminates both infections in more than 90% of the cases. # INTESTINAL SCHISTOSOMIASIS Intestinal schistosomiasis is a disease caused by a parasitic trematode Schistosoma mansoni and Schistosoma japonicum. ## OCCURRENCE Schistosoma mansoni is distributed throughout Africa: There is risk of infection in freshwater in southern and sub-Saharan Africa-including the great lakes and rivers as well as smaller bodies of water. Transmission also occurs in the Nile River valley in Sudan and Egypt. In South America schistosomiasis is present in Brazil, Suriname, and Venezuela. The risk is very low in the Caribbean. ## CYCLE OF INFECTION ### Causative agent: Schistosoma mansoni (S. mansoni). ### Habitat Adult worms inhabit the radicals of the inferior mesenteric veins, draining the large intestine and lower part of the ileum. Rarely worms can be present in the vesical plexus. ### Morphology Adult worms are small in size and have separate sexes. The intestinal caeca re-unite pre-equatorially. Male worms possess a gynaecophoric canal and the testes are globular, small, 6-9 in number behind the ventral sucker. Female worms are longer than males and slender. They lie in the gynaecophoric canal of males (Figure 1). ## Life cycle and mode of transmission Eggs are laid immature in the very fine capillaries of the inferior mesenteric veins. They stretch the capillary wall and then are extruded outside the capillaries to fall in the submucosa of the large intestine and lower part of the ileum. Eggs mature in the intestinal submucosa in six days. They escape to fall in the lumen of the large intestine by the effect of miracidial antigens, egg shell spine, and contraction of the intestinal muscles. Extruded eggs are non-operculated, mature containing a fully developed miracidium and possess a lateral spine. (Figure 2). ## Reservoir of infection Monkeys and rodents are occasionally infected. ## Susceptibility Susceptibility is general ## PATHOLOGY, PATHOGENESIS & MANIFESTATIONS The pathology, pathogenesis and clinical manifestations of bilharzial infection are related to three stages: ### Stage of invasion (Prepatent stage) This can be considered as the incubation period or prepatent stage prior to egg deposition. This includes cercarial penetration, schistosomular migration and maturation. 1. Cercarial penetration can be manifested by pruritus and maculo-papular rash. It develops within few hours of exposure to cercariae in contaminated freshwater. 2. Schistosomular migration and maturation (Katayama fever) (Acute schistosomiasis} It causes generalized allergic reaction and inflammatory reactions in lungs and liver. It occurs most often in travelers or immigrants to schistosome-endemic regions who are exposed to schistosoma antigens for the first time at an older age than usual. It occurs after primary infection with S. mansoni, S. japonicum or, more rarely, S. haematobium as a consequence of schistosome migration, antigen release and immune complex responses. It presents typically with a sudden onset of fever, malaise, myalgia, headache, eosinophilia, fatigue, dry cough, hepatosplenomegaly and abdominal pain. These symptoms are typically seen before oviposition, egg-laying, and the appearance of granulomatous reactions around eggs, which defines the chronic phase of the disease. It usually starts 2-3 weeks after primary infection and lasts 2-10 weeks 3. Stage of established infection = Chronic schistosomiasis This is related to the stage of oviposition and egg extrusion. The eggs are deposited in the submucosa of the large intestine, where they produce the typical bilharzial granuloma which is a local inflammatory response to the eggs (Figure 5). - The eggs are the main cause of serious pathological changes in the human body. - The miracidial antigens stimulate both humoral and cellular immunity. - This stage is manifested by gradual onset of abdominal pain and cramps and dysentery, which is in the form of diarrhea accompanied by tenesmus with mucus and blood in stools. - Other conditions which cause bowel lesions that should be differentiated from intestinal schistosomiasis include: amoebic colitis, bacillary dysentery, ulcerative colitis, tuberculosis, lymphoma and adenocarcinoma. ### Stage of late infection and complications There is progressive formation of fibrous tissue which prevents extrusion of eggs, resulting in complications according to the organs affected. There are intestinal and extraintestinal complications. - Intestinal complications Intestinal polyposis, anal fissures and perianal sinuses. A tender abdominal mass may be felt in left iliac fossa if there is polyposis or bilharzial mass. Severe long-standing polyps may rarely lead to intestinal obstruction (partial or complete), appendicitis or perforation. Protein losing enteropathy may occur secondary to ulcers, fistulae and strictures. - Extra-intestinal complications Hepatosplenic schistosomiasis (described below) - Bilharzial cor pulmonale is the condition of right sided heart failure secondary to fibrosis and sclerosis of the pulmonary artery branches. It occurs in schistosomiasis mansoni, when the portal pressure rises more than the systemic pressure. So, blood will pass from the portal circulation to the systemic circulation across portosystemic shunts carrying S. mansoni ova to reach the lungs. - Anemia: All Schistosoma species cause anemia, malnutrition, and impaired childhood development, as a result of the effect of continued inflammation on normal growth, iron metabolism, physical fitness, and cognitive function. Most anemia in patients with schistosomiasis is anemia of inflammation, linked with blood loss (and high parasitic loads), that contributes to total-body iron deficiency. - Neuroschistosomiasis: Ectopic ova gain access to the central nervous system through the anastomosis in between the lumbar veins, which are tributaries of the inferior vena cava, and the internal vertebral venous plexus. They may deposit and provoke granuloma formation in the adjacent spinal cord, or travel cephalad during coughing or straining, and impinge into the brain tissue. It is more common with schistosomiasis japonicum as the small size of S. japonicum eggs facilitates their journey towards the brain, hence the preference of this species in cerebral schistosomiasis, including the cortex, subcortical white matter, basal ganglia, and internal capsule. On the other hand, myelopathy of the lumbosacral region is more commonly reported with S. mansoni and S. haematobium infection. Neuroschistosomiasis is the most severe clinical syndrome associated with schistosomal infection. Its clinical presentation includes signs and symptoms of increased intracranial pressure, myelopathy, radiculopathy, weakness, sensory loss, and bladder dysfunction. - Glomerulonephritis: Patients with hepatosplenic schistosomiasis can exhibit proliferative glomerulonephritis due to the deposition of immune complexes containing schistosomal antigens. ### Hepatosplenic schistosomiasis Early inflammatory hepatic schistosomiasis characterized by sharp edged left lobe hepatomegaly with or without nodular splenomegaly due to granulomatous early reactions to ova trapped in presinusoidal periportal spaces. Later, fibrotic or chronic hepatic schistosomiasis occurring in a minority of infected patients leading to liver enlargement and periportal fibrosis also called Symmer's pipe-stem fibrosis. This leads to portal hypertension (Figure 6 a), development of portocaval shunts and distribution of eggs into general circulation and ectopic sites. ## Five clinical stages of hepatosplenic schistosomiasis exist: - Hepatomegaly: Liver is enlarged, tender and firm. Spleen may be enlarged due to reticuloendothelial hyperplasia. - Hepatosplenomegaly: Liver is enlarged but not tender. More enlargement of spleen occurs due to congestion (Figure 6 b). - Splenomegaly: Liver becomes shrunken due to fibrosis. The spleen becomes more enlarged and may reach iliac fossa. Splenic rub may be heard with perisplenitis or splenic infarction. - Ascites, abdominal collaterals, hematemesis and melena, neuropsychiatric manifestations due to progression of portal hypertension. - Jaundice, palmar erythema, spider naevi, gynecomastia in males, fetor hepaticus, coma and death due to liver cell failure. ## Classification of hepatosplenic schistosomiasis Hepatosplenic schistosomiasis is classified into three stages according to liver function: - Compensated: May be asymptomatic, some may complain of dyspepsia and flatulence, dragging pain in the left hypochondrium. - Mesenchymal decompensation: Development of portal hypertension. - Parenchymal decompensation: Hepatic cell failure especially with mixed infections. ## Clinical presentation - Symptoms: Hematemesis or melena: May indicate gastroesophageal variceal bleeding or bleeding from portal hypertensive gastropathy. Mental status changes: May indicate the presence of portosystemic encephalopathy. Increasing abdominal girth: May indicate ascites formation. Abdominal pain and fever: May indicate spontaneous bacterial peritonitis, although this disease also presents without symptoms. Hematochezia: May indicate bleeding from portal colopathy. - Signs: Anterior abdominal wall dilated veins: May indicate umbilical epigastric vein shunts. Venous pattern on the flanks: May indicate portal-parietal peritoneal shunting. Caput medusae (tortuous paraumbilical collateral veins; figure 6 c) Ascites and paraumbilical hernia. Splenomegaly. ## DIAGNOSIS ### Clinical diagnosis In an endemic area, a patient complaining of dysentery is suggestive of his infection with S. mansoni. ### Laboratory diagnosis - Direct methods Detection of the characteristic S. mansoni ova by: Stool examination by direct saline smear. In scanty infection, concentration techniques such as formol ether techniques can be used. Kato-Katz fecal examination is recommended by WHO for mapping and field-based control of schistosomiasis. - Rectal swab. - Rectal snip biopsy. - Sigmoidoscopy and biopsy - Liver biopsy. For late stage of infection with fibrous tissue formation direct methods are not suitable but immunological methods are used. ### Immunological methods These tests are used for detecting specific antibodies: - Indirect hemagglutination test (IHAT). - Indirect fluorescent antibody test (IFAT). - Enzyme linked Immunosorbent assay (ELISA): This test can be used for detection of antibodies or circulating antigens in the serum of patients. It can also detect schistosomal antigens in the stool of infected patients. Serological tests for detection of antibodies are unable to discriminate between active infection and past exposure, whereas antigen detection denotes active infection. With advances in parasite antigen isolation and purification, schistosome antigen detection methods in the body fluids of infected individuals were developed. An example of these methods is the use monoclonal antibodies to detect schistosome antigens that are circulating in the blood and excreted in the stool, urine and other body fluid. The most promising and extensively studied are tests that can detect major circulating antigens such as the Circulating Anodic Antigen (CAA) and Circulating Cathodic Antigen (CCA). ### Molecular techniques: DNA detection in serum or stool is being assessed. ## TREATMENT OF SCHISTOSOMIASIS ### Acute schistosomiasis - Cercarial dermatitis: Topical steroids and oral antihistaminics. - Katayama fever: Prednisolone: 40 mg/day for 5-14 days followed by praziquantel to eliminate worms. ### Chronic schistosomiasis Praziquantel is the drug of choice for schistosomiasis. A standard dose of 40 mg/kg is thought effective for treatment of S. haematobium and S. mansoni and can safely be used in pregnancy after the first trimester. For S. japonicum, the recommended dose is 60 mg/kg. ## PREVENTION & CONTROL 1. Reduction of human infection by mass chemotherapy. Treat patients in endemic areas with praziquantel to relieve suffering and prevent disease progression. 2. Regular treatment of high-risk groups such as school age children, women of childbearing age or special occupational groups in endemic areas. 3. Educate the public in endemic areas to seek treatment early and regularly and to protect themselves. 4. Individual protection: prevent exposure to contaminated water (e.g. rubber boots). To minimize cercarial penetration after brief or accidental water exposure, vigorously and completely towel dry skin surfaces that are wet with suspected water. Apply 70% alcohol immediately to the skin to kill surface cercariae. 5. Sanitary sewage disposal, so that viable eggs will not reach bodies of fresh water containing intermediate snail hosts. 6. Treat snail-breeding sites with molluscicides, predators; biological control; water management and engineering. 7. Improve irrigation and agriculture practices; reduce snail habitats by removing vegetation, by draining and filling, or by lining canals with concrete. 8. Clean water supply for drinking, bathing and washing clothes. Effective measures for inactivating cercariae include water treatment with iodine or chlorine. Allowing water to stand 48-72 hours before use is also effective. 9. Travelers visiting endemic areas should be advised of the risks and informed about preventive measures. # URINARY SCHISTOSOMIASIS Urinary schistosomiasis is a disease caused by a parasitic trematode Schistosoma haematobium. ## OCCURRENCE The disease is distributed throughout Africa: There is risk of infection in freshwater in southern and sub-Saharan Africa-including the great lakes and rivers as well as smaller bodies of water. Transmission also occurs in the Nile River valley in Egypt and the Maghreb region of North Africa. It is found in areas of the Middle East and a recent focus of ongoing transmission has been identified in Corsica. ## CYCLE OF INFECTION ### Causative agent: Schistosoma haematobium (S. haematobium) ### Habitat Adult worms inhabit the vesical and pelvic venous plexuses rarely they may be found in the portal blood stream. ### Morphology Adult S. haematobium have the same morphological features as S. mansoni except that they are larger in size and the intestinal caeca unite post-equatorially. Males have 3-5 large testes. In females the ovary is post-equatorial (Figure 7). ## Life cycle and mode of transmission The life cycle is similar to that of S. mansoni with the following differences: - The eggs are laid immature in the very fine capillaries of the vesical plexus. They stretch the capillary wall and then are extruded outside the capillaries to settle in the urinary bladder wall. They mature there in six days. The eggs escape to fall in the lumen of the bladder, by the effect of miracidial antigens, egg shell spine and contraction of the bladder muscles. Extruded eggs possess a terminal spine and pass with the urine (Figure 8). - The intermediate host is snails of the Bulinus species. - The male carries the female in the gynaecophoric canal and migrate in the portal tributaries against the blood stream from the liver to reach the inferior mesenteric veins. Then, the couple migrates to the rectal veins and cross the portosystemic shunts through the inferior rectal vein to reach the vesical and pelvic venous plexus where they settle. ## Reservoir of infection No reservoir host and man is the only known definitive host for S. haematobium. ## Susceptibility Susceptibility is general. ## PATHOLOGY & PATHOGENESIS & MANIFESTATIONS Pathology, pathogenesis and clinical manifestations of bilharzial infection are related to three stages: ### Stages of cercarial penetration, schistosomular migration and maturation The same as S. mansoni but katayama fever is rare in Schistosomiasis haematobium. ### Stage of established infection = Chronic schistosomiasis This is related to the stage of oviposition and egg extrusion. The eggs are deposited in the submucosa of the bladder, where they produce the typical bilharzial granuloma which is a local inflammatory response to the eggs (Figure 9). Living adult worms produce no tissue damage while dead adults produce a local inflammatory reaction consisting of perivascular cellular infiltration. Terminal hematuria appearing 10-12 weeks after infection is the first sign of established infection. Also, dysuria, frequency, and suprapubic discomfort. ### Stage of late infection and complications There is progressive formation of fibrous tissue which prevents extrusion of eggs, resulting in complications according to the organs affected. There are urinary and extra-urinary complications. - Urinary complications Urinary bladder: Polyps, ulcers, calcified bladder (Figure 10), diverticulosis, stones and cancer bladder. The major histological cell type of bladder cancer associated with schistosomiasis of the urinary tract is squamous cell carcinoma (SCC) resulting from chronic inflammation. In industrialized countries (North America and northern Europe), bladder cancer occurs mainly as transitional cell carcinomas (TCC), with a peak incidence in the seventh decade of life. The mechanisms of bladder carcinogenesis include: - Schistosome-induced chronic inflammation and irritation in the urinary bladder. - Nitrate-reducing bacteria, including Staphylococcus aureus, hemolytic Staphylococcus albus, Proteus mirabilis, Klebsiella spp., and Escherichia coli. - Specific genes that underlie neoplastic progression in the development of schistosomal bladder cancer. These include the activation of H-ras, inactivation of p53, and inactivation of the retinoblastoma gene. - Carcinogens associated with traditional foodstuffs have frequently been implicated as causative agents of cancer in Egypt. Ureters: Strictures, obstructive uropathy, hydro-ureters, pyo-ureters. Kidneys: Hydronephrosis, pyonephrosis and impairement of kidney function. Glomerulonephritis: Proliferative glomerulonephritis, with schistosomal antigen deposits, has been identified as a manifestation of early S. haematobium infection. Transient proteinuria, hematuria and hypertension were noticed in infected subjects, and renal biopsy showed mesangial proliferation and infiltration with transit pro-inflammatory blood cells. Spontaneous recovery occurred in most patients. - Extra - urinary complications Bilharzial cor pulmonale is the condition of right sided heart failure secondary to fibrosis and sclerosis of the pulmonary artery branches. It results from shifting of the S. haematobium ova from the pelvic and vesical plexus to the pulmonary artery branches where they settle and produce granulomata and fibrosis. This leads to pulmonary hypertension, right ventricular hypertrophy and failure (Figure 11). ## DIAGNOSIS ### Clinical diagnosis In an endemic area, a patient complaining of terminal hematuria, dysuria and frequency is suggestive of his infection with S. haematobium. ### Laboratory diagnosis - Direct methods Detection of the characteristic eggs in sedimented or centrifuged urine. Microscopic examination of polycarbonate filters for schistosome eggs in the urine, urine dipstick assays for heme, are recommended by WHO for mapping and field-based control of urinary schistosomiasis. - Cystoscopy and bladder biopsy when needed. For late stage of infection with fibrous tissue formation direct methods are not suitable but immunological methods are used. ### Immunological methods (the same as intestinal schistosomiasis) ### Molecular techniques (the same as intestinal schistosomiasis) ## TREATMENT OF SCHISTOSOMIASIS ### Acute schistosomiasis - Cercarial dermatitis: Topical steroids and oral antihistaminics. - Katayama fever: Prednisolone: 40 mg/day for 5-14 days followed by praziquantel to eliminate worms. ### Chronic schistosomiasis Praziquantel is the drug of choice for schistosomiasis. A standard