Schistosomiasis PDF

Schistosomiasis ILOs At the end of this session, the student will be able to: ▪ Describe epidemiological occurrence of the different Schistosoma species worldwide as well as in Egypt. ▪ Recognize the infective stage of Schistosoma and understand the life cycle of its different...

Schistosomiasis ILOs At the end of this session, the student will be able to: ▪ Describe epidemiological occurrence of the different Schistosoma species worldwide as well as in Egypt. ▪ Recognize the infective stage of Schistosoma and understand the life cycle of its different species. ▪ Understand the pathophysiological mechanisms by which Schistosoma species produce pathology. ▪ Link clinical presentation to the infective stage of Schistosoma and duration of illness. ▪ Recognize chronic schistosomiasis as a common cause of hepatosplenomegaly in Egypt. ▪ Associate complications as core-pulmonale and urinary bladder cancer with chronic Schistosoma infection. ▪ Recognize the most common Schistosoma co-infections. ▪ Differentiate between laboratory diagnosis of acute and chronic schistosomiasis. ▪ Identify praziquantel as the drug treatment of choice of schistosomiasis. What is schistosomiasis? Schistosomiasis is a neglected tropical disease (NTD) and one of the most prevalent parasitic diseases worldwide. The three major schistosomes infecting humans are Schistosoma mansoni, Schistosoma haematobium, and Schistosoma japonicum. From a clinical point of view, schistosomiasis is divided into three stages: (i) the first occurs 24 h after the penetration of the cercariae into the dermis called cercarial dermatitis, (ii) acute schistosomiasis appears 3–8 weeks after infection, and (iii) the chronic stage occurs months or years after infection, and is a consequence of the formation of granulomas in the tissues around the schistosome eggs. Life cycle: The schistosome life cycle occurs in 2 hosts: snails and mammals. Asexual reproduction occurs in freshwater snails. In the snail, this begins with the development of miracidia into a sporocyst. Sporocysts multiply and grow into cercariae. Cercariae enter human skin and shed their forked tail, forming schistosomula. The schistosomula migrate throughout the body's tissues through blood circulation. The Schistosomula grow into schistosomes and adult worms.  Adult worms in humans exist in various locations specific to each species. S. haematobium exists in the bladder and ureters, but it can also exist in the rectal venules. S. japonicum exists more frequently in the small intestine. S. mansoni worms can exist in either large or small intestine and they are able to transfer between those sites. Water containing cercariae can cause human schistosomiasis. 1. Acute Schistosomiasis: Cercarial Dermatitis or Swimmer’s Itch Cercarial dermatitis or Swimmer’s itch is reported in 5–100% of exposed travelers; it develops a few hours after freshwater contact carrying infective cercariae, and the affected person develops an itchy maculo-papular rash, limited to areas immersed in water. The itch becomes more intense, and the rash typically develops with papules and vesicles within hours or a few days after exposure. The disease is self-limiting within 1–3 weeks; given the fleeting nature of the condition, itching is sometimes the only finding that patients present. Katayama Syndrome: Katayama fever is currently not used because not all patients present with fever, and most cases are caused by S. mansoni or S. haematobium. Symptoms usually appear between 2 and 6 weeks after exposure during the maturation of adult forms. However, incubation periods of 1 to 12 weeks have been described. In this phase, the schistosomula matures until reaching the adult form, leading to mating and laying the eggs. In nonimmune travelers, the infection is symptomatic in 54–100% of cases. The most frequent symptoms are high fever, asthenia, myalgia, urticaria, and a nonproductive cough. Most patients recover spontaneously after 2–10 weeks, although some develop more severe and persistent disease, with weight loss, diarrhea, diffuse abdominal pain, hepatomegaly, dyspnea, and generalized skin rash. About half of the cases have eosinophilia. Eosinophilia usually appears late, 21 days after fever and up to 47 days (range 25–119) after contact, so its absence does not exclude the diagnosis of acute schistosomiasis and requires repeat laboratory tests in 2–3 weeks.  Classification of acute forms of schistosomiasis: Types of Clinical Manifestations Presentations Local inflammation of the cercariae entry zone, most frequently caused by Swimmer’s itch non-human pathogenic species that cannot migrate Cercarial Maculopapular skin rash. It develops in previously sensitized people when dermatitis they are reinfected by non-human pathogenic species Delayed systemic hypersensitivity reaction (3 and 8 weeks after exposure) It affects more than 50% of infected people. Fever, arthralgia, and cutaneous Katayama vasculitis and eosinophilia are the most common clinical manifestations. syndrome Spontaneous resolution after 2 to 10 weeks A minority develop persistent disease (weight loss, dyspnea and diarrhea, abdominal pain, hepatosplenomegaly) Pulmonary symptoms resulting from the systemic immunoallergic reaction of acute schistosomiasis in non-immune patients. It presents as dyspnea, Pulmonary form bronchospasm, productive cough, hemoptysis, and/or chest pain, which may appear in isolation or within the clinical picture of Katayama fever 2. Chronic Schistosomiasis: Chronic schistosomiasis occurs mainly as a result of granulomatous inflammation induced by the accumulation of eggs released by the parasite in the different tissues, given their ability to produce inflammation and fibrosis. The eggs reach the different tissues after being transported through the portal venous system and embolizing in the liver or spleen or, in the case of passing to the systemic circulation, the lungs, the brain or the spinal cord. 1. Intestinal Schistosomiasis is a very frequent chronic complication that has been described in cases for more than 20 years and is caused by infection with S. mansoni, S. japonicum, S. intercalatum, S. mekongi, and occasionally, S. haematobium. Its severity is related to recurrent exposure and the number of parasite eggs present in the mucosa of the intestinal tract, mainly the colon and rectum, where they cause an inflammatory reaction and the appearance of granulomas, ulcers, and fibrosis. The most common symptoms are nonspecific and include chronic or intermittent abdominal pain, asthenia, weight loss, anorexia, and diarrhea. In severe cases, it may be accompanied by anemia, secondary to bleeding from ulcerations in the colon and rectum (which can mimic chronic colitis of other etiologies, particularly inflammatory bowel disease). Additionally, patients have a higher incidence of colorectal polyps, mainly rectal polyps and granulomatous inflammation can  degenerate into polyps, which is the most common intestinal lesion in chronic intestinal schistosomiasis and even triggers the appearance of dysplasia; however, these polyps were all discovered during colonoscopy and presented as large polyps rather than cecal thickening. 2. Hepatosplenic Schistosomiasis Hepatosplenic schistosomiasis is a heterogeneous condition, ranging from a mildly symptomatic to life-threatening disease. The most common presentation of hepatosplenic schistosomiasis was upper gastrointestinal bleeding leading to severe anemia. An association of HBV or HCV coinfection with severe schistosomiasis has been documented in several studies, and coinfection with hepatitis viruses may accelerate the development of periportal fibrosis and related complications. 3. Urogenital Schistosomiasis The species most frequently implicated at this level is S. haematobium. This is because S. haematobium, unlike other human-infecting schistosome species, mainly migrates to the veins surrounding the bladder (the vesicle venous plexus), thus causing urinary schistosomiasis. The initial lesions are mucosal granulomas that coalesce to form tubercles, nodules or masses that usually ulcerate along the entire urinary tract. The surrounding mucosa is hyperemic. The submucosa and muscle layers are also involved in the inflammatory process, which may lead to transient back pressure if the ureterovesical junctions are affected. Involvement of the submucosa may lead to contraction of the bladder capacity. As they heal with excessive fibrosis, they may lead to strictures, calcifications and urodynamic abnormalities. The characteristic clinical presentation is terminal hematuria, usually associated with an increased frequency of micturition and dysuria, although it can also manifest as pyuria or hematospermia, the latter a common symptom in men. In endemic areas, hematuria is the red flag of schistosomiasis in children aged 5 to 10 years. In the long term, they can cause chronic cystitis and ureterohydronephrosis, as well as papillomas and cancer.  Involvement includes any organ of the genital tract. Female genital schistosomiasis (FGS) is recognized as a common complication of S. haematobium parasitism, occurring in approximately half (33 to 75%) of infected females. 4. Pulmonary Schistosomiasis Chronic Schistosoma infection can induce pulmonary arterial hypertension, a potentially fatal complication. It is assumed that the development of pulmonary hypertension requires hepatosplenic schistosomiasis, which allows portal shunting and egg embolization. The eggs can lodge in pulmonary arterioles and produce pulmonary hypertension and cor-pulmonale. S. mansoni and S. japonicum are more frequently associated with the development of pulmonary hypertension, particularly S. mansoni. This form of chronic pulmonary disease causes dyspnea and cor pulmonale and may result in heart failure. Radiological changes are nonspecific and can include ill-defined nodular, ground glass, or consolidative changes due to migratory parasites or egg deposition with focal granulomatous change. 5. Neuroschistosomiasis: Neuroschistosomiasis can affect any region of the central nervous system (CNS), especially in the spinal cord and brain, and is seen in less than 5% of infected patients. For this to occur, the migration of adult larvae to the CNS and the deposition of eggs are necessary to initiate the chronic granulomatous inflammatory reaction. The manner in which the eggs reach the CNS may be through retrograde venous flow in the Batson vertebral epidural venous plexus or after embolization from portosystemic shunts or from left heart cavities. In addition, adult worms may migrate to settle in sites close to the CNS. The onset of neurological symptoms usually takes place within weeks after infection and progresses in an acute or subacute manner, with the symptoms and signs of the disease progressively worsening. Approximately 90% of patients develop a full neurological picture within 2 months. In cerebral schistosomiasis, the symptoms are caused by granulomatous lesions; by the deposition of eggs, accompanied by edema and mass effects distributed  throughout the cerebral hemispheres; and by vasculitis and thrombosis-type lesions that may be induced by eosinophil toxicity. Depending on the location, it will give a wide variety of symptoms. Diagnosis of schistosomiasis: 1. Identification of eggs in stool or urine: Microscopic identification of eggs in stool or urine is the most practical method for diagnosis. Stool examination should be performed when infection with S. mansoni or S. japonicum is suspected, and urine examination should be performed if S. haematobium is suspected. Eggs can be present in the stool in infections with all Schistosoma species. The examination can be performed on a simple smear (1 to 2 mg of fecal material). Because eggs may be passed intermittently or in small numbers, their detection is enhanced by repeated examinations or concentration procedures, or both. In addition, for field surveys and investigational purposes, the egg output can be quantified by using the Kato-Katz technique (20 to 50 mg of fecal material) or the Ritchie technique. 2. Antibody detection: Can be useful to indicate schistosome infection in people who have traveled to areas where schistosomiasis is common and in whom eggs cannot be demonstrated in fecal or urine specimens. Test sensitivity and specificity vary widely among the many tests reported for the serologic diagnosis of schistosomiasis and are dependent on both the type of antigen preparations used (crude, purified, adult worm, egg, cercarial) and the test procedure. 3. Molecular diagnostics: Polymerase chain reaction (PCR) based testing is accurate and rapid. However, it is not frequently used in countries where the disease is common due to the cost of the equipment and the technical expertise required to run the tests. 4. Laboratory testing: S. haematobium screening in the community can be done by using urine dipstick to check for hematuria, and the stool guaiac test can be used to test for blood in the stool for potential S. mansoni and S. japonicum infection. For travelers or migrants in endemic regions, complete blood count with differential can be used to identify a high level of eosinophil in the blood, which could be indicative of an acute infection. Liver function test can be ordered if hepatosplenic schistosomiasis is suspected, and a subsequent hepatitis test panel can be ordered if liver function test is abnormal. 5. Tissue biopsy: If other diagnostic methods of schistosomiasis have failed to detect the infection, but there is still a high suspicion for schistosomiasis, tissue biopsy from the rectum, bladder, and liver can be obtained to look for schistosome eggs within the tissue samples. 6. Imaging: Imaging modalities such as X-rays, ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) can be utilized to evaluate for severity of schistosomiasis and damages of the infected organs. Treatment of schistosomiasis: Schistosomiasis eradication attempts commonly concentrate on controlling the infection through preventive chemotherapy. Praziquantel is cost-effective for treating schistosomiasis. The World Health Organization recommends a single dose of 40 mg/kg for all species and ages. However, this recommendation has a limitation: praziquantel does not kill immature worms present in the body at the time of treatment. Thus, treatment needs to be repeated after 2 to 4 weeks to increase effectiveness. This disease continues to be among the most alarming diseases in humans.