maculopapular rash (flat and raised lesions) at the sites of cercarial penetration. Skin blisters on the forearm, created by the entrance of Schistosoma parasites Many individuals do not experience symptoms. If symptoms do appear, they usually take 4–6 weeks from the time of infection. The first symptom of the disease may be a general feeling of illness. Within 12 hours of infection, an individual may complain of a tingling sensation or light rash, commonly referred to as "swimmer's itch", due to irritation at the point of entrance. The rash that may develop can mimic scabies and other types of rashes. Other symptoms can occur 2–10 weeks later and can include fever, aching, a cough, diarrhea, chills, or gland enlargement. These symptoms can also be related to avian<unk> , which does not cause any further symptoms in humans. The manifestations of schistosomal infection vary over time as the cercariae, and later adult worms and their eggs, migrate through the body. If eggs migrate to the brain or spinal cord, seizures, paralysis, or spinal-cord inflammation are possible. Acute Infection Manifestation of acute infection from schistosoma include cercarial dermatitis (hours to days) and acute<unk>  (2-8 weeks). Cercarial dermatitis The first potential reaction is an itchy, maculopapular rash that results from cercariae penetrating the skin within the first 12 hours to days of cercarial skin penetration. The first time a non-sensitized person is exposed, the rashes are usually mild with an associated prickling sensation that quickly disappear on its own since this is a type of hypersensitivity reaction. In sensitized people who have previously been infected, the rash can develop into itchy, red, raised lesions (papules) with some turning into fluid-filled lesions (vesicles). Previous infections with cercariae causes a faster developing and worse presentation of dermatitis due to the stronger immune response. The round bumps are usually one to three centimeters across. Because people living in affected areas have often been repeatedly exposed, acute reactions are more common in tourists and migrants. The rash can occur between the first few hours and a week after exposure, and they normally resolve on their own in around 7–10 days. For human<unk> , A similar type of dermatitis called "swimmer's itch" can also be caused by cercariae from animal trematodes that often infect birds. Cercarial dermatitis is not contagious and can not be transmitted from person-to-person. Symptoms may include: * Flat, red rash * Small red, raised pimples * Small red blisters * Prickling or tingling sensation, burning, itching of the skin Scratching the rash can lead to secondary bacterial infection of the skin, thus it is important to refrain from scratching. Some common treatments for itching include corticosteroid cream, anti-itch lotion, application of cool compresses to rash, bathing in Epsom salts or baking soda, and in severe itching cases, prescription strength cream and lotions. Oral antihistamines can also help relieve the itching. Acute<unk>  (Katayama fever) Acute<unk>  (Katayama fever) may occur weeks or months (around 2–8 weeks) after the initial infection as a systemic reaction against migrating schistosomulae as they pass through the bloodstream through the lungs to the liver and also against the antigens of eggs. Similarly to swimmer's itch, Katayama fever is more commonly seen in people with their first infection such as migrants and tourists, and it is associated with heavy infection. It is seen, however, in native residents of China infected with S. japonicum. S. japonicum can cause acute<unk>  in chronically infected population, and it can lead to a more severe form of acute<unk> . Symptoms may include: * Dry cough with changes on chest X-ray * Fever * Fatigue * Muscle aches *Headache * Malaise * Abdominal pain *Diarrhea * Enlargement of both the liver and the spleen *Hives Acute<unk>  usually self-resolves in 2–8 weeks in most cases., but a small proportion of people have persistent weight loss, diarrhea, diffuse abdominal pain, and rash. Complications may include: * Spinal cord inflammation (transverse myelitis) may occur if worms or eggs travel to the spinal cord during this acute phase of infection. Treatment may include: * Corticosteroid such as prednisone is used to alleviate the hypersensitivity reaction and reduce inflammation * Praziquantel can be administered to kill the adult schistosomes to prevent chronic infection in addition to corticosteroid therapy. Praziquantel is not effective to recent infection as it only targets the adult worms, but not the premature schistosomulae. Therefore, a repeat treatment of Praziquantel several weeks after initial infection may be warranted. It is recommended to treat with Praziquantel 4–6 weeks after initial exposure since it targets adult worms. Chronic Infection In long-established disease, adult worms lay eggs that can cause inflammatory reactions. The eggs secrete proteolytic enzymes that help them migrate to the bladder and intestines to be shed. The enzymes also cause an eosinophilic inflammatory reaction when eggs get trapped in tissues or embolize to the liver, spleen, lungs, or brain. The long-term manifestations are dependent on the species of schistosome, as the adult worms of different species migrate to different areas. Many infections are mildly symptomatic, with anemia and malnutrition being common in endemic areas. Intestinal<unk>  The worms of S. mansoni and S. japonicum migrate to the veins of the gastrointestinal tract and liver. Eggs in the gut wall can lead to pain, blood in the stool, and diarrhea (especially in children). Severe disease can lead to narrowing of the colon or rectum. In intestinal<unk> , eggs become lodged in the intestinal wall during their migration from the mesenteric venules to the intestinal lumen, and the trapped eggs cause an immune system reaction called a granulomatous reaction. They mostly affect the large bowel and rectum, and involvement of the small bowel is more rare. This immune response can lead to obstruction of the colon and blood loss. The infected individual may have what appears to be a potbelly. There is a strong correlation between morbidity of intestinal<unk>  and the intensities of infection. In cases of light infections, symptoms may be mild and can go unrecognized. The most common species to cause intestinal<unk>  are S. mansoni and S. japonicum, however, S. mekongi and S. intercalatum can also cause this disease. Symptoms may include: * Abdominal pain and discomfort * Loss of appetite * Mucous diarrhea with or without gross blood * Blood in feces that is not visibly present (fecal occult blood) * Abdominal distention Complications may include: * Intestinal polyps * Intestinal ulcers *Iron deficient anemia * Fistula * Bowel strictures (narrowing of colon or rectum) * Protein-losing enteropathy * Partial or complete bowel obstruction * Appendicitis (rare) Approximately 10-50% of people living in endemic regions of S. mansoni and S. japonicum develop intestinal<unk> . S. mansoni infection epidemiologically overlaps with high HIV prevalence in Sub-Saharan Africa, where gastrointestinal<unk>  has been linked to increased HIV transmission. Hepatosplenic<unk>  Eggs also migrate to the liver leading to fibrosis in 4 to 8% of people with chronic infection, mainly those with long-term heavy infection. Eggs can become lodged in the liver, leading to portal hypertension, splenomegaly, the buildup of fluid in the abdomen, and potentially life-threatening dilations or swollen areas in the esophagus or gastrointestinal tract that can tear and bleed profusely (esophageal varices). This condition can be separated into two distinct phases: inflammatory hepatic<unk>  (early inflammatory reaction) and chronic hepatic<unk> . Most common species to cause this condition are S. mansoni, S. japonicum, and S. mekongi. Inflammatory hepatic<unk>  * This condition occurs mainly in children and adolescents due to early immune reaction to eggs trapped within the periportal and presinusoidal spaces of the liver creating numerous granulomas. Liver function is not affected, and the severity of liver and spleen enlargement is correlated to the intensity of the infection. It is characterized by an enlarged left lobe of the liver with a sharp edge and enlarged spleen with nodules. The enlargement of liver and spleen is usually mild, but in severe cases, they can enlarge to the level of the belly button and even into the pelvis. Caput medusae can occur as a result of the portal hypertension caused by periportal fibrosis Chronic (fibrotic) hepatic<unk>  * This is a late stage liver disease that occurs mainly in young and middle-aged adults who have been chronically infected with a heavy infection and whose immune regulation of fibrosis is not functioning properly. It affects only a small proportion of people who are infected. Liver function and liver architecture are not affected unlike cirrhosis. The pathogenesis of this disease is caused by deposition of collagen and extracellular matrix proteins within the periportal space, which leads to liver portal fibrosis and enlarged fibrotic portal tracts (Symmer's pipe stem fibrosis). The periportal fibrosis physically compress the portal vein leading to portal hypertension (increased portal venous pressure), increased pressure of the splenic vein, and subsequent enlargement of the spleen. Portal hypertension can also increase the pressure in portosystemic anastomoses (vessel connections between the portal circulation and systemic circulation) leading to esophageal varices and caput medusae. These portosystemic
Schistosomiasis
Toxocariasis
Trypanosomiasis
Filariasis
Cyclosporiasis
Cryptosporidiosis
Tylosis
Acariasis