Acute Schistosomiasis (Katayama fever)
Acute schistosomiasis (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 swimmers 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 schistosomiasis in chronically infected population, and it can lead to a more severe form of acute schistosomiasis.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
HivesAcute schistosomiasis 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.
The most common species to cause intestinal schistosomiasis 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 distentionComplications 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 schistosomiasis. S. mansoni infection epidemiologically overlaps with high HIV prevalence in Sub-Saharan Africa, where gastrointestinal schistosomiasis has been linked to increased HIV transmission. Hepatosplenic Schistosomiasis
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 schistosomiasis (early inflammatory reaction) and chronic hepatic schistosomiasis. Most common species to cause this condition are S. mansoni, S. japonicum, and S. mekongi. Inflammatory hepatic schistosomiasis

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.