Th1 helper cell response is prominent releasing cytokines such as IFN-γ during the early phases of infection, and it transitions to Th2 response leading to increase in level of IgE, IL-4, and eosinophils as egg production progresses. In chronic infections, the Th2 response shifts to increasing the level of IL-10, IL-13, and IgG4, which reverses the progression of the granulomas and lead to collagen deposition at the sites of the granulomas. The specific clinical symptoms and severity of the disease this causes depends on the type of schistosome infection, duration of infection, number of eggs, and the organ at which the eggs are deposited. The amount of eggs entrapped in the tissues will continue to increase if the schistosoma are not eliminated. Diagnosis
Identification of eggs in stools
Diagnosis of infection is confirmed by the identification of eggs in stools. Eggs of S. mansoni are about 140 by 60 µm in size and have a lateral spine. The diagnosis is improved through the use of the Kato-Katz technique, a semiquantitative stool examination technique. Other methods that can be used are enzyme-linked immunosorbent assay, circumoval precipitation test, and alkaline phosphatase immunoassay.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 condition was first described between 1888 and 1891. Signs and symptoms
The condition is typically seen in premature infants, and the timing of its onset is generally inversely proportional to the gestational age of the baby at birth (i.e., the earlier a baby is born, the later signs of NEC are typically seen).Initial symptoms include feeding intolerance and failure to thrive, increased gastric residuals, abdominal distension, and bloody stools. Symptoms may progress rapidly to abdominal discoloration with intestinal perforation and peritonitis and systemic hypotension requiring intensive medical support. Cause
The exact cause is unclear. Several risk factors have been implicated:

Maternal factors
Acid-suppressing medications
Chorioamnionitis
Cocaine abuse
In utero growth restriction
Increased body mass index
Intrahepatic cholestasis during pregnancy
Lack of prenatal steroids
Mode of delivery
Placental abruption
Pre-eclampsia
Smoking

Main risk factors
Low birth weight
Prematurity
Formula feeding (bovine based)
Intestinal dysbiosis

Other risk factors
Acute hypoxia
Antibiotic exposure
Blood transfusions
Cardiac anomalies
Neonatal anemia
Poor intestinal perfusion
Prolonged use of indomethacin for patent  ductus arteriosus closure

Diagnosis
Diagnosis is usually suspected clinically, but often requires the aid of diagnostic imaging, most commonly radiography, which can show the intestines and may show areas with death tissue or a bowel perforation.