These conditions decrease the blood flow to vital organs such as the placenta which supplies blood, oxygen, and nutrients to the developing fetus. Decreased blood flow to the fetus causes impaired urine production which leads to reduced amniotic fluid and oligohydramnios. Medications such as angiotensin converting enzyme inhibitors (lisinopril), prostaglandin synthetase inhibitors (NSAIDs, anti-inflammatory steroids), and trastuzumab decrease blood flow to the kidneys of the fetus. When the fetal kidneys are not able to produce adequate amounts of urine, this leads to reduced amniotic fluid or oligohydramnios. Maternal dehydration, especially in the hotter summer months
Infections such as the TORCH infections (toxoplasma gondii, rubella, cytomegalovirus, herpes simplex virus) and parvovirus B19

Fetal
Chromosomal abnormalities such as Down syndrome which are associated with gastrointestinal abnormalities
Congenital abnormalities such as renal agenesis and cystic renal disease are associated with impaired urine production, and posterior urethral valves or urethral atresia which are associated with obstruction of the lower urinary tract
Intrauterine demise
Post-term pregnancy
Rupture of membranes
Intrauterine growth restriction (IUGR) associated with placental insufficiency
Amnion nodosum; failure of secretion by the cells of the amnion covering the placenta

Placental
Placental abruption
Twin-twin transfusion
Placental thrombosis or infarction

Diagnosis
Clinical Manifestation
The volume of amniotic fluid typically increases until 36 weeks and starts decreasing after 40 weeks in post-term gestations. For this reason, discrepancies between fundal height measurements and gestational age can be a clinical indication of amniotic fluid abnormality and should be evaluated by ultrasound. Other common clinical presentations include fetal malpresentation, undue prominence of fetal parts, premature rupture of membranes, and reduced amount of amniotic fluid.
In these individuals, granulomas do not form, and the affected person develops Th2 and Th9 responses, resulting in activation of B lymphocytes, high levels of circulating antibodies, eosinophilia, and hypergammaglobulinemia.Lung involvement subsequently occurs after a dormant phase, manifesting in upper respiratory tract symptoms, and lung infiltrates on imaging. The commonest, chronic form, is almost certainly a reactivation of the disease, and may develop into progressive scarring of the lungs (pulmonary fibrosis).It can cause disease in those with normal immune function, although immunosuppression increases the aggressiveness of the fungus. It rarely causes disease in fertile-age women, probably due to a protective effect of estradiol. Diagnosis
More than 90% of cases can be diagnoses with direct histological examination of tissue, such as sputum, bronchial lavage fluid, exudates and biopsies. Histopathological study with Gomori methenamine silver (GMS) stain or hematoxylin and eosin (H&E) stain revealing large yeast cells with translucent cell walls with multiple buds.In the juvenile form, lung abnormalities are shown in high-resolution CT scans of the lungs, whereas in the chronic form plain X-rays may show interstitial and alveolar infiltrates in the central and lower lung fields.Culture of P. brasiliensis takes between 20 and 30 days, requiring multiple samples and culture media. Initial culture can occur at room temperature, however after growth is noted, confirmation occurs by incubating at to 36-37 degrees to transform the fungus into yeast cells.Antibody detection is useful both for acute diagnosis and monitoring. Gel immunodiffusion is commonly used in endemic areas, diagnoses 95% of cases with high specificity.