Chorioamnionitis, also known as intra-amniotic infection (IAI), is inflammation of the fetal membranes (amnion and chorion), usually due to bacterial infection. In 2015, a National Institute of Child Health and Human Development Workshop expert panel recommended use of the term "triple I" to address the heterogeneity of this disorder. The term triple I refers to intrauterine infection or inflammation or both and is defined by strict diagnostic criteria, but this terminology has not been commonly adopted although the criteria are used.Chorioamnionitis results from an infection caused by bacteria ascending from the vagina into the uterus and is associated with premature or prolonged labor. It triggers an inflammatory response to release various inflammatory signaling molecules, leading to increased prostaglandin and metalloproteinase release. These substances promote uterine contractions and cervical ripening, causations of premature birth. The risk of developing chorioamnionitis increases with number of vaginal examinations performed in the final month of pregnancy, including labor. Tobacco and alcohol use also puts mothers at risk for chorioamnionitis development.Chorioamnionitis is caught early by looking at signs and symptoms such as fever, abdominal pain, or abnormal vaginal excretion. Administration of antibiotics if the amniotic sac bursts prematurely can prevent chorioamnionitis occurrence. Signs and symptoms
The signs and symptoms of clinical chorioamnionitis include fever, leukocytosis (>15,000 cells/mm³), maternal (>100 bpm) or fetal (>160 bpm) tachycardia, uterine tenderness and preterm rupture of membranes. Causes
Causes of chorioamnionitis stem from bacterial infection as well as obstetric and other related factors. Microorganisms
Bacterial, viral, and even fungal infections can cause chorioamnionitis.
These patients are under the risk of severe hyperammonemia during infections that can lead to comatose states.Liver transplant is gaining a role in the management of these patients, with small series showing improved quality of life. Epidemiology
Propionic acidemia is inherited in an autosomal recessive pattern and is found in about 1 in 35,000 live births in the United States. The condition appears to be more common in Saudi Arabia, with a frequency of about 1 in 3,000. The condition also appears to be common in Amish, Mennonite and other populations with higher frequency of consanguinuity. History
In 1957, a male child was born with poor mental development, repeated attacks of acidosis, and high levels of ketones and glycine in the blood. Upon dietary testing, Dr. Barton Childs discovered that his symptoms worsened when given the amino acids leucine, isoleucine, valine, methionine, and threonine. In 1961, the medical team at Johns Hopkins Hospital in Baltimore, Maryland published the case, calling the disorder ketotic hyperglycinemia. In 1969, using data from the original patients sister, scientists established that propionic acidemia was a recessive disorder, and that propionic acidemia and methylmalonic acidemia are caused by deficiencies in the same enzyme pathway. See also
Methylmalonic acidemia
Isovaleric acidemia
Maple syrup urine disease

References
External links
Propionic acidemia at NLM Genetics Home Reference
Propionic acidemia at NIHs Office of Rare Diseases
"Propionic acidemia". Orphanet.