TORCH is an acronym that denotes a chronic nonbacterial perinatal infection. It stands for toxoplasmosis; other infections; rubella virus; cytomegalovirus (CMV); and herpes simplex virus (HSV). "Other" infections include syphilis, hepatitis B, coxsackievirus, Epstein-Barr, varicella-zoster virus (VZV), and human parvovirus B-19. Herpetic disease in the neonate does not fit the pattern of chronic intrauterine infection but is traditionally grouped with the others. This group of infections may present in the neonate with similar clinical and laboratory findings (ie, small for gestational age, hepatosplenomegaly, rash, central nervous system [CNS] manifestations, early jaundice, and low platelets), hence the usefulness of the TORCH concept. Isolation precautions for all infectious diseases, including maternal and neonatal precautions, breast-feeding, and visiting issues, can be found in Appendix F.
Definition. Toxoplasmosis is caused by Toxoplasma gondii, an intracellular parasitic protozoan capable of causing intrauterine infection.
Incidence. The incidence of congenital infection is 1–10 per 10,000 live births. An estimated number of 400–4000 cases of congenital toxoplasmosis occur each year in the United States. Serologic surveys demonstrate that worldwide exposure to T. gondii is high (30% in the United States and 50–80% in Europe).
Pathophysiology.T. gondii is a coccidian parasite ubiquitous in nature. The primary natural host is the cat family. The organism exists in three forms: oocyst, tachyzoite, and tissue cyst (bradyzoites). Cats generally acquire the infection by feeding on infected animals such as mice or uncooked household meats. The parasite replicates sexually in the feline intestine. Cats may begin to excrete oocysts in their stool for 7–14 days after infection. After excretion, oocysts require a maturation phase (sporulation) of 24–48 h before they become infective by oral route. Intermediate hosts (sheep, cattle, and pigs) can have tissue cysts within organs and skeletal muscle. These cysts can remain viable for the lifetime of the host. The pregnant woman usually becomes infected by consumption of raw or undercooked meat that contains cysts or by the accidental ingestion of sporulated oocysts from soil or contaminated food. Ingestion of oocysts and cysts is followed by penetration of gastrointestinal mucosa by sporozoites and circulation of tachyzoites, the ovoid unicellular organism characteristic of acute infections. There are reports of transmission of toxoplasmosis through contaminated municipal water, blood transfusion, organ donation, and occasionally as a result of a laboratory accident. Actual transmission to the fetus is by the transplacental-fetal hematogenous route. In the chronic form of the disease, organisms invade certain body tissues, especially those of the brain, eye, and striated muscle, forming bradyzoites.
Acute infection in the adult is often subclinical (90% of the cases). If symptoms are present, they are generally nonspecific: mononucleosis-like illness with fever, painless lymphadenopathy, fatigue, malaise, myalgia, fever, skin rash, and splenomegaly. The vast majority of congenital toxoplasmosis cases are a result of acquired maternal primary infection during pregnancy; however, toxoplasmic reactivations can occur in immunosuppressed pregnant women and result in fetal infection. About 84% of women of childbearing age in the United States ...
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