This VAP presentation is about the TORCH infections. The objections for this topic are to you name the TORCH infections and know general characteristics of the pathogens, compare and contrast the clinical manifestations of the TORCH infections, identify women at high risk for intrapartum transmission of a TORCH pathogen, and list any available methods of prevention against TORCH transmission. TORCH is an acronym for five infections that can be transmitted transplacentally– Toxoplasmosis, “o” for Other or syphilis, Rubella, Cytomegalovirus, and Herpes simplex virus. Toxoplasmosis is a parasite that exists in three lifeforms– the tachyzoite, which replicates intracellularly, the bradyzoite, which forms cysts, and the spirozoite that is environmentally resistant. The parasite is transmitted in raw or undercooked meat and in cat feces. While the risk of infection is greater beyond 20 weeks gestation, the severity of infection is greater in early pregnancy. Symptoms in infected women include fever, fatigue, muscle pain, maculopapular rash, and posterior cervical lymphadenopathy. However, symptoms only present in a minority of cases. Most infants are also asymptomatic at birth. However, 55% to 85% develop sequelae, including the classic triad of chorioretinitis, hydrocephalus, and intracranial calcifications. Sequelae include decreased birth weight, hepatosplenomagly, jaundice, anemia, and learning disabilities. Maternal infection is diagnosed serologically by measuring IgM and IgG. IgM appears by day 10 after infection and is usually absent by three to four months. In the United States, there is not routine screening of pregnant women. In endemic areas such as France, there are routine screening programs in place. There is no vaccine available for prevention, so the only preventive strategies are lifestyle based such as thoroughly cooking meat and not cleaning the litter box while pregnant. Treatment include spiramycin, pirymethamine, and sulfadiazine. Syphilis is caused by the spirochete Treponema pallidum. Unlike other TORCH infections, most infected infants are symptomatic at the time of birth. And the symptoms manifest as hepatic abnormalities leading to anemia thrombocytopenia, then ascites and hydrops, and possibly intrauterine fetal demise. In pregnant women, there are different phases of presentation. Primary infection presents with a chancre and non-suppurative lymphadenopathy. Secondary syphilis presents with diffuse macular rash, which may involve the palms and soles, petechia, alopecia, condylomata lata, lymphadenopathy, pneumonia, and myocarditis. The third stage is the latent phase. Diagnosis involves direct visualization of the spirochete using darkfield microscopy and serologic testing for antitreponemal antibodies using the VRDL or RPR tests. Fetal infection is suspected with certain ultrasound findings, including a hydrops, ascites, or placental thickening. However, infected fetuses often have normal ultrasounds. Routine screening is recommended in each trimester. Syphilis is transmitted sexually, so the most effective prevention method is barrier contraception. It can be treated in both pregnant and non-pregnant women with IV penicillin G. Penicillin desensitization is recommended in penicillin allergic pregnant women to ensure adequate treatment of the fetus. Rubella, or German measles, is an enveloped single-stranded RNA togavirus. 50% of infections in adults are subclinical. But if there are symptoms, they are usually mild and flu-like with a maculopapular rash that starts on the face and spreads to the trunk and extremities. 80% of pregnant women infected in the first trimester who develop the rash will transmit the virus to their fetus. In infected infants, there’s the classical congenital rubella syndrome, which includes multi-organ manifestations. Opthalmic manifestations include cataracts, congenital glaucoma, and pigmentary retinopathy. Cardiac manifestations include patent ductus arteriosus and pulmonary artery stenosis. Neurologic manifestations include sensorineural deafness, as well as microcephaly and mental retardation. Hepatic manifestations include neonatal purpura, hepatosplenomegaly, and jaundice. And finally, orthopedic manifestations include radiolucent bone disease. There is also an extended rubella syndrome which manifests later in life involving a progressive panencephalopathy and Type 1 diabetes. Maternal rubella infection is diagnosed seriologically. Rubella specific IgM can be detected by ELISA four to five days after onset of rash. While IgG peaks one to two weeks after rash onset. Routine screening is recommended in the first trimester. Rubella infection of the fetus is suspected with particular ultrasound findings, including intracranial calcifications, ventriculomegaly, microcephaly, cardiac malformations, and meconium peritonitis. Rubella can be prevented through vaccination, although it is a live attenuated virus. So it should not be given within one month before or during pregnancy. In the United States, foreign-born pregnant women are at higher risk due to lower vaccination rates. CMV, a member of the herpesvirus family and a double-stranded DNA virus, is the most common congenital infection in the developed world, infecting between a 0.2% and 2% of all neonates. Approximately 15% of pregnant women with primary CMV infection will have mononucleosis-like symptoms. It is a lifelong infection with periods of relative latency in reactivation. When women experience primary infection in pregnancy, the transmission rate is approximately 40%, while the transmission rate and recurrent infection is only a 0.15% to 1%. The risk of transmission is greatest in the third trimester. 10% of infected infants are symptomatic at birth. 50% of symptomatic infants present with cytomegalic inclusion disease. CMV Inclusion disease includes a hepatosplenomegaly, petechial rash, thrombocytopenic purpura, and multi-organ involvement. Late onset sequelae include hearing loss, chorioretinities, and learning disabilities. CMV is the leading cause of congenital hearing loss. Maternal CMV infection is diagnosed seriologically. IgM is formed in primary, recurrent, and re-activated infection. However, IgM is only detected in 75% to 90% of women with acute infection. IgG avidity has been used to improve on the sensitivity of serologic testing, as the ability of an IgG response changes from low to high over a period of weeks to months. The gold standard, however, for diagnosing congenital infection is CMV nucleic acid amplification from amniotic fluid. Ultrasound findings include calcifications of lateral ventricles, ventriculomegaly, hydrops, abdominal and liver calcifications, an echogenic bowel. Largely due to flaws in diagnosing primary infection, routine screening is not recommended. Women from higher socioeconomic status are actually at a higher risk of primary infection because fewer of them are seropositive the general population. There is no currently approved vaccine against CMV. There is also no established treatment in pregnancy, though hyperimmunoglobulin shows some promise. The anti-viral gancyclovir has also been given to infected neonates with some success. HSV is also a member of the herpesvirus family. The transmission rate in maternal primary HSV infection is 30% to 50%, while there is a less than 1% transmission rate with recurrent HSV. Primary infection is symptomatic about one third of the time manifested by itchy or tingling papules that become vasicular and painful. Women may experience flu-like symptoms and other complications, such as hepatitis, encephalitis, or pneumonia. Symptoms are isolated to the eye or mouth in about one third of infected infants, while more serious presentation with CNS disease occurs in another third of cases. Disseminated disease with involvement of multiple organ systems occurs in about 25% of cases with a mortality rate of almost 30%. Diagnosis is accomplished by serology, PCR, or the gold standard cell culture of an active lesion. In part due to the prevalence of HSV, routine screening is not recommended. There is no vaccine, and prevention is centered around safe sexual practices, including barrier contraception. HSV can be treated and/or suppressed with acyclovir or valacyclovir. This summary table shows a comparison between each of the TORCH pathogens, their characteristic neonatal manifestations, and screening recommendations.