AN OVERVIEW OF TORCH INFECTIONS THE TORCH COMPLEXTORCH complex is a medical acronym for a set ofperinatal infections (i.e. infections that are passed from apregnant woman to her fetus). The TORCH infections canlead to severe fetal anomalies or even fetal loss. They area group of viral, bacterial, and protozoan infections thatgain access to the fetal bloodstream transplacentally viathe chrionic villi. Hematogenous transmission may occurat any time during gestation or occasionally at the time ofdelivery via maternal-to-fetal transfusion.
The capitalization "TORCH” consists of :T – TOXOPLASMOSISO – Other infections (Syphilis, Varicella Zoster, Parvovirus B-19, Listerosis & Coxsackie Virus)R – RUBELLAC – CYTOMEGALOVIRUSH – HERPES SIMPLEX VIRUS – 2Hepatitis B may also be included among "other infections",but the hepatitis B virus is a large virus and does not crossthe placenta, hence it cannot infect the fetus unless therehave been breaks in the maternal-fetal barrier, such ascan occur in bleeding during childbirth or amniocentesis.
TOXOPLASMOSISToxoplasmosis is a disease caused by an intracellularparasite TOXOPLASMA GONDII.Human acquisition of the infection occurs by:•Oocyst contaminated soil, salads, vegetables.•Ingestion of raw or undercooked meat containing tissuecysts (Sheep, pigs and rabbits are the most commonmeat sources).•Outbreaks of toxoplasmosis have also been linked to theconsumption of unfiltered water.
•Sera from randomly selected 345 pregnant Nepalese womenaged 16-36 years and 13 women with bad obstetric history(BOH) were tested for the presence of Toxoplasma antibodiesusing microlatex agglutination (MLA) and ELISA methods.•The overall prevalence was 55.4% (191/345).•Prevalence was slightly higher (59.0%) in older age-group(27- 36 years) compared with younger age-group (16-26years) (52.2%).•In patients with an existing HIV infection, toxoplasmosis isan important oppurtunistic infection with considerablemorbidity and mortality especially in the pregnant women.
CLINICAL FEATURES :• In most immunocompetent individuals, includingchildren and pregnant women, the infection goesunnoticed.•In approximately 10% of the patients it causes a self-limiting illness, most commonly in the 25-35 years agegroup.•Painless lymphadenopathy (Local or Generalised) is themost common presenting feature. Cervical lymph nodesare involved in particular. The mesenteric, mediastinal orthe retroperitoneal nodes may also be involved.•Other features include – Malaise, Fever, Fatigue, Musclepain, Sore throat and headache.
• Complete resolution usually occurs within a few months,although symptoms and lymphadenopathy tend tofluctuate unpredictably and some patients do notrecover completely even for a year or more.•Sometimes the patient may also develop encephalitis,hepatitis, pneumonitis and myocarditis.•Retinochoroiditis is nearly always the result of congenitalinfection.
CONGENITAL TOXOPLASMOSIS•Acute toxoplasmosis, mostly subclinical, affects 0.3-1% ofpregnant women, with an approximately 60% transmissionrate to the fetus which increases with increasing gestation.•Primary maternal infection in pregnancy –Infection rate higher with infection in 3rd trimester.Fetal death higher with infection in 1st trimester.•Congenital disease affects approximately 40% ofinfected fetuses, and is more likely to be severe withinfection early in gestation.•Many fetal infections are also subclinical at birth but thelong-term sequelae include hydrocephalus, microcephalyand retinochoroiditis.
INVESTIGATIONS:• In the immunocompetent patient – Serology is oftendone while in the immunocompromised the diagnosisoften requires the direct detection of parasites.•SABIN-FELDMAN DYE TEST (Indirect Fluorescent AntibodyTest) – detects the IgG –Antibody.Recent infection is indicated by a four-fold increase in titrewhile peak titres of 1/1000 or more are reached within 2months of onset of infection.•The detection of Toxoplasma specific IgM-Antibody maybe useful in confirming acute infections. However, falsepositives or persistence of IgM-Antibodies for years afterinfection make interpretation difficult. Negative IgM-Antibody virtually rules out acute infection.
• During pregnancy it is highly critical to differentiatebetween recent and past infection - the presence of high-avidity IgG-Antibodies excludes infection acquired in thepreceding 3-4 months.•If necessary , the presence of Toxoplasma Organisms in alymph node biopsy can be sought for by staining sectionshistochemically with T. Gondii- Antiserum or by the use ofPCR to detect Toxoplasma-specific DNA.
TREATMENT:• In immunocompetent subjects, uncomplicatedtoxoplasmosis is self-limiting and responds poorly to anti-microbial therapy.•In PREGNANT WOMEN with an established recentinfection, SPIRAMYCIN (3g daily in divided doses) shouldbe given until term.• Once fetal infection is established, treatment withSULFADIAZINE AND PYRIMETHAMINE plus CALCIUMFOLINATE is recommended as SPIRAMYCIN does not crossthe placental barrier.
OTHER INFECTIONSVARICELLA ZOSTER• Varicella Zoster is a member of the herpes virus family.•Varicella also known as Chickenpox, is the acute primarydisease.•Incubation Period – 15 days and is communicable 2 daysbefore and 5 days after the onset of rash.•After an initial episode of infection with Varicella Zosterleading to Chickenpox , the virus may persist in a latentstate in the posterior root ganglia of the spinal cord foryear. Reactivation results in Herpes Zoster.
• It is highly contagious, self-limiting disease of childhoodthat is transmitted by respiratory droplets or close contact.•It is usually acquired by 90% of the population before thereproductive age, thus most women are immune beforethey become pregnant.•The incidence of Varicella in pregnancy is 0.7/1000.•CLINICAL FEATURES include vesicular eruptions often onmucosal surfaces first followed by a rapid dissemination ina centripetal pattern. New lesions appear every 2-4 daysand each crop is associated with fever. The rashprogresses from macules to vesicles and then to pustule in24 hours.
•Maternal varicella infection in the first 20 weeks ofpregnancy can cause VARICELLA EMBRYOPATHY alsocalled Congenital Varicella Syndrome in approximately1-2% of cases characterised by hallmark cicatricial lesionsin dermatomal pattern, limb hypoplasia, contractures andcan also involve the eye and central nervous system. Theprognosis is poor if an infant be infected.Diagnosis is byPrenatal Ultrasound and MRI may show Oligohydramnios,IUGR, hydrops, limb deformities and microcephaly.•However, the risk of congenital varicella syndrome isnegligible because antibodies in the maternal bloodprevent the virus from crossing the placenta and infectingthe fetus.•In 1994, Enders and colleagues showed no clinical evidence of infection in infants born to 366women with Varicella Zoster in pregnancy.
DIAGNOSIS : Is primarily clinical, by recognition of the rash. If necessary,it can be confirmed by detection of antigen (DirectImmunofluroscence), PCR or by VIRAL CULTURE of theaspirated Vesicular Fluid.TREATMENT :ACYCLOVIR (800mg 5 times daily at 4 hourly intervals for 7days) or ACYCLOVIR 5mg/kg 8 hourly IV until patient isimproving is a Class-C antiviral agent used in the treatmentof Varicella Zoster. Oral Acyclovir has been shown tosignificantly reduce symptoms, duration and intensity.•Many studies have showed the safety of Acyclovir use in pregnancy. In 1993,Center for Disease Control published data showing no risk of fetalabnormalities in patients exposed in the first trimester receiving Acyclovir.•The newer drugs like VALACYCLOVIR and FAMCYCLOVIR have a better bio-availabilityand a less frequent dosing than Acyclovir with similar efficacy.
PARVOVIRUS B-19 INFECTION :•Parvovirus B-19 virus is a small single stranded DNA virusand has a predilection for rapidly dividing cellsparticularly the erythroblasts. Many infections are sub-clinical.•Incubation Period – 14-21 days.•CLINICAL FEATURES : Prodromal Fever, CoryzalSymptoms, and a characteristic “Slapped-cheek rash”,Impaired Erythropoiesis causing mild anemia andpolyarthropathy.•Trans-placental fetal infection can occur during the firsttwo trimesters of pregnancy with an impact on the fetalbone marrow. It causes 10-15% of non-immune (Non-Rhesus related) HYDROPS FETALIS.
TREATMENT :•Infection is usually self-limiting.•Symptomatic relief from Arthritic symptoms may berequired by the use of analgesics.•Pregnant women should avoid contact with cases ofParvovirus-B19 infection.•If exposed, SEROLOGY should be done to establishwhether they are non-immune.•Passive prophylaxis with NORMAL IMMUNOGLOBIN hasbeen suggested .•The pregnancy should be monitored closely by USG, sothat Hydrops Fetalis can be treated by Fetal Transfusion.
SYPHILIS :• Syphilis is caused by infection, through abrasions in theskin or mucous membranes with the spirochaeteTREPONEMA PALLIDUM.•In adults the infection is usually sexually acquired,however transmission by kissing, blood transfusion andpercutaneous injury have also been reported.•Infection may remain latent throughout or clinicalfeatures may develop at any time.•All women should have syphilis serology carried out inthe first trimester of pregnancy or at the first antenatalvisit.•Women at a risk of acquiring syphilis should have afurther test in the 3rd trimester preferably at 28-30 weeks.
CONGENITAL SYPHILIS –• Congenital Syphilis is rare where antenatal serologicalscreening is practised.•Treponemal infection may give rise to a variety ofoutcomes after 4 months of gestation when the fetusbecomes immunocompetent:1. Miscarriage or Still-birth, Premature or at term.2. Birth of a syphilitic baby (very sick baby withhepatosplenomegaly, bullous rash and perhapspneumonia).3. Birth of a baby with latent infection who either remainswell or develops Congenital Syphilis later in life.
• Syphilis may be divided as Early or Latent Syphilis.•CLINICAL FEATURES :• Incubation period of Early Syphilis is usually 14-28 dayswith a wide range of 9-90 days.• The primary lesion or chancre develops at the site ofinfection usually on the genital area and may also developon the vaginal wall and the cervix.•After 6-8 weeks the treponemes disseminate to produce amulti-system disease. Constitutional features such as fever,malaise and headache are common. Over 75% patientspresent with a rash on the trunk and limbs that laterinvolves the palms and soles.•Generalised non-tender lymphadenopathy is present inover 50% patients.
•Often features such as meningitis, cranial nerve palsies,hepatitis, gastritis, glomerulonephritis and anterior/posterioruveitis are seen.INVESTIGATIONS : SEROLOGICAL TESTS FOR SYPHILIS Non-treponemal ( Non-specific) tests: •Veneral Diseases Research Laboratory ( VDRL ) Test •Rapid Plasma Reagin Test Treponemal (Specific) antibody tests: •Treponemal antigen-based enzyme immuno assay (EIA) for IgG and IgM •T. Pallidum haemagglutination assay (TPHA) •T. Pallidum Particle agglutination assay (TPPA) •Fluorescent treponemal antibody-absorbed (FTA- ABS) test
TREATMENT :•In early latent stage: single dose of 2.4 Million unitsBenzathine Penicillin G IMIn late latent stage: 3 doses of 2.4 million units of BenzathinePenicillin G IM is given. It is given once in a week.•ERYTHROMYCIN STEARATE can be given if there isPenicillin hypersensitivity, but it crosses the placentapoorly. The treatment of syphilis can be consideredadequate if it is completed by at least 30 days beforedelivery or there is a documentef 4-fold drop in RPR titre.
•The newborn baby must therefore be treatedwith a course of Penicillin and considerationgiven to re-treating the mother.•Success has also been achieved withCEFTRIAXONE 250mg IM for 10 days in manycases.All pregnant women testing positive for Syphilis should also be screened for HIV.
COXSACKIE VIRUS INFECTION :• The virus is a member of the Picornaviridae and have asingle-stranded RNA. It may cause clinically inapparentinfection in the mother but may prove fatal to the fetus orthe infant by increasing congenital malformations.•Infection is spread from person to person. The virus ispresent in secretions and body fluids of infected people.•Fetal death may be caused by viraemia resulting inHepatitis, Myocarditis and Encephalomyelitis due toplacentitis and clinical chorioamnionitis.•The virus may be grown from the amniotic fluid or theneonatal spinal fluid.PCR can detect 66-90% of theinfection.
CLINICAL FEATURES : Common Cold, Rash, diarrhoea,sore throat. Severe manifestations include meningitis,encephalitis, severe chest pain, myopericarditis.TREATMENT :•There is no specific medication known to kill theCoxsackie virus.•Fortunately, the body’s immune system is usually able todestroy the virus.•Some reports suggest that there might be a benefit to IVImmunoglobulin which is made from human serum andcontains antibodies.•Treatment for Myocarditis is supportive.
LISTEROSIS :• Recent surveys have shown that 4% of pregnant womenharbor LISTERIA MONOCYTOGENS, a Gram-positivebacteria in the cervix.•Trancplacental infections can occur from an infectedmother.•Such patients have Influenza like symptoms, prematuredelivery and dirty brown amniotic fluid, fever, myalgia,choriamnionitis and abortions.•Babies born to these mothers may get infectedtransplacentally or during delivery with a high morbidityand mortality due to Pyogenic Meningitis.
INVESTIGATIONS :• Diagnosis is made by Blood/CSF Culture, a positivefluoroscent antibody test and culture of stomach content,liquor .TREATMENT :•The most effective regimen consists of IV AMINOPENICILLIN(AMOXYCILLIN/AMPICILLIN) + AN AMINOGLYCOSIDE.•Patients allergic to Penicillin may be given a combinationof Sulfamethoxazole/Trimethoprim.• Dietary precaution : Pregnant women are advised toavoid high-risk products like undercooked chicken, fish, rawvegetables and soft cheese.
RUBELLA :•Rubella, commonly known as German measles, is adisease caused by the rubella virus a togavirus that isenveloped and has a single-stranded RNA genome.•This disease is often mild and attacks often passunnoticed. The disease can last one to three days.Children recover more quickly than adults.•Infection of the mother by Rubella virus during pregnancycan be serious; if the mother is infected within the first 20weeks of pregnancy, the child may be born withcongenital rubella syndrome (CRS), which entails a rangeof serious incurable illnesses. Spontaneous abortion occursin up to 20% of cases. The virus has teratogenic propertiesand is capable of crossing the placenta and infecting thefetus where it stops cells from developing or destroysthem.
•Acquired (i.e. not congenital) rubella is transmitted viaairborne droplet emission from the upper respiratory tractof active cases and replicates in the nasopharynx andlymph nodes.•The virus may also be present in the urine, Faeces and onthe skin. There is no carrier state: the reservoir exists entirelyin active human cases.•The disease has an incubation period of 2 to 3 weeks.•In most people the virus is rapidly eliminated. However, itmay persist for some months post partum in infantssurviving the CRS. These children are a significant source ofinfection to other infants and, more importantly, topregnant female contacts.
CLINICAL FEATURES :•German measles causes symptoms that are similar to theflu. The primary symptom of rubella virus infection is theappearance of a rash (exanthem) on the face whichspreads to the trunk and limbs and usually fades after threedays.•The facial rash usually clears as it spreads to other parts ofthe body. Other symptoms include low grade fever,swollen glands (sub occipital & posterior cervicallymphadenopathy), joint pains, headache andconjunctivitis.The swollen glands or lymph nodes canpersist for up to a week and the fever rarely rises above 38degrees centigrate . The rash disappears after a few dayswith no staining or peeling of the skin.•.
CONGENITAL RUBELLA SYNDROME•Congenital rubella syndrome (CRS) is characterized by: Intrauterine growth restriction Intracranial calcifications Microcephaly Cataracts Cardiac defects (most commonly patent ductus arteriosusor pulmonary arterial hypoplasia). Neurologic disease (with a broad range of presentations,from behavior disorders to meningoencephalitis)Osteitis and hepatosplenomegaly
•Most of these complications develop in infants born tomothers who acquire rubella infection during the first 16weeks of pregnancy.• 90% of infants present with some finding of congenitalrubella if infection occurs within the first 12 weeks, and 20%present with congenital disease if the infection occursbetween weeks 12 and 16.•Cataracts results when infection occurs between the thirdand eighth week of gestation, deafness between the 3rdand 18th week, and heart abnormalities between the 3rdand 10th week.
DIAGNOSIS :•Rubella virus specific IgM antibodies are present inpeople recently infected by Rubella virus but theseantibodies can persist for over a year and a positive testresult needs to be interpreted with caution.• The presence of these antibodies along with, or a shorttime after, the characteristic rash confirms the diagnosis.
TREATMENT :•Rubella infections are prevented by active immunisationprograms using live, disabled virus vaccines. Two liveattenuated virus vaccines, RA 27/3 and Cendehill strains,are effective in the prevention of adult disease.•The vaccine is now usually given as part of the MMRvaccine. The WHO recommends the first dose is given at 12to 18 months of age with a second dose at 36 months.Pregnant women are usually tested for immunity to rubellaearly on. Women found to be susceptible are notvaccinated until after the baby is born because thevaccine contains live virus.
•There is no specific treatment for Rubella; however,management is a matter of responding to symptoms todiminish discomfort.•Treatment of newly born babies is focused onmanagement of the complications.•Congenital heart and cataracts can be corrected bydirect surgery.•Management for ocular congenital rubella syndrome(CRS) is similar to that for age-related maculardegeneration, including counseling, regular monitoring,and the provision of low vision devices, if required.•Rubella infection of children and adults is usually mild, self-limiting and often asymptomatic. The prognosis in childrenborn with CRS is poor.
CYTOMEGALOVIRUS INFECTION :•CMV is a double-stranded DNA herpes virus andrepresents the most common congenital viral infection.•The CMV seropositivity rate increases with age.Geographic location, socioeconomic class, and workexposure are other factors that influence the risk ofinfection.•CMV infection requires intimate contact through saliva,urine, and/or other body fluids.•Possible routes of transmission include sexual contact,organ transplantation, transplacental transmission,transmission via breast milk, and blood transfusion (rare).
•Primary, reactivation, or recurrent CMV infection canoccur in pregnancy and can lead to congenital CMVinfection.•Transplacental infection can result in intrauterine growthrestriction, sensorineural hearing loss, intracranialcalcifications, microcephaly, hydrocephalus,hepatosplenomegaly, delayed psychomotordevelopment, thrombocytopenia and/or optic atrophy.•Vertical transmission of CMV can occur at any stage ofpregnancy; however, severe sequelae are more commonwith infection in the 1st trimester, while the overall risk ofinfection is greatest in the 3rd trimester.•The risk of transmission to the fetus in primary infection is30%-40%.
•The transmission rate to the fetus is between 30-50%according to the Organization of Teratology InformationService (OTIS).•Of those babies who become infected, only 10-15% showsigns of congenital CMV after primary maternal infection.• Congenital CMV affects about 0.2-2.5% of babiesworldwide.•Of these, only 1-10% of the babies born with the CMVinfection will have symptoms at birth and another 10-15%may not show any symptoms at birth, but still may havelong term affects such as hearing loss and learningdisabilities.
DIAGNOSIS & MANAGEMENT :•Serologic testing in women with suspectedCytomegalovirus (CMV)•Amniocentesis•Ultrasonography• Quantitative polymerase chain reaction (PCR) for viralDNA in amniotic fluid•Fetal magnetic resonance imaging (MRI) (consideredbut not recommended)•Intravenous treatment with CMV-hyperimmune globulin•Ganciclovir treatment.
HERPES SIMPLEX VIRUS -2 INFECTION :•Herpes simplex virus (HSV) infection is one of the mostcommon viral sexually transmitted diseases worldwide. Theprimary infection of the mother may lead to severe illnessin pregnancy and may be associated with virustransmission from mother to foetus/newborn.•Since the incidence of this sexually transmitted infectioncontinues to rise and because the greatest incidence ofherpes simplex virus infections occur in women ofreproductive age, the risk of maternal transmission of thevirus to the foetus or neonate has become a major healthconcern.
•A pregnant woman who acquires genital herpes as aprimary infection in the latter half of pregnancy, ratherthan prior to pregnancy, is at greatest risk of transmittingthese viruses to her newborn.•Additional risk factors for neonatal HSV infection includethe use of a foetal-scalp electrode and the age of themother < 21 years.• Herpes Simplex Virus-2 is a DNA virus that belongs toAlphaherpesvirinae family.• HSV-2 is most commonly found in the lumbosacralganglia.•The most important HSV infection during pregnancy is theprimary genital HSV infection.
•Primary HSV infections in pregnant women can result inmore severe diseases than that in non-pregnant ones.• In particular, gingivostomatitis and vulvovaginitisherpetica tend towards dissemination. As a result, womencan develop disseminated skin lesions associated withvisceral involvement such as hepatitis, encephalitis,thrombocytopenia, leucopoenia and coagulopathy.• Although disseminated HSV infection is uncommon inpregnancy, the mortality is about 50%. In particular,pregnant women with primary mucous membraneinfection during the 3rd trimester, have an increased risk fordissemination and they could transmit HSV to their babiesduring vaginal delivery.
•The great majority of recurrent genital herpes is due toHSV-2 because this virus reactivates more frequently thanHSV-1.•Recurrent episodes of HSV infection are characterized bythe presence of antibody against the same HSV type andthe herpes outbreaks are usually mild (7–10 days) with lesssevere symptoms than the first episode.•Prodromal symptoms (itching, tingling, neuralgia) mayoccur hours or days before a recurrent herpes episode.•The apparently asymptomatic phases between clinicaloutbreaks of genital herpes are important, since HSV canreactivate periodically in latently infected cells of sensoryganglia travelling via the neuronal axons back to thegenital mucosa, without clinical signs or symptoms. Thismechanism is known as asymptomatic virus shedding.
•Asymptomatic shedding has been shown to be higher inwomen with HSV-2 infection compared with those withHSV-1.•Although there is a small risk of vertical transmission,recurrent genital herpes must be regarded as the mostcommon cause of neonatal infections and the passagethrough an infected birth canal is the most probableroute of transmission .•In recurrent infections associated with clinical symptoms,the risk of neonatal disease is reduced dramatically byCaesarean section.
DIAGNOSIS :•Clinical diagnosis of genital herpes is limited in accuracy.First, HSV is only one of several diseases characterized bygenital ulcers. More importantly, many persons areunaware that their symptoms are those of herpes.•The typical lesions may not appear, and recurrences maybe at different locations along a dermatome. Women mayexperience only prodromal symptoms, such as burning ortingling; have single ulcers, fissures, or erosion; orexperience erythema or edema as the primary symptom.•Available tests for herpes include both culture and PCR-DNA testing for viral shedding, and the use of blood tests toscreen for previous exposure.
MANAGEMENT :•The American Congress of Obstetricians andGynecologists (ACOG) recommends that women withactive recurrent genital herpes should be offered –•Suppressive viral therapy from 36 weeks until delivery Valacyclovir 500 mg orally BD OR Acyclovir 400 mg orally TDS.•Transplacental infection of the fetus is rare duringpregnancy. Intrauterine HSV infection has uncommonlybeen associated with skin lesions, chorioretinitis,microcephaly, hydranencephaly , and microphthalmia.
•While primary HSV infections in the first trimester areassociated with higher rates of spontaneous abortion andstillbirth, infection later in pregnancy appears more likely tobe associated with preterm labor or growth restriction.•Of greatest concern is the risk of primary infectionacquired at birth which could lead to herpeticmeningitis. The infection rate is 34 to 80% for infants bornvaginally during a primary infection.•Cesarean section is recommended for all women in laborwith active genital lesions or prodromal symptoms such asvulvar pain.For patients with preterm premature rupture of membranes remotefrom term complicated by recurrent maternal HSV infection, the risks ofprematurity should be weighed against the risk of neonatal HSVdisease in considering expectant management. Prophylactictreatment with antiviral agents (eg, acyclovir) may be considered ifexpectant management is chosen.
THE TORCH TEST :•The TORCH test is used to screen pregnant women andnewborns for antibodies to the infectious diseasesincluded in the panel, if either the mother or newborn hassymptoms. The blood test can determine if the person hashad a recent infection, a past infection, or has never beenexposed.•The test is ordered when a pregnant woman is suspectedof having any of the TORCH infections. These infectionscan be serious if they occur during pregnancy becausethey can cross the placenta from the mother to thedeveloping fetus and can cause congenital defects in thenewborn.
•Results are usually given as positive or negative,indicating the presence or absence of IgG and IgMantibodies for each of the infectious agents tested forwith the panel. A "normal" result is negative(undetectable) IgM antibody in the blood of the motheror newborn.•Presence of IgM antibodies indicates either a current orrecent infection. A positive IgM result in a newbornindicates high likelihood of infection with that organism.IgM antibodies produced in the mother cannot cross theplacenta, so presence of this type of antibody stronglysuggests an active infection in the infant. Presence of IgGand absence of IgM antibody in an infant may reflectpassive transfer of maternal antibody to the baby anddoes not indicate active infection in that infant.
•Likewise, the presence of IgM antibody in a pregnantwoman suggests a new infection with the virus orparasite.•Further testing must be done to confirm these resultssince IgM antibody may be present for other reasons.•IgG antibody in the pregnant woman may be a sign ofpast infection with one of these infectious agents. Bytesting a second blood sample drawn two weeks later,the level of antibody can be compared.•If the second blood draw shows an increase in IgGantibody, it may indicate a recent infection with theinfectious agent.
REFERENCES• Davidson’s Principles & Practice of MEDICINE -21st edition •Novak’s Textbook of Obstetrics – 10th edition •TORCH Infections in Pregnancy – Veena Gupta – Jaypee Publication – 2nd edition. •William’s Textbook of Obstetrics – 23rd edition •Article on Torch infections in Pregnancy – THE BRITISH MEDICAL JOURNAL (BMJ)•Article on TORCH INFECTIONS in Pregnancy – AMERICAN COLLEGE OF OBSTETRICS & GYNAECOLOGY (ACOG)