INTRODUCTION:

Congenital defects are an urgent global health priority affecting millions of neonates worldwide, it remains common cause for increasing mortality and morbidity in neonates in the developing and under developed countries. Mutifactorial factors such as genetic inheritance and environmental factors lead to multiple anomalies. Among those Maternal infections are a serious medical condition during pregnancy. TORCH when diagnosed on time and treated properly can lead to healthy offspring. It is potentially harmful during pregnancy, especially at first trimester as organogenesis takes place. The aim of this Case Report is to focus on the underlying factors of torch in development of multiple deformities in neonate.

CASE REPORT:

In the present case report congenital infection is the major cause for the multiple defects in the neonate. A 40-week Female child was born to a G₃P₂L₂A₁, mother through an emergency LSCS with the indication of previous LSCS with VBA failure. Neonate admitted in NICU for evaluation of multiple congenital anomalies. Birth weight is 2060 grams, APGAR score 1 min:7 and 5min:9 score. Child was stable and cried immediately after birth. Initially baby was on Oro-gastric tube feedings with EBF 5ml increased to 10 ml per feed every 2nd Hourly. Significant physical findings included are low hair line, head circumference 30 cms, retrognathia, auricles of ears folded back, depressed nasal bridge, short neck, multiple skin folds back of neck, right rockers bottom foot, overlapping of fingers, deep arm pit. Orthopedic referral was done and revealed the features of bilateral shoulder abduction, right foot- vertical talus, left foot –Congenital Talipes Equino varus (CTEV) atypical, bilateral sprengel shoulder, suggested referral to pediatric orthosurgeon. On the day of admission: vital parameters were HR: 163/min, RR:68/min SPO2:99, on 9^th day HR: 128/ min, RR:38/min, SPO2: 98 weight :2.16 kgs, rooting and sucking reflex normal, moros reflex incomplete. Investigations done on baby to rule out other anomalies. Neurosonogram revealed cortical and basal ganglia calcification probably due to TORCH infections. CT scan brain revealed Corpus calosal agenesis and diffuses multiple calcifications in brain parenchyma and basal ganglia. Infantogram showed shortening of Right proximal femur, narrow space between T1 and T2, bilateral CTEV and no evidence of other skeletal anomalies. 2D ECHO revealed that CAHD, large sub-aortic VSD left to right shunt, tiny mild muscular VSD, Moderate sized OS ASD, Moderate sized PDA, dilated Right atrium and right ventricle, mild TR with mild PAH. CBP-Hb:15.7 gm/dl, rbc:4.58 millions/cumm, Wbc: 23, 100 cells/cumm, platelet count: 2.6 lakhs/cumm, pcv: 48.1%, MCV: 105fl, MCH: 34pg, neutrophils: 75%, Lymphocyte:20%, eosinophils:02%, monocytes:03% . S.calcium:8.6mg/dl, CRP: negative. Treatment prescribed by Neonatologist piptaz, inj. Meropenum, Multidec, Kidrich drops, Tobramycin eye drops. Warmth care, breast feeding on demand. On discharge, baby taking breast feeding; respiratory pattern normal and activity good.

Obstetrical history revealed that mother had spontaneous abortion at 4 months of gestational age. First baby is 2 years old Male child, delivered by LSCS, at term with indication of meconium stained liquor. Present natal history reveals that a 24 year old mother , got admitted in the hospital at 7 months of Gestational age, for 3 days and treated oligohydramnios. Investigations undergone in the present pregnancy showed U/S imaging findings at 27 week of gestation with oligohydramnios(AFI-5 cms), subcutaneous edema noted in the scalp, IUGR. Torch 10 profile done at 28 weeks of Gestational age,Toxoplasmosis IgG Ab: positive, Rubella IgG Ab: positive, Cytomegalovirus IgG Ab:positive.Herpes simplex IgG Ab:positive. Maternal serologies were negative for Hepatitis B surface antigen and HIV antibody. Mother got admitted in labour room at 9 months of gestational age. Stripping done for mechanical dilatation of cervix, mother expelled plenty of candid white discharge and was cleaned with normal saline, due to non progression of labour, mother taken to emergency LSCS.

DISCUSSION:

Infections acquired in utero or during the birth process are a significant cause of fetal and neonatal mortality and an important contributor to early and later childhood morbidity. The infected newborn show abnormal growth, developmental anomalies, or multiple clinical and laboratory abnormalities. The original concept of the TORCH Syndrome refers to infection of a developing fetus or newborn by any of a group of infectious agents. "TORCH" is an acronym meaning (T)oxoplasmosis, (O)ther Agents, (R)ubella (also known as German Measles), (C)ytomegalovirus, and (H)erpes Simplex. Infection with any of these agents (i.e., Toxoplasma gondii, rubella virus, cytomegalovirus, herpes simplex viruses) may show similar symptoms in affected newborns. If a developing fetus is infected by a TORCH agent, the outcome of the pregnancy may be miscarriage, stillbirth, delayed fetal growth and maturation (IUGR), or preterm delivery. In addition, newborns infected by any one of the TORCH agents may develop a similar symptoms and findings. Each infectious agent may also cause additional abnormalities that may vary in degree and severity, depending upon the stage of fetal organogenesis at time of infection and/or other factors. The specific description of the TORCH agents are discussed.

Toxoplasmosis Causative Organism – Toxoplasma gondii. Infections are transmitted by Transplacental, Fecal-oral route, Oocysts excreted in cat feces, found in undercooked meat, contaminated water/soil and unpasteurized goat milk and risk of fetal infection increases with gestational age. Most infants with congenital toxoplasmosis (70-90%) are asymptomatic or without apparent abnormalities at birth. The classic triad of congenital toxoplasmosis consists of chorioretinitis, hydrocephalus and intracranial calcifications. Signs present at birth may include fever, a maculopapular rash, hepatosplenomegaly, microcephaly, seizures, jaundice, thrombocytopenia, and rarely generalized lymphadenopathy. Diagnosis done by definitive Isolating organism from placenta, serum, or CSF also available – PCR and IgM titer (IgG will be elevated if mother is infected regardless of transmission). Management by Pyrimethamine, Sulfadiazine, Leucovorin. Glucocorticoids (Prednisone).

Rubella Causative Organism – Togavirus. Transmitted by Transplacental, Respiratory secretions. Clinical Manifestations are “Blueberry Muffin” rash due to extramedullary hematopoiesis,Cataracts “Salt and Pepper” retinopathy, Radiolucent bone disease (long bones),IUGR, glaucoma, hearing loss, pulmonic stenosis, patent ductus arteriosus, lymphadenopathy, jaundice, hepatosplenomegaly, thrombocytopenia, interstitial pneumonitis, diabetes mellitus. Diagnosis by Culture from blood, urine, CSF, oral/nasal secretions IgM titer.Treatment is Supportive care.

Cytomegalovirus Causative Organism – Human herpesvirus. Transmitted by Transplacental, Perinatal (contact with vagina during delivery or breast milk after delivery),Contact with bodily fluids (urine/saliva). Transmission is possible through reactivation of latent virus (decreased risk of transmission). Clinical Manifestations Majority are asymptomatic at birth Periventricular calcifications, IUGR, developmental delay, microcephaly, sensorineural hearing loss, retinitis, jaundice, hepatosplenomegaly, thrombocytopenia, hypotonia, lethargy, poor suck. Preterm infants may appear septic – apnea, bradycardia, intestinal distension).Postnatal infections are generally asymptomatic. Diagnosis Culture (urine or pharyngeal secretions) PCR. Treatment Studies have shown that gancyclovir can improve hearing loss and neurodevelopmental outcomes and Supportive care.

Herpes Simplex Virus causative Organism – Human herpesvirus 1 and 2. Transmitted by Perinatal (contact with vagina during delivery), Contact after rupture of membranes, direct contact with affected areas. Manifestations include SEM disease (Localized to skin, eyes, and mucosal), Vesicular lesions on an erythematous base. Keratoconjunctivitis, cataracts, chorioretinitis, Ulcerative lesions of the mouth, palate, and tongue. CNS disease Seizure, lethargy, irritability, tremor, poor feeding, temperature instability, full anterior fontanelle, Disseminated disease, Multiple organ involvement (CNS, skin, eye, mouth, lung, liver, adrenal glands), May appear septic – fever/hypothermia, apnea, irritability, lethargy, respiratory distress. Hepatitis, ascites, direct hyperbilirubinemia, neutropenia, disseminated intravascular coagulation, pneumonia, hemorrhagic pneumonitis, necrotizing enterocolitis, meningoencephalitis, skin vesicles. Diagnosis by PCR of CSF, IgM titers, HSV culture of a lesion. Treatment is Acyclovir IV at a dose of 60 mg/kg per day IV divided every eight hours.

In the present case history reveals maternal infection of TRCH Ab are positive and past history of abortion. Neonate has microcephaly, maculopapular rash, intracranial calcifications, congenital heart disease, musculoskeletal deformities and sensorineural hearing loss.

CONCLUSION:

TORCH is set of infections with serious neonatal complications. The neonatal complications are more severe if acquired during early pregnancy and this necessitates early screening before the critical period of fetal organogenesis. Immunization against those infections that are vaccine-preventable would have greater benefit if they were also targeted to young women of reproductive age. Early detection and routine screening in pregnancy may reduce the lifelong disability and trauma to the family.

ACKNOWLEDGEMENT:

The authors are grateful to the authorities of NRIAS, GUNTUR for the facilities.

CONFLICT OF INTEREST:

The authors declare no conflict of interest.

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Received on 10.11.2017 Modified on 26.11.2017

Int. J. Nur. Edu. and Research. 2018; 6(1): 12-14.

DOI: 10.5958/2454-2660.2018.00003.0