 |
|
Letters to the Editor Indian Pediatrics 2002; 39:1167-1168 |
|
Congenital Tuberculosis |
|
Infection with tubercle bacilli either during the intrauterine life or before complete passage through birth canal is termed as congenital tuberculosis. Despite high prevalence of tuberculosis in the world, only 300 such cases have been reported so far in literature and only about 10 cases have made their way into medical records in India(1). We hereby report a case of congenital tuberculosis in a premature infant. The diagnosis could be confirmed only postmortem. A 45 days old male child presented with fever and cough for one month, gradual abdominal distension for three weeks, respiratory distress for two weeks, and had no response to antibiotics. He was born to a second gravida mother at 34 weeks of gestation by normal vaginal delivery. The birth weight was 2.75 kg and there was no perinatal asphyxia. Antenatal period was supervised and uncomplicated. He was given BCG at birth and was exclusively breast-fed. On examination, his weight was 3.2 kg with length of 49 cm and head circumference of 37 cm. The respiratory rate was 74 per minute with subcostal and intercostal recessions. The child had mild pallor, no icterus or superficial lymphadenopathy. BCG scar was absent. Systemic examination revealed diminished air entry in right infrascapular area, bilateral crepitations and hepatosplenomegaly. Hemoglobin was 10 g/dL, total leukocyte count was 8850 per cu mm. with 80% neutrophils and platelet count was 1.5 lacs per cu mm. Liver enzymes were elevated. Chest X-ray revealed extensive bronchopneumonia. Ultrasound revealed hepatosplenomegaly, portal adenopathy and no ascites. Tuberculin test and gastric aspirate for AFB on three occasions were negative. Blood culture was sterile. CSF showed 10 cells, all lymphocyts with normal protein and sugar, negative AFB smear and culture was sterile. Virological and serological tests to rule out toxoplasmosis, herpes, syphilis, CMV and HIV were negative. Blood and urine fungal cultures were sterile. Family screening for tuberculosis was negative. Child was started on cefotaxime and amikacin at admission and in view of progressive pneumonia cloxacillin was added after 48 hours. Antitubercular therapy was started empirically on day 5 of admission because of his worsening clinical status, hepatomegaly with portal lymphadenopathy on ultrasound and chest X-ray findings. However child continued to deteriorate and developed type 2 respiratory failure for which respiratory support was provided. He expired on day 9 of admission. Liver and spleen biopsy revealed multiple small areas of necrosis with large number of acid-fast bacilli without any inflammatory response. Liver also showed diffuse fatty change and spleen showed erythrophagocytosis. A final diagnosis of congenital tuberculosis was thus made. The mother started having malaise and fever after the child’s death and repeat chest X-ray showed pleural effusion and her tuberculin test was strongly positive and sputum for acid fast bacilli was negative. She was started on antituberculosis therapy but she did not agree for undergoing an endometrial biopsy. In 1935, Beitzke presented the following criteria for congenital tuberculosis, (i) tuberculosis must be firmly established in first few days of life, (ii) primary complex in the liver, (iii) if liver is not involved then if lesions are present within first days of life or when extrauterine infection can be excluded with certainty(1,2). Because of rigid nature of Beitzke’s criteria, Cantwell et al(3) proposed a modification at 33rd InterScience Conference of Antimicrobial Agents and Chemotherapy that the infant must have a proven tuberculous lesion and at least one of the following: (i) lesions in first week of life, (ii) primary hepatic complex or caseating hepatic granuloma, (iii) tuberculosis infection of placenta or maternal genital tract, or (iv) exclusion of postnatal transmission by thorough contact investigation(2,3). Our case had caseating hepatic granuloma with portal adenopathy; by either criterion our case qualifies for diagnosis of congenital tuberculosis. Some authors feel that dfistinguishing congenital from early postnatally acquired tuberculosis is a matter of epidemiological importance only and suggest the terminology of perinatal tuberculosis instead of congenital tuberculosis since modes of presentation, treatment and immediate prognosis do not differ(4). Infection has classically been thought to be acquired in three ways (a) transplacentally, with primary complex in liver, (b) aspiration of infected amniotic fluid during passage through birth canal, when lungs are primary focus and (c) ingestion of infected material, where the primary is in the gut(1). In the index case as the primary complex was located in the liver most likely it was a transplacentally acquired disease. The lungs were involved either due to dissemination of disease or aspiration of the infected fluid. Mortality rate is approximately 50%, which underscores the importance of early diagnosis and treatment. The frequency of congenital tuberculosis is probably under-estimated. The importance of early diagnosis and treatment of this condition is crucial because consequences of delayed diagnosis and therapy are serious. Improved screening of women at risk and sensitization of the medical community are necessary. The diagnosis of congenital tuberculosis should be considered in any neonate with pneumonia who fails to respond to conventional treatment, particularly in a child from an ethnic or socioeconomic environment where tuberculosis is prevalent. Munni Ray, Ashish Dixit, *Kim Vaipei, Pratibha D Singhi Departments of Pediatrics and *Pathology, PGIMER, Chandigarh 160 012, India. E-mail: [email protected] |
|
References |
|
|
