|Year : 2016 | Volume
| Issue : 2 | Page : 125-127
Congenital tuberculosis: Presenting as chronic lung disease
Suyog Tannirwar1, Sandeep Kadam1, Sanjay Patole2, Anand Pandit3
1 Department of Neonatology, KEM Hospital, Pune, Maharashtra, India
2 Department of Neonatal Paediatrics, KEM Hospital for Women, Subiaco, City of Perth, Western 6008, Australia
3 Department of Pediatrics, KEM Hospital, Pune, Maharashtra, India
|Date of Web Publication||8-Apr-2016|
Department of Neonatolgy, KEM Hospital, Pune - 411011, Maharashtra
Source of Support: None, Conflict of Interest: None
Congenital tuberculosis (CTB) is a rare entity with 300 cases reported so far and only 12 cases from India. We report an unusual case of multidrug resistant CTB leading to bronchopulmonary dysplasia in the preterm neonate. Baby presented with miliary shadows on chest X-ray with proven diagnosis on bronchopulmonary lavage. This case led to a diagnosis of endometrial tuberculosis in the mother, who looked apparently well.
Keywords: Chronic lung disease, congenital, neonate, tuberculosis
|How to cite this article:|
Tannirwar S, Kadam S, Patole S, Pandit A. Congenital tuberculosis: Presenting as chronic lung disease. J Clin Neonatol 2016;5:125-7
| Introduction|| |
Congenital tuberculosis (CTB) is an unusual problem despite high incidence of tuberculosis (TB) in women of child-bearing age.  The transmission of tubercular bacilli to the fetus occurs by hematogenous spread through the placenta, in utero aspiration and ingestion of infected amniotic fluid or secretions during delivery. Due to the nonspecific presenting signs and symptoms and fatal outcome in the absence of early therapy, one needs to have high index of suspicion.
We report a case of CTB in a 20-day-old preterm, who presented with failure to thrive, respiratory distress, hepatosplenomegaly, and diffuse infiltrates in the chest radiograph. There was no maternal history of TB. Bronchoalveolar lavage (BAL) yielded Mycobacterium tuberculosis. Baby developed chronic lung disease despite early treatment alarming need for surveillance of multidrug-resistant TB to reduce its spread.
| Case Report|| |
This was 35 weeks preterm neonate weighing 1.9 kg born to gravida 4 mothers by normal vaginal delivery. Mother's age was 28 years. She had 2 second trimester spontaneous abortions and a normal child. Antenatal period was uneventful. Baby was initially admitted to the NICU for Preterm care and discharged on day 7 with the uneventful course. Baby presented on day 20 of life with weight loss, respiratory distress, and cough. He weighed 1.5 kg and had tachypnea with subcostal and intercostal recessions. General examination was unremarkable. Systemic examination revealed diminished air entry and crepitations bilaterally and hepatosplenomegaly.
Complete blood cell count and liver function tests were normal. Chest X-ray revealed extensive bronchopneumonia. Ultrasound revealed hepatosplenomegaly, portal lymphadenopathy, and no ascites. Tuberculin test (TT) was negative, and gastric aspirate for acid-fast bacteria (AFB) was negative. Blood and urine culture were sterile. Cerebrospinal fluid showed four cells, all lymphocytes 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. Family screening for TB was negative except for mother. Child was initiated on piperacillin-tazobactam and amikacin on admission. In view of clinical deterioration and progressive pneumonia, antibiotics were changed to vancomycin after 72 h and piperacillin-tazobactam and amikacin were discontinued. BAL was send for AFB staining because of worsening clinical status, hepatosplenomegaly on ultrasound, and chest X-ray findings, which showed 4 + AFB.
Baby deteriorated and developed type 2 respiratory failure for which he was ventilated. Four drugs Antitubercular therapy (isoniazid, rifampicin, ethambutol, and pyrazinamide) were initiated. Baby improved after 7 days of ATT and was extubated. Even after extubation, baby persistently require 1 L/min Oxygen for maintaining SpO 2 >90%. The patient started on the second line Antitubercular drug levofloxacin, linezolid, and amikacin in addition to isoniazid as BAL culture grew multidrug resistant mycobacteria. Baby was diagnosed to have severe bronchopulmonary dysplasia as baby was oxygen dependent until he expired at the age of 5 months. On mother's evaluation, chest X-ray showed hilar adenopathy with positive TT and negative sputum for AFB. She was initiated on Antitubercular therapy after an endometrial biopsy, which showed epithelioid granulomas with langerhans giant cell, caseous necrosis [Figure 1] and endometrial polymerase chain reaction positive for TB.
|Figure 1: Microphotograph of endometrial biopsy showing caseous necrosis and giant cells|
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| Discussion|| |
With increasing rates of TB worldwide, the rate of perinatal TB is also affected.  CTB a rare disease should be distinguished from the more frequent acquired neonatal TB, in which the infant is infected after birth by an adult suffering from contagious pulmonary TB. CTB may occur as a result of maternal TB when the illness involves the genital tract or the placenta. TB bacilli are introduced into the fetus hematologically via the umbilical vein, or infected amniotic fluid which is ingested or aspirated in utero or at birth. 
Revised diagnostic criteria as proposed by Cantwell et al. are proven TB lesions in the infant plus one of the following: (1) Lesions occurring in the first week of life, (2) a primary hepatic complex, (3) maternal genital tract or placental TB, or (4) exclusion of postnatal transmission by a thorough investigation of contacts.
As demonstrated in our patient, CTB is particularly difficult to diagnose. Mothers are often apparently healthy; in one review 24 of 32 mothers were asymptomatic.  According to Cantwell criteria, our case unequivocally qualifies the diagnosis of CTB as there was definite evidence of TB in baby with chest X-ray showing military TB, BAL showing 4+ Acid fast bacilli and proven maternal endometrial infection.
The clinical features of CTB usually present in 2 nd or 3 rd weeks of life and are nonspecific as was seen in our case. Hepatosplenomegaly and respiratory distress are a common manifestation, as seen in this baby.
The miliary pattern in chest radiograph and no response to multiple antibiotics prompted us to evaluate for TB in both baby and mother. We emphasize here that an early diagnosis of congenital TB in neonate is difficult and requires a high index of suspicion.
Our patient had persistent oxygen requirement despite early Antitubercular therapy and good supporting care indicating poor response to Antitubercular drug, emphasizing the need to prevent spread of MDR-TB. The baby was diagnose to have severe bronchopulmonary dysplasia according to NIH consensus definition  as baby was oxygen dependent (O 2 requirement with FiO 2 of 0.4) till he expired at 5 month of age.
CTB is a fatal disease with a high mortality probably related to delay in diagnosis. Our patient's course was marked by military TB, which required intensive second line Antitubercular therapy with linezolid, levofloxacin, amikacin in addition to isoniazid as bug was resistant to rifampicin and pyrazinamide. As the patient was hospitalized until death, compliance was assured.
The diagnosis of CTB should be considered in any neonate with pneumonia who fails to respond to conventional treatment. Mortality with CTB is approximately 50% increasing with MDR-TB emphasizing need for early diagnosis and treatment based on drug sensitivity pattern. As mother is only link in CTB, the even healthy mother should undergo proper evaluation and treatment to reduce the spread of TB. TB is global threat as incidence of MDR-TB is rising; there is a need for better diagnostic and microbiological test for best possible management of MDR-TB.
A high index of suspicion by health professionals, in both the developed and developing world, is required to detect, manage TB in pregnancy and the early newborn period.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Blackall PB. Tuberculosis: Maternal infection of the newborn. Med J Aust 1969;2:1055-8.
Whittaker E, Kampmann B. Perinatal tuberculosis: New challenges in the diagnosis and treatment of tuberculosis in infants and the newborn. Early Hum Dev 2008;84:795-9.
Starke RS, Smith MH. Tuberculosis. In: Remington JS, Klein JO, editors. Infectious Diseases of the Fetus and Newborn. Philadelphia: W.B. Saunders Company; 2001. p. 1184-7.
Cantwell MF, Shehab ZM, Costello AM, Sands L, Green WF, Ewing EP Jr., et al.
Brief report: Congenital tuberculosis. N Engl J Med 1994;330:1051-4.
Ehrenkranz RA, Walsh MC, Vohr BR, Jobe AH, Wright LL, Fanaroff AA, et al.
Validation of the National Institutes of Health consensus definition of bronchopulmonary dysplasia. Pediatrics 2005;116:1353-60.