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Editor—Tuberculosis (TB) in pregnancy is rare and neonatal TB is very rare.1 2 We describe a case of fatal congenital TB resulting from disseminated maternal infection with Mycobacterium tuberculosis.
An otherwise healthy 24 year old Indian woman who had recently emigrated to Australia presented at 33 weeks of gestation with generalised pruritus. Routine antenatal screening tests at 25 weeks of gestation showed nothing untoward. Physical signs were normal, apart from a temperature of 37.5°C. Serum alkaline phosphatase, alanine transferase, total bilirubin and serum bile acid values were all increased. Abdominal ultrasonography showed that the liver and biliary tree were normal.
She was diagnosed as having cholestasis of pregnancy and was started on a course of dexamethasone. Obstetric ultrasonography showed a right pleural effusion in the fetus. There was no maternal serological evidence of recent toxoplasmosis, cytomegalovirus (CMV), rubella or herpes simplex (HSV) infection. A lower segment Caesarean section was performed at 35 weeks of gestation because of preterm rupture of the membranes. A live boy was delivered, weighing 2.2 kg, with an Apgar score of 5 at five minutes. His spleen and liver were enlarged, but he had no peripheral oedema; a right sided pleural effusion was noted on chest x ray picture. The child developed respiratory distress and required ventilation. He had no IgM antibodies toToxoplasma gondii, HSV, rubella and CMV, and no pathogens were isolated from cultures of blood or gastric and endotracheal aspirates. Examination of pleural fluid showed a predominance of mononuclear cells (5.6 × 1010/l). Ziehl-Neelson staining and mycobacterial culture did not indicate acid fast bacilli (AFB).
Despite intensive support, the baby developed increasing consolidation of the right lung and died at 6 days of age. Histological examination of specimens from the right lung, obtained via a core biopsy, showed multiple foci of necrosis, containing numerous AFB (fig 1), but no granulomas. Polymerase chain reaction for mycobacteria was positive forM tuberculosis,3 although tissue was not available for mycobacterial culture.
After delivery, the mother had developed a fever up to 40°C. A chestx ray picture and a thoracic computed tomography scan indicated right pleural effusion with generalised nodular infiltration. No organisms were seen on Gram or Ziehl-Neelson stained films of pleural or bronchoalveolar lavage fluid; cultures for mycobacteria were subsequently negative. An attempted pleural biopsy was unsuccessful. The Mantoux test (10 IU PPD) was negative and dexamethasone had been stopped 10 days before testing.
Tuberculosis was confirmed by visualising caseous granulomas and AFB in the hepatic lobules of liver biopsy specimens obtained six days after empirical antituberculous treatment with isoniazid, rifampicin, pyrazinamide and ethambutol had been started. PCR was positive forM tuberculosis,3 but cultures for mycobacteria were negative. Microscopic examination of the placenta showed areas of intervillitis, and Ziehl-Neelson staining showed that AFB were dispersed throughout the intervillous areas. The patient responded to antituberculous treatment.
Guidelines for prenatal diagnosis of fetal TB are poorly defined. Our findings indicate that TB should be considered when antenatal ultrasonography shows pleural effusion without other features of fetal hydrops, an association that has not been described before.4 Comprehensive histopathological examination of the placenta, including Ziehl-Neelson staining, should be mandatory for the evaluation of unexplained maternal fever, especially in patients at increased risk of TB.
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