A Left apical lung showing diffuse fibroblast plugs in airways with intense interstitial fibrosis and chronic inflammation (H&E, 40x) B The spleen showing a small caseating granuloma (H&E,40x) C The spleen, AFB stain showing one acid-fast bacillus (arrow) (AFB, 1200x) D The liver showing a small necrotizing granuloma (H&E, 100x) E The liver, AFB stain showing one acid-fast bacillus (arrow) (AFB, 1200x) 

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... days after cesarean section the mother developed fever with acute respiratory distress syndrome (ARDS). Possible etiologies included sepsis from chorioamnionitis, chemotherapy-in duced interstitial pneumonitis and lymphomatous involvement. Laboratory investigation for H1N1 in fluenza virus, cytomegalovirus, bacteria, and fungi were all negative. Broad spectrum antibiotics were administered, but with no response in the clinical course. She developed spontaneous pneumothorax and pneumomediastinum from air leak syndrome due to severe diffuse alveolar damage on the 7 th day of admission 15 . Intercostal chest drain insertion was done. Five days later she developed acute respiratory distress syndrome (ARDS) and finally expired due to respiratory failure. Postmortem examination to determine the definite cause of ARDS was performed. Autopsy findings revealed diffuse fibro blast plugging and intensive interstitial fibrosis with chronic inflammation, compatible with organizing stage of diffuse alveolar damage (Fig. 3A). Granulo mas were not seen in the lung. Staining for acid-fast bacilli was negative (not shown). Polymerase chain reaction (PCR) for M. tuberculosis was negative. Lung tissue PCR for H1N1 virus and other com mon 17 viruses were negative. The cause of diffuse alveolar damage was assumed to be from chemo therapy-induced interstitial pneumonitis. Bilateral visceral pleural rupture with subpleural hemorrhage and adjacent microinfarction of distal lungs were noted (not shown), caused by high pressure of distal airway due to intensive fibroblast plugging as a result of severe diffuse alveolar damage. It was called “air leak syndrome” 15 The gastric antrum showed a 3-cm. sub mucosal mass of diffuse large B-cell lymphoma (not shown). Metastasis was present in left liver lobe and lymph nodes from peripancreatic soft tissue, paraaortic and perivesical soft tissue (not shown). Bone marrow involvement was not found, probably representing a response to chemotherapy. Post mortem revealed no granuloma in the bone marrow. Small caseous granulomas with acid-fast bacilli were found diffusely in the spleen (Fig. 3B, 3C) and rarely in the liver (Fig.3D, 3E). Two small caseous granulomas were found in the peripancre atic soft tissue lymph nodes with numerous acid-fast bacilli (not shown). The neonate developed jaundice of prema- turity. Due to the suspicion of chorioamnionitis, prolonged PROM, maternal fever and fetal tachy cardia, she received antibiotic prophylaxis, but still developed neonatal sepsis. Intravenous followed by oral antibiotics were administered. Urine, blood and CSF cultures were negative. She was discharged at age 37 days. Notably, on the postnatal day 40, the neonatologist noticed the maternal autopsy results. Therefore congenital tuberculosis was suspected. Extensive investigations was performed from 49 days of age. Chest radiography was normal. AFB staining from a gastric aspirate was negative. Tuber culin skin test was not conducted since the patient had prior BCG (Bacillus Calmette-Guèrin) vacci nation, which might cause a false positive result 13 . Although the infant had no proven tuberculous lesions, and there were no definite criteria for diagnosing congenital tuberculosis, latent tubercu lous infection was diagnosed as a result of intrau terine tuberculous exposure (see table 1) Antitu berculous monotherpay (isoniazid) was started and continued for 9 months. Recently she experienced failure to thrive according to the head circumference and weight for age were between the 3rd to 10th percentiles. The most likely cause was inadequate feeding. Other organ systems appeared normal. Nutritional supplementation was started. Placental tuberculosis is a rare condition. It was first reported for over a hundred year ago by Aldred et al since 1904, with subsequent studies by Boesaart (1959), Kaplan et al (1980) and Sarkar et al (1996). Most patients were immunosuppressed individuals such as those with hematological malignancy and more recently AIDS 9 . The placenta may be grossly normal or may contain firm, white plaques. Characteristic histopathological findings vary from caseating/non-caseating granu lomas with or without giant cells, in the chorionic villi or intervillous space. Acute intervillositis may be present. Local villous destruction by granulomas may be seen. The decidua may show extensive necrosis, non-specific chronic deciduitis and granu lomas in the placental floor, which suggested direct transmission from decidua to placenta. Acid-fast bacilli may be found in intervillous fibrin, villous stroma or fetal vessels. 10, 11 In fetal infection, caseating granulomas in the lungs and acid-fast bacilli in the liver, spleen, and kidneys could be found 11 . The present case showed a microabscess in the intervillous space with partial villous destruction. Placental TB was diagnosed due to presentation of numerous acid-fast bacilli in the intervillous microabscess (Fig 1C,1D,1E). This case showed maternal disseminated tuberculosis of the liver, spleen, peripancreatic soft tissue lymph nodes and placenta. Despite lack of tissue culture confirmation, PCR from FFPE pre served placental tissue revealed the positive sig nal for Mycobacterium tuberculosis (Fig. 2). Focal tuberculous intervillositis of the placenta suggested hematogenous spread rather than ascending infec - Congenital tuberculosis is a rare condition. Only 300 cases were reported since 1989 and additional 18 cases were reported from 2001 to December 2005 [3]. The modes of transmission are (i) intrauterine: hematogenous via the umbilical vein, aspiration or ingestion of infected amniotic fluid; (ii) intrapartum: aspiration of tuberculosis amniotic fluid or cervicovaginal secretions at birth; (iii) postpartum: breast feeding, inhalation or inges tion of infected respiratory droplets 3, 5,6 . In Thailand, only 9 cases of congenital tuberculosis were reported by Tawee et al , 2003 8 and 1 case by Chulapong et al , 2004 2 . None of these tion via maternal genital tract, since the decidua was normal. Interestingly, the findings lead to a concern of congenital tuberculosis of the infant, possibly transmitted via the hematogenous route during pregnancy. The revised diagnostic criteria for con genital tuberculosis by Cantwell, 1994 was applied (see table 1) 7 . Regardless of the lack of definitive diagnostic criteria including a lack of proven tuber culous lesions in the neonate, and no typical clinical manifestations of tuberculosis in the first weeks of life (such as lymphadenopathy, respiratory distress, hepatosplenomegaly, abdominal distension or abnormal chest radiography), congenital TB was suspected and treated due to the positive diagnosis of placental TB (criterion 3) 14 . reports state placental examination. Disseminated mycobacterial infection is typically associated with defective cellular immunity such as AIDS and lymphoreticular malig nancies, usually when the CD4+ count is <50 μL. In such patients, macrophages are unable to kill the intracellular mycobacteria since they lack of CD4+ T-cells to secrete IFN-gamma and TNF- α. These cytokines are necessary for macrophage activation to against mycobacteria. The relatively impaired cell-mediated immunity in the pregnancy state also leads to susceptibility of tuberculosis 12 . Tuberculosis of the placenta is a rare condition which is usually associated with AIDS and hematological malignancy. Fetal transmission usually occurs via hematogenous route and results in congenital tuberculosis. However, it is difficult to diagnose as the mother may have minimal symp toms and the infant show nonspecific symptoms 3 . If congenital tuberculosis is suspected, full investiga tion should be considered including chest radiogra phy, tuberculin skin test, AFB staining from gastric aspiration, and, if indicated, biopsy of lymph node and liver, CSF culture or polymerase chain reaction (PCR) for tuberculosis are required 3,5, 7, 8, 13 . This case demonstrates tuberculosis of the placenta in the immunocompromised patient due to malignant lymphoma and subsequent chemotherapy shortly before delivery. Congenital tuberculosis was diag nosed on the basis of placental tuberculosis, although the infant lacked signs or a positive laboratory diagnosis of tuberculous infection. The infant sub sequently showed good health and normal develop ment after antituberculous prophylaxis. The authors would like to thank: Wasana Kanoksilp, M.D., instructor of Anatomical Pathology from Department of Pathology Faculty of Medicine, Ramathibodi Hospital,, Mahidol University, Bangkok, Thailand for autopsy consulta tion; Mr. Thanwa Wongsuk, a medical technologist from the same Institute for performing PCR; and the 1st base sequencing Int., Malaysia for the support of PCR ...