Congenital Pulmonary Tuberculosis Associated with Maternal Cerebral Tuberculosis --- Florida, 2002

Persons using assistive technology might not be able to fully access information in this file. For assistance, please send e-mail to: mmwrq@cdc.gov. Type 508 Accommodation and the title of the report in the subject line of e-mail.

In 2002, congenital tuberculosis (TB), a rare disease with nonspecific signs and symptoms, was diagnosed in an infant in Florida. If untreated, congenital TB is fatal, which underscores the importance of suspecting congenital TB in newborns and infants who are at risk and who have unexplained febrile illnesses (1). This report summarizes the investigation of the case in Florida. Health-care practitioners should administer a tuberculin skin test to women who have risks for Mycobacterium tuberculosis infection and treat those who have latent TB infection (LTBI) to prevent maternal and congenital TB disease (2).

In May 2002, a U.S.-born male infant aged 44 days was brought to hospital A after 3 days of respiratory distress and fever. Examination revealed a fever of 103.2^ºF (39.6^ºC), nasal congestion, and bibasilar wheezing. The neck was supple, and no superficial lymphadenopathy was palpable. The abdomen was soft, no hepatosplenomegaly was detected, and ultrasound images of the liver were normal. The chest radiograph showed left lower lobe infiltrates, and the infant was admitted to the hospital for presumptive bacterial pneumonia. The fever continued despite administration of broad-spectrum antibiotics; on hospital day 9, physicians learned that the mother had cerebral TB diagnosed at hospital B approximately 20 days earlier. Gastric aspirates and bronchial washings from the infant yielded acid-fast bacilli (AFB) on smear microscopy and M. tuberculosis by rRNA amplification (Amplified^™Mycobacterium Tuberculosis Direct Test, Gen-Probe, San Diego, California) and by culture. Serology results for human immunodeficiency virus (HIV) antibody were negative. The infant subsequently was administered isoniazid, rifampin, pyrazinamide, and streptomycin. The streptomycin was discontinued when drug-susceptibility studies showed resistance to it. The infant responded favorably to treatment and was discharged after 8 weeks in hospital A. Investigation of potential sources of M. tuberculosis infection other than the mother (i.e., the father, a grandmother, and hospital staff) did not reveal any additional cases of TB disease.

The mother, aged 30 years, was born in Haiti, where TB is prevalent, and had moved to the United States in 1995; she had no children previously. After an uneventful pregnancy, during which she received prenatal care and had negative serology results for HIV antibody, the mother reported having a seizure 1 week before delivery; however, she did not seek medical care. The baby was born at hospital A at full term, with 1-minute and 5-minute Apgar scores of 6 and 9, respectively (normal: 7--10 at 5 minutes), clear amniotic fluid, and a grossly normal placenta. The mother began breastfeeding without difficulty and had no signs or symptoms of mastitis. From the day after delivery, she felt feverish; 3 days later, she had seizures lasting 15 minutes. She was admitted to hospital B, and magnetic resonance imaging showed five inflammatory cortical brain lesions. Histology of a brain biopsy specimen from the mother, obtained 10 days before her infant was admitted to hospital A with respiratory distress and fever, revealed necrotic granulomata and AFB. Cerebrospinal fluid from a lumbar puncture had no white blood cells and normal concentrations of glucose and protein; the results of Gram stain and culture (not performed for mycobacteria) were negative. Culture of her brain tissue yielded M. tuberculosis susceptible to isoniazid, rifampin, and pyrazinamide but resistant to streptomycin. A chest radiograph was normal; the results of AFB smear and culture on the mother's sputum were negative. The uterus was not curetted. The mother recovered fully while receiving isoniazid, rifampin, pyrazinamide, and the anticonvulsant oxcarbazepine. M. tuberculosis isolates from mother and infant were subsequently determined to have identical genotype patterns by IS6110-based restriction fragment length polymorphism.

Two years before her pregnancy, the mother had been administered a preemployment tuberculin skin test with a positive result of 20 mm of induration (>10 mm is positive for persons from countries with high incidence of TB). A chest radiograph was normal, and treatment for LTBI was not prescribed at that time.

Reported by: B Naouri, MD, V Virkud, MD, J Malecki, MD, Palm Beach County Health Dept; J Mateo, MD, Saint Mary's Medical Center, West Palm Beach; M Narita, MD, D Ashkin, MD, H Duncan, MPH, Bur of Tuberculosis and Refugee Health, Florida Dept of Health.

Editorial Note:

The results of the investigation described in this report emphasize the importance of considering congenital TB in a newborn or infant with pneumonia who fails to respond to conventional treatment, particularly if the mother is at risk for TB (e.g., because she emigrated from a country where the disease is prevalent) (2). Congenital TB is rare, but fatal if untreated, and is difficult to diagnose in time to treat successfully without knowledge of a maternal history of TB (3). Two possible routes of M. tuberculosis infection in utero are postulated: 1) hematogenous infection through the umbilical vein, with primary lesions in the liver and sometimes with porta hepatis lymphadenopathy; and 2) prenatal aspiration of infected fluid, with pulmonary and gastrointestinal disease predominating (3,4).

M. tuberculosis infection in utero can be indistinguishable from perinatal or early postpartum infection. The most recent set of criteria for congenital TB requires the infant to have a tuberculous lesion (e.g., infiltrates on the chest radiograph or granulomas) and at least one of the following: 1) onset during the first week of life, 2) a primary hepatic TB complex or caseating hepatic granulomas, 3) infection of the placenta or maternal genital tract, or 4) exclusion of postnatal transmission by a contact investigation (3). In this case, transmission linkage from the mother to the infant was corroborated by the matching drug-resistance and genotype patterns of the M. tuberculosis isolates. The likeliest explanation is that infection was congenital, because the mother had TB during pregnancy and the contact investigation found no alternative sources of infection. The infant came to medical attention at 44 days, later than the typical 1--3 weeks, but still within the widest reported range (1--84 days) for congenital TB (3,4). The mother was not examined for uterine TB, and the placenta was discarded before the infant became ill; no gross abnormalities were noted by physicians. The lack of pulmonary disease in the mother makes airborne spread from her to the infant unlikely. Transmission via breast milk was unlikely because the mother lacked findings of TB mastitis.

The missed opportunity to prevent the infant's TB by treating the mother's LTBI at the time it was diagnosed underscores the need to incorporate treatment plans for persons at risk into preemployment and other health screenings that identify LTBI. Strategies for preventing TB in foreign-born persons are especially important (5). TB-control officials should use epidemiologic history for identifying persons at risk and collaborate with the medical community in finding and treating LTBI to prevent TB disease.

References

Use of trade names and commercial sources is for identification only and does not imply endorsement by the U.S. Department of Health and Human Services.

References to non-CDC sites on the Internet are provided as a service to MMWR readers and do not constitute or imply endorsement of these organizations or their programs by CDC or the U.S. Department of Health and Human Services. CDC is not responsible for the content of pages found at these sites. URL addresses listed in MMWR were current as of the date of publication.

Disclaimer All MMWR HTML versions of articles are electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the electronic PDF version and/or the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices.

Congenital Pulmonary Tuberculosis Associated with Maternal Cerebral Tuberculosis --- Florida, 2002

Editorial Note:

References

**Questions or messages regarding errors in formatting should be addressed to mmwrq@cdc.gov.