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Case Report |
1 Department of Radiology, Mackay Memorial Hospital, No. 92, Sec. 2, Chung-Shan
N Rd., Taipei 10449, Taiwan.
2 Department of Radiology, Taipei Medical University, No. 250, Wu-Hsing St.,
Taipei 110, Taiwan.
Received February 13, 2003;
accepted after revision June 17, 2003.
Address correspondence to S.-L. Shih
(mmhr1{at}seed.net.tw).
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A chest radiograph (Fig. 1A) showed multiple nodules in both lungs. Contrast-enhanced CT scans (Figs. 1B and 1C) revealed pulmonary nodules with a central area of low attenuation and peripheral rim enhancement. Enlarged lymph nodes were shown in the pretracheal and subcarinal regions. Sonography of the abdomen revealed an enlarged liver without evidence of focal lesions.
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Bacterial cultures of blood, CSF, and urine were negative. The patient underwent extensive diagnostic studies, including open lung biopsy. The result of serologic testing for HIV was negative. Smears of gastric aspirates and lung biopsy specimens contained acid-fast bacilli, and cultures were positive for M. tuberculosis. Antituberculous drugs were prescribed on the ninth hospital day. However, her condition continued to deteriorate, and mechanical ventilation became necessary. She died at the age of 52 days.
The patient's mother had normal findings on a chest radiograph and sputum examination, but a purified protein derivative skin test was positive, with 15 mm of induration. Throughout her pregnancy and her daughter's illness, she remained free of symptoms. An endometrial biopsy revealed noncaseating granulomas, in which M. tuberculosis was detected by polymerase chain reaction. We were unable to identify any other infected individuals or caregivers with whom she had contact.
Case 2
An 83-day-old male infant presented with a week-long history of
intermittent fever and poor appetite. Forty days before presentation, he had
been seen in our hospital for constipation and abdominal distention.
Over-the-counter drugs were prescribed, and the patient did not return to the
clinic. Review of the radiograph obtained at that time showed normal lung
fields and hepatosplenomegaly. Abnormal movement of the left lower leg was
also noted before admission.
A physical examination revealed hepatosplenomegaly. Laboratory findings were noncontributory except for abnormal results of liver function tests. The CSF was cloudy and contained 110 WBC/µL, with 90% lymphocytes, 5 RBC/µL, a glucose level of 31 mg/dL, and a protein concentration of 267 mg/dL.
A chest radiograph (Fig. 2A) showed multiple nodules in both lungs. An abdominal sonogram revealed multiple hypoechoic foci in an enlarged liver and spleen. CT scans (Figs. 2B and 2C) of the abdomen showed not only multiple hypodense lesions in the liver and spleen but also paraaortic and porta hepatis lymphadenopathy. We saw hyperattenuating leptomeningeal thickening on unenhanced brain CT scans (Figs. 2D, 2E, 2F), which showed homogeneous enhancement after contrast administration, compatible with meningeal infection. An ischemic infarct was also present in the right middle cerebral artery distribution.
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Bacterial cultures of blood, CSF, and urine were negative. The result of serologic testing for HIV was negative. Despite initial administration of broad-spectrum antibiotics and then empiric antituberculous drugs on the second hospital day, the infant failed to respond to treatment and required mechanical ventilation. No acid-fast bacilli were found on smears of the gastric juice and CSF, but cultures of both were positive for M. tuberculosis. The infant died on the fifth day.
Postmortem examination showed diffuse caseating necrosis involving the liver, spleen, lymph nodes, lungs, meninges, kidneys, adrenal glands, and gastrointestinal tract. Histologic examination revealed abundant acid-fast bacilli, especially in the liver and porta hepatis and paraaortic lymph nodes. Culture of the liver and lung tissues yielded M. tuberculosis.
The mother was asymptomatic, but chest radiography showed fibronodular lesions in both upper lung fields and bilateral pleural effusions. Her purified protein derivative skin test result was positive at 16 mm. The sputum had no acid-fast bacilli and culture findings were negative. An endometrial biopsy revealed normal findings. The mother was given antituberculous therapy. It was difficult to trace other possible infectious contacts.
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Tuberculosis should be suspected in an infant whose response to antibiotic and supportive therapy is poor. Acid-fast stains of smears and mycobacterial cultures from multiple sites are necessary to make a diagnosis. Gastric aspirates, endotracheal aspirates, CSF, or biopsy tissue (e.g., sonographically guided liver biopsy or open lung biopsy) can be useful. An important clue in the diagnosis is a maternal or family history of tuberculosis. However, it is not rare that the diagnosis of infection in the infant leads to the discovery of tuberculosis in the mother, as in our two patients.
The criteria for distinguishing congenital tuberculosis from postnatally acquired tuberculosis were established by Beitzke [4] in 1935. These included isolation of M. tuberculosis from the infant and one of the following: presentation of a primary complex in the liver, tuberculous changes in an affected fetus or in an infant within days of birth, or exclusion of extrauterine exposure. However, these criteria were generated from review of autopsy material and are extremely difficult to meet if the infant survives. In 1994, Cantwell et al. [2] proposed revised criteria to increase sensitivity for antemortem diagnosis. The infant must have a proven tuberculous lesion and at least one of the following: presentation of lesions in the first week of life; presentation of hepatic granulomas, but not necessarily a primary hepatic complex; or confirmation of tuberculosis in the mother's genital tract and exclusion of postnatal exposure by contact investigation. Both our cases met the revised criteria.
Many infants with congenital tuberculosis have abnormal findings on chest radiographs [1, 5], most often a miliary pattern. Hilar and mediastinal lymphadenopathy and parenchymal infiltrates are also common. Some infants with normal findings on chest radiographs early in the course of the disease later develop profound radiologic abnormalities. The multiple pulmonary nodules observed in our patients have not been described previously, and we attribute this finding to the fact that the patients presented late in the course of the disease. CT of the female infant showed pulmonary nodules with peripheral rim enhancement and a central hypodense area, which corresponded to caseating necrosis in the specimen obtained by open lung biopsy. Because of our experience of unusual radiographic findings in the female infant, the male infant was given empiric antituberculous drugs and underwent extensive early examination. When multiple pulmonary nodules are found in any infant, especially one with hepatosplenomegaly, tuberculosis should be in the differential diagnosis.
With the female infant, the mother had no symptoms, no pulmonary parenchymal abnormalities, and no bacilli on acid-fast sputum stain or culture. A survey of individuals with whom she had contact was negative. These factors made extrauterine transmission unlikely. Tubercle bacilli in the endometrial tissue were the only apparent source of exposure for the infant. Imaging studies indicated a primary pulmonary complex with progressive enlargement of parenchymal foci and hematogenous spread to the liver (hepatomegaly without focal lesions on sonography). We believe that the mode of transmission was aspiration of infected amniotic fluid in utero or during labor and delivery.
With the male infant, postnatal exposure was difficult to exclude on clinical grounds. However, when we reviewed serial radiographs of the male infant, it was apparent that hepatosplenic involvement appeared before the pulmonary nodules. The most likely mode of transmission was bacillemia during pregnancy that led to infection of the placenta. We hypothesize that tubercle bacilli first reached the fetal liver via the umbilical vein, forming a primary hepatic complex, which was shown on abdominal CT. This finding merits attention and may make antemortem diagnosis of congenital tuberculosis possible. The lung and meninges were subsequently involved by hematogenous spread. Brain infarction was a sequela of meningeal involvement.
In summary, we described two cases of congenital tuberculosis in infants with intermittent fever, hepatosplenomegaly, and an unusual radiographic presentation (multiple pulmonary nodules). The nodules had central caseating necrosis, presumably due to progressive enlargement of pulmonary foci, either primary (the female infant) or secondary (the male infant). CT may be useful in revealing the primary complex, thus elucidating the mode of transmission without a surgical procedure or autopsy. If a patient has a proven tuberculous lesion and a primary hepatic complex on imaging, the diagnosis of congenital tuberculosis can be made.
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