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Year : 2008  |  Volume : 51  |  Issue : 2  |  Page : 289-291
Congenital tuberculosis with candidal sepsis in a neonate

Department of Microbiology, Lokmanya Tilak Municipal Medical College and General Hospital, Sion, Mumbai - 400 002, India

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About 300 cases of congenital tuberculosis have been reported in the world literature, nevertheless rarely with nonspecific clinical manifestations. Here, we report the case of a premature infant with congenital tuberculosis and septicemia due to Candida krusei, who was treated successfully.

Keywords: Candida septicemia, congenital tuberculosis

How to cite this article:
Wanjari K, Mathur M, Baradkar V P, Kumar S. Congenital tuberculosis with candidal sepsis in a neonate. Indian J Pathol Microbiol 2008;51:289-91

How to cite this URL:
Wanjari K, Mathur M, Baradkar V P, Kumar S. Congenital tuberculosis with candidal sepsis in a neonate. Indian J Pathol Microbiol [serial online] 2008 [cited 2021 Oct 18];51:289-91. Available from: https://www.ijpmonline.org/text.asp?2008/51/2/289/41701

   Introduction Top

Congenital tuberculosis is a rare disease with nonspecific signs and symptoms. If untreated, congenital tuberculosis is fatal, which underscores the importance of suspecting congenital tuberculosis in newborn and infants who are at risk and who have unexplained febrile illness. [1]

Making an early diagnosis of tuberculosis in an infant is difficult and requires a high index of suspicion. [2]

Candida septicemia is common in premature infants. Candida albicans is the commonest species followed by Candida glabrata, Candida parapsilosis a nd Candida krusei. [3] Here, we report a rare case of an infant suffering from congenital tuberculosis along with candida sepsis, which was treated successfully with antitubercular and antifungal drugs.

   Case History Top

A 2-day-old male premature infant (28 weeks) with a birth weight of 1.9 kg was brought to our hospital with fever, respiratory distress syndrome and hyperbilirubinemia. The baby was delivered at home.

This infant was admitted in the Neonatal Intensive Care Unit of our hospital. On examination, he was febrile with a heart rate of 136/min and respiratory rate of 32/min with a palpable liver.

His hemoglobin was 10.5 mg%, TLC 8800/mm 3 with a differential count of polymorphs 45% and lymphocytes 55%. His total bilirubin was 11.5 mg/dl; with direct bilirubin of 1.25 mg/dl and an indirect bilirubin of 10.27 mg/dl. His CSF sample was sent for culture, which revealed normal counts and no growth in culture. C-reactive protein in the serum was 30 mg/liter.

On day 1, he was started on I.V. Calcium gluconate, Aminophylline 1-9 mg, I.V. Amoxycillin + Clavulanic acid (100 mg/kg) and IV Amikacin (15 mg/kg).

On day 2, fluconazole 11mg OD, I.V. meropenem, Inj. dopamine, Inj. Phenobarbitone and Inj. Dobutamine were added. A gastric lavage was performed, which was sent for culture and acid-fast staining. Ziehl Neelsen staining of the fluid showed acid-fast bacilli. Culture for Mycobacterium tuberculosis was positive by the BACTEC MGIT 960 TB system, which later revealed a susceptibility to all the first-line anti-tubercular drugs. The blood culture and sensitivity were performed by the BACTEC system, which yielded the growth of Candida krusei, which was sensitive to Amphotericin B and resistant to fluconazole. Repeated blood culture was done by the conventional method using Brain Heart Infusion Broth (BHIB) as culture media, with blood collected aseptically from different sites repeatedly yielding Candida krusei . Repeated blood cultures and gastric lavage showed similar findings. As the infant was premature, with low birth weight and presented with respiratory distress syndrome (one of the commonest presentations of neonatal sepsis) along with the repeated isolation of Candida krusei from blood culture, a diagnosis of candida sepsis was made. A chest X-ray was performed, which showed multiple nodular opacities scattered in both the lungs, suggestive of miliary tuberculosis [Figure 1]. USG of abdomen showed hepatic granuloma. Based on all these findings, the infant was started with antitubercular treatment, i.e., INH 10mg/kg/day, Rifampicin 20m/kg/day, pyrazinamide 20mg/kg/day and Amphotericin B.

As gastric lavage, smear and culture were positive in early infancy, we suspected it as a rare case of congenital tuberculosis and a retrospective X-ray chest [Figure 2] and HRCT chest of the mother was performed, which showed signs suggestive of miliary tuberculosis [Figure 3], but repeated sputum samples did not reveal AFB and culture for AFB was also negative. The mother, however, refused for an endometrial biopsy. The mother's serum sample was tested for HIV antibodies after pretest counseling and was seronegative. To rule out the probable source of the neonatal candidiasis, the mother was investigated for vaginal candidiasis, but the mother had no symptoms of vaginal candidiasis and the cultures done for candida isolation from the vaginal swabs were negative.

The patient meanwhile responded to the treatment well, which was accompanied by a subsidence of fever and the respiratory distress. A repeat blood culture for fungus was performed after a few days of therapy, which turned out to be negative. After a few weeks of treatment, the baby was discharged on antitubercular therapy. The mother of the baby was also started on anti-tubercular therapy. Repeated follow-up of both mother and infant was done, which showed improvement.

As it was a home-delivered infant and then admitted to our hospital, we tried contact investigation (family screening), but no other source (person) with tuberculosis was found.

As the delivery was performed at home, the placenta was not available for examination and testing for tubercle bacilli or any further investigations. As the mother had miliary tuberculosis and the child was also a case of culture-proven tuberculosis and only 3 days old, we diagnosed this as a case of congenital tuberculosis with candida septicemia.

   Discussion Top

Congenital tuberculosis is a rare disease. [1] Despite the high incidence of tuberculosis in women of reproductive age group, sub-clinical forms of disease during pregnancy and lack of adequate antenatal care in countries with a low development rate, this incidence is expected at 2%, [4] with approximately 340 cases described in literature. [2] Some authors believe that undernotification of cases could explain the phenomenon. The appearance of AIDS has attributed toward an increase in the incidence of tuberculosis in women, thereby increasing the risk of congenital tuberculosis. There are few reports of congenital tuberculosis from India. [5],[6]

Making an early diagnosis in an infant is difficult and requires a high index of suspicion. [4],[5] Respiratory distress, fever and hepatomegaly are nonspecific symptoms and signs that may be present in bacterial sepsis and in other congenital infections such as Cytomegalovirus, herpes simplex virus, HIV, toxoplasmosis and syphilis. [1],[2],[4],[5],[6],[7],[8],[9] Similar presentation was there in our patient. Vilarinho [4] reported congenital tuberculosis in a 2-month-old male infant presenting with fever, dyspnea, anorexia, abdominal distension, anemia and papular erythematous rash. Cantwell et al [9] reported a 24-day-old male infant who presented with a 1-day history of respiratory distress syndrome, vomiting and poor feeding; and physical examination revealed hepatosplenomegaly. Chen et al[7] reported low-grade fever, cough, irritability, abdominal distension and hepatomegaly as presenting signs and symptoms of congenital tuberculosis. Congenital tuberculosis is thought to be acquired in one of the two ways: hematogenous dissemination of Mycobacterium tuberculosis may occur after rupture of a placental tubercle into the fetal circulation, leading to a primary hepatic complex. Alternatively, the fetus may aspirate or swallow infected amniotic fluid or maternal blood, either in utero or during passage through the birth canal, resulting in primary disease in the lungs or gastrointestinal tract. [7] As the determination of the location of primary complex requires open surgical procedures or autopsy, the mode of transmission often may not be determined. [6]

Tuberculosis should be suspected in an infant whose response to antibiotics and supportive therapy is poor. Acid-fast staining of smears and cultures are necessary to make a diagnosis. [7] Gastric aspirate, endotracheal aspirate, CSF, or biopsy tissue (liver or lung biopsy) is useful. In the present case, acid-fast organisms were detected in gastric lavage and the culture for Mycobacterium tuberculosis was positive. However, it is not rare that the diagnosis of infection in the infant leads to the discovery of tuberculosis in the mother, as happened in the present case. In the present case, we suspected tuberculosis in the mother retrospectively; and chest X-ray and CT scan were done, which showed findings suggestive of miliary tuberculosis. Similar findings were reported earlier. [6],[7]

Regarding the possible mode of transmission of tuberculosis, it was probably congenital in the present case because the mother had miliary tuberculosis during pregnancy. The infant came for medical attention in our institute after 3 days of birth, which was within the widest range (1-84 days) for congenital tuberculosis. [7] The mother was not examined for uterine tuberculosis and the placenta was discarded earlier. Due to the lack of open fibrocaseous tuberculosis in the mother and with her being sputum-negative, the airborne spread from her to the infant is unlikely. Transmission through milk was unlikely because the mother lacked findings suggestive of tubercular mastitis. The criteria for distinguishing congenital tuberculosis from postnatally acquired tuberculosis was established by Beitzke in 1935. [8] The criteria requires that the infant has proven tuberculosis lesions and one of the following: presentation of primary complex in the liver, tuberculous changes in affected fetus or infant within few days of birth, or exclusion of extrauterine source. 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[9] proposed a revised criteria, to increase the sensitivity for antemortem diagnosis.

The infant must have proven tuberculosis and at least one of the following: presentation of hepatic granuloma but not necessarily a primary hepatic complex or confirmation of tuberculosis in mother's genital tract and exclusion of postnatal exposure by contact investigation. In the present case, the infant came to us with respiratory distress syndrome; gastric aspirate showed AFB on both smear and culture, X-ray chest showed signs of tuberculosis and the USG abdomen showed hepatic granuloma. Contact investigation done in the present case to rule out other sources of infection symptoms of congenital tuberculosis may be present at birth, but more commonly begin by the second or third week, median age for presentation is 24 days (1-84 days). The signs and symptoms of congenital tuberculosis described are hepatomegaly (76%), respiratory distress (72%), fever (48%), lymphadenopathy (24%), lethargy or irritability (21%), papular skin rash (14%) and jaundice, vomiting, apnea, cyanosis, petechiae, seizures (<10% each). [1],[2],[3],[4],[5],[6],[7],[8],[9] In the present case, similar findings were noted.

The premature infants are prone for sepsis due to immaturity of the immune system. Other predisposing factors are low birth weight, patients on ventilators, patients on central venous catheter and long-term administration of antibiotics. [3] Premature infants with low birth weights have underdeveloped immune response and are hence predisposed to neonatal sepsis by Candida. Candida colonization of the gut starts soon after birth and the administration of antibiotics and other predisposing factors such as prematurity may cause spill-over of the organism into the blood and cause neonatal sepsis. This might have happened in the present case, as the mother was neither suffering from candidal vaginitis nor was she a carrier. [10] The presenting signs are pneumonia (most common), respiratory distress syndrome, meningitis, candiduria and candidemia. [3] Our patient presented with respiratory distress syndrome and candidemia. The clinical presentation is difficult to differentiate from bacterial sepsis. [3] The commonest species of candida known to cause neonatal sepsis are Candida albicans followed by Candida tropicalis, Candida parapsilosis, Candida krusei and Candida glabrata. In our case, Candida krusei was isolated from blood culture, which responded to Amphotericin B treatment, as the repeated blood cultures revealed no growth of Candida species.

To summarize, congenital tuberculosis is a rare disease that is difficult to diagnose due to nonspecific symptoms and a high index of suspicion is required for diagnosis in infants to reduce mortality.

   References Top

1.Snider DE, Bloch AB. Congenital tuberculosis. Tubercle 1984;65:81-2.  Back to cited text no. 1    
2.Crockett M, King SM, Kital I, Jamieson F, Richardson S, Malloy P, et al. Nosocomial transmission of congenital tuberculosis in neonatal intensive care unit. Clin Infect Dis 2004;29:1719-23.  Back to cited text no. 2    
3.Candidiasis in the newborn. Intensive care nursery House staff manual, UCSF Children's Hospital California; 2004. p. 128-30.  Back to cited text no. 3    
4.Vilarinho LC. Congenital tuberculosis: A case report. Braz J Infect Dis 2006;10:368-70.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Balasubramaniam S, Shivram R, Padmasani LN, Nagarju. Congenital tuberculosis. Indian J Pediatr 1999;66:148-50.  Back to cited text no. 5    
6.Ray M, Dixit A, Vaipei K, Singh PD. Congenital tuberculosis. Indian Pediatr 2002;39:1167-8.  Back to cited text no. 6    
7.Chan A, Shih SL. Congenital tuberculosis in two infants. Am J Rotenorol 2004;182:253-6.  Back to cited text no. 7    
8.Beitzke H. Ueber die angeborne. Tuberkuloese Infektion. Ergeb Gesarmten Tuberkulose Forch 1935;7:1-30.  Back to cited text no. 8    
9.Cantwell MF, Shehab ZM, Costello AM, Sands L, Green WF, Ewing EP, et al. Congenital tuberculosis. N Engl J Med 1994;330:1051-4.  Back to cited text no. 9    
10.Rao S, Ali V. Systemic fungal infections in the neonates. J Postgrad Med 2005;51:27-9.  Back to cited text no. 10    

Correspondence Address:
V P Baradkar
Department of Microbiology, LTMMC and LTMGH, Sion, Mumbai - 400 022
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.41701

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  [Figure 1], [Figure 2], [Figure 3]

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