A 3-year-old boy presented with a 3-day history of inability to pass stools, abdominal swelling and bile-stained vomiting. His mother had a history of substance abuse. The pregnancy and delivery had been un-booked. She was diagnosed HIV-positive post-partum and started on antiretroviral therapy (ART). Infant antiretroviral prophylaxis was prescribed for the child. It is not known whether HIV testing of the infant at the time of birth was performed. The mother defaulted her ART and her infant's ARV prophylaxis. The child had no history of contact with a TB source case.
On examination, the child had abdomen distension. He was in shock, pale and severely underweight. The HIV antibody test was positive on two separate samples. The CD4+ lymphocyte count on admission was 56 cells/mL (15%), haemoglobin (Hb) was 5 g/dL and the platelet count was 114 x 109/L. The chest X-ray did not suggest pulmonary TB. Sputum gene Xpert Mycobacterium tuberculosis (MTB)/RIF Ultra was positive for rifampicin-sensitive MTB. The sputum culture grew rifampicin- and isoniazid-sensitive TB. Abdominal radiography and ultrasonography showed distended small-bowel loops with no gas in the rectum, consistent with small-bowel obstruction (Figure 1).
The child was given a blood transfusion and was resuscitated. At laparotomy 3 days after admission, three small-bowel perforations with faecal soiling of the abdominal cavity and 'caseous areas' of the ileum, ascending colon, mesenteric and retroperitoneal lymph nodes were identified. The abdomen was washed with saline and the perforations closed. Histology of the intra-abdominal nodes showed necrotising granulomatous inflammation.
The child was commenced on IV rifampicin, IV moxifloxacin and IV amikacin. On day 3, his creatinine concentration increased from 61 micromol/L to 133 micromol/L. Amikacin was stopped and moxifloxacin dose was adjusted according to the estimated glomerular filtration rate (eGFR) of 26.6 mL/min/1.73 m2. Intravenous meropenem and IV linezolid (LZD) were started. The patient's renal function normalised in the following 12 days. The platelet count and the Hb levels declined, and LZD was discontinued after 10 days. On day 20, ART, namely, IV zidovudine (ZDV or AZT), oral lamivudine (3TC) solution, oral lopinavir or ritonavir (LPV/r) solution and oral ritonavir solution to 'super-boost' the LPV, was introduced. The plasma LPV 'trough' concentration 1 week after starting the ART was therapeutic, namely, Cmin 9.98 mg/L. By day 30, he was tolerating small oral feeds. Intravenous meropenem was stopped and oral isoniazid was started. On day 40, he was settled on oral feeds, and oral rifampicin/isoniazid, pyrazinamide and ethambutol tablets replaced the IV rifampicin and IV moxifloxacin. Intravenous AZT was replaced with abacavir. Liver transaminases had not been significantly altered by the TB therapy or the ART. Four weeks after starting TB treatment, sputum culture was found negative for MTB. Four months after starting ART, the HIV viral load was < 100 copies/mL, and at 12 months the CD4 count was 1111 cells/mL (25%). In total, the patient received approximately 11 months of oral anti-TB therapy. His weight-for-age Z-score 3 months after the completion of the TB treatment was within the normal range, that is, above -2. This had been less than -3 before starting the treatment.