WHO estimates that 8 to 10 million new cases of tuberculosis occur worldwide each year. The disease is responsible for nearly 2 million deaths per year, including 300,000 children. Nearly 60% of cases occur in Africa, where children account for 20% to 25% of cases [1] [2] . Over the last decade, the incidence of tuberculosis has increased, particularly in Africa. This increase is attributed to several factors: the deterioration of the social situation, the mixing of populations linked to armed conflicts, the low capacity of national anti-tuberculosis programs and, above all, the spread of HIV infection [3] [4] . Because of their relative fragility and inescapable contact with adults, children are a prime breeding ground for tuberculosis. However, the diagnosis of childhood tuberculosis, even in its pulmonary form, has been and remains difficult, especially in developing countries, due to the lack of effective means. As if that weren’t enough, the HIV pandemic has altered the epidemiological, clinical and paraclinical profile of tuberculosis throughout the world, presenting the scientific community with numerous challenges, the main ones being the difficulties of diagnosis, treatment and infection control. In countries with limited resources, the number of reported cases of TB-HIV co-infection is constantly increasing, with HIV prevalence among TB-infected children ranging from 10% to 60% [5] . In Mali the frequency of TB-HIV association was estimated at 13% in 2015 (all ages combined) [2] . No case of rifampin-resistant TB-HIV co-infection has ever been reported in an infant in Mali. We report the first case of HIV-tuberculosis pulmonary coinfection resistant to rifampicin in a 19-month-old infant diagnosed at the Pediatrics Department, distric VI Reference Health Center.

This was a 19-month-old male infant admitted to the department for altered general condition and consciousness. He was the second of two siblings, born of a full-term pregnancy, poorly monitored, vaginal delivery with no notion of resuscitation. Breast-feeding was mixed before 6 months, then supplemented by the family dish from 6 months. His psychomotor development was behind his age (he was not yet walking, and his language was only monosyllabic). The family had a low socioeconomic status, no known medical or surgical history, and no history of tuberculosis. According to the story, the onset of the illness was around 10 months ago, marked by fever, cough, dyspnea, anorexia and progressive weight loss, for which the parents had used conventional and traditional medicine without success. As the symptoms persisted, he was referred to us for better management. On initial physical examination, his temperature was 39.9 degree Celcius, he weighed 5.9 kg for a height of 73 cm and a weight/height ratio < −3 Z score indicating severe acute malnutrition. Heart rate was 124 beats/min. He presented with marked paleness of the mucous membranes and severe oral mycosis. Respiratory symptoms included respiratory pauses, respiratory rate 68 cycles/min, intercostal tugging, nasal flaring, oxygen saturation 81% on room air, and crepitus rales in both lung fields. Neurologically, consciousness was impaired, with a Blantyre score of 3. Faced with this picture of pallor, respiratory distress and altered consciousness against a background of severe malnutrition, further investigations (paid for by the parents) were carried out: the blood count showed severe normocytic hypochromic anaemia at 5 g/dl, hyperleukocytosis (18,700/mm³) with neutrophil predominance; hepatic transaminases and creatininaemia were normal; thick drop and malaria RDT were negative; the frontal chest X-ray showed unsystematized parenchymal opacities (Figure 1); HIV serology was positive for HIV1; GeneXpert^® had moderate detection (2+) of Mycobacterium tuberculosis (MTB) with rifampicin resistance (RR). In view of these findings, the diagnosis of HIV1-rifampicin-resistant pulmonary tuberculosis was adopted. Therapeutically, the patient was admitted to the intensive care unit, where he received suctioning, oxygenation and F75 therapeutic milk via nasogastric tube. Antibiotic therapy including Amoxicillin/clavulanic acid 200 mg/kg/day

in 3 intravenous doses and cotrimoxazole 30 mg/kg/day orally was initiated for 10 days without success. Following the diagnosis of tuberculosis and a multidisciplinary consultation between pediatricians and infectiologists, an anti-tuberculosis treatment including 2nd-line drugs was initiated. It combined Bedaquiline (50 mg/d), Moxicillin (10 - 15 mg/kg/d), Linezolide (15 mg/kg/d) + Clofazimine (2 - 5 mg/kg/d), Cycloserine (15 - 20 mh/kg/d) per os through the nasogastric tube. HIV treatment was deferred.

The evolution was marked by persistent fever and worsening respiratory distress. After 30 days of hospitalization and 7 days of anti-tuberculosis treatment, the infant died in respiratory distress.

TB-HIV co-infection is common in children, but remains under-diagnosed. Diagnosis by molecular biology not only provides a diagnosis of certainty, but also looks for antibiotic resistance. Rifampicin-resistant TB-HIV co-infection is rare in children in our context, and especially in infants. Early management before nutritional complications allows simultaneous treatment of tuberculosis and HIV, and is the only survival gas. Efforts are still needed to achieve earlier diagnosis, and the implementation of Prevention of Mother-to-Child Transmission (PMTCT) would be the best strategy for avoiding HIV infection in children.

The information gathered from this patient’s medical record for the writing of this article has been kept confidential.

The authors declare that they have no conflict of interest in relation to this publication.

Maiga, M., Togo, P., Simaga, T., Traoré, M., Konaté, M., Diallo, M., Samaké, A., Keïta, M., Diallo, K.W. and Kassogué, D. (2024) Resistant Pulmonary TB-HIV Co-Infection in an Infant: About a Case. Open Journal of Pediatrics, 14, 420-425. https://doi.org/10.4236/ojped.2024.142041