In Mexico, the number of patients receiving tumor necrosis factor (TNF) blockers continues to grow. We report the case of a 32-year-old man with a history of rheumatoid arthritis, treated with methotrexate, folic acid, hydroxychloroquine and diclofenac for 3 months. Disease activity continued, so we decided to add infliximab (3mg/kg intravenously at weeks 0, 2 and 6, then every 8 weeks), after ruling out suspected latent tuberculosis with negative tuberculin testing and chest X-ray. These 2 aspects, along with the absence of criteria for immunosuppression, and his denial of contact with tuberculosis patients, were taken into account in the decision to not administer isoniazid prophylaxis. After receiving 7 infliximab infusions, the patient moved to New Zealand. Two weeks later he presented in a clinic with a 5-day history of fever 39°C, chills, mainly at night, accompanied by abdominal pain and distension, moderate constipation, and sensation of fullness. Abdominal tomography showed extensive ascites, nodular thickening in the serous membrane, and small mesenteric lymphadenopathies requiring a differential diagnosis with peritoneal cancer and lymphoma. Chest tomography revealed a small right pleural effusion. Ascitic fluid was obtained by abdominal needle aspiration, and incubated for 2 weeks in Mycobacterial Growth Indicator Tube (MGIT) medium. The culture grew an auramine-negative microorganism from the M. tuberculosis complex (MPT64 antigen-positive), later identified on polymerase chain reaction as pyrazinamide-resistant Mycobacterium bovis (M. bovis). QuantiFERON®-TB Gold determination was positive, and adenosine deaminase concentration in ascitic fluid was 66.3U/l. The patient improved after 2 months of treatment with isoniazid, rifampicin and ethambutol, and 7 months of rifampicin and isoniazid, and currently is free of signs and symptoms of active tuberculosis.
Drinking unpasteurized milk contaminated with M. bovis has been associated with tuberculous infection in humans,1 and most cases of peritoneal tuberculosis occur as a result of the hematogenous spread of latent TB.2
Tuberculosis is significantly under-reported in Latin America.3 In Mexico, 10% of cases of mycobacterial infection in immunosuppressed patients seen in tertiary hospitals are caused by M. bovis.4 A recent epidemiological study5 showed that the number of cases of tuberculosis caused by M. bovis in California, USA, rose from 3.4% in 2003 to 5.4% in 2011. It is interesting to note that between 2010 and 2011 either 1 or both parents or caregivers of children with M. bovis infection included in this study were born in Mexico.5
The prevalence of M. bovis in the vulnerable Mexican population must be determined, related risks must be identified, and these risks must be taken into account when deciding on the use of anti-TNF treatments.
I would like to express my thanks to the medical team of the Wellington Hospital, New Zealand, and in particular to Dr Alexis Frangouiles, treating physician in this institution, and to Dr Ketna Parekh, rheumatologist, and Drs Timothy Blackmore and James Taylor (infectious diseases). I would also like to thank our patient for his interest and willingness to share his case for medical and epidemiological purposes.
Please cite this article as: Rodríguez-Orozco AR. Reactivación de infección por Mycobacterium bovis, e inhibidores del factor de necrosis tumoral. El caso de México. Arch Bronconeumol. 2016;52:336–337.