Abstract Pneumocystis jirovecii pneumonia (PJP) is an opportunistic fungal infection that causes severe, life-threatening pneumonia in immunocompromised individuals. The incidence of PJP has declined considerably since the introduction of combination antiretroviral therapy (ART). PJP, which once occurred in 70-80% of people with HIV, is now present in fewer than 1 case per 100 patient-years. Hospitalization rates for PJP in AIDS have also dropped from 31% in the 1980s to less than 3.5% in 2014. Most contemporary series show PJP still occurs as presentation but in a smaller fraction (10%) of all new HIV cases. Here we describe a case of severe PJP complicated by coinfection with Mycobacterium avium complex (MAC) and drug induced thrombocytopenia.A 33-year-old woman with no known HIV history presented with worsening dyspnea and hypoxemia. Two months earlier, she had been treated for community-acquired pneumonia but had persistent respiratory symptoms. On arrival, she was in acute hypoxemic respiratory failure with oxygen saturation in the low 74%. Chest radiograph revealed bilateral moderate-to-large pneumothoraces, and she was intubated with bilateral chest tubes. Computed tomography showed a 5.6-cm thin-walled cavitary lesion in the left lower lobe and multiple bilateral blebs. HIV testing was positive, CD4 90, β-glucan 370, and bronchoscopy confirmed PJP. She was started on sulfamethoxazole-trimethoprim (TMP-SMX) but developed profound thrombocytopenia within days, which resolved after discontinuation and transition to clindamycin and primaquine. She underwent right thoracoscopic drainage of mediastinal air and fluid collection, wedge resection of right upper lobe, and right talc pleurodesis. Due to persistent air leak and ventilator dependence she required tracheostomy. Lung biopsy later grew MAC and started on rifabutin, ethambutol, and azithromycin. PJP remains one of the most frequent opportunistic infections leading to an initial diagnosis of AIDS in individuals with previously unrecognized HIV infection. Spontaneous pneumothorax occurs in about 2-6% of PJP cases, while bilateral involvement is exceedingly uncommon. Concomitant MAC infection is exceedingly rare, with only isolated case reports describing dual infection. In this patient, the coexistence of PJP and MAC likely contributed to extensive lung destruction, recurrent bilateral pneumothoraces, and prolonged critical illness. The additional development of severe TMP-SMX-induced thrombocytopenia—a typically mild and infrequent adverse event—further complicated management. TMP-SMX, the cornerstone of PJP therapy, can rarely cause severe thrombocytopenia, estimated at approximately 2 cases per 1000 patient-years. This case underscores the importance of maintaining a broad infectious differential in severely immunocompromised patients. This abstract is funded by: None
Allonce et al. (Fri,) studied this question.