A 58 year‐old male with recently diagnosed HIV presented with altered mental status in setting of six months progressive cognitive decline, visual hallucinations and paranoia. Patient reported subjective fevers, night sweats, weight loss, and diffuse pruritic rash. On presentation, the patient was somnolent; temperature 98.2, heart rate 95, BP 136/87, SpO2 100% on ambient air. Skin exam revealed diffuse hyperpigmented nodular rash. Neurologic exam revealed waxing and waning alertness, emotional lability, absent focal deficits or meningeal signs. Laboratory analysis revealed normal electrolytes, TSH, B12, folate, RPR/FTA‐ABS, urinalysis, and urine toxicology. Toxoplasma, cryptococcal, and JC Virus serologies were negative. HIV vial load was 1.2 million copies/mL, CD4 count was 2 cells/mL. MRI revealed diffuse white matter changes. LP performed; CSF studies were unrevealing. Blood cultures revealed Staphylococcus Aureus (MSSA) in 1 of 4 initial cultures and 2 of 4 repeat cultures. TTE revealed no valvular abnormalities. Patient was treated with Cefazolin for 6 weeks for presumed Infectious Endocarditis. Opportunistic infection prophylaxis initiated with Azithromycin and Bactrim. Antiretroviral medications were not initiated due to risk of Immune Reconstitution Syndrome. Prurigo Nodularis was treated with topical Triamcinolone. Patient’s mental status remained labile with intermittent aggressiveness, diagnosed as HIV‐associated dementia. Patient was discharged to skilled nursing facility. The patient presented two weeks later with fever to 102.6 and rigors. Infectious workup was unrevealing. AFB blood cultures from initial admission grew Mycobacterium avium complex. Clarithromycin, ethambutol and rifampicin were initiated. The patient defervesced and mental status resolved to baseline within a week.
Symptoms of disseminated mycobacterium avium complex (MAC) infection are non‐specific, including fever, diarrhea, and weight loss. Early diagnosis and treatment are challenging. To our knowledge, there exists no case report documenting disseminated mycobacterium avium complex infection presenting as progressive cognitive impairment. Furthermore, concomitant bacteremia with disseminated MAC infection has not yet been described in the literature. The patient’s significant cognitive improvement after the initiation of disseminated MAC strongly suggests disseminated MAC as the cause of his progressive cognitive decline. Disseminated MAC infection should be considered as etiology of neurocognitive decline or altered mental status in AIDS patients.
Disseminated mycobacterium avium complex infection can cause reversible dementia in AIDS patients.