Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organs. Infectious agents have been implicated in the pathogenesis of SLE. The emergent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces a pro-inflammatory cytokine storm and has been linked to autoimmune phenomena, which can lead to the onset of autoimmune diseases. We report the case of a 70-year-old patient who developed a toxic epidermal necrolysis (TEN)-like subacute cutaneous lupus (SCL) as a severe presentation of SLE, 1 month after SARS-CoV-2 infection. After excluding other causes of SLE, treatment was initiated with a successful outcome.

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The incidence and prevalence of nontuberculous mycobacterial disease is increasing due to enhanced clinician awareness and improved detection methods. The species identification using molecular microbiology techniques allows a better understanding of the differences in pathogenicity and treatment response. A 57-year-old man with a history of B-cell lymphoma in remission was transferred from the hematology department due to fever of unknown origin, night sweats and asthenia. The empirical antibiotic therapy was initiated with no clinical response, and he developed a subacute pneumonia, severe anemia and hepatosplenomegaly. After positive blood, bronchoalveolar lavage and bone marrow cultures, a disseminated Mycobacterium avium-intracellulare complex infection was diagnosed, and the patient began treatment with clarithromycin, rifabutin and ethambutol. Two weeks later, a fourth antibiotic was added, amikacin at first and then linezolid, with slow but gradual improvement. Due to amikacin-related severe kidney injury and linezolid-related severe myelosuppression, the fourth antibiotic was changed to moxifloxacin, which the patient tolerated. After 6 months of therapy, the sensitivity to the regimen was confirmed and the species was identified as Mycobacterium chimaera (MC), using the molecular genetic test GenoType NTM-DR. The blood and tissue cultures were negative after 4 months of therapy, and treatment was continued for 12 months. Although the infection was being treated successfully, the patient's B-cell lymphoma relapsed after 12 months and the patient died. This is a case report of a confirmed severe and disseminated MC infection in an immunocompromised patient using a molecular genetic test, successfully treated using a four-drug regimen.

Mycobacterium szulgai (MS) is a rare and slow-growing type of nontuberculous mycobacteria (NTM), with a human isolation prevalence of less than 0.2% of all NTM cases. MS may cause pulmonary infection, extra-pulmonary localized disease involving the skin, lymph nodes, bone, synovial tissue or kidneys and disseminated infection, when two or more organs are affected. When disseminated infection is present, the patients usually have an underlying immunosuppressive condition. The authors report the case of a 25-year-old patient with systemic lupus erythematosus, presenting with recurrent fever, non-productive coughing, weight loss and asthenia, as well as two violaceous plaques with superficial ulceration in the gluteal region. MS was isolated from the bronchial lavage and skin biopsy cultures, confirming the rare disseminated form of MS infection. After 10 months of follow-up on isoniazid, rifampin, ethambutol and pyrazinamide, no signs of relapse were evident. To date, only 16 other cases of MS disseminated disease have been reported.

A 72-year-old woman was admitted to the hospital because of dorsal, lumbar and lower abdomen pain that had started 4 days before. She had a history of age-related macular degeneration (treated with intraocular bevacizumab). Blood tests showed anaemia, thrombocytopaenia, acute kidney injury, elevated liver enzymes and total bilirubin (mainly because of the indirect fraction). Viral serologies and ADAMTS13 activity levels were normal, and stool testing was negative for Escherichia coli-producing Shiga toxins. E. coli was isolated in urine. Atypical haemolytic uremic syndrome triggered by a urinary tract infection or by the vascular endothelial growth factor-inhibitor bevacizumab were the most likely hypothesis. The patient started urgent plasmapheresis and dialysis that lasted for a total of 18 days. There was complete remission and recovery of kidney function allowing for treatment discontinuation, and she was discharged home. After 6 months of follow-up, she shows no signs of relapse.