On November 25, 2020, a 30-year-old woman with a 13-year history of systemic lupus erythematosus (SLE) exhibited painful leg swelling and was diagnosed with deep venous thrombosis (DVT). She was treated with enoxaparin, followed by an oral anticoagulant (warfarin). Her SLE initially presented as proteinuria, nephritis, and autoimmune hemolytic anemia was well-controlled and stable. She was treated during the last year with mycophenolate mofetil 250mg twice daily, prednisone 20mg/d, and hydroxychloroquine 200 mg/d. Several days following the development of DVT, the patient manifested symptoms of respiratory infection (subfebrile temperature up to 37.3 C, weakness, anosmia). She was tested (PCR of the nasopharyngeal swab) and found to be positive for SARS-CoV-2 on December 8. Due to the mild course of the disease, normal chest radiography, and good oxygen saturation of 99%, she was prescribed therapy and kept in home isolation. Nevertheless, the recovery from COVID-19 was not satisfactory as the patient complained of shortness of breath, persistent dull chest pain, extreme exhaustion, and tachycardia up to 130 bpm for weeks after the onset of the infection. She visited her immunologist on January 21, 2021. The laboratory analyses showed elevated inflammatory markers (CRP 27.5 mg/l [<5 mg/l]), d-dimer 3990 [<500], LDH 589 IU/l, WBC 8.3 x 109/l, Lymphocyte 0.4 x 109/l, and INR 1.93. Immunological analyses (Anti-nuclear antibodies -ANA, anti-Cardiolipin antibodies - aCLA IgM and IgG, anti-beta2 glycoprotein1 - anti-beta2GPI IgM and IgG, lupus anticoagulant - LAC) were negative, total serum IgM and IgG were in the normal range, while total IgA was 0.62 g/l [0.8-2.4]. Computed tomographic pulmonary angiography (CTPA) demonstrated massive pulmonary embolism with the clot at the main branching of the pulmonary artery. She was hospitalized and treated until discharge home on February 8. Due to an allergy to warfarin, she has been prescribed rivaroxaban as further therapy. Two weeks following hospital discharge, the patient's symptoms aggravated as she manifested morning fever up to 39 C, intense fatigue, dry cough, and chest pain. The persistence of these symptoms was the basis for admission to the pulmonology unit on March 12. On admission, she was slightly dyspneic with an oxygen saturation of 95% on room air. She had marked lymphopenia (0.3 x 109/l), elevated CRP (91.9 mg/l), normal procalcitonin (0.05 ng/ml), and anemia (hemoglobin 91 g/L) with high ferritin value (856 mug/l). Initial chest CT scan demonstrated a multilocular irregular cystic formation (45 x 35 x 45 mm) in the right middle lobe adjacent to the visceral pleura, surrounded by a "tree in buds" appearance. It also showed ground-glass opacities (GGO) in both inferior lobes and the right middle lobe with the posterolateral and subpleural distribution. We performed ultrasound-guided lung biopsy to obtain samples to refer to microbiology and cytology analyses. They showed dense infiltration with lymphocytes, erythrocytes, and neutrophils, without malignant cells, while the microbiological culture showed no growth of microorganisms. Fiberoptic bronchoscopy revealed normal findings, and the specimen demonstrated rare neutrophils and Pseudomonas spp. (over 1 million CFU/mL) sensitive to amikacin. Hemoculture was negative, and the infection with Mycobacterium tuberculosis was excluded with smear acid-fast staining, PCR, MGIT culture test, Quantiferon TB Gold blood test, and negative Lowenstein culture growth. Galactomannan antigen (serum and bronchoalveolar) were negative, while serum mannan antigen was positive. The patient was initially treated with broad-spectrum antibiotics (Meropenem and Vancomycin), with the subsequent addition of amikacin and caspofungin. During hospitalization, the patient developed a cephalic vein thrombosis while on anticoagulant therapy, and she was thoroughly investigated for thrombophilia. Her antithrombin III, protein C, and protein S were in the normal range, and Anti-Cardiolipin antibodies (IgG, IgM, IgA) were negative. At the same time, the genetic screening for mutations (factor V Leiden, factor II G20210A, MTHFR, PAI-1) revealed no variants typical for inherited thrombophilia. The patient gradually recovered and was discharged home on April 15. On April 30, she had an episode of seizures with loss of consciousness. She was urgently admitted to the isolation unit of the neurology department of a regional hospital since she tested positive for SARS-CoV-2 again. Brain computed tomography (CT) revealed a solitary lesion with perifocal edema in the right parietal lobe. Antiedematous and anticonvulsant therapy diminished the neurological symptoms, and the patient was planned for referral to a tertiary center for further diagnostics and treatment. It was postponed as she tested positive again, and ordered home isolation. On June 15, the patient underwent brain magnetic resonance imaging (MRI). It showed a 4.6 x 4.3 x 3.9 cm multilocular lesion in the right frontoparietal region with a mass effect on the adjacent lateral ventricle (Figure 1). She tested positive for SARS-CoV-2 the same day and was denied admission to the neurosurgical clinic that offered no isolation ward. Instead, the patient was sent to a COVID hospital. At the time of admission, her symptoms were dry cough, stuffy nose, and mild left-sided weakness. Neurological examination showed subtle left side hemiparesis, right arm pronator drift, positive Mingazzini, and negative Romberg test. Laboratory workup revealed pancytopenia and normal tumor markers. Four days later, the neurological symptoms progressed with the development of holocranial headache, nausea, vomiting, and worsening of hemiparesis. An urgent CT of the brain was done, demonstrating enlargement of the perilesional edema with the shift of midline structures and completely effaced right lateral ventricle. A small lesion with perifocal edema was observed in the left occipital lobe. Right-sided compression of the mesencephalon suggested an imminent transtentorial uncal herniation. The patient was sent for emergency surgery on June 21 as she rapidly deteriorated with the development of a coma and right pupilar dilatation. The thick-walled multilocular abscess was found at surgery, and total excision was performed. Pus aspirated from one of the abscess collections was sent for gram staining and culture. The remaining was sent to histopathology. After the operation, the patient was transferred to the intensive care unit and started treatment with broad-spectrum antibiotics. Her postoperative laboratory was remarkable for severe thrombocytopenia, anemia, hypogammaglobulinemia, and low CD4 lymphocyte count (24/muL). Human immunodeficiency virus infection (HIV) was excluded by repeated testing. She was administered intravenous immunoglobulins (0.4 g/kg daily for 5 days). Hematoxylin-eosin staining revealed necrotizing granulomas, while the histochemical Grocott Methamine Silver staining highlighted the filamentous branching rods (Figure 2). Smears from cultures demonstrated gram-positive, partially acid-fast filaments, and the growth of Nocardia species. She was started on meropenem (3 x 2g) and trimethoprim/sulfamethoxazole (TPM/SMX; 960/4800 mg) via intravenous route while waiting for species determination and susceptibility testing. To transfer the patient to a non-COVID tertiary neurosurgical hospital, we tested her for SARS-CoV2 again, and the PCR result was positive. Final identification of Nocardia cyriacigeorgica was performed with matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS). The susceptibility testing showed that the agent was susceptible to trimethoprim/sulfamethoxazole (TMP/SMX), ceftriaxone, cefotaxime, imipenem, and linezolid. The test demonstrated resistance to ampicillin, amoxicillin/clavulanate, and fluoroquinolones. TPM/SMX was continued as monotherapy after 3 weeks. Neurological deficits before surgery gradually resolved, and the CT of the brain showed significant improvement. Over the next 5 weeks, the patient was tested for SARS-CoV2 seven times, and the result was always positive (Figure 3). The serum sample was tested for antibodies against the spike protein of the virus, and no antibodies were detected. The patient was discharged home on July 30 on an oral TPM/SMX (160/800 mg) for at least 12 months. We decided to prescribe a prolonged course of TPM/SMX because her control CD4 was still low (79/muL), and she needed to continue corticosteroid therapy (prednisone 10mg/d) for SLE. On a follow-up as an outpatient after 1 month, 3 months, and 6 months the patient was in an excellent clinical state, fully active, with no symptoms and neurological deficits.