We report the case of a 10-year-old male patient with bone marrow aplasia secondary to Fanconi anemia who was initially admitted for febrile purulent tonsillitis (no throat culture was performed before antibiotic initiation). Despite several courses of broad-spectrum antibiotic therapy, the clinical course was marked by persistent fever and progressive right-sided orbitofacial cellulitis. Imaging revealed extensive involvement of the right maxillary sinus with orbital extension. The appearance of a necrotic black palatal lesion (eschar) in the setting of profound immunosuppression is highly characteristic, if not pathognomonic, of invasive mucormycosis. Liposomal amphotericin B (5 mg/kg/day) was initiated; however, surgical debridement could not be performed due to severe thrombocytopenia (platelet count of 1,000/mm³). The patient subsequently developed septic deterioration requiring intensive care management and ultimately died. This report highlights the diagnostic challenges and the rapidly progressive course in a severely immunocompromised pediatric patient and emphasizes the importance of early recognition and prompt initiation of antifungal therapy, although management may remain limited in patients with profound cytopenia in whom surgical treatment is not feasible.

Non-tuberculous mycobacteria are increasingly recognized as opportunistic pathogens in solid organ transplant recipients, most commonly causing cutaneous, pulmonary, or disseminated disease. Primary perinephric involvement without evidence of dissemination is exceptionally rare. We report the case of a 34‑year‑old male renal transplant recipient who presented eight months post‑transplant with right iliac fossa pain and fever following minor trauma. Imaging revealed a perinephric collection initially suspected to be a hematoma. Routine bacterial cultures were sterile, and procalcitonin levels were low. Acid‑fast bacilli were detected on the smear, and mycobacterial culture identified Mycobacterium abscessus, a rapidly growing non‑tuberculous mycobacterium. The patient was successfully managed with percutaneous drainage and a tailored multidrug antimicrobial regimen, avoiding aminoglycosides to preserve graft function, although management was complicated by significant drug‑related toxicities and immunosuppressant interactions. This case highlights the importance of considering non‑tuberculous mycobacterial infection in culture‑negative perinephric collections in immunocompromised hosts and underscores the diagnostic and therapeutic challenges posed by Mycobacterium abscessus in renal transplant recipients.

Catheter-related bloodstream infections (CRBSIs) remain a serious complication in patients with hematologic malignancies, regardless of the causative microorganism, although Staphylococcus aureus remains an important pathogen because of its potential for rapid progression and metastatic complications. This report details the case of a 58-year-old man receiving immunochemotherapy for diffuse large B-cell lymphoma who developed fulminant sepsis 72 hours following the implantation of a totally implantable venous access port. The patient presented with high-grade fever, acute confusion, and local signs of port-site infection. Blood cultures confirmed methicillin-susceptible S. aureus bacteremia consistent with a catheter-related source. The diagnosis of secondary acute bacterial meningitis was confirmed by cerebrospinal fluid analysis and culture. Despite prompt initiation of empirical antimicrobial therapy, de-escalation to targeted anti-staphylococcal therapy, and catheter removal, the patient's condition rapidly deteriorated, and the patient died of refractory septic shock. This case highlights the aggressive progression and high mortality associated with S. aureus CRBSI complicated by hematogenous meningitis in immunocompromised patients and illustrates the importance of early recognition, prompt microbiological diagnosis, immediate source control, and vigilant clinical monitoring following catheter placement.

An 80-year-old male patient on maintenance hemodialysis was admitted with "high fever and cough." Pulmonary imaging suggested pneumonia, but his condition deteriorated rapidly despite empirical broad-spectrum antimicrobial therapy (covering bacteria, atypical pathogens, and fungi), progressing to respiratory failure and delirium. He was transferred to the intensive care unit for continuous renal replacement therapy. Routine microbiological tests (blood culture, sputum culture, respiratory pathogen PCR) were all negative. Detailed history revealed that the patient had kept a parrot for over a month prior to illness onset. Metagenomic next-generation sequencing of blood and sputum specimens detected abundant Chlamydia psittaci sequences. Following confirmation, treatment was adjusted to oral minocycline combined with intravenous azithromycin. The patient's temperature gradually normalized, neuropsychiatric symptoms resolved, and pulmonary imaging showed marked improvement, ultimately leading to successful discharge. This case highlights the importance of considering zoonotic pathogens in immunocompromised patients with refractory pneumonia. Detailed history-taking and metagenomic next-generation sequencing (mNGS) technology are crucial for early diagnosis. Early use of mNGS should be strongly considered in immunocompromised patients with severe pneumonia unresponsive to empiric therapy and negative routine workup, particularly when epidemiological clues such as bird exposure are present.

Hantaviruses are enveloped, negative-sense RNA viruses. Rodents serve as natural reservoirs, and spillover into humans causes hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome. While transmission typically occurs by inhaling aerosolized rodent excreta, the Andes virus variant is capable of human-to-human transmission. A recent outbreak involving a person-to-person transmission cluster aboard the cruise ship MV Hondius has underscored the urgency of hantavirus preparedness. Immediate global pandemic risk remains low because sustained transmission requires prolonged close contact, and hantavirus has low environmental stability compared to other RNA viruses with pandemic potential. However, climate change, deforestation, and urbanization increase human-rodent interactions and spillover risks. Additionally, prolonged incubation in immunocompromised individuals, including people with Human Immunodeficiency Virus (PWH) and other chronic conditions, may facilitate viral adaptation, potentially leading to strains with enhanced transmissibility. We review hantavirus classification, epidemiology, transmission dynamics, immunopathology, treatment strategies, the urgent need for global surveillance, and accelerated vaccines and prophylactic development.

A man in his 40s who takes adalimumab for Crohn's disease presented with a 1-day history of fever, headache and rapid onset of agitation with reduced consciousness. He was intubated, and a subsequent lumbar puncture revealed severe Streptococcus pneumoniae meningitis. He was started on antibiotics and steroids; however, on sedation hold, he demonstrated abnormal posturing. Neurological imaging revealed extensive cerebral venous sinus thromboses (CVSTs). He was started on a heparin infusion and transferred to a tertiary neurological centre, where he was managed with a split treatment dose of enoxaparin and a 2-week course of IV ceftriaxone. He was extubated on day 4 of admission and made rapid improvements in cognition and function. This case highlights the importance of considering rare neurological complications in cases of severe meningitis in patients who are immunocompromised, as well as recognising CVSTs as a rare but potentially fatal complication in those with pneumococcal meningitis.

Mycobacterium szulgai is a rare, slow-growing non-tuberculous mycobacterium (NTM), accounting for less than 0.2% of NTM isolates worldwide. It most often presents with pulmonary disease resembling tuberculosis, while disseminated infection is exceptionally uncommon and typically occurs in immunocompromised hosts. We report a 34-year-old male newly diagnosed with advanced HIV infection who presented with painful cutaneous nodular lesions, intermittent fever, anorexia, and significant weight loss. Initial investigations suggested cutaneous nocardiosis or fungal infection, with cultures yielding Aspergillus niger and Corynebacterium species. Despite antifungal and antibacterial therapy, his condition progressed to multifocal cutaneous lesions, oral mucosal involvement, and osteomyelitis of the tibia and fibula. An extended microbiological evaluation of a bone biopsy revealed acid-fast bacilli, and cultures identified M. szulgai via rpoB gene sequencing and matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry (MS). Further imaging and bronchoalveolar lavage confirmed disseminated infection involving lungs, skin, and bone. The patient was treated with rifampicin, ethambutol, and moxifloxacin in combination with antiretroviral therapy. After six months, complete resolution of cutaneous lesions, regression of pulmonary nodules, and normalization of inflammatory markers were achieved. Therapy was planned for 12-18 months. This case underscores the diagnostic complexity of disseminated M. szulgai infection in advanced HIV. Initial misinterpretation as nocardiosis or fungal disease delayed diagnosis, highlighting the importance of extended microbiological workup when conventional therapies fail. Definitive identification through molecular sequencing and MALDI‑TOF MS was crucial. The patient's favorable response to a rifampicin‑based multidrug regimen emphasizes the need for early recognition and prolonged therapy. This report contributes to the limited literature on disseminated M. szulgai and reinforces the importance of considering atypical mycobacteria in immunocompromised patients.

While spinal epidural abscess (SEA) is a well-recognized neurosurgical emergency, its diagnosis remains a formidable challenge when presenting with atypical symptoms such as dysphagia, particularly in patients under anti-tumor necrosis factor (TNF) therapy. This report describes a critical diagnostic trap: a fulminant cervical SEA in a 59-year-old male patient treated with infliximab for ankylosing spondylitis. Despite being afebrile and neurologically intact upon admission, laboratory investigations revealed a massive inflammatory syndrome (C-reactive protein: 282.9 mg/L). His condition rapidly progressed to sudden tetraplegia during diagnostic imaging. MRI confirmed C3-C4 spondylodiscitis with a massive prevertebral and spinal epidural abscess causing critical cord compression (5 mm residual canal). The patient underwent emergency C3-C4 anterior discectomy and abscess drainage. Despite the successful eradication of the methicillin-susceptible Staphylococcus aureus (MSSA) infection, the patient suffered permanent neurological deficits. This case highlights the potent masking effect of anti-TNF therapy on systemic inflammatory signs and the diagnostic challenge of SEA presenting as dysphagia. It underscores that in immunocompromised patients, the absence of fever must not rule out severe infection when neck pain and elevated inflammatory markers are present. Clinicians must maintain a low threshold for emergency MRI, as the therapeutic window for intervention is exceptionally narrow once fulminant neurological deficits manifest.

Capnocytophaga canimorsus is a gram-negative, anaerobic bacillus commonly found in the oral flora of dogs and cats. While often transmitted through animal bites or scratches, severe infections can occur even without documented exposure, particularly in immunocompromised individuals such as asplenic patients. Although rare, mycotic aneurysms caused by C. canimorsus are associated with high mortality. We report the case of a 53-year-old male with a history of splenectomy due to diffuse large B-cell lymphoma, currently in remission, who presented with malaise, fever, dyspnea, and abdominal pain. He rapidly progressed to septic shock and multiorgan failure, including coagulopathy consistent with disseminated intravascular coagulation (DIC). Despite broad-spectrum antibiotics and intensive support, the patient died within hours of admission. Blood cultures later confirmed C. canimorsus bacteremia. Postmortem examination revealed a ruptured aortic aneurysm. This case highlights the fulminant progression of C. canimorsus infection in an asplenic patient, culminating in a fatal aortic aneurysm rupture. Notably, there was no history of animal exposure, reinforcing the need for high clinical suspicion, especially in high-risk populations. Although empiric therapy with beta-lactam/beta-lactamase inhibitors is recommended, early recognition and possible surgical intervention remain crucial for survival. Infections caused by C. canimorsus should be considered in septic patients with risk factors such as splenectomy, even in the absence of animal contact. Rapid deterioration and rare complications, like aortic aneurysm rupture, underscore the importance of early diagnosis and aggressive multidisciplinary management.

Cytomegalovirus (CMV) infections are common worldwide, with clinical manifestations varying from asymptomatic infections in healthy people to life-threatening end-organ dysfunction in immunocompromised patients. Acute CMV infection has been associated with venous thrombosis in immunocompetent patients. We present a rare case of acute superior mesenteric vein (SMV) and portal vein thrombosis in an immunocompetent patient with acute CMV infection. A 28-year-old patient with a past medical history of obesity presented with two days of sharp, 9/10 left upper quadrant (LUQ) pain that radiated to the back, associated with subjective fevers, nausea, and loose stools. The patient was tachycardic, febrile, and tachypneic. Physical examination revealed LUQ tenderness to superficial and deep palpation. Laboratory findings showed leukocytosis with lymphocytic predominance as well as transaminemia. CT of the abdomen/pelvis revealed SMV and portal vein thrombosis, hepatomegaly, and splenomegaly with multiple splenic infarcts. The thrombophilia workup was negative. CMV testing showed positive IgM. CMV polymerase chain reaction was elevated at 1,222 log IU/mL. He was started on ganciclovir and improved clinically. He was discharged on oral ganciclovir and warfarin. This case report emphasizes that, in an immunocompetent patient presenting with acute deep vein thrombosis at unusual sites, a negative thrombophilia workup, and after excluding other risk factors, CMV infection as a triggering etiological factor should be considered.

Coccidioidomycosis is a pulmonary disease caused by the dimorphic fungus Coccidioides, which is endemic to the southwestern United States and South America. Coccidioides grows as septate hyphae in soil and forms spores that can become airborne during mechanical disruption of the soil. In the lungs, the inhaled spores develop into large multinucleated spherules, a unique morphology among medically important Coccidioides species, and reproduce by endosporulation. A hallmark of the host immune response toward endosporulating spherules is the robust recruitment and infiltration of Ly6G[+] neutrophils. However, the effectiveness of Ly6G[+] neutrophils against Coccidioides remains to be studied. Myeloid-derived suppressor cells (MDSCs) are immunosuppressive and share an origin and many phenotypic features with neutrophils. Here, we demonstrated that Ly6G[+] cells, but not Ly6C[+] cells, increased lung expression of the inhibitory programmed death-ligand 1 (PD-L1) in diseased mice. The Ly6G[+]PD-L1[+] cells share common characteristics of granulocytic MDSCs. Bone-marrow-derived GR-1[+] myeloid cells, including both Ly6G[+] and Ly6C[+] cells, suppressed the proliferation of CD4[+] T cells after exposure to spherules. Furthermore, isolated GR-1[+] cells from the lungs and spleens of Coccidioides-infected non-protected mice also suppressed CD4[+] T cell proliferation, thereby diminishing adaptive T cell responses. Adoptive transfer of GR-1[+] myeloid cells isolated from the lungs of Coccidioides-infected mice, or derived from bone marrow exposed to paraformaldehyde-killed spherules, into vaccine-protected recipients exacerbated coccidioidomycosis through the reduction of protective Th1 and Th17 responses. Altogether, we demonstrate that pulmonary infiltration of MDSC-like neutrophils, in non-vaccinated mice, play a detrimental role in coccidioidomycosis by inhibiting protective CD4[+] T cell responses.