搜索结果：Case reports in infectious diseases

Temporal responses of serum iron and ferritin in COVID-19 infection and vaccination remain insufficiently characterized. This case report presents their timeline after SARS-CoV-2 and influenza vaccinations and may serve as a model for future studies. The approach can be extended to cohort studies or investigations of other acute-phase reactants. A vaccination protocol with a defined timeline can provide a template for COVID-19 and long COVID studies. Blood samples were collected from vaccination through 6 weeks postvaccination, focusing on iron metabolism. Prevaccination values served as baseline controls. SARS-CoV-2 mRNA vaccination was administered together with routine seasonal influenza vaccination. Previous influenza vaccinations in this patient were not associated with systemic symptoms such as dizziness or fever; in contrast, the present case exhibited clear reactions, suggesting that the observed alterations in serum iron and ferritin are attributable to the SARS-CoV-2 vaccine. The vaccination induced an abrupt decrease in serum iron and a concomitant increase in ferritin. While ferritin returned to baseline within 6 weeks, iron levels steadily increased to approximately 1.8-fold above baseline values but remaining within the reference interval. The observed decrease in serum iron reflects an iron-withholding response, a well-established host defense mechanism during infections that limits pathogen proliferation. The increase in ferritin requires further interpretation. A hypothesis is presented, but further data are needed to support this mechanism. In future cohort studies, the protocol should include individual prevaccination values so that an additional control group is not necessary. Immune reactions to vaccines can trigger transient changes in serum iron and ferritin that resemble the acute-phase response observed during infections. This case may serve as a template for studying the kinetics of immune responses, where t = 0 is defined by the vaccination time and each patient serves as own control when prior data are available.

Cryptococcal meningitis is a life-threatening opportunistic fungal infection predominantly seen in immunocompromised hosts, yet it is increasingly recognized in apparently immunocompetent individuals. In tuberculosis-endemic regions, its diagnosis is frequently delayed or missed due to overlapping clinical and cerebrospinal fluid findings with tuberculous meningitis. A 44-year-old immunocompetent woman presented with a two-month history of progressive diffuse headache and subjective bilateral lower limb weakness. Neurological examination was unremarkable, and initial cerebrospinal fluid analysis revealed marked hypoglycorrhachia (1 mg/dL), elevated protein (356 mg/dL), and lymphocytic pleocytosis. Brain imaging showed leptomeningeal enhancement without mass lesions. Despite negative microbiological testing for tuberculosis, empirical antituberculous therapy was initiated based on presumptive tuberculous meningitis. Pulmonary imaging demonstrated cavitary nodules and calcified lymph nodes. Lack of clinical improvement prompted further investigation; India ink staining and fungal culture of cerebrospinal fluid eventually confirmed Cryptococcus neoformans infection. The patient had no evidence of HIV, diabetes, or other immunosuppressive conditions. Induction therapy with liposomal amphotericin B and fluconazole was administered, followed by consolidation and maintenance fluconazole. She showed marked clinical and cerebrospinal fluid improvement and was discharged on oral fluconazole with sustained recovery. This case illustrates the diagnostic challenge of cryptococcal meningitis in immunocompetent patients, particularly in settings where tuberculous meningitis is common. Early reliance on India ink staining and fungal culture is essential when initial tuberculosis workup is negative or when response to antituberculous therapy is poor. The incidental detection of HHV-6 DNA likely represented viral reactivation without clinical significance. Cryptococcal meningitis must be considered in immunocompetent patients presenting with chronic meningitis, even in the absence of classic risk factors. Prompt mycological investigation can prevent diagnostic delays and improve outcomes.

Antituberculous drugs carry substantial hepatotoxic risk, most commonly manifesting as idiosyncratic drug-induced liver injury. Although cases of antituberculosis drug-induced liver injury (AT-DILI) have been reported in Ghana, significant challenges remain in its diagnosis, monitoring, and management in low-resource settings. We report the case of a 50-year-old woman who developed severe AT-DILI, initially misdiagnosed as cholecystitis, on a background of chronic hepatitis C infection with established liver cirrhosis. She was referred to the Tamale Teaching Hospital during the continuation phase of first-line antituberculosis therapy, presenting with nausea, anorexia, and right upper quadrant abdominal pain. A clinical examination revealed mild pallor, jaundice, Grade 1 bilateral pitting pedal edema, and moderate ascites. At the referral facility, diagnostic and monitoring constraints were encountered, including the unavailability of liver biopsy, the lack of routine baseline liver function testing, and out-of-pocket costs for serial laboratory monitoring. In addition, the absence of single-drug formulations of isoniazid and rifampicin precluded sequential rechallenges, necessitating rechallenges with a fixed-dose combination during the continuation phase. The patient failed rechallenge and was transitioned to an all-oral second-line antituberculous regimen consisting of bedaquiline, pretomanid, linezolid, and moxifloxacin, alongside direct-acting antiviral therapy for chronic hepatitis C. This resulted in the resolution of liver injury and the successful completion of tuberculosis treatment without complications. This case highlights the diagnostic and management challenges of AT-DILI in low-resource settings, particularly where baseline liver function testing, serial monitoring, and access to single-drug formulations for rechallenge are limited.

Mycoplasma hominis is a fastidious, cell wall-deficient bacterium commonly colonising the lower genitourinary tract. While usually commensal, it can cause opportunistic infections in immunocompromised patients. As it can be difficult to culture on standard mediums and is resistant to many first-line antimicrobials, diagnosis and treatment are often delayed. We report the case of a 31-year-old woman with Stage IVA extranodal marginal zone lymphoma previously treated with bendamustine-rituximab, who presented with fever, suprapubic pain and haematuria in the setting of neutropenia. She developed acute kidney injury and was initially treated for neutropenic sepsis. Computed tomography revealed bilateral hydroureteronephrosis and, subsequently, a right renal lesion concerning for abscess. Despite broad-spectrum empirical therapy, she remained febrile with persistently elevated inflammatory markers. Blood cultures grew Streptococcus mitis in a single bottle, later considered a contaminant. Routine urine cultures were initially negative; M. hominis was identified only after prolonged incubation and directed testing on a urine culture collected on Day 5 of admission. On Day 10 of admission, urine culture identified Mycoplasma hominis. Directed therapy with intravenous clindamycin, doxycycline and levofloxacin led to clinical improvement. She was discharged after 17 days with a combination of oral doxycycline and levofloxacin. She was readmitted shortly afterwards with symptom recurrence and progression of renal abscesses but responded to re-initiation of clindamycin. At outpatient follow-up, she had transitioned to levofloxacin monotherapy with symptomatic improvement, radiological reduction of abscesses, downtrending inflammatory markers and recovery of renal function. This case highlights M. hominis as a rare but important cause of upper urinary tract infection and renal abscess in immunocompromised hosts. Clinicians should suspect atypical pathogens in culture-negative urosepsis unresponsive to empirical antibiotics. Specialised diagnostics are essential for accurate detection, and timely targeted therapy can achieve favourable outcomes even when surgical drainage is not feasible.

Anti-granulocyte macrophage colony stimulating factor (anti-GM-CSF) antibodies, classically associated with pulmonary alveolar proteinosis (PAP), are increasingly recognised as a cause of adult-onset immunodeficiency predisposing to opportunistic infections. Coinfections with multiple opportunistic pathogens in this context are uncommon. We describe a rare case of disseminated Nocardia paucivorans, pulmonary Cryptococcus gattii, pulmonary Mycobacterium chelonae, and subsequent PAP in a patient with high-level anti-GM-CSF antibodies. A 64-year-old man presented with subacute bilateral shoulder pain and was diagnosed with acromioclavicular septic arthritis. N. paucivorans was isolated, and subsequent evaluation demonstrated disseminated infection with numerous brain abscesses, left eye endophthalmitis and pulmonary involvement. Interval computed tomography of the chest revealed new right lower lobe consolidation, a biopsy of which identified C. gattii and M. chelonae. Immunological testing confirmed high-level anti-GM-CSF antibodies. The patient received prolonged combination antimicrobial therapy, including meropenem, ceftriaxone, linezolid, trimethoprim-sulfamethoxazole, moxifloxacin, fluconazole, tigecycline and clofazimine, with clinical and radiological improvement of infectious lesions. Despite microbiological clearance, progressive bilateral ground-glass opacities developed on serial chest imaging consistent with PAP, with no pathogens identified on bronchoscopic sampling. Given minimal respiratory symptoms, PAP-directed therapy was deferred. The patient remains clinically stable on trimethoprim-sulfamethoxazole prophylaxis with ongoing clinical and radiological surveillance. This case illustrates the expanding clinical spectrum of anti-GM-CSF antibody-associated disease and underscores the importance of considering this diagnosis in patients presenting with opportunistic infections, in particular, disseminated nocardiosis or C. gattii infection. It also highlights the need for vigilance in evaluating for coinfections, recognition of PAP as a noninfectious codiagnosis, and the importance of long-term follow-up in affected patients.

Syphilis has become an increasing public health concern in recent times, with rising incidence globally. It is often referred to as the 'great imitator' due to its diverse clinical presentations across multiple stages. Neurosyphilis, a tertiary manifestation of Treponema pallidum infection, can present with neuropsychiatric features including rapid cognitive decline. It remains an important but potentially overlooked cause of cognitive impairment (CI). However, few cases document objective cognitive and functional improvement following treatment, especially within a short time frame. We describe the case of a 67-year-old man with rapid cognitive decline, displaying impairments in various cognitive domains: learning and memory, attention and executive functioning. The presence of Argyll-Robertson pupils combined with positive serological and cerebrospinal fluid testing confirmed a diagnosis of neurosyphilis. Following treatment with intravenous penicillin G, serial cognitive assessment demonstrated objective improvement in his cognition and functioning within 1 month of treatment. Our observation of such an improvement in neurosyphilis-driven CI in this time frame is a finding not commonly documented in associated literature. This case highlights the importance of thorough history taking, including a sexual history, alongside physical examination in diagnosing neurosyphilis. Additionally, it supports the importance of considering neurosyphilis when investigating patients with unexplained cognitive decline and suggests there is a degree of reversibility when treated promptly. Further research is needed to better characterise the treatability of neurosyphilis-related CI.

Necrotizing pneumonia is a severe and potentially fatal complication of community-acquired pneumonia, often associated with toxin-producing or drug-resistant pathogens. Rapid and accurate identification of these pathogens is crucial for timely intervention. Polymerase chain reaction (PCR)-based diagnostic tools, such as the BioFire FilmArray pneumonia panel, have significantly improved early pathogen detection, aiding in prompt and targeted treatment as in the presenting case. We report a case of necrotizing pneumonia in a female adult who presented with severe respiratory distress. Initial testing identified coinfection with influenza and methicillin-resistant Staphylococcus aureus (MRSA) using the BioFire FilmArray pneumonia panel, which provided rapid and precise pathogen detection before admission. The patient developed worsening respiratory failure, requiring mechanical ventilation and intensive care. Despite the severity of the infection, early diagnosis and appropriate antimicrobial therapy tailored to the identified pathogens led to a significant clinical improvement, allowing for a favorable recovery. This case highlights the critical role of rapid molecular diagnostics in the early detection of coinfections in necrotizing pneumonia. The timely identification of influenza and MRSA facilitated targeted antimicrobial therapy, which was instrumental in preventing further complications and improving the patient's prognosis. As PCR-based diagnostics become more widely available, their integration into routine clinical practice can enhance the management of severe pneumonia cases, ultimately leading to better outcomes. Clinicians should maintain a high index of suspicion for coinfections in severe pneumonia and leverage rapid diagnostic tools to guide early and effective treatment strategies.

Actinomycosis is a rare, slow-progressing infection mimicking malignancies by penetrating mucosal barriers and spreading across anatomical planes. While typically affecting the cervicofacial area, it can also involve the thorax and abdomen, with simultaneous hepatic and pulmonary involvement being particularly rare. We report the case of an 85-year-old woman with chronic kidney disease, diabetes, and multiple dental procedures who developed fever, myalgias, and abdominal pain a few weeks after recovering from COVID-19. Diagnostic workup revealed a liver abscess extending into the right perinephric space and a small pleural effusion. Gram stain of abscess aspirate showed Gram-positive, branching filamentous rods, negative on a modified AFB stain. Cultures grew Actinomyces odontolyticus, differing from the more common A. israelii. Her hospital course was complicated by acute hypoxic respiratory failure, with CT showing an expanded, loculated right pleural effusion. Treatment included prolonged antibiotic therapy and interventional radiology procedures for abscess drainage. This case highlights the diagnostic and therapeutic challenges of hepatic actinomycosis caused by A. odontolyticus, particularly when affecting adjacent structures, such as the diaphragm and lung. The infection may have spread hematogenously to the liver with subsequent transdiaphragmatic extension into the thoracic cavity or, alternatively, may have originated from aspiration-related thoracic infection with secondary extension toward the liver. Typically occurring in immunocompetent individuals, this severe presentation may reflect the combined influence of recent COVID-19 infection, chronic comorbidities, and recent dental procedures. This underscores the need for vigilance in recognizing atypical postviral infections and highlights the need for further research into opportunistic bacterial infections following COVID-19-related immune dysregulation.

Pyogenic ventriculitis is a rare and potentially fatal infection of the ventricular system. While most reported cases are nosocomial and catheter-associated, ventriculitis as a complication of community-acquired bacterial meningitis is uncommon, particularly in adults, and carries a poor prognosis. We report the case of an 82-year-old previously healthy and unvaccinated woman who presented with a one-day history of fever, confusion, and purulent left-sided otorrhea on a 2-week background of flu-like symptoms. Cranial computed tomography was consistent with otogenic meningitis complicated by pneumocephalus, and lumbar puncture confirmed purulent meningitis. Empirical therapy for meningitis with ceftriaxone, amoxicillin, metronidazole, and dexamethasone was initiated, and surgical source control of the otogenic focus was performed. Both blood and cerebrospinal fluid cultures grew Streptococcus pneumoniae with a penicillin minimum inhibitory concentration of <&#x2009;0.03&#x2009;mg/L. Serotyping by multiplex PCR with confirmatory Quellung reaction, performed at the Swiss National Reference Center for Invasive Pneumococci, identified Serotype 3. Despite penicillin G monotherapy, fever and impaired consciousness persisted, and repeat imaging revealed meningitis-associated pyogenic ventriculitis with intraventricular debris. Adjunctive rifampicin and a series of cerebrospinal fluid drainage interventions (lumbar drain followed by external ventricular drain) failed to substantially improve neurological outcome. Antibiotic therapy was continued for 9&#x2009;weeks, after which the patient was transferred to long-term institutional care with severe residual neurological impairment. This case illustrates the diagnostic and therapeutic challenges of meningitis-associated pyogenic ventriculitis in adults and the disproportionate severity of disease caused by Serotype 3 S. pneumoniae, whose unusually thick mucoid capsule promotes immune evasion and the formation of viscous purulent debris that hampers source control. The case is consistent with Swiss surveillance data showing that Serotype 3 remains a leading cause of invasive pneumococcal disease in older adults and serves as a sentinel event highlighting persistent gaps in adult pneumococcal immunization.

Cryptococcal neoformans infection of the central nervous system (CNS) is well-documented in Sub-Saharan Africa due to its association with the human immunodeficiency virus (HIV) pandemic. While cryptococcal infections can occur at sites other than the CNS, such as in the bones, these instances are less common and have been inadequately documented in the region. Orthopedic cryptococcal infections arise when the organism is inhaled from the environment and subsequently disseminates from the lungs via the bloodstream to the bones. Due to its low incidence and atypical manifestations, cryptococcal osteomyelitis may be overlooked, leading to delayed treatment and potential complications. This case report describes a 12-year-old female patient who presented with pain and swelling in both knee joints one year after initiating treatment for cryptococcal meningitis, which had been only partially effective. On examination, both knee joints exhibited swelling and tenderness, and imaging revealed bilateral pathological fractures in the distal third of the femurs. Histological analysis demonstrated numerous fungal elements consistent with Cryptococcus neoformans. Treatment was initiated with liposomal amphotericin B at a single dose of 10&#x2009;mg/kg, in conjunction with flucytosine at 100&#x2009;mg/kg/day and fluconazole at 1200&#x2009;mg/day. This was followed by a consolidation phase with fluconazole at 800&#x2009;mg/day, after which the patient was maintained on fluconazole at 200&#x2009;mg/day. After 52&#x2009;weeks of treatment, the patient exhibited a favorable clinical response, with successful union of the fractures. In individuals living with HIV, Cryptococcus neoformans may present atypically with involvement of sites outside the CNS, including the skeletal system. Although cryptococcal osteomyelitis is rare, it should be considered in the differential diagnosis in this population. Favorable outcomes can be achieved with prolonged antifungal therapy.

Differentiating tuberculosis (TB) from sarcoidosis, especially in TB endemic regions, is one of the major clinical challenges because these two diseases may show considerable similarity in terms of clinical manifestations, imaging findings, and granulomatous pattern. In addition, the presence of noncaseating granuloma alone is not sufficient for the definitive diagnosis of sarcoidosis because in some cases, TB may also show granulomas without necrosis. In this report, a 83-year-old man is presented with fever, productive cough, chest pain, weakness, and mild dyspnea, who had a history of pleural and pericardial effusion, with elevated pericardial adenosine deaminase (ADA), a positive tuberculin skin test, and pleural granuloma. The patient was initially treated with anti-TB therapy for probable diagnosis of TB pleurisy and also corticosteroid for probable sarcoidosis, but because of the development of drug-induced hepatitis, treatment was interrupted and modified several times. On subsequent presentation, chest high-resolution computed tomography (HRCT) showed pericardial thickening, pericardial effusion, pulmonary nodules with a perilymphatic distribution, right hilar lymphadenopathy, and a cavitary lesion in the right upper lobe. Sputum smear was 3+ positive for acid-fast bacilli, and anti-TB treatment was reinitiated. Nevertheless, because of the imaging pattern, relative response to corticosteroid, and pathologic findings including non-necrotizing granulomas, the possibility of concurrent sarcoidosis was also raised. After evaluating the possibility of TB progression and the effect of interruptions in anti-TB therapy caused by drug-induced hepatitis, the patient was treated with anti-TB regimen together with prednisolone and later azathioprine. Hence, the clinical case of pulmonary TB and probable sarcoidosis has been described in this study. The patient underwent anti-TB and immunosuppression therapy and experienced significant improvement.

We describe cases of contamination of Mycobacterium ulcerans infections (Buruli ulcer) with Rhodococcus erythropolis, a bacterium of environmental origin that is rarely associated with human infection. The infectious pathogen of Buruli ulcer, Mycobacterium ulcerans, was detected and cultured in vitro from two lesion swabs taken from clinically described Buruli ulcer-like patients (4 and 34&#x2009;years old). Infection by M. ulcerans was confirmed using the WHO-recommended IS2404/IPC-qPCR multiplex analysis of DNA extracts from patient samples, which were subsequently categorized as positive. PCR-positive samples were incubated in L&#xf6;wenstein-Jensen (LJ) culture media, and colony phenotypes characteristic of M. ulcerans were observed 14 days postincubation. However, analysis of culture suspensions by qPCR revealed no M. ulcerans DNA, while Ziehl-Neelsen (ZN) staining showed phenotypes closely related to acid-fast bacilli (AFB) of M. ulcerans. Detected AFBs were not clustered after ZN staining. Further microbial identification and characterization by MALDI-TOF MS and Gram staining revealed the presence of Rhodococcus erythropolis. The identification was confirmed by whole-genome sequencing (WGS) to establish the genomic link between this originally called Mycobacterium erythropolis and M. ulcerans. Analysis of short reads from WGS confirmed the organism as R. erythropolis. When employing the M. ulcerans Agy99 reference chromosome, comparative analysis of whole-genome sequences revealed little genomic relatedness between the two organisms, with an average genome coverage of 5.72%. The study reports the first contamination cases of M. ulcerans-infected lesions with R. erythropolis. Although R. erythropolis did not interfere in the detection specificity of M. ulcerans by IS2404/IPC-qPCR, it completely inhibited M. ulcerans growth in recommended LJ culture media, complicating routine biological diagnosis by culture and microscopy. Hence, Buruli ulcer is likely to be underdiagnosed due to lesion contamination by R. erythropolis and difficulties in M. ulcerans identification in the routine clinical diagnosis procedure.

Descending necrotizing mediastinitis (DNM) is a relatively uncommon complication of deep neck infections. However, with inappropriate use of antibiotics, steroids, or underlying medical problems such as immunocompromised conditions, this type of infection can become life-threatening. We report a case of Ludwig Angina with DNM, diagnosed at the end of December 2019. The subject was a 17-year-old female admitted to the pediatric intensive care unit after two weeks of clinically significant distress and swelling in her neck, tongue, and lips. The predominant underlying oropharyngeal infection originated from the mandibular 3rd molar. The patient was successfully treated due to early diagnosis and adequate medical intervention. Supportive medications were highly effective, including bronchodilators to assist in breathing and improve lung air entry, intravenous glucocorticoids like dexamethasone for their anti-inflammatory effect, and a regimen of antibiotics. No surgical intervention was necessary; the only procedures performed were percutaneous drainage of an abscess in the submandibular area and chest tube insertion for pleural effusion. Early diagnosis and appropriate medical treatment are critical in managing DNM. Supportive medications and minimally invasive procedures can effectively manage the condition, avoiding the need for extensive surgical intervention. This case highlights the importance of vigilant diagnosis and comprehensive medical management in improving patient outcomes.

Suspected macrolide-refractory Mycoplasma pneumoniae pneumonia can be a diagnostic challenge in immunocompromised hosts, particularly after allogeneic stem cell transplantation. Screening serologies may further complicate diagnosis when false-positive or discordant results divert therapy. We report a 63-year-old woman with B-cell acute lymphoblastic leukemia status postallogeneic stem cell transplantation and hypogammaglobulinemia who was transferred for persistent cough, exertional dyspnea, and right upper-lobe consolidation after limited improvement with azithromycin and broad-spectrum antibacterial therapy. Initial and repeat respiratory testing detected M. pneumoniae, while an extensive infectious evaluation was otherwise negative. Coccidioides enzyme immunoassay IgM and IgG were positive, prompting empiric fluconazole, but confirmatory immunodiffusion and complement fixation testing were negative, and the patient lacked epidemiologic risk factors. Following reassessment, fluconazole was discontinued; doxycycline and replacement intravenous immunoglobulin were initiated. Clinical improvement followed, including discontinuation of supplemental oxygen and return to baseline exercise tolerance, although the relative contributions of doxycycline and intravenous immunoglobulin cannot be determined from a single case. This case highlights the need to interpret screening fungal serologies in a clinical and epidemiologic context, confirm positive Coccidioides EIA results, and consider clinically suspected macrolide-refractory M. pneumoniae when respiratory symptoms persist despite macrolide therapy. Molecular resistance testing was not available, so macrolide resistance remained clinically suspected rather than proven.

Pyogenic spondylodiscitis is a rare infection, with cervical spine involvement occurring in only 3%-10% of the cases. Streptococcus gallolyticus subsp. pasteurianus, a normal gut flora component, is a rare causative agent of spinal infections. Here, we report the case of an 88-year-old man with cervical pyogenic spondylodiscitis caused by this organism, complicated by a clinical relapse following a standard antibiotic course. The patient presented with fever and neck pain. Blood cultures revealed Streptococcus gallolyticus subsp. pasteurianus, and cervical magnetic resonance imaging (MRI) revealed spondylodiscitis at the C4-C6 levels. The patient was treated with a 90-day course of antibiotics (46&#x2009;days intravenous and 44&#x2009;days oral), leading to initial clinical and biochemical resolution. However, clinical relapse occurred on day 174, characterized by recurrent neck pain and elevated C-reactive protein levels despite no clear signs of active inflammation on repeat MRI. Extended oral antibiotic therapy was resumed and continued for 9&#x2009;months, resulting in sustained remission without surgical intervention. To our knowledge, only isolated case reports of spinal infections caused by this subspecies have been published, and no prior case has described clinical recurrence. This case suggests that standard antibiotic durations may be insufficient in selected complex or relapsing spinal infections caused by Streptococcus gallolyticus subsp. pasteurianus and highlights the importance of individualized treatment duration and long-term surveillance.

Spinal mucormycosis is an exceptionally rare form of invasive fungal infection, with fewer than 12 confirmed cases reported in the prior literature. Immunocompromised patients are disproportionately affected, and mortality exceeds 50% in this population. Chronic liver disease as a primary predisposing condition is underrepresented in the existing case series. A 54-year-old male with Child-Pugh Grade C chronic liver cirrhosis, diabetes mellitus, and hypothyroidism presented with progressive low back pain and bilateral lower limb weakness of one week duration. Lumbar MRI demonstrated L2-L3 spondylodiscitis with epidural abscess formation, initially attributed to Pott's spine, and antitubercular therapy (ATT) was initiated empirically. Rapid neurological deterioration prompted surgical re-evaluation. The patient underwent an L3 laminectomy with drainage of an L3-L4 anterior epidural abscess. Intraoperative microscopy revealed aseptate ribbon-like hyphae consistent with Mucorales species. Liposomal Amphotericin B (5&#x2009;mg/kg/day), intravenous micafungin, and oral posaconazole were commenced. Antifungal therapy was complicated by progressive nephrotoxicity and hepatic decompensation requiring repeated dose modifications. The patient developed hepatic encephalopathy with sepsis and died on Postoperative day (POD) 12 from multiorgan failure. This case represents the 12th documented instance of spinal mucormycosis and the first attributable to Child-Pugh Grade C liver disease. In tuberculosis-endemic settings, mucormycosis must be considered in the differential diagnosis of apparent Pott's spine in immunocompromised patients, particularly those with progressive neurological deterioration despite empirical ATT. Concurrent hepatic and renal impairment substantially constrains antifungal options and worsens prognosis. Multidisciplinary coordination and early tissue diagnosis are critical to the management of this rare, life-threatening condition.

Staphylococcus aureus, although a common colonizer of skin and mucous membranes in humans, is associated with severe infections in both healthy and debilitated individuals. The mortality induced by invasive MSSA disease is high, especially in patients diagnosed late. In children, skin and joint manifestations are most common. Septic shock is a major contributing factor to early mortality. To date, reported cases of invasive MSSA disease in children are infrequent, especially in Sub-Saharan Africa. We present 4 cases of previously healthy children who presented with various clinical manifestations, but skin lesions and fever were common in all of them. They had multisystem involvement and eventually required aggressive multifactorial therapy. Antibiotic treatment was tailored to the results of antimicrobial sensitivity tests following blood culture. Though the hospital stay was quite long, intensive care and appropriate antibiotics contributed to a good prognosis. In children with invasive MSSA disease, early diagnosis and prompt management are key factors to improved prognosis. Skin lesions with tender joints in a febrile infant should raise suspicion for a staphylococcal infection. Intensive care and infection source control are the cornerstones of the management.

Balamuthia mandrillaris is a rare free-living amoeba that causes granulomatous amoebic encephalitis (GAE), a frequently fatal central nervous system infection. Diagnosis is often delayed because of nonspecific clinical presentation and radiographic findings. We describe a 70-year-old man with recent soil exposure in rural Mexico who developed progressive neurologic decline and multifocal enhancing brain lesions initially concerning for malignancy. Extensive infectious, oncologic, and autoimmune evaluations were unrevealing. Brain biopsy demonstrated dense granulomatous inflammation without identifiable organisms on routine stains. Definitive diagnosis was established via 18S rRNA PCR testing of brain tissue and subsequently confirmed by the Centers for Disease Control and Prevention. A multidrug regimen including miltefosine and investigational nitroxoline was initiated but was complicated by renal and hepatic toxicity. Despite transient radiologic improvement, the patient experienced progressive disease and ultimately died. This case underscores the diagnostic difficulty of Balamuthia encephalitis and highlights the essential role of molecular diagnostics in identifying rare pathogens when conventional testing is inconclusive.

We present a case of acute Candida glabrata prostatitis complicated by secondary candidemia in a 72-year-old man with poorly controlled Type 2 diabetes mellitus and benign prostatic hyperplasia, without classical healthcare-associated risk factors for invasive candidiasis. The patient presented with fever, urinary symptoms, and markedly elevated prostate-specific antigen. Urine and blood cultures confirmed disseminated C. glabrata infection. Despite a comprehensive diagnostic workup, no alternative source of candidemia was identified, supporting primary prostatic infection with secondary hematogenous dissemination. Among the identified predisposing factors was ongoing treatment with dapagliflozin, a sodium-glucose cotransporter 2 inhibitor (SGLT2 inhibitor). While SGLT2 inhibitor use is established as a risk factor for superficial mycotic genitourinary infections, invasive fungal complications remain poorly characterized. This case suggests that the SGLT2 inhibitor-induced glucosuria, in combination with structural urinary obstruction and poorly controlled diabetes, may contribute to invasive fungal infections and highlights the need for clinical vigilance in patients with multiple converging risk factors.