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[This corrects the article DOI: 10.1016/j.idcr.2026.e02612.].
Intestinal tuberculosis (ITB) represents a major diagnostic challenge in endemic regions owing to its substantial clinical and endoscopic overlap with Crohn's disease (CD). This complexity is further amplified when ITB is accompanied by inflammatory musculoskeletal manifestations that resemble axial spondyloarthritis (axSpA), thereby increasing the risk of diagnostic misclassification and potentially hazardous therapeutic decisions, particularly with respect to the use of immunosuppressive agents. A clinical case is presented involving a young woman with chronic diarrhea and progressive inflammatory back pain. The diagnostic workup comprised laboratory investigations, imaging studies, colonoscopy with histopathological analysis, microbiological testing, and longitudinal monitoring throughout the course of anti-tuberculous therapy. Colonoscopy revealed inflammatory lesions suggestive of CD; however, histopathological examination demonstrated large confluent granulomas with central necrosis and acid-fast bacilli (AFB) positivity, establishing the diagnosis of ITB despite initially negative molecular assays and cultures. Radiological findings, inflammatory back pain, and HLA-B27 positivity were consistent with axSpA. Anti-tuberculous therapy led to marked mucosal improvement, although persistent microbiological evidence necessitated extension of treatment duration to nine months. Management of spondyloarthritis was initiated only after adequate control of the tuberculous infection had been achieved. This case underscores the need for heightened vigilance for ITB in patients presenting with Crohn's-like colitis and inflammatory musculoskeletal symptoms in tuberculosis-endemic settings. Histopathological evaluation remains pivotal when microbiological investigations are inconclusive. A stepwise, "infection-first" approach is essential to avoid premature immunosuppression and to ensure safe and effective management of coexisting inflammatory conditions.
Cryptococcal disease typically presents as meningitis in immunocompromised hosts, whereas basal ganglia cryptococcomas causing parkinsonism in immunocompetent patients are uncommon and easily overlooked. We describe a 61-year-old apparently immunocompetent man with subacute meningoencephalitis, abnormal cerebrospinal fluid (CSF), and a pulmonary nodule initially managed as tuberculous meningitis, who subsequently developed severe asymmetric parkinsonism. Neuroimaging later demonstrated diffuse leptomeningeal enhancement and multiple basal ganglia and brainstem cryptococcomas and repeat CSF and lung biopsy confirmed cryptococcosis. Opening CSF pressure was elevated (24 cm H2O). Induction therapy consisted of liposomal amphotericin B (4 mg/kg/day) for two weeks, followed by high-dose fluconazole consolidation; flucytosine was not available in our institution. Despite guideline-oriented antifungal therapy and a levodopa trial, parkinsonism persisted, suggesting possible structural nigrostriatal injury; however, long-term follow-up and functional imaging were not available to confirm irreversibility. Serial CSF findings summarized (Table 1) highlight the importance of repeated lumbar punctures and targeted mycological testing in subacute meningitis with nondiagnostic initial studies. To contextualize this presentation, we reviewed previously reported cases of cryptococcal parkinsonism (Table 2), which delineate a spectrum from fully reversible to L-dopa-responsive or permanently disabling syndromes, largely determined by the extent and localization of basal ganglia involvement and timeliness of treatment. This integrated case and literature review emphasizes that cryptococcosis should be systematically considered in atypical or rapidly progressive parkinsonism with inflammatory CSF and basal ganglia lesions, even in apparently immunocompetent hosts, and underscores the need for early recognition, comprehensive evaluation of pulmonary and CNS disease, and prolonged antifungal therapy to prevent irreversible neurological sequelae.
Nonadherence to trimethoprim-sulfamethoxazole (TMP-SMX) is a known risk factor for nocardiosis treatment failure, often due to adverse effects. However, reports linking relapse to treatment interruption caused by poor adherence are scarce. A 70-year-old male with chronic bronchitis presented with persistent fever, cough, and sputum. Nocardia asiatica was identified. Initial improvement followed a 28-day TMP-SMX course, but the patient discontinued therapy. Multiple readmissions over three years resulted from relapses due to poor adherence. Whole-genome sequencing of isolates from the first and third episodes revealed 99.9% genetic similarity, confirming relapse from the original strain. Only after completing a full six-month TMP-SMX course did the patient achieve sustained remission with no recurrence for five years. This case provides molecular evidence supporting that premature TMP-SMX discontinuation contributed to relapse, emphasizing that adherence is as critical as accurate diagnosis for cure.
Syphilis is a protean infection capable of mimicking various dermatological and systemic diseases, often complicating diagnosis in its later stages. A 26-year-old HIV-negative man with a history of inadequately monitored syphilis presented with headache, cough, and widespread erythematous plaques with central atrophy. Investigations revealed an RPR titer of 1:128 and positive CSF treponemal serology. Chest CT demonstrated peripheral nodular lung consolidations, and ophthalmologic exam showed signs of prior uveitis. A skin biopsy confirmed late-stage syphilis, revealing extensive dermal tuberculoid granulomas and gummatous necrosis. Following a 14-day course of intravenous penicillin G, the pulmonary lesions completely resolved, cutaneous lesions markedly improved, and the RPR titer appropriately declined at the six-month follow-up. This case illustrates a rare presentation of late syphilis with concurrent pulmonary involvement and widespread granulomatous skin lesions, emphasizing the need for clinicians to maintain a high index of suspicion for atypical manifestations of Treponema pallidum.
Pylephlebitis, septic thrombosis of the portal venous system secondary to Klebsiella pneumoniae liver abscess is a rare and potentially life-threatening condition. We present an unusual case of suppurative thrombophlebitis hepatic vein thrombosis in a healthy male who presented with unspecified abdominal pain, fever, and vomiting. He was managed promptly with upfront antimicrobial therapy, and anticoagulation led to an uneventful recovery.
Burkholderia cepacia complex (BCC) comprises environmental non-fermenting Gram-negative bacilli that primarily cause opportunistic infections in immunocompromised individuals. Pericardial infection due to BCC is exceedingly rare, particularly in patients with malignancy. Differentiating infectious from malignant effusions remains a diagnostic challenge, especially in tuberculosis-endemic regions. We report a case of a 50-year-old female presenting with chronic cough, fever, and progressive Grade III dyspnoea requiring oxygen support. Imaging revealed right pleural effusion and pericardial effusion. Cytological examination of pleural fluid demonstrated malignant cells, and immunohistochemistry confirmed lung adenocarcinoma with metastasis. The patient was also HBsAg positive with detectable viral load, representing an additional immunocompromised state.Pericardial fluid culture isolated Burkholderia cepacia complex, while pleural fluid cultures remained sterile. Tuberculosis workup, including Ziehl-Neelsen staining, GeneXpert testing, and adenosine deaminase levels, was negative. Antimicrobial susceptibility testing performed using CLSI 2024 interpretative criteria demonstrated susceptibility to trimethoprim-sulfamethoxazole, levofloxacin, and meropenem; intermediate susceptibility to minocycline; and resistance to ceftazidime. The patient received targeted antimicrobial therapy along with chemotherapy and showed symptomatic improvement with reduced oxygen requirement. Isolation of BCC from a sterile site without prior cardiac intervention raises important questions regarding pathogenesis. Dual immunocompromised states-lung adenocarcinoma with metastasis and chronic hepatitis B infection-likely facilitated opportunistic infection through hematogenous or contiguous spread. Clinical correlation and therapeutic response supported true infection rather than contamination. BCC can rarely cause pericardial infection in patients with malignancy. Comprehensive microbiological evaluation of pericardial fluid is essential even in confirmed malignant effusions to enable accurate diagnosis and targeted therapy.
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Pertussis is a highly contagious infection associated with significant morbidity and mortality in young infants despite widespread vaccination programs. Early recognition and treatment are important to reduce disease severity, shorten symptom duration, and limit transmission. We report the case of a 51-day-old previously healthy boy who presented with a 4-day history of whooping cough, apnea, circumoral cyanosis, post-tussive emesis, and reduced oral intake. Pertussis was confirmed by a nasopharyngeal respiratory multiplex PCR panel detecting Bordetella pertussis. The patient initially received two doses of oral azithromycin (10 mg/kg/dose); however, approximately 20-30 min after the second dose, he developed facial puffiness and lip swelling consistent with a probable immediate hypersensitivity reaction. This complicated management because alternative antimicrobial agents, including trimethoprim-sulfamethoxazole and fluoroquinolones, were considered unsuitable owing to age-related safety concerns and limited clinical applicability. Following multidisciplinary evaluation and individualized risk-benefit assessment, azithromycin desensitization was undertaken. The initial desensitization attempt was discontinued because of recurrent hypersensitivity symptoms, prompting modification of the protocol. A second desensitization attempt using extended infusion and observation intervals was successfully completed. Following tolerance of intravenous azithromycin, the patient was transitioned back to oral therapy and completed the full 5-day treatment course without recurrence of hypersensitivity symptoms or delayed reactions. His cough gradually improved, and apnea episodes resolved before discharge. This case highlights azithromycin desensitization as a potential individualized therapeutic strategy in carefully selected infants with pertussis and suspected macrolide hypersensitivity when safer alternative treatment options are limited. Further evidence is required before broader conclusions regarding safety, efficacy, and reproducibility can be drawn.
Vascular graft infections represent a serious challenge in vascular surgery, characterized by a substantial morbidity and mortality. Listeria monocytogenes is a rare but documented pathogen in prosthetic graft infections. This is an exceedingly rare case of an axillo-femoral graft infection caused by Listeria monocytogenes. We report the case of a 59-year-old male with a complex vascular history, including an axillofemoral bypass, who presented with infectious symptoms and was diagnosed with a late focal infection by Listeria monocytogenes of his vascular graft. Despite the recommendation for a surgical removal of the infected prosthesis, the patient refused and was managed conservatively with long-term antibiotic therapy. This case highlights a rare pathogen in vascular graft infections and the challenges associated with its management in patients with extensive comorbidities. Infections of prosthetic vascular grafts are rare but serious complications. They are associated with high rates of morbidity and mortality, particularly when diagnosis is delayed or surgical management is not feasible. Vascular graft infections with Listeria are uncommon and usually result from hematogenous seeding. The gold standard for treatment of infected vascular prostheses remains a complete surgical excision of the graft, reconstruction of an extra-anatomic bypass, combined with targeted antibiotic treatment.
Mycobacterium brisbanense, a rare, rapidly growing, nontuberculous mycobacterium, is typically associated with respiratory infections. Herein, we report the first known case of peritoneal dialysis (PD)-related peritonitis caused by M. brisbanense in a male patient in his 70 s with end-stage renal disease due to chronic glomerulonephritis and renal sclerosis. Despite initial empirical treatment with cefazolin and ceftazidime for co-isolated bacteria (Staphylococcus warneri and Kocuria marina), the symptoms worsened. A subsequent acid-fast bacillus culture of the PD effluent was positive, and the microorganism was identified as M. brisbanense using time-of-flight mass spectrometry and whole-genome sequencing. Antibiotic susceptibility testing revealed susceptibility to all the following administered agents. The patient was successfully treated by PD-catheter removal and intravenous administration of amikacin, imipenem/cilastatin, and oral azithromycin for 40 days, followed by oral azithromycin and sitafloxacin for 153 days. M. brisbanense is a potential opportunistic pathogen in PD-related peritonitis that requires tailored antimicrobial therapy.
Tuberculosis remains a major global health concern with extrapulmonary manifestations contributing to approximately 15-20% of cases in immune-competent hosts. In 2022, National Tuberculosis Elimination Program (NTEP) reported multidrug resistance in 2.5% of new tuberculosis cases and 13% in previously treated cases. Among extrapulmonary tuberculosis pleural tuberculosis is one of the most common forms. It becomes a diagnostic challenge when microbiological tests are inconclusive. In most developing countries, antitubercular drugs are initiated empirically in patients on the basis of clinical decision. In today's day and age, physicians emphasize more on evidence-based medicine practice. We report a case of a young man who presented with exudative pleural effusion unresponsive to empirical antibiotics. Thoracoscopic pleural crush biopsy showed granulomatous inflammation with caseating necrosis and acid-fast bacilli, confirming tuberculous pleuritis that was multidrug resistant. This case illustrates the role of medical thoracoscopy in patients where suspicions for tuberculosis are raised without clear answers from the initial tests. Relying only on standard antitubercular treatment may delay the detection of underlying drug resistance that is a growing public health challenge. Early tissue diagnosis through thoracoscopy allowed timely identification of multidrug resistance and directed proper management.
To report a case of Fusarium keratitis in an 80-year-old female without typical exogenous or traumatic risk factors, such as ocular trauma, contact lens use, or previous ocular surgery, but with intrinsic ocular surface predisposing factors, and to highlight the diagnostic value of MALDI-TOF MS. Routine bacterial and fungal cultures were performed on ocular secretion samples from the patient. Lactophenol cotton blue staining was used for microscopic examination, and MALDI-TOF MS (Matrix-Assisted Laser Desorption/Ionization-Time of Flight Mass Spectrometry) was employed for rapid and accurate identification of the fungal strain. Clinical data were comprehensively analyzed. White, cotton-like fungal colonies were observed on blood agar and chocolate agar plates. Microscopic examination revealed transparent, septate hyphae and numerous long, oval conidia, initially suggesting Fusarium spp. MALDI-TOF MS analysis showed a high-confidence match with Fusarium solani, and the isolate was interpreted as F. solani / Fusarium solani species complex (FSSC) based on morphology and MALDI-TOF MS. This study highlights the clinical value of MALDI-TOF MS in the identification of pathogens in complex ocular infections. Despite the absence of typical exogenous or traumatic risk factors, the patient developed rapidly progressive invasive keratitis. This case suggests that intrinsic ocular surface abnormalities in older adults, including tear film instability, epithelial barrier impairment, and corneal nerve degeneration, may lower the threshold for fungal infection. The possible contribution of immunosenescence should be interpreted only as contextual background and remains to be validated in future studies.
African tick bite fever (ATBF) is a spotted fever group rickettsiosis caused by Rickettsia africae and is often identified among travelers returning from sub-Saharan Africa. Clinical presentation may be mild or nonspecific, often delaying diagnosis despite characteristic findings such as inoculation eschars. A 52-year-old male presented to the preoperative holding area prior to a scheduled left-sided inguinal hernia repair after recently returning from a game-hunting trip to Africa. During preoperative intake, he was noted to have a fever of 106 °F despite being otherwise asymptomatic. Physical examination revealed two black eschars on the patient's back and right shin. Given the presence of high-grade fever, the scheduled procedure was canceled, and the patient was discharged for outpatient evaluation. He was subsequently treated with a 10-day course of doxycycline for suspected African tick bite fever. At two-week follow-up, the patient remained asymptomatic, his fever had resolved, and repeat preoperative evaluation was unremarkable. Surgical repair of the inguinal hernia was performed without complications. Although laboratory confirmation was not obtained, the clinical presentation, including characteristic eschars, high-grade fever, and recent travel to sub-Saharan Africa, was highly suggestive of ATBF. This case underscores the importance of maintaining clinical suspicion for ATBF in returning travelers and highlights the diagnostic value of inoculation eschars, even in the absence of systemic symptoms. Early recognition of suspected ATBF and empiric doxycycline therapy may result in rapid clinical improvement and help prevent unnecessary delays in care.
Chronic rhinosinusitis (CRS), defined as persistent inflammation of the sinuses lasting longer than 12 weeks, and recurrent acute rhinosinusitis (RARS), characterized by multiple distinct episodes of acute bacterial sinusitis within a year, are among the most common chronic illnesses in the US. Several risk factors, including gastroesophageal reflux disease (GERD) are associated with CRS and RARS. For exacerbations of CRS and recurrent episodes of RARS, antibiotic therapy is the mainstay of treatment; however, a significant subpopulation of patients remain resistant to treatment, despite rigorous and prolonged treatment. Consequently, patients experience frequent recurrences and more complex infections involving multiple organisms. Multidrug resistant bacterial strains, such as methicillin-resistant Staphylococcus aureus (MRSA), are increasingly implicated in treatment failure. Thus, there is a need for new therapies to treat patients with CRS and RARS effectively. Omadacycline is a tetracycline derivative antibiotic approved by the FDA to treat adult patients with community-acquired bacterial pneumonia and acute skin and skin structure infections. Omadacycline has broad spectrum activity against select pathogens and was proven to be effective against select multidrug resistant bacteria, including MRSA. Presented here are three cases of patients with underlying GERD and polymicrobial chronic sinusitis involving MRSA, along with several gram-negative enteric organisms, who were successfully treated with omadacycline after many years of recurrent infections. Omadacycline was shown to be an oral option for patients with infectious exacerbations of CRS and RARS involving antibiotic resistance and was well tolerated. These findings suggest that further investigation of omadacycline in this setting is warranted.
Levofloxacin and other fluoroquinolones are widely used antibiotics, though they can cause rare immune-mediated adverse events. We report a man in his late 50 s with long-standing type 2 diabetes mellitus and a new plantar foot wound who was prescribed oral levofloxacin for presumed soft-tissue infection. Within 48-72 h of starting levofloxacin, he developed rapidly progressive palpable purpura that began on the upper extremities and spread to the lower extremities up to the thighs, with intense pruritus, migratory arthralgias, and bullous lesions on the distal lower extremities and right upper extremity. He had no mucosal involvement and no pulmonary or gastrointestinal symptoms. Dermatologic evaluation favored small-vessel vasculitis; systemic corticosteroids were initiated and the patient was transferred for further management. Skin biopsy demonstrated leukocytoclastic vasculitis with leukocytoclasis and fibrinoid necrosis of superficial dermal vessels. Direct immunofluorescence showed perivascular IgG and C3 without IgA deposition. Workup revealed elevated inflammatory markers, elevated serum IgA, positive p-ANCA with negative MPO and PR3, probable mixed cryoglobulins, and mild hematuria and proteinuria without casts; nephrology assessed low likelihood of clinically significant renal vasculitis. Levofloxacin was discontinued and a short corticosteroid taper was completed, with steady improvement of rash and stable renal function. This case highlights the recognition and evaluation of suspected fluoroquinolone-associated cutaneous small-vessel vasculitis and the importance of early biopsy of fresh lesions when IgA vasculitis is considered.
Rifampicin-induced purpura is a rare hypersensitivity reaction encountered during anti tubercular therapy (ATT). We report a 43-year-old male with cervical tubercular lymphadenitis who developed purpuric lesions with distinctive orange-colored serous discharge over the left lower limb after initiation of ATT. Investigations excluded thrombocytopenia and systemic vasculitis. A temporal relationship between drug intake and symptom onset confirmed rifampicin as the causative agent. Prompt withdrawal of rifampicin and initiation of systemic corticosteroids led to complete resolution of the lesions. This case highlights the need for vigilance regarding rare dermatological adverse effects in patients on ATT and the importance of prompt clinical recognition to prevent serious complications.
Subdural empyema (SDE) is a neurosurgical emergency with 6-15% mortality. Culture-negative cases pose significant diagnostic and therapeutic challenges. A 51-year-old male with chronic alcohol abuse presented with high fever (39°C), severe headache, meningismus, and altered mental status (GCS 13). CSF analysis revealed protein 28 g/L (60-fold elevated), uncountable cells due to viscous fluid, and Gram-positive cocci. Initial non-contrast CT suggested chronic subdural hematoma, but surgical exploration revealed frontal subdural empyema with frank purulent discharge. All cultures (pus, CSF, blood, urine) were negative despite elevated inflammatory markers (CRP 303 mg/L, PCT 2.12 ng/mL, WBC 16.7 × 10⁹/L). Treatment with surgical drainage and combination antibiotics (meropenem with linezolid) achieved complete recovery after 24 days. This case emphasizes the diagnostic challenges of distinguishing subdural hemorrhage from empyema on a CT scanner, the critical importance of early surgical intervention, and the necessity of broad-spectrum empirical antibiotics, with consideration of molecular diagnostics when cultures are negative.
Streptococcus pneumoniae remains a leading cause of invasive bacterial infection worldwide and is classically associated with community-acquired pneumonia. However, fulminant pneumococcal septic shock in the absence of radiographic pneumonia is uncommon and may delay diagnosis and treatment. We present the case of a 48-year-old immunocompetent female who developed severe septic shock secondary to Streptococcus pneumoniae bacteremia despite initially negative chest imaging for focal pneumonia. The patient presented with profound hypotension, lactic acidosis, thrombocytopenia, acute kidney injury, and acute hypoxic respiratory failure requiring vasopressor support and intensive care admission. Blood cultures grew Streptococcus pneumoniae. Initial chest radiography and computed tomography angiography of the chest demonstrated no focal consolidative pneumonia, although delayed bibasilar pulmonary infiltrative changes developed later during hospitalization. Extensive evaluation did not identify alternative infectious sources including endocarditis or meningitis. The patient improved rapidly with aggressive resuscitation and targeted antimicrobial therapy. This case highlights the importance of recognizing invasive pneumococcal disease even in the absence of classic radiographic findings and emphasizes that early imaging may underestimate evolving pulmonary infection in severe sepsis.
This report describes a case of Cryptococcus gattii meningitis in an immunocompetent man that was initially misdiagnosed as Epstein-Barr virus meningitis and treated with steroids. The diagnostic challenges and radiographic findings are presented. It highlights the importance of maintaining a high index of suspicion for C. gattii meningitis in immunocompetent individuals presenting with subacute meningitis and pulmonary masses.