Congenital syphilis remains a preventable but underrecognized condition in Nepal, where routine antenatal screening is limited to the first visit. We report five infants with diverse clinical manifestations, including hydrops fetalis, bullous lesions, bone involvement, and persistent rhinitis. Four were classified as highly probable and one as possible congenital syphilis according to the 2021 CDC criteria. Four mothers had initially negative screening results, highlighting the possibility of infection acquired later in pregnancy. Due to penicillin unavailability, all infants received ceftriaxone despite limited supporting evidence. The cases emphasize the importance of appropriate repeat maternal testing, follow-up and treatment of seropositive mothers, systematic infant evaluation, and reliable access to penicillin.
Very rarely, live attenuated varicella zoster virus (VZV) vaccine recipients develop herpes zoster (HZ) without a preceding history of clinical varicella. A 14-month-old girl without prior varicella developed vesicles on her right arm and back. She received zoster vaccine live (ZVL) on the right arm 65 days earlier. A rapid immunochromatographic VZV antigen detection kit (DermaQuick VZV, Maruho, Osaka, Japan) was positive. Because PCR strain typing was not performed, the causative agent could not be definitively identified as the vaccine strain; therefore, breakthrough varicella or HZ due to wild-type VZV could not be completely ruled out. Based on the clinical and laboratory findings, she was diagnosed with HZ. Weight-adjusted oral valacyclovir was initiated at 200mg four times daily for seven days. At seven-day follow-up, the vesicles had resolved into erythema and erythematous papules accompanied by desquamation in some areas. Assuming the HZ in our current case originated from the ZVL strain, it is hypothesized that the administered virus replicated locally in the skin, traveled retrogradely via sensory nerves to establish latency, and subsequently reactivated to cause HZ in the dermatome that corresponded to the injection site. Clinicians should include HZ in the differential diagnosis when they encounter a unilateral vesicular eruption in an immunocompetent infant with no history of varicella. DermaQuick, a simple and minimally invasive method, is extremely useful for rapidly diagnosing such cases.
Acute otitis media (AOM) is a common infection, whereas peripheral facial nerve palsy is an uncommon extracranial complication in the post-antibiotic era. We report the case of a 53-year-old immunocompetent man who developed acute suppurative otitis media complicated by ipsilateral peripheral facial nerve palsy following an upper respiratory tract infection. The illness began with sore throat and cough during Hajj and progressed to severe right-sided otalgia, followed by complete right lower motor neuron facial weakness despite sequential empirical oral antibiotics. On return to Pakistan, otoscopy demonstrated a bulging, pulsating opaque tympanic membrane. Laboratory investigations revealed neutrophilic leukocytosis with normal glycated hemoglobin. Computed tomography of the temporal bones showed acute right oto-mastoiditis with middle ear opacification, an air-fluid level within the mastoid, and subtle possible erosive change along the lateral facial nerve canal without intracranial extension. The patient was treated conservatively with intravenous ceftriaxone, oral corticosteroids, and early structured facial physiotherapy. Facial nerve function improved by approximately 70% within 10 days and recovered completely by day 25 without surgical intervention. This case highlights the importance of recognizing facial nerve palsy as a rare but potentially reversible complication of AOM. It also emphasizes the increased burden of upper respiratory tract infections during mass gatherings and the need for early otologic and neurological evaluation in pilgrims presenting with persistent otalgia or new facial asymmetry to facilitate timely treatment and favorable outcomes.
Ocular toxoplasmosis is the most common cause of infectious posterior uveitis worldwide and may lead to irreversible visual impairment when the macula is involved. Definitive diagnosis remains challenging because clinical manifestations overlap with those of other infectious and inflammatory retinal disorders. We report a case of active ocular toxoplasmosis involving the fovea in an immunocompetent 44-year-old man presenting with progressive unilateral visual loss and central scotoma. Ophthalmic examination revealed keratic precipitates, mild vitritis, and a yellow-white inflammatory lesion involving the macular region. Fluorescein angiography demonstrated progressive hyperfluorescent staining, and optical coherence tomography showed a hyperreflective subfoveal lesion. Serological testing was positive for anti-Toxoplasma gondii IgM and IgG antibodies. Intraocular fluid analysis demonstrated positive anti-Toxoplasma IgG, while metagenomic next-generation sequencing (mNGS) directly identified Toxoplasma gondii DNA, providing molecular evidence supporting the diagnosis. The patient denied cat ownership or close feline exposure but reported occasional consumption of raw salmon. Treatment consisted of oral trimethoprim-sulfamethoxazole combined with methylprednisolone and two intravitreal injections of clindamycin plus dexamethasone. Significant regression of the retinal lesion was observed after treatment. This case highlights the diagnostic value of intraocular fluid mNGS in ocular toxoplasmosis and emphasizes the importance of considering ocular toxoplasmosis in patients presenting with posterior uveitis involving the macula, even in the absence of traditional epidemiological risk factors.
Drug-induced liver injury (DILI) is an important and frequently under-recognized cause of acute hepatitis. Antibiotics represent one of the most commonly implicated drug classes. Azithromycin, a widely used macrolide antibiotic, is generally well tolerated; however, rare cases of idiosyncratic hepatotoxicity have been reported in the literature. This report describes a case of azithromycin-induced acute hepatocellular liver injury in a previously healthy 20-year-old male who developed jaundice, elevated aminotransferases, and hyperbilirubinemia within three days of initiating a standard three-day course of oral azithromycin 500mg once daily (cumulative dose 1,500mg) prescribed for an upper respiratory tract infection. Biochemical analysis demonstrated a hepatocellular pattern of injury, confirmed by an R-value of 10.6 (ALT/ULN ÷ ALP/ULN), which exceeds the threshold of 5 required for this classification according to international guidelines. Viral hepatitis and autoimmune etiologies were excluded, and the patient specifically denied the use of dietary supplements, vitamins, bodybuilding or protein powders, and herbal remedies. Causality was assessed using the Roussel Uclaf Causality Assessment Method (RUCAM); on recalculation using the 2016 updated criteria, the score is 6, consistent with a probable causal relationship. The patient recovered fully with supportive care following prompt drug discontinuation, with normalization of liver function tests within eight weeks. This case highlights the importance of accurate biochemical classification of DILI, rigorous causality assessment, and heightened clinical vigilance when prescribing azithromycin even under standard guideline-recommended dosing regimens in young patients without pre-existing liver disease.
Background Herpes zoster ophthalmicus is caused by reactivation of varicella-zoster virus in the ophthalmic division of the trigeminal nerve. Optic neuritis is an uncommon but vision-threatening complication, and bilateral optic nerve involvement in immunocompetent individuals is exceptionally rare. Case Presentation A 40-year-old immunocompetent man presented with acute right frontal and periorbital pain followed by a vesicular rash in the right ophthalmic division, including Hutchinson’s sign. Initial visual acuity was normal, and oral valacyclovir was started. Within days, he developed rapidly progressive visual loss in the right eye with optic disc edema and right optic nerve enhancement on orbital magnetic resonance imaging. Cerebrospinal fluid analysis and systemic autoimmune and infectious workups were unrevealing. After admission, oral valacyclovir was switched to intravenous acyclovir, and oral corticosteroid therapy was initiated. On the following day, visual acuity in the right eye declined to light perception, and the previously unaffected left eye developed decreased visual acuity, impaired color vision, and visual field defects. Corticosteroid treatment was therefore escalated to intravenous methylprednisolone pulse therapy. Because of subsequent bilateral visual deterioration, intravenous immunoglobulin was added and administered for 5 days. Despite partial radiologic improvement, vision in the right eye progressed to permanent no light perception. Left eye visual acuity partially recovered to 0.9 (approximately 20/22 Snellen) at follow-up. Conclusion This case highlights the fulminant course of herpes zoster ophthalmicus-associated optic neuritis and shows that bilateral optic nerve involvement may occur even in immunocompetent patients. Early recognition, close monitoring of both eyes, and prompt escalation of therapy are critical when optic nerve involvement is suspected.
Mycoplasma hominis is a fastidious, cell wall-deficient bacterium that typically colonizes the genitourinary tract but can cause invasive extragenital infections in immunocompromised hosts. Such infections have been reported primarily in patients receiving rituximab; however, they have not been previously described with obinutuzumab therapy. We report a case of M. hominis septic arthritis of the shoulder in a 70-year-old man with chronic lymphocytic leukemia/small lymphocytic lymphoma treated with Obinutuzumab. The patient presented with several months of progressive shoulder pain and radiographic evidence of rapidly destructive arthritis. Repeated joint aspirations and early cultures were negative, and he required multiple surgical washouts because of extensive purulence and periarticular abscess formation. Extended incubation of synovial fluid and tissue cultures ultimately identified M. hominis. Antimicrobial therapy was transitioned to levofloxacin and doxycycline, which were administered for six weeks with good tolerance and sustained clinical improvement. At follow-up, the patient remained free of recurrent infection with gradual recovery of shoulder function. This case highlights M. hominis as an emerging opportunistic pathogen in patients receiving newer anti-CD20 monoclonal antibodies and expands the recognized infectious complications of obinutuzumab-induced B-cell depletion. Because M. hominis lacks a cell wall, routine diagnostic methods and empiric β-lactam therapy may be ineffective, resulting in diagnostic delays. Awareness of this organism and early consideration of targeted therapy are critical to improving outcomes in immunocompromised patients.
Invasive aspergillosis is a rare and often life-threatening manifestation of Aspergillus fungal infection affecting multiple organs. It tends to occur in immunocompromised patients, such as those with haematological malignancy receiving immunosuppressive treatments. Although pulmonary infection following inhalation is the principal route of acquisition, angioinvasive dissemination may result in involvement of multiple highly vascular organs, including the eye, myocardium and brain. This case report describes an 83-year-old man with chronic lymphocytic leukaemia (CLL) receiving the bruton tyrosine kinase (BTK) inhibitor acalabrutinib, who presented with left-sided Aspergillus fumigatus panuveitis and was subsequently diagnosed with disseminated invasive aspergillosis involving the lungs, myocardium and brain. Pulmonary nodules identified on prior surveillance imaging suggested the lungs as the most likely portal of entry, with subsequent haematogenous dissemination to the eye, heart and central nervous system. Cardiac involvement manifested as myocardial infiltration with high-grade 2:1 atrioventricular block. Diagnosis was established using ocular culture and Polymerase Chain Reaction (PCR) confirming Aspergillus fumigatus, positive serum beta-D-glucan and multimodality imaging. The patient was treated initially with intravenous liposomal amphotericin B, before transition to oral isavuconazole following multidisciplinary specialist review. Despite treatment, the patient deteriorated with evidence of progressive disseminated disease. He was eventually palliated due to poor predicted prognosis, and subsequently died. This case highlights the importance of recognising disseminated invasive aspergillosis in patients receiving BTK inhibitor therapy, appreciating that ocular involvement commonly represents haematogenous dissemination rather than the primary site of infection, and considering early multidisciplinary assessment with prompt antifungal therapy when cardiac or central nervous system involvement is suspected.
Visceral leishmaniasis is a vector-borne disease caused by protozoan parasites of the genus Leishmania and is endemic in parts of East Africa, including Ethiopia. Coinfection with HIV is associated with atypical clinical manifestations, reduced serologic sensitivity, and frequent relapse. We describe a 48-year-old Ethiopian man with a five-month history of dysphagia, odynophagia, and progressive weight loss. Examination revealed hepatosplenomegaly, and laboratory testing showed anemia and thrombocytopenia. Upper gastrointestinal endoscopy demonstrated multiple ulcerated, mass-like growths of the lower esophagus causing luminal narrowing; biopsy revealed numerous Leishmania amastigotes exhibiting the “marquee sign.” Splenic and bone marrow aspirates were negative for parasites. Subsequent HIV testing was positive, with a CD4+ count of 133 cells/µL, representing the first indication of previously undiagnosed HIV infection. The patient was treated with intravenous liposomal amphotericin B and antiretroviral therapy, with marked clinical improvement; repeat endoscopy and biopsy after treatment showed resolution of the esophageal lesions and clearance of the parasite. This case illustrates that esophageal involvement, although rare, may be the initial presentation of visceral leishmaniasis and can unmask previously undiagnosed advanced HIV infection. Clinicians practicing in leishmania-endemic regions should consider this diagnosis in patients with unexplained esophageal masses, particularly when biopsies for malignancy are inconclusive.
Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy. While ICIs have shown efficacy across a range of malignancies, they have also been associated with immune-related adverse events (irAEs) and there is increasing concern that ICIs may predispose patients to opportunistic infections. We report six cases of clinically significant nontuberculous mycobacterial (NTM) infections occurring during or after ICI therapy. Key findings include the prevalence of underlying lung disease in patients diagnosed with NTM infection (including primary pulmonary malignancy or metastases), predominance of anti-PD-1/PD-L1 exposure in our cohort, wide range of NTM species identified, wide temporal windows between ICI therapy and NTM infection, and overall good outcomes after NTM-directed therapy with four of five patients who received NTM-directed therapy alive at one year after NTM diagnosis. We recommend that clinicians maintain a high index of suspicion for NTM infections in the differential for patients who have received ICI therapy and we recommend ongoing investigation into the potential correlation between ICI therapy and NTM infection.
Background Polymicrobial pneumonia caused by multiple pathogens is increasingly recognized in immune compromised individuals with comorbidities such as type 2 diabetes mellitus (T2DM). The immunocompromised state associated with T2DM predisposes patients to polymicrobial opportunistic infections, including multidrug-resistant bacteria and fungi. Prompt laboratory diagnosis and organism-specific treatment are critical for optimal outcomes.Case presentation:We report the case of a 53-year-old male with newly diagnosed T2DM who presented with a three-month history of left-sided chest pain, dry cough, dyspnoea, and persistent fever. Initial empirical antibiotic therapy with intravenous ceftriaxone was ineffective. Computed tomography (CT) with contrast imaging revealed a massive loculated left pleural effusion with compressive atelectasis. Analysis of microbiological culture and sensitivity results revealed a polymicrobial infection involving multidrug-resistant Klebsiella pneumoniae, Enterobacter spp with inducible AmpC resistance, and fluconazole-susceptible dose dependent Candida glabrata. Based on the laboratory results, intravenous meropenem, high dose antifungal therapy, and subsequent oral fluconazole were recommended and led to successful treatment. Glycaemic control was concurrently optimized with insulin therapy and initial random blood sugar levels were 16.7 mmole per l, and at discharge was 9.3 mmoles per l. Conclusion This case emphasizes the importance of considering polymicrobial infections in diabetic patients presenting with unresolving pneumonia. Early use of imaging and microbiological analysis of the pleural fluid enabled prompt identification of the polymicrobial causative organisms, guiding tailored antimicrobial therapy. Multidisciplinary management is essential in improving outcomes in such complex cases.
We report a case of secondary haemophagocytic lymphohistiocytosis (HLH) triggered by confirmed typhoid fever (Salmonella Typhi) in a 23-year-old Senegalese man. The initial radiological presentation suggested ileo-caecal tuberculosis. Thus, persistent fever, marked hyperferritinaemia and systemic inflammation raised suspicion of HLH, confirmed by bone marrow examination demonstrating hemophagocytosis. The H-Score was 206, corresponding to 88–93% probability. Blood cultures isolated ciprofloxacin-susceptible Salmonella Typhi. Fluoroquinolone monotherapy led to complete clinical and biological remission without the need for immunosuppression. This case underscores the importance of including typhoid fever in the differential aetiology of HLH in endemic settings, and of early H-Score calculation to expedite diagnosis.
Cholera is an infectious disease caused by Vibrio cholerae which has caused several global pandemics since 1817. Currently, Japan is not a cholera-endemic country, and only a few cases of imported disease are reported annually. Vibrio cholerae is classified into more than 200 serogroups according to the differences in the O antigen on the cell surface, and only the O1 or O139 groups that produce cholera toxins are called cholera.We report a case in which toxigenic Vibrio cholerae O1 was detected in a 64-year-old Japanese traveler returning from Delhi, India, who presented with diarrhea without rice-water stools. Multiple potential diarrheal pathogens were simultaneously detected, including Clostridioides difficile toxin A/B and pathogenic Escherichia coli (E. coli) including enteroaggregative, enteropathogenic, and enterotoxigenic E. coli, making definitive attribution of symptoms to a single pathogen difficult by Genetic testing (BioFire FilmArray Gastrointestinal Panel).This case highlights the diagnostic uncertainty that arises with multiplex PCR-based stool testing: while such panels improve detection sensitivity, distinguishing true infection from colonization remains a clinical challenge. Clinicians should integrate laboratory findings with travel history and clinical course rather than relying solely on molecular test results.
Background Severe mpox is increasingly reported in people living with HIV (PLHIV). While immune reconstitution inflammatory syndrome (IRIS) is well-characterised in other opportunistic infections, its role in the acute clinical course of mpox remains poorly understood. Case presentation A 42-year-old man from eastern South Kivu, Democratic Republic of the Congo (DRC), with newly diagnosed HIV initiated tenofovir/lamivudine/dolutegravir. Two weeks later, he developed severe disseminated clade I mpox, confirmed by PCR, with more than 250 polymorphic lesions. Around day 7 of admission, while afebrile, he experienced paradoxical clinical worsening with confluent hemorrhagic and necrotic plaques, which were highly suggestive of mpox-associated IRIS. A pragmatic management protocol consisting of a 6-week tapered course of oral prednisone, broad-spectrum oral antibiotics (levofloxacin and clindamycin), high-dose acyclovir, and supportive care led to progressive skin healing and clinical recovery while ART was continued. He was discharged after 62 days at the family's request. Unfortunately, 3.5 weeks post-discharge, he died at home following the application of traditional topical preparations to residual lesions. Conclusions This case highlights the need to consider mpox-associated IRIS in the differential diagnosis of unexplained clinical worsening of mpox in PLHIV who recently initiated ART. Although definitive confirmation of IRIS was not possible because of limited immunological investigations, the temporal association with ART initiation and the clinical course were consistent with this diagnosis. This case underscores the need for standardized diagnostic criteria, prospective evaluation of adjunctive anti-inflammatory therapies, and strengthened post-discharge community follow-up in resource-limited settings.
Cefiderocol (CFDC) is a siderophore cephalosporin with activity against multidrug-resistant Gram-negative pathogens, and it is considered a treatment option for refractory Gram-negative infections. Because CFDC is primarily eliminated by the kidneys, dose individualization is required in patients with renal impairment and in those receiving renal replacement therapy. During continuous hemodiafiltration (CHDF), drug clearance is influenced not only by residual renal function but also by dialysis and filtration flow rates and membrane characteristics; thus, careful determination of dose and dosing interval is necessary. However, real-world evidence on CFDC dosing during CHDF, particularly for prolonged courses, remains limited. We report a case of refractory Pseudomonas aeruginosa bacteremia in a patient with an implanted left ventricular assist device receiving CHDF, successfully managed with a 55-day course of CFDC using a dosing strategy tailored to CHDF settings.
Pyogenic granuloma is a benign vascular lesion that sometimes originates from the inferior turbinate. We report a case of a 57-year-old man with a pyogenic granuloma arising from the right inferior turbinate that caused secondary sinusitis with symptoms resembling chronic rhinosinusitis. The patient had a domestic cat and frequently allowed the cat to lick his face. Endoscopic examination revealed a large nasal lesion covered with purulent exudate, and the lesion was surgically resected at its pedicle. Tissue culture yielded Pasteurella multocida and Group G Streptococcus, indicating secondary polymicrobial infection of the pyogenic granuloma. The patient recovered without postoperative complications. This case highlights an unusual secondary infection of a nasal pyogenic granuloma with the zoonotic pathogen P. multocida following close contact with a domestic cat.
Wohlfahrtiimonas chitiniclastica (W. chitiniclastica) is an emerging zoonotic Gram-negative pathogen. Over 40 human infections have been documented worldwide. Poor hygiene conditions and chronic wounds are recognized as high-risk factors for infection. We report a case of W. chitiniclastica infection in a patient with a sprain complicated by type 2 diabetes mellitus. Due to suboptimal glycemic control during the early hospitalization period, the wound progressed to an active infection. This case indicates that W. chitiniclastica may possess virulence capable of causing severe local and systemic infections in diabetic patients. Clinically, diagnosis should be confirmed through pathogen detection, and early intervention may reduce the occurrence of serious complications.
Background Cervicofacial cellulitis (CCF) is a severe deep neck infection involving the cervical fascial spaces, most commonly of odontogenic origin. It may rapidly extend to adjacent compartments and lead to life-threatening complications such as mediastinitis, necrotizing fasciitis, and septic shock. In immunocompromised patients, particularly those infected with human immunodeficiency virus (HIV), the clinical course may be more aggressive due to impaired cellular immunity. Aim This study aims to report two cases of severe cervicofacial cellulitis revealing previously undiagnosed HIV infection and to emphasize the importance of early diagnosis and multidisciplinary management. Cases We describe two patients who presented with extensive cervicofacial cellulitis complicated by mediastinal extension and systemic involvement. Both required urgent contrast-enhanced computed tomography, broad-spectrum intravenous antibiotics, and extensive surgical drainage. In the first case, the infection progressed to septic shock and necrotizing fasciitis. The causal tooth was extracted during surgery. Microbiological cultures isolated Klebsiella pneumoniae and α-hemolytic Streptococcus. In both cases, HIV infection was diagnosed during hospitalization. Conclusion Cervicofacial cellulitis may represent the first clinical manifestation of undiagnosed HIV infection. Severe or atypical deep neck infections should prompt systematic HIV screening. Early imaging, targeted antimicrobial therapy guided by microbiological findings, and coordinated surgical and medical intervention are essential to improve patient outcomes.
Chikungunya fever is a mosquito-borne viral illness that is increasingly recognized for its atypical and multi-organ involvement. Although self-limiting, it can affect multiple organ systems, including the nervous and ocular systems. Ocular manifestations, particularly retinitis with retinal detachment, are vision-threatening. Recent outbreaks in endemic regions have demonstrated an expanding clinical spectrum, with increasing reports of severe and atypical complications. We report a pediatric case presented with chikungunya infection and concurrent UTI with septicemia. Visual impairment was noted, progressing to bilateral vision loss. Ophthalmic findings showed posterior segment involvement with extensive retinitis with retinal detachment, consistent with post-chikungunya viral retinopathy. Despite treatment with antivirals and corticosteroids, recovery was minimal, resulting in irreversible retinal damage. This case highlights the importance of prompt clinical evaluation and early ophthalmic referral to recognize chikungunya-associated retinitis. Severe bilateral retinitis with early profound visual impairment in pediatric chikungunya is uncommon, emphasizing the need for increased clinical awareness.
