In July 2022, an outbreak characterized by fever, diarrhea, and mortality occurred among suckling calves at a beef calf-rearing farm in Tottori Prefecture in Japan. A monophasic variant of Salmonella enterica serovar Typhimurium (Salmonella 4,[5],12:i:-) was subsequently isolated from a deceased calf. In August 2022, a persistently infected (PI) calf with bovine viral diarrhea virus (BVDV) was identified and subsequently euthanized. Between June and September 2022, the median number of treatments administered per month per calf in the calf-hutch area tended to be higher (P<0.20) and the mortality rate was significantly higher (P<0.05) compared with the same period in 2021. In this outbreak, the PI calf introduced to the farm likely transmitted BVDV to other suckling calves; the resulting immunosuppression may have exacerbated the clinical manifestations of concomitant Salmonella 4,[5],12:i:- infection, leading to substantial production losses on the farm. To our knowledge, this is the first report of a herd-level concurrent infection with BVDV and Salmonella 4,[5],12:i:- in Japan.

A previously healthy woman in her early 30s developed rash, fever and arthralgia 3 weeks after SARS-CoV-2 infection, rapidly progressing to multiorgan failure. Laboratory studies revealed severe thrombocytopenia (23×109/L), microangiopathic haemolytic anaemia, acute kidney injury and ferritin >100 000 ng/mL. Kidney biopsy demonstrated thrombotic microangiopathy with negative antinuclear antibody, supporting atypical haemolytic uraemic syndrome (aHUS). Concurrently, low haptoglobin, elevated lactate dehydrogenase (2500 U/L), interleukin-2 receptor (18 644), triglycerides (425 mg/dL) and splenomegaly supported haemophagocytic lymphohistiocytosis (HLH). Despite plasmapheresis, corticosteroids, etoposide, eculizumab and continuous renal replacement therapy, she died 7 weeks after SARS-CoV-2 infection. Autopsy confirmed aHUS with extensive thrombotic microangiopathy and HLH with bone marrow haemophagocytosis. This case underscores the importance of recognising concurrent aHUS and HLH after COVID-19, as complement-mediated injury and hyperinflammation may produce catastrophic outcomes.

A preadolescent HIV-positive girl from Southern Africa presented to a public healthcare facility with fever and unilateral facial and neck swelling. Clinical examination revealed generalised lymphadenopathy, hepatosplenomegaly, hypertension and haematuria. A provisional diagnosis of poststreptococcal glomerulonephritis was made; however, when the patient displayed no clinical improvement on supportive treatment, she was referred to a tertiary hospital for further evaluation. The peripheral blood smear showed marked agglutination, which improved on warming. Serum protein electrophoresis demonstrated a monoclonal protein, yet the bone marrow plasmacytosis of 30% was polyclonal and human herpesvirus 8 negative. Subsequently, a lymph node biopsy confirmed a diagnosis of plasmacytic idiopathic multicentric Castleman disease. The atypical presentation contributed to delayed diagnosis and prompted unnecessary invasive investigations in a paediatric patient.

Brazilian spotted fever, caused by Rickettsia rickettsii, is a life-threatening tick-borne disease endemic to southeastern Brazil and is associated with high mortality when treatment is delayed. Central nervous system involvement poses a particular diagnostic challenge because of nonspecific early symptoms and frequent misdiagnosis as dengue or leptospirosis. We report a case illustrating characteristic neuroimaging findings and therapeutic considerations in rickettsial encephalitis. We describe the clinical course, cerebrospinal fluid (CSF) findings, magnetic resonance imaging (MRI) findings, serologic results, and treatment response in a 23-year-old man who presented with febrile encephalopathy in an endemic region of Brazil. The patient had a five-day history of fever, erythematous macules, and progressive encephalopathy. CSF analysis showed elevated protein and lymphocytic pleocytosis. MRI showed T2/fluid-attenuated inversion recovery hyperintensities with restricted diffusion involving the bilateral corticospinal tracts and the splenium of the corpus callosum, forming a "boomerang" pattern. Clinical improvement followed initiation of empirical doxycycline and pulse methylprednisolone. Serologic testing supported the diagnosis of R. rickettsii infection with a positive immunoglobulin M titer of 1:512. Follow-up MRI showed near-complete lesion resolution at 4 months, with a residual splenial lesion persisting at 18 months. This case illustrates the importance of recognizing characteristic MRI patterns, including the "starry sky" and "boomerang" signs, as diagnostic clues in rickettsial encephalitis, even when the classic triad is incomplete. Early empirical doxycycline remains critical for neurologic outcomes, and adjunctive corticosteroids may have a role in selected cases when immune-mediated central nervous system injury is suspected.

Tuberculous meningitis (TBM) is a severe and often fatal form of extrapulmonary tuberculosis. We describe a case in which the initial cerebrospinal fluid (CSF) analysis showed no specific abnormalities, but a diagnosis was established after repeat CSF evaluation. A 41-year-old female presented with a 10-day history of persistent fever and headache. Initial CSF analysis demonstrated an opening pressure of 150 mmH2O, a white blood cell (WBC) count of 10/μL, a glucose level of 50 mg/dL, and a protein level of 31.4 mg/dL. Despite treatment with an antiviral agent and doxycycline, her symptoms did not improve. A repeat CSF analysis demonstrated an opening pressure of 120 mmH2O, an elevated WBC count of 140/μL (55% lymphocytes), a glucose level of 52 mg/dL, and an elevated protein level of 201.6 mg/dL, which was highly suggestive of TBM. This case highlights the importance of repeat CSF analysis based on clinical judgment when diagnosing TBM.

French Guiana (FG), an Amazonian French territory, represents a unique ecological and epidemiological setting for tick-borne diseases (TBDs). In contrast to mainland France, where TBDs are well-documented, data from FG remain scarce. We carried out a systematic review using the PRISMA criteria for our search of the PubMed, ScienceDirect, and SciELO data bases. We identified 68 articles, of which 43 met our inclusion criteria. Data from FG were compared with those originating from mainland France. Albeit highly prevalent in Europe, and notwithstanding detection of a distinct Borrelia species in bird-associated ticks, there have been no confirmed autochthonous cases of Lyme disease in French Guiana. Conversely, Q fever occurs more frequently in this overseas territory than in mainland France, even though its causative agent, Coxiella burnetii, has been detected only one time in a local tick. While Rickettsia spp. are widely present in tick populations, no human rickettsiosis has been reported. As for Anaplasma and Ehrlichia spp., they have been identified in wildlife, domestic animals, and ticks, but with only one documented human case of chronic anaplasmosis, which was caused by a novel species, Candidatus Anaplasma sparouinense. Other pathogens, including Babesia, Bartonella, and filarial nematodes, have been detected in animals or ticks, but without evidence of human infection. Of note, emerging conditions have been described, one example being alpha-gal syndrome, an allergy triggered by tick bites to mammalian meat. To summarize, available data remain limited, and in all likelihood, the burden of TBDs in FG is underestimated. Integrated research combining human, animal and environmental surveillance is needed to more precisely characterize epidemiology, assess risks, and facilitate preventive strategies.

Dengue virus (DENV) infection causes a broad spectrum of clinical manifestations, ranging from self-limiting dengue fever (DF) to life-threatening severe dengue (SD). Increased vascular permeability and endothelial dysfunction are hallmarks of SD and contribute to plasma leakage, shock, and multi-organ injury, yet the underlying mechanisms remain incompletely understood. Here, we integrated dynamic bulk and single-cell RNA sequencing data from peripheral blood mononuclear cells (PBMCs) of dengue patients at different disease stages to investigate the mechanisms associated with disease progression. Complement-related signatures were prominently altered in patients with dengue with warning signs (DWS) and SD, with monocytes emerging as a major cellular source of increased C1Q genes (C1QA, C1QB, and C1QC) expression. These findings implicated monocyte-derived C1q and classical complement pathway activation in dengue progression. Using a severe dengue mouse model, we further demonstrated systemic complement activation and deposition of the terminal complement effector membrane attack complex (MAC), which was associated with microvascular endothelial damage and multi-organ injury. Importantly, inhibition of the classical complement pathway with C1INH (C1 esterase inhibitor) significantly alleviated vascular barrier dysfunction and multi-organ injury in severe dengue mice. Collectively, our findings identify monocyte-derived C1q and dysregulated classical complement activation as important contributors to vascular endothelial and multi-organ injury in SD and suggest that targeting the classical complement pathway may represent a potential therapeutic strategy for severe dengue.

Severe fever with thrombocytopenia syndrome virus (SFTSV), a World Health Organization (WHO) priority pathogen, causes hemorrhagic fever with up to 30% case fatality and lacks approved vaccines or therapeutics. Here, we isolated Gc-specific monoclonal antibodies H2, H4, and H12. H2 potently neutralized endemic Chinese SFTSV strains but failed against the heterologous NB24 strain. Mutational analysis identified Arg577 within Gc domain I as a critical residue essential for H2 binding. Reverse genetics demonstrated that Arg577 is both necessary for H2 binding and sufficient to confer neutralization susceptibility. Beyond immune recognition, residue 577 critically governed viral replication fitness and pathogenesis. In virulent HBMC, Arg577 was essential for efficient replication, assembly and overall viral fitness; in attenuated NB24 (native lysine), introducing Arg577 enhanced progeny production and virulence. Combining H2 with H12 overcame H2's narrow neutralization, achieving broad protection. Our study establishes Arg577 as a central regulator of SFTSV pathogenicity and informs dual-antibody therapy development.

Extraction-string ureteral stents facilitate non-cystoscopic removal after ureteroscopy, but concerns remain regarding postoperative infection and accidental dislodgement. We evaluated whether extraction-string stents were associated with postoperative infection after flexible ureteroscopic lithotripsy (fURSL) in a cohort restricted to procedures with the distal Double-J (D-J) stent portion positioned within the bladder. This retrospective observational study included 102 procedures in 92 unique patients: 58 extraction-string and 44 conventional non-string procedures. Postoperative infection was defined as fever > 38 °C or a positive postoperative urine culture during the stent-indwelling period. Propensity scores incorporated age, sex, positive preoperative urine culture, preoperative pyuria, and procedure laterality. Stabilized inverse probability of treatment weights were truncated at the 1st and 99th percentiles; effective sample size was 85.38. Crude postoperative infection occurred in 8/58 (13.8%) extraction-string and 6/44 (13.6%) non-string procedures. After weighting, estimated infection rates were 13.6% and 8.8%, respectively (OR 1.64, 95% CI 0.50-5.44; P = 0.416). Fever, positive postoperative urine culture, postoperative pyuria, and postoperative day 1 pain did not differ significantly. Sensitivity analyses accounting for repeated procedures and propensity-model specification were consistent with the primary analysis. Extraction-string stent use was not significantly associated with postoperative infection after fURSL; however, the limited number of events and wide confidence intervals preclude exclusion of a clinically meaningful difference.

Salmonella Typhi is an invasive pathogen with sustained bacteraemia and intracellular persistence, requiring therapy that achieves systemic exposure and intracellular penetration. Clinical efficacy should remain central to therapeutic decision-making, while pharmacokinetic/pharmacodynamic (PK/PD) analyses provide complementary insights into dose optimization and the pharmacological limitations of candidate therapies. Oral therapy remains central to typhoid fever management, particularly in South and Southeast Asia, where most patients are managed in the outpatient setting. However, the emergence of MDR and extensively drug-resistant (XDR) S. Typhi has substantially narrowed the available oral treatment options. Azithromycin remains the only widely available oral agent with established clinical efficacy, but emerging resistance threatens its continued utility. Several alternative oral agents, including mecillinam, faropenem, tebipenem, fosfomycin and β-lactam/β-lactamase inhibitor combinations, demonstrate favourable in vitro activity against S. Typhi. However, robust clinical efficacy and contemporary PK/PD data are lacking to support their use against MDR and XDR S. Typhi. Addressing these evidence gaps through integrated PK/PD investigations and prospective clinical trials will be essential to expand the oral therapeutic armamentarium for typhoid fever.