A globally prevalent human cytomegalovirus (HCMV), capable of establishing a lifelong infection in the host, exists in a latent state and can reactivate. Viral transmission can occur through contact with the bodily fluids of infected individuals, such as saliva, semen, urine, and breast milk. The infection is usually asymptomatic. However, immunocompromised individuals are more prone to experience severe complications, including pneumonia, organ damage, and retinitis. Because of high levels of HCMV in breast milk, breastfeeding by seropositive mothers may lead to viral transmission, which is most hazardous in low-birth-weight and very preterm infants. During infection, thrombocytopenia and inflammation of the lungs, liver, retina, and meninges may occur. To date, risk mitigation strategies have included pasteurization of breast milk. HCMV latency is defined as the presence of the viral genome in the infected cell without the production of infectious viral particles. This state is regulated by viral proteins, such as LUNA, UL138, and US28, as well as viral miRNAs, which silence transcription of immediate-early genes. The virus also avoids eliciting an immune response by suppressing the MHC class II presentation, utilizing viral IL-10 homologs, and impairing T-cell recognition. The reactivation of HCMV can be triggered by cellular differentiation or by the release of inflammatory cytokines, leading to the re-expression of viral IE genes and subsequent viral replication. This review summarizes the current knowledge of HCMV's molecular biology and pathogenesis, emphasizing the interplay between viral and host factors during latency and reactivation. It also highlights the importance of milk-mediated infection and its implications for neonatal health.

Pneumocystis jirovecii pneumonia (PJP) remains a life-threatening lower respiratory tract infection associated with respiratory failure in patients with impaired T-cell immunity. Its incidence is increasing in non-HIV patients, who typically experience a more severe disease course and poorer outcomes than HIV patients. Keeping a high level of suspicion for PJP when confronted to an immunocompromised patient presenting with an acute respiratory failure (ARF) is essential to start promptly the treatment and thereby reduce associated morbidity and mortality.

Despite the decline of the global peak of COVID-19, SARS-CoV-2 continues to circulate, evolve, and undergo immune escape, posing persistent threats, particularly to older adults, individuals with comorbidities, and immunocompromised populations. Although existing vaccination strategies have substantially reduced the risks of severe disease, hospitalization, and death, their ability to block infection and transmission remains limited, and protection wanes over time. Current heterologous booster strategies still rely largely on combinations of different parenteral vaccine platforms. Although these regimens can enhance systemic humoral and cellular immunity, they are insufficient to robustly induce upper respiratory mucosal immunity, thereby limiting their role in early infection control and interruption of transmission. Because respiratory mucosal vaccines target the natural entry site of SARS-CoV-2, they have the potential to induce secretory IgA, tissue-resident memory immune cells, and local immune memory, offering distinct advantages in compensating for the shortcomings of conventional heterologous boosting. Combining heterologous boosting with respiratory mucosal delivery may further enhance the control of viral infection, early replication, and subsequent transmission while preserving systemic immunity, thereby providing more comprehensive immune protection for high-risk populations. However, this strategy still faces challenges related to mucosal barriers, delivery efficiency, adjuvant safety, manufacturing scale-up, and incomplete clinical evaluation frameworks. Future high-quality studies focusing on high-risk populations are needed to clarify its value in preventing infection, protecting against severe disease, and providing long-term protection.

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.

Renal transplant patients (RTPs) receiving immunomodulatory therapy are at increased risk of severe complications from COVID-19 and other infections. This study aimed to identify immune and proteomic biomarkers associated with COVID-19 in RTPs to improve disease characterization and support future diagnostic and therapeutic strategies.

Pseudomonas aeruginosa is a major opportunistic pathogen frequently associated with nosocomial infections, such as pneumonia, urinary tract infections, and wound infections, particularly in immunocompromised or hospitalized patients. These infections are often difficult to treat due to the pathogen's intrinsic antibiotic resistance and biofilm-forming ability. Therefore, rapid and selective detection of P. aeruginosa is essential for early diagnosis and effective infection control. In this study, a novel surface-imprinted MIP design uniquely combines methacrylamide (MAM), acrylamide (AAM), and vinylpyrrolidone (VP) monomers to generate recognition cavities that are complementary to the surface morphology and physicochemical properties of Pseudomonas aeruginosa cells. Unlike traditional MIP approaches, this surface imprinting strategy provides improved stability and reproducibility, without relying on biological recognition elements like antibodies or aptamers. This novel approach enabled us to achieve an ultralow LOD of 1 CFU/mL over a linear range of 1-10[4] CFU/mL, demonstrating excellent analytical performance. In addition, the sensor exhibited good reproducibility with an RSD of 5-12%. The novelty of this work lies in the use of a surface-imprinted MIP strategy combined with a multi-monomer system to enhance bacterial recognition and sensing performance. Overall, the proposed MIP-based electrochemical biomimetic sensor offers a rapid, cost-effective, and portable platform with strong potential for the detection of P. aeruginosa in clinical and environmental applications.

Pneumocystis is an opportunistic fungal pathogen that causes severe Pneumocystis pneumonia (PCP) in immunocompromised individuals and laboratory animals. Three host-specific species-Pneumocystis murina (P. murina), Pneumocystis carinii (P. carinii), and Pneumocystis jirovecii (P. jirovecii)-are closely associated with infections in humans and laboratory animals. However, the conventional method, microscopic staining, suffers from low sensitivity, operator-dependent subjectivity, and inability to differentiate species, highlighting the urgent need for a multiplex qPCR assay. In this study, we established a multiplex qPCR method targeting the mtLSUrRNA gene of P. murina, the TS gene of P. carinii, and the mtSSUrRNA gene of P. jirovecii. Primers and probes were designed and optimized using a matrix approach. The method was systematically evaluated for sensitivity, specificity, and reproducibility using recombinant plasmid standards and laboratory animal samples. Validation was performed on 260 mouse lung samples, 30 P. murina-positive samples, 25 rat lung samples, 6 rat bronchoalveolar lavage fluid (BALF) samples, and 8 P. carinii-positive samples. Results were compared with single-plex qPCR and staining microscopy (performed on 68 mouse lung samples, 38 Pneumocystis-positive samples). The limits of detection (LOD) were 5 copies/μL for P. murina, 6 copies/μL for P. carinii, and 8 copies/μL for P. jirovecii. Standard curves showed excellent linearity (R2 ≥ 0.999) with amplification efficiencies of 90-110%. No non-specific reactions were observed with 22 common pathogens, and intra-/inter-group coefficients of variation (CV%) were below 1%. Moreover, interference testing revealed minimal matrix effects on the amplification system and no mutual interference among the primers and probes. The multiplex qPCR detected all 38 positive samples (100%), showing 100% concordance with single-plex qPCR, whereas Giemsa staining detected none (0%) and toluidine blue staining only 60% (3/5) of the tested positives, suggesting that the multiplex qPCR achieved higher detection rates than staining microscopy. In conclusion, this novel multiplex qPCR method offers high sensitivity, specificity, and reproducibility, providing a sensitive and specific tool for laboratory animal health monitoring and epidemiological surveillance. Its clinical application for human PCP diagnosis requires further validation with authentic human specimens.

Serratia spp., particularly Serratia marcescens, have emerged as clinically important opportunistic pathogens and are increasingly recognized as causes of healthcare-associated infections, especially among critically ill and immunocompromised patients. Their remarkable ecological adaptability, persistence in hospital environments, and capacity to acquire multiple antimicrobial resistance determinants have contributed to the global emergence of multidrug-resistant strains and complicated therapeutic management. This review aims to comprehensively analyze the epidemiology, virulence mechanisms, antimicrobial resistance patterns, and current and emerging therapeutic strategies associated with Serratia spp. The manuscript is based on a critical review and analysis of previously published literature retrieved from electronic scientific databases focusing on clinically relevant Serratia spp. infections and resistance trends. The reviewed literature demonstrates that Serratia spp. combine intrinsic resistance mechanisms, particularly inducible chromosomal AmpC β-lactamases, with acquired resistance determinants including extended-spectrum β-lactamases, carbapenemases, aminoglycoside-modifying enzymes, and plasmid-mediated quinolone resistance. Horizontal gene transfer and biofilm formation further enhance bacterial persistence, dissemination, and adaptation within healthcare settings. Clinically, these pathogens are associated with device-related infections, bloodstream infections, pneumonia, urinary tract infections, and hospital outbreaks, where increasing multidrug and carbapenem resistance significantly limits therapeutic options. Novel β-lactam/β-lactamase inhibitor combinations and cefiderocol represent promising therapeutic approaches, although treatment success remains highly dependent on accurate identification of underlying resistance mechanisms. This review highlights the growing public health importance of Serratia spp. and underscores the need for improved surveillance, molecular diagnostics, antimicrobial stewardship, and the development of innovative therapeutic strategies in the context of the evolving antimicrobial resistance crisis.