Biofilms are complex communities of microorganisms enclosed in a self-produced matrix of extracellular polymeric substances consisting of polysaccharides, proteins, lipids and extracellular DNA. These biofilms can form on a variety of surfaces and pose a major challenge in both the medical and industrial sectors as they can harbor pathogenic microorganisms. In healthcare, biofilms form on hospital surfaces, medical devices, patient tissue and implants and contribute to persistent infections that are difficult to treat. In the food industry, biofilms on processing equipment and food matrices can also lead to contamination and pose a serious threat to public health through foodborne diseases. The bacteria embedded in biofilms are much more tolerant to antimicrobial treatments than their planktonic counterparts, necessitating the development of new strategies to combat biofilm-associated infections and contamination. As biofilms mature, they become even more resistant to conventional treatments, making prevention strategies particularly important. This review focuses on enzyme-based strategies that have been developed over the last decade to inhibit biofilm formation. Key approaches such as disruption of microbial signaling pathways and degradation of biofilm matrix components are highlighted, offering promising ways to prevent biofilm-related problems in both medicine and industry.

Pertussis or whooping cough is a highly contagious, vaccine-preventable, respiratory disease caused by Bordetella pertussis, and transmitted through the respiratory tract (aerosol). According to the reports of the World Health Organization and Centers for Disease Control and Prevention, the incidence of pertussis shows periodical variations in certain regions of the world. As humans are the sole reservoir of this bacteria complete vaccination against pertussis and high vaccination coverage is of utmost importance for reducing the incidence and severity of the disease. Two types of pertussis vaccine are available: whole-cell (wP) and acellular pertussis (aP) vaccine. wP contains whole nonviable bacteria, while aP usually contains two or more protein components. These protein components include inactivated pertussis toxin, filamentous hemagglutinin, pertactin, and fimbriae. The acellular vaccine was developed in response to reports of adverse reactions upon administering the whole-cell vaccine in certain countries. Both vaccines are usually formulated with diphtheria and tetanus toxoids, and more recently a trend of combining more antigenic sources such as Haemophilus influenzae type b, hepatitis B, and inactivated poliovirus vaccine has been accepted in many countries, including Serbia. The wP vaccine stimulates a strong immune response more similar to infection, while the response to aP vaccine differs in this respect. Due to the difference in the types of immune response predominating with different types of pertussis vaccines, there are differences in the duration of protection, and it has been reported that wP induces more durable protection. For countries that have adopted aP increased monitoring is advised as well as the inclusion of booster doses. The special focus is on the vaccination of pregnant women to protect the newborns. Incited by the recent surge in pertussis cases in Serbia here we provide a comprehensive literature overview of pertussis vaccines.

Streptococcus pneumoniae is an opportunistic bacteria causing non-invasive and invasive infections. Introduction of pneumococcal conjugate vaccine (PCV) into national immunization program heavily affects serotype distribution and reduces antibiotic resistance. The aim of the study is to examine serotype distribution antimicrobial susceptibility of non-invasive Streptococcus pneumoniae isolates in Belgrade, Serbia. Non-invasive isolates included in this study are part of a collection of National Reference Laboratory for streptococci, that were obtained from January to December of 2022. Typing of clinical isolates was performed using multiplex PCR method. Susceptibility to antibiotics was tested using disc-diffusion method of antibiogram by EUCAST standard. Results: A total of 155 isolates were obtained, 102 (65.8%) from children ≤5 years and 53 (34.2%) from people >5 years. Isolates were obtained from: middle ear aspirates (n=110, 71%), tracheal aspirates (n=18, 11.6%), sputum (n=17, 10.97%), sinus aspirates (n=4, 2.58%), and eye swabs (n=6, 3.87%). The most frequent serotypes were: 3 (n=25, 16.1%), 11A (n=19, 12.3%), 15A (n=15, 9.7%), 19F (n=12, 7.7%), and 10A (n=11, 7.1%). Coverage of PCV10 and PCV13 was 23.89% and 48.41%. The most common resistance was to erythromycin (n=43, 27.7%), nonsusceptibility penicillin was observed in 18.1% of isolates (R=2, 1.3% and I=26, 16.8%), and 42 (27.1%) were resistant to tetracycline. The cMLS phenotype was the most common type of macrolide resistance (90.7%). A total of 39 (25.2%) MDR isolates were detected. Serotype 19F was observed as the most resistant (75% resistant to erythromycin and clindamycin, 41.6% nonsusceptible to penicillin). The changes in serotype distribution and the prevalence of antimicrobial resistance in non-invasive pneumococcal strains should be closely monitored in response to the implementation of PCV and eventual PCV change.

People with diabetes, particularly those with poorly controlled blood glucose levels, exhibit a 1.5 to 4-fold increased susceptibility to bacterial infections. This heightened vulnerability is primarily attributed to immune system dysfunctions exacerbated by hyperglycaemia. Impaired neutrophil and macrophage function, altered T-cell responses, and compromised skin and mucosal barriers all contribute to an impaired immune defence, increasing both the frequency and severity of infections. Hyperglycaemia directly affects neutrophil functions such as migration, phagocytosis, and apoptosis, while also promoting excessive neutrophil extracellular trap (NET) formation. Macrophages in diabetes tend to favour a pro-inflammatory M1 phenotype, impairing their ability to effectively clear pathogens. Additionally, T-cell dysfunction and altered antibody responses hinder adaptive immunity. Furthermore, the hyperglycaemic environment supports bacterial growth and enhances the virulence of pathogens such as Staphylococcus aureus and Group B Streptococcus , which thrive in this altered metabolic state. These bacteria produce various virulence factors that contribute to chronic infections and worsened outcomes. Collectively, the interplay of immune dysfunction and hyperglycaemia leads to an increased risk of persistent and severe infections in individuals with diabetes, necessitating a deeper understanding of the underlying mechanisms to improve clinical outcomes.

Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) represent highly prevalent human pathogens with high global prevalence rates of approximately 67% (HSV-1) and 13% (HSV-2). Manifestations of HSV-1 and HSV-2 infections include vesicular changes on the lips, genital herpes, herpetic stromal keratitis (HSK), eczema herpeticum, and systemic disease in newborns.