Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition, primarily affecting young individuals, with a significant impact on their quality of life due to recurrent, painful nodules, abscesses, and oozing sinus tracts, primarily affecting intertriginous areas. The pathogenesis of HS is multifactorial, involving a complex interplay between genetic predisposition, immune dysregulation, microbial, and environmental factors. While it is known that cutaneous and gut microbiome contribute to innate immune dysregulation in HS, their precise involvement in disease pathogenesis remains unclear. Despite several studies investigating the microbiome of HS lesions, either by culture-dependent or independent methods, there is no data available on the interplay between bacterial virulence profiles, clinical manifestations, and the host immune response. This study aimed to explore the phenotypic and genotypic resistance and virulence profiles of microorganisms isolated from HS lesions (including the expression of soluble virulence factors and the ability to develop biofilms), with a special focus on Staphylococcus aureus (S. aureus), one of the most frequent infectious agents of HS. A total of 92 bacterial strains, belonging to 20 different bacterial species, were isolated from the HS lesions of 23 patients. The strains of Staphylococcus, Corynebacterium, and Enterococcus expressed the highest levels of soluble virulence factors, such as hemolysins, lecithinase, and lipase, which are involved in bacterial persistence, local invasivity, and tissue damage. Moreover, a significant variation among bacterial species was noted regarding the capacity to develop biofilms, with a potential impact on disease chronicization, bacterial tolerance to antibiotics, and immune defense mechanisms. The genetic characterization of methicillin-resistant staphylococci revealed the presence of adhesins, hemolysin and enterotoxin genes as well as methicillin and macrolides resistance genes. Our findings highlight the critical role of virulence determinants, including bacterial biofilms, in HS pathogenesis, emphasizing the need for targeted therapeutic strategies to disrupt biofilms and mitigate infection severity.

Background: The increasing incidence of infection with Gram-negative bacilli (GNB) producing broad-spectrum β-lactamases, such as extended-spectrum β-lactamases (ESBLs), cephalosporinases (AmpCs), and carbapenemases, has become a great clinical concern. AmpCs are found in many clinically relevant Enterobacterales, where they may compromise the effectiveness of most β-lactams, including carbapenems when associated with an impaired outer membrane. Detection and distinction between these resistance mechanisms are crucial for antimicrobial therapy and for implementation of proper infection control procedures to prevent further spread. Methods: The disk diffusion antibiogram using Mueller-Hinton agar (MHA) supplemented with cloxacillin (MHC), which inhibits AmpCs, was validated to identify AmpC-producing Enterobacterales (AmpC-PE). As cloxacillin is not available in several countries, we investigated the use of oxacillin as an alternative compound to inhibit AmpCs. The ability of MHA supplemented with oxacillin (MHO) to distinguish between carbapenem-resistant Enterobacterales (CREs) due to AmpC hyperproduction and the presence of a carbapenemase has particularly been investigated. Results: MHOs containing several concentrations of oxacillin were compared to MHA and MHC containing 250 mg/L cloxacillin (MHC250). A set of well-characterized Enterobacterales with different β-lactam resistance mechanisms were evaluated. MHO containing 300 mg/L of oxacillin (MHO300) gave similar results to MHC250. Conclusions: The use of MHO300 proved to be efficient in inhibiting AmpCs, allowing differentiation between AmpC hyperproducers and carbapenemase producers. In addition, the use of MHO300 allowed detection of resistance mechanisms hidden by AmpCs, such as ESBLs.

Background: Neisseria meningitidis (meningococcus) is a Gram-negative bacterium that colonises the nasopharynx of about 10% of the healthy human population. Under certain conditions, it spreads into the body, causing infections with high morbidity and mortality rates. Although the capsule is the key virulence factor, unencapsulated strains have proved to possess significant clinical implications as well. Meningococcal meningitis is a primarily human infection, with limited animal models that are dependent on a variety of parameters such as bacterial virulence and mouse strain. In this study, we aimed to develop a murine Neisseria meningitidis meningitis model to be used in the study of various antimicrobial compounds. Method: We used a capsule-deficient Neisseria meningitidis strain that was thoroughly analysed through various methods. The bacterial strain was incubated for 48 h in brain–heart infusion (BHI) broth before being concentrated and injected intracisternally to bypass the blood–brain barrier in CD-1 mice. This prolonged incubation time was a key factor in increasing the virulence of the bacterial strain. A total of three more differently prepared inoculums were tested to further solidify the importance of the protocol (a 24-h incubated inoculum, a diluted inoculum, and an inactivated inoculum). Antibiotic treatment groups were also established. The clinical parameters and number of deaths were recorded over a period of 5 days, and comatose mice with no chance of recovery were euthanised. Results: The bacterial strain was confirmed to have no capsule but was found to harbour a total of 56 genes coding virulence factors, and its antibiotic susceptibility was established. Meningitis was confirmed through positive tissue culture and histological evaluation, where specific lesions were observed, such as perivascular sheaths with inflammatory infiltrate. In the treatment groups, survival rates were significantly higher (up to 81.25% in one of the treatment groups compared to 18.75% in the control group). Conclusion: We managed to successfully develop a cost-efficient murine (using simple CD-1 mice instead of expensive transgenic mice) meningococcal meningitis model using an unencapsulated strain with a novel method of preparation.

Background: Neisseria meningitidis (meningococcus) is an aerobic Gram-negative bacterium that accounts for a large number of bacterial meningitis cases worldwide. It is a strict human pathogen that is easily spread between hosts via aerosols. Although up to 15% of young adults and children carry meningococci in the nose and throat, few transient carriage cases develop into an actual case of meningitis. However, those that do frequently lead to the patient's death within one or two days after the onset of disease. To better study this illness and test possible treatments, meningitis animal models were developed throughout the years, from as early as 1976. Methods: We tried to find a stable and cost-effective animal meningitis model by querying the Pubmed database using two sets of keywords, going through all the results and choosing one protocol that best fit our needs. Results: After analysing 665 results, we comprised a list of 20 meningococcal meningitis murine models that had varying similarities between them, in the end deciding on the most efficient one. Conclusions: We chose and further described the model presented in the article „Inducing Meningococcal Meningitis Serogroup C in Mice via Intracisternal Delivery” by Chiara Pagliuca et al. in 2019.

Leishmaniasis has the paradoxical reputation of being both an emerging and a neglected disease. If we look at the seriousness of some clinical forms, the lack of training in microscopic diagnosis, the lack of reagents for immunological tests and the precariousness of the therapeutic arsenal in many cases, as well as the morbidity and mortality figures, we can only try to better understand and offer solutions to improve the situation. In the current conditions of global warming, humanitarian crises that generate waves of refugees and the existence of latent outbreaks of canine leishmaniasis in a country where the sand fly lives undisturbed, I believe that this letter could increase the degree of concern about this disease. Leishmaniasis refers to a group of parasitic diseases transmitted by a kinetoplastid flagellate named Leishmania. More than 50 genera are recognized, but the taxonomic situation is subject to a series of controversies. Of the 20 most frequently encountered species over half are zoonotic. The protozoan causes three primary pathological forms: the two “Old World” diseases known as visceral leishmaniasis (black fever/kala azar) and cutaneous leishmaniasis (Aleppo button, Biskra button, Jericho button) as well as mucocutaneous leishmaniasis which is specific to the Americas (also called the “New World” diseases).

The following clinical images were obtained during the investigation of a case involving a 57-year-old female patient who, nine years ago, underwent surgery for a uterine fibroid. Post-surgery, she developed a wound infection along with wound dehiscence and eventration. Multidrug-resistant Staphylococcus aureus was identified. Antibiotic treatment was initiated, and over time, the patient underwent several surgical interventions to correct the dehiscence and address the recurrent S. aureus infection.