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Volume 14, January
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Pathogens, Volume 14, Issue 2 (February 2025) – 11 articles

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23 pages, 2336 KiB  
Review
Understanding the Molecular Interactions Between Influenza A Virus and Streptococcus Proteins in Co-Infection: A Scoping Review
by Askar K. Alshammari, Meshach Maina, Adam M. Blanchard, Janet M. Daly and Stephen P. Dunham
Pathogens 2025, 14(2), 114; https://doi.org/10.3390/pathogens14020114 - 24 Jan 2025
Abstract
Influenza A virus infections are known to predispose infected individuals to bacterial infections of the respiratory tract that result in co-infection with severe disease outcomes. Co-infections involving influenza A viruses and streptococcus bacteria result in protein–protein interactions that can alter disease outcomes, promoting [...] Read more.
Influenza A virus infections are known to predispose infected individuals to bacterial infections of the respiratory tract that result in co-infection with severe disease outcomes. Co-infections involving influenza A viruses and streptococcus bacteria result in protein–protein interactions that can alter disease outcomes, promoting bacterial colonisation, immune evasion, and tissue damage. Focusing on the synergistic effects of proteins from different pathogens during co-infection, this scoping review evaluated evidence for protein–protein interactions between influenza A virus proteins and streptococcus bacterial proteins. Of the 2366 studies initially identified, only 32 satisfied all the inclusion criteria. Analysis of the 32 studies showed that viral and bacterial neuraminidases (including NanA, NanB and NanC) are key players in desialylating host cell receptors, promoting bacterial adherence and colonisation of the respiratory tract. Virus hemagglutinin modulates bacterial virulence factors, hence aiding bacterial internalisation. Pneumococcal surface proteins (PspA and PspK), bacterial M protein, and pneumolysin (PLY) enhance immune evasion during influenza co-infections thus altering disease severity. This review highlights the importance of understanding the interaction of viral and bacterial proteins during influenza virus infection, which could provide opportunities to mitigate the severity of secondary bacterial infections through synergistic mechanisms. Full article
(This article belongs to the Section Viral Pathogens)
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<p>Illustration of primary IAV infection and secondary Streptococcus infection. The ciliated epithelial cells and underlying mucosal layers are damaged due to the sialidase activity of the viral NA. Viral infections impair the immune response, induce apoptosis, and cause inflammation, leading to tissue damage. This will enhance susceptibility to secondary bacterial infection 3–7 days post-viral infection. Created with BioRender.com.</p>
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<p>Flowchart summarising the process of the literature identification, screening, and selection for the scoping review.</p>
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<p>Direct interactions between Influenza A virus (IAV) and Streptococcus during co-infection. (<b>A</b>) Streptococcus adhesion to host epithelial cells, facilitated by viral factors during co-infection. (<b>B</b>) Co-infection of Influenza A virus (IAV) and Streptococcus, where viral particles enhance bacterial colonisation on host tissues. (<b>C</b>) Receptor binding between viral proteins and bacterial surface components, promoting bacterial adherence to host cells. (<b>D</b>) Virion stability is affected by bacterial interaction, which may facilitate the persistence of viral particles on host cells and enhance co-infection severity (Created with BioRender.com).</p>
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13 pages, 603 KiB  
Article
Yeast Strains as Probiotic and Postbiotic Agents for the Agglutination of Enteric Pathogens: A Preventive Approach
by Michelle Cerdán-Alduán, Josune Salvador-Erro, Ana Villegas-Remírez, David García-Yoldi, Ana Ceniceros, Yadira Pastor and Carlos Gamazo
Pathogens 2025, 14(2), 113; https://doi.org/10.3390/pathogens14020113 - 24 Jan 2025
Viewed by 139
Abstract
This study evaluates the potential of various yeast strains as probiotic and postbiotic agents for agglutinating enteric pathogens, offering a preventive approach to gastrointestinal infections. Different yeast species were tested in vitro against a range of pathogenic bacteria, including enterotoxigenic Escherichia coli ETEC, [...] Read more.
This study evaluates the potential of various yeast strains as probiotic and postbiotic agents for agglutinating enteric pathogens, offering a preventive approach to gastrointestinal infections. Different yeast species were tested in vitro against a range of pathogenic bacteria, including enterotoxigenic Escherichia coli ETEC, Shigella flexneri, Salmonella enterica serovar Typhimurium, and Salmonella enterica serovar Enteritidis, to assess their capacity for pathogen agglutination. Additionally, inactivated yeasts were obtained using a novel chemical treatment and employed to explore their efficacy as postbiotic agents. The results suggest that both live and inactivated yeasts are able to agglutinate the different pathogens, potentially limiting bacterial colonization. Notably, we also demonstrated that Wickerhamomyces anomalus, Saccharomyces cerevisiae, and Pichia fermentans, exhibiting agglutination activity, were capable of reducing bacterial adhesion to HeLa cells in vitro. This research highlights yeast’s probiotic and postbiotic potential and supports the development of novel yeast-based products for preventing enteric infections. Full article
(This article belongs to the Section Vaccines and Therapeutic Developments)
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<p>Detection of yeast mannoproteins with fluorescently labeled concanavalin A by flow cytometry. The results of mean fluorescence intensity (MFI) for each strain, live or inactivated with either chemical (BEI/FA) or heat (HT) methods, are shown (*, <span class="html-italic">p</span> &lt; 0.05, **, <span class="html-italic">p</span> &lt; 0.01, ***, <span class="html-italic">p</span> &lt; 0.001, ****, <span class="html-italic">p</span> &lt; 0.0001). Error bars represent SD (<span class="html-italic">n</span> = 3).</p>
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<p>Ability of yeast strains to inhibit <span class="html-italic">Escherichia coli</span> ETEC adhesion to HeLa cells<b>.</b> Percentage (%) reduction in bacterial adhesion to HeLa cells compared to untreated (yeast-free) ETEC control (*, <span class="html-italic">p</span> &lt; 0.05). Error bars represent SEM (<span class="html-italic">n</span> = 3).</p>
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19 pages, 1589 KiB  
Review
Pathogenic and Protective Roles of Neutrophils in Chlamydia trachomatis Infection
by Zoe E. R. Wilton, Andzoa N. Jamus, Susan B. Core and Kathryn M. Frietze
Pathogens 2025, 14(2), 112; https://doi.org/10.3390/pathogens14020112 - 23 Jan 2025
Viewed by 270
Abstract
Chlamydia trachomatis (Ct) is an obligate intracellular pathogen that causes the most commonly diagnosed bacterial sexually transmitted infection (STI) and is a leading cause of preventable blindness globally. Ct infections can generate a strong pro-inflammatory immune response, leading to immune-mediated pathology in infected [...] Read more.
Chlamydia trachomatis (Ct) is an obligate intracellular pathogen that causes the most commonly diagnosed bacterial sexually transmitted infection (STI) and is a leading cause of preventable blindness globally. Ct infections can generate a strong pro-inflammatory immune response, leading to immune-mediated pathology in infected tissues. Neutrophils play an important role in mediating both pathology and protection during infection. Excessive neutrophil activation, migration, and survival are associated with host tissue damage during Chlamydia infections. In contrast, neutrophils also perform phagocytic killing of Chlamydia in the presence of IFN-γ and anti-Chlamydia antibodies. Neutrophil extracellular traps (NETs) and many neutrophil degranulation products have also demonstrated strong anti-Chlamydia functions. To counteract this neutrophil-mediated protection, Chlamydia has developed several evasion strategies. Various Chlamydia proteins can limit potentially protective neutrophil responses by directly targeting receptors present on the surface of neutrophils or neutrophil degranulation products. In this review, we provide a survey of current knowledge regarding the role of neutrophils in pathogenesis and protection, including the ways that Chlamydia circumvents neutrophil functions, and we propose critical areas for future research. Full article
(This article belongs to the Special Issue Host Immune Responses to Intracellular Pathogens)
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<p>Schematic illustrating how <span class="html-italic">Chlamydia</span> infections can activate neutrophils, which can contribute to pathology and host tissue damage. Top: Epithelial cells are infected with <span class="html-italic">Chlamydia</span>, which causes the release of pro-inflammatory cytokines and chemokines such as IL-8, IL-6, GM-CSF, and CXCL1. These cytokines and chemokines promote the adhesion of circulating neutrophils to endothelial cells. The circulating neutrophils then undergo conformational change that allows them to exit the bloodstream and enter the site of <span class="html-italic">Chlamydia</span> infection. The cytokines also promote the activation and survival of present neutrophils. These activated neutrophils increase production of ROS, which can cause directly oxidative damage to host cells. ROS can also damage host cells by promoting neutrophil phagocytosis, degranulation, and NET release. (<b>A</b>) Neutrophil degranulation can damage host cells by releasing of MMPs, such as MMP-9, which can disrupt the basal lamina that the FRT epithelial cells are anchored to. This can cause the epithelial cells to disseminate, potentially allowing spread of the infection. In addition, degradation of the basal lamina by MMPs can promote fibrosis during tissue repair. MMPs are also able to regulate different chemokines and cytokines, which can increase neutrophil recruitment to the site of infection. (<b>B</b>) <span class="html-italic">Chlamydia</span> can survive in neutrophils for several hours; therefore, neutrophil phagocytosis can contribute to pathology by allowing <span class="html-italic">Chlamydia</span> to disseminate to other areas of the FRT by utilizing neutrophils as a method of transportation and protection against immune surveillance. Infected neutrophils can also die in response to infection, thus releasing DAMPs that promote macrophage activation and cytokine release. Several of these macrophage-secreted cytokines can promote neutrophil recruitment, thus triggering a positive feedback loop. (<b>C</b>) NET release can directly and indirectly damage host cells. NET release causes histones and anti-microbial products to be released into the extracellular space, where they can be cytotoxic to other cells and/or function as DAMPs to promote a pro-inflammatory environment. Macrophages also release pro-inflammatory cytokines in response to NETs, promoting neutrophil influx.</p>
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<p>Schematic illustrating neutrophil-mediated mechanisms of protection against <span class="html-italic">Chlamydia</span>. Neutrophils can provide protection by three main mechanisms: degranulation, phagocytosis, and NET release. (<b>A</b>) During degranulation, neutrophils can release human cathelicidin LL-37, which has strong anti-<span class="html-italic">Chlamydia</span> activity. Lactoferrin is also released during degranulation, which can block entry of <span class="html-italic">Chlamydia</span> into host cells and decrease the secretion of pro-inflammatory cytokines during infection, potentially reducing tissue damage. (<b>B</b>) Neutrophils can also provide protection against <span class="html-italic">Chlamydia</span> infection by phagocytosing and killing the engulfed bacteria in the presence of IFN-γ and <span class="html-italic">Chlamydia</span>-specific antibodies. (<b>C</b>) NET release, which can directly kill and/or prevent the dissemination of pathogens, is another way that neutrophils might provide protection.</p>
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<p>Schematic illustrating how <span class="html-italic">Chlamydia</span> can disrupt neutrophil-mediated protection. (<b>A</b>) CPAF can cleave the FPR2 receptor on the surface of neutrophils, which disrupts PI3K and MAPK signaling. The disruption of these signaling pathways can prevent neutrophils from degranulating or performing NET release. Another mechanism of anti-neutrophil activity by CPAF is the degradation of LL-37. This prevents LL-37 from being able to perform anti-<span class="html-italic">Chlamydia</span> functions, enhancing host cell infection. (<b>B</b>) Pgp3 can form a stable complex with LL-37, limiting the anti-<span class="html-italic">Chlamydia</span> functions of LL-37. The presence of Pgp3 can directly interfere with LL-37’s ability to prevent <span class="html-italic">Chlamydia</span> infection in host cells, and Pgp3/LL-37 complexes can delay neutrophil migration to the site of infection. Pgp3, free or complexed with LL-37, promotes the release of the pro-inflammatory cytokines IL-6 and IL-8 by neutrophils, which can contribute to the pro-inflammatory environment at the site of infection. (<b>C</b>) CT135 can destroy neutrophils that have taken up <span class="html-italic">Chlamydia</span> EBs. The presence of CT135 can trigger neutrophil cell death through TLR2/MyD88 signaling, which triggers the NLRP3 inflammasome. This results in the release of pro-inflammatory cytokines, such as IL-1β, and DAMPs, such as extracellular ATP. Macrophages can recognize the presence of extracellular ATP through the P2X7 receptor, which results in inflammasome activation and the release of pro-inflammatory cytokines, such as IL-1β. (<b>D</b>) cHtrA can cleave LL-37, thus preventing the anti-<span class="html-italic">Chlamydia</span> functions of LL-37. In addition, cHtrA can also degrade ECM components, which could promote <span class="html-italic">Chlamydia</span> spreading as infected cells are released and travel through the FRT.</p>
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21 pages, 700 KiB  
Review
Cariogenic Microbiota and Emerging Antibacterial Materials to Combat Dental Caries: A Literature Review
by Jingwei Cao, Qizhao Ma, Jia Shi, Xinyue Wang, Dingwei Ye, Jingou Liang and Jing Zou
Pathogens 2025, 14(2), 111; https://doi.org/10.3390/pathogens14020111 - 23 Jan 2025
Viewed by 420
Abstract
Dental caries is the most common oral disease in the world and a chronic infectious disease. The cariogenic microbiome plays an important role in the process of caries. The ecological imbalance of microbiota leads to low pH, which causes caries. Therefore, antibacterial materials [...] Read more.
Dental caries is the most common oral disease in the world and a chronic infectious disease. The cariogenic microbiome plays an important role in the process of caries. The ecological imbalance of microbiota leads to low pH, which causes caries. Therefore, antibacterial materials have always been a hot topic. Traditional antibacterial materials such as cationic antibacterial agents, metal ion antibacterial agents, and some natural extract antibacterial agents have good antibacterial effects. However, they can cause bacterial resistance and have poor biological safety when used for long-term purposes. Intelligent antibacterial materials, such as pH-responsive materials, nanozymes, photoresponsive materials, piezoelectric materials, and living materials are emerging antibacterial nano-strategies that can respond to the caries microenvironment or other specific stimuli to exert antibacterial effects. Compared with traditional antibacterial materials, these materials are less prone to bacterial resistanceand have good biological safety. This review summarizes the characteristics of cariogenic microbiota and some traditional or emerging antibacterial materials. These emerging antibacterial materials can accurately act on the caries microenvironment, showing intelligent antibacterial effects and providing new ideas for caries management. Full article
(This article belongs to the Special Issue Oral Microbes and Oral Diseases)
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<p>Schematic diagram of emerging antibacterial materials for dental caries.</p>
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15 pages, 1253 KiB  
Case Report
A One Health Zoonotic Vector Borne Infectious Disease Family Outbreak Investigation
by Edward B. Breitschwerdt, Ricardo G. Maggi, Charlotte O. Moore, Cynthia Robveille, Rosalie Greenberg and Emily Kingston
Pathogens 2025, 14(2), 110; https://doi.org/10.3390/pathogens14020110 - 23 Jan 2025
Viewed by 322
Abstract
This study reinforces the value of a One Health approach to infectious disease outbreak investigations. After the onset of neuropsychiatric symptoms in their son, our investigation focused on a family composed of a mother, father, two daughters, the son, two dogs, and a [...] Read more.
This study reinforces the value of a One Health approach to infectious disease outbreak investigations. After the onset of neuropsychiatric symptoms in their son, our investigation focused on a family composed of a mother, father, two daughters, the son, two dogs, and a rabbit, all with exposures to vectors (fleas and ticks), rescued dogs, and other animals. Between 2020 and 2022, all family members experienced illnesses that included neurological symptoms. Prolonged menorrhagia (130d) in the youngest daughter ultimately resolved following antibiotic administration. One dog was diagnosed with a splenic hematoma and months later spinal histiocytic sarcoma. The father, both daughters, and one dog were seroreactive to multiple Bartonella spp. antigens, whereas the mother and son were not seroreactive. Bartonella quintana DNA was amplified from specimens obtained from all family members. Based upon DNA sequencing, infection with B. quintana was confirmed for the mother and both pet dogs. Bartonella henselae DNA was amplified and sequenced from the youngest daughter, the son, and one dog (co-infected with B. quintana), and from Ctenocephalides felis collected from their pet rabbit. All five family members and one dog were infected with Babesia divergens-like MO-1. Both parents were co-infected with Babesia microti. Droplet digital PCR supported potential infection with a Borrelia species in three family members. This study provided additional case-based evidence supporting the role of stealth Babesia, Bartonella, and Borrelia pathogens as a cause or cofactor in neurological and neuropsychiatric symptoms. We conclude that a One Health investigation approach, particularly for stealth vector borne pathogens such as Babesia, Bartonella, and Borrelia spp., will enhance clinical and epidemiological understanding of these organisms for animal and human health. During outbreak investigations it is critical to document travel and vector exposure histories, symptoms, and pathology in pets and human patients, contact with rescued, wild, or feral animals and perform diagnostic testing that includes family members, pets, and vectors. Full article
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Graphical abstract

Graphical abstract
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<p>Microbiological testing approach used in this study. <span class="html-italic">Bh</span>: <span class="html-italic">Bartonella henselae</span>; <span class="html-italic">Bvb</span> I or II: <span class="html-italic">Bartonella vinsonii</span> subsp. <span class="html-italic">berkhoffii</span> genotype I or II; <span class="html-italic">Bk</span>: <span class="html-italic">Bartonella koehlerae</span>; <span class="html-italic">Bq</span>: <span class="html-italic">Bartonella quintana</span>.</p>
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<p>Historical timeline for the youngest son who was 10 years old at the time of this investigation in August 2022. His illness and neurological symptoms reportedly predated the onset of neurological symptoms in other family members.</p>
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27 pages, 1663 KiB  
Review
Ligands for Intestinal Intraepithelial T Lymphocytes in Health and Disease
by Akanksha Hada and Zhengguo Xiao
Pathogens 2025, 14(2), 109; https://doi.org/10.3390/pathogens14020109 - 23 Jan 2025
Viewed by 287
Abstract
The intestinal tract is constantly exposed to a diverse mixture of luminal antigens, such as those derived from commensals, dietary substances, and potential pathogens. It also serves as a primary route of entry for pathogens. At the forefront of this intestinal defense is [...] Read more.
The intestinal tract is constantly exposed to a diverse mixture of luminal antigens, such as those derived from commensals, dietary substances, and potential pathogens. It also serves as a primary route of entry for pathogens. At the forefront of this intestinal defense is a single layer of epithelial cells that forms a critical barrier between the gastrointestinal (GI) lumen and the underlying host tissue. The intestinal intraepithelial T lymphocytes (T-IELs), one of the most abundant lymphocyte populations in the body, play a crucial role in actively surveilling and maintaining the integrity of this barrier by tolerating non-harmful factors such as commensal microbiota and dietary components, promoting epithelial turnover and renewal while also defending against pathogens. This immune balance is maintained through interactions between ligands in the GI microenvironment and receptors on T-IELs. This review provides a detailed examination of the ligands present in the intestinal epithelia and the corresponding receptors expressed on T-IELs, including T cell receptors (TCRs) and non-TCRs, as well as how these ligand-receptor interactions influence T-IEL functions under both steady-state and pathological conditions. By understanding these engagements, we aim to shed light on the mechanisms that govern T-IEL activities within the GI microenvironment. This knowledge may help in developing strategies to target GI ligands and modulate T-IEL receptor expression, offering precise approaches for treating intestinal disorders. Full article
(This article belongs to the Section Immunological Responses and Immune Defense Mechanisms)
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<p>Availability of potential ligands and the possible expression of T-IEL receptors in steady-state and disease conditions. This diagram illustrates the crucial roles of ligand availability and receptor expression on T-IELs within the intestinal epithelial environment under both steady-state (<b>left</b>) and disease (<b>right</b>) conditions. Under steady-state conditions, specific ligands and their corresponding receptors are essential for preserving T-IEL populations, preventing microbial invasion, maintaining immune tolerance, conducting immune surveillance, sustaining the integrity of the epithelial barrier, and communicating with the enteric nervous system, ultimately maintaining homeostasis. In contrast, during disease conditions, changes in ligand availability and ligand-receptor interactions aid in eliminating pathogens, stressed and malignantly transformed cells, as well as in promoting tissue repair and healing. TCR, T cell receptor; PRR, pattern recognition receptor; TLR, toll-like receptor; AhR, aryl hydrocarbon receptor; IL, interleukin; MHC, major histocompatibility complex; HVEM, herpesvirus entry mediator receptor; GLP, glucagon-like peptide; VIP, vasoactive intestinal peptide; eCIRP, extracellular cold-inducible RNA-binding protein; JAML, junctional adhesion molecule-like; CAR, coxsackievirus and adenovirus receptor. Created in BioRender.com (accessed on 15 January 2025).</p>
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14 pages, 1479 KiB  
Article
Introduction of a Divergent Canine Parvovirus Type 2b Strain with a Dog in Sicily, Southern Italy, Through the Mediterranean Sea Route to Europe
by Francesco Mira, Giovanni Franzo, Giorgia Schirò, Domenico Vicari, Giuseppa Purpari, Vincenza Cannella, Elisabetta Giudice, Martino Trapani, Anna Carrozzo, Giada Spene, Virginia Talarico and Annalisa Guercio
Pathogens 2025, 14(2), 108; https://doi.org/10.3390/pathogens14020108 - 23 Jan 2025
Viewed by 288
Abstract
Despite over four decades since its emergence, canine parvovirus type 2 (CPV-2) remains a relevant disease for dogs. Few studies, primarily only recent ones based on phylodynamic and phylogeography approaches, have highlighted the impact of rapid and long-distance transport of dogs on the [...] Read more.
Despite over four decades since its emergence, canine parvovirus type 2 (CPV-2) remains a relevant disease for dogs. Few studies, primarily only recent ones based on phylodynamic and phylogeography approaches, have highlighted the impact of rapid and long-distance transport of dogs on the CPV-2 spreading dynamics. The present study reports the genomic characterization of a CPV-2 strain detected in a dog introduced into Italy from the coasts of North Africa through the Mediterranean Sea route to Europe. The nearly complete CPV-2 sequence was obtained and analyzed. The viral isolate was characterized as a CPV-2b variant, showing genetic signatures distinct from those of CPV-2 strains detected to date in Europe. Phylodynamic and phylogeographic approaches revealed a close correlation with CPV-2 strains recently reported in the Middle East (Turkey and Egypt), which likely originated or co-evolved from Asian ones. It is at least suggestive that the inferred spreading pattern overlaps with the routes often followed by migrants travelling from Asia and Middle East to Europe, passing through Africa. This evidence for the introduction of CPV-2 via the Mediterranean Sea route to Europe highlights the relevant role of the dog movements in the global spread of emerging or re-emerging viral pathogens. Full article
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<p>A schematic representation of the CPV-2 genome: the upper lines (<b>A</b>) represent the complete encoding nucleotide length (4269 nucleotides) of the genome, excluding the 5′ to the 3′ UTRs, and the relative positions of the NS1 and VP2 genes; the middle ((<b>B</b>), in blue) and lower ((<b>C</b>), in red) lines represent the relative positions of the described amino-acid changes in the NS1 and VP2 gene sequences, respectively.</p>
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<p>Maximum clade credibility tree of CPV2 strains based on VP2 sequence. Countries where the virus ancestors were estimated to circulate are color-coded. The branch length is scaled in time (years). The clade including the sequence obtained in the present study (highlighted in yellow) is reported in the right insert. Tree nodes are annotated with the estimated year.</p>
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<p>Geographical map of the Mediterranean basin, including year and country of detection of the most related CPV-2b strain to the one described in this study (strain IZSSI_2024PA10625), spreading from Africa to Italy. For each strain, the strain name and the accession number were provided. Each strain refers to the following references: (from Egypt) strain EGY/2019/39-517 [<a href="#B43-pathogens-14-00108" class="html-bibr">43</a>], EGY-FVMVL-18/2019 [<a href="#B44-pathogens-14-00108" class="html-bibr">44</a>]; (from Turkey) CPV-2b-O1-TR [<a href="#B45-pathogens-14-00108" class="html-bibr">45</a>], Turkey_Izmir_2, and Turkey_Ankara_2 [<a href="#B46-pathogens-14-00108" class="html-bibr">46</a>]. The main image was obtained from Google Earth (Google Landsat / Copernicus Data SIO, NOAA, U.S. Navy, NGA, GEBCOInst. Geogr. NacionalGeoBasis-DE/BKG (©2009) Mapa GISrael).</p>
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15 pages, 1872 KiB  
Article
Antimicrobial Resistance, Virulence Gene Profiling, and Spa Typing of Staphylococcus aureus Isolated from Retail Chicken Meat in Alabama, USA
by Rawah Faraj, Hazem Ramadan, Kingsley E. Bentum, Bilal Alkaraghulli, Yilkal Woube, Zakaria Hassan, Temesgen Samuel, Abiodun Adesiyun, Charlene R. Jackson and Woubit Abebe
Pathogens 2025, 14(2), 107; https://doi.org/10.3390/pathogens14020107 - 22 Jan 2025
Viewed by 387
Abstract
Antibiotic-resistant Staphylococcus aureus (S. aureus) in retail meat poses a public health threat requiring continuous surveillance. This study investigated the frequency of isolation, toxin genes, and antibiotic resistance profile of S. aureus recovered from retail poultry meat samples and presented results [...] Read more.
Antibiotic-resistant Staphylococcus aureus (S. aureus) in retail meat poses a public health threat requiring continuous surveillance. This study investigated the frequency of isolation, toxin genes, and antibiotic resistance profile of S. aureus recovered from retail poultry meat samples and presented results beneficial to public health interventions. Of 200 samples collected, 16% (32/200) tested positive for S. aureus, and these were recovered from thigh 37.5% (12/32), wing 34.4% (11/32), gizzard (15.6% (5/32), and liver 12.5% (4/32) samples. Findings of spa typing analysis revealed that 68.8% (22/32), 18.8% (6/32), 9.4% (3/32), and 3.0% (1/32) of the isolates belonged to the spa types t267, t160, t548, and t008, respectively. For antibiotic susceptibility testing, 12.5% (4/32) of the isolates were resistant to only penicillin, but one isolate (1/32; 3%) showed resistance to the antibiotics penicillin, erythromycin, ampicillin, and oxacillin. PCR analysis revealed that 9.4% (3/32) of the isolates carried the mecA gene associated with methicillin-resistant Staphylococcus aureus (MRSA) isolates. One MRSA isolate was identified as a t008 spa type, and harbored a 26,974 bp-sized plasmid, which was the source of its resistance to penicillin, ampicillin, erythromycin, and oxacillin. The staphylococcal enterotoxin (SE) genes seg, sei, sek, seb, selm, and seln were also identified among the isolates, and mostly the antimicrobial and enterotoxin genes were carried on plasmids of the isolates. This study raises awareness on the continuous circulation of pathogenic microbes like S. aureus in retail poultry meat. Full article
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<p>A pie chart showing the proportions of <span class="html-italic">S. aureus</span> isolated from various chicken meat parts. Each section of the chart shows the percentage of isolates recovered from the given chicken part, and the corresponding proportions are shown in brackets.</p>
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<p>A cluster dendrogram with a heatmap showing the presence or absence of antimicrobial genes in various samples. Sample identifiers are shown to the right and antimicrobial genes (<span class="html-italic">tetA</span>, <span class="html-italic">tetM</span>, <span class="html-italic">ermA</span>, <span class="html-italic">mecA</span>, <span class="html-italic">norA</span>, <span class="html-italic">blaZ</span>, and <span class="html-italic">chlA</span>) are shown at the bottom of the diagram. Red and blue depict the presence and absence, respectively, of the corresponding genes in the isolates of the samples.</p>
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<p>A cluster dendrogram with a heatmap showing the resistance or susceptibility of samples to antibiotics. Sample identifiers are shown to the right and the antibiotics (penicillin (pen), ampicillin (amp), erythromycin (ery), and oxacillin (oxa) are shown at the bottom of the diagram. Red and blue depict resistance (Resis) and susceptibility (Susc) to the corresponding antibiotic by the isolate from the samples.</p>
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<p>A cluster dendrogram with a heatmap showing the presence or absence of staphylococcal enterotoxin genes in samples. Sample identifiers are shown to the right, and the enterotoxin genes <span class="html-italic">seg</span>, <span class="html-italic">sei</span>, <span class="html-italic">sek</span>, <span class="html-italic">seb</span>, <span class="html-italic">selm</span>, and <span class="html-italic">seln</span> are shown at the bottom of the diagram. Red and blue depict the presence and absence, respectively, of the corresponding genes in the isolates of the various samples.</p>
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<p>Dendrogram tree based on spa typing results of isolates from samples. The various spa types and their associated samples are shown to the right. The spa types t548, t160, t267, and t008 are also represented by the colors violet, red, green, and yellow.</p>
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25 pages, 1927 KiB  
Review
Understanding Host–Pathogen Interactions in Congenital Chagas Disease Through Transcriptomic Approaches
by Tatiana M. Cáceres, Luz Helena Patiño and Juan David Ramírez
Pathogens 2025, 14(2), 106; https://doi.org/10.3390/pathogens14020106 - 22 Jan 2025
Viewed by 369
Abstract
Chagas disease, caused by Trypanosoma cruzi, is a parasitic zoonosis with significant health impacts, particularly in Latin America. While traditionally associated with vector-borne transmission, increased migration has expanded its reach into urban and non-endemic regions. Congenital transmission has become a critical route [...] Read more.
Chagas disease, caused by Trypanosoma cruzi, is a parasitic zoonosis with significant health impacts, particularly in Latin America. While traditionally associated with vector-borne transmission, increased migration has expanded its reach into urban and non-endemic regions. Congenital transmission has become a critical route of infection, involving intricate maternal–fetal immune interactions that challenge diagnosis and treatment. This review synthesizes findings from three RNA-seq studies that explore the molecular underpinnings of congenital Chagas disease, emphasizing differentially expressed genes (DEGs) implicated in host–pathogen interactions. The DAVID tool analysis highlighted the overexpression of genes associated with the innate immune response, including pro-inflammatory cytokines that drive chemotaxis and neutrophil activation. Additionally, calcium-dependent pathways critical for parasite invasion were modulated. T. cruzi exploits the maternal–fetal immune axis to establish a tolerogenic environment conducive to congenital transmission. Alterations in placental angiogenesis, cellular regeneration, and metabolic processes further demonstrate the parasite’s ability to manipulate host responses for its survival and persistence. These findings underscore the complex interplay between the host and pathogen that facilitates disease progression. Future research integrating transcriptomic, proteomic, and metabolomic approaches is essential to unravel the molecular mechanisms underlying congenital Chagas disease, with a particular focus on the contributions of genetic diversity and non-coding RNAs in immune evasion and disease pathogenesis. Full article
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<p>Life cycle. (<b>A</b>) The life cycle of <span class="html-italic">T. cruzi</span> alternates between vertebrate hosts and the triatomine insect vector. In vertebrates, metacyclic trypomastigotes invade host cells, where they differentiate into intracellular amastigotes, the replicative stage. Amastigotes multiply and transform into cell-derived trypomastigotes, which are released into the bloodstream to infect new cells or be ingested by a triatomine during a blood meal. In the triatomine, trypomastigotes differentiate into epimastigotes in the midgut, where they replicate and eventually transform into infective metacyclic trypomastigotes in the rectal ampoule, completing the cycle. (<b>B</b>) Mechanisms of congenital transmission of <span class="html-italic">T. cruzi.</span> During pregnancy, <span class="html-italic">T. cruzi</span> can be transmitted to the fetus through two mechanisms: (1) reactivation of infection: pregnancy-related hormones stimulate amastigotes in maternal tissues to transform into cell-derived trypomastigotes (CDTs), which are released into the maternal bloodstream. These CDTs can cross the placenta, enter fetal circulation, and spread the infection to fetal organs. (2) Direct transmission: CDTs circulating in the maternal blood invade trophoblastic cells in the placenta, crossing the placental barrier to enter the fetal bloodstream and infecting fetal tissues.</p>
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<p>Host–pathogen interactions during congenital <span class="html-italic">T. cruzi</span> infection. This figure illustrates the interactions between the <span class="html-italic">T. cruzi</span> parasite and chorionic villi, emphasizing key molecular and cellular mechanisms: the interaction between surface molecules of <span class="html-italic">T. cruzi</span> and Toll-like receptors (TLRs) on trophoblastic cells initiates signaling cascades that increase cyclic AMP (cAMP) levels and activate the MAPK/ERK1/2 pathway (1). This pathway orchestrates multiple cellular responses, including the production of pro-inflammatory cytokines such as IL-6 and TNF-α, along with the generation of reactive oxygen species (ROS) (2). These inflammatory mediators exacerbate placental tissue damage and create a microenvironment conducive to parasite persistence. Additionally, <span class="html-italic">T. cruzi</span> infection triggers the activation of caspase-8, which facilitates the detachment of infected trophoblastic cells. This detachment contributes to cell turnover (3) and forms structural discontinuities in the placental barrier, allowing deeper parasite infiltration. The parasite also induces the overexpression of matrix metalloproteinases (MMP-2 and MMP-9), enzymes that degrade key components of the basal lamina, such as collagen types I and IV and fibronectin. This degradation disrupts the basal lamina’s structural integrity (4), enhancing parasite transmigration toward fetal tissues. Finally, <span class="html-italic">T. cruzi</span> calcireticulin (TcCRT) binds to C1q, a component of the complement system. This interaction promotes parasite opsonization, increasing its uptake by host cells (5). Concurrently, TcCRT disrupts the classical complement pathway, impairing the host’s immune response and facilitating parasite survival (6).</p>
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<p>Functional categories of differentially expressed genes in the placental environment during <span class="html-italic">Trypanosoma cruzi</span> infection. This figure highlights the functional categories of differentially expressed genes (DEGs) involved in the interaction between <span class="html-italic">Trypanosoma cruzi</span> and the placental environment, which plays a critical role in the congenital transmission of Chagas disease. Up-regulated genes are shown in green boxes, while down-regulated genes are in red boxes, illustrating the biological processes activated or suppressed during infection. Background colors within the boxes correspond to the sources of the transcriptomic data, providing a clear link to the original studies and integrating findings across multiple investigations to offer a comprehensive overview of the key transcriptomic changes induced by <span class="html-italic">T. cruzi</span> [<a href="#B56-pathogens-14-00106" class="html-bibr">56</a>,<a href="#B57-pathogens-14-00106" class="html-bibr">57</a>,<a href="#B83-pathogens-14-00106" class="html-bibr">83</a>].</p>
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11 pages, 270 KiB  
Article
Using an Aqueous Suspension of Duddingtonia flagrans Chlamydospores and a Hexane Extract of Artemisia cina as Sustainable Methods to Reduce the Fecal Egg Count and Larvae of Haemonchus contortus in the Feces of Periparturient Ewes
by Héctor Alejandro de la Crúz-Crúz, Rosa Isabel Higuera-Piedrahita, Alejandro Zamilpa, Yazmín Alcalá-Canto, Ana Yuridia Ocampo-Gutiérrez, Luis David Arango-de la Pava, María Eugenia López-Arellano, Daniel Hernandez-Patlan, Jorge Alfredo Cuéllar-Ordaz and Pedro Mendoza-de Gives
Pathogens 2025, 14(2), 105; https://doi.org/10.3390/pathogens14020105 - 21 Jan 2025
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Abstract
This study evaluated the effectiveness of Duddingtonia flagrans chlamydospores and an Artemisia cina hexane extract in reducing Haemonchus contortus fecal egg counts and larvae in periparturient ewes. This study involved five groups of four ewes: a control group, an ivermectin group, an A. [...] Read more.
This study evaluated the effectiveness of Duddingtonia flagrans chlamydospores and an Artemisia cina hexane extract in reducing Haemonchus contortus fecal egg counts and larvae in periparturient ewes. This study involved five groups of four ewes: a control group, an ivermectin group, an A. cina oral extract group, a D. flagrans group, and a combined treatment group. Treatments began two weeks before delivery, with ivermectin administered 15 days before delivery. Fecal samples were collected every fifteen days to estimate parasite egg counts per gram of feces (EPG) and assess larvae reductions. The results showed very low EPG values for ivermectin and D. flagrans treatments (175 and 150, respectively). The control and combined treatment groups had EPG values rise to 3000 and 4100 by day 15. The EPG values for the A. cina group reached 850 and 533 in later samplings. Throughout the study, the D. flagrans and A. cina groups maintained low EPG values, with the highest recorded values being 50 and 0, respectively. All treatments significantly reduced the larvae in the fecal cultures: D. flagrans (97.4% reduction), ivermectin (91.4%), Artemisia cina (89.9%), and the combined treatment (84.3%). Full article
15 pages, 1226 KiB  
Review
Preventing RSV Infection in Children: Current Passive Immunizations and Vaccine Development
by Pius I. Babawale, Iván Martínez-Espinoza, Alaine’ M. Mitchell and Antonieta Guerrero-Plata
Pathogens 2025, 14(2), 104; https://doi.org/10.3390/pathogens14020104 - 21 Jan 2025
Viewed by 452
Abstract
Human respiratory syncytial virus (RSV) is a leading cause of acute respiratory tract infection and lower respiratory tract infection, associated with high morbidity and mortality in young children, the elderly, and immunocompromised individuals. Initial attempts to develop an RSV vaccine in the 1960s [...] Read more.
Human respiratory syncytial virus (RSV) is a leading cause of acute respiratory tract infection and lower respiratory tract infection, associated with high morbidity and mortality in young children, the elderly, and immunocompromised individuals. Initial attempts to develop an RSV vaccine in the 1960s were faced with a setback due to the enhanced RSV disease developed by vaccinated children. More recent advancements have led to the generation of RSV vaccines for older adults and pregnant women. However, there are still no commercially available RSV vaccines for infants. This work summarizes the current passive immunizations and the ongoing efforts to develop an RSV vaccine for infants. Full article
(This article belongs to the Special Issue Updates on Pediatric Infectious Diseases)
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<p>Prophylactic approach of RSV vaccine and mAb for children. (<b>a</b>) RSV F protein initial precursor (pre-F; F0), which is later cleaved by a furin-like protease into F1 and F2 that form the post-fusion conformation. The Pre-F protein structure was modeled using 5K6C of the RCSB Protein Data Bank [<a href="#B40-pathogens-14-00104" class="html-bibr">40</a>] and post-F protein using 3RRR of the RCSB Protein Data Bank [<a href="#B41-pathogens-14-00104" class="html-bibr">41</a>]. (<b>b</b>) Prophylactic mAb (palivizumab and nirsevimab), and the maternal vaccine (RSVpreF, Abrysvo) targeting different antigenic sites of RSV pre-F and post-F protein. (Created with <a href="http://Biorender.com" target="_blank">Biorender.com</a>).</p>
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<p>RSV vaccines and mAbs for children in clinical trials. Active clinical trials for pediatric RSV vaccine and mAb therapies with outlines of the platforms and components utilized in each therapy, the corresponding trial stages, target age groups, and clinical trial identification numbers. (Created with <a href="http://Biorender.com" target="_blank">Biorender.com</a>).</p>
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