Most surveys of pathogens in red foxes (Vulpes vulpes) have focused on particular agents. The aim of this study was to verify, with bacteriological and molecular analyses, the occurrence of the main bacterial and protozoan pathogens that are able to infect canids, in red foxes regularly hunted in Central Italy. Spleen, brain, kidney and fecal samples from red foxes were submitted to bacteriological and/or molecular analyses to detect Salmonella spp., Yersinia spp., Listeria monocytogenes, Brucella spp., Ehrlichia canis, Anaplasma phagocytophilum, Coxiella burnetii, Leptospira spp., Neospora caninum, Hepatozoon canis, Babesia spp. and microsporidia. Two (9.1%) strains of Yersinia enterocolitica biotype 1 and 2 (9.1%) of Yersinia frederiksenii were isolated from 22 fecal samples. Among the 22 spleen samples, seven (31.8%) were PCR-positive for H. canis and 3 (13.6%) for Babesia vulpes. Kidneys from two (2.9%) foxes, among 71 tested, were PCR-positive for L. interrogans. Even though the analyses were carried out on a small number of animals, the results suggested that red foxes from the selected geographic area may act as reservoirs of some investigated pathogens.

Bacterial and protozoan agents can determine abortion and other reproductive disorders in domestic ruminants, but data regarding their occurrence in wild ruminants are scanty worldwide, including in Italy. The aim of this retrospective study was to verify the occurrence of the main bacterial and protozoan abortive agents in 72 spleen samples previously collected from roe deer (Capreolus capreolus) living in mountain areas of Central Italy. All samples were collected and submitted to DNA extraction for other investigations. Molecular analyses were carried out on the DNA samples to detect Brucella spp., Chlamydia abortus, Coxiella burnetii, Salmonella enterica, Listeria monocytogenes, Neospora caninum, and Toxoplasma gondii. Three (4.16%) roe deer resulted PCR positive for C. burnetii and one (1.38%) for T. gondii. These findings suggest that roe deer living in the investigated areas do not act as important reservoirs of the searched agents. However, the tested animals lived in a closed area without contact with domestic animals that are usually involved in the epidemiology of the investigated pathogens. Monitoring of wild ruminants is pivotal to verify changes in the epidemiological scenario from a One Health perspective, too.

Wild ruminants often harbor pathogens transmissible to other animals and humans, but their epidemiological role is not always defined for all microorganisms. In this survey, spleens, kidneys, and hearts sampled from 162 fallow deer (Dama dama) were subjected to molecular analyses to detect bacterial (Anaplasma phagocytophilum, Borrelia burgdorferi s.l., Brucella spp., Chlamydia abortus, Coxiella burnetii, Francisella tularensis, Leptospira spp.) and protozoan (piroplasms, Neospora caninum, Toxoplasma gondii) pathogens. Five (3.08%) spleens were positive for A. phagocytophilum, and twelve (7.40%) spleens were positive for Theileria cervi. The remaining pathogens investigated were not detected, and no coinfections were found. The analyzed animals do not seem to have a relevant role in the spreading of these pathogens; however, monitoring is pivotal to understand the epidemiological scenarios and take appropriate preventive measures in areas frequently visited by people.

In order to assess the spreading of tick-borne bacteria and protozoa in a protected area largely frequented by people and in which numerous domestic and wild animals live, molecular analyses were carried out in ticks collected from fallow deer (Dama dama) to detect Anaplasma phagocytophilum, Borrelia sp., Coxiella burnetii, Francisella tularensis, Hepatozoon sp., and piroplasms. A total of 148 tick pools, for a total of 475 ticks collected from fallow deer and identified as female adult Ixodes ricinus, were submitted to DNA extraction and different PCR assays. One hundred and two (68.92%) pools were positive for one or more pathogens: three (2.02%) for C. burnetii, 21 (14.19%) for Borrelia sp., 35 (23.64%) for piroplasms, and 87 (58.78%) for A. phagocytophilum. All tick pools were negative for F. tularensis and Hepatozoon sp. Sixty-seven (45.27%) pools were positive for only one investigated pathogen, whereas in 35 (23.64%) pools DNA of two or more pathogens were found. Sequencing analyses identified 28 piroplasm amplicons as Theileria sp. OT3 and seven amplicons as possible Theileria cervi. Sequencing of the 21 Borrelia amplicons identified six samples as B. miyamotoi and eight as B. lusitaniae, whereas seven amplicons had 100% homology with a Borrelia sp. found in France and 99.37% with a B. theileri strain detected in Zambia. Monitoring tick-borne pathogens in ticks is pivotal to assess the spread of these microorganisms, the evolution of their epidemiology, and the risk of infections for animals and humans.

Equine sarcoid is the most common cutaneous neoplasm of equids and represents a distinctive model of virus-associated tumor persistence. Although bovine papillomaviruses, particularly BPV-1 and BPV-2, are recognized as the main etiological agents, viral infection alone does not fully explain the clinical heterogeneity, frequent recurrence, and limited spontaneous regression of these lesions. This review summarizes current evidence on the molecular and cellular mechanisms underlying equine sarcoid pathogenesis, with emphasis on the interaction between BPV infection, host signaling pathways, tumor microenvironment dynamics, and multi-omic evidence of host regulatory networks. BPV oncoproteins, especially E5, promote fibroblast transformation through PDGFβR activation, downstream PI3K/AKT, MAPK and p38 signaling, altered cell survival, and immune evasion mediated by impaired antigen presentation. However, sarcoid persistence appears to depend on broader host-driven processes, including extracellular matrix remodeling, activated fibroblastic and myofibroblastic phenotypes, chronic inflammatory signaling, and ineffective immune clearance. Recent transcriptomic and epigenomic studies further indicate that long non-coding RNAs, DNA methylation changes, circulating microRNAs, and recently identified virus–host chimeric transcripts may contribute to stabilization of the neoplastic phenotype and may represent future biomarkers. Overall, this review proposes a virus-initiated, host-sustained conceptual framework for equine sarcoid pathogenesis, in which viral oncogene activity and host tissue reprogramming cooperate to promote lesion persistence, recurrence, and therapeutic resistance.