The discovery and clinical deployment of antibiotics marked a paradigm shift in combating bacterial infections, profoundly benefiting human medicine, veterinary health, and agricultural productivity. However, pervasive overuse in both the clinical and livestock sectors has precipitated an alarming acceleration of antimicrobial resistance, now recognized as a critical global health threat. Compounding this crisis, livestock-associated resistant pathogens persistently colonize the food production continuum, enabling zoonotic transmission through animal-derived products and endangering public health, food safety, and human survival. This review delineates current insights into bacterial resistance mechanisms and evaluates innovative countermeasures, aiming to inform future antimicrobial development and resistance containment strategies.

Under modern intensive and large-scale animal farming practices, the high animal density and confined spaces have progressively elevated the risk of disease transmission while complicating epidemic prevention and control. Current estimates indicate that over 70% of animal disease risks stem from viral infections, primarily transmitted via aerosol pathways. Such aerosol-mediated transmission not only triggers concentrated disease outbreaks within farms but also endangers farm workers and adjacent environments, thereby amplifying prevention challenges and substantially impeding the sustainable development of livestock industries. Therefore, this review systematically expounds the sources, hazards, and influencing factors of microbial aerosols in livestock farming environments. Furthermore, it proposes targeted prevention and control measures to address these challenges, aiming to provide theoretical and practical insights for enhancing disease prevention and promoting the healthy development of the livestock industry.

Porcine epidemic diarrhea virus (PEDV), the causative agent of porcine epidemic diarrhea (PED), induces vomiting, watery diarrhea, and severe dehydration in pigs. It exhibits particularly high lethality in neonatal piglets, posing a significant threat to the global swine industry and inflicting substantial economic losses. The host innate immune system serves as the primary defense against viral invasion; however, PEDV employs multiple strategies to evade this response. This review systematically summarizes the multiple molecular mechanisms by which PEDV evaded the host’s innate immunity, including interfering with host intracellular signaling pathways by virally encoded proteins, antagonizing the host’s antiviral factors and related immune genes to suppress the innate immune responses, and regulating the autophagy process of the host cells, thereby achieving the escape of the host’s innate immunity. A comprehensive understanding of how PEDV subverts innate immunity is crucial for developing effective control strategies and therapeutics. This review aims to provide novel insights and potential targets for combating PED.

In May 2025, a female giraffe in poor body condition died unexpectedly at a zoo in Henan Province, China. A bacterial strain, designated HN-1, was isolated from the heart, liver, spleen, lungs, and kidneys of the deceased animal. After 24 h of incubation at 37 °C on Luria–Bertani (LB) agar, the colonies appeared round, smooth, pale yellow, translucent, and raised. Gram staining revealed that the isolate was a Gram-positive, rod-shaped, and non-spore-forming bacterium. Based on 16S rRNA gene sequencing, the strain showed more than 99.7% homology with reference sequences of E. mexicanum from various sources in GenBank. The results of the susceptibility test showed that E. mexicanum was susceptible to levofloxacin, clindamycin, chloramphenicol, trimethoprim, rifampicin, tetracycline, minocycline, gentamicin, erythromycin, and doxycycline, but resistant to oxacillin, penicillin, ciprofloxacin, and linezolid. These findings provide valuable insights for the diagnosis and treatment of infections caused by E. mexicanum in giraffes.

In May 2025, a female giraffe in poor body condition died unexpectedly at a zoo in Henan Province, China. A bacterial strain, designated HN-1, was isolated from the heart, liver, spleen, lungs, and kidneys of the deceased animal. After 24 hours of incubation at 37°C on Luria–Bertani (LB) agar, the colonies appeared round, smooth, pale yellow, translucent, and raised. Gram staining revealed that the isolate was a Gram-positive, rod-shaped, and non-spore-forming bacterium. Based on 16S rRNA gene sequencing, the strain showed more than 99.7% homology with reference sequences of E. mexicanum from various sources in GenBank. The results of the susceptibility test showed that E. mexicanum was susceptible to levofloxacin, clindamycin, chloramphenicol, trimethoprim, rifampicin, tetracycline, minocycline, gentamicin, erythromycin, and doxycycline, but resistant to oxacillin, penicillin, ciprofloxacin, and linezolid. These findings provide valuable insights for the diagnosis and treatment of infections caused by E. mexicanum in giraffes.

Coronaviruses are a group of widespread infectious pathogens that pose a serious threat to human and animal health. Corona Virus Disease 2019, instigated by severe acute respiratory SARS-CoV-2, has presented an unprecedented challenge to global public health in recent years. The host innate immune system is the first line of defense against pathogens, which plays a key role in inhibiting the initial infection of viruses and regulating the initiation and development of acquired immunity. However, coronaviruses can suppress the host’s innate immune response through their unique immune escape mechanisms, which is one of the key strategies for coronavirus pathogenesis. This review focuses on the host’s innate immune sensors, innate antiviral immune responses, and the mechanisms employed by coronaviruses to evade and suppress the innate immune system. And we hope that it will contribute to a comprehensive understanding of the escape mechanism of coronaviruses regarding innate immunity and the pathogenesis of coronaviruses.