Department of Animal Sciences, University of Florida, Gainesville 32611.
Division of Animal Sciences, University of Missouri, Columbia 65211.
J Dairy Sci. 2022 Oct;105(10):8586-8589. doi: 10.3168/jds.2021-21433. Epub 2022 Aug 31.
Environmental effects on pathogen abundance and access are precursors to mastitis. Indeed, high heat and humidity, and unsanitary housing and equipment, are associated with greater pathogen load and exposure. Although less is known about effects of environment on a cow's ability to resist infection, several indicators suggest that it can affect pathogen responses. Mastitis incidence and bulk tank somatic cell count vary with season, typically peaking in summer. Recent controlled studies have revealed that heat stress exposure results in changes in the microbiome of the cow and her environment, which may relate to negative effects on milk quality and cow health. Alternatively, specific pathogen loads may vary based on housing dynamics rather than associations with physical environment. Indeed, housing-related stressors, such as overcrowding and social group challenge, influence secretion of glucocorticoids, thus affecting pathogen resistance in the cow. Two key seasonal variables are photoperiod and temperature, specifically the heat stress consequent to elevated temperature and humidity. Shifts in light duration regulate immune function in other species, but apparently have limited effect on udder health of lactating cows. In contrast, in dry cows, short days increase peripheral blood mononuclear cell number and are associated with lower somatic cell count in the next lactation, compared with long days. With heat stress, elevated body temperature directly affects expression of immune-related genes in mammary tissue. Responses depend on duration of exposure and feature acute upregulation of immune-signaling pathways, followed by enrichment of other immune-related pathways after prolonged exposure. Most responses are transient and recover within 1 wk. Functionally, heat stress impairs some aspects of acquired immunity in dry cows, including antigen responses and lymphocyte proliferation, but apparently not innate immune function. However, heat stress in late gestation reduces neutrophil phagocytosis and killing in vitro, and neutrophils in circulation are reduced in vivo as are responses to pathogen challenge in the subsequent lactation. A holistic understanding of the complex interplay of environment, pathogens, and host is needed to inform advances in this area.
环境对病原体数量和接触的影响是乳腺炎的前兆。事实上，高温高湿以及不卫生的住房和设备与更大的病原体负荷和暴露有关。虽然关于环境对牛抵抗感染能力的影响知之甚少，但有几个指标表明它可能会影响病原体的反应。乳腺炎的发病率和牛奶体细胞计数随季节而变化，通常在夏季达到高峰。最近的对照研究表明，热应激暴露会导致牛及其环境的微生物组发生变化，这可能与牛奶质量和牛健康的负面影响有关。或者，特定的病原体负荷可能会根据住房动态而变化，而不是与物理环境相关。事实上，与住房相关的压力源，如过度拥挤和社会群体挑战，会影响糖皮质激素的分泌，从而影响牛的病原体抵抗力。两个关键的季节性变量是光周期和温度，特别是与高温和高湿度相关的热应激。光照时间的变化调节了其他物种的免疫功能，但对泌乳奶牛的乳房健康显然影响有限。相比之下，在干奶牛中，短日照天数会增加外周血单核细胞数量，并与下一泌乳期的体细胞计数较低相关，而长日照天数则相反。在热应激下，体温升高直接影响乳腺组织中与免疫相关的基因表达。这些反应取决于暴露的持续时间，其特征是急性上调免疫信号通路，然后在长时间暴露后富集其他与免疫相关的途径。大多数反应是短暂的，在 1 周内恢复。从功能上讲，热应激会损害干奶牛某些获得性免疫功能，包括抗原反应和淋巴细胞增殖，但显然不会损害先天免疫功能。然而，妊娠后期的热应激会降低体外中性粒细胞的吞噬和杀伤作用，体内循环中的中性粒细胞减少，随后的泌乳期对病原体挑战的反应也减少。为了在这一领域取得进展，需要全面了解环境、病原体和宿主之间的复杂相互作用。
