The effects of climate changes and, in particular, global warming on health status of livestock have not been considered with the same attention as given to humans (http://www.who.int/globalchange/climate/en/). However, it is assumed that as in the case of humans, climate changes can affect the health of livestock and poultry, both directly and indirectly. Direct impacts include temperature-related illness and death, and the morbidity of animals during extreme weather events. Indirect impacts follow more intricate pathways and include those deriving from the influence of climate on microbial density and distribution, distribution of vector-borne diseases, host resistance to infections, food and water shortages, or food-borne diseases. Some general concepts of livestock environment and health have been presented by Simensen (1984) and these may serve as a guide to management of disease during climate change.
A series of studies carried out in dairy cows indicated a higher occurrence of mastitis during periods of hot weather (Giesecke 1985; Smith et al. 1985; Morse et al. 1988; Waage et al. 1998; Cook et al. 2002; Yeruham et al. 2003). However, the mechanisms responsible for the higher occurrence of mastitis during summer have not been elucidated. The hypothesis to explain these observations include the possibility that high temperatures can facilitate survival and multiplication of pathogens (Hogan et al. 1989) or their vectors (Chirico et al. 1997), or a negative action of heat stress on defensive mechanisms (Giesecke 1985).
During summer, ketosis is more prevalent due to increased maintenance requirements for thermoregulation and lower feed intake (Lacetera et al. 1996), and the incidence of lameness increases as a consequence of metabolic acidosis (Shearer 1999). Furthermore, analysis of metabolic parameters in the blood of dairy cows indicates that high environmental temperatures may be responsible for alteration of liver function, mineral metabolism and oxidative status (Bernabucci et al. 2002) (Table 7.1), which may also lead to animals having clinical or sub-clinical disease.
Results from an epidemiology study carried out in California (Martin et al. 1975) documented higher mortality rates of calves born during summer. Others
Table 7.1 Effects of high environmental temperatures on blood indexes of energy and mineral metabolism, liver function and oxidative balance in dairy cows (Adapted from Lacetera et al. 1996; Ronchi et al. 1999, Bernabucci et al. 2002)
Energy metabolism Body condition score Glycemia
Non esterified fatty acids
Mg Na K Cl
CAB (Na + K - Cl) Oxidative balance Pro-oxidants (TBARS, ROMs) Antioxidants (GSH, Thiols)
Loss Decrease Increase Increase
Decrease Decrease Increase
Decrease/increase Decrease/increase Decrease/no changes Decrease
Increase Decrease have reported that heat stress may be responsible for impairment of the protective value of colostrum both in cows (Nardone et al. 1997) and pigs (Machado-Neto et al. 1987), and also for alteration of passive immunization of calves (Donovan et al. 1986; Lacetera 1998). On the other hand, results on the negative influence of heat stress on colostral immunoglobulins may provide an explanation for the higher mortality rate of newborns observed during hot months.
Several studies have assessed the relationships between heat stress and immune responses in cattle, chickens or pigs. However, results of those studies are conflicting. In particular, some authors reported an improvement (Soper et al. 1978; Regnier and Kelley 1981; Beard and Mitchell 1987), others described an impairment (Regnier and Kelley 1981; Elvinger et al. 1991; Kamwanja et al. 1994; Morrow-Tesch et al. 1994), and others indicated no effects (Regnier et al. 1980; Kelley et al. 1982; Bonnette et al. 1990; Donker et al. 1990; Lacetera et al. 2002) of high environmental temperatures on immune function. Recently, in a field study carried out in Italy during the summer 2003 (Lacetera et al. 2005), which was characterized by the occurrence of at
Days relative to calving
Fig. 7.1 DNA synthesis in peripheral blood mononuclear cells (PBMC) isolated from spring (solid line) or summer (dotted line) cows. The PBMC were stimulated with concanavalin A. Values are the means ± SEM of the optical density (OD). Asterisks indicate significant differences (P < 0.01) (Adapted from Lacetera et al. 2005)
least three heat waves, there was a profound impairment of cell-mediated immunity in high yielding dairy cows (Fig. 7.1). Interestingly, such results suggest that immunosuppression during hot periods may be responsible for the failure of vaccine interventions and for reduced reliability of diagnostic tests based on immune system reaction (i.e., tuberculin skin test). The large variety of experimental conditions in terms of species, severity and length of heat stress, recovery opportunities, and also of the specific immune functions taken into consideration are likely to explain the discrepancy among results of different studies. In addition other factors such as pho-toperiod may impact on immune function (Auchtung et al. 2004).
Global warming will affect the biology and distribution of vector-borne infections. Wittmann et al. (2001) simulated an increase of temperature values by 2°C. Under these conditions, their model indicated the possibility of an extensive spread of Culicoides imicola, which represents the major vector of the bluetongue virus. The distribution of ticks and flies is also likely to change.
Another mechanism through which climate changes can impair livestock health is represented by the favorable effects that high temperature and moisture have on growth of mycotoxin-producing fungi. Their growth and the associated toxin production are closely correlated to the degree of moisture to which they are exposed, which itself is dependent on weather conditions at harvest, and techniques for drying and storage (Frank 1991). With regard to alteration of animal health, mycotoxins can cause acute disease episodes when animals consume critical quantities. Specific toxins affect specific organs or tissues such as the liver, kidney, oral and gastric mucosa, brain, or reproductive tract. In acute mycotoxicoses, the signs of disease often are marked and directly referable to the affected target organs. Most frequently, however, concentrations of mycotoxin in feeds are below those that cause acute disease. At lower concentrations, mycotoxins reduce the growth rate of young animals, and some interfere with native mechanisms of resistance and impair immunologic responsiveness, making the animals more susceptible to infection. Studies have shown that some mycotoxins can alter lymphocyte functions in domestic ruminants through alteration of DNA structure and functions (Lacetera et al. 2003, 2006; Vitali et al. 2004).
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