Insights
In order to maximise production results in the livestock industry, it is important to understand the challenges that animals face.
Solutions through the feed can support growth, health and overall performance. Let’s delve into the fascinating world of animal nutrition and its importance in agriculture.
Mycotoxins – a force to be reckoned with!
Mycotoxins are a diverse group of toxic secondary metabolites produced by various filamentous fungi, primarily belonging to the genera Aspergillus, Penicillium, and Fusarium. Common mycotoxins of concern in livestock production include aflatoxins, ochratoxin A, fumonisins, zearalenone, and trichothecenes. These compounds frequently contaminate feed ingredients during cultivation, harvest, transport, or storage, particularly under conditions of high humidity and temperature that favor fungal growth.
Ingestion of mycotoxin-contaminated feed can lead to a wide spectrum of adverse physiological effects in animals, depending on the type and concentration of toxin, duration of exposure, and species susceptibility. Documented effects include gastrointestinal disturbances, hepatotoxicity, nephrotoxicity, reproductive failures, immune suppression, and reduced feed efficiency. Chronic exposure, even at subclinical levels, can compromise productivity and predispose animals to secondary infections due to impaired immune competence.
Ensuring the production and provision of high-quality, contaminant-free feed is therefore essential for maintaining animal health and performance. Preventive strategies include implementing good agricultural and storage practices, routine monitoring for fungal and mycotoxin contamination, and the use of mycotoxin detoxifying agents or binders in feed formulations. Such integrated control measures are critical to safeguard livestock welfare, productivity, and the safety of animal-derived food products.
Endotoxins: Inducers of inflammation
Endotoxins, also known as bacterial lipopolysaccharides (LPS), are potent inflammatory mediators derived from the outer membrane of Gram-negative bacteria. Upon release into the gastrointestinal lumen or systemic circulation, these molecules are recognized by pattern recognition receptors such as Toll-like receptor 4 (TLR4), which initiate strong innate immune responses in livestock. While this activation is essential for pathogen defense, excessive or chronic stimulation can have detrimental physiological consequences.
The inflammatory cascade triggered by LPS involves the release of cytokines, acute-phase proteins, and reactive oxygen species, which collectively impose significant metabolic costs on the host. Energy and nutrients are diverted from productive functions, such as growth, lactation, and reproduction, toward sustaining the immune response. This metabolic shift, often described as the “cost of inflammation,” reduces feed efficiency and overall performance.
Prolonged endotoxin-induced inflammation disrupts intestinal structure and function, leading to impaired barrier integrity, increased permeability, and reduced nutrient absorption. These pathophysiological changes not only compromise animal health and welfare but also result in measurable declines in productivity and profitability in intensive livestock systems. Effective management of endotoxin exposure and modulation of inflammatory responses are therefore key to maintaining optimal gut health and performance.
Impact of heat stress on poultry
Heat stress is a major environmental challenge in poultry production, particularly in regions with high ambient temperatures or inadequate ventilation. Exposure to elevated temperatures disrupts thermoregulatory mechanisms, leading to increased body temperature, dehydration, and substantial physiological strain. These conditions are associated with elevated mortality rates, reduced growth performance, diminished feed efficiency, and declines in both meat and egg quality.
The detrimental effects of heat stress extend beyond productivity losses to encompass profound alterations in physiology, health, welfare, and behavior. Birds subjected to chronic thermal stress exhibit changes in endocrine and metabolic function, altered feeding behavior, and impaired intestinal integrity. These disruptions collectively compromise nutrient absorption and energy utilization, reducing overall performance.
At the cellular level, heat stress induces oxidative stress through excessive generation of reactive oxygen species (ROS), overwhelming the antioxidant defense systems. This imbalance contributes to cellular damage, inflammation, and immunosuppression, making birds more susceptible to infections and disease. Consequently, managing heat stress through environmental control, nutritional interventions, and genetic selection for thermotolerance is essential to sustain poultry health, welfare, and productivity under modern production conditions.
Ear necrosis in pigs – A multifactorial problem.
Ear necrosis is a multifactorial condition observed in pigs, characterized by the progressive degeneration of tissue at the ear tips, where peripheral blood circulation is naturally limited. The condition manifests as discoloration, ulceration, and eventual blackening of the affected tissue due to localized ischemia and necrosis. It is most commonly reported in growing and finishing pigs, particularly under intensive production conditions.
Although the precise etiology of ear necrosis remains complex, it is widely recognized as being closely associated with stress-related factors. Contributing elements can be broadly categorized into nutritional, environmental, and health-related factors. Poor housing conditions, crowding, thermal stress, and inadequate hygiene have been implicated in exacerbating its occurrence, often through their effects on immune and vascular function.
Among the major biochemical contributors, mycotoxins and endotoxins play a critical role. These toxins, frequently co-occurring in livestock environments, can impair vascular integrity, promote systemic inflammation, and compromise skin health. Their synergistic action increases the susceptibility of ear tissue to necrosis, highlighting the need for comprehensive management strategies focused on feed quality, toxin control, and stress reduction to prevent the onset and progression of the condition.