Calf diarrhea is a disease that causes serious economic losses in livestock farms due to its effect on treatment costs and mortality rates. Viral, bacterial, and protozoal pathogens are major causes of this disease, often occurring as mixed infections
1-5. Neonatal calf diarrhea, frequently caused by Escherichia coli, Cryptosporidium spp., rotavirus, and coronavirus, is highly prevalent during the first four weeks following birth
6. In neonatal calves with diarrhea, electrolyte losses such as bicarbonate (HCO
3-), chloride (Cl), sodium (Na), potassium (K) and hydrogen (H) are observed along with fluid loss (7, 8). In addition to fluid electrolyte loss, decreased milk intake, changes in intestinal flora, metabolic acidosis, hypothermia, septicemia and azotemia are also observed
2,3,9-12. In healthy calves, venous pH ranges between 7.35 and 7.45. A venous pH below 7.35 indicates acidosis. Diarrhea is particularly recognized as the primary factor leading to metabolic acidosis observed in calves
13,14. Metabolic acidosis typically arises as a result of hyponatremia, the accumulation of D-lactate and volatile fatty acids, or intestinal HCO
3- loss, all of which contribute to the development of symptoms
15. In dehydrated calves, inadequate perfusion leads to reduced acid secretion in the kidneys, while tissue hypoxia results in the formation of lactic acid, further contributing to the development of metabolic acidosis
4,16. In the case of metabolic acidosis, respiratory compensation results in a decrease in partial arterial pCO
2. Metabolic acidosis, characterized by HCO
3- depletion, excessive acid production, and impaired renal acid excretion, is a critical and commonly observed condition in diarrheic calves
17. The acidosis observed in diarrhea is associated with intestinal HCO
3- loss and the accumulation of organic acids such as L-lactate and D-lactate
18,19. Additionally, diarrhea is frequently accompanied by significant electrolyte imbalances. Although there is a reduction in the total body K levels, an increase in blood K concentration is observed in diarrheic calves
18,20. Moreover, moderate L-lactic acidosis may develop in both healthy and diarrheic calves due to dehydration
21,22. In metabolic acidosis, particularly in cases of elevated plasma D-lactate concentrations, the central nervous system becomes progressively depressed over time. This condition is further characterized by a reduction in the suckling reflex, ataxia, recumbency, coma, and ultimately, death
3. In calves with severe diarrhea, it is reported that mortality is more often attributable to metabolic acidosis rather than dehydration
8.
The severity of acidosis and base deficit can be accurately determined using a blood gas analyzer23. The assessment of acid-base imbalances and the degree of dehydration is crucial for determining the treatment protocol and ensuring effective therapeutic management7. A blood gas analyzer measures parameters such as blood pH, pCO2 (mmHg), and HCO3- (mmol/L). These parameters allow the determination of whether the acid-base imbalance is acidemia or alkalemia and whether the underlying issue is respiratory or metabolic in origin24.
Oxidative stress refers to an imbalance between oxidants and antioxidants, skewed towards an excess of oxidants. This condition is primarily characterized by lipid peroxidation and the generation of reactive oxygen species (ROS) or free radicals, resulting in cellular damage within the organism. When the body’s defense mechanisms against oxidative stress fail, oxidative damage occurs in cells, resulting in significant disruptions in bodily functions. Oxidative stress plays a critical role in the pathogenesis of numerous diseases, including aging, cardiovascular diseases, cancer, sepsis, degenerative neurological disorders, renal failure, infertility, and various muscle and liver diseases25,26. Under normal conditions, there is a balance between oxidant and antioxidant systems within the organism. In the case of oxidative stress, this balance is disrupted, leading to an increase in the number of oxidants27,28. Free oxygen radicals function in two significant ways. First, they act on the fatty acids present in the cell membrane, leading to the generation of new radicals. Second, they incorporate released hydrogen atoms, converting them into lipid peroxides29. Malondialdehyde (MDA), a lipid peroxide product, causes alterations such as disruption of ion transport, enzyme activities, and the integrity of the cell membrane 30. Therefore, MDA measurement is utilized to assess the severity of cellular damage31. Catalase (CAT) and glutathione peroxidase (GSH-Px) reduce hydrogen peroxide (H2O2) to water and atomic oxygen. Glutathione (GSH), as a substrate in the redox cycle, plays a crucial role in scavenging hydroxyl radicals and singlet oxygen. In addition to directly neutralizing free radicals, GSH also exerts enzymatic effects in collaboration with GSH-Px. The primary function of GSH is to maintain enzymes and other cellular components in their reduced state within cells32. Superoxide dismutase (SOD) is the primary detoxification enzyme within cells and is known to play a central role in defense against ROS33,34.
The aim of this study was to investigate the etiology of diarrhea in neonatal calves and to determine the relationship in blood gas and oxidative stress parameters.
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