The objective of this study was to characterize oligofructose-induced acute rumen lactic acidosis and its consequences in zebu cattle. We used 29 Nellore heifers which were submitted to experimental induction of laminitis by oligofructose excess. During the induction period, the animals underwent clinical examination, including laminitis diagnosis (hoof pressure testing and locomotion score) and blood and ruminal fluid sampling every six hours (over the initial 24 h) and every 12 h (up to 72 h), after the highest dose. Almost half of the animals (48.1%) required treatment with bicarbonate and saline to correct metabolic acidosis and dehydration. Due to this treatment, the animals were analyzed in treated (n = 13) and non-treated (n = 14) groups. The induction model promoted marked reduction in rumen pH, rumen anaerobiosis, carbon dioxide pressure, and increase in rumen lactate, blood osmolarity, and cortisol concentration. The animals treated had lower values of rumen pH and marked dehydration, evidenced by the increase in globular volume and serum urea. The clinical condition caused by excess oligofructose is severe, with the differential of the appearance of ephemeral fever and respiratory compensation against systemic acidosis, in addition to the frequent appearance of laminitis.

This study aimed to characterize oligofructose-induced laminitis in zebu cattle and comparatively evaluate four different diagnostic methods for laminitis. A total of 29 rumen-cannulated Nelore heifers, weighing 474.5 ± 58.5 kg were used. Laminitis was experimentally induced by intraruminal administration of 0.765 g/kg oligofructose twice daily for three consecutive days, followed by a single dose of 10.71 g/kg oligofructose on the fourth day. The animals were evaluated before administration of the highest dose of oligofructose (basal) and every six hours for up to 24 hours (6, 12, 18, 24 hours) and thereafter, every 12 hours for up to 72 hours (36, 48, 60, 72 hours) post-induction. The following diagnostic methods were used: hoof pain sensitivity test (hoof-testing), locomotion scoring, hoof infrared thermography, and force platform. Diagnosis of laminitis was confirmed after two positive responses to hoof pressure testing. Using a receiver operator characteristic (ROC) curve, we defined the appropriate cutoff for infrared thermography and force plate as 30˚C and < 24%, respectively. From the 29 heifers, 27 developed laminitis (93.1%) which occurred between 24 h to 72 h in the digits from two limbs, with more frequent sensitivity in the lateral digits. Locomotion analysis detected twenty-eight heifers with laminitis and showed that a greater (P = 0.006) number of animals had lameness in two limbs (n = 13; 56%). Using hoof-testing as gold standard for the diagnosis of laminitis the locomotion score displayed 100% sensitivity, 97% specificity and 98% accuracy; infrared thermography showed 96% sensitivity, 63% specificity, and 75% accuracy whilst force plate had 76% sensitivity, 82% specificity and 79% accuracy. This suggests that, for the diagnosis of laminitis in cattle, pain evaluation is more efficient. Considering the difficult to evaluate pain sensitivity in Nelore animals, filmed locomotion score, infrared thermography and force plate methods can be indicated for noninvasive lameness detection in beef farms.

We evaluated the clinical aspects and feeding behavior of cattle with subacute ruminal acidosis (SARA) caused by short-chain fatty acids (SCFAs). Ten healthy Nelore heifers were subjected to an adjusted SARA induction protocol using citrus pulp (CP). Clinical examinations were performed at baseline and at 3, 6, 9, 12, 15, 18, and 24 h intervals after induction, with ruminal fluid, blood, and feces sampling. The animals’ feeding behavior was evaluated on, before, and for 3 days after SARA by observing the animals every 5 min for 24 h. The dry matter intake (DMI) was recorded daily. The ruminal pH during SARA was always lower than baseline, with an acidotic duration of 547 ± 215 min, a minimum pH of 5.38 ± 0.16, and an average pH of 5.62 ± 0.1. SARA was mainly caused by SCFAs (maximum 118.4 ± 9.3 mmol/L), with the production of l-lactic acids (7.17 mmol/L) and d-lactic acids (0.56 mmol/L) 6 h after the experiment began. The DMI was reduced by 66% and 48% on days 1 and 2, respectively, and returned to normal levels on day 3. SARA caused a reduction in feed intake and rumination time, as well as an increase in the time spent in decubitus on days 1 and 2. These results were influenced by the ruminal pH, ruminal movement, and osmolarity. Furthermore, SARA caused different degrees of depression, which became more pronounced with higher ruminal lactic acid concentrations.

The purpose of this work was to determine a radiographic standard of normality for lateral and medial ungulae in 3‐year‐old bovine females of the Nellore breed. Twenty‐six cows underwent radiographic exposure of the medial and lateral ungulae of the hindlimbs and forelimbs; abaxioaxial projections were used. The images were analyzed; distances were measured between the dorsal surface of the distal phalanx and the surface of the hoof capsule. The two angles formed, i.e., an angle between the dorsal surface of the distal phalanx and a line parallel to the sole (inner), and an angle between the dorsal surface of the hoof and a line parallel to the sole (outer), were also recorded. The results suggested a standard of normality for the proximal, middle and distal distances of the ungulae of the forelimbs: 0.96 ± 0.12 cm. For the measurement of hindlimbs, except for the distal distances of the side ungulae, the suggested value was 1.02 ± 0.14 cm; for the distal measurement of the lateral ungulae of the hindlimbs, the value was 1.09 ± 0.12 cm. For inner and outer angles, the values were 36.45° ± 4.4° for the medial ungulae of the forelimbs and 42.50° ± 3.8° for other ungulae of the forelimbs and hindlimbs (standard deviations of the values suggested for the angles should be used as variations between different animals, limbs and ungulae; they should not be used between angles of the same ungula).

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