Three-related cats were evaluated for a history of short-strided gait and temporary recumbency after startle. Neurological examination, electromyography (EMG), muscle biopsies, and a chloride voltage-gated channel 1 (CLCN1) molecular study were performed. Clinically, all 3 cats presented myotonia with warm-up phenomenon and myotonic discharges during EMG examination. Muscle biopsies showed normal muscle architecture and variation in the diameter of myofiber size with the presence of numerous hypertrophic fibers. The molecular study revealed a missense variant (c.991G>C, p.Ala331Pro) in exon 9 of the CLCN1 gene, responsible for the first chloride channel extracellular loop. This mutation was screened in 104 control phenotypically normal unrelated cats, and all were wildtype. The alanine at this position is conserved in ClC-1 (chloride channel protein 1) in different species, and 2 mutations at this amino acid position are associated with human myotonia. This is the third CLCN1 mutation described in the literature associated with hereditary myotonia in cats and the first in domestic animals located in an extracellular muscle ClC-1 loop.

In a randomized controlled trial, we evaluated the effects of five oral electrolyte solutions (OESs) with different compositions of water, electrolyte, and acid-base balances of diarrheal neonatal calves. Osmotic diarrhea and dehydration were induced with sucrose in milk, spironolactone, and hydrochlorothiazide for 48 h in thirty 10-day old Holstein healthy calves with 43.5 ± 3.80 kg BW who were fed with natural milk. They were allocated to five treatment groups (n=6) based on the administered OES (commercial: OES A, B, C, D; and non-commercial: OES UEL). On the day of treatment, the calves received 6L of OES in two doses apart from milk intakes. Venous blood samples were collected at -48h (start of induction), -24h, 0h (start of the treatment day), 8h, 16h, 24h, 48h, and 72h. TPP, glucose, D-lactate, L-lactate, pH, pCO2, HCO3 -, BE, Na+, K+, Cl-, SID3, SIG, AG, Atot and percentage change in plasma volume (%PV) were measured or calculated and analyzed by two-way repeated measures ANOVA. All the calves developed osmotic diarrhea, mild to moderate dehydration, hyponatremia, relative hyperchloremia, and moderate to severe metabolic acidosis. The tested OESs were well accepted by the calves and effective in reversing dehydration, electrolyte imbalances, and metabolic acidosis. OES D did not completely correct hyponatremia, and SEO B caused transient hyperglycemia. It has been concluded that all the tested OESs are safe and effective for the treatment of diarrhea in calves with moderate degrees of dehydration and metabolic acidosis, which indicates that they have proper compositions for this purpose.

Sucrose- and diuretics-based protocols are widely used to induce osmotic diarrhea and dehydration in calves, but they fail to cause metabolic acidosis. In previous studies, calves were fed milk replacers and deprived of water. In this study, we assessed the water, electrolyte, and acid-base imbalances in calves that were fed whole milk and were not completely deprived of water during the induction period. Healthy, male Holstein calves aged 10-12 days were assigned to two groups: free access to water (FWG; n=17) and water deprivation at night (DWG; n=21); and osmotic diarrhea was induced with sucrose added to milk, spironolactone (2mg kg^-1) and hydrochlorothiazide (2mg kg^-1) orally every 8h for 48h. pH, pCO₂, HCO₃^-, BE, Na⁺, K⁺, Cl^-, SID₃, TPP, AG, A_tot, glucose, L-lactate, D-lactate, SIG, and percentage change in plasma volume were measured in venous blood samples taken at 0, 24, and 48h. Data were analyzed using two-way repeated measures ANOVA. Calves showed diarrhea, mild (FWG) to moderate (DWG) dehydration, hyponatremia, and moderate (FWG) to severe (DWG) metabolic acidosis. AG and D-lactate levels were higher and SIG was lower in the DWG, and there was no hyper-L- or D-lactatemia. The magnitude of metabolic acidosis was similar to that observed in natural cases of diarrhea. The protocol for inducing osmotic diarrhea and dehydration should be applied to calves that are fed whole milk and are not completely deprived of water.