(a) Structure and function of sweat glands (10 marks) (b) Role of antimuscarinic agents in anaesthesia (10 marks) (c)…

(a) Structure and Function of Sweat Glands

Sweat glands (glandulae sudoriferae) are simple coiled tubular exocrine glands situated within the dermis or hypodermis. Morphologically and functionally, they are differentiated into epitrichial (apocrine) and atrichial (eccrine) types. Apocrine glands open primarily into hair follicles and dominate across domestic mammals, whereas eccrine glands open directly onto the epidermal surface, localized mainly in specialized glabrous areas such as footpads in canines and the porcine snout.

Physiologically, these glands serve thermoregulation, excretion, and chemical signaling. Evaporative heat dissipation varies widely across species: equines possess profusely active, adrenergic-innervated apocrine glands rich in latherin protein, making cutaneous evaporation their primary cooling mechanism. In contrast, cattle possess moderately developed glands, and sweating accounts for the larger share of their evaporative heat loss in hot conditions, supplemented by panting, while pigs and dogs possess poorly functional sweat glands over the general body. Besides evaporative cooling, sweat glands facilitate electrolyte balance through regulated excretion of sodium, potassium, chloride, and urea, alongside secreting species-specific pheromones.

(b) Role of Antimuscarinic Agents in Anaesthesia

Antimuscarinic drugs, primarily atropine sulphate and glycopyrrolate, act as competitive antagonists at postganglionic muscarinic acetylcholine receptors (M₁–M₃). In veterinary pre-anaesthetic protocols, they are employed to counteract vagally mediated reflex bradycardia induced by endotracheal intubation, visceral traction, or concurrent administration of potent anaesthetic agents like alpha-2 agonists and opioids. Furthermore, they diminish excessive salivary, pharyngeal, and tracheobronchial secretions, thereby maintaining airway patency during general anaesthesia.

However, their routine administration warrants clinical caution due to adverse effects. Antimuscarinics cause sinus tachycardia, reduce cardiac efficiency, and induce gastrointestinal hypomotility, predisposing ruminants to ruminal atony and equines to cecal impaction or colic. Glycopyrrolate offers advantages over atropine as it does not cross the blood-brain or placental barriers and lacks central nervous system toxicity. In species with endogenous atropinase, such as certain breeds of rabbits, glycopyrrolate is preferred for reliable muscarinic blockade.

(c) Hypocalcemic Tetany in Milch Cattle

Hypocalcemic tetany, closely associated with the onset of parturient paresis (milk fever), represents a critical metabolic disturbance occurring around peripartum. The sudden diversion of serum ionic calcium into colostrum exceeds physiological homeostatic adaptation, resulting in severe acute hypocalcemia (below 5.0 mg/dL). This gap arises because bone mobilization mediated by parathyroid hormone (PTH) and renal activation of 1,25-dihydroxycholecalciferol require 24 to 48 hours to reach compensatory levels.

Clinically, a brief initial phase of hyperexcitability and muscle tetany rapidly progresses to sternal recumbency, marked by the characteristic "S-bend" lateral deviation of the neck, progressive flaccid paralysis, ruminal tympany, loss of pupillary light reflex, and hypothermia (subnormal rectal temperature). Untreated cases deteriorate into lateral recumbency, coma, and circulatory failure. Emergency therapy requires the slow intravenous administration of calcium borogluconate (20–25% solution), accompanied by strict cardiac auscultation to prevent fatal arrhythmias or cardiac arrest caused by hypercalcemic cardiotoxicity.

(d) Thiamine Deficiency in Poultry

Thiamine (Vitamin B₁) deficiency in poultry induces severe metabolic failure in the central nervous system due to the impairment of thiamine pyrophosphate-dependent enzymes, namely pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase. Etiologically, it occurs due to dietary insufficiency, presence of heat-labile thiaminases in feed ingredients like raw fish meal, or competitive antagonism caused by prolonged administration of the coccidiostat amprolium.

Pathologically, energy deprivation and lactic acidosis trigger neuronal degeneration and peripheral nerve myelin degeneration (avian polyneuritis). Chicks exhibit profound neurological manifestations within weeks, classically displaying the pathognomonic "star-gazing" posture characterized by severe cervical opisthotonus, progressive ascending leg weakness, ataxia, loss of righting reflexes, and blindness. High mortality occurs due to dehydration and inability to access feed. Therapeutic administration of parenteral thiamine hydrochloride produces rapid reversal of neuromuscular signs if intervened before irreversible central neuronal necrosis sets in, necessitating subsequent dietary supplementation and careful regulation of coccidiostats.

(e) Neurological Implications of Rabies in Domestic Animals

Rabies is a neurotropic lyssaviral encephalitis, almost invariably fatal once clinical signs appear, affecting all warm-blooded domestic species. Following inoculation via saliva, the virus ascends centripetally along peripheral motor and sensory axoplasm to the dorsal root ganglia and spinal cord, culminating in widespread central nervous system replication and descending migration via cranial nerves to salivary glands. Histopathologically, the presence of intracytoplasmic, eosinophilic Negri bodies within hippocampal pyramidal cells and cerebellar Purkinje neurons represents the pathognomonic lesion.

Clinically, domestic animals exhibit either the furious form (hyperexcitability, unprovoked aggression, hyperaesthesia, loss of fear, altered vocalization, and pharyngeal paralysis preventing deglutition) or the dumb/paralytic form (dropping of the lower jaw, excessive salivation, ascending flaccid paraplegia, and respiratory arrest). Domestic animals act as critical transmission vectors at the human-animal interface. In India, tackling the disease necessitates integrated rabies surveillance and synchronized vaccination under the One Health-based National Action Plan for Dog Mediated Rabies Elimination (NAPRE, 2021), which targets zero dog-mediated human rabies deaths by 2030.