(a) Enlist the cranial nerves of bovines. Discuss the origin, distribution and functions of the vagus nerve. (20 marks) (b)…

(a) Cranial nerves of bovines; origin, distribution and functions of the vagus nerve (20 marks)

Bovines have twelve pairs of cranial nerves:

1. I Olfactory (sensory, smell).
2. II Optic (sensory, vision).
3. III Oculomotor (motor, most eye muscles, pupil constriction and lens accommodation).
4. IV Trochlear (motor, dorsal oblique muscle).
5. V Trigeminal (mixed; ophthalmic, maxillary and mandibular branches; sensation of the face and motor to the chewing muscles).
6. VI Abducens (motor, lateral rectus and retractor bulbi).
7. VII Facial (mixed; facial muscles, taste from the tongue front, salivary and lacrimal glands).
8. VIII Vestibulocochlear (sensory, hearing and balance).
9. IX Glossopharyngeal (mixed; taste and sensation of the tongue back and pharynx, parotid gland).
10. X Vagus (mixed, see below).
11. XI Accessory (motor, trapezius, sternocephalic and brachiocephalic muscles).
12. XII Hypoglossal (motor, tongue muscles).

Vagus nerve:

• Origin: from the lateral surface of the medulla oblongata, caudal to the glossopharyngeal nerve, by several rootlets. Its nuclei are the nucleus ambiguus (motor to the pharynx, larynx and oesophagus), the dorsal motor nucleus (parasympathetic to the viscera), and the nucleus of the tractus solitarius (visceral sensation). It leaves the skull through the jugular foramen.
• Course and distribution: in the neck it runs with the sympathetic trunk as the vagosympathetic trunk beside the common carotid artery. Branches: pharyngeal, cranial laryngeal (with the external branch to the cricothyroid muscle) and the recurrent laryngeal nerve (the left hooks round the aortic arch, the right round the subclavian artery) to the larynx and oesophagus; then cardiac and pulmonary branches in the thorax. The dorsal and ventral vagal trunks accompany the oesophagus through the diaphragm and supply the reticulum, rumen, omasum and abomasum, and also the liver, pancreas, and the small and part of the large intestine, through the coeliac and cranial mesenteric plexuses.
• Functions: motor to the muscles of the pharynx, larynx and oesophagus (swallowing and voice); parasympathetic slowing of the heart, bronchoconstriction, and stimulation of gastrointestinal secretion and motility, including the ruminant forestomach contractions; sensory from the larynx (cough), the pharynx, and the thoracic and abdominal viscera, including baroreceptors, chemoreceptors and stretch receptors of the rumen.
• Clinical: vagal indigestion in cattle (damage to the vagal branches causes forestomach motility failure and distension), and recurrent laryngeal damage.

(b) Principles of chemotherapy for neoplastic diseases in animals (15 marks)

Chemotherapy uses cytotoxic drugs to kill tumour cells while sparing normal ones. Its principles are:

• Log-kill hypothesis: each dose kills a constant fraction of cells, not a fixed number, so repeated cycles are needed to reduce the cell number to a very low level, and cure requires killing every clonogenic cell.
• Growth kinetics: small tumours have a large growth fraction and are most sensitive (Gompertzian growth), so treatment is best begun early or as an adjuvant after surgery or radiotherapy, when little disease remains; bulky tumours respond poorly.
• Cell cycle: some drugs are cell-cycle specific (antimetabolites in S phase, such as methotrexate and cytarabine; vincristine in M phase), while alkylating agents (cyclophosphamide, chlorambucil) and anthracyclines (doxorubicin) and platinum drugs act throughout the cycle.
• Combination chemotherapy: drugs with different mechanisms and different toxicities are combined to raise cell kill and delay resistance, for example CHOP (cyclophosphamide, doxorubicin, vincristine, prednisolone) for canine lymphoma.
• Dose and schedule: doses by body surface area (mg/m²), close to the maximum tolerated, given in cycles with rest periods so normal tissue (marrow, gut) recovers; check the blood count before each dose.
• Drug resistance, which grows with tumour size and treatment; sanctuary sites such as the brain.
• Toxicity monitoring and supportive care: bone marrow suppression, vomiting, alopecia, cardiotoxicity (doxorubicin), haemorrhagic cystitis (cyclophosphamide), and platinum toxicity in cats.
• Safety of staff and owners in handling and disposal of cytotoxic drugs; informed consent; the goals of cure, remission or palliation, with quality of life; and response assessment (complete or partial remission).

(c) Meningitis in cattle: aetiology, pathogenesis, clinical findings, diagnosis and treatment (15 marks)

Meningitis is inflammation of the meninges (the leptomeninges).

Aetiology: mainly bacterial. In calves, it follows septicaemia from Escherichia coli, Salmonella, streptococci and Trueperella pyogenes, with failure of colostrum transfer. In older cattle, Histophilus somni causes thromboembolic meningoencephalitis, and the bacteria may spread from otitis, sinusitis, dehorning wounds or skull injury. Listeria monocytogenes causes encephalitis, and viruses (rabies, bovine herpesvirus) cause encephalitis.

Pathogenesis: bacteria reach the meninges by the blood, or by direct extension. They lodge in the choroid plexus and meninges, and endotoxin and inflammatory mediators increase vascular permeability, giving a purulent exudate in the subarachnoid space, cerebral oedema and raised intracranial pressure, obstruction of the flow of cerebrospinal fluid (CSF), vasculitis and thrombosis, and ischaemia of the brain.

Clinical findings: fever, depression, hyperaesthesia, a stiff neck with the head drawn back (opisthotonos), head pressing, tremors, convulsions, nystagmus, blindness, then recumbency, coma and death. Calves also show signs of septicaemia (navel ill, diarrhoea, joint ill, hypopyon).

Diagnosis: history and signs; CSF analysis (turbid, with high protein, high neutrophil count and low glucose), with culture and sensitivity; blood culture and blood count; the serum immunoglobulin level of calves; and post-mortem histopathology. Differentials are polioencephalomalacia, listeriosis, rabies, lead poisoning and hypomagnesaemia.

Treatment: early, high doses of antibiotics that cross the blood-brain barrier (a third-generation cephalosporin such as ceftiofur, florfenicol, trimethoprim-sulfonamide, or ampicillin) by injection; an anti-inflammatory (flunixin); reduction of brain pressure (mannitol, hypertonic saline); anticonvulsants such as diazepam; fluids and nutrition; and prevention by adequate colostrum and hygiene.