Vetnews | Mei 2024 40 « BACK TO CONTENTS oxidative phosphorylation in helminths and there is a similarity in mechanism of action in myelin resulting in myelin spongiosis. The toxic effects include degeneration and gliosis of the CNS, retina, and optic nerve, resulting in blindness and even death. The other common presenting clinical signs of closantel toxicity in sheep are inappetence, paresis, ataxia, recumbency and blindness. Swollen optic discs with several small papillary and peripapillary haemorrhages have been recorded in fundoscopic examination. The optic nerve diameter physically increases in size. Over time, there is generalized retinal and optic disc atrophy producing irreversible blindness. There are certainly some practical ways that a farmer could reduce the chance of causing a toxicity problem in a group of animals. These include: • Weigh – don’t guess. Underestimating the weight of sheep is a common cause of under-dosing. Select and weigh the biggest sheep in the group to determine the correct dose –if there is a wide range of weights, consider splitting the group into different weight groups and dose accordingly rather than dosing to the heaviest animal and administering too much closantel to small animals. • Calibrate and maintain the drench gun. Always check the dosing gun is delivering the right amount before you start drenching. Adjust the gun until the dose delivered is correct and re-check the accuracy of the gun at regular intervals. • Drench correctly. The drenching technique is a vital part of ensuring that the wormer does its job effectively. Pregnancy Toxaemia: Pregnancy toxaemia is a metabolic disorder of pregnant small ruminants. It occurs during the final stage of gestation as the result of inadequate nutrition [inappropriate metabolism of carbohydrates and fats] usually because of insufficient energy density of the ration and decreased rumen capacity as a result of foetal growth. The disease is characterized by hypoglycaemic encephalopathy, with a variety of behavioural and neurologic clinical signs, as well as by increased concentration of beta-hydroxybutyrate in blood and possibly urine. In the case of negative energy balance, this increased mobilization may overwhelm the liver’s capacity and result in hepatic lipidosis, with subsequent impairment of function. Overconditioned animals may have decreased appetites, and adipose mobilization quickly overwhelms the liver’s capacity, resulting in hepatic lipidosis. Affected sheep may show an unsteady walk, appear dull, and are usually anorexic. Vision may be impaired and this may extend to blindness. The mortality rate is about 80%, with death usually occurring in from 2 – 10 days. Taenia: Taenia multiceps is a cestode that typically affects the central nervous system (CNS) of livestock, particularly the brain and spinal cord. Although the life cycle may be complex it can be summarised by eggs being released by the host in faeces into the environment. The eggs are ingested and hatch in the GIT and the parasites penetrate the intestinal lining and reach the CNS via the bloodstream where it then encyst and mature over months. As the cyst in the brain increases in volume, clinical signs may start developing and can include depression, moving in a circle, head deviation, ataxia and blindness. The neurological signs are determined by the location, number and size of the cyst(s) in the CNS. It may form cysts in other tissues like muscle, subcutaneous and peritoneal areas. It is this part of the lifecycle that may result in visual problems. The author has seen a young blind hyena caught in an electric fence that eventually had an MRI and a large brain taenia cysts was seen on the MRI and confirmed at necropsy. Thromboembolic meningoencephalitis: Meningitis, encephalitis, and encephalomyelitis are terms used to describe inflammatory conditions of the meninges, brain, or brain and spinal cord, respectively. Causes of meningitis, encephalitis, and meningoencephalitis include bacteria, viruses, fungi, protozoa, rickettsia, parasite migrations, chemical agents, and idiopathic or immune-mediated diseases. Depending on the causal agent, the extent and speed of onset, and the location of the inflammation, clinical signs can vary from subtle to dramatic, and therapies can have varied successes. Accurate diagnosis is dependent on quality neurologic (including ocular) examinations and supported by CSF analysis and imaging, in particular MRI. Although the latter are unlikely to occur in a production animal system, the importance of postmortem examinations cannot be underestimated, because historically, many zoonotic agents have manifested as meningoencephalitis in people and animals. In ruminants, generally, bacterial infections are more common than other causes of meningitis or encephalitis. These may include Histophilus and Listeriosis. Bacteria can arrive in the CNS either as a result of local trauma or by direct extension, as occurs with puncture wounds from fighting, sinusitis after dehorning (cattle), otitis media or -interna, spinal column inflammation (salmonellosis in cattle). Hematogenous spread, as septic emboli from suppurative lesions in other locations of the body (endocarditis or arthritis in cattle, navel-ill in ruminants) or as bacteremia that leads to CNS vascular damage (Histophilus somni in feedlot cattle), is also well documented as a mode of bacterial entry to the CNS. Whereas these latter lesions lead to blood-brain barrier damage, penetration of an intact blood-brain barrier can also occur by cells harbouring intracellular bacteria such as Mycobacterium spp, Regulars I Ophthalmology Column
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