Bacterial Meningoencephalitis - Cattle
Also Known As: Meningitis — Encephalitis — Septicaemia — Bacteraemia — Navel Ill
Caused By: Escherichia coli — Haemophilus somnus — Listeria monocytogenes — Arcanobacterium pyogenes — Mannheimia haemolytica — Streptococcus spp. — Pasteurella spp. — and many other opportunistic bacterial species.
Meningoencephalitis encompasses inflammation of both the meninges (meningitis) and brain (encephalitis). The two often occur simultaneously, as once the blood: brain barrier is penetrated, both structures are accessible and vulnerable.
Infection originates most commonly from haematogenous spread after bacteraemia has occurred, but can also be produced from severe head injuries and thermonecrosis after disbudding/dehorning procedures.
The clinical signs of meningitis often precede those of encephalitis and may dominate for the duration of the illness.
Disease is most commonly seen in neonatal calves as a result of haematogenous spread of navel infection but can also occur in adult animals, especially Haemophilus somnus. Failure of maternal antibody transfer through inadequate colostrum intake in the first six hours of life is a large contributor to susceptibility to septicaemia and concurrent meningoencephalitis.
Neonates of other species, particularly lambs and foals, can also be affected similarly.
The signs of meningitis are often earlier and more pronounced than those of encephalitis and usually include pyrexia, hyperaesthesia, neck rigidity and painful paraspinal muscular spasms.
Encephalitis often adds depression, blindness, opisthotonus, paresis/paralysis which may be progressive, ataxia, cranial nerve deficits, seizures and changes in mentation.
CSF analysis is the preferred method of diagnosis, usually revealing a raised total protein and a sometimes positive culture result. The latter is definitive although sometimes difficult to obtain. In farm species however, clinical signs are often used for a presumptive diagnosis and treatment instigated appropriately.
A blood culture will confirm bacteraemia which in the presence of neurological signs can confirm a suspicion of bacterial meningitis. This will also allow the causative agent and its sensitivity profile to be identified.
On necropsy, the meninges and parenchyma are infiltrated by leucocytes and the subarachnoid space is inflamed, often along its entire length. Perivascular cuffing often features extensively. Blood vessels within and associated with the CNS may show evidence of vasculitis. End-stage disease features areas of necrosis and malacia with a mixed inflammatory infiltrate.
Listeriosis also causes its own pathognomic pathology.
Early and aggressive therapy is imperative for a successful outcome.
Prolonged antibiotic therapy is often required and an agent should be chosen that is ideally bacteriocidal and also has good blood: brain barrier penetration. Ampicillin, metronidazole, tetracyclines, trimethoprim-sulphonamides, fluoroquinolones and third generation cephalosporins have all been used with success. Licensing for food production animals should also always be considered.
Affected neonates also require attentive nursing in the form of nutritional support, fluid therapy, protection from self-trauma and maintenance of temperature and acid: base balance.
Treatment is sometimes combined with corticosteroids to reduce cerebral inflammation, but this should be implemented with care due to immunosuppressive effects,
Anticonvulsants can also be used when seizures are prolonged or repetitive.
Minimising perinatal stress, ensuring colostrum quality and intake and maintaining hygienic conditions for neonates at parturition and also during husbandry and surgical procedures are all vital measures to prevent septicaemia and concurrent bacterial meningoencephalitis.
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Haskell, S (2008) Blackwell’s Five-Minute Veterinary Consult: Ruminant. Wiley-Blackwell, Oxford, p104-105.
Merck Veterinary Manual, Meningitis and Encephalitis, accessed online 24/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/101600.htm
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