EQUINE VETERINARY EDUCATION / AE / OCTOBER 2014
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Clinical Commentary Improving survival in bacterial meningitis
R. J. Hepburn B&W Equine Hospital, Berkeley, UK. Corresponding author email:
richard.hepburn@bwequinevets.co.uk
Meningitis describes inflammation of the 3 membranes (dura mater, arachnoid and pia mater) collectively known as meninges, that surround the brain and spinal cord, and the subarachnoid space they delineate. In horses bacterial meningitis is rare, with a prevalence of 0.04% reported in a referral hospital population (Toth et al. 2012). Aetiologically it can be split into traumatic inoculation (fracture of the cranial vault, basioccipital/basisphenoid bones, temporohyoid oestoarthropathy); ascending infection from adjacent sites (cranial bones, vertebrae, paranasal sinuses, oral cavity and ocular structures); or haematogenous spread, which is more common in neonates where the umbilical remnant structures represent a significant portal for bacteraemia (Foreman and Santschi 1989; Santschi and Foreman 1989; Pellegrini-Masini and Livesey 2006). In some cases, the origin of the central nervous system (CNS) infection may never be defined, which should prompt investigation of a potential immunodeficiency (Newton 1998; Pellegrini-Masini et al. 2005). In this edition, Hepworth et al. (2014) describe a case of
bacterial meningitis that developed 3 days after ocular trauma, and in which identical isolates of Escherichia coli were cultured from nasal and palpebral abscesses as well as from the cerebrospinal fluid. This raises the question of which was the origin of the CNS infection. Meningitis from haematogenous spread is possible in the horse from both the periorbital tissues and the paranasal sinuses as both ultimately drain into the deep facial veins, which connect with the ventral venous sinuses that are enclosed between the meningeal and periosteal layers of the dura on the floor of the middle cranial fossa (Smith et al. 2004). However, horses usually have a severe infectious process, which in the case of sinusitis can also lead to direct erosion through the thin walls of the sphenopalatone sinus, rather than the focal nasal abscess described by Hepworth et al. (2014). Meningitis has also been described in 3 horses via direct extension of a periocular infection along the optic nerve, 2 with presumptive periocular trauma and one with exophthalmous (Smith et al. 2004). Confusingly in man, disseminated infection can actually occur as a consequence of bacterial meningitis, as bacteria pass through the pores of the arachnoid villi, enter the venous sinuses and then the systemic circulation (Quagliarello and Scheld 1992). Whatever the route of CNS infection, the rapid evolution of this case from uncomplicated periocular trauma to life threatening meningitis highlights the need for clinicians to be able to identify uncommon conditions and institute appropriate diagnostic techniques and treatments, in order to offer the best prognosis. Bacterial meningitis cases can present with evidence of an
infectious or traumatic disease of the head or cervical spine, exophthalmos/enophthalmus, lameness, fever of unknown origin, weight loss, cervical pain or reduced neck flexion; all typically of short duration (<15 days) (Smith et al. 2004;
Pellegrini-Masini and Livesey 2006). Neurological deficits are variable and reflect multifocal CNS inflammation of varying intensity and location. They include forebrain signs (altered mental status, seizures, apparent blindness, head pressing, aggressive behaviour, disorientation, inability to initiate walking); brainstem signs (cranial nerve deficits such as blindness, head tilt, strabismus, nystagmus, anisocoria, facial nerve paralysis, muzzle fasciculation/hyperaesthesia, dysphagia); vestibular dysfunction and gait changes (multilimb ataxia, dysmetria, paresis and varying degrees of muscle atrophy) (Pellegrini-Masini and Livesey 2006). A recent retrospective of 28 cases of meningitis found abnormal mental status in 71%, cranial nerve deficits in 71% and vestibular dysfunction in 46% of horses (Toth et al. 2012). Systemic signs such as fever, anorexia, lethargy, generalised weakness and recumbency are also common. The most important clinicopathological findings are leucocytosis, neutrophilia, hyperfibrinogenaemia and hyperglobulinaemia. Lymphopenia and hypoalbuminaemia have been reported in cases with common variable immunodeficiency (Pellegrini- Masini et al. 2005; Toth et al. 2012). It is also important to appreciate that the complete blood count may initially be normal. It is this author’s experience that the acute phase protein serum amyloid A can be elevated in equine bacterial meningitis, although this is not reported in the literature; it has been reported in dogs with bacterial meningitis (Christensen et al. 2012). Diagnostic imaging should cover all cranial and cervical
structures that may provide a portal of bacterial entry and should include: plain latero-lateral, oblique lateral and dorsoventral radiography of the skull (paranasal sinuses, cranial vault and skull base), and latero-lateral views of the cervical spine, sufficient to recognise fractures, sinusitis, osteomyelitis and pneumocephalus (Mitchell et al. 2006; Toth et al. 2012). Temporohyoid osteoarthropathy is more effectively diagnosed by guttural pouch endoscopy or computed tomography; the latter can also identify skull fractures, but has poor sensitivity for meningitis itself (Walker et al. 2002; Mitchell et al. 2006; Hilton et al. 2009; Lacombe et al. 2010). In man and small animals, magnetic resonance imaging is the ideal imaging modality for meningitis, with similar findings reported in a foal; however, the access to magnetic resonance imaging for mature equine intracranial disease is limited (Hecht and Adams 2010; Viu et al. 2012). The gold standard diagnostic test is cerebrospinal fluid
(CSF) cytology and bacteriological culture, which should be performed on all horses suspected of having meningitis. A sample should be obtained aseptically from either the atlanto-occipital or lumbosacral site. Grossly, the CSF is often xanthochronic, reflecting blood-brain barrier (BBB) disruption of several hours duration (Johnson and Constantinescu 2000). A neutrophilic pleocytosis (with or without degenerative
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