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EQUINE VETERINARY EDUCATION / AE / OCTOBER 2014
Direct pupillary light reflex was present in the right eye, but the consensual response was absent. The left eye exhibited no direct or consensual PLR, no menace, and no dazzle response, implying complete loss of vision in the left eye. Atropine administration on Day 3 may have influenced the pupil’s reactivity, however, instillation of pilocarpine into the eye failed to alter the pupil’s appearance. While all ERGs (rod function, combined rod-cone function and flicker) recorded from the left eye demonstrated normal wave form, the amplitudes of the flicker and flash ERGs recorded from the left eye were lower than those of the right eye. Implicit times of all components of the ERG were comparable between the left and the right eye (Fig 2). These findings were suggestive of normal retinal function in the left eye therefore visual deficits and lack of PLR in the left eye were not associated with a retinal lesion. Based on the unilateral blindness with relatively normal retinal function, a lesion affecting the left optic nerve or visual pathway within the CNS caused the blindness. The horse was switched to oral enrofloxacin on Day 16 (7 mg/kg per os,q.24 h ¥ 10 days) and remained on flunixin meglumine until Day 17 at which point he was discharged.
Outcome
The horse’s neurological deficits continued to improve and a follow-up examination 2 weeks after discharge revealed the horse to be much brighter and more active. The owner reported that the horse had adjusted well to the loss of vision in the left eye, and was still eating and drinking normally. Ophthalmological examination revealed that the pupil of the left eye was still fixed, dilated and unresponsive to light, despite no additional atropine administration. The right eye had an intact menace and direct PLR, both were absent in the left eye. Fundic examinations in both eyes were normal. Consensual PLRs were absent bilaterally. The periocular swelling had markedly decreased, although the horse could not open the left eye completely, probably due to facial nerve paresis. A very mild muzzle deviation to the left remained, but was improved. Complete blood count at this time was within normal limits. Collection of CSF to evaluate for resolution of the meningitis was offered, but declined by the owner. Oral enrofloxacin (7 mg/kg bwt per os, once daily) was continued for another 10 days and discontinued. Communication with the owner 2 months later indicated that the horse was doing well and had returned to training. The owner still believed the horse to be unilaterally blind at this time.
Discussion
Bacterial meningitis is a rare condition in the horse and typically warrants a grave prognosis. A recent retrospective study of 28 horses with meningitis or meningoencephalitis, 19 of which had a bacterial aetiology, documented a mortality rate of 96.4% (Toth et al. 2012). The resolution of signs and return to function of affected animals, as in this case discussed here, has rarely been reported. Anamnesis often reveals prior trauma or illness, but acute onset of neurological signs with no obvious aetiology has also been reported (Newton 1998; Mitchell et al. 2006). Haematogenous spread of infection into the CNS is well-documented in septic foals, but rare in the mature horse (Viu et al. 2012). Bacterial isolates from the CSF of horses with meningitis have included Stapylococcus aureus (Mitchell et al. 2006), Escherichia coli (present case, Toth et al. 2012), nonhaemolytic Streptococcus (Smith et al. 2004),
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Streptococcus equi ssp. zooepidemicus (Smith et al. 2004; Pusterla et al. 2007), Klebsiella pneumoniae (Timoney and McArdle 1983; Smith et al. 2004), Actinobacillus equuli (Smith et al. 2004), Pasteurella caballi (Smith et al. 2004) Actinomyces sp. (Rumbaugh 1978), Fusobacterium sp. (Toth et al. 2012), Corynebacterium psuedotuberculosis
(Toth et al. 2012),
Bacteroides sp. (Toth et al. 2012), and Capnocytophaga canimorsus (Toth et al. 2012). In addition, Streptococcus equi ssp. equi has been reported to cause brain abscesses following respiratory infection (Allen et al. 1987; Kaplan and Moore 1996; Smith et al. 2004; Finno 2006; Toth et al. 2012). The case presented here is unique in that the precise origin
of bacterial entry into the CNS was unknown, although haematogenous spread from the nasal or periorbital abscesses are likely sources, supported by the identical banding patterns of E. coli from the pulsed field gel electrophoresis between the 3 samples. This route of infection differs from the more typical extension of infection from a skull fracture or paranasal sinus. Veterinary and human literature has documented meningitis resulting from extension from cranial nerves (Durand et al. 1993; Smith et al. 2004). Although there was no evidence of intraocular disease, it remains plausible that the marked periocular swelling and subsequent palpebral abscess formation presented a focus for the initial extension to the CNS via the optic nerve. In reported cases of bacterial meningitis following trauma, infection most often extends either from a paranasal sinus or via bacterial translocation from periorbital tissues along the optic nerve (Smith et al. 2004). A retrospective study of 5 mature horses with bacterial meningitis documented that 2 horses had evidence of temporohyoid osteoarthropathy, which may ultimately have precipitated a fracture and breach of the calvarium (Mitchell et al. 2007). Another retrospective study of 7 horses that developed bacterial meningitis following trauma to the head found that 6 out of the 7 horses had paranasal sinus or periorbital origins of infection supporting extension of infection from more distal regions of the head (Smith et al. 2004). Based on multiple radiographs of the periorbital and guttural pouch regions in this case no fractures were noted in the skull but a strong likelihood existed that a fracture may still have been present. Computed tomography would have been the ideal imaging modality, with higher sensitivity, but was declined by the owner. Haematogenous spread of bacteria from the nasal
abscess or local extension from the periorbital infection could be supported by the identical banding pattern and antimicrobial susceptibility of the E. coli cultured from the CSF, nasal abscess and ventral palpebral abscess. Although the nasal abscess was not noted at initial examination, the enlargement of the right submandibular lymph node suggests that the abscess was developing at presentation and the suspected trauma may have been incidental. Haematogenous spread of bacteria from nasal mucosa and paranasal sinuses into the CNS is a well-recognised cause of meningitis and brain abscesses in man (Mathisen and Johnson 1997; Gallagher et al. 1998; Jones et al. 2002; Furr 2008; Honda and Warren 2009). Nasal septal abscesses leading to meningitis in man have been associated with immune deficiencies, although this was considered unlikely in this case (Debnam and Gillenwater 2007). Meningitis can also arise secondary to chronic paranasal sinusitis in people as a result of septic thromboemboli formation following cavernous sinus thrombosis, as an extension of infection to the dura and
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