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change), increased total protein, elevated creatinine kinase activity and reduced glucose (<50% serum glucose) are all typical findings (Furr and Tyler 1990; Toth et al. 2012). Gram staining may show low numbers of bacteria, but an absence does not rule out bacterial meningitis and so all samples should be cultured in enriched media. Repeated CSF sampling for cytology and culture may be required to confirm the neurological diagnosis and isolate the causal organism. Polymerase chain reaction assays for common bacteria are available and could be a useful test on CSF (Toth et al. 2012). The ability of antibiotics to enter the CNS is determined by
their permeability across the BBB, with highly lipophilic, low molecular weight drugs undergoing rapid transcellular diffusion, whereas large hydrophilic molecules undergo minimal paracellular transport (Pellegrini-Masini and Livesey 2006). The severity of meningeal inflammation is variable; therefore it is impossible to predict any improvement in penetration of antimicrobials that normally do not cross the BBB. A more effective approach is to use an agent that readily crosses the normal BBB, leading to known CSF concentrations that can be related to bacteriological sensitivity results. Drugs with good CNS penetration are the fluoroquinolones, imipenem, third and fourth generation cephalosporins (ceftiofur and cefquinome), metronidazole, rifampin, doxycycline, and chloramphenicol; drugs with moderate penetration include penicillins and potentiated sulphonamides; those with poor CNS penetration are aminoglycosides, second generation cephalosporins, macrolides and oxytetracycline (Pellegrini-Masini and Livesey 2006; Mitchell et al. 2007). Inflamed CSF has elevated protein levels, which may decrease the activity of highly protein bound drugs such as ceftiofur. Chosen antimicrobials should ideally have a bactericidal rather than bacteriostatic action at concentrations achievable in CSF, as the CNS has low numbers of macrophages and T-lymphocytes, no traditional antigen-presenting cells, and negligible concentrations of complement, all of which limit its ability to mount an effective phagocytic response (Brass 1994; Furr et al. 2001; Pellegrini-Masini and Livesey 2006). A 4-day course of dexamethasone can reduce mortality in human meningitis when given concurrently with the first dose of antimicrobial, but not if it is started afterwards (Townsend and Scheld 1996). Dexamethasone reduces meningeal inflammation, stabilising the BBB and limiting permeability changes, which highlights the need for an antimicrobial with good penetration of the normal CNS. Cases with severe depression or frequent seizure activity may have elevated intracranial pressure, which can be seen as ophthalmoscopically as papilloedema and ultrasonographically as an enlarged hypoechoic optic nerve (Stone 2009). This author recommends treatment with intravenous mannitol (Cornelisse et al. 2001). One question arises from the case of Hepworth et al.
(2014): if antibiotic therapy was instituted for the periocular swelling could the meningitis have been prevented? Meningitis is an uncommon condition with high mortality, therefore could preventative therapy be rationalised? Unfortunately there is minimal equine evidence to answer this question: Smith et al. (2004) found that 4/7 horses received antibiotics for their primary condition but still developed meningitis. A recent Cochrane Intervention Review of antibiotic prohylaxis in cases of basilar skull fractures in man, also failed to show any benefit of antibiotic prophylaxis (Ratilal et al. 2011). A better approach to improve survival in equine
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bacterial meningitis is surely early recognition, prompt referral and effective treatment with a combination of CNS penetrating antimicrobials and appropriate corticosteroids.
Author’s declaration of interests No conflicts of interest have been declared.
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