Septic Meningoencephalomyelitis

Outline

Definition
Pathophysiology
Signalment
Signs
Causes
Risk Factors

BASICS

Definition

Septic meningoencephalomyelitis is defined as bacteria-associated inflammation of the CNS.

Pathophysiology

Microbial invasion of the CNS occurs with hematogenous spread, traumatic injury, or via an ascending infection. Hematogenous spread is the most common and is associated with immunosuppression/immunodeficiency and sepsis. Following bacterial invasion, inflammation leads to increased permeability of the BBB, vasculitis, cerebral edema, and, occasionally, hydrocephalus.

Systems Affected

CNS

Signalment

Young foals, but adult horses may be affected.

Signs

Historical Findings

Inadequate passive transfer of maternal immunoglobulin, prematurity, and other illnesses are important historical factors in foals
Infection within the head such as sinusitis and thrombophlebitis, bacteremia, or head trauma are other important historical factors

Physical Examination Findings

Fever (not always present), lethargy, and behavioral changes (aimless walking, somnolence, abnormal vocalization, lack of affinity for the mare) characterize the early stages
Later, tactile and auditory hyperesthesia over the entire body and a stiff and extended neck posture may be noted
CNS pain is often manifested by reluctance to move the head or neck and trismus (spasms of the muscles of mastication)
Signs progress to loss of the suckling reflex, cranial nerve abnormalities, ataxia, paresis, and blindness. Recumbency, coma, seizures, and death quickly follow

Causes

The bacteria involved are those most commonly associated with neonatal sepsis including coliforms, Salmonella spp., and Klebsiella spp.
Adult horse meningitis has been associated with a wide variety of organisms; however, Streptococcus equi and Actinomyces spp. predominate

Risk Factors

Include those that are associated with septic conditions of foals—maternal uterine infection, premature placental separation, poor hygiene during parturition, failure of passive transfer of maternal immunoglobulins, etc. A risk factor in adults is the hypogammaglobulinemia associated with CVID.

Diagnosis ⬆ ⬇

DIAGNOSIS

Early diagnosis and aggressive treatment are essential
A CBC may reveal a neutrophilic leukocytosis, but neonatal foals frequently have neutropenia with sepsis. Adults with CVID may have marked lymphopenia with hypoglobulinemia on chemistry profile. Additional testing is required to demonstrate low IgM and IgG
In acute cases, CSF contains high neutrophils and protein. In protracted and treated cases mononuclear cells often predominate. Low glucose (compared with blood) and high lactate are consistent with CNS sepsis
Blood and CSF culture and Gram stain

Differential Diagnosis

Viral encephalomyelitis, hepatic encephalopathy, intoxication.

Treatment ⬆ ⬇

Medications ⬆ ⬇

MEDICATIONS

Drug(s) of Choice

Most antibiotics are likely to get into the CSF as the BBB is damaged
Third-generation cephalosporins, such as cefotaxime and ceftriaxone, have good CNS penetration; however, they are expensive. Ceftiofur is a third-generation cephalosporin that is inexpensive; however, its penetration into the CNS is questionable
The fluoroquinolones are efficacious but adverse effects on cartilage must be considered in foals
Potentiated sulfonamides have good CNS penetration but resistance is common. Chloramphenicol has good CNS penetration, but is bacteriostatic and human health concerns such as aplastic anemia should be considered
Antimicrobial administration must begin immediately and be broad spectrum. A combination of potassium penicillin G (22 000 U/kg IV every 6 h), ceftiofur (2.2–5.0 mg/kg IV every 12 h), or ampicillin (22 mg/kg IV every 8 h) plus amikacin (25 mg/kg IV every 24 h) or gentamicin (6.6 mg/kg IV every 24 h) provides a good initial regimen
Additional therapy including caloric, fluid, electrolyte, respiratory, and thermic support is essential
Seizures may be managed with diazepam (5–20 mg IV) and repeated as necessary in 50 kg foals. Intractable seizures may require phenobarbital (10–20 mg/kg diluted in saline and administered slowly over 15 min IV every 12 h)
Corticosteroids (e.g. dexamethasone 0.1 mg/kg IV) may be given initially, preferably beginning 30 min before antimicrobials. NSAIDs should be administered to mitigate effects of inflammation and fever
Drugs to resolve secondary problems should be considered (e.g. antiulcer medications, ocular medications)