TiHo Bibliothek elib - Tierärztliche Hochschule Hannover

Falldarstellung
bacterial growth (Dewey 2008). Systemic immune cells are able to penetrate an
intact BBB and enter the perivascular and subarachnoid spaces, and can serve as a
protective immunologic surveillance of the CNS (Zachary 2006). A complex system
of chemokine and cytokine gradients interact with leukocytes of the systemic immune
system to direct physiologic and pathologic leukocyte trafficking and cellular
migration of the CNS (Zachary 2006). However, as a result of the physiological and
anatomic barriers, a response from the systemic immune system may occur well after
an infection has been established (Dewey 2008). Additionally, in immune
compromised dogs, BA may be more likely to develop (Smith et al. 2007). Once
inflammation is underway, a disruption in the BBB resulting in hemorrhage and
edema may occur (Zachary 2006).
Life threatening neurologic dysfunction can be a sequela of bacterial brain infections.
Clinical signs depend on the area of CNS involved and may be focal or multifocal
with signs associated with meningitis (Lorenz et al. 2011). Neurological signs are
usually acute, progressive in nature, and unilaterally localized (Tipold 1997). Cerebral
abscesses are destructive, and cause progressive focal neurological deficits due to
development of a mass effect and capsulated accumulation of purulent material
within the CNS. In addition to focal signs, they may cause generalized neurological
deterioration due to increased intracranial pressure or as the result of the
involvement of bacterial toxins (Dewey 2008). Animals with a forebrain lesion may be
presented with seizures, behavior changes and hyperesthesia (Tipold 1997).
Brainstem abscesses can lead to severe neurologic complications due to their
anatomic location and the interference with vital centers. In humans abscesses tend
to elongate in the brainstem instead of expanding laterally. Therefore, the clinical
findings may be confusing (Kastenbauer et al. 2004). With brainstem involvement,
changes in mentation, gait abnormalities, proprioception deficits, and cranial nerve
deficits may occur. Additionally, vestibular syndrome may be seen (Tipold 1997).
Clinical signs of central vestibular syndrome consist of vestibular ataxia to rolling in
one direction, nystagmus, abnormal head posture, nausea and vomiting, altered
mental status, cerebellar signs, and evidence of ipsilateral hemiparesis and postural
reaction deficits as seen in the case presented here (Munana 2004).
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