23.18A ).Multifocalgraymatterandwhitematternecrosisisseen,oftenassociatedwithneuronophagia,thephagocytosisofneuronaldebris,aswellaslocalizedcollectionsofmicrogliatermedmicroglial nodules (see
Fig.23.18B ).Inseverecases,theremaybeanecrotizingvasculitiswithassociatedfocalhemorrhages.
HSV-1 encephalitis may occur in any age group but is most common in children and young adults. It typically manifests with alterations in mood, memory, and behavior, reflecting involvement of the frontal and temporal lobes. Recurrent HSV-1 encephalitis is sometimes associated with inherited mutations that interfere with Toll-like receptor signaling (specifically that of TLR-3), which has an important role in anti-viral defense.
Fig.23.18C ).Theinfectionisnecrotizingandoftenhemorrhagicinseverelyaffectedregions.Perivascularinflammatoryinfiltratesusuallyarepresent,andlargeeosinophilicintranuclearviralinclusions(CowdrytypeAbodies)canbefoundinbothneuronsandglialcells.
HSV-2 also affects the nervous system, usually in the form of meningitis in adults. Disseminated severe encephalitis occurs in many neonates born by vaginal delivery to women with active primary HSV genital infections.
Varicella-zoster virus (VZV) causes chickenpox during primary infection, usually without any evidence of neurologic involvement. The virus establishes latent infection in neurons of dorsal root ganglia. Reactivation in adults manifests as a painful, vesicular skin eruption in the distribution of one or a few dermatomes (shingles). This usually is a self-limited process, but there may be a persistent pain syndrome in the affected region (postherpetic neuralgia).
http://ebooksmedicine.net
VZV also may cause a granulomatous arteritis that can lead to tissue infarcts. In immunosuppressed patients, acute herpes zoster encephalitis can occur. Inclusion bodies can be found in glial cells and neurons.
CMV infects the nervous system in fetuses and immunosuppressed individuals. All cells within the CNS (neurons, glial cells, ependyma, and endothelium) are susceptible to infection. Intrauterine infection causes periventricular necrosis, followed later by microcephaly with periventricular calcification. When adults are infected, CMV produces a subacute encephalitis, which is also often most severe in the periventricular region. Lesions can be hemorrhagic and contain typical viral inclusion–bearing cells.
Poliovirus is an enterovirus that most often causes a sub-clinical or mild gastroenteritis; in a small fraction of cases, it secondarily invades the nervous system and damages motor neurons in the spinal cord and brain stem (paralytic poliomyelitis). The loss of motor neurons results in a flaccid paralysis with muscle wasting and hyporeflexia in the corresponding region of the body. In the acute disease, death can occur from paralysis of respiratory muscles. Long after the infection has resolved, typically 25 to 35 years after the initial illness, a poorly understood post-polio syndromeof progressive weakness associated with decreased muscle bulk and pain may appear. The re-emergent weakness has the same distribution as the prior polio infection.