Case 180727-1

two-year-old, male castrated pug

Approximately three months prior to presentation, the patient experienced multiple seizure episodes and was diagnosed with granulomatous meningoencephalitis (GME)/necrotizing meningoencephalitis (NME). The patient was medically managed with multiple anti-epileptic drugs. A couple of days prior to presentation, the owners sedated the patient during a cross-country flight and the patient never recovered. He remained obtunded, and began to show signs of increased respiratory effort. The patient’s mentation improved slightly over the course of two days, but he remained dyspneic and eventually went into cardiac arrest.

No significant lesions.

One section of cerebral cortex is examined in which the white matter is multifocally rarefied to cavitated. Cavitations are surrounded by marked numbers of micoglia, reactive astrocytes, characterized by an open chromatin pattern, and gemistocytes. There is mild gliosis and reactive astrocytosis within the adjacent grey matter. Meningeal vessels are surrounded by small numbers of lymphocytes and plasma cells (perivascular cuffing).

None.

Brain, frontal lobe: Severe, asymmetrical, bilateral, multifocal leukoencephalomalacia with gemistocytic astrocytosis

Three idiopathic encephalopathies recognized in dogs are necrotizing meningoencephalitis (NME), granulomatous meningoencephalitis (GME) and necrotizing encephalitis (NE). The three entities are distinguished from one another through variances in lesion distribution and inflammatory cell populations. Historically, the three entities were also distinguished by breed disposition, however recent retrospective studies have shown that breed disposition is not as reliable as we once believed and multiple breeds are susceptible to multiple entities. For example, although NME used to be referred to as pug dog encephalitis, we now know that many other breeds get NME and pugs can get GME and NE as well as NME. Each of the three entities have been reported in a wide age range of dogs, from young adults to aged animals.

In this case, the multifocal, bilaterally asymmetrical distribution of the white matter cavitations and bordering gemistocytes are consistent with NE, where malacia is appreciated within only the cerebral white matter and not the cerebral cortex or meninges. Interestingly, a section of this patient’s mesencephalon, which was not provided in this conference, exhibited multifocal gliosis and edema within the white matter. These additional histopathologic findings are not classically identified in NE and may represent earlier lesions on the disease spectrum or an entirely different etiology, such as a metabolic disturbance. Necrotizing meningoencephalitis is also multifocal and bilaterally asymmetrical. However, while NE affects only the white matter, NME may affect the meninges, white matter and grey matter. Some reports suggest that the cortical grey matter is the most severely affected region in NME. Another distinction is the inflammatory population; NE is defined by large numbers of gemistocytic astrocytes while NME is defined by lymphocytes, plasma cells and microglia that are diffuse or forming perivascular cuffs. Granulomatous meningoencephalitis may also involve the grey matter, white matter and meninges, although the white matter is typically the most severely affected. Additionally, as the name suggests, GME is defined by prominent perivascular cuffs and focal aggregates of macrophages that may form “granuloma-like” lesions.

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