Case 180511-1

Six-year-old, male rabbit

Approximately one and a half weeks prior to presentation, the owners heard thrashing in another room and found the patient laterally recumbent and obtunded. The patient recovered after about 2 hours and was mostly normal. However, he was tilting slightly to one side and occasionally “gazing upward”. On the day of presentation, the owners found the patient thrashing, laterally recumbent and minimally responsive. The patient was presented in a similar condition with no pupillary light reflex in the right eye, which progressed to absent pupillary light reflexes in both eyes. The patient was placed in a cage and minutes later was found dead. The rDVM reported that the patient was serologically negative for Encephalitozoon cuniculi.

There were no significant gross findings.

One section of brain, including hippocampus and thalmus, is examined. The section of thalamus has an irregularly-shaped, fairly-well demarcated, rarefied focus with severe vacuolation, marked gliosis and infiltration by large foamy macrophages (interpreted as gitter cells). Granulocytes are also scattered within the affected region. A few axons in the area are swollen and hypereosinophilic axons (spheroids). A small number of neurons in the region are angular, hypereosinophilic and have condensed nuclei. There are scattered foci of hemorrhage. Immature blood vessels are present within the lesion. At the periphery of the rarefied focus, a small artery is occluded by a thrombus.

None.

Brain (thalamus): arterial thrombosis with severe regionally extensive encephalomalacia.

This case was chosen because it is an excellent example of how histologic findings can be used to approximate the chronicity of a cerebral infarct. Within the first 12 hours following the inciting vascular event, the affected neuronal tissue is characterized by edema, gliosis and chromatolysis. Acidophilic neuronal necrosis may take up to a day to develop and is frequently associated with pyknosis. After 12 to 24 hours, polymorphonuclear leukocytes invade the tissue. Between one to two days following the stroke, microglial are activated and macrophages infiltrate the tissue. The macrophages will persist for the remainder of the patient’s life but will decrease in number. After about five days, the polymorphonuclear leukocytes are cleared and replaced by a reactive astrocytosis. After seven days, neovascularization occurs and is frequently accompanied by hemorrhage. The edema is progressively cleared and increasing numbers of gitter cells infiltrate the lesion. In this case, hemorrhage, neovasculariation and gitter cells are consistent with a one to two-week-old lesion. This apparent age of the lesion is consistent with the patient’s first “thrashing” event approximately one and a half weeks prior to death. However, the presence of heterophils and neuronal necrosis within the lesion suggests that a second, nearby vascular event occurred only one to two days prior to death, which is consistent with the patient’s second “thrashing” event.

This case was chosen because it is an excellent example of how histologic findings can be used to approximate the chronicity of a cerebral infarct. Within the first 12 hours following the inciting vascular event, the affected neuronal tissue is characterized by edema, gliosis and chromatolysis. Acidophilic neuronal necrosis may take up to a day to develop and is frequently associated with pyknosis. After 12 to 24 hours, polymorphonuclear leukocytes invade the tissue. Between one to two days following the stroke, microglial are activated and macrophages infiltrate the tissue. The macrophages will persist for the remainder of the patient’s life but will decrease in number. After about five days, the polymorphonuclear leukocytes are cleared and replaced by a reactive astrocytosis. After seven days, neovascularization occurs and is frequently accompanied by hemorrhage. The edema is progressively cleared and increasing numbers of gitter cells infiltrate the lesion. In this case, hemorrhage, neovasculariation and gitter cells are consistent with a one to two-week-old lesion. This apparent age of the lesion is consistent with the patient’s first “thrashing” event approximately one and a half weeks prior to death. However, the presence of heterophils and neuronal necrosis within the lesion suggests that a second, nearby vascular event occurred only one to two days prior to death, which is consistent with the patient’s second “thrashing” event.

References