BRAIN DAMAGE BY EXTRACTS OF PARASITISED ANNUAL RYEGRASS (LOLIUM RIGIDUM) IN NURSLING RATS

Abstract

Summary Extracts of annual ryegrass. (Lolium rigidum) infected with Anguina sp., and Corynebacterium sp. and associated with an outbreak of annual ryegrass toxicity in sheep, were administered to 2‐week‐old rats by a single intraperitoneal injection. Rats that received a lethal dose of toxin developed neurological signs including incoordination and convulsions from the second day and most died between 2 and 7 days after injection. Histologically, the brains showed widespread lesions of focal necrosis consistent with anoxia. Peripheral circulation rate was greatly reduced after 3 days and gangrene of the tail and hind legs developed in some rats, Evidence of restricted blond How was also seen in kidneys, lungs and bruin. It was concluded that the toxin contains a long‐acting vasoconstrictor.

TOXICITY STUDIES OF THE TOXINS ISOLATED FROM ANNUAL RYEGRASS (LOLIUM RIGIDUM) INFECTED BY CORYNEBACTERIUM RATHAYI

“…Gangrene of limbs or tails, as reported by Peterson and Jago (1977), did not occur in this study, and there was a ten-fold range in the LD50 estimations of the individual toxins. Histopathological changes of varying degree, but qualitatively similar to those reported by Peterson and Jago (1977), were found in all rats which died or exhibited clinical signs. Lesions were also observed in 13 surviving, treated rats in which tremors or convulsions were not observed (Table 1).…”

“…Neurological signs of ARGT in the rats (Peterson and Jago, 1977) were observed after treatment with all corynetoxins tested but only at the higher dose rates. Each of the toxins elicited similar clinical signs which varied in degree and were not seen until approximately 36 h after treatment.…”

“…The remaining 20 brains were cannabalised, damaged during removal or processed unsatisfactorily. Transverse sections taken from 3 or 4 levels of each brain were examined and scored for degree of haemorrhage, focal necrosis, malacia, cell infiltration and gliosis (Peterson and Jago, 1977). Brains from 9 sheep which manifested clinicat signs were fixed by immersion or perfusion (Berry et al, 1980) and processed routinely for HE sections.…”

“…Oral administration of toxic ryegrass to sheep, or intraperitoneal (IP) injection of crude extracts to 2-week-old rats, causes lesions in the central nervous system (CNS) which may be due to vasoconstriction (Peterson and Jago, 1977;Berry, Howell and Cook, 1980). However, damage caused by ingested toxic ryegrass also occurs in other body systems, particularly the ovine liver, in which histological and ultrastructural changes suggest a cytotoxic effect (Berry etal, 1982).…”

Review of corynetoxins poisoning of livestock, a neurological disorder produced by a nematode‐bacterium complex

“…Some blood vessels in the brain were also not cleared of this tracer, although occluded vessels had no particular association with haemorrhagic or necrotic lesions. No evidence of vascular damage was found in conventionally stained brains, except in large, advanced necrotic lesions where injury to blood vessels may have been the result rather than cause of the malacia 54 . These nursling rat brains were not examined ultrastructurally and haemorrhages may have been due to a direct effect of the toxin on cerebral endothelium rather than being secondary to ischaemia‐hypoxia 54 .…”