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Production Animal Clinical Toxicology

Sudden Death: Cyanogenetic Glycosides


Plants | Epidemiology | Pathogenesis | Clinical Signs | Clinical Pathology | Necropsy | Diagnosis | Treatment | Control


Return to Production Animal Clinical Toxicology Index


Plants

Sorghum spp. - grain and forage

Sorghum halepense - Johnson grass

Sorghum halepense - click for larger image

Cynodon spp. - blue couch

Brachyachne spp. - native couches

Eremophila maculata - native fuschia

Eremophila maculata - click for larger image Eremophila maculata - click for larger image

Some acacias - e.g. Acacia glaucescens

linseed meal/cake - esp. immature seeds

Heterodendrum oleifolium - rosewood

Heterodendrum oleifolium - click for larger image

Epidemiology

animal factors

  • aggravated if animals hungry, resulting in rapid ingestion, or under stress of droving or mustering
  • animals recently introduced to area may be more susceptible than indigenous populations
  • more common in ruminants than monogastrics - related to low activity of beta-glycosidase at low pH.

plant/environmental factors

  • 2 enzymes required; both usually in same plant
  • may also be in ruminal microbes
  • glycoside --->(beta-glycosidase)--->(lyase)--->HCN
  • glycoside levels most important:
    • high in young plants, rapidly growing green shoots
  • plants wet with dew/light rain
  • glycoside levels can increase transiently:
    • frosted/wilted plants
    • plants treated with herbicides
    • in addition, in these plants there is an increased spontaneous breakdown to HCN

Pathogenesis

  • HCN released either enzymatically or spontaneously
    • rapid absorption in rumen
    • can be metabolised by liver, but if release excessive cytochrome oxidase can be inhibited
  • blocks cellular respiration - histotoxic anoxia
  • myocardium tissue most severely affected; cardiac failure and cerebral anoxia
  • toxic dose 2 mg/kg bodyweight - large amount of toxic plant needs to be ingested

Clinical Signs

  • sudden death
  • bright red mucosae and blood from high levels of oxyHb
  • respiratory distress
  • muscular twitching; staggering gait
  • spasm
  • dilated pupils; pronounced bloat
  • coma, death

Clinical Pathology

  • generally nonspecific

Necropsy

  • blood may be brighter in colour; may clot poorly
  • generally nonspecific

Diagnosis

  • history; red venous blood
  • picrate paper test - plant material or ruminal contents
  • some labs may do muscle levels but these levels rapidly decline

Treatment

  • Na nitrite/Na thiosulphate: CN- binds preferentially to MetHb; CN- slowly released from cyano MetHb to combine with thiosulphate.

Control

  • grazing management
  • test graze




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Last Modified: Tuesday 08 July, 2008
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