Sudden Death in Cattle

Infectious

Clostridial

Significant types in Australia

Black Leg (C.Chauvoei, C. Feseri)

Tetanus (C.tetani)

Malignant Oedema (C.septicum, C.Feseri, C.Sordelli)

Clostridial Myositis

Pathogenesis

Rapid death through invasion of tissue and toxin production which accelerates tissue death and bacteria production (positive feedback)


Endotoxaemia from absorption of toxins which are normally present in the GIT

Severe toxaemia through excessive endotoxin production

Pseudo blackleg -> more cellulitis focussing on the connective tissue (limited spread until excessive pressure from increase vasculature separates muscle fibre and further devitalizing of tissues

Activation of latent bacteria through abnormal tissue environment (low O2) -> rapid proliferation and toxin production

Diagnosis

Blackleg

Clinical signs ->Dullness lameness inappetence very painful, crepitus is a differing feature compared to malignant oedema -> progress to signs of systemic endotoxemic shock

Post mortem -> hind leg will be fully extended very rapid autolysis and gas production deep red swollen dry muscle identified

Treatment

Requires rapid antimicrobial treatment as death can occur within 12 - 24 hoours of infection

Malignant oedema

Clinical Signs -> Rapid swelling of area with large fluid accumulation and indenting on palpation hot and painful to touch

Post mortem -> discolouration of skin large gelatinous exudate in connective tissue -> muscle lesions are less extensive than in blackleg with muscle being dark red and moist instead of dry

Tissue for histopathology -> muscle or liver

IMPORTANT -> C.Chauvoei does not appear to proliferate out of wound site after death however pathogens associated with Malignant oedema are naturally present in decomposing tissue


Is good to make diagnosis of black leg in alive animal with crepitus and swelling in leg and examination of lesion however a range of factors intramuscular wound with increased autolysis of body and time since death need to be considered when confirming death by malignant oedema

Cattle can be vaccinated with vaccine 2 over 4 - 6 weeks with annual booster immunity does not occur until 7 - 10 days therefore more deaths may occur

Black Disease (C. Novyi)

Pathogenesis

Diagnosis

Caused by C. Novyi infection of the liver which alings with migration of liver fluke through the organ causes tissue damage

Anaerobic environment activates latent spores

Clinical signs -> depressed, unwilling to move , abdominal pain with brown mucous membranes

Post mortem -> venous congestion after death causes carcass to blacken with macroscopically visual liver necrosis sourounded by hyperaemic inflammation

Gram stain or fluorescent antibody staining on impression smears

Treatment

Antibiotics -> high doses of procaine penicillin

Vaccination of clostidials and fluke treatment

Anthrax

Pathogenesis

Highly environmental resistant spores gain entry into the body through inhalation of invasion of cuts or wounds

Not generally assumed to be a cause of sudden death

Diagnosis

Post Mortem -> Blood pooling out of nose, if carcass is opened large volumes of red/brown fluid is seen in thoracic and peritoneal cavity

Sample of blood for ICT test (can get false negative after 48 hours) followed by blood samples sent to lab

Clinical signs -> pyrexia muscle tremors terminal covulsions , dyspnea, ruminal stasis

Treatment

Antibiotics high dosage

Vaccine 10 days after antibiotics can give double dose to increase resistance

Prevention -> burn bodies of infected animals

Toxicities

click to edit

Lead Poisoning

Diagnosis

Clinical signs -> Neurological signs 12 - 24 hours before death unless per-acute includes salivating, ruminal atony, ataxia

Treatment

Thiamine recommended it make lead more soluble in vasculature therefore able to excrete

Measurment of lead levels in whole blood heparin tubes 0.2> mg/L is normal >0.35mg/L strongly indicative of poisoning blood lead levels fluctuate and may not always be diagnostic

Pathogenesis

Post mortem -> macroscopic lesions in brain are mild include oedema , congestion of vessels, yellowing and flattening of the gyri

Urea

Pathogenesis

Excessive intake of urea causes an increase in rumen PH resulting in increased ammonia production. isn't all utilised by microbes and leaks into circulation excessive amount in the vasculature overloads capacity for metabolism, bypass liver accumulating to cause neurological signs

Diagnosis

Clinical signs -> occur 20 mins after poisoning include hypersensitivity to stimuli, aggitation, salivating, frothing of nose and ears, teeth grinding twitching of ear severe abdominal pain and muscle fasciculation

If unsure about access to urea can measure concentration >10mmol/L in blood must assess in live animal with samples being stored on ice as protein breakdown produces ammonia

Treatment

Oral acids to reduce PH in rumen and minimise absorption of ammonia in rumen or woth cold water -> repeat treatments are often necessary as ammonia production continues

Mortaility rate is high and treatment is often unseuccesful

Organophosphates

Diagnosis

Clinical Signs -> Salivation, muscle fasciculation, a typical grunting dyspnea, muscle stiffness, progression to paralysis

Can sample whole blood for cholinesterase activity sample must be chilled

Post mortem -> no macroscopic lesion son post mortem samples can still be taken for toxicity diagnosis

Pathogensis

Inhibition of cholinesterase which causes an increase in acetylcholine at the synapses -> Causes increase in bronchi constriction in additon to excess mucous production with added smooth muscle fasciculations progressing in to convulsion and paralysis

Plant

Nitrate/Nitrite

Pathogenesis

Nitrate converted to nitrite in rumen then to ammonia -> excessive nitrite accumulation causes oxidation haemoglobin into methhaemoglobin which can no longer transport oxygen

Dyspnea occurs when there is 30% conversion to methhaemoglobin hypoxia and death occur around 70% -> maximum concentration usually occur at 5 hours post ingestion

Factors effecting high nitrate concentrations in the plant

Low Photosynthesis/energy reserves (requires energy to convert nitrate to ammonia) -> low sunlight, cold stress, insect damage, drought

Plant characteristics -> lush low fibre, young plants
(annual ryegrass, sorghum, Brassica, cereal grasses)

Excessive Nitrate -> Application of fertiliser (takes 4 days for plants to uptake fertiliser maximum concentrations around 10 days may take up to 6 weeks before return to safe values)

Diagnosis

Treatment

History -> Cattle being placed on pasture that has been recently fertilised or have rapid growth after stunting

Clinical signs -> Dyspnea , Brown Blood/Mucous membranes, abdominal pain, salivation , ataxia -> terminal clonic convulsions

Carful removal of animals from pasture and feed high quality hay

treatment with methylene blue 4 - 6 mg/kg (as a 2 - 3% solution) -> very reactive to tissue can cause serious necrosis if given extravasculalrly
-> not registered for food producing animals therefore withholding periods are up to veterinary (suggested 4 days milk , 180 days meat may be only as long as 14 but better safe then sorry)

Cyanide

Pathogenesis

Consumption of cyanogenic glycoside found in plants are converted in the rumen to hydrogen cyanide -> limits red blood cells ability to release O2 to tissue causing hypoxia

Diagnosis

Clinical Signs -> Dyspnea, restless then progress to recumbency mucous membranes are bright pink with blood being cherry red

Samples -> rumen contents (must be assessed within 1 hour) , heparinised whole blood, liver , prussic acid field test (used on rumen contents, muscle liver or plants -> paper goes brown)

Treatment

Sodium Nitrite -> 16 -20 mg 10% solution it is rare to have sodium nitirite readily available and death can occur within 1 hour of ingestion

Blue - Green Algae

Fluroacetate poisoning

Common plants to contain high Cyanide are sorghum and other sorghum like grasses e.g. sudan grasses

Pathogenesis

Treatment

Diagnosis

Blocks Krebs cycle and the animals ability to undergo cellular respiration and metabolism -> results in cardiac arrythmias and eventual cardiac arrest

Fluroacetate is naturally occurring compound in Australian vegetation and is very palatable -> Acacia georginae , Gastolobium spp and Oxylobium ( most are confined to WA and northern NT and QLD

Clinical signs -> Depression, dyspnea weakness -> progress to ataxia , sweating and gastrointestinal irrtation

Samples -> rumen contents , liver , kidney analysis for compound

No specific treatment therefore should just manage symptoms

Diagnosis

Treatment

Pathogenesis

No treatment -> prognosis grave if clinical signs displayed

Clinical Signs

Neurotoxin (Fast Death Factor Syndrome) (30 mins) Anatoxins produced by the algae that have strong neurotoxic effects

Hepatotoxins (Slow Death Factor Syndrome) -> causes progressive sinusoidal endothelium breakdown and petechial haemorrhage and necrosis leading to death

Hepatotoxic -> jaundice and photosensitisation

Neurotoxic -> Nervousness, ataxia, salivation, recumbency, GIT irritation, dyspnea

Visual observation of blooms -> Identification of blooms on water source or assesment of blooms microscopically -> progression to assay test

Post mortem

Neurotoxic -> no macroscopic lesions

Hepatotoxic -> extensive liver necrosis (swollen, pale-or haemorrhagic may be excess of clotted yellowish fluid in cavity

Is absorbed through the intestinal wall after ingestion

Selenium

Treatment

Atropine sulphate in large doses until effect (0.25 mg/kg - double normal dose rate) and removal of pour on where feasible with detergent -> treatment may have to be repeated 4 - 5 hours

Paspalum

Treatment

Pathogenesis

Diagnosis

click to edit

PEM (Sudden death syndrome)

click to edit

Phalaris

Diagnosis

Treatment

Pathogenesis

Sudden Death -> accumulation of ammonia due to inability to process nitrogen producing PEM like lesions

Incoordination -> due to accumulation of indole alkaloids within the bloodstream -> dependent on consumption

Clinical signs and history of being on phalaris pasture

Post mortem -> histopathology will see greenish/grey pigmentation in the body tissue especially the brain and kidney

Can supplement chronic incordination cases with cobalt however best treatment is to remove them from the paddock