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
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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
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PEM (Sudden death syndrome)
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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