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Sudden Death in Cattle ((Lead Poisoning (Diagnosis (Clinical signs ->…

- - - - Black Leg (C.Chauvoei, C. Feseri)
        
        Clostridial Myositis
        
        Pathogenesis
        
        Severe toxaemia through excessive endotoxin production
        
        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
        
        Tissue for histopathology -> muscle or liver
        
        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
        
        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
        
        Treatment
        
        Requires rapid antimicrobial treatment as death can occur within 12 - 24 hoours of infection
        
        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
      - Tetanus (C.tetani)
        
        Not generally assumed to be a cause of sudden death
      - Malignant Oedema (C.septicum, C.Feseri, C.Sordelli)
        
        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
      - Black Disease (C. Novyi)
        
        Pathogenesis
        
        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
        
        Diagnosis
        
        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
  - - - Highly environmental resistant spores gain entry into the body through inhalation of invasion of cuts or wounds
    - - 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
    - - Antibiotics high dosage
      - Vaccine 10 days after antibiotics can give double dose to increase resistance
      - Prevention -> burn bodies of infected animals
- - - - 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
        
        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
      - Treatment
        
        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)
    - - 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
        
        Common plants to contain high Cyanide are sorghum and other sorghum like grasses e.g. sudan grasses
      - 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
    - - Diagnosis
        
        Clinical Signs
        
        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
      - Treatment
        
        No treatment -> prognosis grave if clinical signs displayed
      - Pathogenesis
        
        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
    - - Pathogenesis
        
        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
      - Treatment
        
        No specific treatment therefore should just manage symptoms
      - Diagnosis
        
        Clinical signs -> Depression, dyspnea weakness -> progress to ataxia , sweating and gastrointestinal irrtation
        
        Samples -> rumen contents , liver , kidney analysis for compound
    - - Treatment
      - Pathogenesis
        
        PEM (Sudden death syndrome)
      - Diagnosis
    - - Diagnosis
        
        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
      - Treatment
        
        Can supplement chronic incordination cases with cobalt however best treatment is to remove them from the paddock
      - 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 -> Neurological signs 12 - 24 hours before death unless per-acute includes salivating, ruminal atony, ataxia
      - 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
      - Post mortem -> macroscopic lesions in brain are mild include oedema , congestion of vessels, yellowing and flattening of the gyri
    - - Thiamine recommended it make lead more soluble in vasculature therefore able to excrete
    - - Is absorbed through the intestinal wall after ingestion
  - - - 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
    - - 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
    - - 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
  - - - 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
    - - 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
    - - 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