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DDx for paralysis/reduced mobility in Australian macropods (Non-infectious…
DDx for paralysis/reduced mobility in Australian macropods
Parasitic
Endoparasites
Globocephaloides
Blood feeding intestinal parasite causing anaemia and hypoproteinaemia
Mainly juvenile kangaroos, usually mortalities in Autumn (joeys emerge from pouch in Summer but don't acquire infection until Autumn)
Coccidia
Typically Eimeria
Mainly occurs in hand-reared juvenile kangaroos. Faeco-oral transmission
Depression, lethargy, abdominal discomfort, anorexia, bloody diarrhoea, dehydration.
Fascioliasis
Higher prevalence in macropods grazing with ruminants
Causes cholangiohepatitis
One of the most pathogenic parasites of marsupials
Protozoan parasites
Piroplasms
Transmitted by ticks
Babesia invades RBCs, Theileria invades RBCs and lymphocytes
Relatively non-pathogenic unless immunosuppressed, but may be anaemia and depression
Babesia and Theileria
Toxoplasma
Toxoplasma gondii
All mammals affected as intermediate hosts (encysts in brain, liver and muscle tissue), but only cats are definitive hosts (shed oocysts in faeces, but also develop extra-intestinal tissue cysts)
Intermediate hosts (e.g. rabbits, birds, rodents), become infected after ingesting soil, water or plant material contaminated with oocysts. After ingestion, the oocysts form tachyzoites which localise in neural and muscle tissue, developing into tissue cyst (schizont) bradyzoites. Cats ingest these bradyzoites after consuming intermediate hosts harbouring tissue cysts. The cat may also become infected by directly consuming sporulated oocysts.
Oocysts shed in cat faeces sporulate (become infective) after 1-5 days.
Clinical signs: dyspnoea, tachypnoea, coughing, depression, anorexia, lymphadenopathy, diarrhoea, neurological signs, ocular lesions (usually in cats - keratitis, uveitis, chorioretinitis).
Diagnosis: PCR (faeces, tissues, aqueous humor, CSF, respiratory secretions) most reliable way, or histopathology (ID tissue cysts).
Prevention of zoonotic infection: Daily changing of cat litter box, feed cats only cooked meat, wear gloves when gardening (limits contact with oocysts), keeping hunting cats indoors.
Coccidia (as mentioned)
Ectoparasites
Tick paralysis
Ixodes holocyclus
Ascending flaccid paralysis progressing to recumbency and respiratory failure
Non-infectious
Musculoskeletal
Capture myopathy
Syndrome: damage to skeletal/cardiac muscle following intense physical activity (chase, restraint, transport).
Pathogenesis
Prolonged sympaticotonus reduces tissue perfusion, causing excessive ATP consumption and lactic acidosis. This leads to CVS collapse, muscular compartment syndrome (muscles swell and ischaemia occurs), acute renal failure (myoglobinuric nephrosis and ischaemia)
Syndrome sub-classifications
Peracute death: mainly results from metabolic acidosis and shock (cardiac fibrillation due to hyperkalaemia)
Delayed peracute death: sudden death after a second episode of exertion/stress due to pre-existing cardiac lesions which increase sensitivity to hyperkalaemia/acidosis.
Muscle damage: due to reduced tissue perfusion, acidosis and ATP depletion. Arteriolar vasoplegia due to prolonged sympaticotonus, coupled with local lactic acid accumulation, leads to arteriolar dilation. Venules remain constricted (more resistant to lactic acid), resulting in congestion, hypoxia, rhabdomyolysis, and obstructive and cardiogenic shock (decreased cardiac return and output).
Compartment syndrome: mainly in muscles bound by tight fascia (hind-limb adductors of macropods, deep pectoral muscles of birds). Intramuscular oedema due to lactic acid accumulation leads to pressure buildup, compressing venous supply. Arterial integrity remains, resulting in massive oedema, congestion and rhabdomyolysis.
Myoglobinuric nephrosis: rhabdomyolysis results in massive myoglobinaemia. Myoglobin is acutely toxic to cells of the PCT and loop of Henle.
Clinical signs
Initially: tachycardia, tachypnoea, hyperthermia
Later: depression, ataxia/stiff gait, pulmonary oedema, muscle tremors pigmenturia (myoglobinuria).
Potential death weeks later due to cardiomyopathy (delayed peracute death).
Treatment and prevention
Sedation prior to/immediately following capture
Darting prior to capture (tiletamine/zolazepam - 'Zoletil' 5-7 mg/kg IM). Tiletamine (dissociative) provides amnesia, analgesia and immobilisation. Zolazepam (benzodiazepine derivative) provides muscle relaxation and tranquilisation.
Immediate administration of IM diazepam (0.1-2 mg/kg) following capture, coupled with other preventative measures.
IV catheter placement
Fluid therapy (isotonic balanced crystalloids). Promotes haemodynamic stabilisation and diuresis (to prevent myoglobinuric nephrosis).
Dantolene sodium (1 mg/kg IV). Skeletal muscle relaxant.
Sodium bicarbonate administration: typically not recommended due to formation of CO2 from the buffering reaction in blood (patients with respiratory compromise may not be able to offload this). Reserved for SEVERE metabolic acidosis (based on BG analysis).
Flunixin meglumine. Prevents cell damage.
Active cooling
Damp towels, cool packs, if outdoors move into the shade.
Covering eyes/ears immediately following capture (e.g. towels, bags) and performing further procedures in a quiet environment to reduce stress. Minimise handling by having all necessary equipment at hand.
Nutritional myopathy (Vit E/Se deficiency or 'White Muscle Disease')
Degeneration and calcification of skeletal muscle
Ataxia progressing to hindlimb paralysis with muscle wasting
Trauma
Metabolic
Starvation
Dehydration
Vitamin E/Se deficiency (as mentioned)
Toxic
Steroidal saponins
Witch grass, hairy panic grass, caltrop
Saponins form crystals within the bile cannaliculi and induce hepatocyte damage. Results in an inability to conjugate phylloerythrin (a metabolite of chlorophyll) within bile. Phylloerythrin is photodynamic and enters the blood, resulting in hepatogenous photosensitisation.
Results in dermatologic/ocular lesions: anorexia, lethargy and jaundice, exudative dermatitis of ear margins, eyelids, muzzle, scrotum, and corneal opacity (due to oedema/inflammation).
Phalaris toxicity
Indole alkaloids interfere with serotonin (inhibitory neurotransmitter) & catecholamine metabolism.
Late Summer/Autumn or when hungry animals graze phalaris pastures that have been stressed by frosts/lack of water etc.
Mainly EG kangaroos and Red-necked wallabies (SE Australia & Tas)
Ataxia, head tremors, weight loss, collapse.
Sodium fluoroaceate (1080)
Sodium fluoroacetate is metabolised to fluorocitrate, which inhibits the Krebs cycle, depleting tissues of energy stores (particularly those which high energy demand - heart, brain, kidneys, liver). Citrate also chelates with serum calcium (seizures).
Hyperexcitability, aimless hopping, hyperaesthesia, vomiting, hypersalivation, urination, defecation, mydriasis, hyperthermia, and epileptiform convulsions or seizures.
Lantana toxicity
Also leads to hepatogenous photosensitisation.
Miscellaneous
Poor dentition
Bacterial/viral
Generalised diseases
Macropod herpesvirus
Only reported in captive kangaroos, wallabies, quokkas, bettongs and potoroos
Fever, conjunctivitis, cutaneous and mucosal erythema, incoordination, dyspnoea and oral/cloacal vesiculation and ulceration
Tamar Sudden Death Syndrome
Orbivirus-associated disease
Reported in captive tammar wallabies in eastern Australia
Lethargy, weakness, lateral recumbency, muscle fasciculations, tachypnoea
Tyzzer's disease
Clostridium piliforme
Uncommon but fatal disease of marsupials, spread mainly by rodent faeces. Causes hepatic/cardiomyocyte necrosis.
Acute death, diarrhoea, weakness, altered behaviour, fever, dyspnoea, jaundice, anorexia, convulsions
Typically seen in captive juvenile Australian mammals (kangaroos, wombats, koalas, possums)
Botulism
C. botulinum produces neurotoxin that blocks ACh release at motor nerve endings (also smooth muscle paralysis and failure of parasympathetic function)
Sources of toxin include poultry litter, rotting animal carcases and plant matter. Spores may be found in contaminated soil and waterways.
Ascending flaccid paralysis, but no loss in skin sensation or rise in temperature. Also excessive salivation and mydriasis.
Death occurs due to respiratory paralysis
Detection of toxin in the peripheral blood/serum, GIT contents or feed is confirmative.
Tetanus
C. tetani (drumstick-shaped G -ve bacteria) produces tetanospasmin & tetanolysin. Tetanospasmin spreads via local motor nerves to the spinal cord and inhibits release of inhibitory neurotransmitters (GAB, glycine) from presynaptic nerve endings.
Muscle stiffness, hyperaesthesia, anxious expression with erect ears, lockjaw, hypersalivation, recumbency, tetanic spasms, opisthotonus.
Culturing of wounds and Gram staining
Treatment: toxin neutralisation (antitoxin), preventing toxin production (wound debridement and antibiosis), muscle relaxation (ACP, diazepam)
Opthalmic diseases
Viral chorioretinitis
Orbivirus (Wallal serogroup) and Warrego virus
Transmitted by culcoides (biting midges) present in northern Australia
Most common in western grey kangaroos, but also eastern grey, red and euro kangaroos
Associated with large numbers of deaths
Apart from blindness there are few external signs of eye disease
Stumbling, changes in tapetal reflectivity, but animal can move freely
DDx: Toxoplasmosis, head trauma
Gastroenteric diseases
Salmonellosis & Campylobacteriosis
Clinically indistinguishable (rely on culture for diagnosis)
Semi-formed to haemorrhagic diarrhoea, anorexia, dehydration, lethargy
Appropriate husbandry (including consistency in feeding times, volume, composition and temperature of milk feeds) and reduced environmental stressors help prevent the development of clinical signs in asymptomatic carriers.
Gastric amoebiasis
Diagnosed be demonstrating Entamoeba cysts in faeces via faecal flotation or smear.
Weight loss, diarrhoea, anorexia, bloat, possible sudden death.
Euthanasia methods in macropods (Code of Practice for Injured, Sick
and Orphaned Macropods - NSW Office of Environment and Heritage)
When to euthanase?
Likely imminent death regardless of treatment
Suffering from chronic, un-relievable pain/distress
Carrying a disease that poses a health risk to wild animals
Ability to consume food unaided is impaired due to injured jaw/missing teeth
No suitable release location
Locomotion/ability to escape predators is impaired
Ability to see/hear/smell/taste/feel is permanently impaired
Advanced age renders it unable to survive in its environment
How to euthanase?
Aim is to minimise pain/distress prior to and during the process, and establish a rapid loss of consciousness immediately followed by death.
Sedation with subsequent barbiturate overdose is ideal
Other methods: shooting into head/heart, blunt force trauma to skull with a single blow
A macropod that requires euthanasia should not be exposed to additional stressors such as large numbers of onlookers, people touching it, loud noises or extremes of temperature
Carcass disposal
If suspected disease contamination or exposure to chemicals (e.g. barbiturates), the carcass must be incinerated or buried at a depth that will prevent scavengers from reaching it.