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29 Cards in this Set
- Front
- Back
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Chain of transmission |
Agent Portal of Entry Susceptible host Animal-to-Animal transmission Reservoir Portal of Exit |
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Reservoir host |
Species that keep virus at low levels in the environment |
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Direct transmission routes |
Sexual contact Skin to skin Sneezes/ coughs Mucous membrane to mucous membrane Blood |
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Indirect transmission routes |
Waterborne Airborne Foodborne Vectorborne Objects/ fomites |
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What causes rabies? |
Negative strand RNA viruses belonging to the Lyssaviruses |
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How does transmission occur? |
Exposure to infectious saliva |
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Why does incubation period for rabies vary? |
Site of Infection Amount of virus Virus strain |
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Explain how rabies infects you. |
Virus enters body and binds to cell receptors Virus replicates in striated muscle cells/ directly infects nerve cells Virus travels via retrograde axoplasmic transport mechanisms to CNS Rapid virus replication occurs Virus moves via anterograde axoplasmicflow within peripheralnerves This leads to infection of adjacent non-nervous tissues Death by respiratory failure. |
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Rabies Prodromal phase |
Aggressiveness in tame animals Daytime behaviour in nocturnal animals Abnormalities in appetite |
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Rabies Excitative phase |
Severe agitation and aggressiveness Hydrophobia - death by dehydration |
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Rabies Paralytic phase |
Inability to swallow - leads to foaming saliva Paralysis - death |
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Method for diagnosing rabies |
Fluorescent antibody test |
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Control of canine rabies |
Vaccination of pets and high risk groups Mass vaccination programs (mainly dogs) Dog population control (neutering) |
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Causes of cell death |
Chemical Hypoxia Infections Physical Genetics/ age Immune response Nutrition |
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Injury mechanisms in reversible changes |
Decreased ATP Mitochondrial damage Increased intracellular calcium Increased free radicals Increased cell membrane permeability |
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Injury mechanisms in irreversible changes |
Mitochondrial irreversibility Irreversible membrane defects Lysosomal defects |
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What is oxidative stress? |
accumulation of free radicals |
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How do free radicals damage cells? |
Membrane lipid peroxidation Interaction with proteins DNA damage |
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How are free radicals removed? |
Spontaneous decay Antioxidants Storage proteins Enzymes |
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Morphological events of apoptosis |
Cell shrinkage Organelle reduction Mitochondrial leakage Chromatin condensation Nuclear fragmentation Membrane blebbing and changes |
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What is necrosis? |
Death of groups of contiguous cells in tissue or organ |
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Liquefactive necrosis |
Complete dissolution of necrotic tissue, due to massive infiltration by necrophils |
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Caseous necrosis |
Accumulation of debris within an area of necrosis |
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Signs of hyperthyroidism |
Weight loss Increased food consumption Loss of appetite Vomiting Weakness Decreased activity |
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Treatments for hyperthyroidism |
Antithyroid Drugs
Radioactive iodine therapy Surgical Thyroidectomy |
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Signs of hypothyroidism |
Hair loss Weight gain Lethargy Slow heart rate High blood cholesterol |
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What causes hyperthyroidism in cats? |
Over production of thyroid hormones T3 and T4 |
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What is Addisons disease caused by? |
disruption to adrenal gland |
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How is Addisons disease cured? |
Hormone replacement therapy Fluid therapy |
