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26 Cards in this Set
- Front
- Back
- 3rd side (hint)
What two factors determine disease outcome
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Host - defense capabilities
Agent - destructive capacity |
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What factors affect host defense capabilities
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Mucosal barrier, age influence, nutrition, pre-existing disease, local factors, genetic abnormalities of neutrophils, other genetic diseases
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Side 2: What is a mucosal barrier
Side 3: Where are some sites it may be found |
Type of epithelium covering surface and providing a physical barrier
Additional features - cilia, mucous secretion |
Skin, respiratory system, urinary system, GI tract
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What are some defense mechanisms of the GI tract
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Saliva, mucus, resident flora and fauna, gastric pH, secretory Ig, vomiting, liver and pancreatic secretions, intestinal enzymes, epithelial turnover, peristalsis (diarrhea), adaptive immune system
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Age influence
Side 2: what are some properties of the fetus or neonate Side 3: What are some properties of the geriatric animal |
Decreased vascular responsiveness, unresponsive to some mediators, decreased circulating WBCs, immature neutrophils/MP, decreased blood clearance of bact
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Decreased responsiveness of immune system, decreased rate of fibroblast proliferation
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What are some outcomes of poor nutrition
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Atrophy of lymphoid tissue in lymphoid organs resulting from protein deficiency
poor wound healing related to vitamin C or zinc deficiency |
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What are the properties of Hyperadrenocorticism (Cushing's disease)
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Gluconeogenesis but decreased flucose uptake by cells, vascular endo altered permeability and decreased response to mediators, decreased emigration and chemotaxis of WBCs, lysosomal membrane stabilized, decreased PG lvls, lymphocytolysis, decreased lymphocytic proliferations, decreased healing response
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Side 2: What is Diabetes mellitus
Side 3: What are some properties |
Increased production and under utilization of glucose
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Decreased: phagocytosis, chemotaxis, blood supply
Glycosylation of important proteins interferes with function of many cell types |
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Side 2: what breed is associated with cyclic neutropenia
Side 3: what breed is granulocytopathy associated with |
Grey collies
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Irish setters
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Side 2: What breed is associated with defective neutrophil bactericidal activity
Side 3: What breed is associated with C3 deficiency |
Doberman pinschers
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Brittany spaniels
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Side 2: What is Pelger-Huet anomaly
Side 3: What species are associated |
Failure of granulocytes to become multilobed
(neutrophil hyposegmented) |
Dogs and cats
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Side 2: What is Chediak-Higashi syndrome
Side 3: What breeds are associated with cell adhesion defects |
WBC abnormalities - contain large granules (characteristic)
Seen in a variety of animals (defective phagocytosis) |
Holstein cattle and Irish setters
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What are some host agent interactions
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Cytolytic killing of phagocytes by bacteria, prevention of phagolysosome fusion, bacteria survival in phagolysosomes, encapsulation, adaptation to environment, development of antigenic variance, antigenic mimicry, immunosuppression, immune interference
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Side 2: What is the importance of cytolytic killing of phagocytes
Side 3: What are some examples of bacteria and the toxins they produce |
In process of killing phagocytes, lysosomal enzymes are released causing tissue necrosis and permitting diffuse spread of bact
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Streptococci - streptolysins
Staphylococci - alpha toxins Pasteurella hemolytica - leukotoxins Corynebacterium ovis |
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Side 2: What is the mechanism for prevention of phagolysosome fusion
Side 3: What is formed if an immune response is provoked |
Engulfed bact reamin in phagosome but don't stimulate lysosomal fusion and discharge - pahgolysosome not formed
Bact persist in dormant state |
If provoke an immune response - DTH (delayed type hypersensitivity) - Granuloma formaion
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What are the mechanisms for which the following organisms prevent phagolysosome fusion
Side 2: toxoplasma gondii Side 3: Mycobacterium bovis |
Phagocytized and remain inert until replicates itself causing cell lysis
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Survives in phagosome but stimulates marked DTH response causing granulomatous inflammation
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What are the mechanisms for which Rhodococcus equi prevents phagolysosome fusion
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Survives in phagosome but may elicit a marked suppurative response
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Side 2: What is the mechanism by with bacteria survive in phagolysosome
Side 3: What are some examples |
Agents have a complex cell wall that resists digestive enzymes of WBCs
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Mycobacterium avium and leprae
Listeria monocytogenes Brucella abortus - resides in ER; cell wall inhibits myeloperoxidase activity |
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Side 2: What is the mechanism of encapsulation
Side 3: what are some agents with this ability |
Disease agents survive in hostile intracellular and extracellular sites by secreting a thick glycoprotein capsule
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Streptococci equi, Escherichia coli, Pasteurella multocida, Cryptococcus neoformans
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Side 2: What is the mechanism by which agents adapt to the environment
Side 3: What are some examples |
Agents modify their environment in host tissues by releasing products to make local environment favorable for their survival and replication
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Helicobbacter pylori - secretes urease (urea-ammonia) making site more alkaline and locally buffering stomach acid
Enteric bact - regulates local pH in gut by secreting decarboxylases |
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Side 2: What is the mechanism of antigenic variance
Side 3: What are the outcomes of this |
Capacity to vary surface antigens, bypassing the secondary immune response
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Marked primary immune response having a marked lympho-plasmacytic response
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What are some agents with the ability to cause antigenic variance
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Viruses - Ovine progressive pneumonia virus, equine infectious anemia virus
Baceria - Campylobacter fetus Protozoa - Trypanosomes (blood and tissue), Plasmodium (malaria) |
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Side 2: What is the mechanism of antigenic mimicry
Side 3: What are some agents with this ability |
Agents absorb host antigens on surface membranes so they are not recognized as 'foreign'
Provoke an attenuated chronic inflammatory response |
Haemonchus contortus ('barber pole' worm)
Shistosomes (blood flukes) Cysticercus (larval stage of some cestodes) |
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Side 2: What are the two mechanisms of immunosuppression
Side 3: What does it look like |
Killing lymphocytes
Inhibiting lymphocyte function |
Infectious lesion is one of necrosis but with little inflammatory response
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Side 2: What are some viral agents with the ability to cause immunosuppresion
Side 3: What is a parasitic agent |
Canine distemper virus, canine/feline parvovirus, felin leukemia/immunodeficiency virus, Bovine viral diarrhea virus, Hog cholera virus, New castle disease virus
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Demodex folliculorum (dog mite)
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Side 2: What is immune interference
Side 3: Give an example of an agent with this property |
Immune response is regulated by the organism
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Leishmania organisms - may induce 'class switching' (TH1 to TH2) - avoiding cell mediated immunity
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