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Gen Path > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

What is the function of the immune system?

A

to protect animals from pathogens and prevent the development of cancers

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2
Q

What are the two components of the immune system?

A
  1. innate immunity

2. adaptive immune system

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3
Q

What are two characteristics of the innate immune system?

A
  1. it is present before infection occurs and does not need to have previous exposure to the pathogen
  2. it is able to recognize microbes and protect multicelluar organisms from infections
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4
Q

What are the 4 major components of the innate immune system?

A
  1. barriers:
    • physical barriers:
      1. physiological barriers (pH, temperature)
      2. static barriers (epithelial surfaces)
      3. kinetic barriers (cilia clearing the resp tract or peristalsis)
    • biological barriers : normal flora that competes and inhibits with microbes
    • chemical barriers: hydrochloric acid killing microbes
  2. Acute phase response: acute phase proteins, systemic reactions like fever, anorexia, chills, and systemic hypoferremia (withholding iron from pathogens and decreasing the production of free radicals)
  3. Humoral innate immunity:
    - microbicidal components like MAC or defensins and lysozymes secreted
    - microbiostatic components (stops the growth of microbes) like metal binding proteins
    - opsonins: lectins like mannose binding lectin, C reactive proteins
    - acute phase proteins
  4. Cellular innate immunity:
    - phagocytes
    - natural killer cells
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5
Q

What are two characteristics of adaptive immunity?

A
  1. stimulated by previous exposure to microbes (has memory)
  2. capable of also recognizing non microbial substances like antigens

-it is slower to develop (if no memory) but much more effective

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6
Q

What are the two main types of adaptive immunity? (what cell types)

A
  1. cellular immunity (T lymphocytes). it defends against intracellular microbes that have been presented to it from the B cells
  2. humoral immunity (b lymphocytes). defends against extracellular microbes and their toxins by recognizing the microbes, binding to them, engulfing and degrading them so that the microbe can be presented to the T cell
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7
Q

What are the two types of immune deficiency disorders?

A
  1. primary (inherited) immunodeficiency - rare in animals

2. secondary (acquired) immunodeficiency - much more common in animals

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8
Q

Name some primary immunodeficiencies

A
  1. Chediak-Higashi syndrome
  2. Leukocyte adhesion deficiency
  3. Severe combined immunodeficiency (SCID)
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9
Q

Describe Chediak-Higashi syndrome

A
  • occurs in Hereford cattle and Persian cats
  • there is abnormal lysosomal binding so what is being phagocytosed isn’t being killed
  • may also get abnormal pigmentation of melanocytes so get albino animal
  • microscopically, there will be large neutrophils and large granules within them because it is unable to degrade anything
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10
Q

Describe Leukocyte adhesion deficiency

A
  • occurs in irish setters and Holsteins
  • there is a defect in b2 integrin so the neutrophils within the blood vessels are unable to bind to the endothelial cells and exit into the infected tissue. Since they are unable to decrease the infection there is still stimulus to increase the amount of neutrophils
  • get persistent neutrophilia
  • cattle can develop severe gingivitis, oral ulcers etc and abscesses that lack pus formation
  • histologically there is lower amount of neutrophils in tissue and high amounts within the blood
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11
Q

Describe SCID

A
  • occurs in Arab foals, dogs and cats
  • there is a defect in both the humoral and cell mediated acquired immune system
  • in Arabs, it doesn’t show up until the foal does not have passive immunity any more so it results in fatal respiratory and GIT infections
  • will have small or absent thymus
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12
Q

Name some secondary immunodeficiencies

A
  1. failure of passive transfer
  2. animal immunodeficiency viruses
  3. lymphotropic viruses
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13
Q

Describe failure of passive transfer

A
  • most common immunodeficiency disorder!
  • neonates rely heavily on immune protection from their mothers colostrum and milk (esp. horses and ruminants because their placenta is impermeable to immunoglobins). these neonates are both hypogammaglobulinemic so they need colostrum to get immunoglobins within the first 24 hours.
  • if they fail to do so then they have a high chance of getting septicaemia, meningitis polyarthritic or polyserositis
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14
Q

Describe animal immunodeficiency viruses

A
  • FIV: when they get the virus, there is an asymptomicatic period while there is progressive loss of T lymphocytes, resulting in immunodeficiency with chronic and recurrent infections which are eventually fatal. First sign may appear as gingivitis
    • biting is main mode of transmission
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15
Q

Describe lymphotropic viruses

A

Bovine viral diarrhea virus (BVDV). present in 40% of herds

  • both epitheliotropic and lymphotropic
  • causes erosions of upper alimentary tract like mouth esophagus and rumen, interdigital areas and causes lymphoid depletion
  • get corrugation of intestine
  • if cow that is normal gets virus then there may not be any symptoms but if an immune difficient cow gets it while she is pregnant then there may be various signs depending on stage in pregnancy

Canine parvovirus and feline panleukopenia affect proliferating cells.

  • destoys cryptal epithelial cells in small intestine (because they divide), and bone marrow cells (causing a lack of WBC) and peyers patches
  • get bloody diarrhea, hyperaemia and ulcerated intestinal tract
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16
Q

What are some other causes of immunodeficiency?

A
  • steroid induced immunosuppression
  • malnutrition
  • age
  • chemotherapy
  • radiation therapy
17
Q

What are the two categories of excessive immunity? Describe them

A
  1. hypersensitivity: exaggerated immunological reaction to normal, harmless antigen stimulus resulting in injury to the host (type I and IV)
  2. Autoimmune disease: antibodies or T cells are reactive against self antigens (type II and III)
18
Q

Describe type I reaction

A
  • immediate hypersensitivity
  • mediated by histamine that is released when mast cells or basophil antibodies bind to the antigen (allergen). The mast cells and basophils are sensitive to the allergen
  • can be systemic or local
  • ex/ insect bite, food allergy, anaphylaxis
19
Q

Describe type II reactions

A
  • autoimmune reaction
  • antibodies on cytotoxic T cells bind to self antigens on self cells causing an immune response and cell destruction because it activates compliment, antibody-dependent cell mediated cytotoxicity or anytbosy-dependent cell dysfunction
  • ex/ myasthenia gravis, pemphigus
20
Q

Describe type III reactions

A
  • autoimmune reaction
  • large amount of immune complexes deposit themselves into tissue allowing complement to generate cytokines, attracting neutrophils to the area
  • ex/ equine purpura hemorrhagica
21
Q

Describe type IV reactions

A
  • hypersensitivity reaction
  • delayed hypersensitivity
  • an antigen sensitizes a T cell causing the release of cytokines which attract macrophages and other leukocytes that are cytotoxic
  • ex/ granulomatous diseases (TB)
22
Q

Describe Atopy

A
  • type I hypersensitivity reaction
  • affects mostly the skin in dogs, cats and horses
  • allergen is believed to enter through respiratory tract
  • it is inherited problem that results in development of immediate hypersensitivity to antigens by producing excess IgE. When IgE is coupled to the antigen it results in degranulation of mast cells and basophils
  • lesions: erythema (redness from capillary dilation), urticaria (eruption of itching dermal edema) and self inflicting trauma by licking and rubbing
23
Q

Describe food hypersensitivity dermatitis

A
  • non seasonal
  • in young dogs
  • type I or type IV reaction to food antigens
  • lesions: erythema, urticaria, self inflicting trauma
24
Q

Describe Pemphigus

A
  • type II reaction
  • development of antidesmosomal auto-antibodies that bind to desmosomal proteins, causing the cells to break apart on the skin and form intraepithelial blisters
  • lesions: intraepithelial pustules or erosions following pustular ruptures
25
Q

Describe acquired myasthenia gravis

A
  • type II reaction
  • systemic muscular autoimmune diease
  • mediated by antibody dependent disfunction => autoantibodies develop against ACH receptors, blocking the receptors so that ACh cannot react with them
  • CS: muscle weakness and fatigue after exercise and resolves with rest
  • adult dogs affected
  • may also present with megaesophagus with or without aspiration pneumonia
26
Q

Describe iso-immune thrombocytopenia in piglets

A
  • there is mixing of sow and piglet blood when the piglet is in utero. The sow develops anti-platelet antibodies against the platelet antigens that the piglet got from boar.
  • when the piglet ingests the colostrum from the sow when it is born, the colostrum has the anti platelet antibodies that the sow produced. these bind to the piglets platelets, resulting in destruction of platelets
  • causes a thrombocytopenia and widespread hemorrhages
27
Q

Describe idiopathic immune mediated haemolytic anemia (IMHA)

A
  • most common in dogs
  • autoantibodies develop against own erythrocytic antigens.
  • the erythrocytes that are coated by IgG are phagocytosed by macrophages (in spleen mostly) or lysed by complement
  • lesion: regenerative anemia (trying to replace RBC), icterus, centrilobar hepatic necrosis (b/c hypoxia) enlarged spleen (b/c full of macrophages) and spherocytes (small RBC b/c part of it got phagocytksed)
  • spherocytes are the hallmark of IMHA
  • if complement destroys them = intravascular hemolysis. get red urine and serum
  • if macrophages destroy them = extravascular hemolysis. get low amount of RBC
28
Q

Describe Equine purpura haemorrhagica

A
  • type III reaction
  • may occur after a horse is infected by strangles.
  • horse gets a high level of antigen (protein M) antibody (IgA and IgM) complexes in the circulation
  • these complexes are deposited in vessel walls and result in complement coming to destroy the cells that are in that location resulting in vasculitis, generalized edema and hemorrhagic purpura because the lack of endothelial integrity
29
Q

describe feline infectous peritonitis (FIP)

A
  • type III reaction
  • progressive fatal immune mediated disease of cats caused by corona virus
  • virus is spread systemically by infected macrophages
  • virus and antibody complexes are deposited on venular walls causing complement to come and destroy the cell walls
  • if cell mediated immunity (CMI) is strong and rapid, virus will be contained and eradicated
  • if CMI is moderately strong, there will be a dry form with granulomatous and pyogranumomatous infiltrate in may organs
  • if CMI is weak, then fibrinous education of serosal cavities
30
Q

what is an amyloid?

A

-a pathologic proteinaceous substance that is resistant to degradation and is between cells in tissues and organs

31
Q

describe amyloidosis

A
  • when there is a build up of amyloid in your system
  • clinical dx: morphological identification in biopsy by light microscope
  • amyloid is amorphous, esosinophilic and extracellular
  • deposits have uniform b pleated sheets
32
Q

What are the 3 types of amyloid?

A
  1. AA: most common systemic form in animals. originates from serum amyloid a (an acute phase protein). concentration increases during an inflammatory disease so it is commonly seen with chronic infectious disease
  2. AL: rarely seen in animals
  3. IAPP: relatively common in older cats and is associated with diabetes mellitus. it is a normal component secreted with insulin by b cells
33
Q

describe renal amyloiosis

A
  • animals that have this progressively tend to die with renal failure and uraemia
  • kidneys get enlarged, pale yellow brown
  • amyloid accumulates in glomeruli and interferes with normal filtration, resulting in proteinuria
  • it also interferes with blood supply to the entire nephron and renal tubular atrophy with uraemia occurs

Gen Path (10 decks)

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