Inflammation/Immunopathology Labs

Question 1

What is “Navel ill”?

Answer 1

• Omphalophlebitis - inflammation of the umbelical vein
• Occurs in neonates
  
  • often assoc. with failure of passive transfer
• Contamination of umbilicus can lead to septicemia
  
  • A. pyogenes, F. necrophorum, …
• Affected calves get fibrinopurulent polyarthritis, hepatic abscesses, umbical abscesses, pneumonia, meningitis, rumenitis, among others

Question 2

What is the pathogenesis of Navel ill?

Answer 2

1. Dirty environment, +/- failure of passive transfer, & regressing umbilicus
2. omphalophlebitis
3. Liver abscesses
4. Hematogenous dissemination
5. Septicemia

Question 3

what is an abscess

Answer 3

• a collection of neutrophils, accompanied by liquefactive necrosis of the associated tissue, usually surrounded by a fibrous capsule

Question 4

What is a granuloma

Answer 4

• nodule comprised of macrophages
  
  • also often lymphocytes and epithelioid macrophges
• With caseous necrosis of affected tissue
• usually surrounded by fibrous capsule
• No necrossis = granulomatous

Question 5

What is Bovine bronchopneumonia

Answer 5

• common in cattle, particularly after stressful events
• Affect the cranioventral regions of the lungs
• Major bacterial causes:
  
  • mannheimia haemolytica, histophilus somni, pasteurella mutocida, mycobacteria, and trueperella pyogenes

Question 6

What is the Pathogenesis of Brochopneumonia?

Answer 6

1. Stree event
2. Decreased immunity - bacteria colonize and proliferate
3. tissue destroying inflammatory respone in bronchi & alveoli
4. Suppurative or fibrinous broncopnumonia

Question 7

What is Johnes Disease?

Answer 7

• Affects ruminants
• Casued by mycobacterium avium paratubercuosis
• Fecal-oral transmission
• Infection occurs young, diseae manifests later (years)

Question 8

What are the clinical signs of Johnes disease?

Answer 8

• Weight loss
• Diarrhea
• Decreased milk production, good appetite

Question 9

What is the pathology of Johnes disease?

Answer 9

• Lymphogranulomatous inflammation in the intestin, lymphatics and ln
• mineralization in the aorta
• Muscle atrophy and serous atrophy of fat

Question 10

What is Murine Respiratoy Mycoplasmosis?

Answer 10

• M. pulmonis - ubiquitous in pet rats
  
  • mitogenic for B-cells actts as a superantigen
    
    • BALT hyperplasia
• Development of clinical disease differs rat to rat
  
  • some never
  • co infection with other respiratory diseases may worsen Murine
• Chonic pulmonary inflammaitno and degeneraion
  
  • suppurative bronchopneumonia
  • Bronchiectasis

Question 11

What is the pathogenesisof Murine Respiratory Mycoplasmosis?

Answer 11

1. Initial infection with Mycoplsma pumonis
2. Bacteria colonizes apical cell membrane o ciliated repiatory epithelium
3. Interference with mucociliary clearance
4. Chronic neutrophil cheomtazis and lysosome exudate
5. Weakening of bronchiolar walls and distension / rupture of airways (bronchiectasis)
6. Airway inflammation and blockage, atelectasis

Question 12

What is traumatic reticulopericarditis?

Answer 12

• Most common in dairy cattle
• cause - perforation of reticulum by a foreign body
• poor prognosis
• other syndromes may occur depending on what the foreign body perforates into
  
  • Pleural or peritoneal adhesions
  • Hepatic abscesses

Question 13

What are the initial clinical features of Traumatic retculopericarditis?

Answer 13

• Acute remenoreticular atony
• Dramatic drop in milk prodution
• Cranial abdominal pain
• Fever

Question 14

What is the pathogenesis of traumatic reticulopericarditis?

Answer 14

1. Ingestion of sharp foreign body
2. Enters reticulum
3. REticular contractions force object through wall
4. Introduction of ingesta/bacteria into abdomen
5. Object migrates and pierces pericardium and myocardium

Question 15

Whate is immune mediated Hemolytic anemia?

Answer 15

• exact cause not fully unerstood
  
  • erythrocyte surfat altered by drug or infectious agent
  • Could be true autoimmune disease due to breakdown of self recognition or lteration of erythrocyte self-antigen
• TYPE II hypersnsitivity against erythrocytes
  
  • Spherocytes, anemia, hyperbilirubinemia, icterus
  • Premature removal of damaged RBCs by spleen
    
    • extravascular hemolysis
  • Destruction o RBC by complement
    
    • intravascular hemolysis
• Antibody-coated RBC become sticky and auto-agllutinate
• Clumps activate platelets and coagulation resulting in thromboemboli
  
  • main cause of death

Question 16

Where can IMHA occur

Answer 16

• Hemorrhage can occur in multiple orangs/tissues
  
  • coul be secondary to anti-coagulatn (heparin) or anti-platelet (aspirin) therapy to preent erythrocyte autoagglutintion/thromboembolism
  • This could be due to consumption coagulopathy and DIC
  • Coudl be due to concurrent immune-mediated thrombocytopeni

Question 17

What is the pathogenesis of IMHA/

Answer 17

1. Unknown inciting cause
2. Immune sytem attacks RBCs
3. Premature destruction of RBC
4. Hemolysis
   
   1. Intravascular
      
      1. release of hemoglobin into circulation
         
         1. icterus
   2. extravascular
      
      1. anemia

Question 18

What is Severe Combined immunodeficiency (SCID)?

Answer 18

• Autosomal recessive disorder of Arabian/Arabian crosses
  
  • results in severe lymphopenia
• lyphopenia occurs because failure to produce funcitonal T- and B-lymphocytes
  
  • cannot generate approprate immune response
  • Defects due to spontaneous mutation in gene encoding the subunit of DNA-dependent protein kinase (DNA-PKcs)
• Recurrent infections are typical
  *

Question 19

What is Rhodococcus equi?

Answer 19

• Causes pneumonia and colitis
• Widespread in the environment and seologic evidence of infection is common, but disase is not common
  
  • affects immunocomprimised/young
• Likely aerosol exposure
  
  • Suppurative bronchopneumoiana
    
    • abscesses
      
      • pyogranulomatous nodule
• Swallowed R.equi from lungs most likely initiants colitis
  
  • R equi enter GALT associated Mcells to initiate colitis and mesenteric lymphadenitis

Question 20

What is feline infectious peritonitis?

Answer 20

• Casused by mutated feline enteric coronavirus
  
  • localized TYPE III hypersensitivity
• Formation of granulomas and effusion are commonly observerd
  
  • classic lesion is goled-yellow fluid in abdominal or thoracic cavity
• Clinically: immunoglobulins are usually high, albumin low
• Lesions tend to be perivascular and lymphocyte/plasma cell rich histologically
• Risk factors: age, multicat households
• Differentials: neoplasia, systemic fungal infection

Question 21

What is the pathogenesis of FIP

Answer 21

1. fecal oral transmission
2. Enteric coronavirus enters the body
3. Emutates witin the body
4. replicates in macrophages
5. systemi disaese, FIP, Type III hypersensitivity

Question 22

How is a scar formed

Answer 22

1. in areas of irreversibl injury, granulation tissue can form
   
   • transient fibrovascular tissue that forms to help resulvean area of irreversible injuty
2. Fibroblasts produce collagen
3. Collagen coss-link, remodel, and cotnracts to miimize area of damage
   
   • metalloproteinases, myofibroblast contraction, and alteration in cross-linking
4. Regression of bloodvessels and fbroblasts
5. Fribrosis/ scar tissue
   
   • no longer inflammatino

Question 23

What is pyometra

Answer 23

• Commonly caused by E. coli
• higest risk during diestrs, when progesterone is high
• Pus accumulation in te uterine lumen and dilaiton
• Requires medical attention

Question 24

How does progesterone cause suscptibility to infection?

Answer 24

• Inreased endometrail growth and glandular sections
• Continued closure of cervix
• decreased migraiton of neutrophils to uterus, reduced phagocytosis of uterine bacteria
• Bacteial colonizaitno and infiltration leads to bacterial infection

Question 25

What is the pathogenesis of pyometra?

Answer 25

1. Diestrus
2. prolonged and large amount of progesterone
3. Fluid accumulation in endometrial glands
4. cystic endometrial hyperplasia
5. uterine drainage hindered by progesterone inhibiting myometrial contractility
6. abnormal uterine environment
7. bacterial conlonization
8. Bacterial overgrowth pyometra
9. Type III hypersensitivity reaction

Question 26

How does pyometra lead to glomular disease?

Answer 26

1. Chronic infection, high level of bacterial antigens
2. Antigens = antibody production
3. immune complexes in circulation
   
   • have slidgh antigenexcess
     
     • too sall for phagocytosis to big for filtration by glomerulus
4. immune complezes become stuck in glomeruli and activate complement and nutorphils
   
   • glomerulitis and progessive renal failure

Type III hypersensitibity