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Module 16 > Pathology of Viral Infections, Equine Grass Sickness and Displacements > Flashcards

Pathology of Viral Infections, Equine Grass Sickness and Displacements Flashcards

1
Q

what are the defence mechansisms of saliva (3)

A
  1. flushing action –> potential pathogens are cleared from the oropharynx
  2. protective coating of the mucosa
  3. contains antimicrobial lysozyme, lactoferrin, lactoperoxidase and immunoglobulins
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2
Q

what paneth cells

A

antimicrobial peptides and proteins

lysozyme, secretory phospholipase A2, alpha-defensins, cryptidins

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3
Q

what are the defence mechanisms of the GI system (16)

A
  1. saliva
  2. gastric pH
  3. paneth cells
  4. intestinal proteolytic enzymes
  5. intestinal biotransforming and metabolic enzymes
  6. extra-intestinal secretions from liver and pancreas
  7. mucus (contains phages destroying bacteria)
  8. vomiting
  9. high rate of epithelial turnover
  10. increased peristalsis
  11. shedding of receptor-laden ALP and catalase-containing vesicles from microvilli
  12. phagocytes and other effector cells within submucosa
  13. innate lymphoid cells
  14. kupffer cells (liver)
  15. adaptive immune system
  16. secreted immunoglobulins
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4
Q

what are the functions of resident commensal bacteria and protozoa (6)

A
  1. 100 trillion (anaerobic) bacteria
  2. compete for nutrients
  3. compete for attachment sites
  4. promote immune system maturation
  5. bacteriocins
  6. biotransformation
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5
Q

describe the mucosal associated lymphoid tissue immune function (5)

A
  1. sampling actions from the gut lumen
  2. processing by mucosal dendritic cells
  3. transport to lymph nodes
  4. presentation to T-cells and activiation
  5. B-cell stimulation
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6
Q

what do specialized M cells in the dome region of intestinal mucosa do (7)

A
  1. antigen uptake
  2. processing
  3. presentation
  4. stimulation of B cell response
  5. plasma cells
  6. antibody production
  7. secretion through intestinal epithelium
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7
Q

describe the pathology of canine parvovirus (5)

A
  1. oronasal exposure
  2. virus uptake in tonsil epithelium and peyer’s patches
  3. infection of lypmhocytes nad viral replication
  4. systemic dissemination (lymphocytes and cell-free viremia)
  5. final target crypt enterocytes in small intestines

viral replication in rapidly dividing cells

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8
Q

what does canine parvovirus cause in rapidly dividing cells

A

necrosis or rapidly dividing cells

lymphoid tissue necrosis/depletion

crypt enterocyte necrosis

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9
Q

what does CPV-2 infection cause

A

villous atrophy results from inability to replace enterocytes from crypts

necrosis of crypt epithelial cells leads to crypt dilation

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10
Q

what are the clinical signs of canine and feline parvoviral infections (7)

A
  1. pyrexia
  2. depression
  3. inappetance
  4. vomiting
  5. diarrhea (hemorrhagic)
  6. dehydration
  7. anemia
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11
Q

what pathology is shown

A

diffuse mucosal necrosis

dog parvoviral enteritis

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12
Q

what are 6 key histological features of parvoviral enteritis

A
  1. necrosis of crypt epithelial cells
  2. dilation of crypts with intraluminal sloughed degenerate/necrotic cells
  3. intranuclear viral inclusions detectable only in the early phase
  4. atrophy of villi resulting from destruction of crypt epithelium
  5. necrosis of lymphoid tissue in Peyer’s patches
  6. epithelial regeneration – late phase –> damaged crypts may be lined by extremely flattened cells (squamous metaplasia) and by scattered large bizarre cells with swollen nuclei and prominant nucleoli
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13
Q

what histological features are seen here

A

shortening and loss of villi on surface

dilation of crypts with slough cell and debris in lumen

flattened cells attempting regeneration

minimal presence of inflammatory cells in mucosa

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14
Q

what are the gross pathologic lesions associated with

A

feline panleukopenia virus

segmental necrotizing and hemorrhagic enteritis

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15
Q

what are the histopatholigical findings seen on here

A

crypts containing sloughed necrotic enterocytes

lined by flattened epithelial cells or bizarre cells with enlarged nucleus

intranuclear basophilic viral inclusion bodies (rarely seen)

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16
Q

what does coronavirus cause in pigs

A

procine epidemic diarrhea virus (PEDV)

transmissible gastroenteritis virus (TGEV)

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17
Q

what does porcine epidemic diarrhea virus (PEDV) and transmissible gastroenteritis virus (TGEV) cause

A

severe diarrhea in suckling piglets up to 100% mortality in piglets <10-14 days

piglets less resistant to dehydration and hypoglycemia –> blunting and fusion of villi in the small intestine

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18
Q

what does bovine coronavirus virus (BCoV) cause

A

diarrhea in neonatal calves

lesions in small intestine and colon –> malabsorptive diarrhea

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19
Q

what is winter dysentery

A

syndrome in adult cattle due to BCoV

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20
Q

what does winter dysentry cause

A

high morbidity (50-100%) but low mortality (<2%)

blood tinged diarrhea, drop in milk production

lesions mostly restricted to colon

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21
Q

what is the clinical presentation of equine coronavirus (5)

A
  1. fever
  2. colic
  3. anorexia
  4. acute neurologica deficits
  5. head pressing, aimless circling, depression/lethargy with severe hyperammonemia
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22
Q

what gross pathological changes can be seen with equine coronavirus infections

A

small intestine –> red ringed fluid contents

jejunum and ileum –> diffuse red discoloration of the mucosa and thin, friable, finely granular, adherent, brown to gray pseudomembranes

or more severe mucosal ulcerative lesions

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23
Q

what histopathological changes can be seen in equine coronavirus (7)

A
  1. necrotizing enteritis with marked villous attenuation
  2. epithelial cell necrosis at the tips of the villi
  3. neutrophilic and fibrinous exudation (pseudomembrane formation)
  4. crypt necrosis (and possible crypt abscesses)
  5. mitothrombosis and hemorrhage
  6. possible intracytoplasmic inclusions in enterocytes
  7. viral antigen identified by immunochemistry
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24
Q

what is the mechanism of hyperammonia and encephalopathy in the absence of liver disease

A
  1. overgrowth of urease producing bacteria –>
  2. abundant ammonia production from degradation of proteins and endogenous urea –>
  3. disruption of normal intestinal mucosal barrier –>
  4. excessive ammonia absorption from the intestinal lumen into the circulation
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25
Q

what is a distinctive histopathological feature of equine enteric hyperammonemia and enteric encephalopathy

A

in the horse brain there is type II alzheimer astrocytes

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26
Q

what does rotavirus cause in foals

A

major cause of diarrhea <3-4 months

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27
Q

what is also observed in rotavirus infections

A

co infections with other pathogens salmonella, cryptosporidium, and equine coronavirus

28
Q

where does the rotavirus infect

A

in the enterocytes in the small intestine

29
Q

what does rotavirus cause

A

villous atrophy and fusion (similar to rotavirus and coronavirus infection in other species)

30
Q

what does equine adenovirus (EAdV) 1 cause

A

upper resp tract infection in foals <3 months of age

31
Q

what does equine adenovirus (EAdV) 2 cause

A

GI tract infecitons

32
Q

what pathological changes does EAdV cause (4)

A
  1. necrosis and ulceration in distal esophagus and non-glandular gastric mucosa
  2. intestinal lumen soft semi fluid ingesta
  3. typical adenoviral inclusions (intranuclear) at all levels of small intestine (most commonly located in the villus epithelial cells, less often in the crypts)
  4. villous atrophy in small intestine
33
Q

what is equine grass sickness

A

disorder affected the autonomic nervous system

34
Q

what areas of the ANS does equine grass sickness affect

A

postglanglionic sympathetic and parasympathetic neurones

prevertebral and paravertabral ganglia

cranial nerve nuclei of the brainstem

35
Q

what are the causative factors/agents in equine grass sickness (4)

A
  1. oxidative stress
  2. fungal toxins
  3. changes in weather
  4. exposure to C. botulinum type C –> role yet unproven
36
Q

why might pasture grasses with rapid growth or exposed to suden weather changes

A
  1. reduced concentration of antioxidants
  2. increased concentration of glutamate and aspartate (excitotoxic amino acids)
  3. increased concentration of malonate (neurotoxic substance)
37
Q

what are risk factors of equine grass sickness

A
  1. strong association with grazing
  2. recent move to new pasture and premises
  3. age –> higher incidence in 2-7 year old
  4. seasonal peak between spring and early summer
  5. higher herbage Fe, Pb, As, Cr concentrations –> oxidative stress
  6. abundance of Ranunculus species in pasture
  7. cooler dryer weather and irregular frost grounds
  8. low serum antibodies to Cl. botulinum type C and Cl. novyi type A surface antigens and Cl. botulinum toxoid

however causal or contributory role of Cl. botulinum still unconfirmed

38
Q

what are the acute/subacute forms (1-2/2-7 days duration) (8)

A
  1. progressively severe tympany
  2. attempts to swallow painful –> reverese peristalsis in the esophagus
  3. swallowing avoided –> drooling
  4. stomach distended with pale tan mucinous fluid sometimes more watery with fibrous material
  5. gastric rupture possible
  6. excess fluid in small intestine

7. large intestine impacted with dry contents

  1. fecal pellets in the small colon are small and dry (may have a surgace blackened by a small amount of blood/sloughed necrotic mucosa)
39
Q

what is the chronic form (>7 days duration) (2)

A
  1. markedly reduced alimentary contents in the stomach
  2. hypertrophy of intestinal musculature (often most prominent in the jejunum)
40
Q

what are the clinical sigsn of equine grass sickness

A

dull, patchy sweating and colic episodes regurgitation of green material from nostrils

41
Q

what are the pathological lesions seen here

A

equine grass sickness

fecal pellets small and dry covered with blackish strands of blood/necrotic mucosa

42
Q

what are the neuronal degenerative changes seen in equine grass sickness (6)

A
  1. chromatolysis = dispersion and loss of nissl substance (neuronal RER)
  2. cytoplasmic swelling and vacuolation
  3. peripheral displacement of the nucleus
  4. overt neuronal necrosis and loss
  5. satellite cell proliferation in affected ganglia
  6. formation of eosinophilic bodies/spheroids
43
Q

what are cajal cells

A

peacemaker cells of intestinal muscular layers

decreased number in equine grass sickness

44
Q

what histopathological changes are seen here

A

neuronal chromatolytic degeneration with loss of nissl substance and cytoplasmic vacuolation

45
Q

what are dislocations, displacements and strangulation seen in bovine

A
  1. right abomasal displacement and volvulus
  2. intestinal torsion/volvulus
  3. intestinal intussusception
46
Q

what are dislocations, displacements and strangulation seen in equine (4)

A
  1. gastric dilation and rupture
  2. intestinal herniation through Winslow’s foramen
  3. intestinal strangulation by pedunculated lipomas
  4. intestinal intussusception
47
Q

what are dislocations, displacements and strangulations seen in dogs

A
  1. gastric dilation and rupture
  2. intestinal torsion/volvulus
  3. intestinal intussusception
48
Q

what are predisposing factors for gastric dilation and volvolus

A

large deep chested breeds

rapid food intake

post prandial exercise

49
Q

what is the pathogenesis of GDV (6)

A
  1. gastric dilation resulting from accumulation of gas/fluid/food
  2. obstruction of cardia –> preventing eructation/emesis
  3. obstruction of pylorus –> preventing transit of ingesta
  4. recurrent dilation + overfeeding + post-prandial exercise + possible genetic predisposition
  5. stretching and relaxation of the gastro-hepatic ligament
  6. gastric rotation (180 to 360 clockwise on the ventrodorsal axis with ventral view of the abdomen)
50
Q

what other complications can occur with GDV

A
  1. displacement of spleen
  2. twisted esophagus
51
Q

how does the pylorus move during GDV (4)

A
  1. pylorus moving cranially towards midline
  2. pylorus and antrum ventral and cranial to the body of the stomach
  3. pylorus and antrum moving toward the left side of the abdomen and shifting dorsally
  4. pylorus and antrum displaced dorsally on the left side of the abdomen (rotation complete)
52
Q

what are the consequences of GDV (12)

A
  1. vascular stretching and compression
  2. decreased venous drainage
  3. congestion, hypoxia
  4. hemorrhagic infarction of the gastric wall
  5. possible hemoperitoneum
  6. alteration of gastric mucosal barrier & secretion
  7. acid-base and electroylte imbalance
  8. progressively increased intra-gastric pressure
  9. anit-peristaltic waves and atony
  10. decreased portal venous return
  11. pancreatic ischemia
  12. release of myocardial depressent factor –> CV collapse and circulatory shock
53
Q

what is primary dilation in the horse caused by (3) ,

A
  1. excess fermentable carbohydrates
  2. sudden access to lush pastures with rapid intake of large amounts of food
  3. excess water intake
54
Q

what is secondary dilation in the horse

A

intestinal obstruction or colic with ileal paralysis

55
Q

what is secondary dilation possibly caused by in the horse

A

grass sicknesss

56
Q

in which does rupture occur –> primary or secondary dilation in the horse

A

it can occur with both

57
Q

where does the rupture occur in primary or secondary dilation in horses

A

usually occurs along the greater curvature parallel to the omental attachment

58
Q

what is the sequela following gastric rupture in the horse

A

gastric content released into the omental bursa or the abdominal cavity

peritonitis –> septic shock –> acute death

59
Q

what is an intestinal volvulus

A

twisting of an intestinal segment on its mesenteric axis (small intestine, horse colon, especially left colon)

60
Q

what is a intestinal torsion

A

rotation of a tubular organ along its long axis (cecum of cattle and horse)

61
Q

what are the sequeala following a volvulus or a torsion (5)

A
  1. compression of mesenteric veins (and arteries) –> occlusion of thin walled veins
  2. thick walled mesenteric arteries are more resistant to pressure and occlusion
  3. blood still pumped into local circulation of the twisted segment but cannot be drained

4. edema –> congestion –> hemorrhage –> necrosis

  1. stasis of contents with toxemia and possible bacteremia resulting from necrosis of the affected segment
62
Q

what is a colonic torsion in horses

A

rotation of the colon resulting in strangulation

63
Q

what is the pathogenesis of intestinal loop herniation through epiploic foramen of winslow (6)

A
  1. epiploic foramen of winslow (normally small and slit like) may be dilated
  2. portion of small intestine, usually distal jejunum and ileum pass down into the omental bursa
  3. incarceration through the epiploic foramen
  4. compression of blood vessels
  5. impaired venous drainage
  6. severe congestion progressing to hemorrhage infarcation
64
Q

what is the pathogenesis of intestinal loop strangulation by pedunculated lipomas in horses (5)

A
  1. lipomas arising within the mesenteric adipose tissue frequently characterized by a long peduncle
  2. tumours may be mobile and wrap around intestinal loops
  3. the intestinal loops become incarcerated
  4. blood vessel compression with imparied venous drainage
  5. hemorrhagic infarction of the strangulated loops
65
Q

what is an intestinal intussusception

A

portion of intestine telescoped into the immediately distal segment of intestine

66
Q

what are intestinal intussusceptions caused by (4)

A

intestinal irritation and hypermotility secondary due to:

  1. enteritis
  2. foreign bodies (linear FBs, strings, ropes)
  3. parasites
  4. neoplasms
67
Q

what is the pathogenesis of intesintal intussusceptions (5)

A
  1. enlarged thickened segments of intestines
  2. red to black discolouration depends on degree of vascular compromise (congestion –> hemorrhage –> necrosis)
  3. vascular mesentery pulled into the intussusceptions (enveloping portion)
  4. compression of thin walled veins and then arteries
  5. congestion, edema, fibrin exudate, ischemic necrosis may occur in both the intussuscipiens and in the intussusceptum

Module 16 (26 decks)

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