Pathology of viral infections, equine grass sickness & intestinal displacements Flashcards
Outline Antibody secretion in Gastrointestinal System
Specialized cells in MALT, sample antigens from the GI lumen
Antigen-presenting cells (APCs) capture and present these antigens to immune cells within MALT and GALT.
B cells encountering antigens in MALT and GALT become activated and undergo differentiation.
Activated B cells differentiate into plasma cells, specialized for antibody secretion.
Plasma cells in MALT and GALT predominantly secrete immunoglobulin A (IgA) antibodies.
IgA plays a crucial role in mucosal immunity by neutralizing pathogens, preventing their attachment to epithelial cells, and promoting their clearance.
Canine Parvovirus 2 (CPV-2) infects…?
infects canids (and cats, especially big ones!)
Feline Panleukopenia Virus (FPV, CPV-1) infects…?
Felidae, raccoons, mink
Outline CPV and FPV ROI
- Oronasal exposure
- Viral uptake tonsil epithelium and Peyer’s patches
- infection of lymphocytes and viral replication
- systemic dissemination (lymphocytes and cell-free viraemia)
- Final target for virus is rapidly dividing crypt enterocytes in small intestine
- Necrosis of rapidly dividing cells
Canine and Feline Parvoviral infections non-specific clinical signs
pyrexia
depression
inappetance
vomiting
diarrhoea
dehydration
anaemia
6 key histological features of Parvoviral enteritis
- Necrosis of crypt epithelial cells
- Dilation of crypts with intraluminal sloughed degenerate/necrotic cells
- Intranuclear viral inclusions (detectable only in the early phase)
- Atrophy of villi (resulting from destruction of crypt epithelium)
- Necrosis of lymphoid tissue in Peyer’s patches
- 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 prominent nucleoli
histological features of Feline Panleukopaenia Virus
crypts containing sloughed necrotic enterocytes
lined by flattened epithelial cells or bizarre cells with an enlarged nucleus
intranuclear basophilic viral inclusion bodies (rarely seen)
Virus that affect pigs of any age, severe diarrhoea in suckling piglets
up to 100% mortality in piglets <10-14 days
Coronaviruses
Porcine Epidemic Diarrhoea Virus (PEDV)
Transmissible Gastroenteritis Virus (TGEV)
Virus that Common cause of diarrhoea in neonatal calves and Lesions in small intestine and colon
Bovine Coronavirus (BCoV)
Virus that has High morbidity (50-100%) but low mortality (<2%)
Blood-tinged diarrhoea, drop in milk production
Lesions mostly restricted to colon
Winter dysentery
Syndrome in adult cattle due to BCoV
Clinical presentation of Equine coronavirus
Fever
Acute colic
Anorexia
Acute neurologic deficits
(head pressing, aimless circling, depression/lethargy)
with severe hyperammonaemia
(677 mmol/L, normal range 60 mmol/L)
Outline Equine adenovirus (EAdV)
EAdV-1= upper respiratory tract infections in foals <3 months of age
EAdV-2= gastrointestinal tract infections
necrosis & ulceration in distal oesophagus & non-glandular gastric mucosa
Equine grass sickness is also known as
Equine Dysautonomia
Where does equine grass sickness affect
Disorder affecting the autonomic nervous system
postganglionic sympathetic and parasympathetic neurones
prevertebral and paravertebral ganglia
cranial nerve nuclei of the brainstem
Hypotheses on causative factors / agents of Equine grass sickness
oxidative stress
fungal toxins
changes in weather
exposure to C. botulinum type C (?)
Equine grass sickness risk factors
Strong association with grazing
Recent move to new pasture and premises
Age: higher incidence in 2–7-year-old animals
seasonal peak between Spring and early Summer
higher herbage Fe, Pb, As, Cr concentrations
Buttercups n pasture
cooler dryer weather and irregular ground frost
Clinical signs of Equine grass sickness
dull, patchy sweating, episodes of colic, reflux of gastric contents from nostrils
Outline the acute form of EGS
Progressively severe tympany (swelling of the abdomen with air or gas.)
Swallowing painful= Reverse peristalsis in the oesophagus
Swallowing avoided causing drooling
stomach distended with pale tan mucinous fluid sometimes watery with fibrous material
Gastric rupture due to excess fluid in the small intestine
Large intestine impacted with dry contents
faecal pellets in the small colon are small and dry (may have a surface blackened by a small amount of blood / sloughed necrotic mucosa)
Outline the chronic form of EGS
markedly reduced alimentary contents in the stomach
hypertrophy of intestinal musculature (most prominent in the jejunum)
What is the defining features for histopathological diagnostic confirmation for EGS
chromatolysis= dispersion and loss of Nissl substance
cytoplasmic swelling and vacuolation
peripheral displacement of the nucleus
decreased numbers of interstitial cells of Cajal
Dilation
widen or enlarge an opening or hollow structure beyond its usual size
Volvulus
twisting of an intestinal segment on its mesenteric axis (small intestine, horse colon; especially left colon)
Torsion
rotation of a tubular organ along its long axis (caecum of cattle and horse)
Dog – gastric dilatation and volvulus predisposing factors
Large deep-chested breeds
(Irish setter, Dobermann, Great Dane, others)
Rapid food intake
Post-prandial exercise
Pathogenesis of dog GDV
Gastric dilatation resulting from
accumulation of gas / fluid / food
obstruction of cardia= preventing eructation/vomiting
Obstruction of pylorus= preventing transit of ingesta
- Recurrent dilation + overfeeding + post-prandial exercise
+ possible genetic predisposition - stretching & relaxation of the gastro-hepatic ligament
- gastric rotation
Dog – gastric dilatation and volvulus- Consequence
Decreased venous drainage
Congestion, hypoxia
Haemorrhagic infarction of the gastric wall
decreased portal venous return
pancreatic ischaemia causing release of myocardial depressant factor
results in cardiovascular collapse & circulatory shock
Cause of horse primary dilation
excess fermentable carbohydrates
sudden access to lush pastures with rapid intake of large amounts of food
excess water intake
Cause of horse secondary dilation
intestinal obstruction or colic with ileal paralysis
manifestation of acute Equine Grass Sickness
Mechanisms of dog GDV
Pylorus moving cranially towards midline
Pylorus & antrum becoming ventral and cranial to the body of the stomach
Pylorus & antrum moving toward the left side of the abdomen and shifting dorsally
Pylorus and antrum displaced dorsally on the left side of the abdomen (rotation complete)
Explain why in the Horse –volvulus of the ileum can cause haemorrhagic infarction
compression of mesenteric veins but thick walled mesenteric arteries are more resistant to pressure and occlusion. blood still pumped into local circulation of the twisted segment but cannot drain
oedema> congestion > haemorrhage > necrosis
Explain the cause of intestinal loop strangulation by pedunculated lipomas
lipomas arising within the mesenteric adipose tissue
frequently characterised by a long peduncle
tumours may be mobile and wrap around intestinal loops
the intestinal loops become incarcerated
blood vessels compression with impaired venous drainage
haemorrhagic infarction of the strangulated loops
