CNS & Enteritis Flashcards

1
Q
Avian encephalomyelitis (AE)
Pathogen
A

• Picornaviridae, Enterovirus
– 1-2 weeks of age
– „epidemic tremor”
• Nonsuppurative encephalomyelitis/encephalitis = lymphocytes and histiocytes (not heterocytes)
– Cerebellum, medulla, spinal cord (ventral horn)
– Neuronal degeneration, gliosis, mononuclear perivasculitis
– Lymphoid tissue proliferation (glandular, gizzard, heart muscle, pancreas)

Major lesions in CNS
In different areas of the CNS
(basal part of the brain, medulla oblongata, cerebellum, cervical & lumbal part of the myelon):
• neuron degeneration
• focal gliosis
• perivascular lymphohistiocytic infiltration

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2
Q
Avian encephalomyelitis (AE)
Pathogenesis
A

Per os infection
viraemia → the virus reaches the target organs (inflammatory cell infiltration)
– propria of the proventriculus
– myocardium
– interstitium of the pancreas
-gizzard
• in these organs focal lymphocytic infiltration develops
• epidemic tremor
(head, neck)
• later ataxia
Occasionally central opacity (blindness) and/or uveitis is developed

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3
Q

Arthritis and tenosynovitis

caused by Orthoreoviruses

A

• infectious synovialitis
• orthoreoviruses like to proliferate on synovial membranes
– mainly the trypsin-sensitive strains
– the trypsin-resistant viruses start to proliferate in the mucous
membrane of the intestinal tract
• Infection:
– in ovo
– per os from the infected birds (• orofecal)
• Other (trypsin-sensitive) strains enter through the airways or skin
1) proliferation in the port of entry
2) viraemia – unnoticed in most of the birds
3) during viraemia reach the joints, tendon sheaths and bursa
4) proliferate
• acute serous, sero-fibrinous(-purulent) inflammation, later chronic
• Appearance: chicken, hen, turkey, goose, Muscovy duck
• Secondary: Staphylococcus aureus, Mycoplasma synoviae

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4
Q

Disease in geese and Muscovy

ducks caused by orthoreoviruses

A
• Pathogen:
– different strain of orthoreovirus
• Infection: same
• Pathogenesis: similar
• no lesions develop in the gut
• the viraemia by orthoreoviruses is fatal
– mainly in young animals
• arthritis and tenosynovitis also occurs
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5
Q

Pathology of the small intestine

Viral enteritides

A
• Parvovirus enteritis
• Adenovirus enteritis
• Astrovirus enteritis
• Reovirus enteritis
• Rotavirus enteritis
• Coronavirus enteritis
• PEMS
– poult enteritis mortality syndrome (young turkeys)
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6
Q

General pathogenesis of viral

enteritides

A

Multiplication of the virus takes place in the epithelial cells of the intestinal villi (villus-atrophy)
– in the enterocytes
• degeneration of the enterocytes occurs due to destruction of the enterocytes
• decreased production of enzymes
– malsecretion
• abnormal digestion processes
– maldigestion
• imperfect, incomplete absorption
– malabsorption
Because of malsecretion, maldigestion and malabsorption
• osmotically active decomposition products are produced
• these substances bind fluid
– increased fluid amount in the intestines- osmotic diarrhoea=> ORANGE
-faecal balls on the toes

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7
Q

General pathogenesis of viral
enteritides
Outside the intestines

A

due to malnutrition
viraemia follows the proliferation
– feathering problems (helicopter feather)
– osteopathies
• ricketts and other diseases
– dyschondroplasia, epiphysiolisis (bone is bending and cartilage)
– vitamin E deficiency
– atrophy of the immune organs
Runting-stunting (syndrome), maldevelopment

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8
Q

Enteric disease complex in chickens

A
– Clinical symptoms
– In the flock
» Huddling, litter ingestion
» Diarrhoea consequences
» Poor production, fail to grow
» Heterogenous flock
Runting-Stunting Syndrome (RSS)
– Cause
– Not completely cleared
– Several factors
» VIRUSES
Astroviridae
Coronaviridae
Reoviridae
Rotaviridae
PARVOVIRIDAE
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9
Q

Pathogenesis of enteric diseases

A
• Dilatation of the intestinal loops
– Changes in the quality of the content
=>Maldigestion-malabsorption
syndrome
• Villus degeneration
– Destruction of the epithelial layer
» Villus denudation
» Villus atrophy / fusion
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