1
Q
Where abouts in the Gastrointestinal tract are you likely to find Haemonchus?
A
Abomasum
2
Q
Where abouts in the GIT are you likely to find Trichostrongylus?
A
Small intestine
3
Q
How are clinical signs of parasitic gastroenteritis (PGE) caused?
A
- Removal of something (metabolites, blood)
- Damage to gut lining with loss of body fluids (PLGE -> hypo-proteinaemic oedema)
- Interference with digestion & absorption (damage)
- Blockage of something (gut, bile ducts)
- Irritation of gut-larvae in mucosa -> diarrhoea, XS secretion
- Migration through gut wall -> Ill-thrift, diarrhoea, anaemia, more specific signs.
4
Q
What is stomatitis?
A
Diffuse inflammation of the oral cavity mucosa
5
Q
What are some defence mechanisms of the oral cavity?
A
- Tough stratified squamous epithelium
- Rapid epithelial regeneration
- Resident microflora occupy attachment sites
- Taste buds reject potential toxins
- Saliva contains digestive enzymes
- Salivary pH
- Swallowing, flushing action
- Mucosal secretions provide physical and chemical protection (IgA and lysozyme)
6
Q
What are some defence mechanisms of the GIT?
A
- Saliva
- Resident microflora
- Low gastric pH
- Secreted immunoglobulins
- Vomiting
- Intestinal proteolytic enzymes
- Submucosal phagocytes
- Rapid epithelial turnover
- Increased peristalsis -> diarrhoea
- Adaptive immunity
7
Q
What are the causes of stomatitis?
A
Direct injury
- foreign body (needle, grass seed, bones)
- ingested chemicals (detergents, other caustics)
Systemic or local disease
- Viruses (FMD, blue-tongue, rinderpest*[no longer exists])
- Autoimmune disease (pemphigus)
- Uraemia (syndromes associated with renal failure)
8
Q
What are the various types of Stomatitis?
A
- Vesicular Stomatitis
- Catarrhal Stomatitis
- Erosive/Ulcerative Stomatitis
- Necrotising Stomatitis
- Papular Stomatitis
- Eosinophilic Granuloma Complex
9
Q
What is an example of a virus causing vesicular stomatitis in ruminants?
A
FMD -> affects clovel-footed animals (ruminants & pigs)
- wt loss from inability to eat
- high production losses
- Currently exotic to aust.
- can affect the lips, buccal mucosa, tongue, coronet, interdigital skin & udder)
- main routes of infection are inhalation & ingestion
- causes viraemia, localises in lymphoid tissue and epithelial tissue
10
Q
Give an example of a disease that causes supporative stomatitis in ruminants?
A
- Actinobacillosis (‘wooden tongue’)
- tongue enlarged, firn, diffuse, fibrous proliferations & many
granulomas - Multifocal, well demarcated yellow lesions in the retropharyngeal lymph node
11
Q
Eosinophilic Granuloma Complex commonly occurs in what species?
A
Cats
- lesser dogs
- often seen in cats with hypersensitivity disorders or allergies
- thought to be hypersensitivity or autoimmune rxn + genetic component
- Identifiable lesions:
1. Indolent (rodent) ulcer
2. Eosinophilic (linear) granuloma
3. Eosinophilic plaque
12
Q
What are some developmental abnormalities of the oral cavity?
A
- Cleft lip = Cheiloschisis
- Cleft palate = Palatoschisis
- Malocclusions names according to position of mandible (Brachygnathia = parrot mouth, short mandible; Prognathia = elongated mandible)
- Characteristic breeds e.g. brachycephalic causes dysphagia
13
Q
List common neoplasias/hyperplasia of the oral cavity in companion animals.
A
- Gingival hyperplasia -> gingival overgrowth
- Epulis = excessive growth of gingiva
- Viral papillomas
- Neoplasia -> oral melanoma; fibrosarcoma; SCC; chondrosarcoma; osteosarcoma
14
Q
What are the 3 mechanisms of diarrhoea?
A
- Osmotic
- Secretory
- Increased permeability
15
Q
What clinical signs are apparent with intestinal disease?
A
- Diarrhoea
- Vomiting
- Abdominal pain
- Wt loss
16
Q
What are the 4 possible intestinal obstructions?
A
- Stenosis & Atresia
- Extrinsic Obstruction
- Functional Obstruction
- Intestinal Displacements
17
Q
Stenosis & atresia of the GIT tract can be due to:
A
- Congenital atresia
- Acquired due to intramural lesion
- Foreign bodies
- Parasites
- Impaction of the colon
- Impaction of the caecum
18
Q
What are possible extrinsic obstructions of the GIT?
A
- Neoplasm
- Abscesses
- Peritonitis
- Fibrous adhesions
19
Q
Displacements of the Intestine
A
- Herniation: Internal herniation (displacement of intestine through a normal or pathological foramen inside the abdomen e.g. epiploic foraemn entrapment in horses or mesenteric tears
20
Q
Describe simple gut formation. (development of GIT)
A
- Formed during folding of embryonic disc.
- gut lumen derived from cavity of yolk sac
- part of yolk sac cavity is incorporated into the folding embryonic disc (body) as the lumen of the primitive gut
21
Q
Name the simple gut wall layers. (what they are formed from)
A
Endoderm -> epithelial lining
Splanchnic mesoderm -> remainder of wall
22
Q
Describe the formation of the liver.
A
Arise from the foregut.
- Diverticula from the hepatic diverticum include the ventral pancreatic diverticulum & the cystic diverticulum (gall bladder)
- Primordial liver: composed of hepatic diverticulum (endoderm forms hepatocytes, bile caniculi & hepatic ducts; splanchnic mesoderm forms the CT framework of the liver)
- Expansion of hepatic diverticulum -> engulfs vitelline and umbilical veins (-> hepatic sinusoids); Ductus venosus (within liver primordium) links umbilical v with caudal vena cava.
- Primordial liver expands through ventral mesentery & contacts septum transversum.
- Liver surface remains adherent to diaphragm in adult
23
Q
Describe the formation of the pancreas.
A
Foregut –> Ventral & Dorsal diverticulum.
Fusion of the 2 diverticula makes the pancreatic body & lobes
- Occurs as gut wall expands
- Duel origin reflected in presence of 2 pancreatic ducts in horse & dog ( major duodenal papilla and minor duodenal papilla) whereas 1 pancreatic duct regresses in pigs, ruminants & cats
24
Q
What structures are associated with the foregut?
A
oesophagus, lungs, stomach, pancreas & liver
25
Outline the histogenesis of the intestinal wall.
- Temporary occlusion of gut lumen
o Proliferation of endodermal cells --> occlusion
o Occurs toward end of embryonic period of development
o Vacuoles form shortly thereafter & fuse--> recanalization
- Villi formation & cellular differentiation
- Functional maturation of cell types.
26
What are features of the non-spore forming anaerobes?
- Major shareholders (80%) within normal flora (skin, MM, URT, LG-UT)
- outnumber the facultative anaerobes 5:1 on mucocutaneous surfaces
- seen clinically in mixed infections
- similar susceptibility pattern to antibacterial drugs
27
Some examples of NSFAs (gram -Ve, gram +Ve)
G-ve:
- Bacteroides
- Porphyromonas
- Prevetella
- Fusobacterium
Gram +Ve:
- Proprionibacterium
- Lactiobacillus
- Eubacterium
- Bifidobacterium
- Actinomyes (some)
- Peptostrep.
- Peptococcus.
28
Where do the NSFA cause ds?
1. at sites where they are part of the normal flora e.g. periodontal
2. extension of the normal flora into sterile area e.g. pleuropneumonia, hoof abscess
3. traumatic instillation into distant sites
29
what are some pre-disposing factors for NSFA-associated ds?
- Breakdown of normal host defences e.g. penetrating foreign body
- Change in association between normal flora e.g. overgrowth of some members
- Poor blood supply & tissue necrosis e.g. trauma, tumours
- Decreased host resistance e.g. cancer, chemo
- Prior use of Abs
- Overwhelming contamination of normally sterile area e.g. aspiration pneumonia
- Prior infection with aerobes/facultative anaerobes e.g. pyometra
30
List the differences in gingivitis and periodontitis.
Gingivitis:
- Reversible inflammation of gingiva
- Bacteria in gingival sulcus stimulate inflammatory rxn
- Gram +ve bacteria predominate in gingivitis
- If left untreated > irreversible changes = periodontitis
Periodontitis
- Irreversible destruction of the tooth’s supporting structures
- Switch to primarily Gram -ve bacteria
- Inflammatory rxn > periodontal soft tissue damage and alveolar bone loss
- Clinical signs -> pus, abscess on every tooth root, X ray shows bone recession
31
what bacteria causes wooden tongue?
Actinobacillus ligniersii
- Gram -Ve rods (coccobacili)
- normal flora of oropharynx & rumen
- facultatively anaerobic
- oxidase +
- mainly seen in ruminants
32
Describe the lesions caused by bacteria causing 'wooden-tongue'
o Produces hard tumour-like masses -> Pyogranulomatous abscesses (chronic)
o Head, neck and tongue (where it lives)
o Predominately soft tissue, not bone
o Tongue painful & wood like
o Dysphagia -> weight loss, loss of production
o Drooling, tongue protrusion and submandibular swelling
o Abscesses begin as a firm nodule that may ulcerate
o Commonly see external draining tract/sinus. Discharge = pale, with small, hard grey-white granules
-> Granules = ‘sulphur granules’ aka ‘club colonies’ = aggregates of bacteria + calcium phosphate
o May disseminate via regional lymphatics to involve internal organs such as lung
o Abscesses contain thick, viscous pus together with small, hard grey-white granules called “sulphur granules” or “club colonies”
-> Granules are aggregates of bacteria + calcium phosphate
33
FMD is apart of what virus family?
Picornaviridae
34
What species of bacteria cause lumpy jaw?
Actinomyces spp. - mainly A. bovis - gram +ve filamentous rod - normal flora of oral cavity
- pyogranulomatous inflammation in boney tissues/jaw
- Not as common as Wooden Tongue
35
Outline the pathogenesis of CAV1 (infectious canine hepatitis)
- Oronasal exposure
- Initial replication in local lymphoid tissue
- Viraemia disseminates virus systemically
o Virus replication in vascular endothelium and parenchymal cells -> haemorrhage and necrosis [particularly the liver (hepatic); can die suddenly (systemic ds)]
- Severity of disease depends on host immune response
- Virus shed in faeces, urine, saliva
- Localises in kidneys --> prolonged urinary shedding --> oronasal exposure
36
Discuss the characteristics of the virus causing FIP?
- Induced by FIP virus (FIPV) = a mutant form of Feline Coronavirus
o Mutates from avirulent enteric biotype (FECV) to virulent biotype (FIPV) within an individual cat
o No treatment
o Usually causes a mild gastrointestinal ds
- Enveloped virus
o Large glycoprotein spikes (peplomers)
o Relatively stable in environment (for an enveloped virus)
- RNA genome
o High mutation rate >> quasispecies
o Genetic recombination can occur
- Most commonly causes self-limiting enteric ds in cats (FECV)
o FECV can mutate within individual cats to become FIPV
37
Discuss the pathogenesis of FIP.
- FECVs mutates to FIPV in an individual cat and causes them to lose their tropism for intestinal cells while gaining macrophage tropism
- FIP required:
o Systemic infection with FIPV
o Sustainable replication of FIPV in monocytes
o Activation of these FIPV-infected monocytes
o Ultimate target cell is not just any macrophage, but a distinct population seen in the lining of blood vessels in the membranes covering the lungs, abdo organs, brain and eyes
o Infected monocytes mediate a granulomatous phlebitis and periphlebitis through interaction with endothelial cells
o Cytokines and adhesion molecules produced by the activated macrophages cause systemic damage to vascular endothelium (immune-mediated)
o FIPV infection also results in depletion of other WBCs natural killer cells & T reg cells usually involved stopping infection
38
What are some definitive tests to diagnose FIP?
1. Immunocytochemistry (direct immunofluroescence [IFA]) on effusions
2. Immunohistochemistry (IHC) on tissue
39
What are common causes of non-infectious GIT disease?
- . Simple Indigestion
- Free gas bloat
- Frothy bloat
- Reticulitis
- Vagal indigestion
- Ruminal acidosis
- Abomasal displacement
DOG, Derm
flashcards
Decks in class (6)
# Cards
