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GI LA > Small and Large Intestinal Disease > Flashcards

Small and Large Intestinal Disease Flashcards

1
Q

Describe the locations of the most severe lesions in DPJ

A
  • duodenum and proximal jejunum

- may extend proximally to gastric mucosa and aborally to LI mucosa and submucosa

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2
Q

Describe the microscopic lesions associated with DPJ

A
  • varying degrees of mucosal and submucosal hyperaemia with oedema
  • more severe lesions include villous degeneration with necrosis and more severely, sloughing of villous epithelium
  • lamina propria, mucosa and submucosa may have varying degrees of granulocyte infiltration (predominantly neutrophils)
  • muscular layers and serosal surfaces contain small haemorrhages
  • proximal SI serosal fibrinopurulent exudate is common finding in more severe cases
  • can have evidence of multiple organ involvement - can have hepatic changes including hepatocellular vacuolization, cholestasis, inflammatory infiltrate and biliary hyperplasia
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3
Q

Describe the possible mechanisms of development of hepatic disease in DPJ?

A
  • ascending infection by way of the common bile duct
  • local absorption of endotoxin via portal circulation
  • systemic consequences of endotoxin absorption
  • metabolic imbalances such as acidaemia
  • hypoperfusion or hypovolaemia
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4
Q

Which infectious agents have been proposed to play a role in DPJ?

A
  • Salmonella spp. (although Salmonellosis not consistently identified in majority of cases)
  • Clostridium spp.
  • Fusarium spp.
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5
Q

List possible predisposing factors for DPJ

A
  • recent dietary change with abrupt increase in dietary concentrate - may cause intraluminal microbial imbalances
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6
Q

Name the two intracellular processes that control intestinal secretion.

A
  • cyclic nucleotide (cAMP & CGMP) system

- calcium system

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7
Q

List the common clinical pathology findings in peritoneal fluid of horses with DPJ

A
  • protein concentration higher than in horses with SI obstruction (often > 3.5g/dL)
  • mild to moderate increase in WCC (usually < 10000/microliter)
  • disproportionate increase in total protein concentration relative to TNCC - probably by leakage of blood or plasma into peritoneal cavity without significant stimulus for leukocyte chemotaxis
  • usually yellow and turbid - in severe cases, diapedesis can occur, resulting in serosanguinous colour
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8
Q

Discuss the suggested mechanisms for increased abdominal fluid protein concentration in DPJ

A
  • serositis associated with inflamed intestine

- SI distension causing passive congestion and increased capillary hydrostatic pressure of visceral peritoneal vessels

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9
Q

Discuss the pathophysiology and predisposing factors for development of ileus in DPJ

A
  • involves primary and secondary dysfunction of the central, autonomic and enteric nervous systems
  • peritoneal inflammation
  • inflammatory cell migration/activation within the muscularis
  • SI mechanical distension
  • endotoxin absorption
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10
Q

Describe the difference in clinical signs between DPJ and SI obstructive lesions

A
  • signs of acute abdominal pain typically subside after gastric decompression - then display lethargy, general malaise
  • degree of SI distension on rectal exam is less, particularly following gastric decompression
  • colour and odour of gastric reflux can be similar but horses with DPJ tend to have larger volume (>4-20L with each decompressive effort)
  • temperature often 38.6 - 39.1
  • brick-red mm, lethargy, decreased to absent gut sounds, prolonged CRT, tachycardia, tachypnoea
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11
Q

Describe the haematology and biochemical abnormalities in horses with DPJ

A
  • normal, decreased or increased WCC
  • abnormalities in leukogram more common than in horses with SI obstructive lesions
  • increased PCV and TPP reflective of volume depletion
  • biochemical changes: hyponatraemia, hypochloraemia, hypokalaemia, prerenal azotaemia, elevated liver enzymes (GGT, AST, ALP)
  • metabolic acidosis with high anion gap - loss of enteric bicarbonate through evacuation of gastric reflux and hyperlactataemia from poor tissue perfusion and hypovolaemia
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12
Q

Describe the ultrasonographic findings in DPJ

A
  • gastric distension
  • duodenal distension
  • segments of SI containing hypoechoic to anechoic fluid
  • wall of SI can be normal or thickened with time
  • peristalsis decreased, normal or increased
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13
Q

Define malabsoprtion

A

The impairment of digestive and absorptive processes arising from functional or structural disorders of the SI and related organs, including the pancreas, liver and biliary tract

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14
Q

List the carbohydrate absorption tests used for the diagnosis of IBD in horses

A

1) oral glucose tolerance test - 1g/kg glucose administered as 20% solution via NGT following overnight fast (14-16hrs)
- blood glucose measured at 30min intervals for 180mins; then at 60min intervals until 360mins
- max plasma glucose level (> 85% baseline) reached by 120mins in healthy horses
- 15-85% baseline = partial malabsorption
- < 15% baseline = total malabsorption
- abnormal OGTT result and weight loss can occur in horse as a transient event and without significant morphologic changes in SI
- immediate dietary history, gastric emptying rate, intestinal transit, age and hormonal effects influence glucose peak and curve shape
- prolonged fasting results in delayed and slightly lower peak
- also affected by content of NSC and fat in diet and other disorders such as PSSM
2) D-Xylose absorption test
- 0.5g/kg D-xylose administered as 10% solution via NGT
- same fasting and blood collection as OGTT
- peak plasma D-xylose b/w 20-25mg/dL b/w 60-90 mins
- not confounded by hormonal effects or mucosal metabolism
- altered by diet, length of fasting and age, gastric emptying rate, intestinal motility, intraluminal bacterial overgrowth and renal clearance
- abnormal tests likely indicates abnormal mucosal SA or permeability

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15
Q

Discuss the features of lactase deficiency in foals

A
  • secondary lactase deficiency can occur when a SI disorder damages epithelial cells, resulting in decreased brush border disaccharidase activity
  • typically rotavirus
  • also reported secondary to clostridial enteritis in foals
  • can perform oral lactose tolerance test - 1g/kg lactose monohydrate as 20% solution via NGT; same blood sampling as OGTT; plasma glucose typically peaks 1hr after lactose administration (range 30-90mins) with mean increase of 77mg/dL
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16
Q

Discuss the findings on diagnostic workup in horses with alimentary lymphosarcoma

A
  • anaemia, thrombocytopenia, neutrophilia or neutropenia, hypoalbuminaemia with hyperglobulinaemia with normal or elevated serum protein
  • rectal palpation may reveal intra-abdominal masses, mainly enlarged mesenteric lymph nodes
  • abdominocentesis and rectal biopsy not sensitive indicators of disease
  • carbohydrate absorption tests: partial to total malabsorption indicative of the severely reduced SA resulting from significant villous atrophy and extensive mucosal or transmural infiltration
  • early confirmation necessitates ex lap to obtain multiple intestinal and LN biopises
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17
Q

List the disorders associated with MEED (multisystemic eosinophilic epitheliotropic disease)

A
  • chronic eosinophilic gastroenteritis
  • eosinophilic granulomatosis
  • chronic eosinophilic dermatitis
  • basophilic enterocolitis
  • MEED encompasses disorders characterised by predominant eosinophilic infiltrate in the GIT, associated LN, liver, pancreas, skin and other structures
  • accompanied by some degree of malabsorption and enteric protein loss (diarrhoea common)
  • liver and pancreatic involvement —–> maldigestion may contribute to wasting disease
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18
Q

Describe the skin lesions commonly seen in horses with MEED

A

Exudative dermatitis and ulcerative coronitis

19
Q

List the diagnostic workup findings in MEED

A
  • systemic eosinophilia RARE
  • hypoalbuminaemia
  • elevations in GGT and ALP
  • carbohydrate absorption tests: reduced or normal peak concentration delayed to at least 180mins
  • morphologic changes less pronounced in SI than LI - severe segmental or multifocal granulomatous lesions with mucosal and transmural thickening and extensive ulceration (likely cause of diarrhoea)
  • SI lesions predominate segmentally in proximal duodenum and distal ileum
  • significant hyperkeratosis of fundic region may contribute to gastric muscle contractile disruption
  • biopsies of rectal mucosa or skin, liver, intestinal tract and LN may assist diagnosis
20
Q

Discuss the causes of MEED

A
  • cause is unknown
  • could represent chronic, ongoing, immediate hypersensitivity reaction against undefined antigens ingested or excreted into lumen from parasitic, bacterial or dietary sources
  • infectious agents have not been identified
21
Q

What is the causative organism of proliferative enteropathy (PE)?

A

Lawsonia intracellularis

  • obligate, intracellular, gram negative bacteria
  • found in cytoplasm of proliferative crypt epithelial cells of jejunum and ileum
22
Q

What are the diagnostic tests for PE?

A
  • may suspect based on clinical signs and severe hypoalbuminaemia in a weanling
  • faecal PCR for bacterial DNA
  • serum immunofluorescence assay or immunoperoxidase monolayer assay (IMPA) for antibodies against the organism
  • IMPA may be more sensitive - titers > or equal to 1:60 considered positive
  • submission of both tests (PCR + IMPA) recommended; both tests lack sensitivity esp early in course of disease (serology) or with prior antimicrobial therapy (faecal PCR)
  • not typically associated with abnormal carbohydrate absorption tests
  • PM diagnosis: characteristic mural thickening and intracellular bacteria within apical cytoplasm of proliferating crypt epithelial cells using silver stains, PCR or immunohistochemical testing
23
Q

What is the common treatment for PE?

A
  • IV oxytetracycline
  • may follow with oral doxycycline
  • duration of tx usually 2-4 weeks
24
Q

Which species of Salmonella are most frequently isolated from horses

A
  • gram negative facultatively anaerobic bacteria
  • S.enterica serovar group B commonly infect horses
    • S. enterica var. typhimurium and S. enterica var. agona
    • s. enterica var. typhimurium is most pathogenic serotype in horses and is associated with higher case fatality rate
25
Q

What environmental factors or stresses may increase susceptibility to S. enterica infection?

A
  • high ambient temperature —-> peak incidence in late summer and autumn
  • transportation
  • antibiotic administration before or during hospitalisation
  • gastrointestinal or abdominal sx
  • general anaesthesia
  • pre-existing GIT disease (eg. colic, diarrhoea)
  • presence of leukopenia or laminitis during hospitalisation
  • prolonged hospital stay
  • change in diet
  • immunosuppression
  • foals with gastrointestinal dz more likely to shed S. enterica organisms than are adult horses with GIT dz
26
Q

What host factors restrict gastrointestinal colonisation and invasion by pathogens?

A
  • gastric pH
  • commensal GIT flora - secrete bacteriocins, SCFAs and other substances; compete for nutrients and space esp. on mucosa
  • GIT motility
  • mucosal barrier
  • mucosal immunity - mucosal antibody secretion and enterocyte-derived cationic peptides
27
Q

What are the features of S.enterica that allow it to invade and survive?

A
  • capable or surviving and multiplying within macrophages, rendering humoral (non cellular) immune systems ineffective
  • ability of S. enterica to cause enterocolitis depends on ability to invade GIT mucosa
  • invasion of GIT mucosa occurs preferentially through specialised enterocytes called M cells that overlay intestinal lymphoid tissue
  • —-> self induced uptake via apical membrane of M cell, often killing the cell in the process
  • S. enterica then invades neighbouring cells via basolateral membrane
  • virulent S. enterica have invasion mechanism involving generation of a Type III secretory system that enables virulence gene products to be injected directly into enterocytes
  • virulence proteins injected into enterocyte —-> induce cell to engulf bacteria by macropinocytosis
  • virulence gene products also induce enterocyte chloride and fluid secretion and upregulate enterocyte transcription of inflammatory cytokines and chemokines that trigger mucosal infl. response
28
Q

What are the important defense mechanisms against dissemination and systemic infection by S.enterica?

A
  • specific cellular immunity
  • protective immunity may be induced by oral inoculation with small numbers of virulent organisms but duration of immunity not known
  • oral and parenteral vaccines using killed or attenuated organisms and bacterial products effective only against homologous organisms
29
Q

What are the causes of diarrhoea associated with virulent S. enterica.

A
  • a S. enterica cytotoxin inhibits protein synthesis in mucosal cells, causing morphologic damage and altered permeability
  • produce an enterotoxin that increases secretion of chloride and water by colonic mucosal cells (by increasing cAMP concentrations)
  • ability to invade enterocytes and trigger infl. reaction - infl. cytokine and chemokine production —> recruitment of leukocytes esp neutrophils and activation of resident macrophages and mast cells
  • products of activated leukocytes include prostaglandins, leukotrienes, reactive O2 metabolites and histamine —-> potent stimulators of chloride secretion in colon
  • enteric nervous system integrates the diverse processes of pathogen recognition, triggering of infl. response and induction of enterocyte fluid secretion
30
Q

What are the four clinical syndromes of S. enterica infection in horses?

A

1) inapparent infections with latent or active carrier states
- can be activated to clinical dz in compromised horses
- latent infections can become active infections under certain conditions (transportation stress, AB tx)
2) depression, fever, anorexia and neutropenia without diarrhoea or colic
- good px and usually recover in several days without specific tx
3) fulminant or peracute enterocolitis with diarrhoea
4) septicaemia (enteric fever) with or without diarrhoea
- mostly restricted to neonatal foals and is uncommon in adult horses

31
Q

How is S. enterica infection diagnosed?

A
  • analysis of five daily faecal cultures using enrichment techniques - sensitivity can be as low as 30-50%; concurrent culture of rectal biopsy specimens may increase sensitivity to 60-75%
  • Faecal PCR is most sensitive and rapid detection method esp. if early in dz - up to 100% sensitivity and 98% specificity
  • detection of organisms not necessarily proof of dx but PPV of either positive PCR or culture is high in horses with compatible clinical signs
32
Q

What are possible complications of S. enterica infection?

A
  • MODS
  • vascular leak syndrome with peripheral and organ oedema
  • laminitis
  • ARF
  • venous thrombosis and septic phlebitis
  • irreversible PLE or chronic malabsorption
  • pulmonary aspergillosis
  • gastrointestinal infarction
33
Q

List the factors which may increase clostridial numbers in the GIT

A
  • dietary factors
  • colic
  • antibiotics esp those administered orally or recycled via enterohepatic system
  • —-> C. difficile likely to be most important cause of antibiotic-induced enterocolitis in the horse
34
Q

Describe the roles of Clostridium difficile toxins A and B in enterocolitis in horses

A
  • Toxin B: potent cytotoxin in vitro but role in enterocolitis is less clear thatthat of toxin A
  • Toxin A: enterotoxin that induces an infl. response with hypersecretory diarrhoea; induces neutrophil influx into intestinal tissue, mast cell degranulation and secretion of prostaglandins, histamine, cytokines and 5-HT by these activated leukocytes; products of neutrophils and mast cells have significant role in vasodilatory and secretory responses in intestine
35
Q

Describe the role of the enteric nervous system in C. difficile enterocolitis

A
  • ENS is central to the induction of intestinal inflammation and mucosal secretion by toxin A
  • toxin A stimulates substance P-containing afferent sensory nerve fibres —-> in turn stimulate mast cell degranulation, recruitment and activation of PMN and vasodilation
  • Toxin A-induced stimulation of enterocyte secretion can occur via secretomotor neuronal stimulation by substance P-containing sensory neurons or products of mast cells and PMN
  • mast cell degranulation, PMN influx and enterocyte secretion are all abolished by neural blockade or depletion of substance P
  • toxin A induced necrosis of enterocytes likely exposes afferent neurons to the noxious milieu of the intestinal contents
36
Q

Describe the aetiology of equine coronavirus

A
  • Coronaviruses: members of Coronaviridae family - single-stranded, positive-sense, nonsegmented, enveloped RNA viruses
  • Coronaviridae subdivided into two subfamilies - Torovirinae and Coronavirinae
  • Coronavirinae contains 4 genera defined on basis of serological cross-reactivity and genetic differences: Alpha-, Beta-, Delta- and Gamma-coronavirus
  • Equine coronavirus classified within the Betacoronavirus genus
37
Q

Describe the important epidemiology of Equine coronavirus

A
  • sporadic or epizootic
  • case number higher during colder months but cases occur year around
  • widespread across lower 48 states of USA
  • predominantly reported in adult horses
  • more common in riding, racing and show horses than in breeding animals
  • frequent circulation of ECoV b/w asymptomatic young animals and adult resident horses, conferring protection against clinical disease in adult horses
  • suspected faeco-oral transmission
  • variable morbidity rate; low mortality rate
  • incubation time: 2-3 days
  • outbreak duration: 2-3 weeks
  • period of illness: few days - 1 week
  • faecal shedding can range between 3 and 25 days
  • not known how long it can survive in environment and potentially act as source of infection
  • ECoV can occur in one or more horses on a farm with no recent exposure to new horses - could be explained by indirect ECoV transmission by nonequine animal species or colder weather may allow increased faecal replication of virus from chronically infected horse
38
Q

What clinical signs are associated with ECoV

A
  • anorexia
  • lethargy
  • fever
  • diarrhoea (less frequent)
  • colic
  • GIT signs generally preceded by systemic signs of anorexia and fever
  • neurological signs - circling, head pressing, ataxia, proprioceptive deficits, nystagmus, recumbency and seizure
  • clinical disease apparent in 10-83% of ECoV infected horses but some horses remain asymptomatic after infection
39
Q

How is ECoV diagnosed?

A
  • clinical signs compatible with ECoV infection
    +
  • neutropenia and/or lymphopenia (not a classical viral CBC)
    +
  • exclusion of other infectious causes
    +
  • molecular detection of ECoV in faeces
40
Q

List the biochemical abnormalities which may occur in ECoV infection

A
  • may be unremarkable
  • elevation of total and indirect bilirubin due to partial or complete anorexia
  • electrolyte changes consistent with enterocolitis
  • transient elevation of liver enzymes and renal parameters (suggestive of prerenal azotaemia)
  • measure blood ammonia concentratons if concurrent signs of encephalopathy - hyperammonaemia likely due to increased ammonia production within or absorption from GIT due to gastrointestinal barrier breakdown
41
Q

Describe the molecular techniques for diagnosis of ECoV

A
  • faecal quantitative PCR (qPCR)
  • 90% accuracy b/w clinical status and PCR detection
  • may be negative in peracute stages of infection or in horses with ileus and colic - retest in a suspected index case at later time point or collect multiple samples for pooled sampling
  • usually shed in faeces 3-4 days post infection and continue shedding for 12-14 days post infection
  • PM diagnosis: qPCR of faeces, SI tissue, GIT content; can also collect formalin fixed intestinal tissue samples for immunohistochemistry and direct fluorescent antibody testing using BCoV reagents
42
Q

Discuss the differences in ECoV infection in foals and adult horses

A
  • high and similar frequency of ECoV shedding detected in healthy foals and foals with GIT diseases
  • ECoV likely commonly circulates among young horses with subclinical dz
  • all ECoV infections in foals with GIT dz associated with coinfections whereas healthy foals infected with ECoV displayed moninfection
  • in foals, pre-existing ECoV infection may predispose to opportunistic secondary viral, bacterial or protozoal infections
  • vast majority of adults: ECoV is a monoinfection
43
Q

Describe the pathology associated with ECoV infection in adult horses

A
  • severe, diffuse, necrotising enteritis
  • marked villous attenuation
  • epithelial cell necrosis in tips of villi
  • neutrophilic and fibrin extravasation into SI lumen (pseudomembrane formation)
  • crypt necrosis
  • microthrombosis
  • haemorrhage
44
Q

Discuss the important biosecurity recommendation in outbreaks of ECoV infection.

A
  • routine management practices should be aimed at reducing likelihood of introducing and disseminating ECoV at any horse-based premises
  • horses developing or presenting with fever, anorexia and lethargy with or without enteric signs should be strictly isolated until dx is secured
  • once ECoV infection confirmed, strict isolation procedures (footbaths, PPE) and secondary quarantine of source stable of particular horse should be employed
  • infected horses may need to be isolated for > 14 days after cessation of clinical signs
  • post infection testing of clinical cases to prevent viral spread to other horses
  • all newly arrived horses on a farm should be isolated for at least 3 weeks
  • separate equipment for care of infected animals
  • vans and trailers thoroughly cleaned and disinfected (susceptible to common disinfectants)
  • examination of at risk horses for clinical signs of dz - twice daily rectal temp
  • importance of retesting in horses that are negative initially, particularly if not passing normal amounts of faeces

GI LA (9 decks)

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