C23 Gastrointestinal Pathology VI Flashcards

1
Q
  • All parasites are more common than the diseases they cause
    o Helminthiasis = ?
    o Helminthosis = ?
A
  • All parasites are more common than the diseases they cause
    o Helminthiasis = infection with parasites
    o Helminthosis = disease caused by parasitic infection
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2
Q

Helminths: general considerations
* 5 categories of pathologic effect:
- strategy
- pathogenicity
- possible sequelae
- examples

A
  1. Live free in lumen, compete for nutrients
    - pathogenicity: Low unless very high burdens
    - possible sequelae: Physical obstruction
    - eg. Cestodes, some adult nematodes (ascarids)
    <><><><>
  2. Blood loss via direct consumption or mucosal damage
    - pathogenicity: Moderate-high
    - possible sequelae: Anemia
    - eg. Nematodes
    <><><><>
  3. Protein-losing gastroenteropathy due to inflammation
    - pathogenicity: Moderate
    - possible sequelae: Wasting, anorexia
    - eg. Nematodes, some trematodes
    <><><><>
  4. Physical trauma to gut wall due to adult feeding or larval emergence
    - pathogenicity: Moderate-high
    - possible sequelae: Perforation, adhesions
    eg. Nematodes and trematodes
    <><><><>
  5. Damage to sites distant from gut, usually migrating larvae
    - pathogenicity: Moderate-high
    - possible sequelae: Depends on tissue
    - eg. Mostly nematodes, some cestodes
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3
Q

Diagnosing helminthosis requires three criteria:

A

1) Helminth is present in sufficient numbers to cause disease
2) Lesions typical of the helminth are present
3) The clinical syndrome is compatible with the pathology caused by the helminth

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4
Q

Nematodes
* Nematodes of herbivores tend to have similar direct life cycles…

A

GIN eggs on pasture, from poop
> infective larvae in grass
> ingested
> winter: hypobiosis
> adult GINs
> ~21 dats
<><><><>
Mixed infections are typical

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5
Q

Nematodes
* Ostertagiosis
- agent in cattle and sheep?
- geography
- signs
- pathogenesis, lesions

A
  • Ostertagiosis: Ostertagia ostertagi in cattle, Teladorsagia circumcincta in sheep
    o Important abomasal parasite in temperate regions
    o Subclinical production losses, clinical diarrhea, wasting, death
    <><><><>
  • Infective larvae invade gastric glands
  • Cause inflammation, mucous metaplasia, and glandular hyperplasia before emerging
  • Adults live in lumen (too small to see easily)
    <><>
  • Thickened mucosa at sites of larval penetration In heavy infection, ‘Morocco leather’
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6
Q

Nematodes
* Ostertagiosis
- type I and II disease
> age groups, what happens
> signs
- Dx
<><>
- when can we see type II and I
- diarrhea?
- PM lesions

A

o Type I disease: young animals under high challenge
o Lots of worms develop at once, causing chronic gastritis
<><>
o Type II disease: yearlings, due to synchronous emergence of hypobiotic larvae o Acute gastritis that can be fatal
<><>
- damaged gland > Reduced acid, Leakage of pepsinogen into bloodstream > Diarrhea (cows only), Loss of appetite, wasting
<><>
Confirm via abomasal pH, worm count (must digest to see larvae), plasma pepsinogen
<><><><>
o Periparturient rise in females when hypobiotic larvae resume development (type II)
o Disease in adults and young animals on contaminated pasture (type I)
o NO DIARRHEA
<><>
- carcass pallor
- Hydropericardium +/- ascites, hydrothorax

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7
Q

Nematodes
* Haemonchosis
- species, agents
- geography
- feeding
- environmental survival
- signs in acute and chronic cases? burdens?

A
  • Haemonchosis: H. contortus in small ruminants, H. placei in cattle
  • can also affect llamas
    o Major abomasal pathogen in tropical areas and climates with warm summers
    o Adults and late-stage larvae are voracious blood feeders (~0.05 mL/worm/day)
    o Able to survive environmental extremes via hypobiosis
    <><><><>
    Aka barberpole worm Large adults (~2 cm)
    <><><><>
    Acute/peracute: heavy burdens
  • Severe anemia and hypoproteinemia
  • May die suddenly and before patency
  • Weak, exercise intolerant
    <><>
    Chronic: lower burdens
  • Bottle jaw (edema) due to hypoproteinemia more common than in acute cases
  • Death due to iron deficiency
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8
Q

Nematodes
* Trichostrongylus spp.
- mostly what agent
- species?
- anatomic location? signs?
- pathogenesis
- clinical signs due to…
- signs? why?
- Dx

A

sheep, cattle
<><><><>
* Trichostrongylus spp.: mostly T. colubriformis
o Infects SI, causing production loss, ill thrift, diarrhea, death
o Larvae tunnel in epithelium and adults remain partly embedded
o Causes villus atrophy and hyperplastic crypts
o Clinical signs due to loss of plasma into gut, gross lesions are nonspecific
o May see edema and effusions in non-dehydrated animals due to hypoproteinemia
<><>
typical GIN eggs in feces

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9
Q

Nematodes
* Trichostrongylus axei
- species?
- anatomic location
- mechanism?
- lesions
- signs?
- Ddx?
<><>
- in the horse?
- lesions?

A
  • sheep, cattle
  • Trichostrongylus axei
    o Abomasal/gastric nematode, often mixed infection but high solo burdens pathogenic o Similar mechanism of pathology to T. colubriformis
    o Mucous metaplasia/hyperplasia forms raised white plaques or nodules
    o May cause achlorhydria in heavy infection, causing diarrhea (especially in cattle)
    o Plasma pepsinogen increases, causing inappetence and wasting
    o Main differential is ostertagiosis, but intraepithelial location is distinctive
    <><><><>
    Horse:
    o Uncommon, usually in horses grazed with ruminants
    o Stomach lesions are commonly seen in chronic infections
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10
Q

Nematodes
* Strongyloides spp.
- who is affected?
- forms?
- parasitic forms are always ___
- free living issues?
- go through what tissues?
- cause what issue with heavy burdens? how?
<><>
horse
pig
cat
dog
cattle
sheep
- what strongyloides spp., and what do they cause in each?
<><>
-eggs?

A

o Different species affect all domestic mammals, free-living and parasitic forms
o The parasitic forms are all female (parthenogenesis)
o Free-living forms undertake sexual reproduction and larvae penetrate skin
o Migrate through lungs before reaching gut via mucociliary escalator
o Tunnel in epithelium at junction of villus and crypt, causing crypt atrophy and inflammation in heavy burdens
<><><><>
Horse: S. westeri
- Diarrhea
- Fatal in high burdens
<><>
Pig: S. ransomi
- Diarrhea
<><>
Cat: S. felis
- Pneumonia (migration)
<><>
Dog: S. stercoralis
- Commonly fatal in puppies up to 2-3 months old
- Blood-tinged diarrhea, dehydration, emaciation
<><>
Sheep and cattle: S. papillosus
- Diarrhea
- Sometimes death
<><><><>
Larvated eggs (unlike other nematodes)

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11
Q

Nematodes
* Nematodirus spp.
- species
- amatomic location?
- temperature
- pathogenesis
- disease course
- lesions

A
  • sheep, cattle
    o Infects proximal SI, often needs cold exposure for eggs to hatch
    o Larvae mature in deep mucosa, then emerge to coil around villi -> malabsorption
    o Annual disease in youngstock: severe dark green diarrhea, anorexia, wasting, death
    o Nonspecific gross lesions (‘cotton wool’ appearance of adults)
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12
Q

Nematodes
* Oesophagostomum spp.
- species
- pathogenesis?
- lesions
- possible outcomes
- possible signs
- cattle vs pig dz

A
  • sheep, (cattle, pigs)
    o Larvae encyst deep in mucosa, producing
    inflammatory nodules
    o Resembles pimples up to 1 cm projecting
    from serosa with caseous contents
    o Usually incidental but can cause
    adhesions or peritonitis
    o Adults in colon lumen cause anorexia,
    diarrhea, ill thrift
    o In cattle, larvae cause protein loss
    o Mild and subclinical in pigs
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13
Q

Nematodes
* Cooperia spp.
- species
- location
- winter
- pathogenesis, signs

A

o Most important in cattle, infects upper SI, capable of hypobiosis
o Coils around villi like Nematodirus spp. -> inappetence, poor growth, diarrhea
<><>
- can also affect sheep

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14
Q

Nematodes
* Chabertia ovina
- appearance
- pathogenesis
- signs
- species

A

o 1-2 cm long, thick nematode of colon, feeds on plugs of mucosa
o Hemorrhage and protein loss due to physical trauma
o Nonspecific clinical signs (ill thrift, diarrhea +/- blood)
- sheep, cattle

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15
Q

Nematodes
* Strongyles in the horse
- common in what anatomic locations?
- two subfamilies, what they feed on, notes

A
  • Strongyles are common in the cecum and colon and fall into two subfamilies:
    o Strongylinae (large strongyles): mostly Strongylus spp., blood or plug feeders with
    extensive extraintestinal migratory phase
    o Cyathostominae (small strongyles): 8 genera, adults feed on gut contents so cause
    limited pathology but synchronous larval emergence can be damaging
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16
Q

Nematodes
* Large strongyles in the horse
- which is most important
> common?
> issues?
> signs?
> lesion?

A

o Strongylus vulgaris most important
o Once rare due to anthelmintics but becoming more common due to resistance o Larvae cause endarteritis of cranial mesenteric artery
o Can cause colic due to colon infarction (mostly in young horses)
o Eventually return to gut via arteries and rupture into the lumen
o Feeding of adults causes anemia and ill thrift
<><>
- verminous arteritis does not always cause infarction

17
Q

Nematodes
* Large strongyles - S. edentatus
- common? problematic?
- what it causes?
- lesions?

A

o S. edentatus is now uncommon and largely considered incidental
o Migrates through liver – implicated as cause of fibrous tags (but these are common
despite the nematode being rare)
o Hemomelasma ilei may also be related to large strongyles (controversial)
<><>
- Raised, subserosal hemorrhagic plaques on antimesenteric border of ileum +/- colon
- Incidental finding

18
Q

Nematodes
* Small strongyles in horses
- how common?
- pathogenicity? resistance?
- larva? in what age group?
- life strategy?
- morbidity, mortality? why?
- clinical signs?
- lesions?

A

o Common, >50 species, adults are nonpathogenic, anthelmintic resistance widespread o Larval cyathostominosis seen in horses >1 year old, limited resistance to reinfection
o Larvae can undergo hypobiosis during winter and emerge in spring
o Significant morbidity and mortality due to synchronous re-emergence of larvae from
mucosa but nonspecific clinical signs (diarrhea, edema, anorexia)
o May see tiny (mm) red-black nodules in the mucosa
> Each of these is an encysted larva!

19
Q

Nematodes
* Hookworms - Ancylostomatidae
- where do adults feed? which are zoonotic?

A

o Adults feed in SI, all are zoonotic (mostly cutaneous larval migrans)

20
Q

Nematodes
Ancylostoma caninum
- host
- route of infection
- pathogenesis

A

Dogs
<><>
Route of infection:
- Oral (direct to gut)
- Skin penetration (via blood to lungs then gut) - Lactogenic (dormant larvae move from muscles of bitch to mammary gland)
- Transplacental
<><>
Pathogenesis:
- Ingest large tissue plug, penetrate deep into mucosa and produce anticoagulant to facilitate blood feeding
- Blood loss (0.2 mL/worm/day) leads to anemia and hypoproteinemia

21
Q

Nematodes
Uncinaria stenocephala
- host
- route of infection
- pathogenesis

A

Dogs
<><>
Route of infection:
- Mostly oral
- Percutaneous inefficient
- NOT lactogenic or placental
<><>
Pathogenesis:
- Not a blood feeder – less pathogenic
- Malabsorptive protein loss can cause hypoproteinemia but not anemia
- Lethargy, inappetence, ill thrift

22
Q

Nematodes
Bunostomum spp.
- host
- route of infection
- pathogenesis

A

Ruminants
<><>
Route of infection:
- Oral and percutaneous only
<><>
Pathogenesis:
- Similar to Ancylostoma caninum but longer prepatent period

23
Q

Nematodes
* Ancylostoma caninum
- puppies more prone to what?
- fatal? age? route of infection?
- death timing? skin?
- adult appearance, burden
- signs, lesions

A

o Suckling puppies more prone to nonregenerative anemia due to poor iron reserves
o Fatal disease most common in 2-3 week old pups infected via milk
o May die before patency, sometimes causes dermatitis in contaminated environments
o Adults are 1-1.5 cm and red (as few as 20 may cause death of young pups)
<><>
- Pallor, subcutaneous edema and cavity effusions, lung hemorrhages, cachexia (chronic)

24
Q

Nematodes
- Ascarids cause disease via…..
- ascarid life cycle

A
  • Ascarids cause disease via larval migration and adults in the SI
    <><>
  • unembryonated egg in feces
    > infective egg with L3 larva
    > ingestion of infective egg
    > larva migrate to bronchi and are swallowed
    > hatched larvae penetrate the large intestinal wall and migrate via the liver to the lungs
    => reach liver via portal circulation
    > coughed, swallowed
    > larvae establich in the small intestine and become patent at week 6-8
25
Q

Nematodes
* Ascaris suum
- size, life cycle
- housing?
- heavy infection outcome
- light infection outcome
- lesions? species?

A

o Large (up to 40 cm), direct life cycle
o Uncommon in housed pigs
o Heavy infection can cause obstruction
o Lighter infection can cause inappetence
or may have little clinical effect
o Larval migration causes liver and lung
hemorrhages
o Can also cause lung lesions in other
livestock species, may even cause fatal
pneumonia in calves
o ZOONOTIC
<><>
- Milk spotted liver: healed (fibrotic) migratory lesions
> Not clinically significant, financial losses due to condemnation
- May cause respiratory signs (dyspnea, colloquial ‘thumps’)

26
Q

Nematodes
* Parascaris equorum
- life cycle
- age
- signs, outcomes
- size, what they do
- immune response?

A

o Similar life cycle and pathology to A. suum
o Common in foals, causes ill thrift, sometimes obstruction, intussusception, perforation
o Large, up to 50 cm, does not cause protein loss but reduces feed intake
o Larvae killed by immune response during migration in yearlings and adults