C22 pt 2

Question 1

Yersiniosis
- gram
- how to tell apart species
- epidemiology, weather
- shedding, outbreaks

Answer 1

• Gram negative, Y. enterocolitica and Y. pseudotuberculosis
  o Must culture to tell apart (cold enrichment used)
• Epidemiology poorly understood, survives cold weather
  o Shed by carriers or wildlife, outbreaks usually under stressful conditions

Question 2

Yersiniosis
- pathogenesis

Answer 2

1. Invade enterocytes or M cells over Peyer’s patches
2. Recruit neutrophils (local suppurative inflammation)
3. Dissemination via lymphatics and portal vein
4. Chronic cases: giant cells wall off lesions (pseudotuberculosis)

Question 3

Yersiniosis in calves and deer?
- lesions
- less common presentations

Answer 3

• May cause fulminant fibrinous or fibrinohemorrhagic enterocolitis with diarrhea, mesenteric lymphadenitis, peritonitis, septicemia
• Hepatitis, abortion, mastitis, pneumonia less common

Question 4

Yersiniosis in lambs, calves, piglets
- signs
- lesions

Answer 4

• Sometimes causes gradual onset diarrhea and ill thrift
• Thickened mesenteric lymphatics and enlarged, edematous LNs
• Fluid GI contents

Question 5

Lawsonia intracellularis
- type of bacteria
- how to isolate
- causes what lesions? anatomic location
> symptoms
- mostly in what animals?

Answer 5

• Microaerophilic, nonflagellated, Gram -, curved or S-shaped rod
• Obligate intracellular pathogen – must use cell culture to isolate
• Causes proliferation of crypts in distal SI and/or LI
  o Loss of functional surface area causes diarrhea
  o Ill thrift and wasting due to protein loss
  <><>
  Mostly: piglets, foals
• also can infect dogs, rabbits, hamsters, ferrets

Question 6

Lawsonia intracellularis in piglets
* Porcine proliferative enteropathy (PPE)
- how important, geographic spread
- age
- severity
- mortality
- signs
- disease depends on…
- cells infected? adeonomatosis formation?
- lesions
> where
- shedding
- serosa appearance
- most common cause of what in pigs
<>
- PM

Answer 6

o Globally prevalent and important disease, mostly weaned pigs but anytime 3 weeks +
o Varying severity (subclinical to reduced growth to severe weight loss and diarrhea)
o Can have high mortality due to progressive cachexia, hemorrhage, or perforation
o Disease depends on interaction with other gut bacteria
<><><><>
1. Actively taken up by enterocytes
2. Replicate in dividing cells, causing proliferation of poorly differentiated cells (mechanism not known)
3. Elongation and branching of crypts/glands, mucosal thickening and villus atrophy
> Result is adenomatosis = thickened plaques on mucosa
<><><><>
o Lesions are most consistent in the ileum but can extend to the cecum and spiral colon
o Shedding persists for weeks after infection
o Cerebriform appearance of serosa is almost pathognomonic
o The most common cause of necrotic enteritis in pigs, necrosis can be superficial or full thickness and may progress to stricture
<><><><>
- Irregular mucosal thickening with folds and ridges
- May have ulcerated foci
- Coagulative necrosis with diphtheritic membrane

Question 7

Lawsonia intracellularis in piglets
* Proliferative hemorrhagic enteropathy (PHE)
- severity
- age, morbidity, mortality
- PM appearance, lesions
<>
- histo

Answer 7

o Severity ranges from acute exsanguination to gradual melena/hematochezia
o More common in young adults, sporadic and low morbidity but half of cases may die
o Pale carcasses with blood on perineum, cerebriform ileal serosa with bloody contents
<><><><>
- Silver stain shows bacteria
- Curved rods in apical cytoplasm
- Minimal inflammation

Question 8

Lawsonia intracellularis in foals
- what disease
- age
- signs
- gross lesions?
- origin?

Answer 8

• Equine proliferative enteritis (EPE)
  o Mostly seen in weanling foals: fever, lethargy, weight loss, diarrhea, hypoproteinemia
  o Gross lesions in ileum can be subtle to nonexistent
  o Severe or chronic cases resemble PPE in pigs (thickening, fibrinonecrotic membrane)
  o Possibly originated from a rodent reservoir?

Question 9

Spirochetal colitis in piglets
* Swine dysentery - agent?
- bacteria type
- age, infectivity
- transmission, outbreaks
- pathogenesis?
- morbidity, mortality, immunity
<>
- signs
- lesions
- anatomic location

Answer 9

Swine dysentery: Brachyspira hyodysenteriae
o Gram -, anaerobic, oxygen-tolerant, beta-hemolytic spirochete
o Highly infectious disease of weaned pigs (mostly 8-14 weeks old)
o Feco-oral transmission with outbreaks after introduction of carriers
o Pathogenesis poorly understood (invades enterocytes and produces endotoxin)
o Up to 90% morbidity and 30% mortality, usually produces immunity after recovery
<><><><>
- Fever, poor growth
- Watery malabsorptive diarrhea +/- blood, mucus, fibrin
- Cecum and spiral colon ONLY
- Erosion is limited to the epithelium because it does not invade deeper
- Often lots of mucus, fibrin, and hemorrhage, sometimes pseudomembranes

Question 10

Spirochetal colitis
* Porcine intestinal spirochetosis - agent
- bacteria property
- comparison to swine dysentery
- anatomic location
- lesions? histo?

Answer 10

• Porcine intestinal spirochetosis: Brachyspira pilosicoli
  o Weakly beta hemolytic, milder disease than swine dysentery, wider host range
  o Transient watery to mucoid diarrhea without blood, poor weight gain
  o Unlike swine dysentery, can colonize long term and does not elicit protective immunity
  o Lesions limited to cecum and colon
  <><>
• Severe case – fibrin mixed with necrotic debris on surface
• False brush border (early infection)

Question 11

Clostridial disease
- bacterial characteristics
- what’s needed for disease?
- species, mostly
- in circulation?

Answer 11

• Gram + rods, often commensals, some change needed to favour disease (diet, antibiotic treatment, reduced motility, other pathogens, etc)
• Disease mostly seen in herbivores and sometimes dogs
• Called enterotoxemia if produce toxins that are absorbed into circulation

Question 12

Clostridial disease
* Braxy
- agent?
- toxin and disease process
- species, age
- lesions
<>
- other disease causing claustridua
> blackleg
> botox
> Tyzzer’s

Answer 12

• Gram + rods, often commensals, some change needed to favour disease (diet, antibiotic treatment, reduced motility, other pathogens, etc)
• Disease mostly seen in herbivores and sometimes dogs
• Called enterotoxemia if produce toxins that are absorbed into circulation
• Braxy: C. septicum or C. sordelli
  o Sporadic, predisposing factors unknown
  o Toxin production leads to rapid onset of clinical signs and death
  <>
• lambs > calves
  <>
• Thickened, red, edematous, often emphysematous abomasum
  <><><><>
  Other possible clostridial diseases
  o C. chauvoei in tongue (’blackleg’)
  o C. botulinum (toxin ingestion and paralysis)
  o C. piliforme (Tyzzer’s disease, the only Gram - clostridium) sometimes causes mild enteritis

Question 13

Clostridium perfringens
- virulence due to?
> toxins, 4 types
> when are they produced
- Dx
<><>
- Toxinotypes
- toxins
> which are present in which types?
- effects of toxins
- which in healthy animals?
- which not in NA?

Answer 13

• Virulence is primarily due to 4 major toxins used to define toxinotypes
  o All are produced during active growth, if no toxins = nonpathogenic
  o Culture alone is not enough for diagnosis (some toxinotypes are commensals) – must
  demonstrate presence of toxin in gut contents
  <><><>
  TOXINOTYPES:
• A, C, D, E
  > type E common in healthy animals
  > Type B not present in NA
  <><><><>
  TOXINS
  Alpha - Cell membrane damage and necrosis
  > in every toxinotype
  <><>
  Beta - Pore-forming, causes intestinal necrosis. Inactivated by trypsin.
  > type B, C
  <><>
  Epsilon - Pore-forming, increases vascular permeability. Activated by enzymes including trypsin.
  > type B, D
  <><>
  Iota - Interferes with actin causing cell death. Activated by enzymes.
  > type E
  <><><><>
  Type A: alpha
  Type B: alpha, beta, epsilon
  Type C: alpha, beta
  Tye D: alpha, epsilon
  Type E: alpha, iota

Question 14

Clostridium perfringens A
- common? found where?
- causes what in wounds
- poultry dz
- canine dz
- calf dz

Answer 14

• Most common as a commensal and in the environment
• Cause of gas gangrene in wounds (like other Clostridia)
• Necrotic enteritis in poultry (implicated but not proven in other species)
• Cause of some cases of canine gastrointestinal hemorrhage syndrome
  o Peracute cases: sudden death with profuse bloody diarrhea
• Abomasitis and tympany in calves, especially ruminal drinkers
  o Reddening and ulcers; also common in normal calves

Question 15

Clostridium perfringens C
- geography
- what animals? why?
- colostrum impact
<>
- common? difference from other toxotypes?
- Dx, toxin?
<>
- signs, progression
- anatomic location

Answer 15

• Worldwide distribution, disease mostly in neonatal livestock and foals
  o Recall beta toxin is sensitive to trypsin – neonates have less trypsin
  o Colostrum also inhibits trypsin activity (to protect immunoglobulins)
  <><><><>
• Unlike other toxinotypes, uncommon in healthy animals
  o Need to isolate beta toxin to confirm disease, but toxin is unstable so absence does not rule it out as a cause
  <><><><>
• Disease similar in all species, usually within first hours to days of life
  o Acute necrohemorrhagic enteritis, can resemble venous infarction
  o Occasionally affects feedlot calves and adult sheep (‘struck’)
• Jejunum and ileum most affected

Question 16

Clostridium perfringens D
- small ruminant dz?
- toxin? lesions?
- associated risk
- presentation in sheep, goats
- subacute and chronic form name

Answer 16

• Enterotoxemia (pulpy kidney disease) is an important problem in small ruminants
  o Sometimes also affects cattle
  <>
• Most of the lesions are due to epsilon toxin
  o Absorbed and reaches brain, lungs, kidneys; damages endothelium
  <>
• Often associated with history of high grain or concentrate feeding but reason unclear o Poorly digested starch reaching small intestine?
  <>
• Varying presentations depending on age and species of host…
  o Usually no diarrhea or mucosal damage in sheep, necrotizing lesions in goats
  o Subacute and chronic forms also called focal symmetrical encephalomalacia (FSE)

Question 17

Clostridium perfringens D
- sheep, age affected and signs
- goats, signs
> vaccine, signs
<>
- lesions

Answer 17

• Lambs > 2 weeks old and kids: acute course
  o Found dead or brief neurologic signs
  o Endocardial hemorrhage, edematous lungs
  <>
• Adult sheep: usually subacute to chronic
  o Neurologic signs (FSE), not usually diarrheic
  <><><><>
• Adult goats: subacute
  o Hemorrhagic diarrhea, colic, convulsions
  o Death in 2-4 days, brain lesions less common than sheep
  <>
• Vaccinated adult goats: chronic
  o Watery diarrhea with blood and mucus, colic, anorexia
  <><><><>
• Good fat stores
• Straw coloured serosal fluid that clots when exposed to air
• Fibrinonecrotic enteritis in goats

Question 18

Clostridium difficile
- species
- where it lives
- what it does
- gut distribution
<>
- toxins, what they do
<>
- carriers
- toxinotyping

Answer 18

• horse, pig, rabbit, dog, cat, ostrich
  <><><><>
• Lives in soil and gut, common cause of hospital or antibiotic-associated diarrhea
  o Variable distribution in gut depending on age and species
  <><>
• 2 toxins produced, A (enterotoxin) and B (enterotoxin and cytotoxin)
  o Disable cell signalling pathways, interfere with cytoskeleton, promote release of
  inflammatory mediators
  o Result: apoptosis and inflammation with fluid gut contents
  <><>
• Carrier state is uncommon, but toxinotyping needed to rule out nontoxigenic strains

Question 19

Clostridium difficile in the horse
- age, lesion location
- signs, severity, mortality
- looks like?
- Ddx
- lesions

Answer 19

• Any age affected, lesions anywhere from the small intestine to the colon
  o Foals <1 month old mostly SI, older horses mostly colon
  <><>
• Variable clinical signs and severity
  o Diarrhea (consistent), fever, colic, injected mucous membranes, shock, DIC
  o Mortality 0-42%, lesions almost identical to C. perfringens C (can occur together)
  o Other differentials: salmonellosis, Potomac horse fever, NSAID toxicity
  <><>
• Multifocal hemorrhage/hyperemia
• Thickened by edema
• Pseudomembrane and watery contents

Question 20

Paratuberculosis (Johne’s)
- bacteria?
- Dx
- species

Answer 20

• Mycobacterium avium subspecies paratuberculosis (MAP)
• Slowgrowing–PCRtoconfirm
• Epidemiology best characterized in cattle, likely similar in other species
• Also occurs in these species:
• pigs, rabbits, sheep, deer, horses, llama, (humans?), (Other species infected but no disease)

Question 21

Paratuberculosis (Johne’s)
- infectious dose
- route of infection
- pathogenesis
- if infection is not cleared…. what hapens?
<><><><>
4 stages of infection
- which is most important source of infection?

Answer 21

• Infectious dose is higher for adults than neonates
  o Usually infection of calves via feco-oral or contaminated milk/colostrum
  o Enters via M cells or enterocytes over Peyer’s patches, invades macrophages
  o Prevents phagolysosome fusion to survive, triggers proinflammatory cell-mediated
  response that may clear infection
  o If infection is not cleared, eventually shifts to ineffective antibody-mediated response
  at the start of clinical disease
  <><><><>
• 4 stages of infection
  Most important source of infection!
  1) Silent: Infected but not shedding
  2) Subclinical: Infected and progressive shedding but no signs, lasts 2-5 years
  3) Clinical: Infected, shedding, signs present, rare in cows <2 years old
  4) Advanced clinical: Terminal stages of disease
  <><>
  Subclinical stage is the most important source of infection

Question 22

Paratuberculosis (Johne’s)
- lesions, anatomic location
- signs and lesions

Answer 22

• Lesions mostly seen in the ileum, colon, and draining lymph nodes
  o Granulomatous enteritis and villus atrophy, protein loss = wasting
  o Malabsorption and inflammatory secretion overload resorption = diarrhea
  <><><><>
• ‘Hosepipe’ diarrhea and wasting
• Keep eating and may have intermittent or progressive diarrhea for weeks before cachexia and wasting begin
• Mineral plaques in aorta
• Diffuse mucosal thickening into transverse rugae
• Lymphangitis (thickened lymphatics) characteristic, may eventually involve lymph nodes

Question 23

Paratuberculosis (Johne’s)
- in sheep and goats
> susceptibility
> incubation
> progression
> disease presentation
> lesions? histo?

Answer 23

• More susceptible than cows (especially goats), shorter incubation period o Exposure to higher doses in early life leads to faster progression
• Disease mostly in adults, chronic wasting without diarrhea
  o GI lesions sporadic and milder than cows, often few bacteria
  <><>
• skinny animals but lack of fecal soiling
• Acid-fast stain to show bacteria in cells – useful in all species

Question 23

Rhodococcus equi in foals
- where is it found?
- most important as what type of pathogen?
- lesions? why?
- bacteria in what cells?
- signs
<>
- also infects what animals

Answer 23

• Opportunist, normal flora in soil and GI tract, most important as a respiratory pathogen
  o 50% also have dose-related GI tract lesions
  o Likely due to swallowing bacteria-laden exudates coughed up from lungs
• Bacteria found inside macrophages
  <><><><>
• Pyogranulomatous typhlocolitis +/- lymphadenitis
• May form abscesses or cause peritonitis
• Crater-like ulcers that are worst over Peyer’s patches
• Mostly affects cecum and colon
• Causes chronic diarrhea, wasting
  <><><><>
  Also infects pigs, cattle, goats, humans (immunocompromised)

Question 24

Neorickettsiosis in horses
* Aka Potomac horse fever
- agent
- type of pathogen
- where it replicates
- geography
- life cycle / vector / route of infection

Answer 24

• Aka Potomac horse fever, caused by Neorickettsia risticii
  o Obligate intracellular pathogen that replicates in phagosomes
  o Originally described around the Potomac River but now widespread in North and
  South America
  <><><><>
• Flukes are the vector for the bacterium
• Infected mayflies drown in horse water buckets etc
• Accidentally ingested by horses
  <><><><>
• snail eats egg
  > cercariae leaves snail
  > infects aquatic insect > metacercaria
  > insect may be eaten by horse, which becomes accidental host

Question 25

Neorickettsiosis in the horse
- incubation, when are clinical signs?
- signs?
- severity? mortality?
- Dx
- lesions
- lesion location

Answer 25

• Incubation period 9-14 days, diarrhea occurs 1-3 days after onset of fever
• Variable severity, up to 30% mortality if untreated, confirm with PCR
• Endotoxic lesions, leukopenia, depression, inappetence, colic, lameness
  <><><><>
• Liquid, red-brown, foul smelling colon contents
• May have clusters of small (few mm) ulcers
• R dorsal colon worst
• Laminitis

Question 26

Campylobacter spp.
- pathogenesis
- signs in chickens, pigs
- signs in dogs, foals, lambs

Answer 26

o Attach to and invade enterocytes, pathology due to toxin production
o Chickens asymptomatic (C. jejuni), pigs asymptomatic or diarrheic (C. coli)
o Mild diarrhea in dogs, foals, weaned lambs

Question 27

Enterococcus spp.
- type of bacteria, can behave like what other bacteria sometimes?
- which ones can affect all species?

Answer 27

o Gram + cocci, mostly commensal but sometimes behaves like EPEC
o E. durans and E. hirae can affect any species

Question 28

Bacteroides fragilis
- type of bacteria
- some secrete what? consequence?

Answer 28

o Non-spore forming obligate anaerobe, usually commensal
o Some secrete a protease that damages enterocytes, but don’t adhere to mucosa