Test 3- Helicobacter and Lawsonia

Question 1

Helicobacter

Answer 1

Spiral-shaped or curved, flagellated, Gram negative

Originally classified as Campylobacter

Associated with gastrointestinal tract of humans and animals

In humans, H. pylori may cause:

– Persistent gastritis
– Peptic ulcer disease
– Gastric adenocarcinoma (?)

– Gastric mucosal-associated lymphoma (?)

In animals, disease spectrum of various species ranges from asymptomatic to gastritis to cancer

Question 2

Virulence Factors

Answer 2

• Flagella

–———-Provide motility for penetration of mucus and adherence to gastric epithelia

• Urease
–——– Hydrolyzes urea to ammonium

———————The ammonium neutralizes gastric acids

–———- Associated with inflammation

• Adhesins
–———— Sialic acid-binding adhesin (SabA)
–————- Blood group antigen-binding adhesin (BabA)

• LPS

——- Endotoxin; pro-inflammatory cytokine
–——- O-repeats prevent complement attachment

• Cytotoxin associated gene pathogenicity island (Cag PAI)

–———- Codes for T4SS
• Allows CagA protein into host cells

• Vacuolating Cytotoxin(Vac)

– Disrupts epithelial cell barrier

– Pro-inflammatory

• Cytolethal Distending Toxin (CDT)

– Very similar to that from C. jejuni

Question 3

Growth Characteristics

Answer 3

Microaerophilic (not aerobic)

Optimal grow at 37 ̊C

Flat, non-pigmented, non-hemolytic colonies

Slow growing

Fastidious(Selectivemedia)

– Vancomycin
– Amphotericin
– Trimethoprim

– Cefsulodin
– Lysed horse blood

Question 4

Ecology

Answer 4

Reservoir

– Gastric mucus layer of many animals- in the CRYPTS

– >50% of humans carry H. pylori

– 80-100% of dogs and cats are infected with at least one Helicobacter species

– 60% of slaughtered pigs infected with H. suis

Transmission
– Oral-oral and fecal-oral, perhaps

Zoonotic Potential

– Some evidence that humans and their pets are infected with similar strains

Question 5

Pathogenesis

Answer 5

Still not perfectly understood

The organism alters gastric physiology

————–– Urease

The organism adjusts to the gastric environment for persistence/colonization

Chronic inflammation- Hallmark of the disease

Pathological Changes

–—— Gastric pathological changes
——————— Hyperplasia, reduction of mucus, degeneration of glands, necrosis, variable inflammation

——–– Hepatic

———————-Inflammatory and necrotizing lesions

Question 6

Laboratory Diagnosis

Answer 6

• Stained smears of gastric mucosa

–———- Difficult (but not impossible) to identify organisms

• Urease test
• Difficult to isolate in culture

• Molecular methods

——– PCR

–——- Western Blot
–——– FISH (fluorescence in situ hybridization)

Question 7

Treatment and Control

Answer 7

• Controversial

– Most infections are subclinical

• Resistance to antimicrobials develops quickly
• Combination therapies seem effective

– Amoxicillin and metronidazole
– Amoxicillin and clarithromycin

– Bismuth subsalicylate(peptiobismol), omeprazole and/or famotidine for clinical gastric infections

Question 8

Lawsonia intracellularis

Answer 8

Lawsonia intracellularis

– Gram‐negative; Curved rods

Lawsonia

– Causes Porcine Proliferative Enteropathy

• Porcine

• Equine
• Other mammals, especially rodents

– May be associated with wet‐tail in hamsters

• Birds

– Obligate intracellular pathogen of enterocytes

• Apical cytoplasmic area

– Worldwide distribution

Question 9

Lawsonia generals

Answer 9

• Typical Gram negative

– Proper LPS

• T3SS
– Unknown role for effectors

• Reservoir

– Intestinal tract and environment

Lawsonia

– Rodents are possible reservoirs on horse and pig farms

• Transmission

– Fecal‐oral

Question 10

Pathogenesis of Lawsonia

Answer 10

• Interaction with unknown natural flora are required for disease

– Experimental inoculation of germ‐ free swine does not lead to disease

• Microbes escape the phagocytic vacuole, multiply, and inhibit host‐ cell maturation

– Enterocyte division continues and daughter cells are infected

• Usually affects distal jejunum and ileum
• Minimal to moderate inflammation

– Neutrophils, macrophages, and lymphocytes

Question 11

Answer 11

Lawsonia

thickened muscoa because Lawsonia causes the cells to multipy faster

“garden-hose”

Question 12

Dx and Immunity of Lawsonia

Answer 12

• Specific IgA response occurs

Lawsonia

• Recovered pigs are resistant to reinfection

• Diagnosis:
– Stained smears of intestinal mucosa

– Histological evidence of proliferative changes

– Immunohistochemical stains
– Isolation is not feasible for diagnosis
– PCR

Question 13

Treatment of Lawsonia

Answer 13

• Treatment:
– Tetracyclines

– Tylosin
– Tiamulin
– Lincomycin
– Carbadox (where available)

• Vaccine
– Oral vaccine; live attenuated – Available and commonly used