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24 Cards in this Set

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What general type of dz is associated with Aeromonas, vibrio, and plesiomonas?

Why are these three in the same category?
These are vibrio species.

Genera associated with ___waterborne__ infections
Major problems in aquatic species.
Also human problems-
1°: Vibrio cholerae, V. parahaemolyticus, V. vulnificus.
Vibrios are very important in __marine__ ecology
Bioluminescence, etc.
What are the characteristics and top three species of Campylobacter?
Kampylos= curved.

small, comma-shaped gram-negative rods

oxidase positive, catalase positive, _microaerophilic__ (this is the key term to associated with campylobacter - thrive in low oxygen, critical to ability to diagnose)

Several species, a couple are most common:

C. jejuni

C. coli

C. fetus

C. jejuni and C. fetus have more than one subspecies.
What is the physiology and structure of Camplyobacter species? What is the gram stain? Are they motile? In what oxygenic atmosphere do they thrive?
1. small (0.2 X 0.5-1 µm) Gram-negative curved (seagull) rod (0. 3 to 0.6 µm, small, will pass through 0.45 mm filters)

2. motile -single unipolar flagellum or 2 bipolar flagella. _corkscrew_-like darting motility in phase or darkfield microscopy.)

3. microaerophilic and capnophilic (likes CO2). C. jejuni = ~6% O, 10% CO84% nitrogen for best growth.
What are the primary hosts, dz, and reservoirs for the three campylobacter species?
Primary host Disease Reservoir
1. C. jejuni Humans, dogs gastrointestinal chickens
2. C. coli Humans gastrointestinal pigs
3. C. fetus
subspecies fetus intestinal tract of abortions sheep
sheep, goats, cattle still births cattle
subspecies venerealis cattle venereal disease cattle
reproductive tract transmitted bovine
infertility
sporadic abortion in cattle
Is Campylobacter zoonotic?
Serious __zoonotic__ problem.
Chickens, turkeys and raw milk are the main sources of Campylobacter spp.. Healthy pigs, cattle, dogs, cats and wild birds are also sources.
Surface waters such as rivers, lakes, etc., can be contaminated, and inadequately chlorinated water supplies have been known to cause widespread outbreaks of campylobacteriosis. Raw food materials likely to be contaminated: Chicken, turkey and other poultry; less commonly pork, beef and raw milk.
Is Campylobacter commensal in chickens?

What kills them better, heat or cold?
Yes - that's why it is so closely related to poultry.

Bacteria survive for several months in frozen minced meat
and poultry.

Campylobacters are very _heat_ sensitive: for example,
a ten-fold reduction in count takes approximately 6
seconds at 60°C.

Organism can survive for 5 weeks in water

or milk at 4°C.

Take home: Very sensitive to heat and drying, survives
well in a __cold, moist__ environment.
If C. jejuni is sensitive to stomach acids, how can it get through the stomach?

What is it's incubation period
Incubation period 24-72 hours

Disease can result from as few as 500 organisms.

Pathogen must survive the stomach but can inside
_undigested food_. Once past the stomach, organism
resides in the mucosal layer of the small intestine-
flagellar motility facilitates a corkscrewing into the
mucosae. One to 7 days after ingestion, disease will
result.

80% of patients may remain asymptomatic.

In those that are not, ten bowel movements a day. may
show grossly bloody stools.

Can last longer than 1 week.
What are the virulence factors of C. jejuni?
A.  Colonization aided by flagella
B. Adhesins
CadF (Campylobacter adherence to fibronectin) = 37 kDa protein
PEB1 = 28 kDa protein
JlpA = jejuni lipoprotein A = 42.3 kDa lipoprotein
C. Invasins - Cia proteins - invades mucosal surfaces of jejunum, ileum and colon.
• requires de novo protein synthesis
• facilitated by secreted proteins (type III), which presumably alter host cell signaling
• uptake requires host cell participation (microfilaments and microtubules)
D. Cytolethal distending toxin (CDT)
• CDT toxin is encoded by three adjacent genes termed cdtA, cdtB, and cdtC,
which encode proteins of approximately 30, 29 and 21 kDa,
• induces progressive cell distention (elongation and swelling to nearly 5 times
its normal size)
• causes cells to irreversibly arrest in the G2/M transition phase of the cell cycle
• prevents dephosphorylation of CDC2. CDC2 is the catalytic subunit of the cyclin-
dependent kinase and must be activated (dephosphorylated) for cells to enter
mitosis

CAMPY HAS A TOXIN THAT MESSES WITH THE HOST CELL CYCLE.
Can C. jejuni be treated with antibiotics?
VI. Treatment
1. Antibiotics (macrolide = erythromycin) will reduce severity and duration of disease,
and decreases the period of communicability.
2. Alternative = fluoroquinolone = ciprofloxacin / tetracyclines
3. Fluid and electrolyte replacement
Is Baytril used in poultry production?
No because of resistance, those it evidently is an effective treatment of the birds.

http://www.foodsafetynews.com/2010/10/straight-talk-about-feeding-antibiotics-to-animals/
How are Guillian-Barre Syndrome and Campylobacter connected?
Guillian-Barre Syndrome: an example of _chronic_ disease resulting from _actue_ infections.

Guillain-Barre syndrome (GBS), a neurologic disease that
produces ascending paralysis, affects people all over the
world. Usually fades with time.

Acute infectious illnesses precede 50%-75% of the GBS cases. Campylobacter infection is strongly associated with GBS. Evidence: Serologic surveys have demonstrated that sera from GBS patients contain anti-Campylobacter jejuni antibodies, consistent with recent infection. Culture studies have proven that a high proportion of GBS patients have C. jejuni in their stools at the time of onset of neurologic symptoms. Neurologic symptoms are more severe and more likely to be irreversible when GBS is preceded by C. jejuni infection. One of every 1058 Campylobacter infections results in GBS, and 1 of 158 Campylobacter type O:19 infections results in GBS.

Why does only a specific strain cause this?

humans have the exact same epitope that campylobacter jejuni has on its surface.

We will mount an immune response to the pathogen via innate and acquired means, but a small proportion of the immune response will be directed toward our own neurons.
What is the key difference between c. fetus and the other two (c. jejuni and c. coli)?
C. fetus = S-layer protein = a high mwt proteinaceous surface protein

• provides serum resistance
• prevents the binding of complement component C3b
• mutants lacking the S-layer have reduced virulence in a murine mouse model

This means that this pathogen can go systemic and can cause septicemia and infection where the other two campy's can't
What is the pathway that C. fetus would take to cause abortion?
Campylobacter fetus subspecies fetus
•  fecal-oral route of transmission
• colonizes intestinal tract of sheep, goats, cattle
• bacteremia
•  Organism becomes localized in the uterus - necrotic placenta (placentitis)
•  Abortion in late pregnancy - still born lambs
•  Can get necrotic lesions evident on the surface of the liver
•  Recovered ewes are immune for at least 3 yrs
What is the pathway that C. veneralis would take to cause infertility?
Campylobacter fetus subspecies venerealis
•  sexual transmission from an asymptomatic (carrier) bull to a cow
•  Also via artificial insemination, but semen prep conditions can kill the campy
•  Venereal disease = uterine invasion = infertility for 3 to 5 months until natural immunity develops (IgA in the vagina, IgG in the uterus). Will cause abortions in fertilized cows, more commonly infertility.
•  About 1/3rd of cows become carriers as the organism can persist in the vagina due to antigenic variation of the S-layer
Are the C. fetus subspecies treatable by antibiotics?
Campylobacter fetus subspecies fetus
•  Vaccination of ewes with a C. fetus subspecies fetus bacterin
(before and after mating, and a booster after the 2nd month of gestation)
•  Chlortetracycline to control outbreaks of abortion

Campylobacter fetus subspecies venerealis
•  Dihydrostreptomycin (administered either systemically or topically to bulls)
•  Interuterine administration of dihydrostreptomycin
•  Vaccination with a bacterin.
What is the aerotolerant Campylobacter?
Arcobacter

New genus of aerotolerant Campylobacter

May be associated with late term abortions in several species…. Common in bird tissue?

May be associated with human diarrheas, possibly zoonotic.

Possible cause of abortions, if no other cause can be ID’d.
What vibrio is commensal to the mammalian stomach?
Helicobacter species - rides the fine line between commensal and pathogen

•  Cultured from many mammalian __stomach_

•  Many different species.

•  H. mustelae: ferrets

•  H. pullorum: Chickens

•  __liver__ involvement: some species associated with liver disease in some animals

•  Mice and H. hepaticus, H. bilus

•  Helicobacter: Liver necrosis, abortions in sheep-crosses placenta

•  MAJOR HUMAN PATHOGEN: H. pylori-

May be ancestral in sheep
What is the physiology and virulence of helicobacter? What is it's key enzyme?
A.  Gram-negative, curved, spiral shaped bacterium.
C.  Highly motile with cork screw motion.
Lophotrichous flagella- penetration of mucin
C.  Microaerophilic.
E.  Highly active __urease__ enzyme.
Activity can be detected within minutes of inoculating test medium.
E. Other virulence factors: Cag pathogenicity island, cell
cycle toxins, adhesins (binds blood groups).
How do the virulence factors of Helicobacter function? (MAFU)
Virulence factors
A. Urease
1. Neutralizes gastric acid creating a relatively alkaline microenvironment.
•  Urea is hydrolyzed to ammonia (NH3) and carbon dioxide CO2
2. NH3 is:
•  Toxic to eukaryotic cells.
•  Proinflammatory - Stimulates monocyte and neutrophil chemotaxis.
3. Urease negative mutants cannot colonize.
B. Flagella
1. Aids in penetration of the gastric mucin layer.
C. Adhesins
1. Multiple--some use blood group antigens as receptors.
Example: BabA binds to Lewis b antigen (a carbohydrate found on
epithelial cells).
D. Mucinase
1. Degrades gastric mucin.
2.  Reduces the viscosity of the mucus.
How do you diagnose the presence of Helicobacter in the human stomach?
Urease converts urea to ammonia (basic) and CO2

Swallowing carbon-labeled urea, cleaved by urease. leads to the production of CO2 that is breathed out the lungs.
What did Koch use to make his postulates?

And for good measure, what are they?

What does this have to do with Barry Marshall?
Anthrax

1. The specific organism should be shown to be present in all cases
of animals suffering from a specific disease, but should not be found
in healthy animals.

2. The specific microorganism should be isolated from the
diseased animal and grown in pure culture on artificial laboratory
media.

3. This freshly isolated microorganism, when inoculated into a healthy nonimmune laboratory animal, should cause the same
disease seen in the original animal.

4. The microorganism should be reisolated in pure culture from
the experimental infection.

Barry decided to this experiment on himself.

Postulate 1. H. pylori associated with ulcer lesions. (Previously done)
Postulate 2. It could be isolated in pure culture. (Previously done)
• Checked stomach beforehand to make sure he was ulcer-free.
• Drank Helicobacter culture
Postulate 3. One week later experienced vomiting and nausea.
Postulate 4. Second week had biopsy taken of an inflamed lesion and isolated H. pylori from lesion.
Are ulcers curable?

What's their relationship with cancer?
Major concept: ulcers were curable,
gastric cancer was infectious in nature.
Where do Helicobacter live?
In the stomach.

There is evidence that they cause ulcer-like symptoms in multiple species.

Responsible for 90% of gastric and duodenal ulcers.
Each year, over 7 million Americans suffer from H. pylori related disease.
Helicobacter spp. present in 40-100% of cats
Other helicobacter in dogs, pigs, birds, nonhuman primates,
Horses and cows (cow milk and kid’s infections by Helicobacter)…?
How is Helicobacter spread?

How does it cause ulcers and cancer?
Probably spread host to host by fecal-oral route. This however is not clear.

H. pylori messes with the chemical environment (making it more acidic) disturbing the lining to cause ulcers. And messes with the eukaryotic cell cycle to cause neoplastic processes.

30% of US population infected

Duodenal (top of small intestine) ulcers:
•! Of that 30%, about 1% per year develop duodenal ulcer;
•! Nearly all persons with duodenal ulcer are colonized

Gastric ulcers:
•! 70% of persons with gastric ulcers are colonized with H. pylori.
Gastric adenocarcinomas:
• Most gastric adenocarcinomas and lymphomas are concurrent with or preceded by an infection with H. pylori.