3. Vibrio, Campylobacter, & Helicobacter

Question 1

Vibrio is gram ()?, oxidase ()?

Answer 1

Gram negative, oxidase positive

Question 2

Are vibrio motile or nonmotile, where are they found?

Answer 2

Motile, in water

Question 3

Vibrio bacteria is classified into 1. Non- halophilic / 2. Halophilic. What does each of them include?

Answer 3

• Non- halophilic ~ V. cholerae

* halophilic ~ V. parahemolyticus / V. vulnificus

Question 4

Is V.cholarae transmitted via a vector or just by drinking contaminated water?

Answer 4

Just by drinking contaminated water!

Question 5

V. Chlorae is a gram negative () shaped bacilli? Capsulated or not?

Answer 5

Comma shaped, NON- capsulated

Question 6

Is V.cholerae aerobic or anaerobic?

Answer 6

Aerobic .

Question 7

What is the enrichment media of v.cholerae?

Answer 7

Alkaline peptone water.

Question 8

What’s the selective media of v. Cholerae?

Answer 8

TCBS media (thiosulphate citrate bile sucrose agar)

Question 9

What color colonies does v. Cholerae have ?

Answer 9

Yellow colonies (sucrose fermenting colonies

Question 10

What’re the biotypes of v.cholerae?

Answer 10

Classical and El Tor

Question 11

What’re the somatic (0) antigen structure?

Answer 11

V.cholerae; O1 antigen structure

Non O1V.cholerae: no O1 antigen

Question 12

What is v.cholerae pathogenesity?

Answer 12

The causative agent of choler a in humans.
Causes irreversible activation of cAMP
Produces enterotoxin

Question 13

V. Choleral non - 01 (wl out somatic antigen)

Answer 13

Causes mild, bloody diarrhea
May produce toxins
Can cause epidemics

Question 14

Is v. Parahemolyticus salt-tolerant? And what does it cause?

Answer 14

It is salt-tolerant\halophilic vibrio.

Causes food poisoning. (Acute gastroenteritis)

Question 15

Is v. Parahemolyticus transmitted through a vector or just by contaminated water?

Answer 15

It is related to ingestion of sea good (fish and shellfish) (there is a vector)

Question 16

Is V. vulnificus a halophilic or non-halophilic vibrio?

Answer 16

Halophilic.

Question 17

Acute diarrhea caused by v.vulnificus following consumption of?

Answer 17

Shellfish

Question 18

Does campylobacter bacteria multiply in food (salmonellosis)?

Answer 18

No

Question 19

C. Jejuni and c. Coli pathogenesis ?

Answer 19

Commonest cause of infective diarrhea / invasive disease

Question 20

Complications of c. Jejuni and c. Coli?

Answer 20

• G1 hemorrhage
• Toxic megacolon
• Hus ( hemolytic uritic syndrome)
• Reactive arthritis (having an infection away from the original place of infection)
• Pyogensitonsiitis

Question 21

What’s the selective media of C.jejuni and c.coli?

Answer 21

Charcoal - based media containing antibiotics (to prevent the growth of unwanted bacteria)

Question 22

C. Jejuni and c-coli require microaerophilic environment for growth (high conc. Of CO2)

Answer 22

C jejuni is the commenest hydrolyse hippurate in 90-95% of infections.

Question 23

What’s helicobacter pylori?

Answer 23

Gram negative spirally-shaped
Microaerophilic
Man (only resevoir)
Oral-oral or fecal-oral rout for transmission.

Question 24

Helibacter pylori liveonly in?

Answer 24

Gastric mucosa .

Question 25

Minority of patients w/ helicobacter pylori develop ?

Answer 25

Peptide ulcer

Question 26

Long standing infection of helicobacter pylori is associated with?

Answer 26

Gastric cancer

Question 27

What are the non-invasive tests for helicobacter pylori?

Answer 27

1) serology: ELISA

2) urea breath:

Question 28

What’re some invasive tests for helicobacter pylori?

Answer 28

1- microscopy
2 - culture
3 - biopsy urease test: small portion of the biopsy put in a small quantity of urease solution (indicator, amonia production and change in pH

Question 29

What bacteria is actively involved in peptic ulceration?

Answer 29

H pylori

elimination of infection allows healing w/ out recurrence

Question 30

What’s the pathogenic mechanism of peptic ulceration

Answer 30

• The production of amonia by urease causes ionic changes in the mucus layer.
• production of toxins as lipopolysaccharide that activates inflammatory cells
• stimulation of an auto- immune response by production of antigens that cross-react w/ antral gastric antigens
• the degradation of mucus by a protesse