Vibrio, Camplyobacter, & Helicobacter

Question 1

Describe the characteristics of Vibrio Cholera.

Answer 1

Gram -

Curved rod

Facultive anaerobe

Has a single, polar flagellum

Chemoorganotrophic

Optimal growth is 20-30 degrees

Question 2

What does chemoorganotrophic mean?

Answer 2

These are organisms that organisms which oxidize the chemical bonds in organic compounds as their energy source

Question 3

How are different subsets of cholera divided?

Answer 3

Biotype (Biovar) - Different strains of the same bacterial species distinguished by a group of phenotypic or genetic traits.

Serogroup - Bacteria of the same species with different antigenic determinants on the cell surface.

V. cholera has more than 150 different serogroups but only two cause epidemic disease.

Question 4

How many chromosomes does V. cholera have?

Answer 4

Two circular chromosomes

Chromosome 1 is for larger cell functions / housekeeping

Chromosome 2 is smaller and carries integron island genes a/ antibiotic resistance genes

Question 5

How is Cholera spread?

Answer 5

Fecal-oral route

Question 6

What is the pathogenesis of V. cholera?

Answer 6

Cholera disease begins with the ingestion of contaminated water or food.

Those bacteria that survive the acidic conditions in the stomach are able to colonize the small intestine.

Question 7

What is responsible for the severe diarrhea that is characteristic of Cholera disease?

Answer 7

Cholera toxin (CT)

Question 8

What are the characteristics of Cholera Toxin?

Answer 8

Cholera toxin is a proteinaceous enterotoxin that is secreted by V. cholera.

Question 9

Describe the make up of Cholera Toxin?

Answer 9

Cholera toxin is made up of five (5) B subunits and Two (2) A subunits

Question 10

How does Cholera Toxin work?

Answer 10

The five B subunits bind to GM1 gangliosides on the intestinal cell membrane.

The two A subunits ribosylate the ADP on the GTP=binding protein.

This ribosylation activates membrane-associated adenylate cyclase which converts ATP to cAMP.

Elevated levels cAMP induces the secretion of NaCL and HCO₃ while inhibiting the absorption of these compounds.

This change in ion concentration in the lumen of the intestine leads to the secretion of large amounts of H₂O and electrolytes.

This ten leads to the watery diarrhea that is characteristic of Cholera.

This ultimately leads to death by dehydration if these imbalances are not corrected.

Question 11

What antigens are present in V. cholera?

Answer 11

O and H antigens but ONLY O antigens are useful in distinguishing pathogenic V. cholera species.

Question 12

What are the two biotypes (subdivisions) of the species of V. cholera?

Answer 12

There are two biotypes: Classic and El Tor

Question 13

What are outbreaks of Cholera due to?

Answer 13

Undercooked, contaminated seafood and contaminated water.

Question 14

How can V. cholera be identified?

Answer 14

V. cholera grows on standard media such as blood agar and MacConkey agars.

Thiosulfate-citrate-bile salt & sucrose media can also help with the isolation of V. cholera

Question 15

Is V. cholera oxidase positive or negative?

Answer 15

V. cholera is oxidase positive.

Question 16

How is Cholera treated?

Answer 16

Fluid and electrolyte replacement

Antibiotics are of limited value because they are flushed out with the diarrhea

Question 17

How is Cholera diagnosed?

Answer 17

Cholera is usually diagnosed based on the characteristics of the diarrhea.

Question 18

What are the characteristics of Campylobacter and Helicobacter?

Answer 18

These are Gram - and have a helical / spiral morphology. They also tend to be pleomorphic (Become coccoid when exposed to O² or prolonged culture time)

The shape of the bacteria help to facilitate penetration and colonization of mucosal environments

They are Microaerophilic and do not ferment or oxidize carbohydrates.

Question 19

Describe the history and characteristics of Campylobacter.

Answer 19

First isolated as Vibrio fetus in 1909 from spontaneously aborted livestock

Was not officially recognized as Campylobacter enteritis until 1970. Isolated from feces.

This is the most common form of acute, infectious diarrhea in developed nations. Has a higher incidence than Salmonella and Shigella combined.

Question 20

Describe the morphology and physiology of Campylobacter.

Answer 20

Small and thin (0.2 - 0.5 um X 0.5 - 5.0 um)

Helical (Spiral or curved)

Have a typical ‘gull-winged’ appearance with a typical Gram - cell wall

They have a tendency to form coccoid & elongated shapes when in prolonged cell culture or exposed to O₂

Have a distinctive, darting motility due to long, sheathed polar flagellum

Microaerophillic & capnophillic (5% O₂, 10% CO₂, & 85% N₂)

Thermophilic (42 - 43 ^o C)- This happens to be the body temp. of the natural avian reservoir

Question 21

What are the three most important Campylobacter species that are associated with human diseases?

Answer 21

C. jejuni - The reservoir are poultry, pigs, cattle, dogs, cats, birds, minks, rabbits, insects and it causes gastroenteritis, septicemia, meningitis, spontaneous abortion, and Guillain-Barre syndrome.

C. coli - Reservoir is pigs, poultry, cattle, sheep and birds. Causes all of the diseases that C. jejuni causes except for Guillain-Barre.

C. fetus - The reservoir is cattle and sheep. Causes all of the same diseases as C. jejuni except for Guillain-Barre.

Question 22

What is Guillain-Barre Syndrome (GBS)?

Answer 22

This is a low-incidence, self-limited autoimmune disease that is associated with Campylobacter jejuni infection.

Question 23

How does GBS start?

Answer 23

Specific bacterial O-antigens cross react with surface components of peripheral nerves. (Antigenic mimicry)

The immune system responds to this cross-reaction.

This causes an acute inflammatory demylenating neuropathy in 85% of the cases due to cross reaction with Schwann cells or myelin.

Question 24

Discuss the epidemiology of Campylobacteriosis.

Answer 24

Zoonotic infection

Birds are the reservoirs

Causes spontaneous abortions in cattle, sheep, and swine but usually asymptomatic in animals.

Humans acquire this via teh ingestion of contaminated food, esp. chicken, milk, or water. Fecal-oral transmission occurs as well.

Infectious dose is reduced by foods that neutralize gastric acids (Milk).

Contaminated polutry accounts for more than 1/2 of cases in developed countries.

Peak incidence occurs in children below 1 year of age and young adults 15-24 years of age.

In developing nations, this disease is hyperendemic with symptomatic disease occuring in young children and persistent, asymptomatic carriage in adults.

Question 25

What are the virulence factors associated with Campylobacter?

Answer 25

Endotoxin

Flagellum - Motility

Adhesins - Mediate attachment to mucosa

Invasins

S-layer protein in C. fetus

GBS is associated with C. jejuni serogroup O19

Extracellular virulence factors include enterotoxins and cytopathic toxins

Question 26

Discuss the pathogenesis and immune response to Camplyobacter.

Answer 26

Infectious dose and host immunity determine whether gastroenteric disease develops.

Some people infected with as few as 500 organisms while others need 106 colony forming units.

Pathogenesis is not fully understood

No good animal model exists

Damage to mucosal surfaces of the jejunum, ileum, and colon

Inflammatory process is consistent with invasion of the organisms into the intestinal tissue

Strains that are non-motile & adhesin-lacking strains are avirulent

Question 27

How are Camplyobacter species identified in a laboratory?

Answer 27

Examination of feces
& rectal swabs

Blood draws for C. fetus

Take care to avoid oxygen exposure

Selective isolation by filtration of stool specimen (0.45 um filter)

Enrichment broth & selective medias

Hippurate hydrolysis

Susceptibility testing (Nalidixic acid and Cephalothin)

Question 28

How Camplyobacter species treated?

Answer 28

Gastroenteritis from Camplyobacter species is usually self-limiting

Replinish fluids and electrolytes

Antibiotics can shorten the excretion period

Controls should be directed at domesticated animals to interrupt transmission to humans

To treat Guillain-Barre Syndrome, provide supportive care but intensive care is needed for up to 33% of cases

Question 29

Describe the history and taxonomy of Helicobacter.

Answer 29

First observed in 1983 in the stomachs of patients with type B gastritis (pylorus)

The important human pathogens are:

H pylori (Humans and no animal reservoir)

H cinaedi (Male homosexuals and rodents) - Colonize intestinal tract

H fenneliae (Male homosexuals and rodents) - Colonize intestinal tract

Question 30

What makes H. pylori and important human pathogen?

Answer 30

H. pylori is associated with chronic gastritis.

The stomachs of many animal species are also colonized.

Urease+ (Gastric strains only)

Mucinase+

Catalase+

Highly motile

Question 31

What is the morphology and physiology of Helicobacter?

Answer 31

Gram -

Helical 9Spiral or curved)

Cells become rod-like or coccoid on prolonged culture

Produce urease, mucinase, and catalase

H. pylori is lophotrichous with 4 to 6 sheathed flagella on one end.

Single polar flagella on H. fennellae and H. cinaedi.

Question 32

What is the epidemiology of Helicobacter infection?

Answer 32

See family clusters

Orally transmitted person-to-person (?)

~ 20% below age 40 are infected

~50% above age 60 are infected

H. pylori is uncommon in young children

In U.S., 30% of total population is infected and about 1% per year develop duodenal ulcer

Low socioeconomic status is a risk factor for infection

Hyperendemic in developing nations; most adults are infected but have no disease due to protective immunity

Question 33

Where does Helicobacter colonize?

Answer 33

Mucosal lining of stomach and duodenum in humans and animals

Most gastric adenocarcinomas and lymphomas are concurrent with or preceded by an infection with H. pylori

Question 34

What are the virulence factors for Helicobacter?

Answer 34

Multiple polar, sheathed flagella

Adhesins - Hemagglutinins

Mucinase - Degrades gastric mucus and causes localized tissue damage

Urase - Converts urea to bicarbonate and ammonia; this neutralizes the local acidic environment and causes localized tissue damage

Acid-inhibitory proteins

Question 35

How are Helicobacter infections treated?

Answer 35

Proton pump inhibitors

One or more antibiotics - Clarithromycin, amoxicillin, metronidazole

Bismuth compound

It should be noted that inadequate treatment results in the recurrence of symptoms