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Transcript
Vibrio Infections
Michael Addidle
Vibrios
Taxonomy
Species
Genera
V. cholerae
V. vulnificus
Family
Vibrios
V. parahaemolyticus
Vibrionaciae
Non-enteric,
fermentative, gramnegative rods that are
oxidase positive and
motile by means of a
polar flagella
Aeromonas
Plesiomonas
(amongst others)
Vibrios
• Most vibrios require saline for growth.(halophilic).
However Vibrio cholerae & Vibrio mimicus can survive in
both saltwater and freshwater.
• Prefer alkaline environments.
• Flourish in shallow waters with temperatures greater
than 20 degrees. Ie Estuarine environments in the
summer.
• Survive quite happily in filterfeeding shell fish, such as
oysters and pipis.
• Greater than 90% of clinical disease due to vibrios in NZ
occurs during the summer months.
Vibrio cholerae
Aetiological agent of cholera
Divided into Serogroups on basis of O (somatic
antigen)
Only serogroups 01 and 0139 are associated with
epidemic and pandemic cholera. Often clinically more
serious because of production of classical cholera
toxin.
Vibrio cholerae: bacteriology
• Curved gram negative
bacillus
• Single polar flagellum
• Flagellar H antigen and
somatic O antigen.
• O antigen used to classify
V. cholerae into
serogroups (01 and 0139
are most well known)
• Two biotypes of 01
(classical and El Tor)
History of Cholera
• “Cholera like illness” described by Hippocrates circa
500 BC
• Cholera means “flow of bile”
• The Italian doctor Filippo Pacini was the first to
discover the cholera bacterium (Vibrio cholerae) in
1854 when cholera hit Florence.
• The first recorded cholera pandemic of 1817-1823
spread from India to Southeast Asia, Central Asia,
the Middle East and Russia.
• 1961-1970s - Seventh pandemic began in
Indonesia, called El Tor. Has since spread to many
countries.
Epidemiology of Vibrio cholerae
•
•
•
•
•
Large infective dose required. Person to person
spread uncommon. Most common where poor
sanitation and in particular where mass
displacement of population has occured
Usually acquired through contaminated food or
water. Avoidance of unboiled water, ice cubes, food
from street vendors, undercooked seafood.
To cause infection, organisms must first pass the
highly acidic secretions in stomach. (alkaline
loving) Infecting dose 10,000,000,000 orgs
Therefore people with gastrectomy or on ant- acids
are more susceptible. 100-1000 orgs.
Incubation period few hours to 5 days.
Vibrio cholerae: Pathogenicity
• Classical cholera 01/0139 strains usually produce a
classical toxin. Non 01/0139 strains usually don’t
• Classical Cholera toxin:- Non-invasive, consists of A
and B subunits. B subunit facilitates binding and A
subunit activates Adenylate Cyclase, leading to
increase in cAMP in enterocyte.
• cAMP leads to increased Chloride excretion from the
enterocyte and decreased sodium reabsorption,
leading to osmotic gradient, and water passes out of
the cells into the intestinal lumen. “Rice water stool”
• Many non-01/0139 strains are “non-toxigenic”.
Actually other toxins some of which are invasive.
It has also been hypothesized that the cystic fibrosis genetic mutation has
been maintained in humans due to a selective advantage: heterozygous
carriers of the mutation (who are thus not affected by cystic fibrosis) are
more resistant to V. cholerae infections.
“Cholera gravis”
•Most people asymptomatic or mild illness
only. However shed bacteria for 1-2 wks into
the environment.
• Severe illness, dehydration renal failure,
metabolic acidosis and death.
Diagnosis of Cholera
• In epidemic “field situation”, dark field or wet film
showing motile comma shaped bacteria usually
sufficient. Motility inhibited by specific anti-sera.
• Stool can be cultured in Alkaline Peptone water
to select out vibrios.
• TCBS (Thiosulphate Citrate Bile Salts) agar or
Tellurite Taurocholate Gelatin Agar (TTGA).
• Yellow oxidase positive colonies are suspicious
• Suspicious colonies confirmed using API20E
• V cholerae 01 and 0139 strains can be detected
with specific anti-sera.
• Latex agglutination, EIA or PCR can be used to
look for cholera toxin
TCBS Medium
The high concentrations of thiosulfate and citrate and the strong alkalinity of this medium
largely inhibit the growth of Enterobacteriaceae. Ox bile and cholate suppress
primarily enterococci. Any coliform bacteria, which may grow, cannot metabolize
sucrose. Only a few sucrose-positive Proteus strains can grow to form yellow,
vibrid-like colonies
Treatment of Cholera
• Aggressive rehydration is necessary for
serious cases.
• Tetracyclines are the drug of choice.
However in some parts of the world,
resistance is becoming a problem.
Quinolones also have good activity.
• In pregnant and breastfeeding women,
and children, Azithromycin is useful.
Cholera Vaccine
• Parenteral whole cell killed vaccine is
available. Only 50% protection from 01 for
6 months, not recommended by WHO
• Oral, killed, whole cell vaccine licensed for
use in Europe, 1-2yrs protection after 2
doses.
Vibrio vulnificus
• First identified in the 1970s, can cause serious
wound infections and septicaemia.
• Usually infects patients with
immunocompromise, particularly patients with
underlying liver disease.
• V. vulnificus found commonly in saltwater
estuarine environments. (Isolated from virtually
all oysters harvested in the Chesapeake Bay
and the United States Gulf Coast when water
temperatures exceeded 20ºC)
Vibrio vulnificus: Pathogenicity Factors
• Polysaccheride Capsule
Anti-capsular antibodies are
protective
• Iron
– Bacterial growth in human serum is directly
related to percentage transferrin saturation
with iron.
Vibrio vulnificus Infection:
Acquisition
• Eating uncooked shellfish(especially in
summer)
• Wading in shallow estuarine environments
where patient has skin breaks to the legs.
Risk Factors for Vibrio
vulnificus septicaemia
• Alcoholic cirrhosis — 31 to 43 percent
• Underlying liver disease including cirrhosis
(unspecified etiology) and chronic hepatitis — 24
to 31 percent
• Alcohol abuse without documented liver disease
— 12 to 27 percent
• Hereditary hemochromatosis — 12 percent
• Chronic diseases such as diabetes mellitus,
rheumatoid arthritis, thalassemia major, chronic
renal failure, "preleukemia", and lymphoma — 7
to 8 percent
Diagnosis of Vibrio vulnificus
Infection
•
•
•
•
Severe clinical picture
Blue Green colonies on TCBS agar
Halophilic
API20E will give you a good idea, but other
Vibrio species closely related biochemically.
Treatment of Vibrio vulnificus Infection
• Should consist of a 3rd generation
Cephalosporin and a Tetracycline
• Newer fluoroquinolones also effective.
• Macrolides probably are also effective.
Vibrio parahaemolyticus : What
diseases does it cause?
• Causes seafood associated diarrhoeal
illness(usually oysters), and less commonly
wound infections & septicaemia.
• Pathogenicity associated with production of a
thermostable haemolysin (Vp-TDH) in most
cases.
• A lot of V. parahaemolyticus bacteria don’t
contain pathogenicity factors and are nonpathogenic.
Vibrio parahaemolyticus
How is it diagnosed and treated?
• TCBS agar. Alkaline peptone water may be used
as an enrichment broth, particularly when
culturing stools.
• Non-sucrose fermentor, therefore blue-green
colonies on TCBS.
• API 20 E ID, ?with additional NaCl
• Clinically significant isolates will generally either
be haemolytic or be urease positive.
• Again treatment of severe disease should
involve a 3rd generation cephalosporin and oral
tetracycline
Other Vibrios
V. fluvialis
V. mimicus
V. furnissii
V. Hollisae
V. alginolyticus
V. damsela
Diarrhoeal Illness
Wound Infections
Summary
• Vibrios can cause serious disease. The main
three are V.cholerae, V. vulnificus & V.
parahaemolyticus.
• Appropriate plates should be set up when
clinically suspected.
• Reasonably easy to identify to Vibrio genus
level, more difficult sometimes to get the
species.