Microsoft powerpoint - the genus vibrio_web [režim kompatibility]
THE GENUS VIBRIO, CAMPYLOBACTER CAM AND ASSOCIATED BACTERIA (AEROMONAS, HELICOBACTER, PLESIOMONAS) General Characteristics of Vibrio, Aeromonas and Plesiomonas
· Gram-negative· Facultative anaerobes· Fermentative bacilli · Polar flagella · Oxidase positive
Ø Formerly classified together as Vibrionaceae
· Primarily found in water sources · Cause gastrointestinal disease
l Vibrio, Campylobacter, Aeromonas, Plesiomonas and Helicobacter species are gramnegative rods, that are all widely distributed in nature.
– Vibrio sp. are found in marine and surface waters. Some of
them can cause a disease in man as well as in marine vertebrates and invertebrates. Vibrio cholerae produces an enterotoxin that cause cholera, a profuse watery diarrhea that can rapidly lead to dehydration and death.
– Aeromonas sp. is found predominantly in fresh water and in
– Plesiomonas sp. exists in both cold- and warm-blooded
animals, including many domesticated animals.
– Campylobacter sp. is a common cause of enteritis in humans.
Less commonly, Aeromonas sp. and rarely, Plesiomonas sp. have been associated with diarrheal disease in humans.
– Helicobacter pylori has been associated with gastritis and ulcer
The VIBROS
l Among common pathogenic vibrio species belong:
– V. cholerae, V. parahaemolyticus, V. vulnificus,
V. alginolyticus, V. mimicus.
– into non-halophilic vibrios, including V. cholerae, that
are able to grow in media without added salt,
– and halophilic species which do not grow in these
media, they require higher contents of salt. The VIBROS
l Morphology:
– gramnegative rods, non-spore forming, motile (polar flagellum)
Vibrio The VIBROS pathogenity
l V. cholerae serotype O1 causes cholera in humans, while
other vibrios may cause sepsis, enteritis and other infections.
– V. cholerae serotype O1: epidemic and pandemic cholera
– V. cholerae serotype non O1: choleralike diarrhea, mild diarrhea,
– V. parahaemolyticus: gastroenteritis, possibly extraintestinal
– other (V. mimicus, V. vulnificus.): ear, wound, soft tissue and
other extraintestinal infections, all uncommon
Vibrio cholerae
l Gramnegative, slim, curved rods about 2 to 4 mm long.
l Cell may be linked end to end, forming "S" shapes and
l They are non-spore forming and do not form a capsule.
l Cholera vibrios are motile with a single polar
flagellum. Their motility is extremely rapid.
lThe bacterium Vibrio cholerae
– Humans are one of the reservoirs of this
– It is also often found in the aquatic
environment and is part of the normal flora of brackish water.
– It is often associated with algal blooms
(plankton), which are influenced by the water temperature.
lCholera in the world Vibrio cholerae
l V. cholerae can grow aerobically or anaerobically on a
l Vibrios grow at a very high pH (8.5 to 9.5) and are rapidly
l In alkaline peptone water they produce a turbidity and
surface membrane in six hours of incubation.
l V. cholerae grows in convex, smooth, round colonies on
l Vibrios grow well on thiosulfate-citrate-bile-sucrose
(TCBS) agar on which they form yellow colonies.
l Vibrios are oxidase-positive, which differentiates them from
enteric gramnegative bacteria grown on blood agar.
l V. cholerae strains produce catalase. Vibrios form acids
Vibrio cholerae is divided biotypes
– causes severe forms of cholera with a high
– does not hemolyse on blood agar,– does not agglutinate chicken, sheep or human
– it is susceptible to polymyxin B.
– all the properties has just opposited as given above. Vibrio cholerae antigenic structure
l Many cholera vibrios share a single heat-labile
flagellar H antigen. Antibodies to the H antigen are probably not involved in the protection of susceptible host organisms.
l V. cholerae has cell wall lipopolysaccharides that
confer serological specifity as somatic O antigens. There are more than 140 antigens. Vibrio cholerae antigenic structure
l V. cholerae strains causing classical epidemic
cholera belong into the O1 group. They are classified as V. cholerae O1.
l Strains of other serogroups are classified as V. cholerae non O1 or non-agglutinated vibrios s.c. NAG vibrios (they do not agglutinate in anti-O1 serum) or non-cholera vibrios s.c. NCV. Many of these vibrios may cause diarrhea in humans as s.c. cholera-like disease or gastroenteritis of travellers. Vibrio cholerae antigenic structure
l The V. cholerae serogroup O1 antigen has
determinants A, B, C that make possible further subdivison into three serologic subtypes:
Vibrio cholerae toxicity
– it has only a negligible significance as a virulence factor.
– it is a main factor of pathogenity,– it is heat-labile protein which can be changed by formol into
– synthesis of cholera toxin is controlled by chromosomal
gene. Its molecule is a complex of multiple polypeptide chains organized into a toxic unit A, consisting of A1 and A2 subunits, and unit B. Vibrio cholerae toxicity
l The B unit mediates tight binding to a cell wall ganglioside
of enterocytes in the small intestine. It means
subunit B, which promotes entry of subunit A into cell.
l Activation of subunit A1 yields increased levels of
intracellular cyclic AMP (adenosine monophosphate) and results in prolonged hypersecretion of water and electrolytes. There is increased sodium-dependend chloride secretion, and absorption of sodium and chloride is inhibited. Diarrhea occurs - as much as 20 - 30 L/day -with resulting dehydratation, shock, acidosis and death. Vibrio cholerae toxicity
l V. cholerae is pathogenic only for humans. Cholera is not
an invasive infection. The microorganism do not reach the blood stream but remain within the intestinal tract.
l Although cholera toxin is the most important virulence
factor, the motility and the production of mucinase and other proteolytic enzymes contribute to the ability of V. cholerae to colonize.
l The microorganism can colonize the entire intestinal tract
from the jejunum to the colon and can multiply to high numbers. An alkaline environment is ideal for bacterial growth. Vibrio cholerae
l Incubation:
– several hours to 5 days (usually 2-3 days)
l Symptoms:
– diarrhea and other (vomiting, pain in the
abdominal region, hypotermia, hypotension, anuria, metabolic acidosis and others)
Vibrio cholerae
l In the treatment of cholera absolute priority must be
given to the replacement of fluid and electrolytes.
l Antimicrobial therapy shortens the duration
diarrhea and reduces the period of excretion ofV. cholerae in the stools of cholera patients.
– tetracyclines have been used most frequently (tetracycline
for 3 days), although chloramphenicol, fluoroquinolones,cotrimoxazole and others have also been effective. Vibrio cholerae
l Transmission:
– Epidemic cholera is spread primarly by contaminated
water and food, most commonly during the warmmonths of the year. Cholera vibrios can be transmittedby direct contact with patients and carrriers.
l Morbidity:
l Mortality:
– About 50% in classical V. cholerae,– only 1% in V. cholerae El tor.
lThe genus AEROMONAS
– Aeromonas hydrophila is the most important
species from this genus causing disease in humans.
– The strains have been associated with diarrhea.
lThe genus PLESIOMONAS
– Plesiomonas sp. is most common in tropical and
– Plesiomonas shigeloides can cause diarrhea. Characteristics and epidemiology of Aeromonas spp.
Ø Gram-negative facultatively anaerobic bacillusØ Motile species have single polar flagellum
(nonmotile species apparently not associated with human disease)
Ø 16 phenospecies: Most significant human
pathogens A. hydrophila, A. caviae, A. veronii biovar sobria
Ø Ubiquitous in fresh and brackish waterØ Acquired by ingestion of or exposure to
Characteristics of Plesiomonas spp.
· Oxidase positive· Multiple polar flagella (lophotrichous)· Single species: Plesiomonas shigelloides· Isolated from aquatic environment (fresh or
· Acquired by ingestion of or exposure to
contaminated water or seafood or by exposure to amphibians or reptiles
· Self-limited gastroenteritis: secretory, colitis or
· Variety of uncommon extra-intestinal infections
The genus CAMPYL CAM OBACTER
l Campylobacter jejuni has emerged as a common human
pathogen, causing mainly enteritis and occasionally systemic invasion.
l The medically important Campylobacter species:
– C. fetus subspecies fetus
l septicemia in debilitated and immunocompromised patients
– C. cinaedi, C. fennelliaeThe genus CAMPYL CAM OBACTER
l Rehydrationl Most patients do not require antibotics
– exceptions: high fewer, bloody stool, prolonged
illness (more than 1 week), pregnancy, HIV and other immunosuppressed states
l Erytromycin 2x500 mg p.osl Ciprofloxacin 2x500 mg p.os
The genus HELICOBACTER
l Helicobacter pylori is associated with antral gastritis and
apears to be important in the pathogenesis of ulcer disease.
l It is motile and a strong producer of urease.
l It is present on the gastric mucosa of less than 20% of
persons under age 30, but increases in prevalence to 40-60% of persons age 60.
l In developing countries, the prevalence of infection may
The genus HELICOBACTER
– Combination of two of the following three antibiotics
(amoxicillin, clarithromycin, metronidazole, tetracycline) plus omeprazole.
– Resistence of H. pylori to antibiotics in the Czech
Republic: Antibiotic Resistance (in %) The genus HELICOBACTER
– amoxicillin + clarithromycin + omeprazol– metronidazol + clarithromycin + omeprazol– metronidazol + tetracycline + omeprazol
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