Microsoft powerpoint - the genus vibrio_web [režim kompatibility]

General Characteristics of Vibrio,
· 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 cold-blooded animals. – 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.
l The genus can be divided: – 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.
– gramnegative rods, non-spore forming, motile (polar flagellum) l Vibrio cholerae serotypes V. cholerae food associated diarrheal disease V. vulnificus wound infection, sepsis V. alginolyticus otitis externa, wound infection The VIBROS
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, rarely extraintestinal infection – V. parahaemolyticus: gastroenteritis, possibly extraintestinal – other (V. mimicus, V. vulnificus.): ear, wound, soft tissue and other extraintestinal infections, all uncommon 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
– Annually 5-7 million cases, 100,000 deaths worldwide.
l V. cholerae can grow aerobically or anaerobically on a variety of simple media.
l Vibrios grow at a very high pH (8.5 to 9.5) and are rapidly killed by acid conditions.
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 nutrient or blood agar.
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 without gas from a many sugars.
Vibrio cholerae is divided
l Cholera biotype: – 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.
l El tor biotype: – all the properties has just opposited as given above.
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.
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.
l The V. cholerae serogroup O1 antigen has determinants A, B, C that make possible further subdivison into three serologic subtypes: – A,B (s.c. Ogawa) – A,C (s.c. Inaba) – A,B,C (s.c. Hikojima) – 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.
l The B unit mediates tight binding to a cell wall ganglioside of enterocytes in the small intestine. It means that ganglioside G serves as the mucosal receptor for 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.
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.
– 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) 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.
– 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:
– In epidemics 1-5%.
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.
Plesiomonas sp. is most common in tropical and subtropial areas. – Plesiomonas shigeloides can cause diarrhea.
Characteristics and epidemiology of
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 contaminated water or food 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
l Campylobacter jejuni has emerged as a common human pathogen, causing mainly enteritis and occasionally systemic invasion.
l The medically important Campylobacter species: – C. jejuni l diarrhea (common) – C. fetus subspecies fetus l septicemia in debilitated and immunocompromised patients – C. coli, C. laridisC. cinaedi, C. fennelliae l infections in homosexual man The genus CAMPYL
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 be 80% or higher in adults.
– Combination of two of the following three antibiotics (amoxicillin, clarithromycin, metronidazole, tetracycline) plus omeprazole.
– Resistence of H. pylori to antibiotics in the Czech Resistance (in %)
– amoxicillin + clarithromycin + omeprazol– metronidazol + clarithromycin + omeprazol– metronidazol + tetracycline + omeprazol


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