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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. fennelliae The 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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Doi:10.1016/j.theriogenology.2004.03.002

Increasing feed intake in late gestation does notaffect plasma progesterone concentration in the sowaSchool of Biology, University of Leeds, Leeds LS2 9JT, UKbDepartment of Agriculture, Food and Nutritional Science, University of Alberta, Edmonton, Alta., CanadaReceived 10 February 2003; received in revised form 20 February 2004; accepted 14 March 2004Rate of decline in plasma progester

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