Basic features of Vibrio
- Curved gram-negative bacilli
- Facultative anaerobes
- Highly motile: 1–3 polar flagella
- Non-spore forming
- Oxidase positive
Major pathogenic species
- Vibrio cholerae (V. cholerae)
- V. vulnificus
- V. parahaemolyticus
Biochemistry and growth characteristics
- Halophilic: require sodium chloride (NaCl) for growth
- Acid labile: grows well in alkaline media
- Thiosulfate-citrate-bile-sucrose (TCBS) agar:
- V. cholerae ferments sucrose → forms yellow colonies
- V. parahaemolyticus and V. vulnificus do not ferment sucrose → form green colonies
- V. parahaemolyticus exhibits the Kanagawa phenomenon:
- Beta-hemolytic on blood agar if isolated from human host
- Non-hemolytic if from non-human sources
- V. cholerae: found in brackish and marine waters
- V. vulnificus and V. parahaemolyticus: shellfish
Clinical Relevance of Vibrio cholerae
- Primarily occurs in areas with limited access to clean water
- Endemic in some countries in Africa and Asia
- Cholera affects only humans.
- Through contaminated food or water
- Fecal-oral route (person-to-person)
- Not all strains are pathogenic.
- Pathogenesis is determined by production of cholera toxin (CT):
- Carried by a lysogenic bacteriophage (CTXΦ)
- Heat-labile enterotoxin: composed of 1 A subunit (toxic domain) and 5 B subunits (receptor-binding domain)
- B-subunit binds to the mucosal receptor ganglioside monosialotetrahexosylganglioside (GM1).
- CT is internalized by endocytosis: The A1 subunit of the toxin activates adenylyl cyclase, which converts adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP).
- cAMP causes chloride secretion into lumen and inhibition of sodium absorption.
- Water follows the osmotic gradient and moves into the lumen, resulting in watery diarrhea with electrolyte concentrations isotonic to those of plasma.
- Stool contains large amounts of sodium, chloride, bicarbonate, and potassium with few cells.
- O lipopolysaccharide antigens:
- Confer serologic specificity; > 200 serotypes
- Only strains of O1 (classic and El Tor biotypes) and O139 serogroups cause epidemic and pandemic cholera (they are the most virulent).
- Fimbriae (pili):
- Aid in attachment to the intestinal mucosa
- V. cholerae does NOT invade the intestinal mucosa.
- Co-expressed (co-regulated) with cholera toxin and needed for adherence, biofilm formation, colonization, and as receptors for the bacteriophage that carries the genes for cholera toxin
- Because V. cholerae are acid labile, a high inoculum is required to overcome the acidity of the gastric mucosa. The infectious dose is reduced:
- In hypochlorhydric persons
- In those using antacids
- When gastric acidity is buffered by a meal
- The higher the bacteria number, the more severe the symptoms.
- Incubation period: 1–2 days
- Fluid loss originates in the duodenum and upper jejunum; the ileum is less affected.
- The colon is relatively insensitive to the toxin, but the large volume of fluid overwhelms its absorptive capacity.
About 50% of infections with classic V. cholerae are asymptomatic and 75% of infections with El Tor biotype of V. cholerae are asymptomatic.
- May be mild, moderate, or severe
- Clinical presentation of severe, secretory diarrhea:
- Typically painless, without tenesmus
- “Rice-water” stool (non-malodorous, watery stool with flecks of mucus)
- Stool output can reach as high as 1 L/hour in severe cases (the most of any other infectious diarrhea).
- Vomiting: may precede or follow the onset of diarrhea
- Consequences of severe, secretory diarrhea:
- Profound fluid and electrolyte loss → “isotonic dehydration”:
- A type of dehydration most frequently caused by diarrhea
- Occurs when the net losses of water and sodium are in the same proportion as normally found in the extracellular fluid
- Metabolic acidosis due to loss of bicarbonate
- Acute kidney injury (acute renal failure) is a possible complication.
- Symptoms and signs depend on volume contraction (severity of hypovolemia):
- < 5% of normal body weight (NBW): thirst
- 5%-10% of NBW: postural hypotension, weakness, muscle cramps, tachycardia, ↓ skin turgor, dry oral mucosa
- > 10% of NBW: oliguria, weak pulses, sunken eyes (sunken fontanelles in infants), wrinkled skin, somnolence, coma
- In severe cases, quick progression to hypovolemic shock and death if not treated urgently
- Profound fluid and electrolyte loss → “isotonic dehydration”:
- Not uncommon in children
- Probably from vomitus aspiration
Mortality in untreated patients is up to 50%-70% (but < 1% with prompt electrolyte and fluid replacement).
- Aggressive oral rehydration therapy with electrolytes
- Antibiotics may be used to shorten duration of diarrhea, most often doxycycline.
- Clean water supply and appropriate sanitation are the keys to prevention.
- General precautions for the prevention of travelers’ diarrhea:
- Avoidance of tap water, food from street vendors, raw or undercooked seafood, and raw vegetables
- Non-bottled water should be treated with chlorine or iodine, filtrated, or boiled.
- Killed whole-cell oral vaccines are recommended by the World Health Organization for residents in endemic areas.
- For U.S. travelers to high-risk areas at high risk for exposure:
- A live oral vaccine against serotype O1 is available (“Vaxchora”).
- The vaccine lacks the gene that encodes for the cholera toxin.
- Stool culture (the gold standard) on selective media (TCBS or taurocholate-tellurite-gelatin agar):
- V. cholerae produces yellow colonies (due to sucrose fermentation).
- Non-sucrose fermenting vibriones (e.g., most strains of V. parahaemolyticus and V. vulnificus) produce green colonies.
- Gram stain and biochemical testing of isolates: All vibriones are oxidase positive.
- Serotyping with specific antisera
- Stool microscopic examination: only a few neutrophils because the intestinal wall is not invaded
- Rapid antigen-detection tests:
- Crystal VC: detects O1 and O139 antigens
- Cholkit: detects O1 antigen
- Molecular testing (e.g., polymerase chain reaction (PCR): limited to epidemiologic research and surveillance)
Clinical Relevance of V. vulnificus and V. parahaemolyticus
- The leading cause of shellfish-associated deaths in the United States
- Wound infections:
- Associated with hand injuries while opening oysters, or leg lacerations during boating activities
- May cause hemorrhagic bullae
- May range from mild cellulitis to severe necrotizing infections
- Primary septicemia:
- Associated with ingestion of raw or undercooked shellfish, most commonly oysters
- More common in those with chronic, underlying conditions:
- Liver disease (alcoholics, cirrhosis)
- The leading cause of foodborne illness in Japan (especially shellfish)
- Also associated with diarrhea, wound infections, and septicemia
- Same risk factors as V. vulnificus
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