Vibrio

Vibrio is a genus of comma-shaped, gram-negative bacilli. It is halophilic, acid labile, and commonly isolated on thiosulfate-citrate-bile-sucrose (TCBS) agar. There are 3 clinically relevant species. Vibrio cholerae (V. cholerae) is found in brackish and marine waters. Vibrio cholerae is associated with cholera, which causes severe, secretory “rice-water” diarrhea. The other 2 species are Vibrio vulnificus (V. vulnificus) and Vibrio parahaemolyticus (V. parahaemolyticus), which are transmitted through raw or undercooked shellfish and are associated with wound infections, septicemia, and diarrhea.

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Classification

Gram negative bacteria classification flowchart

Gram-negative bacteria:
Most bacteria can be classified according to a lab procedure called Gram staining.
Bacteria with cell walls that have a thin layer of peptidoglycan do not retain the crystal violet stain utilized in Gram staining. These bacteria do, however, retain the safranin counterstain and thus appear as pinkish-red on the stain, making them gram negative. These bacteria can be further classified according to morphology (diplococci, curved rods, bacilli, and coccobacilli) and their ability to grow in the presence of oxygen (aerobic versus anaerobic). The bacteria can be more narrowly identified by growing them on specific media (triple sugar iron (TSI) agar) where their enzymes can be identified (urease, oxidase) and their ability to ferment lactose can be tested.
* Stains poorly on Gram stain
** Pleomorphic rod/coccobacillus
*** Require special transport media

Image by Lecturio.

General Characteristics

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

Reservoirs

  • V. cholerae: found in brackish and marine waters
  • V. vulnificus and V. parahaemolyticus: shellfish

Clinical Relevance of Vibrio cholerae

Epidemiology

  • Primarily occurs in areas with limited access to clean water
  • Endemic in some countries in Africa and Asia
  • Cholera affects only humans.

Transmission

  • Through contaminated food or water
  • Fecal-oral route (person-to-person)

Pathogenesis

  • 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.

Clinical presentation

About 50% of infections with classic V. cholerae are asymptomatic and 75% of infections with El Tor biotype of V. cholerae are asymptomatic.

Diarrhea:

  • 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

Pneumonia:

  • Not uncommon in children
  • Probably from vomitus aspiration
cholera diarrhea rice water

Typical cholera diarrhea that looks like “rice water”

Image: “Here, a cup of typical “rice-water” stool from a cholera patient shows flecks of mucus that have settled to the bottom” by CDC. License: Public Domain

Management

Mortality in untreated patients is up to 50%-70% (but < 1% with prompt electrolyte and fluid replacement).

Treatment:

  • Aggressive oral rehydration therapy with electrolytes
  • Antibiotics may be used to shorten duration of diarrhea, most often doxycycline.

Prevention:

  • 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. 
  • Vaccines:
    • 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.

Diagnosis

  • 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

V. vulnificus

  • The leading cause of shellfish-associated deaths in the United States
  • Diarrhea
  • 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)
      • Hemochromatosis

V. parahaemolyticus

  • The leading cause of foodborne illness in Japan (especially shellfish)
  • Also associated with diarrhea, wound infections, and septicemia
  • Same risk factors as V. vulnificus

References

  1. Aryal, S. (2018). Thiosulfate-citrate-bile salts-sucrose (TCBS) Agar. https://microbenotes.com/thiosulfate-citrate-bile-salts-sucrose-tcbs-agar/
  2. Morris J.G. (2020). Vibrio parahaemolyticus infections. UpToDate. Retrieved January 3, 2021, from https://www.uptodate.com/contents/vibrio-parahaemolyticus-infections 
  3. Morris J.G. (2019). Vibrio vulnificus infections. UpToDate. Retrieved January 3, 2021, from https://www.uptodate.com/contents/vibrio-vulnificus-infections
  4. LaRocque R., Harris J.B. (2018). Cholera: Microbiology and pathogenesis. UpToDate. Retrieved January 3, 2021, from https://www.uptodate.com/contents/cholera-microbiology-and-pathogenesis
  5. LaRocque R., Harris J.B. (2020). Clinical features, diagnosis, treatment, and prevention. UpToDate. Retrieved January 3, 2021, from https://www.uptodate.com/contents/cholera-clinical-features-diagnosis-treatment-and-prevention
  6. Walder, M.K., Ryan, E.T. (2018). Cholera and Other Vibrioses. In Jameson, J.L., et al. (Ed.), Harrison’s Principles of Internal Medicine (20th ed. Vol 1, p. 1186–1192).
  7. Riedel, S., Hobden, J.A. (2019). In Riedel, S, Morse, S.A., Mietzner, T., Miller, S. (Eds.), Jawetz, Melnick, & Adelberg’s Medical Microbiology (28th ed, pp. 261–266).
  8. Liu, D. (2015). Toxin-Associated Gastrointestinal Disease. In Molecular Medical Microbiology (2nd ed., Vol. 2, pp. 971–977).
  9. Severin, G. B., et al. (Ed.) (2018). Direct activation of a phospholipase by cyclic gmp-amp in el tor vibrio cholerae. Proceedings of the National Academy of Sciences, 115(26), E6048–E6055. https://doi.org/10.1073/pnas.1801233115

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