Notes
Cholera & Related Illnesses
Sections
Vibrio
Gram-negative rods.
Facultatively anaerobic
Oxidase-positive
Polar flagella facilitate rapid motility.
Found in water, especially estuaries and coastal waters, because salt is required for growth.
Upon ingestion, pathogenic strains cause gastrointestinal disease.
Vibrio cholerae
Causative agent of cholera.
Ingested as free-living cells, micro-colonies, or as biofilms in contaminated foods or water.
Sensitive to stomach acids; infection typically requires exposure to a large quantity. However, individuals with impaired stomach acid production are vulnerable to lower infectious doses.
Gastroenteritis caused by Vibrio cholerae causes mild to severe vomiting and watery diarrhea.
In severe cases, the profuse stool has a characteristic milky-white "rice water" appearance.
Prevention:
Proper sanitation and thorough cooking of food can prevent cholera epidemics.
Vaccination can help prevent worsening conditions in areas where cholera is endemic.
Treatment:
Infected patients should be given antibiotics, such as tetracycline, to avoid dehydration and death.
Cholera epidemics: Vibrio cholerae O1 and O139
Vibrio cholerae O1 is further subdivided into biotypes and serotypes.
Biotypes: Classical and El tor
Serotypes: Ogawa and Inaba; Hikojima is thought to be a hybrid transitional state.
Severe fluid loss leads to dehydration, which can result in metabolic acidosis, hypokalemia, hypovolemic shock, cardiac arrhythmia, and renal failure.
Cholera is endemic in some parts of the world; asymptomatic carriers contribute to its maintained presence.
Cholera outbreaks occur in areas where humanitarian and/or environmental crises lead to overcrowding and poor sanitation.
Acquisition of Virulence Factors:
We show how Vibrio cholerae O1 and O139 acquire the virulence factors that promote severe gastroenteritis.
Horizontal gene transfer is key to this process.
First, we draw a couple of small intestine epithelial cells and indicate the intestinal lumen.
Then, we draw a non-pathogenic Vibrio cholerae bacterium.
Its chromosomal DNA has already acquired Vibrio Pathogenicity Island -1 (VPI-1), which carries genes for Toxin co-regulated pili.
Toxin co-regulated pilus is a type of bundle-forming pilus that promotes microcolony formation, which is important for Vibrio cholerae colonization.
This pilus is also a receptor for bacteriophage CTXφ, which injects DNA into the V. cholerae microbe.
Without the pathogenicity island and toxin co-regulated pilus, the bacteriophage would not be able to attach to the microbe and transfer DNA.
Next, we show that the CTX prophage has been integrated into the chromosomal DNA.
The CTX prophage triggers production of cholera toxin, which interacts with binding sites on the small intestine epithelial cells.
Cholera toxin increases cyclic AMP, which leads to water and electrolyte secretion into the lumen.
Profuse watery diarrhea ensues.
The CTXφ prophage also carries genes for two additional toxins:
Accessory cholera enterotoxin (ACE) contributes to water and ion secretion; some authors report that this enterotoxin, alone, can induce gastroenteritis.
Zona occludens toxin (ZOT) disassembles epithelial tight junctions, which increases intestinal permeability.
Neuraminidase increases the availability of cholera toxin binding sites on host cells
The nanH gene that codes for this enzyme is carried separately.
Non-O1 and non-O139 Vibrio cholerae strains can cause mild diarrhea.
Virulence factors of these strains vary.
Non-O1 strains have polysaccharide capsules that facilitate spread beyond the intestine.
Various toxins, including heat-stable enterotoxin, induce diarrheal symptoms.
Vibrio parahaemolyticus & Vibrio vulnificus
Associated with gastroenteritis, septicemia, and wound infections.
Vibrio parahaemolyticus
Lives as free cells in contaminated food and water; Halophilic ("Salt-loving;" growth on most media requires the addition of sodium chloride).
Virulence factors:
Type three secretion systems inject protein effectors into host cells.
Thermostable Direct Hemolysin (TDH) and TDH-Related Hemolysin (TRH) are enterotoxins that increase intestinal fluid secretion; they also act as cytotoxins that affect other host cells.
Thermostable direct hemolysins produce beta hemolytic halos when grown on Wagastuma blood agar; this is called the Kanagawa phenomenon. However, be aware that strains carrying only the TDH-related hemolysin (TRH) gene are Kanagawa phenomenon-negative, but can still cause gastroenteritis. Thus, the absence of beta hemolysis does not necessarily mean that the strain is non-pathogenic.
Plastic motility: with a single flagellum, it moves as a rapid swimmer cell. In more viscous environments, the microbe produces multiple lateral flagella and moves as a swarmer cell.
Capsule synthesis is also up- or down-regulated in response to environmental changes.
Vibrio vulnificus
Associated with warm saltwater; halophilic.
Ferments lactose, which can aid in its identification.
Strains can be further classified into three biotypes.
Risk factors: More likely to cause infections in males; it has been suggested that estrogen has protective effects.
- Individuals with elevated free iron levels are also more susceptible to infection, likely because Vibrio vulnificus thrives in iron-rich environments.
Overall, Vibrio vulnificus is responsible for most sea-food related deaths in the U.S.
Virulence factors:
A polysaccharide capsule protects from host immune responses
Proteases break down host tissues
Hemolysins release iron from host storage
Cytolysins cause cell death
Endotoxin comprises LPS; triggers cytokine release.
V. parahaemolyticus & V. vulnificus Infections
Infection is more common in individuals with immunodeficiencies and/or liver disease, which is associated with decreased neutrophil activity.
Self-limiting Gastroenteritis is associated with consumption of raw oysters that are contaminated with Vibrio parahaemolyticus.
Vibrio parahaemolyticus is associated with more than half of all cases of seafood-borne bacterial gastroenteritis.
Results from consumption of shellfish, especially raw oysters.
Symptoms include watery diarrhea, abdominal cramps, nausea, vomiting, headache, and fever.
Fortunately, gastroenteritis is preventable by cooking, which kills the bacteria.
In most cases, gastroenteritis is self-limiting.
Septicemia is associated with consumption of raw oysters that are contaminated with Vibrio vulnificus.
In the bloodstream, Vibrio vulnificus triggers a systemic inflammatory response; the bacteria are protected their polysaccharide capsules, but massive release of pro-inflammatory cytokines damages the host.
Gastrointestinal symptoms followed by chills, fever, and septic shock are associated with septicemia.
The mortality rate is high; in some reports, more than half of infected patients die.
Treatment:
Antibiotics
Wound infections occur after exposure to contaminated water.
Mild infections can lead to cellulitis; this is more common when Vibrio parahaemolyticus is the causative agent.
Severe cases can lead to necrotizing fasciitis; this is more common when the wound is infected by Vibrio vulnificus.
Treatment:
Antibiotic administration; if necrotic tissue is present, surgical debridement is also necessary.
References
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