Vibrio cholerae (Cholera)

20,131views

Vibrio cholerae (Cholera)

Oral Microbiology

Oral Microbiology

Polymerase chain reaction (PCR) and reverse-transcriptase PCR (RT-PCR)
Gel electrophoresis and genetic testing
ELISA (Enzyme-linked immunosorbent assay)
Karyotyping
DNA cloning
Fluorescence in situ hybridization
Light microscopy and staining methods
Introduction to the immune system
Innate immune system
Complement system
T-cell development
B-cell development
MHC class I and MHC class II molecules
T-cell activation
B-cell activation, differentiation, and contraction
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
Antibody classes
Somatic hypermutation and affinity maturation
VDJ rearrangement
Contracting the immune response and peripheral tolerance
B- and T-cell memory
Anergy, exhaustion, and clonal deletion
Vaccinations
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity
Bacterial structure and functions
Staphylococcus epidermidis
Staphylococcus aureus
Staphylococcus saprophyticus
Streptococcus viridans
Streptococcus pneumoniae
Streptococcus pyogenes (Group A Strep)
Streptococcus agalactiae (Group B Strep)
Enterococcus
Clostridium perfringens
Clostridium botulinum (Botulism)
Clostridium difficile (Pseudomembranous colitis)
Clostridium tetani (Tetanus)
Bacillus cereus (Food poisoning)
Listeria monocytogenes
Corynebacterium diphtheriae (Diphtheria)
Bacillus anthracis (Anthrax)
Nocardia
Actinomyces israelii
Escherichia coli
Salmonella (non-typhoidal)
Salmonella typhi (typhoid fever)
Pseudomonas aeruginosa
Enterobacter
Klebsiella pneumoniae
Shigella
Proteus mirabilis
Yersinia enterocolitica
Legionella pneumophila (Legionnaires disease and Pontiac fever)
Serratia marcescens
Bacteroides fragilis
Yersinia pestis (Plague)
Vibrio cholerae (Cholera)
Helicobacter pylori
Campylobacter jejuni
Neisseria meningitidis
Neisseria gonorrhoeae
Moraxella catarrhalis
Francisella tularensis (Tularemia)
Bordetella pertussis (Whooping cough)
Brucella
Haemophilus influenzae
Haemophilus ducreyi (Chancroid)
Pasteurella multocida
Mycobacterium tuberculosis (Tuberculosis)
Mycobacterium leprae
Mycobacterium avium complex (NORD)
Mycoplasma pneumoniae
Chlamydia pneumoniae
Chlamydia trachomatis
Borrelia burgdorferi (Lyme disease)
Borrelia species (Relapsing fever)
Leptospira
Treponema pallidum (Syphilis)
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Coxiella burnetii (Q fever)
Ehrlichia and Anaplasma
Gardnerella vaginalis (Bacterial vaginosis)
Viral structure and functions
Varicella zoster virus
Cytomegalovirus
Epstein-Barr virus (Infectious mononucleosis)
Human herpesvirus 8 (Kaposi sarcoma)
Herpes simplex virus
Human herpesvirus 6 (Roseola)
Adenovirus
Parvovirus B19
Hepatitis B and Hepatitis D virus
Human papillomavirus
Poxvirus (Smallpox and Molluscum contagiosum)
BK virus (Hemorrhagic cystitis)
JC virus (Progressive multifocal leukoencephalopathy)
Poliovirus
Coxsackievirus
Rhinovirus
Hepatitis A and Hepatitis E virus
Influenza virus
Mumps virus
Measles virus
Respiratory syncytial virus
Human parainfluenza viruses
Dengue virus
Yellow fever virus
Zika virus
Hepatitis C virus
West Nile virus
Norovirus
Rotavirus
Coronaviruses
HIV (AIDS)
Human T-lymphotropic virus
Ebola virus
Rabies virus
Rubella virus
Eastern and Western equine encephalitis virus
Lymphocytic choriomeningitis virus
Hantavirus
Prions (Spongiform encephalopathy)
Candida
Plasmodium species (Malaria)

Transcript

Watch video only

Content Reviewers

Cholera is a contagious infection caused by the bacteria Vibrio cholerae, which can in turn cause severe gastroenteritis and excessive watery diarrhea for several days.

Rapid dehydration and electrolyte imbalances can be fatal as suspected in the deaths of James K. Polk, the 11th President of the United States; and Charles the Tenth, King of France.

V. cholerae is a gram-negative, curved bacteria which looks like little red or pink comma-shapes on a gram stain.

It’s positive for oxidase and grows in alkaline media.

It has pili and a single polar flagellum, kind of like a tail, at one end which it uses for movement through the gastrointestinal tract.

It’s a facultative anaerobe so that means it can undergo respiratory and fermentative metabolism.

Transmission of V. cholerae typically occurs through a fecal to oral route.

This includes consuming untreated sewage water, and anything that comes in contact with it, like raw or undercooked fish including shellfish; and improper hygiene, like a lack of hand washing after a bowel movement.

Cholera tends to be more common in developing countries and places lacking advanced sanitation and sewage treatment facilities, with high rates in some locations in Africa and South America.

People who have low gastric acidity or have an O-blood type are particularly at risk for a severe infection.

Now, when V. cholerae enters the stomach it shuts down protein production to conserve energy and nutrients, and to survive the acidic environment.

But once V. cholerae is in the intestines, it uses its flagella to move toward the intestinal walls; propel through the mucous layer on top of the epithelial cells lining the intestines; and attach to the finger-like cellular projections, called villi, on the surface of the epithelial cells.

There, V. cholerae can begin to multiply and produce toxins.

And though V. cholerae does not enter the epithelial cells itself, the toxins do and they can cause a lot of trouble.

Now, the exact toxins produced can depend on the strain of V. cholerae.

Some strains produce toxins that won’t cause any, or maybe just mild clinical symptoms.

But some strains produce cholera enterotoxin, also called choleragen, which is most often the cause significant clinical symptoms.

When cholera enterotoxin enters the epithelial cells, it leads to the ADP-ribosylation of the Gs alpha subunit of G-protein.

So, this causes the G-protein to becomes permanently activated and it keeps activating a membrane-bound protein called adenylate cyclase.
This protein in turn leads to an overproduction of the intracellular secondary messenger protein, cyclic adenosine monophosphate, or simply cAMP.

Increase in cAMP causes chloride channels on the cells to increase the secretion of chloride into the lumen while inhibiting the channels that let sodium and chloride back into the cell.

Key Takeaways

Vibrio cholerae is a bacterium that causes cholera, a severe and contagious diarrheal disease. Cholera is transmitted through contaminated water or food and is most common in areas with poor sanitation and limited access to clean drinking water.

Some strains produce cholera enterotoxin, which acts on the intestinal epithelial cells in the small intestine, causing over-activation of the enzyme adenylate cyclase. This leads to an increase in the intracellular levels of cyclic AMP (cAMP) in the intestinal cells, which in turn leads to the secretion of large amounts of water and electrolytes into the intestinal lumen, resulting in the characteristic watery diarrhea of cholera.

Patients most often present with voluminous, profuse, watery diarrhea, vomiting, and dehydration, all of which lead to fatal dehydration and electrolyte imbalances. Treatment involves rehydration therapy to replace all the fluids and electrolytes that are lost through diarrhea. In severe cases, antibiotics such as tetracyclines, ciprofloxacin, or trimethoprim-sulfamethoxazole may be necessary.