LECTURE Flashcards
(124 cards)
V. cholerae: common name
“Kommabacillus”
V. cholerae: habitat
human colon
Man is the only known reservoir of V. cholerae. Human carriage may persist after untreated infection for months after infection; however, permanent carrier state is rare. They can survive and grow in fresh and brackish water.
V. cholerae
V. cholerae: transmission
fecal-oral route.
The most common source of infection is contaminated water. Food, especially shellfish (contaminated from contaminated waters) eaten
raw, have also been a source of infection.
V. cholerae
Cholera, which is also known as
Asiatic cholera or epidemic cholera
The incubation period of Cholera is [?] depending on the size of the inoculum ingested.
12 hours up to 3 days
Symptoms include sudden onset of nausea, vomiting, abdominal cramps and profuse “rice water” diarrhea (stool resembles water in which the rice has been boiled) that may be as many as 10 to 30 per day, containing mucus, epithelial cells, and large numbers of species
Cholera
In severe cholera, infected individual can lose several liters of fluid, as much as [?]. If left untreated, it can result in a rapid fluid and electrolyte loss that leads to dehydration, hypovolemic shock, metabolic acidosis, and death in a matter of hours.
20-30 liters per day
To cause disease, cells of V. cholerae must adhere to the gastric and intestinal mucosal epithelial cells of the host; two properties that aid in the penetration of the protective mucin layer that coats the surface of the gastroenteric mucosa.
Motility and mucinase
The cholera toxin is a heat-labile enterotoxin, the genes for which are encoded in a lysogenic phage.
Choleragen (cholera toxin)
Cholera is consists of 2 subunits:
A (active) subunits and binding (B) subunits
The A subunit is composed of two peptides:
A1 with toxin activity
A2
it activates adenylate cyclase, causing increased levels of cyclic adenosine monophosphate (cAMP) and hypersecretion of electrolytes (Na+, K+, HCO3−) and water out of the cell and into the lumen of the intestine. The net effect is that the gastrointestinal tract’s absorptive ability is overwhelmed, resulting in the massive outpouring of watery stools
A1 with toxin activity
facilitates penetration of the A1 subunit into the enterocyte
A2
[?] binds the A2 subunit to the GM1 ganglioside receptor on the cell membrane of the enterocytes. There are five B subunits per toxin molecule, arranged in a ring around a central core that contains the enzyme A1.
B subunit
Heat-labile substances that are found in all V. cholerae strains
H antigen
Cell wall lipopolysaccharides that confer serologic specificity to the bacterial cells
O antigen
V. cholerae strains are designated into 3 major serogroups based on agglutination with V. cholerae O1 polyvalent antiserum.
Serogroups of V. cholerae
- Is agglutinated by V. cholerae O1 antiserum
V. cholerae O1
- Is NOT agglutinated by V. cholerae O1 antiserum
V. cholerae non-O1
- Is NOT agglutinated by V. cholerae O1 antiserum
V. cholerae O139
There are two biotypes of V. cholerae serogroup O1 based on their differences in biochemical characteristics, which is associated with how they differ with respect to the severity of the disease they can cause.
Biotypes of V. cholerae O1
caused the epidemic cholera from early 1800s to early 1900 – during this time, there were 6 waves of cholera pandemic that spread across the world.
Classical strain of V. cholerae