Biology 216 - Lect 19
Cholera/ETEC
Nobel Prize in physiology/medicine this year?
Family: Vibrionaceae - Gm- curved rods, Ox+;
Members: Vibrio, Aeromonas, Plesiomonas
I. Non-cholera vibrios
A. V. vulnificus - wound infections
B. V. parahaemolyticus - grow in salt water
estuaries, halophilic.
Contaminate foods and grow very quickly.
#1 food illness in Japan - sushi
Acute GI
II. Vibrio cholerae - explosive life-threatening diarrhea.
Prototypic enteropathy - Other studies based on this
(ex. ETEC, Salmonella.....)
A. Bacteriology -
Sequenced: http://www.tigr.org/tdb/CMR/gvc/htmls/SplashPage.html
2 chromosomes
1. Serotypes based on O-Ag (O-1 agglutinable -
epidemic; NAGs most tox-; O-139)
O-1 Ag - 3 serotypes (Inaba, Ogawa, Hikojima)
2. Biotypes of O-1Ag - Different biochems (HA, VP,
phage sensitivity, polymyxin B)
Classical and El Tor
B. Cholera toxin - responsible for entire disease;
Prototype enterotoxin (E. coli, Campy...)
Genes found in lysogenic phage in chromosome
(phage can be recovered)
1. 1959 soluble toxin; Before i.p. in mouse gave
no response; ligated ileal loop
2. Structure - 1A (enzymatic ADP-ribosylating),
5B (bind GM1 ganglioside - sugar/lipid)
ctxA-ctxB single operon - differ in rbs efficiency
toxR - transcriptional activator.
3. MOA - modifies intestinal epithelial cell to excrete;
Does not kill; MOA OTB;Y-1 adrenal,CHO
C. Pathogenesis - 7th great pandemic -
began 1961 (Asia-> Africa) -
40,000/yr, under reported probably 1 million.
1991 Peru >300K. Now spread through latin and
south America (> 1 million)
Began with Chinese frigate in Lima, sewage
dumped, fish -> sewage
Decreased chlorination of sewage.
1. Transmission - 10(8) ie no direct transmission;
Ingestion of food, water, vegetable,
Found in shellfish and plankton beds.
2. Pass stomach (bolus); Gastric barrier; achlorhydria
and bicarb increase infection.
3. Colonize and multiply in small intestine
(draw lumen, crypts, villi, microvilli, mucus)
Role for motility, mucinase, attachment
4. Cholera toxin - electrolyte efflux, water, diarrhea
(rice water stool), vomit, no damage
May lose 20 liters/day for 3 days.
5. Dehydration - sunken tissues (face, washer
woman hand), hypovolemic shock.
6. 3 - 5 days vibrios detach. 60 % mortality
untreated; 1 % if treated.
7. 1f - 20 % carriers after disease (carriage is
the rule/disease is a mistake)
D. Lab diagnosis
1. History, stool appearance, Fl-Ab of stool in epidemics.
2. Isolation and ID - TCBS (thiosulfate citrate bile sucrose),
usually pure culture, biochem
E. Treatment
1. Replace fluid and electrolytes - iv (2 liter/hr);
WHO Oral rehydration pack (ORP)
Gatorade; cholera cot
2. Antibiotics - eliminate carrier state;
Some effect on course of disease.
3. Exptl drugs based on MOA - chlorpromazine
(conc in sm intest; inhibit Ad cyclase)
F. Prevention
1. Sewage disposal - flush toilet; treat and
disinfect sewage (Peru); controllable
2. Travelers to endemic areas - avoid vegetables;
raw seafood, tap water and ice, fruit
3. Vaccines: Old vaccine is ip killed V. cholerae - ineffective.
Need immune response at site of infection,
not circulating Ab.
Live attenuated vaccines: M13 (reverted);
Texas star S/R; A-B+ recombinant
Recombinant A-B+ (gene replacement HgR insert).
S. typhi carrying cloned genes.
New - oral rCTB + 4 killed strains
II. ETEC - First in swine piglets (plasmid, K88, LT, ST);
1/2 billion humans/year (CFA, LT, ST)
Tijuana trots, Montezuma's revenge; mild to cholera-like.
A. LT and CT - Ouchterlony
MOA identical
Clements purification of LT on A5M (galactose)
B. ST - small MW non-immunogenic protein
MOA - activates guanylate cyclase and
blocks absorption of electrolytes
Now found in Yersinia and other bacteria
C. Lab diagnosis -
Biochemically identical to other E. coli;
Certain serotypes;
Need for rapid determination of ETEC
(DNA hybridization to plasmid; ELISA toxin)
D. Treat same as cholera
E. Control - Diarrheal disease in WHO #1 target
Exptl vaccines - LT/ST conjugates;
Cloned into S. typhi
A subunit as mucosal adjuvant to stimulate
local immune response.