Vibrionaceae, Helicobacter pylori

Vibrionaceae

curved gram-negative, commonly found in saltwater, gram-negative

Vibrionaceae virulence factors

highly motile with single polar flagellum

Vibrio cholerae

low tolerance acid but tolerate alkaline conditions (pH 8-9)., water usually bit alkaline

rapid onset, suspected cases cultured

Vibrio cholerae serotypes

150 + anitgens, but only 2 cause cholera (O1 and O139)

O1

El Tor variant

O139

encapsulate → more resilient and protected, bengal, new and virulent

O1 and O139

contain TCP and CT

TCP

toxin co-regulated pilus

CT

cholera toxin, similar to LT

Vibrio cholerae dormant form

survive in environment associated with chitin exoskeleton of shellfish and plankton

Vibrio cholerae signs/symptoms

vomiting, painless diarrhea → “rice water” 10-20L/day

voluminous, odorless, may have mucus flecks

Loss of water causes loss in blood volume making it harder for blood to circulate and causes low bp

rapid pulse, wrinkled skin, sunken eyes, Blue death: cyanosis

Dehydration, hypertension, death

Blue death

1854 severe cholera outbreak in London proposed by John Snow as water-brone leading to better sanitation

Vibrio cholerae transmission

contaminated water, incubates for 2 days so traveling can cause imported cases

Vibrio cholerae endemic

india, africa, haiti

Vibrio cholerae pandemic

spans decades, 8 in the last 2 centuries

brought into western hemisphere (1911)

seen in gulf coast (1970s): undercooked shellfish

Vibrio cholerae epidemic

1991 Latin America: 21 countries

Peru 1/2million cases, 4500 deaths in 2. years

Cholera toxin pathogenesis 1

penetrates mucous using flagellum to reach epithelial layer

Cholera toxin pathogenesis 2

induces secretion of cholera toxin that binds to epithelial cells

Cholera toxin pathogenesis 3

subunit B binds to glycolipids brining bacterium and host closer

Cholera toxin pathogenesis 4

subunit A penetrates host membrane, cascade of molecular events resulting in higher cAMP

Cholera toxin pathogenesis 5

high levels of cAMP → acts on CFTR protein → Cl- ions into intestinal lumen

Cholera toxin pathogenesis 6

Osmotic gradient pulls Na+ and H2O out of cell into lumen causing dehydration

Vibrio cholerae treatment

rehydration therapy, antibiotics may shorten duration and transmission

Vibrio cholerae immunity

• natural infection can lead to lasting immunity

• Low gastric acid can make a person less susceptible

• IgG against LPS

• IgA in gastrointestinal tract

Vibrio cholerae prevention

water sanitation

proper cooking of shellfsih

vaccines: in trail for years but lack of funding

H.pylori

gram-negative bacilli

causative agent of most gastric ulcers and adenocarcinomas

H.pylori transmission

fecal-oral gastric secretions, infects 1/3 of population and cause clinical disease in a small portion

H.pylori proteins of interest

urease, vacuolating cytotoxin

Urease

H.pylori degrades urease producing ammonia and carbon dioxide that creates a local basic pH env

H.pylori diagnosis

breath test

endoscopy with biopsy and culture

serologic test

Breath test

1. baseline breath sample measures CO2

2. Second sample is taken after C13 urea which is labeled naturally occurring non-radioactive carbon isotope is ingested

H.pylori signs and symptoms

gastric pain, nausea

H.pylori treatment

antibiotics and bismuth salts (pepto Bismal)