Enteric Bacteria: Shigella, Salmonella, Yersinia, Klebsiella, Rods

Shigella

strictly human disease, invasion enteric pathogen, closely ralted to E.coli but lack flagella. low infecting dose

900 million causes and about 110,00 deaths/year, 14,000 cases in the U.S.

Low infecting dose

colonizes GI tract, gram-neg

Shigella complications

dysentery and blood diarrhea, secondary attack rates in families (40%), high mortality 20%

Shigella sanitary practices

determine incidence, war and natural disasters can cause outbreaks

Shigella manifestations

fever, malaise, watery diarrhea, fever, dysentery, crampling/straining→ tenesmus

inflammation

Shigella treatment

resolve in 2-5 days

self-limiting, antibiotics shorten illness and spread

fluid and electrolytes

Shigella prevention

good hygiene, vaccines (in trial)

Shigella virulence factors

shigellosis, enterotoxin produces diarrhea

Shigella dampens immune system

acid-resistant

invasion causes destruction of enterocytes → ulcers

OSP5 protein inhibits expression of IL8 gene and inhibits immune response

Salmonella

non typhoid gastroenteritis, typhoid fever, systemic infection of PMN, carrier state- bacteria in gall bladder, disease of industrialized nations, infecting dose is higher institutional outbreaks common, human carries (5%), gram-negative, bacilli

Salmonella serotypes

many salmonella enteric, vary in preferred host

S. enteridits

human and other animals

S. typhimurium

humans, other animals

S. typhi

humans, higher primates

Salmonella food borne

intestinal infections, eggs and potato salad, seasonal outbreaks

modern food processing and delivery facilitate spread

Salmonella virulence factors

pili, flagella

Typhoid Mary

asymptomatic carrier, isolated by force, live typhoid bacteria in gall bladder, bacteria may be able to hide in macrophages

Shigella pathogenesis 1

shigella attaches to epithelial cells of colon

Shigella pathogenesis 2

shigella triggers endocytosis

Shigella pathogenesis 3

shigella multiplies in cytosol

Shigella pathogenesis 5

abscess forms as epithelial cells thus avoiding immune defense

Shigella pathogenesis 4

shigella invades neighboring epithelial cells, thus avoiding immune defense

shigella pathogenesis 6

shigella enters the blood vessel quickly phagocytized and destroyed

Salmonella pathogenesis 1

salmonella attached to epithelial cells lining small intestine

Salmonella pathogenesis 2

salmonella triggers endocytosis

Salmonella pathogenesis 3

salmonella multiples with food vesicle

Salmonella pathogenesis 4

salmonella kills host cell inducing fever, cramps, diarrhea

Salmonella pathogenesis 5

bacteremia salmonella moves into bloodstream

salmonella gastroenteritis treatment

antibiotics are of limited use, may increase carrier state

Salmonella typhoid fever treatment

antibiotics indicated, fever abates in 3-5 days, well in 2 weeks reduced mortality 20% to 2%

Salmonella prevention

sanitation, vaccines (moderately effective 50%-70%) only lasts a few years)

Yersinia

gram negative, facultative anaerobic bacteria

Y. pestis

plague, rodents, natural reservoir, fleas are vector

Y. enterocolitica

gastroenteritis, may be associated with chron’s disease

Yersimia pathogenesis: invasion of M cells 1

porte formation in macrophage

Yersimia pathogenesis: invasion of M cells 2

inhibition of phagocytosis and TMF production

Yersimia pathogenesis: invasion of M cells 3

local and systemic dissemination

Yersimia pathogenesis: in invasion of M cells 4

apoptosis of macrophage, release bacteria

Klebsiella

non-motile, gram-neg, facultative bacteria, diplo-cocci, opportunistic pathogen

Found everywhere in nature, natural flora: nost, mouth, GI tract

In GI tract, enteric, but get into lungs → pneumonia