Download Enterobacteriaceae (Intro and E. coli)

Enterobacteriaceae
Chapter 31
Introduction
“Enteric Bacteria”
Gram-negative rods
Ubiquitous
Cause 30%-35% of all septicemias, more
than 70% of UTIs, and many intestinal
infections
 Pathogens:
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 Normal flora – opportunistic infections
 Animal reservoirs
 Human carriers
 Box 31-1
BOX 31-1. Common Medically
Important Enterobacteriaceae
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Citrobacter freundii, Citrobacter koseri
Enterobacter aerogenes, Enterobacter cloacae
Escherichia coli
Klebsiella pneumoniae, Klebsiella oxytoca
Morganella morganii
Proteus mirabilis, Proteus vulgaris
Salmonella enterica
Serratia marcescens
Shigella sonnei, Shigella flexneri
Yersinia pestis, Yersinia enterocolitica, Yersinia
pseudotuberculosis
Physiology and Structure
 Facultative anaerobes
 Ferment glucose, are catalase
positive, and oxidase negative
 Lactose fermenting strains (e.g.
Escherichia, Klebsiella, Enterobacter)
 Non-lactose fermenting (e.g.
Salmonella, Shigella, and Yersinia)
Differentiating Similar Strains
Antigen detection
 O polysaccharides
 Part of LPS
 Capsular K
 Flagellar H proteins
 E. coli O157:H7
Pathogenesis and Immunity
Common virulence factors
 Endotoxin
 Lipid A portion of LPS causes many of the systemic
manifestations of infection
 Capsule
 Interferes with antibody binding
 Capsular antigens are hydrophilic (phagocytic cell
surface is hydrophobic)
 Poor antigenicity
 Antigenic phase variation
 Capsular K and flagellar H antigens are under genetic
control
 Can be expressed or not expressed
Pathogenesis and Immunity
 Sequestration of growth factors
 Iron: Bacteria produce competitive
siderophores or iron-chelating
compounds, hemolysins
Escherichia coli
Pathogenesis (Box 31-3)
 Adhesins: Essential for colonization
 Prevents the organism from being
flushed out of the urinary or
gastrointestinal tract
 Exotoxins
 Specific target tissue
 Result in altered cell function or cell
death
Epidemiology and Clinical Diseases
 Many infections are endogenous (septicemia and
UTI’s)
 Septicemia-originate from UT or GI infections leading
to intraabdominal infection
 Neonatal meningitis, Intraabdominal infections
 UTIs-originate in the colon -> contaminate urethra ->
ascend into the bladder
 Production of adhesins
 ~80% of all community-acquired UTIs
 Gastroenteritis-caused by five major groups
 May include: watery diarrhea, abdominal cramps,
fever, and vomiting
 (Table 31-1)
Gastroenteritis (ETEC)
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Estimated 80,000 cases in US travelers annually (650
million worldwide)
In small intestine; watery diarrhea, cramps, vomiting, fever
Occurs in developing countries usually in children or
travelers (traveler’s diarrhea)
1-2 day incubation, 3-4 duration
Infectious dose is high so person to person spread does not
occur
Two classes of enterotoxins: heat-labile (LT-I, LT-II) and
heat-stable (STa, STb)
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LT-I increases secretion of chloride and inhibits absorption of
sodium and chloride (the same as cholera toxin)
STa causes a hypersecretion of fluids
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Both contributing to watery diarrhea
Disease similar to cholera, but milder
Gastroenteritis (ETEC)
Imodium mode of action:
http://en.wikipedia.org/wiki
/Loperamide
Gastroenteritis (EHEC)
 73,000 cases with 60 deaths annually
 In large intestine; vomiting, abdominal cramps, fever
 Severity ranges from diarrhea to hemorrhagic
colitis (bacterial dysentery)
 3-4 day incubation, 4-10 day duration
 Infectious dose is less than 100 bacteria, O157:H7
serotype is the most common
 Read text page 329
 Shiga toxins (Stx-1, Stx-2)
 Bind to 28S rRNA and disrupt protein synthesis
 Tissue destruction leads to the symptoms (bloody
diarrhea)
Gastroenteritis (EHEC)
 Spinach Outbreak Information
 http://www.cdc.gov/mmwr/preview/
mmwrhtml/mm55d926a1.htm
 http://www.cfsan.fda.gov/~dms/spin
acqa.html#howmany
Salmonella Characteristics
 Similar to E. coli except no lactose
fermentation
 Historically there have been many
different species (~2000)
 All are really one species:
 Salmonella enterica
Salmonella Virulence factors
 Box 31-2 and 31-5
 Some bacteria can survive stomach
acid
 Able to enter M cells (peyer’s
patches)
 Cause cell death and spread to
surrounding cells.
 Figure
Salmonella
Epidemiology
 Colonize virtually all animal species
Salmonella Diseases
(Gastroenteritis)
 Most common form of disease
 40,000 cases in the US in 2004
 Mostly spread by eating contaminated food
(Poultry, eggs, dairy products)
 Can be fecal-oral in children
 Infectious dose 106 to 108
 Symptoms 6-48hrs after consumption
nausea, vomiting, non-bloody
diarrhea, fever, abdominal cramps
 Usually ends without intervention in a week
or less
Salmonella Diseases
(Typhoid Fever)
 Typhoid Fever
 Human reservoir (person-to-person spread)
 Pass through intestinal lining and engulfed
by phagocytes
 Replicate in liver, spleen, bone marrow
 Cause fever, myalgia, gastroenteritis
 Asymptomatic colonization (1-5% patients)
 Story Time - “Typhoid Mary”
Salmonella Treatment
 Preventative - safe food preparation
 Antibiotics not recommended for enteritis
 Typhoid Fever - antibiotics
Shigella
 Characteristics
 Gram - facultative anaerobe, rod
 DNA hybridization reveals they’re actually
biogroups of E. coli.
 Don’t ferment lactose
 Intracellular pathogen
Shigella Virulence Factors
 Adhere to, invade, and replicate in M cells
(Peyer’s Patches).
 Spread to macrophages and cause lysis of
phagocytic vacuole
 They then replicate in the cytoplasm
 Cause apoptosis, and release of IL-1β which
attract polymorphonulear leukocytes which
destroy intestinal tissue.
 Shiga toxin—disrupts protein synthesis
 Remember E. coli O157:H7
Shigella Epidemiology
 Estimated 450,000 cases in U.S.
(2003)
 150 million world wide
 Spread by fecal oral route (yummy).
 Primarily a pediatric disease
 70% occur in children 15 and under.
 Highest risk in daycares, nurseries,
custodial institutions
 Low infectious dosage (~200 cells)
Shigellosis
 Symptoms appear 1-3 days after ingestion
 Begin with watery diarrhea.
 Progress to abdominal cramps and pus in
bloody stool.
 Usually clears up on its own
 Antibiotics are given to reduce the chance of
spread
 Small percentage of asymptomatic
colonization
Yersinia Species
 Y. pestis – causes the plague
 Highly virulent pathogen causing a systemic
disease
 Y. enterocolitica - causes enterocolitis
Yersinia Virulence Factors
Found on plasmids
Capsule
Antiphagocytic proteins
Proteins which cause apoptosis in
macrophages
 Proteases which inactivate compliment
proteins
 Fibrinases which break down blood clots
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Yersinia Epidemiology
 Humans are accidental hosts
 Most infections in other animals are fatal (not
normal flora)
 Y. enterocolitica
 Reservoir rabbits, rodents, pigs, livestock
 Primarily in colder climates
 90% infections associated with ingestion of
contaminated meat, milk, water
 Mostly in children
Yersinia entercolitica
 Symptoms include: diarrhea, abdominal
pain, fever
 Can mimic acute appendicitis
 Usually lasts 1 to 2 weeks
 Because of growth at low temperature
(4°C) can spread in blood products
Yersinia pestis Epidemiology
Sylvatic Plague
 Reservoir is small
mammals,
livestock etc.
 Too widespread for
animal control
 Can spread by
eating
contaminated food
Yersinia Pestis Epidemiology
Urban plague
 Reservoir is rats,
transmitted by
fleas
 Rare due to good
hygiene, and rat
control
 Three great
pandemics.
Plague History
 Egypt 541 AD. lasted 200yrs
 Spread to most of the “old world”
 Killed a majority of the population
 1320s, over 5 year period 25 million
died in Europe (30-40% of
population)
 China 1860s spread world wide
 About 10 cases in the U.S. per year
 Sylvatic plague
Yersinia Diseases
Bubonic Plague
incubation of no more than 7 days
cause bubos (swelling of lymph
nodes) in groin and armpit
75% mortality in untreated cases
Yersinia Diseases
Pneumonic Plague
short (2-3 day) incubation
fever, malaise, pulmonary signs
highly infectious
90% mortality for untreated patients
Yersinia Treatment
 Y. pestis–streptomycin, tetracyclines,
chloroamphenicol
 Enteric infections usually clear on
there own
 Urban plague is controlled by
reducing the rodent population