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: Normal flora – opportunistic infections Animal reservoirs Human carriers

Box 31-1

BOX 31-1. Common Medically Important Enterobacteriaceae 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 ImmunityCommon 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) 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) LT-I increases secretion of chloride and inhibits absorption of

sodium and chloride (the same as cholera toxin) STa causes a hypersecretion of fluids

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/m

mwrhtml/mm55d926a1.htm

http://www.cfsan.fda.gov/~dms/spinacqa.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

SalmonellaEpidemiology

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 consumptionnausea, 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

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 dayscause bubos (swelling of lymph nodes) in groin and armpit75% mortality in untreated cases

Yersinia Diseases

Pneumonic Plagueshort (2-3 day) incubationfever, malaise, pulmonary signshighly infectious90% 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