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131 Cards in this Set

  • Front
  • Back
1) antibiotics
2) surgical treatments
3) indwelling devices
4) chronic illness
5) chemo-immunosuppression
6) immunosuppression due to infection (ie AIDS)
these pathogens show LESS SPECIALIZED adaptations to the host than other pathogens

only capable of causing infection when host defenses are compromised
NOSOCOMIAL infections
those that occur in the hospital (hospital-aquired infections)

often multiply (antibiotic) resistant
-LPS (involved in symptomotology)
Virulence Factors
contribute to the disease caused by the bacterium

(can include variety of different types of molecules, toxins and cell surface structures)
factors or pathways that are required for an organism to cause disease
virulence determinants or pathogenesis

**may not be specific to bacterium-host interactions
mechanism by which gram-negative bacteria cause disease
continues to be elucidated

often the immune response to Gram-negative cell components, such as LPS, cause symptoms
surface-attached microbial communities (~65% nosocomial infections are thought to be biofilm-related)

Biofilm formation is particularly relevant in device related infections

*biofilm bacteria have increased resistance to a range of antimicrobial agents and are often associated with the production of large quantities of polysaccharides
bacteria that causes most gram-negative infections
E. coli
types of infections caused by E. coli
1) GI
2) UTI
3) Bacteriemia
4) Meningitis
Opportunistic Gram-negative bacteria causing UTIs
E. coli
Klebsiella pneumonia
**Enterbacter cloacae
Proteus mirabilus
**Pseudomonas aeruginosa
Serratia marcescens
Opportunistic Gram-negative bacteria causing Respiratory infections
**Pseudomonas aeruginosa
**Enterbacter cloacae
Legionella pneumophila
3 characteristics of E. coli that contribute to its pathogenicity
1. CAPSULAR ANTIGEN (known significance in neonatal meningitis)
2. PILI (mediates invasion/adhesion esp in UTIs)
3. EXOTOXIN (principal cuase of GI symptoms)
Uropathogenic E. coli
cause of 95% of all non-hospital aquired UTIs
E. coli
frequency of UTIs among american women
60% have at least one in lifetime

11% have at least one per year
Opportunistic gram-negative bacteria associated with infections in burns and wounds
Klebsiella pneumoniae
Pseudomonas aeruginosa
Enterbacter cloacae
Legionella pneumophila
bacteria that:
-is part of our normal flora (0.1% of total enteric bacteria)
-synthesizes Vitamin K
-protects against other pathogens
E. coli
route of UTI caused by UPEC
ascending route of infection
why are women more susceptible to UTI than men?
due to presence of bacteria on the vulvar and perirectal areas and the short length of the female urethra

urethral massage or sex can contribute to infection by bacteria
a bacteriurial infection requires what concentration of bacteria in urine?
10^5 bacteria/ ml urine
syndrome involving dysuria (burning feeling during urination)
-frequency, urgency, occassionally suprapubic tenderness
-typically invovles infection of lower UT (but may include upper UT as well)
acute pylenophritis
results from UTI that has disseminated to the kidney

the clinical syndrome characterized by:
flank pain, tenderness and fever, dysuria, frequency and urgency
how do most UTIs resolve?
most are acute and self-limiting

however, 27-44% of infected women will experience at least one recurrence w/in 6 months, despite antibiotic therapy
what might contribute to persistant UTIs?
formation of "pods" or biofilm-like structures that form within epithelial cells of the Urinary tract

UPEC is able to invade epithelial cells and replicate within the cells
what influences the location of colonization of Uropathogenic E. coli?
TYPE OF ADHESIN elaborated by a particular E. coli strain

P pili (MR): pyelonephritis/cystitis
Prs pili (MR): cystitis
Type 1 pili (MS): cystitis
S pili (MR): cystitis
F adhesin (MR): pyelonephritis
Dr adhesin (MR): cystitis

MS= mannose sensitive, MR= mannose resistant
how is adherence (such as that involved in UPEC colonization) commonly measured?
by hemagglutination assay
almost 100% of these are colonized with bacteria within 3 days
urinary catheters
P pili present on UPEC associated with pyelonephritis mediate attachment of bacteria to what?
P blood group globoseries Gal-Gal constituent of glycolipids present on uroepithelial cells and erythrocytes
Pap genes (of a chromosomally located operon) encode all of the functions necessary for the biogenesis and function of what system?
the P pilus system
What is phase variation and what is its function?
stochastic switching of a phenotypic trait to provide phenotypic diversity inside and outside the host
-Goal: one varient is better able to survive and proliferate
-Controlled by: variety of mechs, strand slippage, methylation, recombination
-Influenced by enviro factors (temp, carborn source)
Mechanisms that control phase variation
strand slippage
leading cause of nosocomial bactemia
E. coli

(usually via urinary route, rarely via GI)
2 major routes of E. coli invasion
indwelling devices and UTI

mechanisms by which it crosses from UT into blood is not known (might invovle ability to invade host cells)
bacterimia caused by UTI most often occurs when
urinary flow is obstructed
E. coli associated with bacteremia have what critical traits?
SERUM RESISTANCE (ciritcal and correlated with production of K1 capsule)
systemic reaction to endotoxin or LPS (perhaps most toxic component of most bacteremic isolates of E. coli and is life-threatening)
most common neonatal pathogen, leading cause of neonatal meningitis
E. coli K1
E coli K1 is isolated from what percentage of healthy individuals?
how does E. coli colonize in newborns?
can colonize within hours of birth via vertical transmission from the mom or nursery staff
Pathogenesis of Neonatal meningitis caused by E. coli K1
1) colonize host mucosal surfaces
2) translocate ax to bloodstream
3) survive transport through bloodstrem (serum resistance important)
4) cross the blood-brain barrier and survive in CSF
5) proliferate and cause tissue damage
virulence determinants of E. coli causing neonatal meningitis
1) K1 polysialic acid capsule = MAJOR determinant
2) other determinants include S. Fimbriae, siderophores, etc...
general characteristics of bacterial capsule
1) outermost strucutre on bacterial surface
2) typically glycoconjugates
3) allow organism to evade nonspecific host immune defenses
4) primarily an anti-phagocytic mechanism
features of the K1 capsule
1) polysialic acid capsule, nearly identical to that of Neisseria meningitidis
2) sialic acids are constituents of most host glycoproteins and glycolipids, which may explain absence of effective immune response against E. coli K1
what feature of the K1 capsule may play a role in ineffective immune response against E. coli K1?
made of polysialic acid (also a constituent of most host glycoproteins and glycolipids)
Main contributor to pathogenicity of Klebsiella pneumoniae
reduced phagocytosis
reduced complement susceptibility

(can also be used to help id K pneumoniae based on a mucoid colony)
how does Enterbacter cloacae differ from Klebsiella pneumoniae?
E. cloacae is MOTILE and generally less heavily encapsulated
Enterobacter cloacae infection occurs in what setting?

associated with what type of infections?
occurs in hospital, 2ndary to antibiotic therapy

associated with burn, wound, respiratory and urinary infections
blood group type with increased susceptibility to E. coli UTIs and pyelonephritis
P1 blood group individuals (express P1 determinants in uroepithelium) appeart to be predisposed relative to P2 individuals
Serratia marcesens infections are seen secondary to what?
infections are seen secondary to:
-INSTRUMENTATION (tracheotomy, catheter, etc..)
pneumonia often contracted after use of contaminated respirator
How is Serratia marcesens different from other enterobacteriaceae?
less likely to colonise the GI tract and more associated with respiratory and urinary tract than other enterobacteriaceae

(GI tract is important reservoir among neonates)
outside the hospital setting, this bacteria has been associated with heroin addicts
in out-patient setting serratia marcesens is associated with what condition?
Septic arthritis

(also pink stuff in shower)
characteristics of Serratia marcescens that may influence its pathogenicity
production of Ig-specific protease

swarming motility
Prodigiosins produced by Serratia give rise to
a characteristic color
Proteus vulgaris and Proteus mirabalis are a frequent cause of what type of infection?
2 characteristics of Proteus vulgaris and Proteus mirabalis pathogenicity

UREASE SYNTHESIS (causes accumulation of ammonia)
bacteria that synthesizes UREASE, contributing to pathogenesis
Proteus vulgaris and Proteus mirabalis
P. aeruginosa acute infections include:
1) bacteremia in immunosuppressed
2) eye infections
3) burn infections
chronic infections by P. aeruginosa generally occur where? associated with what?
generally occur in the lung

in association with respiratory disease (eg CF) or implanted medical devices
bacteria that grows in biofilms in CF patients
p. aeruginosa
how is p. aeruginosa detected in blood culture?
requires aerobic incubation (since cannot ferment sugars= obligate aerobe) can grow via anaerobic respiration with nitrate as an electron acceptor, or ferment the amino acid arginine
factors that contribute to P aeruginosa pathogenicity:
1. Grows readily under various conditions (few nutrients, low temps)
2. Endotoxin
3. Plasmid content (antibiotic resistance)
4. Exotoxin- cytotoxic exotixin (ExoA,S,T, and U)
5. Elastases and phospholipases
6. Alginate capsule slime may block phagocytosis in chronic infections
7. biofilm formation
** Pili (type IV) = important virulence factors
Exotoxins involved in P aeruginosa pathogenicity
ExoA: ADP-ribosylates EF-2, stops protein syntehsis and elicits apoptosis
ExoS&T: ADP-ribosylating enzymes that target host regulatory proteins
ExoU: cytotoxic, phospholipase activity; causes irreversible cell-membrane damage and rapid necrotic death
Exotoxin: ExoA
ADP-ribosylates elongation factor 2 (EF-2), which stops protein synthesis and elicits apoptosis of affected cells
Exotoxins: ExoS and ExoT
ADP-ribosylating enzymes that target host regulatory proteins
Exotoxin: ExoU
cytotoxic, has phospholipase activity; causes irreversible damage to cellular membranes and rapid necrotic death
Legionella pneumophila was first identified where/when
19776, outbreak of penumonia among American Legion conference attendees
characteristics of 1976 Legionella pneumophila outbreak
1. large population (>189 people) affected
2. geographically circumscribed
3. significant mortality (15%)
4. large population at risk, elderly
5. Well publicized
characteristics of Legionella pneumophila organism:
-strict growth requirements, slow growing, rarely isolated from patients, in nature found in water of cooling towers
-resides within amoeba (or free-living in biofilms)
-gram negative pleomorphic rod
-intracellular growth
Legionella pneumophila route of infection
airborn route from environmental contamination (not usually person to person)
Legionella pneumophila incubation period
2-10 days
most infections caused by Legionella pneumophila are:
probably clinically insignificant (cold-symptoms)
why do most Legionella pneumophila outbreaks occur in summer and early fall?
because AC and heating units are a common reservoir
in early stages of Legionella pneumophila infection what is induced in M0s and alveolar epithelial cells
Legionella pneumophila induces apoptosis in M0s and alvelolar epithelial cells

2nd phase of necrosis induced by a pore-forming activity takes place in infected human phagocytes
principal clinical symptom in serious cases of Legionella pneumophila infection
fever, chills and a cough that may be dry or produce sputum

difficult to distinguish Legionnaire's disease from other types of pneumonia by symptoms
test of choice to Dx Legionnaires disease

most useful tests detect the bacteria in sputum, find Legionella antigens in urine samples, or compare Ab levels to Legionella in 2 blood samples obtained 3-6 weeks apart
how are gram-negative opportunistic pathogens differentiated in the clinical laboratory
since most are facultative anaerobes, they are distinguished by:
*their ability to ferment lactose
lactose fermenting gram-negative opportunistic pathogens
E. coli
K pneumonia
Enterobacter cloacae
Enterohemorrhagic E. coli
O157:H7 (as foodbourne pathogen)
Surface determinants of E. coli
O-antigen: LPS
H-antigen: Flagella (peritrichous)
K antigen: Capsule
Virulence factors of intestingal pathogenic E. coli isoaltes:
Toxins LT and ST; Shiga-like toxins
Endotoxin (LPS)
Nutrient update systems (siderophores)
Hemolysins and cytotoxins
K1 capsule
virulence factors of E. coli are typically chromosomally encoded, except for:
heat labile toxin (LT) and head stable toxin (ST) which are generally encoded on plasmids

Shiga-like toxin is encoded on a lysogenic phage similar to phage lambda
Adhesins involved in E. Coli colonization
{colonization factor antigens (CFAs)
and bundle forming pili (BFP)} and
E. coli's H-antigen
pertrichous Flagella
epidemiology of E. coli:
Primary source:
other sources
Contaminated Farm products
Primary source: cattle fecal contamination
Ground beef, undercooked hamburger, leafy vegetables, unpasteurized juice, dairy, vegetable products
2ndary person to person spread via pools
petting zoos, etc..
clinical manifestations of E. coli infections
asymtomatic carrier
diarrhea, frequently bloody
severe cramping abdominal pain
vomiting (50% of cases)
Hemolytic uremic syndrome (HUS) {~7% of cases: hemolytic anemia, thrombocytopenia, acute renal failure, esp. susceptible: toddlers and eldery}
O antigen 157
H antigen 77
E. coli O157:H7
s[ecofoc serogroup based on LPS and flagellear antigens
Colonization factors of E. coli O157:H7
delivered by the Type III secretion system
attaching and effacing lesion
A college student comes into the clinic complaining of eye irritation. This individual wears contact lenses. Culture of the eye reveals a Gram negative rod that produces a greenish pigment and grows at 42C.
Pseudomonas Aeruginosa
An individual who was using a urinary catheter subsequently complains of discomfort urinating. Culture reveals a Gram-negative, motile rod.
E. coli
Elderly individual returned from college reunion. Complains of flu-like symptoms, but recovers quickly upon antibiotic treatment. No patient samples are culture positive.
Legionnaires Disease
Enterohemorrhagic E. coli (EHEC)
infects what organ?
large intestine
Bloody diarrhea
-Organism invades mucosal cells but does not become systemic
-Although the organism does not become systemic, the toxins can spread
-Hemolytic uremic syndrome (HUS) acute renal failure caused by Shiga-like toxin
Enteropathogenic E. coli (EPEC) infects what organ?
small intestine
Enteroaggregative E. coli (EAEC) affects what organ?
small intestine
Enteroinvasive E. coli (EIEC) affects what organ?
large intestine
Enterotoxigenic E. coli (ETEC) affects what organ?
small intestine
Forming attaching/effacing lesions (E. coli pathogenesis)
Type II seretion system (proteins to host cells)
LEE (locus of enterocyte effacement, creation of pathogenicity island)
Intimate attaching: Tir intimin complex
Effacing: destruction of host cell microvilli
Type III Secretion Systems
A type III secretion system is a specialized form of secretion wherein a protein moves across the bacterial cytoplamic and outer membrane AND across a host cell membrane

A type III secretion system allows the bacterium to deliver proteins to the host cytoplasm
Type III Secretion system:
likely evolved from what apparatus?
can translocate what?
requires direct contact with what?
Likely evolved from the flagellar export apparatus
The type III secretion system can translocate many different types of effectors
Requires direct contact with the host cell
Type II secretion system is found only in what type of bacteria?
-only in gram negatives (but not in all species or strains)
- to date, only found in plant and animal pathogens
-usually present on mobile genetic elements (plasmids and transposons) in pathogenicity islands
how is the Type II secretion system regulated?
by low calcium
by cell contact
LEE (Locus for enterocyte effacement)
the pathogenicity island that encodes the T3SS, intimin, and tir
the 2 components to type III secretion systems
"secretion apparatus" used to deliver
"effector proteins" to the host cell altering its biology {Tir, Intimin, other proteins involved in recruitment/transduction)
-also called verotoxin
-encoded on a phage
-comprised of 2 subunits
-interferes with protein syntehsis via its RNA cleavage activity (subunit A) and may impact cytoskeleton (subunit B)
Shiga-like toxin
EspA forms what?
type III filaments
EspB and D from what?
pores in eukaryotic membranes
Mechanims by which E. coli alters/ subverts host cell biology
by causing actin polymerization and pedestal formation

(via Intimin on E coli binding Tir on host cell)
origin of shiga-like toxin virulence
Functions of Shiga-like toxin
Subunit A: interferes with protein syntehsis via its RNA cleavage (RNAse) activity (A subunit)

Subunit B: may bind to lipid component of euk cell membrane, remodels cytoskeleton and redistributes actin-binding proteins
Shiga-Like Toxin receptors
Binds to Gb3/CD77 glycolipid receptor

difference between cattle and humans?
RTX or hemolysin
pore forming protein that inserts into host cell membranes

common in strains of E coli that cause meningitis
Emergence of O157:H7 can be explained by

O55:H7 (frequent cause of infantile diarrhea, acquired additional virulence factors; Type III Secretion machinery, Intimin, effector proteins, Shiga Toxin (phage encoded) and hemolysin (
type of E. coli
causes Bloody diarrhea

Organism invades mucosal cells but does not become systemic

Does not possess Shiga toxin, HL or ST toxins

causes Childhood diarrhea similar to EPEC

Somewhat more aggressive than EPEC due to different colonization factors that lead to more aggressive epithelial cell attachment

Roles of toxins not known
EAEC Enteroaggregative E. coli
Traveler's Diarrhea

Virulence factors include plasmid encoded:
fimbriae (colonizes the small intestine)
heat-labile toxin (LT) (with essentially the same structure as cholera toxin)
heat stable toxin (ST)
Enterotoxigenic E. coli (ETEC)
ETEC Exotoxins
Heat Labile toxin (LT)
heat stable toxin (ST)
Heat-Labile Enterotoxin (HL (?LT))
produced by ETEC
-similar to cholerae toxin
causes a watery, bloody diarrhea
-target is adenylate cyclase: leads to increased cAMP levels resulting in excess chloride ion secretion and blocking of Na ion uptake
-overall consequence of these physiological changes is a net loss of fluid and electrolytes into lumen of the gut
Heat-stable toxin
produced by ETEC
alters cGMP levels with similar outcome to the heat-labile enterotoxin
main virulence factors of EHEC
-Intimin/Tir pedestals, Shiga-like toxin, hemolysin, evolved from EPEC
main virulence factors associated with EPEC pathogenesis
-Intimin/Tir pedestals, toxins?
main virulence factors associated with EAEC pathogenesis
-No A/E lesions, heat stable toxin, hemolysin
main virulence factors associated with EIEC pathogenesis
-non-fibrial adhesins
main virulence factors associated with ETEC pathogenesis
LT and ST toxins
Diagnosis of E. coli infection:
biochemical id based on:
carbohydrate fermentation patters and other reactions
-lactose fermentation is notable among intestingal pathogens
E. coli is Lac +, easily discerned on EMB or MacConkey agar, whereas salmonella and shigella are Lac -
-Sorbitol MacConkey Agar Dx test for O157:H7
O157:H7 is sorbitol-negative (colorless), while commensal E. Coli stains are sorbitol-positive
Serological Dx for O157:H7
direct or latex agglutination tests (to id O157 Antigen)

or H7 serological analysis
Dx of other diarrheagenic E. coli
serotyping-pulsed field gel electrophoresis

PCR analysis for virulence factors (e.g. BFP)
causes 73,000 cases of infection and 61 deaths each year on average in the US.
E. Coli
factors contributing to emergence of infectious diseases caused by foodborne pathogens
-HUMAN DEMOGRAPHICS: industrialized nations, advancing age (nursing homes), underlying chronic disease (HIV)
-BEHAVIOR (fresh fruit/veggie consumption, eating away from home)
-INDUSTRIAL TECH (mass produciton and bredding facilities)
-MICROBIAL ADAPTATION (including resistance)
-ECONOMIC DVPT/LAND USE (manure disposal)
How could switching to hay 5 days before slaughter could reduce E. coli numbers significantly?
grain produces a low pH in the rumen and this pre-adapts E. coli to smoach acid shock- they survive better

Hay leads to a higher pH, no adaptation and lower survival

Problem: switching to hay lowers yield and the beef industry opposes this