Gm- Opportunists Flashcards
List 7 commonly isolated Gram negative bacteria that often grow as opportunists in debilitated
patients.
Escherichia coli Pseudomonas aeruginosa Klebsiella pneumoniae Enterobacter cloacae Serratia marcesens Proteus vulgaris & Proteus mirabilis Acinetobacter baumanii
Explain how specific known properties of each organism can contribute to its ability to cause infections.
Antibiotic resistance
Biofilms
List three diagnostic critera for diagnosis of Gram negative opportunists.
Diagnostics:
- –Colony morphology
- –Selective medium
- –Biochemical tests
Explain how infections by Gram negative opportunists are prevented and the role of antibiotics in controlling infections.
Treatments: Abx used dependent on infecting microbe and site of infection
Prevention: many things in combination need to be used to prevent infections
- –Control underlying compromising factors
- –Reduce catheter usage, increase hygiene
- –Decontamination of medical equipment
- –Cleaning of hospital spaces
- –Handwashing and glove use!
List three things that can increase risk of infection by opportunistic pathogens
- Decreased/altered immune function: chronic disease, chemo/immunosuppressive therapies, antibiotics
- Alterations in innate protective mechanisms
- Breach of physical barriers: surgery, indwelling catheters
What are opportunistic pathogens? What bacteria typically cause them?
Pathogens that can only cause disease in compromised people
Typically caused by Gm- bacteria
What are some sources of opportunistic pathogens?
Everywhere! Water, soil, vegetables, us
HOSPITALS!
What general virulence factors are associated with opportunistic infections? (4)
LPS -> systemic response if in bloodstream
Adhesins: cell-surface structures that mediate colonization
Nutrient acquisition factors
Toxins
What can contribute to pneumonia from opportunistic pathogens? (5)
Lung/heart disease, cancer Surgery Lying on back for a long time Mechanical ventilation Sedation
What are nosocomial infections? How can they be prevented?
Infections acquired in hospitals
Handwashing!
Name two important opportunistic pathogens with high INNATE resistance to antibiotics. Why are they so resistant?
Pseudomonas aeruginosa
Acinetobacter baumanii
Resistant because they grow in soil and have to compete with Abx producers in soil
What are biofilms? Why are they important? Where do they form?
Single or mixed species films of bacteria on a surface that increase their resistance to Abx
Form on catheters, sutures, chronic wounds, lung infections, endocarditis, UTIs
–65% of nosocomial infections are biofilm-related
How are biofilms formed?
Organic layer on catheter -> surface-associated cells -> ECM -> induction of biofilm Abx resistance genes
What is quorum sensing? What does it have to do with virulence factors?
A way for bacteria to talk to one another using chemicals that will indicate that they are surrounded by a certain number of organisms of the same type
Bacteria generally only induce virulence factors when they are at high density
What are three infections that can be caused by commensal E. coli?
UTIs
Bacteremia
Meningitis
Uropathogenic E. coli: epidemiology, including number of serotypes
Cause most UTIs
-Catheters important source of infection
-Women more susceptible than men
Only a few serogroups cause infection
Uropathogenic E. coli: how does infection occur?
Invasion and spread of bacteria into UT
Uses adhesins to aid in colonization and ascension of urethra
—Different strains = diffferent types = different colonizable locations
Form biofilms -> persistent infections
Uropathogenic E. coli: what are clinical symptoms? How many bacteria must be present to have a diagnosable infection?
Need 10^5 bacteria/ml in urine
Cystitis (inflammation of bladder)
- -Dysuria (burning during urination)
- -Frequent/urgent urination
Acute pyelonephritis (kidney infection)
- -Flank pain and tenderness
- -Fever
- -Dysuria (burning during urination)
- -Frequent/urgent urination
Uropathogenic E. coli: how is it treated?
Acute and self-limiting
Treat pyelonephritis with Abx
Commonly reoccur: human behavioral, biofilm formation
Uropathogenic E. coli: what is the P-pili? What does it bind to?
Binds to glycolipids found on human P blood group (Gal-Gal moiety)
- -Common in PYELONEPHRITIS
- -Different individuals have different P blood groups -> different susceptibility to P-pili/E. coli UTIs
Uropathogenic E. coli: what are type I pili?
Mannose-binding pili - allow them to bind mannose on host uroepithelial cells
–Common in CYSTITIS
E. coli bacteremia: epidemiology, pathogenesis
Leading cause of nosocomial bacteremia
–Commonly invades through IV catheters or UTIs with obstructed urine flow
E. coli bacteremia: how does it resist serum?
Produces K1 capsule: polysialic acid capsule (same as N. meningitidis)
–Sialic acid is on host glycoproteins/lipids, so no effective immune response
E. coli bacteremia: what is its most dangerous virulence factor?
LPS! Life-threatening
E. coli meningitis: what is it? What virulence factors are important for it? Briefly describe its pathogenesis.
Causes meningitis in neonates
Main virulence factor = K1 polysialic acid capsule (escapes phagocytosis)
–Siderophores very important
Proliferates in CSF -> inflammation, tissue damage
Pseudomonas aeruginosa: what range of infections can it cause?
Infections of burns, eyes, wounds, catheters, implants
Pneumonia, especially ventilator-associated
Bacteremia in immunocompromised patients
Pseudomonas aeruginosa: role in cystic fibrosis
Forms biofilms -> recalcitrance and resistance
Infects more than 80% of CF patients
Die in mid-30s due to inflammation/infection
Cannot be cleared
Pseudomonas aeruginosa: how does it evolve in chronic infections (CF)? (may not be important)
Produces alginate slime that may block phagocytosis (very mucousy)
Pseudomonas aeruginosa: virulence factors (5)
LPS
Extracellular elastases (proteases) and phospholipases
T3SS exotoxins:
–ExoA. Inhibits protein synthesis.
–ExoS and ExoT. Exoenzymes that modify host cell regulatory proteins
–ExoU. Phospholipase activity within host cell
Pyocyanin
Pseudomonas aeruginosa: why does it produce a green color?
Blue-green pigment = toxin called pyocyanin
–Affects host cell function, generates ROS
Klebsiella pneumoniae: clinical syndromes
Pneumonia when other conditions are present --Associated with alcoholism --Red currant jelly sputum UT, wound infections Diarrhea by enterotoxigenic strains Bacteriemia and meningitis
Klebsiella pneumoniae: virulence factors
CAPSULE:
- -Reduced phagocytosis and complement susceptibility
- -Produces mucoid phenotype
Enterobacter cloacae: epidemiology
Hospital-associated!
- –Associated with burns, wounds, respiratory/UT/catheter associated infections
- –Forms biofilms
Virulence factors unknown
Serratia marcesens: epidemiology, virulence factors
Very common enterobacteriaciae ---Produces a red color when grown (pink color on showers, water bottles!) - likes water Most common in respiratory/UT infections ---Can colonize joints, most tissues Generally seen secondary to immune problems, instrumentation, Abx use Virulence factors: ---MS-fimbrae ---Proteases ---Siderophores ---Swarming motility (see Proteus)
Proteus vulgaris & mirabilis: clinical syndromes, virulence determinants (2)
Commonly causes UTIs
Virulence determinants:
–Flagella (swarm motility- make a surfactant, then swim through it)
–Urease production: can contribute to stone formation due to urine pH change
Acinetobacter baumanii: characteristics, epidemiology
Similar to P. aeruginosa (non-fermenter) ---Oxidase negative ---Short rod ---Increasingly multi-drug resistant Causes nosocomial infections, especially with indwelling devices
UPEC: virulence factors (5)
Pili LPS Capsule Motility Exotoxins (including hemolysin)
Classify P. aeruginosa’s oxygen usage.
Obligate aerobe (cannot ferment sugars)
Acinetobactor baumanii: virulence factors (4)
Capsular polysaccharides
Adhesins
Proteolytic/lipolytic enzymes
LPS
E. coli: energy metabolism
Facultative anaerobe
E. coli: lactose fermenting?
Positive
K. pneumonia: energy metabolism
Facultative anaerobe
K. pneumonia: lactose fermenting?
Positive
S. marcescens: energy metabolism
Facultative anaerobe
S. marcescens: lactose fermenting?
Negative
E. cloacae: energy metabolism
Facultative anaerobe
E. cloacae: lactose fermenting?
Positive
P. mirabilis: energy metabolism
Facultative anaerobe
P. mirabilis: lactose fermenting?
Negative
A. baumanii: energy metabolism
Non-fermenter
A. baumanii: lactose fermenting?
Negative
P. aeruginosa: energy metabolism
Obligate aerobe
P. aeruginosa: lactose fermenting?
Negative
What is CRE?
Carbapenem-resistant enterobacteriaceae
