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151 Cards in this Set
- Front
- Back
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Opportunistic pathogens
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Those capable of causing infection only when host defenses are compromised. These pathogens show less specialized adaptations to the host than other pathogens.
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True or false:
The increased use of antibiotics decreases the predisposition to an opportunistic infections. |
False.It increases
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True or false:
The increased scope of surgical treatments, implants, and transplants has predisposed patients to an opportunistic infections. |
True
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True or false:
Now that we have the increased capacity to sustain the chronically ill, there are more individuals who are predisposed to an opportunistic infection. |
True
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True or false:
Immunosuppression due to a primary infection such as AIDS has resulted in increased clinical cases of opportunistic infections. |
Tre
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Nosocomial
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Opportunistic infections that occur in the hospital or hospital-acquired infections
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What is the best way to avoid nosocomial infections?
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Washing hands
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What often causes the symptoms of Gm- infections?
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Endotoxin or LPS
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What are biofilms?
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Surface-attached microbial communities
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True or false:
~65% of total nosocomial infections are thought to be biofilm-related. |
True
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Do biofilm bacteria increase resistace to a range of bacterial agents?
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Yes
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Give 7 examples of opportunistic pathogens
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E. coli, Klebsiella pneumoniae, Enterobacter cloacae,Proteus vulgaris, Proteus mirabilis, Serrata marcesens, Pseudomonas aeruginosa, Legionella pneumophila
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Opportunistic pathogens that commonly cause urinary tract infection
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E. coli
Klebsiella pneumoniae Enterbacter cloacae Pseudomonas aeruginosa |
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Opportunistic pathogens that commonly cause respiratory infection
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Pseudomonas aeruginosa
Enterobacter cloacae |
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Opportunistic pathogens that commonly cause infections in burns and wounds
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Klebsiella pneumoniae
Pseudomona aeruginosa Enterobacter cloacae |
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Give two bugs that are part of normal flora but are also opportunistic pathogens.
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E. Coli
Enterobacter cloacae |
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E. Coli is the most common cause of Gram negative infections. E. Coli can cause:
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1. GI infection
2. UTI 3. Bactremia 4. Meningitis |
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Name three virulence factors of E. Coli.
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Capsular antigen (K Ag)
Pilli Exotoxin |
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Capsular antigen of E.Coli is associated with what kind of infection.
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Neonatal meningitis
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Pili of E. Coli is associated with what kind of infection.
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UTI and GI infection
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Exotoxin (proteins produced by bacteria)of E. Coli is associate with what kind of infection.
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Principal cuase of GI tract symptoms
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True or false:
More than one serogroups of E.Coli are associated with UTI. |
True
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Are E. Coli adhesins mannose-sensitive like other UTI-causing agents?
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Yes
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What is the laboratory diagnostic factor for UTI?
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> 10^5 bacteria/ml in urine
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Cystitis
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Describe the syndrome involving dysuria (burning feeling dring urination), frequency, urgency and occasionally suprapubic tenderness. Typically involves lower UTI
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Acute pylenophritis
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UTI disseminated to the kidney. Results in a clinical syndrome characterized by flank pain, tenderness and fever, dysuria, frequency and urgency
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Do UPEC invade epithelial cells? What are the consequences?
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Yes, it may lead to persistent infection
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Do UPEC form pods?
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Pods are biofilm-like structures. Persistent infection by UPEC may be due to the formation of pods.
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Can UPEC resolve on its own?
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Yes, typically, UTI by UPEC are sel-limiting. However, some women (27~44%) experience at last one recurrence of symptoms despite of antibiotic therapy.
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P-pili is associated with what type of infection?
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Pyelonephritis/ cystitis
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Prs pili are associated with
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cystitis
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Type I pili are associated with...
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cystitis
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S pili are associated with...
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cystitis
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F adhesin is associated with...
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Pyelonephritis
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Dr adhesin is associated with...
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cystitis
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Which type of pili/ fimbriae of E. Coli is mannose-sensitive?
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Tye 1 pili are the only pili that are mannose-sensitive.
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What is a common measure of adherence of pili?
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Hemagglutination
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Describe the mechanism of attachment of bacteria by P pili.
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P pili bind to glycolipids found on the huma P blood groups.
P1 individuals with certain P1 determinants are predisposed to E. Coli UTI. |
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Describe phase variation of pili.
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Stochastic switching of a phenotypic trait to provide
phenotypic diversity inside and outside the host. Mechanisms include strand slippage, recombination, methylation Influenced by environmental factors –Temperature »No pili produced at 25C, some cells produce pili at 37C. –Carbon source |
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Which two adhesin of E.Coli are associated with pyelonephritis?
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P pili/fimbriae and F nonfimbrial adhesin
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True or false:
E. Coli is a major cause of bacteremia, and is the leading cause of nosocomial bactremia. |
Tre
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True or false:
E. Coli entering the host via certain routes are more likely to be invasive. |
True
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What are the two routes that promote E. Coli invasion?
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UTI (especially when urinary flow is obstructed) and catheters
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Describe the pathogenesis of E. Coli bacteremia.
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1. Colonization host mucosal surface
– Pili and lectins 2. Translocation across surfaces into the bloodstream (mechanism not defined) – UTIs – Use of indwelling devices such as intravenous catheters 3. Survival in bloodstream (importance of serum resistance) |
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What is the biggest danger of Gm- bacteremia?
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Systemic reaction to endotoxin or LPS
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True or false:
Bacteremia frequently arise from GI infection of E. Coli. |
False
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What is the most common neonatal pathogen?
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E. Coli
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Is neonatal meningitis frequently caused by E.Coli K1?
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Yes
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What might be contributing to the serum resistance of E. Coli in bacteremia and neonatal meningitis?
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K1 capsule (composed of polysaccharides) allow the organism to evade nonspecific host immune defenses
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What are K1 capsule made of?
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Polysialic acid capsue. Sialic acids are constituents of most host glycoproteins and glycolipids.
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What are the virulence factors of neonatal meningitis?
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1) K1 polysialic acid capsule is the major determinant.
2) other determinants include S fimbriae, siderophores, etc. |
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Describe the pathogenesis of neonatal meningitis caused by E. Coli.
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Colonization host mucosal surface
• Translocation across surfaces into the bloodstream (mechanism not defined) • Survival in bloodstream (importance of serum resistance) The K1 capsule is a key virulence determinant here. • Cross the blood-brain barrier and survive in CSF. Proliferate and cause tissue damage |
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What are the characteristics of Klebsiella pneumoniae? (x3)
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1. Capsule
2. Non-motile 3. Mucoid colony due to capsule |
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What are the diseases frequently caused by Klebsiella pneumoniae?
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UTI
Wound infection Diarrhea by endotoxin strains |
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How do Enterobacter cloacae differ from Klebsiella?
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Enterobacter are motile and less heavily encapsulated.
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How does capsule increase pathogenesity of organism?
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1. Reduced phagocytosis
2. Reduced complement susceptibility |
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True or false:
Infections by Enterobacter cloacae are associated with burn, wound and respiratory and urinary infections. |
True
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True or false:
Enterobacter cloacae accounts for many hostpial acquired infections, expcially those associated with IV tubing. |
True
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Proteus vulgaris and proteus mirabilis frequently cause:
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UTI
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What contribute to the pathogenicity of Proteus vulgaris and proteus mirabilis?
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1. Flagella
2. Urease synthesis --> break-down urea to NH3 and CO2 and make urine alkaline |
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True or false:
Infection by Serratia marcesens are seen secondary to broad spectrum antibiotic therapy or secondary to instrumentation. |
True
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What disease is frequently caused by Serratia?
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Pneumonia
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How are serratia marcesens different from other enterobacteriaceae?
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Serratia is different from the other enterobacteriaceae in that it is more often associated with the respiratory and urinary tract
• less likely to colonize the GI tract • The GI tract is important reservoir among neonates |
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Which populations are associated with Serratia infections?
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Heroin addicts
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True or false:
In out-patient setting Serratia is associated wth septic arthritis. |
True
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Special pathogenicity of Serratia
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Ig-specific protease
Swarming motility |
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Pseudomonas aeruginosa can cause infections such as...
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Bactremia in immune compromised patients
Eye infections Burn infectins Pneumonia Chronic infections in association with cystic fibrosis |
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True or false:
P. aeruginosa can cause both acute and chronc infections. |
True
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What is the important diagnostic point of P. aeruginosa?
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It canNOT ferment sugars, detection in blood culture requires aerobic incubation.
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True or false:
P. aeroginosa is an obligate aerobe, thus cannot grow in anaerobic condition. |
False: P. aeroginosa can grow via anaerobic respiration with nitrate as an electron aceptor or ferment the amino acid arginine
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7 virulence factors of P. aeruginosa
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• Growth characteristics
• Endotoxin • Plasmid content that increase antibiotic resistance • Exotoxins that act within host cells •Pili (type IV)•Extracellular elastases and phospholipases •Alginate slime capsule may blocks phagocytosis (mucoid colony)•Biofilm formation |
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What do P. aeruginosa infect?
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Infects burns, eye wounds, catheters, implants
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What are the three exotoxins produced by P. aeruginosa important in pneumonia?
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Exo A, Exo S and Exo T, Exo U
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Exo A
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Stops protein synthesis and elicit apoptosis of affected cells
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Exo S and Exo T
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Exoenzyme is an ADP-ribosylating enyme that
targets cellular regulatory proteins |
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Exo U
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Cytotoxic
Has phospholipase activity Causes irreversible damage to cellular membanes and rapid necrotic death |
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Pneudomonas aeruginosa in clinic presentations
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• Bacteremia
• Eye infection • Burns • Intubated patients • Implant infections |
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True or false:
There is a high assoiation between CF and chroni P. aeruginosa infection. |
True.
Individuals with CF are susceptible to a chronic bacterial infections – P.a. infections occur in more than 80% of individuals • Patients usually die of respiratory failure in their mid-30’s due to damage from infection and from inflammation • Infections cannot be cleared by any current antimicrobial therapies |
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What might be contributing to the P. aeruginosa infection in CF patients?
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Evidence suggests that P. aeruginosa biofilm formation in the CF lung contributes to the inability to treat these infections
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What is the route of transmission for Legionella pneumophila?
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Air-borne
NOT human to human contact |
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Are most Legionella pneumophila infections asymptomatic?
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Yes
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What is the principal presentation of Legionella pneumophila in clinic?
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Pneumonia (serious case)
Cough, fever, muscle ache (cold symptoms) |
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How do you diagnose Legionella pneumophila?
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Direct fluorescent antibody test.
The most useful tests detect the bacteria in sputum, find Legionella antigens in urine samples, or compare antibody levels to Legionella in two blood samples obtained 3 to 6 weeks apart. |
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Are the common Gm- opportunisti pathogens usually anaerobes?
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No, most are facultative anaerobes.
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How do Pseudomonas aeruginosa metabolize their energy?
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They are categoricaly obligate aerobes; however, they can grow with nitrate a an alternative e- acceptor and grow on arginine fermentively.
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Name three Gm- opportnistic pathogens that fement lactose
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E. Coli
Klebsiella pneumonia Enterobacter cloacae |
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Name four Gm- opportunistic pathogens that cannot ferment lactose.
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Serritia marescens
Proteus mirabilis Legionella pneumophila Pseudomonas aruginosa (obligate aerobe) |
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Are E.Coli Gm- or +?
Are they rod-shaped or cocci? |
Gm-
Rod |
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Which virulent form of E. Coli causes enterohemorrhagic infection?
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E.Coli O157:H7 as foodborne pathogen
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Name the three surface antigenic determinants of E.Coli/ typical Gm- bacteria
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LPS (O-Ag)
Flagella (H-Ag) Capsule (K-Ag) |
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Are virulence factors of intestinal patogens encoded on chromosome of bacteria or on plasmid?
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Most are encoded chromosomally except for the heat labile toxin (LT) and heat stable toxin (ST) which are generally encoded on plasmid
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True or false:
Shiga-like toxin is encoded on a lysogenic phage that is similar phage lambda. |
True
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What is Shiga-lik toxin?
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It's LT and ST toxin that is specific to intestinal isolates.
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Which one of our normal flora synthesize vitamin K?
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E. Coli
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Which strain of E. Coli cause GI infection?
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Enteropathogenic E.Coli (EEC)
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What proportion of diarrhea in the developing countries result from EEC?
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25~50%
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List some virulence factors of intestinal pathogenic isolates
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fimbrial adhesin, nonfimbrial adhesin, Shiga-like toxins, endotoxin (LPS), siderophores, hemolysins, cytotoxins, K1 capsule
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List some common sources of EHEC.
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Most illness is associated with eating undercooked,
contaminated ground beef. Leafy vegetables are the second most common source Unpasteurized apple cider/juice, raw milk/dairy products, vegetables Person-to-person contact is also an important mode of transmission. |
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Is EHEC the only E.Coli strain that cause GI infection?
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No, there are several other strains: Enterohemorrhagic E. coli (EHEC), Enteropathogenic E. coli (EPEC), Enteroaggregative E. coli (EAEC), Enteroinvasive E. coli (EIEC), Enterotoxigenic E. coli (ETEC)
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What part of GI system does EHEC affect?
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Large intestine
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Give a clinical range of EHEC infection.
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•Asymptomatic carrier
•Diarrhea, frequently bloody •Severe, cramping abdominal pain •Vomiting in about 50% of cases |
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What are some major symptoms of EHEC?
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Bloody diarrhea
Severe, cramping abdominal pain HUS (hemolytic uremic syndrome)- inclue hemolytic anemia, thrombocytopenia, acute renal failure |
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Which virulence factor of EHEC cause hemolytic uremic syndrome?
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Shiga-like toxin
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What part of pathogenesis distinguish EHEC from non-hemorrhagic pathogens?
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EHEC invades the mucosal cells of GI tract. However, it usually does not become systematic.
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What determine serogroups of E. Coli?
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O-antigen and H-antigen
e.g. O157:H7 |
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Describe T3SS (type III secretion system) of E. Coli
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T3SS allows bacteria to deliver proteins to the host system. The genes are encoded on LEE (Locus for enterocyte effacement),a part of pathogenicity island.
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What does Tir do?
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Tir is a T3SS-secreted bacterial protein that is delivered to the surface of the host cell to allow E.Coli attachment.
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What does Intimin do?
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Intimin a Tir-binding protein that allow the E.Coli attachment to the host cell.
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What does Esp A do?
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Esp A forms Type III filaments building T3SS between the host and E.Coli
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What does Esp B and D do?
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They form pores in the eukaryotic membrane.
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LEE is thought to be acquired by E. Coli O157:H7 via....
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stabile toxin phage
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Describe a typical pathogenesis of EHEC inection.
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1) Attaching via pili and effacing (destruction of host villi)
2) Injecting bacterial proteins such as Intimin/Tir 3) Actin polymerization and pedestal formation |
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How is T3SS regulated?
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low calium and cell contact. The latter is required for T3SS activation.
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True or false:
T3SS is found in all Gm- bacteria but not in Gm+. |
False: T3SS is found only in Gm- bacteria; however, not all species have T3SS
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Which virulence factor causes bloody diarrhea?
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Shiga-like toxin, a.k.a., verotoxin
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How does Shiga-like toxin kill host cell?
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Shiga-like toxin, made up of two subunits, cleaves RNA via RNAase activity (subunit A) and interfere with ctoskeleton (subunit B)
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To what does Shiga-like toxin bind?
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Gb3/CD77 glycolipid receptor
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Which populations are more susceptible to hemolytic ureic syndrome caused by EHEC?
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Young children and elderly
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Give two examples of EHEC enterotoxin.
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Shiga-like toxin
Hemolysin |
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How do hemolysins cause toxicity to cells?
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Forms pore that insert into a host cell membrane
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True or false:
Hemolysin is encoded on plasma |
True
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E. Coli strain associated with infantile diarrhea ad its virulent component
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Enteropathogenic E. Coli (EPEC)
Forms A/E lesions, no known hemolysin, no shiga-like toxin or others |
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Is EHEC invasive?
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Yes, moderately.
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Is enteroaggregative E. Coli invasive?
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No, it's non-inasive. It produces a heat stable-like toxin and hemolysin
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What clinical manifestatio is common in manifestation of EAEC?
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persistent diarrhea in children
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Describe the pathogenesis of enteroinvasive E. Coli (EIEC) that is different from EHEC
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Non-fimbrial adhesin
Replicate within enterocytes leading to lysis No shiga-like toxin |
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Are enterinvasice E. Coli an important cause diarrhea?
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Yes
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Which strainof E.Coli is the major cause of diarrhea worldwide?
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Enterotoxigenic E. Coli (ETEC)
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ETEC has what virulent factors?
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Fimbrial adhesins, LT and ST
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True or false:
ETEC cause watery diarrhea with no inflammation |
True
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Which enteropathogenic E. Coli infect large intestine?
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Invasive ones that cause bloody diarrhea
EHEC EIEC |
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Which enteropathogenic E. Coli infect small intestine?
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Non-invasive ones that cause watery diarrhea
EPEC EAEC ETEC |
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How is EPEC transmitted?
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via person-to-person route
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True or false:
Enteroinvasive E. Coli infection is a very common cause of bloody diarrhea. |
False, it's quite rare.
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How can you differentiate the cause of bloody diarrhea between EIEC and EHEC infections?
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EIEC do not produce Shiga-like toxin and has non-fimbrial adhesins
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How are EIEC invasive?
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They invade entrocytes and replicate within the host leading to lysis. Note that there is no toxin involved.
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Which two enteropathogenic E.Coli strains cause A/E lesions?
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EHEC and EPEC
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A/E lesions refers to...
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the destruction of host microvilli due to the intimate adherence of E.Coli
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Which is more aggresive in its pathogenesis? EPEC or EAEC?
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EAEC due to different adhesion factors that lead to more aggressive attachment.
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Name three virulent factors of ETEC.
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Fimbrae
ST (heat stable toxin)and LT (heat labile toxin) |
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True or false:
LT is similar to cholerae toxin. |
True
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What type(s) of diarrhea does LT cause?
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both watery and bloody
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What is the target of LT?
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adenylate cyclase which increases the activity of cAMP. The increased cAMP activity results in the increased activity of chloride efflux ion pump, leading to excess Cl- loss and blockage of Na+ intake. Overall, net loss of fluid and electrolytes to gut lumen
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What is he target of HT?
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cGMP, the consequence and route are similar to LT
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Major virulent factors of EHEC
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Intimin/Tir pedestals (A/E lesions), Shiga-like toxin, hemolysin, evolved
from EPEC |
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Major virulent factors of EPEC
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Intimin/Tir pedestals (A/E lesion)
No known toxins |
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Major virulent factors of EAEC
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No A/E lesions, heat stable toxin, hemolysin
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Major virulent factors of EIEC
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non-fibrial adhesins
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Major virulet factors of ETEC
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LT, ST and fimbrial adhesins
No inflammation Diarrhea majorly due to loss of fluid and electrolytes to the gut lumen |
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What are the main diagnostic tools for O157:H7?
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•Sorbitol MacConkey Agar
–O157:H7 is sorbitol-negative –Commensal E. coli strains are sorbitol-positive •Direct or latex agglutination tests •Confirmation by biochemical tests •PCR •H7 serology and toxin analysis |
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Is O157:H7 sortbitol-negative or -positive? What about commensal E. Coli?
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O157:H7 are sorbitol-negative (colorless)
Commensal E. Coli are sorbitol-positive. |
