URINARY TRACT INFECTIONS
ESCHERICHIA COLI: UTI's
Epidemiology / At Risk:
#1 organism responsible for UTI's.
Organisms originate from endogenous flora.
Manifestations: UTI
Dysuria, Frequency, Urgency
Cystitis, Urethritis
Pyelonephritis
Processing:
Specimen: Mid-stream clean catch
Catheter
Suprapubic aspiration
Stain: Gram-stain with one or more organisms per oil-immersion field is diagnostic.
Culture: Enteric Selective Medium (lactose).
Identification:
Lactose-Positive
Typical E. COLI Profile: O126:B4:H15:F1,P+
All E. COLI have F1 (mannose-sensitive) pilus
P+ means the Pyelonephritis antigen is present.
B4 represents subtype of flagellar antigens
H15 is another flagellar antigen
Virulence:
P-Antigen (Pili): Mannose-resistant F2-10 antigen that is associated with pyelonephritis.
K-Antigen (Capsule): Associated with adherence to transitional epithelium.
O-Antigen: Cell-wall polysaccharide.
Treatment: No treatment if asymptomatic
PROTEUS VULGARIS, MIRABILIS: Family Proteaceae, Gram-negative rods
Epidemiology / At Risk: Hospital-acquired UTI, catheterized.
Found in soil, water, and decaying organic matter.
10-15% of hospital-acquired UTI's
Wound infection
Manifestations:
UTI: Bacteriuria, dysuria, frequency, urgency, pyelonephritis, prostatitis.
Processing:
Specimen:
Stain:
Culture: Swarming Growth, many flagella and highly motile, forming rings of growth.
Identification:
Urease(+): Key test.
Weil-Felix Test: Cross-reaction of Proteus with the Rickettsia, to test for a Rickettsial infection. No longer used.
Species:
P. Vulgaris: Positive for metabolizing tryptophan ------> indole
Ampicillin-resistant. Use aminoglycoside and then wait for sensitivity tests.
P. Mirabilis: Negative for metabolizing tryptophan ------> indole
Treated with Ampicillin
Virulence:
Urease: Key virulence. Makes alkaline urine (more ammonia) ------> calculi and kidney stones.
A pH>8 in urine is suspicious for Proteus.
Flagella: Peritrichous flagella enables retrograde invasion of urinary tract.
Pili: Adhesin in renal pelvis.
Treatment:
P. Vulgaris: Ampicillin-resistant
P. Mirabilis: May be treated with Ampicillin.
PSEUDOMONAS AERUGINOSA: Family Pseudomonaceae, Gram (-) Rod.
Name-Derivation:
Epidemiology / At Risk: 3rd most common cause of UTI's.
Manifestations: Opportunistic
UTI's
Burn Infection: Leads to bacteremia and sepsis.
Bacteremia: Immunocompromised
Endocarditis
Pneumonia: Especially in Cystic Fibrosis patients.
Luminal infection is leads to buildup of mucus and pus.
micro-abscesses and necrosis can result.
Otitis Externa: Swimmer's ear
Eye infection: Conjunctivitis, keratitis, endophthalmitis.
Processing:
Specimen: Take blood to test for bacteremia
Clean-catch urine for UTI
Sputum for CF patient
Surface swab of burn
Stain: Direct microscopy not helpful.
Culture: Blood agar shows smooth, beta-hemolytic, blue-green (due to pyocyanin) colonies.
Sputum colonies from CF patient will be mucoidy, because of the presence of Alginate which sticks to the glycocalyx of epthelial cells.
Identification:
Strict Aerobe, thus they are non-fermenting of all sugars.
Oxidase (+) -- cytochrome oxidase; again, strict aerobes.
Juicy-Fruit Smell
Bug-Typing: Pyocins are used in hospitals to type-strains. These are proteins made by one strain of Pseudomonas that is lethal to another strain of Pseudomonas. This property allows for mapping of infections by different strains.
Virulence:
Cell-Associated
Pigments:
Pyocyanin: It is an effective antibiotic against Staph Aureus, thus it overtakes Staph in CF lung infections.
Pyoverdin:
Helps to acquire iron.
Ciliostatic.
Flagella: Adhesin in the urinary tract.
Pili: Adhesin to skin and upper respiratory tract.
Toxins
Exotoxin A: AB-Toxin acts similar to Diphtheria toxin. Especially toxic to liver cells (as compared to Diphtheria which likes heart, nerve, kidneys).
Fragment-A: Transfers ADP to Elongation-Factor 2 (EL-2) ------> inhibit protein synthesis.
Exotoxin S: General AB-cytotoxin that targets a lot of cells. ADP-ribosyl transferase that interrupts protein synthesis.
beta-Hemolysin: Consists of Phospholipase-C and Glycolipid, which act synergistically to lyse RBC's.
Enzymes
Alkaline Protease: Ruins PMN interaction with antibodies, thus preventing opsonisation and making a vaccine difficult.
Alginate: In CF patients, this sticts to the glycocalyx and is toxic to PMN's, resulting in the mucoidy colony.
Elastase: Responsible for the toxic effects of the bug.
Attacks elastin in vessels and lung.
Damages cornea
Causes pinpoint hemorrhages in skin
Impairs PMN function.
Vaccine / Prevention: Under develpoment, but not much progress.
Treatment: Highly drug-resistant. Big problem.