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532 Cards in this Set
- Front
- Back
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These are the three (not very effective) approaches to prevent endotoxic shock
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1. Antibodies (vs. TNFa, LPS)
2. Competitive inhibition of LPS binding to macrophage receptors, and LPS binding proteins 3. Inhibition of synthesis of LPS by gram- bacteria |
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These are elements of gram+ bacteria that can elicit endotoxin-like reactions in patients
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Teichoic acid, peptidoglycan
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This is one way to screen for LPS contamination
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Limulus polyphoemus (horseshoe crab) amoebocyte agglutination test
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LPS tests are typically performed in these cases
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LPS tests are performed on products at their site of manufacture; they are NOT routinely performed in the clinical lab, and rarely on patient samples (it is easier to culture bacteria than to detect LPS directly)
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What is the sensitivity of LPS screening by horseshoe crab amoebocyte agglutination?
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Picograms
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These toxins are denatured by boiling
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Exotoxins
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These toxins are /not/ denatured by boiling
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Endotoxins
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These toxins are antigenic
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Exo- and endotoxins both.
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These form toxoids
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Exotoxins (but NOT endotoxins)
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These toxins are characterized by low potency
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Endotoxin
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These toxins are characterized by high potency
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Exotoxins
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These toxins are highly specific
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Exotoxins
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These toxins have low specificity
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Endotoxins
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These toxins usually act via enzymatic mechanisms
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Exotoxins
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These are occasionally but not always pyogenic
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Exotoxins
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The mortality rate caused by endotoxic shock
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20-80% (depending on the patient's condition and the gram negative organisms, eg, different mortality rates can be partially explained by different O-antigens between microbes)
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The amount of time it takes for endotoxic shock to develop
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24 hours, but usually much longer
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The number of deaths in the US due to gram negative sepsis each year
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20,000
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This is the toxic portion of LPS
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Lipid A
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This is the antigenic portion of LPS
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O-antigen
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The function of LPS in gram negative bacteria
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Protection from predators, and permeability barrier to serum and antibiotics by increasing the negative charge of the membrane
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Bacteremia vs septicemia
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Bacteremia is simply the PRESENCE of bacteria in the blood, whereas septicemia is the GROWTH of, or INFECTION by, bacteria in the blood; both are assocated with septic shock
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Septic shock vs toxic shock
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Septic shock requires that bacteria are still in the blood, whereas toxic shock only requires a toxin be present, though bacteria may also be present. Patients can go into shock AFTER the bacteria are cleared; toxins remain or the cascade of events that characterize endotoxic shock have already been initiated
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Laboratory tests for gram negative bacteremia/septicemia
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Bacterial culture of three independent blood samples taken over a period of time in both aerobic and anaerobic conditions (two cultures for each blood sample), or direct culture of echthyma gangrenosum (black necrotic skin lesions) instead of culturing from the blood
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Echthyma gangrenosum
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A cutaneous infection characterized by black necrotic lesions on the skin
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Pseudomonas aeruginos
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Most commonly associated with echthyma gangrenosum
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Typical bacteria involved in gram negative infections
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1. E-coli, 2. Neisseria, 3. Pseudomonas aeruginosa
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What does "rough" mean in the context of gram negative bacteria?
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No O-antigen, and/or no outercore polysaccharides
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T/F: The physiological effects caused by LPS require living bacteria
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False
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Primary symptoms of endotoxic shock syndrome
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Fever; chills; hyperventilation; change in mental status; cool, pale extremities
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Clinical signs and complications of endotoxic shock syndrome
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Tachycarida; warm hypotension (esp standing BP); bleeding; leukopenia; thrombocytopenia; skin lesions; organ failure: lungs (cyanosis, acidosis), kidneys (oliguria, anuria, acidosis), liver (jaundice), heart (CHF)
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Gram negative sepsis is most common in these individuals
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Immunocompromised patients, debilitated or trauma patients
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Ineffective ways to prevent endotoxic shock
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Antibodies vs TNFa or LPS; Competitive inhibition of LPS binding to LBP or macrophage LPS receptors; inhibition of LPS synthesis by microbes
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These are elements of gram positive bacteria that can elicit endotoxin-like symptoms
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Teichoic acid, peptidoglycan (via Toll receptors)
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Limulus polyphoemus (horseshoe crab) amoebocyte agglutination test
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LPS is screened for in IV fluids and other materials via this method
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LPS tests are typically performed in these situations, and not in these
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Solutions for hospital use (eg, transfusions) and medical products at the site of manufacture; they are NOT routinely used in the clinical lab or on patient samples because it is easier to detect the bacteria direclty now that they can be cultured in as little as 6-12 hours
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These toxins are proteins, not lippopolysaccarides
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Exotoxins
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These toxins are usually denatured by boiling
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Exotoxins
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These toxins are resistant to boiling
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Endotoxins
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These toxins are antigenic
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Both exotoxins and endotoxins
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These toxins form toxoids
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Exotoxins
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These toxins are not very potent
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Endotoxins (>100 micrograms)
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These toxins have a relatively high potency
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Exotoxins (1 microgram)
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T/F: Exotoxins are 100 times more potent than endotoxins
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True
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These toxins have a high degree of specificty
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Exotoxins
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These toxins have a low degree of specificity
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Endotoxins
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These toxins typically exhibit enzymatic activity
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Exotoxins
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These toxins are occassionally but not always pyogenic
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Exotoxins
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These toxins are always pyogenic
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Endotoxins
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These toxins are coded for by genes located in a plasmid or bacteriophage
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Exotoxins
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These toxins are coded for by genes located in the bacterial genome
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Endotoxins
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These toxins induce the secretion of antitoxin antibodies in the host
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Exotoxins
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These toxins are poorly antigenic
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Endotoxins
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There are vaccines against these toxins
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Exotoxins (through toxoids), but NOT endotoxins (no toxoids)
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Toxic shock vs septic shock
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In septic shock, bacteria are in the blood; in toxic shock, toxins are in the blood. Blood cultures are therefore usually positive in septic shock, and negative in toxic shock
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These bacteria have capsules (K antigens)
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E. coli. Typeable H. influenzae. Meningococcus.
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These toxins associated with E. coli are plasmid encoded
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Heat labile (LT) and heat stable (ST) toxins
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Shiga-like toxin / Verotoxin
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E. coli toxin. Encoded on a lysogenic phage similar to phage lambda. Two subunits. Interferes with protein synthesis via RNA cleavage activity of the A subunit, and may interfere with host cell cytoskeleton via activity of its B subunit
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Siderophore
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E. coli bacterial protein. Responsible for uptake of nutrients such as iron in intestinal pathogenic isolates
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The primary source of enterohemorrhagic e. coli
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Cattle fecal contamination
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The second most common source of enterohemorrhagic e. coli
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Leafy vegetables
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Less important sources of enterohemorrhagic e. coli
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Unpasteurized cider/juice, raw milk/dairy products, vegetables (spinach); person-to-person, contaminated wading pools, petting zoos, etc.
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This bacteria causes an infectious disease characterized by asymptomatic carriers, bloody diarrhea, severe abdominal pain, vomiting in 50% of the cases, and hemolytic uremic syndrome (HUS) in 7% of cases
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Enterohemorrhage e. coli
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HUS
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(Hemolytic uremic syndrome) Characterized by hemolytic anemia, thrombocyutopenia, acute renal failure. Preschool children and the eldery are especially susceptible. Associated with 7% of cases of enterohemorrhagic e. coli infections
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E. coli O157:H7
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Enterohemorrhagic e. coli
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H antigen
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Flagella
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E. coli O55:H7
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An example of horizontal evolution among e. coli. Enteropathic e. coli, causing infantile diarrhea and has LEE insertion sites, thought to have aquired the ST phage and perhaps other elements that altered the O antigen
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Type III secretion system (T3SS)
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E. coli. Secretion of bacterial proteins through the bacterial cytoplasm, bacterial OM, and host cell cytoplasm through an "injection needle", allowing delivery of bacterial proteins to host cytoplasm
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LEE
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Locus of enterocyte effacement
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Tir
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Secreted via T3SS. Allows E. coli attachment to epithelium
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Intimin
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Located on E. coli (EHEC only) surface membrane. Binds Tir
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Components of E. coli LEE pathogenicity island (responsible for E. coli colonization)
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T3SS, Intimin, Tir
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Capable of recruitment of host cell actin, causing altered morphology. Impact signal transduction pathways to form A/E lesions
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E. coli bacterial proteins
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Beta-hemolysin
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This is a membrane-bound toxin of E. coli. Important for nutrient acquisition and cytotoxic pore formation in cells
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EHEC
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Enterohemorrhage E. coli (O157:H7)
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EPEC
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Enteropathogenic E. coli
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EAEC
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Enteroaggregative E. coli
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EIEC
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Enteroinvasive E. coli
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ETEC
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Enterotoxigenic E. coli
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Large intestine (food borne pathogen), moderately invasive, produces Shiga-like toxin, forms attaching and effacing (A/E) lesions and is complicated by hemoyltic uremia
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EHEC
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Small intestine (major cause of infantile diarrhea), forms A/E lesions; no hemolysin, shiga-like toxin or other toxins identified
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EPEC
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Small intestine, no A/E lesions, non-invasive, produces ST-like toxin, hemolysin, causes persistent diarrhea in children
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EAEC
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Large intestine (important cause of diarrhea), non-fimbrial adhesins, intracellular (replicate within enterocytes leading to lysis), no shiga toxin
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EIEC
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Small inestine (major cause of diarrhea worldwide), fimbrial adhesins, non-invasive, produces LT and/or ST, watery diarrhea, no inflammation
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ETEC
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EMB
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Selects for Lac+ pathogens
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MacConkey agar
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Selects for Lac+ pathogens
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Fermentation pattern common among intestinal pathogens
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Lactose
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Lactose negative pathogens
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Salmonella and Shigella
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Lactose positive pathogens
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E. coli
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Sorbital MacConkey Agar
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Used to distinguish pathogenic O157:H7 EHEC (negative testing) from commensal E. coli strains (positive testing)
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Diagnostic tools for O157:H7 E. coli
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Sorbitol MacConkey Agar; O157 antigen identification via serologic testing by direct or latex agglutination; H7 antigen identification; biochemicals
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Diagnostic tools of diarrheagenic E. coli
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Serotyping by pulsed field gel electrophoresis; PCR analysis of virulence factors
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Factors contributing to emerging infectious diseases
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Advancing age, chronic disease (eg, HIV), mass production of food, role of travel and commerce in transmission, microbial adaptation, etc.
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These bacteria are enterics (Enterobacteriaceae)
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E. coli, Salmonella, Shigella
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These bacteria are facultative anaerobes that ferment glucose
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Enterics
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These bacteria lack cytochrome oxidase and are therefore "oxidase negative"
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Enterics
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These bacteria reduce nitrates to nitrites
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Enterics
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These bacteria produce H2S
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Salmonella
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These bacteria have flagella (H antigen)
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E. coli, Salmonella
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These antigens are described as either Phase I or Phase II antigens
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H antigens
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Vi antigen
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Unique among S. typhi; a capsule-associated antigen
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These bacteria ferment glucose
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Salmonella. Shigella. Gonococcus. E. coli. Etc etc
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Number of species of Salmonella
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1500 species / serotypes
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Four species of Salmonella
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Typhi (one serotype), choleraesuis (one serotype), enteritidis (many serotypes), paratyphi
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Common and rare cause of typhoid fever
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Salmonella typhi, Salmonella paratyphi
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Specimens of this bacteria are recovered from patient's feces, blood or urine
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Salmonella
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Identified by sera against O, H and Vi antigen
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Salmonella typhi (most hospital labs carry sufficient variety of antisera to idenfity O antigens)
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Requires a high inoculum for disease (10e5 CFU)
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Salmonellosis
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Requires only a low inoculum of disease
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Shigella
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Salmonellosis syndromes
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Gastroenteritis, enteric fevers, and septicemias (most serotypes only cause gastroenteritis)
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These bacteria are facultative intracellular organisms
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Salmonella typhi and paratyphi
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Salmonellosis with an incubation period of 7-20 days
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Enteric fever (Typhoid)
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Salmonellosis with an incubation period of 8-48 hours
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Gastroenteritis
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Salmonellosis with abrupt onset and a rapid-rise fever
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Septicemia
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Salmonellosis with insidious onset and a gradual fever with a high plataeu lasting for several weeks
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Enteric fevers (eg, typhoid)
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Salmonellosis with abrupt onset, low fever and 2-5 day duration
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Gastroenteritis
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Salmonellosis with positive blood cultures
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Enteric fevers (1st through 2nd week of disease), Septicemia (during high fever)
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Salmonellosis rarely characterized by positive blood culture
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Gastroenteritis (only 5-10%)
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Salmonellosis with positive stool cultures -- diagnosis is absolutely dependent on finding the pathogen in feces or fecal swab
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Gastroenteritis
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Salmonellosis with stool culture that is often missed early on in disease
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Enteric fevers (Typhoid)
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Salmonellosis with stool culture that is only occasionally positive
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Septicemia
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Leukopenia is common in this disease
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Typhoid fever
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10% of untreated cases die of complications resulting from bowel perforation
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Typhoid fever
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Osteomyelitis may occur in patients with sickle cell anemia who contract these infectious diseases (2)
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Typhoid fever, septicemia (children)
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Diarrhea is usually absent, but abdominal tenderness and distention present
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Typhoid fever
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Malaise, anorexia, headache, followed by onset of fever with stepwise (contrast to rapid rise) increase to ~104 F
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Typhoid fever
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Many infections may be subclinical
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Typhoid fever
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This salmonellosis may cause enlargement of liver and spleen
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Typhoid fever
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This is the infectious path of Salmonella typhi
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Multiply within mononuclear cells of Peyer's patches --> enter blood via lymphatics through the thoracic duct --> disemmination to spleen, bone marrow and always the gall bladder / endotoxin is released in the blood causing some symptoms of typhoid fever
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Stool cultures are missed in this disease because GI symptoms do not appear until later
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Typhoid fever
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Stool cultures become positive then negative then positive again
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Typhoid fever (in the late stage, S. typhi is excreted into the intestine from the gall bladder)
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This disease is spread by 3% of infected patients who excrete the pathogen from suppurative focus in biliary tract, especially a problem in communities with poor sewage disposal
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Typhoid fever
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Febrile agglutinins
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Test for O and H agglutinins of S. typhi between 1st and 3rd week of infection
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Treatment for S. typhi infection
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First line therapy: fluoroquinolones (cirproflaxin), third generation cephalosporins (ceftriaxone). Second line therapy: chloramphenicol, amipicillin, trimethoprim plus sulfa. Treatment for chronic carrier state: ampicillin, ciproflaxin; or cholecystectomy (gall bladder removal)
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Some chloramphenicol resistance has been seen among these pathogens
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S. typhi
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Infects only man, not animals
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S. typhi. Pertussis. Diphtheria.
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Circulating antibodies to this pathogen are not entirely protective
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S. typhi
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Vaccine is a 4-dose, oral, live vaccine not to be given to children under the age of 6 with 50-80% success
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S. typhi (Typhoid)
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Vaccine is an intramuscular, Vi capsular polysaccharide vaccine administered 2 weeks before exposure with 50-80% success
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S. typhi
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Old vaccine is a saline suspension of killed pathogen that causes several adverse reactions in 10-30% of recipients
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S. typhi
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Accounts for 5-10% of salmonella infections
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Septicemia
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Disease characterized by high fever and bacteremia without GI involvement
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Salmonella choleraesuis
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This salmonellosis is rare but may occur in patients with underlying chronic diseases or immune deficiencies (eg, sickle cell anemia, cancer, young children)
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Septicemia
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Disease characterized by local abscesses, cholecystitis, pericarditis, meningitis, osteomyelitis
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Septicemia (system wide inflammation)
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Most common form of salmonella infection
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Gastroenteritis
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This disease is confined to the GI tract, and therefore blood cultures are often negative (90-95%)
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Gastroenteritis
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Salmonella typhimurium
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Most common cause of gastroenteritis
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This disease is characterized by sudden onset with headache, chills, abdominal pain, nausea, vomitting, diarrhea, often accompanied by fever
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Gastroenteritis
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Gastroenteritis
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Enterocolitis caused by salmonella
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This disease is self-limiting and usually lasts just 1-4 days
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Gastroenteritis (caused by salmonella)
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This disease has an animal reservoir
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Gastroenteritis caused by salmonella (eg, poultry, eggs, pork, dog food, domestic turtles, pork sausage)
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This disease is common in both developed and developing countries
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Gastroenteritis
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This disease is common in developing but not developed countries
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Typhoid
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This serotype is most frequently involved in egg contamination (0.005% to 5% of eggs entering the food supply)
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Salmonella enteritidis
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This disease can be transmitted by fruits
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Salmonella gastroenteritis
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This disease is treated by replacement of fluids and electrolytes
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Salmonella gastroenteritis and other diarrheal diseases
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This enteric bacteria is non-motile
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Shigella (lacks flagella)
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Production of gas from glucose can distinguish these two bacteria from one another
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SALMONELLA produces gas whereas SHIGELLA does not, though both are able to ferment glucose
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Production of H2S can distinguish these two bacteria from one another
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SALMONELLA produces H2S whereas SHIGELLA does not
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Gram negative bacillus, non-motile enteric bacteria
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Shigella
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This species of bacteria is more difficult to recover from feces than Salmonella
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Shigella
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There are four serotypes (A,B,C and D) of this bacteria
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Shigella
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Shigella serological group A
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S. dysenteriae
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Shigella serological group B
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S. flexneri
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Shigella serological group C
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S. boydii
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Shigella serological group D
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S. sonnei
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This serological group of Shigella is most common (75% of cases) in the USA, followed by these ones
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Group D, S. sonnei is the most common in the USA, followed by Groups B and C (flexneri and boydii, resp.)
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This serological group of Shigella is most common outside of the USA
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Group A, dysenteriae
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This bacteria has no animal reservoir
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Shigella. Contrast to Salmonella.
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Transmission is via "food, feces, fingers, flies"
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Shigella
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This bacteria has an incubation period of 1-4 days
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Shigella
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This is how Shigella invades its host
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Via the intestinal epithelium.
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This bacteria grows within host cells during infection
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Shigella
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This bacteria rarely causes bacteremia
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Shigella (rarely penetrates beyond the submucosa). Therefore blood cultures will be negative. Pertussis also never causes bactermia; it is confined to the respiratory tract.
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This bacteria causes bacteremia in 5-10% of cases
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Salmonella
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This bacteria can initiate disease at very low inoculum
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Shigella (as few as 100 bugs). This is possible because they are able to resist stomach acids. This explains why Shigellosis can be easily transmitted by the fecal-oral route.
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This bacteria invades cells at the terminal ileum and colon
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Shigella
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This bacteria produces bloody diarrhea by mucosal ulcerations with PMN and bacteria enmeshed in fibrin
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Shigella (because it invades at the terminal ileum and colon)
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This bacteria produces Shiga toxin
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Shigella dysenteriae
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Shiga toxin
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Cytotoxin with two subunits. Subunit B encodes a receptor for binding to intestinal epithelial cells. Subunit A binds host cell ribosomes leading to cell death. Shiga toxin also blocks fluid absorption in the intestine by killing absorptive epithelial cells (leading to diarrhea); bloody diarrhea is caused by invasion and blockage of fluid secretion. Contrast this with cholera toxin which causes active fluid secretion
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These two factors influence the severity of Shigellosis
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The species (dysenteriae is most severe), and the age of the patient
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This bacteria causes diarrhea by preventing absorption of fluid, and this one causes diarrhea by actively secreting fluid
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Shigella. Cholera.
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Invasiveness and toxin both play a role in the pathogenesis of diseases caused by this bacteria
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Shigella
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Non-protective serum agglutinins appear in the blood during convalescence in this bacterial infection
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Shigella
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Diarrhea is watery at first, but later contains blood and mucus
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Bacillary dysentery caused by Shigella dysenteriae
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The presence of this in the stool will indicate invasive disease
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PMNs
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Diarrhea is usually self-limiting lasting a few days, and rarely fatal
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Bacillary dysentery caused by Shigella dysenteriae
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Outbreak caused by the same strain is characterized by a spectrum of severity among patients
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Bacillary dysentery caused by Shigella dysenteriae
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Gram negative rods, non lactose fermenting, produce no gas, no H2S, non-motile
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Shigella
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Gram negative rods, non lactose fermenting, produces gas, H2S, motile
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Salmonella
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Gram negative rods, lactose fermenting, capsular
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E. coli
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This bacteria has many strains that carry R factors for ampicillin resistance
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Shigella
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Shigella vaccine
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Little immunity and not very effective. Live, avirulent oral vaccines have not proven successful
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Intracellular bacteria
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Rickettsia (obligate), Chlamydia (obligate), Mycobacterium leprae (obligate), Mycobacterium tuberculosis (facultative), Shigella (facultative), S. Typhi (facultative), a.o.
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These bacteria were originally mistaken for viruses because of their small size
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Rickettsia and chlamydia (both are obligate intracellular bacteria)
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Elementary bodies
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Stage one of the Chlamydia life cycle. Small, non-multiplying bodies with a rigid bacteria-like cell wall. This form transmits the infection from cell to cell and from person to person. They enter host cells by inducing phagocytosis, and can enter cells that are not normally phagocytic.
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Initial bodies / Reticulate bodies
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Stage two of the Chlamydia life cycle. Larger, actively multiplying, lacks rigid cell wall, non-infectious.
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These bacteria can enter, via phagocytosis, cells that are not normally phagocytic
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Chlamydia and Rickettsia
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This bacteria cannot synthesize ATP
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Chlamydia (therefore relies on host cells--obligate intracellular)
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Three species of chlamydia
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Psittaci, pneumoniae, trachomatis
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Pathogenesis of psittacosis
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Generalized infection, the agent can be recovered from blood or sputum. Most patients have fever and headache, but the most severe and distinct sign is extensive interstitial pneumonia.
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This bacteria is naturally a parasite of birds, and infections are caused by inhalation of bird feces
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Chlamydia psittaci
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|
|
This bacteria causes a significant fraction (10%) of pneumonia in adults, and is spread directly from person to person as respiratory aerosols
|
Chlamydia pneumoniae
|
|
|
This is the most common venereal disease
|
Nongonococcal urethritis (caused by Chlamydia trochomatis)
|
|
|
This bacteria exists as different serotypes that cause various diseases
|
Chlamydia trachomatis
|
|
|
C. trachomatis causes these two diseases and three clinical presentations
|
Trachoma, lymphogranuloma venereum. Inclusion conjunctivitis, newborn infant pneumonia, urethritis
|
|
|
This bacteria responds well to tetracyclines, though azithromycin may be the preferred treatment
|
Chlamydia
|
|
|
This disease is characterized by asymptomatic males and females
|
Nongonococcal urethritis (caused by Chlamydia trochomatis)
|
|
|
This disease may be characterized by purulent urethral discharge
|
Nongonococcal urethritis
|
|
|
This bacteria causes about half of the cases of nongonococcal urethritis
|
C. trachomatis
|
|
|
Nongonococcal urethritis
|
Disease caused by C. trachomatis. Grows in cervical cells of asymptomatic females and elsewhere; increases likelihood of HIV transmission
|
|
|
50,000 infections result in sterility every year
|
Nongonococcal urethritis (Chlamydia trochomatis)
|
|
|
This bacteria can cause ectopic pregnancies by this disease process
|
C. trachomatis. Nongonococcal urethritis
|
|
|
Asymptomatic at-risk women of child-bearing years should be screened by PCR of urine specimens for this bacteria.
|
C. trachomatis
|
|
|
This disease is treated with a single high dose of azithromycin
|
Nongonococcal urethritis (Chlamydia)
|
|
|
Inclusion conjunctivitis
|
Neonate disease caused by C. trachomatis infection from mother to child at birth (perinatal), and, rarely, by environmental contamination (eg, swimming pools). Can also be contracted by adults and adolescents as an STD.
|
|
|
Infant pneumonia
|
Neonate disease caused by C. trachomatis infection, usually secondary to ocular disease
|
|
|
Trachoma (caused by C. trochomatis)
|
Chronic reinfection of the conjunctiva causes an infolding of the eyelashes that results in corneal scarring and blindness
|
|
|
This disease is transmitted mechanically (eg, finger to eye) and by flies under conditions of poor hygiene, and is prevalent in tropical Africa and Asia
|
Trachoma (caused by Chlamydia trochomatis)
|
|
|
Treatment for diseases caused by chlamydia
|
Tetricycline and azithromycin
|
|
|
This disease is characterized by a painless papule progressing to an ulcerating vesicle that appears two weeks after exposure; four weeks after exposure the disease may progress to a painful suppurating disease of regional lymph nodes
|
Lymphogranuloma venereum
|
|
|
Frei test
|
Intradermal injection of heat-killed LGV. DTH indicates prior or current disease
|
|
|
Different serotypes of this bacteria cause different diseases
|
C. trachomatis
|
|
|
Lab diagnosis of Chlamydial infections
|
Comparison of acute and convalescent antibody titers (as in virology); inoculation of cultured cells to produce inclusion bodies by staining
|
|
|
These bacteria belong to the same family and both cause interstitial pneumonia transmitted by respiratory infections
|
C. psittaci and C. pneumoniae
|
|
|
This bacteria is a parasite of arthropods
|
Human disease-causing Rickettsia (Q fever is an exception--not transmitted by arthropods)
|
|
|
This bacteria is an obligate intracellular bacteria that can synthesize its own ATP
|
Rickettsia
|
|
|
This bacteria has a slow division time (about one day)
|
Rickettsia
|
|
|
This bacteria enters host cells via phagocytosis, expending its own energy in the process
|
Rickettsia
|
|
|
This bacteria lyses the host cell to release its progency
|
Rickettsia
|
|
|
This bacteria causes primary epidemic typhus
|
Rickettsia prowazekii
|
|
|
This disease requires louse control for its prevention
|
Primary epidemic typhus (caused by R. prowazekii)
|
|
|
Route of infection of Rickettsia prowazekii
|
Body louse punctures skin and defecates into the wound. Bacteria multiply first in capillary endothelial cells.
|
|
|
Incubation period of primary epidemic typhus
|
10 days
|
|
|
Pathogenesis of primary epidemic typhus
|
Abrupt onset of fever and severe intractable headache. A rash follows 4 to 7 days later. Frequently fatal except in children. A toxin may be responsible
|
|
|
This disease is frequently fatal if untreated, except in children
|
Primary epidemic typhus (caused by R. prowazekii)
|
|
|
This is the treatment for primary epidemic typhus
|
Tetracycline
|
|
|
Weil-Felix Reaction
|
Obsolete, non-specific serological test for primary epidemic typhus. Based on agglutination of OX-19 strain of Proteus, the gram negative bacterium. This is an example of two unrelated organisms sharing cross-reacting antigens.
|
|
|
Liver function tests are often elevated in this disease
|
Primary epidemic typhus (caused by R. prowazekii). Also Q fever, Ehrlichosis. RICKETTSIA diseases.
|
|
|
Brill-Zinsser Disease
|
A recrudescent disease of R. prowazekii, esp in immunocompromised hosts
|
|
|
This bacteria remains in the host even after recovery from primary infection, and can cause disease decades later
|
R. prowazekii
|
|
|
This disease is something to consider in patients formerly living in Russia or Eastern Europe
|
Brill-Zinsser Disease
|
|
|
This bacteria has an animal reservoir of flying squirrels
|
R. prowazekii
|
|
|
Endemic murine typhus
|
Caused by R. typhi. Milder version of primary epidemic typhus
|
|
|
This bacteria has as its usual hosts squirrels and rats
|
Rickettsia typhi
|
|
|
This disease has an endemic foci with rat as the normal host on Atlantic and Gulf seaboard, and with ground squirrel as the normal host in the southwestern USA
|
Endemic murine typhus
|
|
|
Rocky Mountain Spotted Fever
|
Caused by Rickettsia rickettsii.
|
|
|
This disease is characterized by fever, headache, arthritic pains and abdominal pain with nausea and vomiting
|
Rocky Mountain spotted fever
|
|
|
Incubation period of Rocky Mountain spotted fever
|
One week or less
|
|
|
This disease is characterized by a rash that begins on the hands and feet and spreads rapidly to the trunk. Lesions on the palms and soles is characteristic
|
Rocky Mountain spotted fever
|
|
|
This disease is characterized by a mortality rate of 20% in untreated adults
|
Rocky Mountain spotted fever
|
|
|
This bacteria is transmitted from tick to tick via the transovarian route
|
Rickettsia rickettsii
|
|
|
This disease is mostly acquired in the eastern half of the USA
|
Rocky Mountain spotted fever. Transmitted by forest ticks in the east, and dog ticks in the west
|
|
|
This bacteria causes Rickettsial pox
|
Rickettsia akari
|
|
|
This disease is systemic (fever, chills, headache rash), and the rash resembles that of chicken pox
|
Rickettsial pox
|
|
|
This disease is transmitted from mouse to mouse mite to human
|
Rickettsial pox (caused by R. akari)
|
|
|
Outbreaks of this disease are usually confined to a single building
|
Rickettsial pox
|
|
|
This bacteria causes Q fever
|
Coxiella burnetii
|
|
|
This disease is characterized by interstitial pneumonia, fever, headache, and elevated liver function tests (LFTs). Some patients have a rash
|
Q fever
|
|
|
This disease is transmitted in a spore-like stage
|
Q fever
|
|
|
This disease is transmitted to sheep, goats, cows and cats via ticks, and then to humans via placental tissue
|
Q fever
|
|
|
This disease is something to consider in patients with occupational exposure to animals
|
Q fever
|
|
|
Ehrlichosis
|
Two types: Monocytic and Granulocytic. Tick-borne disease.
|
|
|
This disease is characterized by fever, lymphocytopenia, and elevated LFT due to liver damage
|
Ehrlichiosis
|
|
|
Treatment for ehrlichiosis
|
Tetracycline
|
|
|
Vector for R. prowazekii
|
Human louse
|
|
|
Vector for R. typhi
|
Flea
|
|
|
Vector for R. rickettsii
|
Tick (dog or other)
|
|
|
Vector for R. akari
|
Mouse mite
|
|
|
Vector for Coxiella burnetii
|
None (respiratory infection of humans)
|
|
|
Vector for ehrlichiosis diseases
|
Tick
|
|
|
Gram positive rods, pleomorphic, non spore-forming, club-shaped
|
Corynebacteria
|
|
|
These bacteria are normal inhabitants of our skin and throat
|
Corynebacteria diphtheroids (all non-diphtheriae corynebacteria)
|
|
|
This bacteria causes diphtheria
|
Corynebacteria diphtheriae
|
|
|
This bacteria is unique in its arrangement in a non-orderly array suggestive of Chinese characters
|
Cor. diphtheriae
|
|
|
An example of a gram positive rod that does NOT form spores
|
Corynebacteria
|
|
|
Diphtheria transmission
|
Humans are the only natural host. Transmission by respiratory droplets.
|
|
|
Incubation period of diphtheria
|
2-5 days in the throat
|
|
|
This disease is characterized by a local inflammatory response with fever, cough and sore throat that leads to the formation of a gray pseudomembrane
|
Diphtheria
|
|
|
This disease is also seen as a necrotizing skin infection spread by contact in the tropics (and sometimes elsewhere)
|
Diphtheria
|
|
|
These three diseases are caused by Salmonella
|
Enteric fever, septicemia, gastroenteritis
|
|
|
This disease is the main disease caused by Shigella
|
Bacillary dysentery
|
|
|
This bacteria does not produce a systemic infection but does produce systemic symptoms
|
Corynebacteria diphtheria
|
|
|
This diseae may result in myocarditis, CHF, renal tubular necrosis, and nervous system disorders leading to weakness or paralysis
|
Corynebacteria diphtheria
|
|
|
Enterotoxins
|
Exotoxins (NOT endotoxins) produced in the GI tract
|
|
|
Conversion
|
Describes transfer of bacteriophage genes to the bacterial genome
|
|
|
Transduction
|
Describes transfer of bacterial genes between bacteria via bacteriophages
|
|
|
Bacteriophage beta
|
A temperate phage that carries the diphtheria toxin. An example of conversion.
|
|
|
These toxins have two domains, one that binds to a specific cell surface receptor of host cells, and a separate toxic domain that detaches following endocytosis of the toxin and enters the cytoplasm while the other domain remains in the endosome.
|
Diphtheria toxin, Pseudomonas toxin
|
|
|
These toxins block eukaryotic protein synthesis by inactivating EF2
|
Diphtheria toxin, Pseudomonas toxin
|
|
|
Toxoid
|
Formaldehyde treated exotoxin. Useful in prepartion of vaccines.
|
|
|
DPT
|
Combined vaccine against diphtheria, pertussis (whooping cough) and tetanus. Protection lasts at least 10 years.
|
|
|
This bacteria is detected by growth on tellurite and Leoffler media, and metachromatic granules
|
Corynebacteria diphtheria
|
|
|
This disease is diagnosed by presence of exotoxin demonstrated in lab animals following intradermal injection of cultured inoculum
|
Diphtheria
|
|
|
Treatment for diphtheria
|
Antitoxin and penicillin. Horse or human antitoxin neutralize the free toxin. Penicillin eliminates bacteria that would otherwise continue to produce toxin.
|
|
|
Once a major disease in the USA, now drastically reduced in incidence as a result of vaccination
|
Diphtheria
|
|
|
Schick test
|
Skin test for antibodies to diphtheria toxin
|
|
|
Skin test, toxin reagent
|
Positive response indicates no previous infection--there are no antitoxins in the serum to counter the effects of the toxin
|
|
|
Skin test, DTH-inducing antigen reagent
|
Positive response indicates previous infection--there are already cytotoxic T-cells specific for the anitgen that can react with it to cause a response
|
|
|
Positive test indicates NO previous infection
|
Skin test for diphtheria
|
|
|
Positive test indicates previous infection
|
Skin test for TB
|
|
|
Schick test
|
Skin test for antibodies to diphtheria toxin
|
|
|
Skin test, toxin reagent
|
Positive response indicates no previous infection--there are no antitoxins in the serum to counter the effects of the toxin
|
|
|
Skin test, DTH-inducing antigen reagent
|
Positive response indicates previous infection--there are already cytotoxic T-cells specific for the anitgen that can react with it to cause a response
|
|
|
Positive test indicates NO previous infection
|
Skin test for diphtheria
|
|
|
Positive test indicates previous infection
|
Skin test for TB
|
|
|
This bacteria's name is a misnomer--it was once thought to cause flu epidemics, but was later recognized as a secondary invader
|
Haemophilus influenzae
|
|
|
Small, gram-negative, non-motile, encapsulated bacillus (or coccobacillus) with complex nutritional requirements
|
Haemophilus influenzae
|
|
|
This bacteria was previously the most common cause of bacterial meningitis in children under 4 years of age
|
Haemophilus influenzae
|
|
|
Hib
|
Haemophilus influenzae type B. 60% of children infected with H. influenzae develop meningitis. 3-6% death rate.
|
|
|
This disease occurs only in humans
|
Bacterial meningitis caused by Hib
|
|
|
This bacteria produces an IgA protease
|
Haemophilus influenzae. Neisseria. E. coli.
|
|
|
This disease starts as a nasopharyngitis with otitis media or sinusitis, and may be followed by bacteremia
|
Bacterial meningitis caused by Hib
|
|
|
This disease has a sudden onset and may be fatal within 24 hours
|
Epiglottitis caused by Hib
|
|
|
This bacteria can cause cellulitis (face) or childhood pyarthoris (pus in joint) or pneumonia
|
Hib
|
|
|
Quellung
|
Capsular swelling. Used in the identifcation of different serotypes of capsular microorganisms
|
|
|
This bacteria exists as six serotypes (A,B,C,D,E,F)
|
Haemophilus influenzae
|
|
|
These serotypes of this bacteria have hexose in their capsules
|
Haemophilus influenzae types A,C,D,E,F
|
|
|
This serotype of this bacteria has ribose in its capsule
|
Haemophilus influenzae type B
|
|
|
These bacteria are facultative anaerobes
|
Enterics (E. Coli, Salmonella, Shigella), Haemophilus, etc.
|
|
|
This bacteria requires two growth factors
|
Haemophilus influenzae
|
|
|
Growth factor X
|
Hemin, precursor for heme groups of respiratory enzymes. Growth factor for Haemophilus influenzae
|
|
|
Growth factor V
|
NAD or NADP. Growth factor for Haemophilus influenzae.
|
|
|
This bacteria does not grow on fresh blood agar, and chocolate agar is used for culture instead
|
Haemophilus influenzae
|
|
|
This bacteria is very susceptible to disinfectants and drying
|
Haemophilus influenzae
|
|
|
This bacteria may appear as satellite colonies surrounding other bacterial colonies that secrete growth factors
|
Haemophilus influenzae. (Staphylococci and Streptococci secrete hemolysins and release their own growth factors to support H. influenzae growth.)
|
|
|
Sugar fermentation reactions are not of diagnostic use in identifying this bacteria
|
Haemophilus influenzae
|
|
|
Passive immunity to this infectious agent acquired from mother lasts only a few months
|
Hib and nontypeable Haemophilus influenzae
|
|
|
Incidence of disease caused by this bacteria falls off in children at 3-4 years of age due to acquired active immunity from asymptomatic infections
|
Hib
|
|
|
Hib vaccine
|
Conjugate CAPSULAR vaccine introduced in 1988. Capsular proteins are conjugated to diphtheria toxoid
|
|
|
Diagnosis is by blood and spinal fluid culture on a special agar plate and incubated in a carbon dioxide incubator
|
Meningitis caused by Hib
|
|
|
Treatment for Hib meningitis
|
Ampicillin. Third-generation cephalosporins. Augmentin (ampicillin and clavulanate combination).
|
|
|
Corticosteroids used during antibiotic treatment reduce residual neurological damage in treatment of this disease
|
Meningitis caused by Hib
|
|
|
Prophylaxis for Hib meningitis
|
Rifampin. Single dose of cirpoflaxin or ceftriaxone (cephalosporin).
|
|
|
Typeable vs. non-typeable
|
Describes Haemophilus influenzae. Typeable refers to capsular. Non-typeable lack capsule.
|
|
|
Transmission of Hib
|
Respiratory aerosols, esp between children
|
|
|
Most common cause of otitis media in children
|
Streptococcus pneuomniae
|
|
|
Second most common cause of otitis media in children
|
Non-typeable Haemophilus influenzae
|
|
|
This bacteria is generally restricted to the respiratory tract and infections of the ear (non-systemic)
|
Non-typeable Haemophilus influenzae
|
|
|
This bacteria causes respiratory tract infections in patients with underlying respiratory issues (COPD, chronic bronchitis, CF), sinusitis, conjunctivitis and otitis media
|
Non-typeable Haemophilus influenzae
|
|
|
Hap
|
Adhesin found among typeable and nontypeable Haemophilus influenzae
|
|
|
HMW1/2
|
Adhesin found in most nontypeable but not typeable Haemolophilus influenzae
|
|
|
Hia
|
Adhesin expressed in most nontypeable Haemolphilus influenzae that lack HMW1/2
|
|
|
Hsf
|
Adhesin of typeable strains of Haemophilus influenza that is a homologue of Hia
|
|
|
LPS
|
Adhesin that binds to platelet activating factor (PAF) receptor
|
|
|
Three ways of invasion of non-typeable Haemophilus influenzae
|
Macropinocytosis. Paracytosis (movement between cells of epithelium to invade sub-epithelial space; unknown OM protein is implicated). LPS binding to PAF receptor.
|
|
|
This bacteria colonizes the nasopharynx with preferential adhesion to respiratory mucus, non-ciliated cells and damaged epithelium
|
Non-typeable Haemophilus influenzae
|
|
|
Immunity to this bacteria seems to be strain specific--variation in OM proteins
|
Non-typeable Haemophilus influenzae
|
|
|
Non-typeable Haemophilus influenzae vaccine
|
Does not exist
|
|
|
20-35% of isolates of this bacteria are resistant to amoxicillin
|
Non-typeable Haemophilus influenzae
|
|
|
Treatment for otitis media and sinusitis caused by non-typeable Haemophilus influenzae
|
Amoxicillin (orally), sometimes also with beta-lactamase inhibitor (eg, clavulanate), or ceftriaxone
|
|
|
Top reason for the prescription of antibiotics in the US
|
Otitis media and sinusitis caused by non-typeable Haemophilus influenzae
|
|
|
This bacteria can cause persistent and recurrent infections, possibly due to its ability to form an antibiotic resistant biofilm, or its ability to invade host cells
|
Non-typeable Haemophilus influenzae
|
|
|
This bacteria is responsible for chancroid, an emerging STD in the US that is common in Africa and Asia
|
Haemophilus ducreyi
|
|
|
This bacteria produces a purulent conjunctivitis and is common in hot climates
|
Haemophilus aegypticus ("Koch-Weeks bacillus")
|
|
|
This bacteria is an occasional cause of pharyngitis and bacterial endocarditis
|
Haemophilus parainfluenzae
|
|
|
Four specis of Haemophilus
|
H. influenzae, H. ducreyi, H. aegypticus, H. parainfluenzae
|
|
|
Whooping cough
|
Bordetella pertussis
|
|
|
This disease begins with mild upper respiratory symptoms (catarrhal stage) followed by acute inflammation of trachae, bronchi and bronchioles with paroxysmal cough (paroxysmal stage)
|
Whooping cough
|
|
|
Whooping cough lasts this long
|
1-4 weeks
|
|
|
Small, gram-negative cocco-bacillus
|
Bordetella pertussis
|
|
|
This bacteria is a strict aerobe
|
Bordetella pertussis. Pseudomonas aeruginosa.
|
|
|
This bacteria requires very fresh media for growth (most labs have switched to PCR for detection)
|
Bordetella pertussis
|
|
|
This bacteria is found only in humans
|
Bordetella pertussis
|
|
|
Bordetella pertussis expresses these toxins
|
Pertussis toxin. Adenylate cyclase toxin. Dermonecrotic toxin. Tracheal cytotoxin.
|
|
|
Pertussis toxin
|
ADP-ribosylating toxin affecting adenylate cyclase, PLC and ion channels, causing lymphocytosis, histamine sensitization and enhanced insulin secretion. Causes a rise in cAMP by ribosylating (thereby deactivating) G-proteins involved in the inhibition of adenylate cyclase.
|
|
|
Cholera toxin
|
ADP-ribosylating toxin affecting adenylate cyclase. Causes a rise in cAMP by ribosylating (thereby increasing the activity of) G-proteins involved in the stimulation of adenylate cyclase.
|
|
|
Adenylate cyclase toxin
|
Calmodulin-stimulated. Impairs leukocyte function and may cause cell death by causing a rise in cellular [cAMP]. A toxin of Bordetella pertusis.
|
|
|
Dermonecrotic toxin
|
Mouse lethal toxin. Heat-labile toxin (LT). Causes vascular smooth muscle contraction resulting in ischemic necrosis of lung tissue. Toxin of B. pertussis.
|
|
|
Trachael cytotoxin
|
Causes ciliostasis and inhibits DNA synthesis. Kills trachael epithelial cells.
|
|
|
T/F: Bacteremia can result from Bordetella pertusis infection
|
False. Organisms remain in the respiratory tract
|
|
|
T/F: Bordetella pertussis can cause pneuomnia
|
True.
|
|
|
FHA
|
Filamentous hemagglutinin. Pilus-like filaments found on Bordetella pertussis
|
|
|
Pertactin
|
Surface molecule of Bordetella pertussis that aids in colonization
|
|
|
T/F: Bordetella pertussis features pili
|
True.
|
|
|
"Two component" system
|
Sensor and promoter. Controls virulence gene expression in Bordetella pertussis, and is being identified in many other pathogenic bacteria. Consists of a transmembrane sensor protein that detects environmental cues, and a cytoplasmic response regulator proteins (promoters)
|
|
|
Whooping cough
|
Bordetella pertussis
|
|
|
This disease begins with mild upper respiratory symptoms (catarrhal stage) followed by acute inflammation of trachae, bronchi and bronchioles with paroxysmal cough (paroxysmal stage)
|
Whooping cough
|
|
|
Whooping cough lasts this long
|
1-4 weeks
|
|
|
Small, gram-negative cocco-bacillus
|
Bordetella pertussis
|
|
|
This bacteria is a strict aerobe
|
Bordetella pertussis
|
|
|
This bacteria requires very fresh media for growth (most labs have switched to PCR for detection). Boudet-Gengou complex media.
|
Bordetella pertussis
|
|
|
This bacteria is found only in humans
|
Bordetella pertussis
|
|
|
Bordetella pertussis expresses these toxins
|
Pertussis toxin. Adenylate cyclase toxin. Dermonecrotic toxin. Tracheal cytotoxin.
|
|
|
Pertussis toxin
|
ADP-ribosylating toxin affecting adenylate cyclase, PLC and ion channels, causing lymphocytosis, histamine sensitization and enhanced insulin secretion. Causes a rise in cAMP by ribosylating (thereby deactivating) G-proteins involved in the inhibition of adenylate cyclase.
|
|
|
Cholera toxin
|
ADP-ribosylating toxin affecting adenylate cyclase. Causes a rise in cAMP by ribosylating (thereby increasing the activity of) G-proteins involved in the stimulation of adenylate cyclase.
|
|
|
Adenylate cyclase toxin
|
Calmodulin-stimulated. Impairs leukocyte function and may cause cell death by causing a rise in cellular [cAMP]. A toxin of Bordetella pertusis.
|
|
|
Dermonecrotic toxin
|
Mouse lethal toxin. Heat-labile toxin (LT). Causes vascular smooth muscle contraction resulting in ischemic necrosis of lung tissue. Toxin of pertussis.
|
|
|
Trachael cytotoxin
|
Causes ciliostasis and inhibits DNA synthesis. Kills trachael epithelial cells. Toxin of B. pertussis.
|
|
|
T/F: Bacteremia can result from Bordetella pertusis infection
|
False. Organisms remain in the respiratory tract
|
|
|
T/F: Bordetella pertussis can cause pneuomnia
|
True.
|
|
|
FHA
|
Filamentous hemagglutinin. Pilus-like filaments found on Bordetella pertussis
|
|
|
Pertactin
|
Surface molecule of Bordetella pertussis that aids in colonization
|
|
|
T/F: Bordetella pertussis features pili
|
True.
|
|
|
"Two component" system
|
Sensor and promoter. Controls virulence gene expression in Bordetella pertussis, and is being identified in many other pathogenic bacteria. Consists of a transmembrane sensor protein that detects environmental cues, and a cytoplasmic response regulator protein (promoter)
|
|
|
Incubation period of Bordetella pertussis
|
7-10 days
|
|
|
Bordetella pertussis vaccine
|
New acellular vaccines are safer ("aP" in "TDaP"). Contains PT, FHA, pertactin and pili virulence factors
|
|
|
T/F: Immunization or infection with Bordetella pertussis confers lifelong immunity
|
False.
|
|
|
Incidence of this disease increased after a precipitous decline due to risks associated with its vaccine
|
Whooping cough.
|
|
|
This vaccine can cause encephalopathy and permenant neurologic sequelae, thus it is phased out
|
Early pertussis vaccine (DTP)
|
|
|
T/F: Bordetella pertussis (whooping cough) is transmitted by aerosolized droplets and is very contagious
|
True.
|
|
|
It takes several weeks for children to produce antibodies to this infectious agents
|
Bordetella pertussis (whooping cough). Long duration (1-4 weeks).
|
|
|
This disease frequently is fatal for infants because passive immunity confered by Ab transmitted across the placenta are not sufficient
|
Whooping cough (B. pertussis)
|
|
|
This disease is characterized by lymphocytosis
|
Whooping cough (B. pertussis)
|
|
|
This bacteria has a large generation time (colonies grow very slowly)
|
Bordetella pertussis
|
|
|
Treatment for Bordetella pertussis
|
Erythromycin (penicillin, ampicillin are ineffective)
|
|
|
Species of Bordetella
|
B. pertussis, B. parapertussis, B. bronchiseptica
|
|
|
This bacteria causes respiratory illness in animals and only occasionally in humans
|
Bordetella bronchiseptica
|
|
|
T/F: Bordetella pertussis is the only species of Bordetella that produces pertussis toxin
|
True.
|
|
|
Major common and uncommon infections associated with Haemophilus influenzae
|
Meningitis, epiglottitis, pneuomia, otitis media. Less common: arthritis, osteomyelitis
|
|
|
Minor infection associated with Bordetella pertussis
|
Pneuomonia
|
|
|
Bordet-Gengou complex medium
|
Used for growth of Bordetella pertussis
|
|
|
Virulence factors of Haemophilus influenzae
|
Caspule, pili, IgA protease
|
|
|
Virulence factors of Bordetella pertussis
|
FHA, pili, pertactin, numerous toxins
|
|
|
Two species within the Neisseria genus
|
1. Neisseria meningitidis (meningococcus), 2. Neisseria gonorrhoeae (gonococcus)
|
|
|
Gram-negative, oxidase positive diplococci, adjacent sides slightly flattened
|
Neisseria (N. gonorrhoeae, N. meningitis)
|
|
|
Thayer-Martin selective medium
|
Isolates Neisseria meningitidis and gonorrhoaeae. Chocolate agar, vancomycin, colistin, nystatin. Vancomycin is anti-gram+, colisitin is anti gram- enteric, nystatin is anti-fungal
|
|
|
T/F: Drying, heat, and disinfectants are all effective ways of killing Neisseria
|
True.
|
|
|
Human pathogen only
|
Neisseria
|
|
|
This is how to distinguish between meningococcus and gonococcus
|
Sugar fermentation tests with glucose, maltose, lactose and sucrose
|
|
|
Neisseria that ferments glucose only
|
Gonococcus
|
|
|
Neisseria that ferments glucose and maltose only
|
Meningococcus
|
|
|
Neisseria that ferments glucose, maltose and lactose but not sucrose
|
Non-pathogenic Neisseria
|
|
|
Neisseria that ferments sucrose
|
None
|
|
|
Secretes IgA protease
|
Neisseria
|
|
|
LOS
|
Found on Neisseria. Lipid-oligosaccharide. No "O" side chains ("rough")
|
|
|
T/F: Unlike LPS, LOS is not endotoxic, and does not mediate resistance to serum bactericidal activity
|
False.
|
|
|
This bacteria's endotoxin damages cell walls of small vessels
|
Meningococcus
|
|
|
This bacteria lives in the nasopharynx and is present in about 5% of the general population
|
Meningococcus
|
|
|
This bacteria multiplies outside of cells, but not once phagocytosed
|
Meningococcus (contrast to gonococcus)
|
|
|
Neisseria that is encapsulated
|
Meningococcus
|
|
|
Serogroups of N. meningitidis
|
A,B and C are the important ones
|
|
|
This bacteria is characterized by smooth colonies, though on artificial media rough colonies are often produced
|
Meningococcus
|
|
|
Transmission of meningococcus
|
Person-to-person via respiratory droplets
|
|
|
This bacteria may only cause a mild pharyngitis and fever
|
Meningococcus
|
|
|
This bacteria may progress from the nasopharynx into the blood stream in a small percentage of infected people
|
Meningococcus
|
|
|
Incubation period of meningococcal meningitis
|
Up to 1 week
|
|
|
T/F: Maternal antibodies are ineffective against meningococcus.
|
False. Protective maternal antibodies are effective in preventing infection, thus it is not common among neonates.
|
|
|
This disease sees increased predilection among children below the age of five
|
Meningococcal meningitis
|
|
|
Organotropism
|
A characteristic of some bacteria that localize preferentially to specific organs. Meningococcus localizes to meninges.
|
|
|
Sites of localization of meningococcus
|
Meninges (major), but also skin, eyes and lung
|
|
|
Waterhouse-Friderchsen syndrome
|
Adrenal failure, circulatory collapse and shock with rapid death. Caused by excessive bacteremia.
|
|
|
T/F: Waterhouse-Friderchsen syndrome is a common occurence in meningococcal meningitis
|
False. It is an uncommon occurrence
|
|
|
This disease is characterized by outbreaks when diverse groups are brought together and previously unencountered serotypes are present
|
Meningococcal meningitis
|
|
|
This disease is characterized by patechiae followed by large areas of ecchymosis
|
Meningococcal meningitis
|
|
|
The infectious agent in this disease can be cultured from blood, CSF, and nasopharyngeal secretions
|
Meningococcal meningitis
|
|
|
T/F: Capsule antigens in CSF is a bad sign
|
True.
|
|
|
Treatment for meningococcal meningitis (2)
|
IV penicillin. Third generation cephalosporins (cefttriaxone)
|
|
|
Prophylaxes for meningococcal meningitis (2)
|
Rifampicin (tendency to be secreted into the saliva). Ciproflaxin (very potent).
|
|
|
This is not recognized by C3b and therefore does not stimulate recruitment of phagocytes
|
Sialic acid, a component of Type B meningococcal capsule and K1 capsule of some E. coli
|
|
|
T/F: Always take an LP of febrile neonates
|
True. It is essential to test CSF for meningococcal meningitis.
|
|
|
Meningitis caused by these bacteria (2) is the most difficult to diagnose in children
|
Haemaphilus influenza, streptococcus pneumoniae
|
|
|
This bacteria can be seen by gram stain in fluid of purulent exudate in infected individuals
|
Gonococcus
|
|
|
This Neisseria can be seen inside of epithelial and phagocytic (monocyte) cells
|
Gonococcus
|
|
|
This bacteria lives primarily in the GU tract
|
Gonococcus
|
|
|
T/F: Endotoxin is not a major factor in the disease state of meningococcus
|
False. It is a major factor in meningococcus infection, but not gonococcus
|
|
|
This Neisseria does not have a capulse
|
Gonococcus
|
|
|
Opthalmia neonatorium
|
Perinatal infection of conjunctiva in newborns.
|
|
|
Gonococcus vaccine
|
Does not exist
|
|
|
Incubation period of gonorrhoeae
|
2-3 days in males. Up to 10 days in females
|
|
|
This bacteria colonizes its host by intracellularly penetrating epithelial cells to reach sub-epithelial tissue
|
Gonococcus
|
|
|
More female than male carriers of this disease are asymptomatic
|
Gonorrhoeae. (1-10% of male carriers are asymptomatic, and an even greater percentage of females)
|
|
|
These bacteria cause the two most prevalent communicable bacterial diseases of humans
|
Neisseria gonorrhoeae and Chlamydia trachomatis
|
|
|
Arthritis-dermatitis syndrome
|
A complication of gonorrhoeae. May occur even without GU symptoms
|
|
|
This bacteria can cause chronic pelvic inflammatory disease in females
|
Gonococcus
|
|
|
Diagnosed by identification of gram negative diplococci within PMNs
|
Gonococcus
|
|
|
Treatment for gonorrhoeae
|
IM ceftriaxone (and 10 days oral tetracycline or doxycycline for chlamydia). One assumes chlamydia is present in cases of gonorrhoeae simply because it is a more prevalent STD.
|
|
|
STD of highest incidence
|
Chlamydia
|
|
|
Prophylaxis is mandatory for this disease
|
Opthalmia neonatorum caused by gonococcus.
|
|
|
Prophylaxis for opthalmia neonatorum
|
Tetracycline or erythromicin ointment, or dilute silver nitrate.
|
|
|
Recommended treatment regimens of this disease have changed several times in the last 10 years because of drug resistance
|
Gonorrhoeae
|
|
|
Diagnosis of this disease is difficult in chronic cases
|
Gonorrhoeae
|
|
|
PPNG
|
Plasmid-mediated penicillinase producing Neisseria gonorrhoeae
|
|
|
TRNG
|
Plasmid-mediated tetracycline resistant Neisseria gonorrhoeae
|
|
|
CRMNG
|
Chromosome-mediated resistant Neisseria gonorrhoeae. Multiple resistance to penicillin, tetracycline and some cephalosporins, related to mutations affecting permeability
|
|
|
Major infections of meningococcus (2)
|
Meningitis, septicemia
|
|
|
Major infections of gonococcus (2)
|
Gonorrhoeae, pelvic inflammatory disease (PID)
|
|
|
Virulence factors of meningococcus
|
Capsule, IgA protease, pili, LOS
|
|
|
Virulence factors of gonococcus
|
IgA protease, pili, LOS
|
|
|
This bacteria causes urethritis in men and PID in women
|
Gonococcus
|
|
|
Meningococcal vaccine
|
Available for capsule types A,C,Y and W-135, but NOT type B
|
|
|
Gram negative opportunistic pathogens
|
E. coli, Klebsiella pneumonia, Serratia marcescens, Enterbacter cloacae, Proteus mirabilis, Legionella pneumophila, Pseudomonas aeruginosa
|
|
|
These pathogens show less specialized adaptations to the host than other pathogens
|
Opportunistic pathogens
|
|
|
Nosocomial infections
|
Hospital-aquired infections. 65% of them involve biofilm formation
|
|
|
Most of this general type of bacteria form biofilms
|
Gram negative opportunistic pathogens
|
|
|
Diseases caused by E. coli
|
Gastrointestinal infections, urinary tract infections (UTIs), bacteremia, meningitis
|
|
|
Virulence factors of E. coli
|
Capsular antigen (important in neonatal meningitis), pili, exotoxin, cell-surface adhesins (eg, mannoside binding in UPEC)
|
|
|
UPEC
|
Uropathogenic E. coli. Causes UTIs. Capable of intracellular growth (in urinary tract epithelium)
|
|
|
This bacteria causes 95% of all non-hospital acquired UTIs
|
Uropathogenic E. coli
|
|
|
Cystitis
|
Syndome involving dysuria (burning pee), frequency, urgency and occasional suprapubic tenderness. No fever, contrast to pyelonephritis. Typical of LOWER urinary tract infections, but may also include UPPER
|
|
|
Mannosides
|
Important cell surface molecule of uroepithelial cells that are binding targets for UPEC
|
|
|
Acute pylenophritis
|
Results when UTI disseminates to kidney. Syndrome involving flank pain, tenderness, fever, dysuria, frequency and urgency
|
|
|
Type 1 pili
|
Notable for being mannose sensitive. Found in UPEC
|
|
|
UPEC E. coli adhesins
|
P pili and F adhesin can cause pyelonephritis. Prs, Type 1, S pili and Dr adhesin can cause cystitis. Only Type 1 pili are mannose sensitive.
|
|
|
P pili
|
Feature of UPEC, causes pyelnephritis. Attaches to P blood group globoseries Gal-Gal constituents of glycolipids on uroepithelia cells and erythrocytes. Coded by an OPERON
|
|
|
Stochastic switching
|
"Phase variation". Epigenetic and genetic phenotypic trait changes contributing to diversity and survival of a species of bacteria.
|
|
|
Gram-negative bacteremia
|
Main cause is E. coli. Systemic reaction to endotoxin (LPS). Septic (endotoxic) shock.
|
|
|
Leading cause of neonatal meningitis
|
E. coli
|
|
|
K1 capsule
|
Virulence factor of some E. coli. Nearly identical to the meningococcal capsule. Consist of sialic acids, which are also present in host cells and therefore are poor antigenic determinants.
|
|
|
Klebsiella pneumoniae
|
Red capsule. Non-motile. Causes primary pneumonia in alocholics, diabetics, etc. Also a cause of meningitis, bacteremia, etc.
|
|
|
Enterobacter cloacae
|
Contrast to Klebsiella: motile, thinner capsule. Associated with burn, wound, respiratory and urinary tract infections. With E. agglomerans, associated with IV tubing contamination affecting hundreds of patients in 25 hospitals.
|
|
|
Proteus vulgaris, Proteus mirabilis
|
Frequent cause of UTI. A notable feature is UREASE SYNTHESIS that can raise the pH of urine to precipitate salt and stone formation in the urinary tract in chronic infections
|
|
|
Serratia marcesens
|
Pneumonia. Less likely to colonize GI tract than other enterobacteriaceae. More associated with URINARY TRACT and RESPIRATORY TRACT. Associated with HEROIN addicts. Also associated with SEPTIC ARTHRITIS. Can produce IgA-specific proteases.
|
|
|
Pseudomonas aeruginosa
|
FORMS BIOLFILMS--the model organism for studying biofilms. Gram negative, obligate aerobe (cannot ferment sugar, but can grow via anaerobic resp. with nitrate instead of oxygen), opportunistic bacteria. Able to grow at temperatures as low as 4 C. Causes acute and chronic infections. Acute: Bacteremia (immunocompromised patients), eye infections, burn infections. Chronic: respiratory infections.
|
|
|
This bacteria can grow at temperatures as low as 4 C
|
Pseudomonas aeruginosa
|
|
|
This bacteria has a high natural resistance to many of the antibiotics used to treat other gram negative pathogens
|
Pseudomonas aeruginosa
|
|
|
Exotoxins secreted by P. aeruginosa
|
ExoA: Stops protein synthesis by ribosylating EF-2; ExoS and ExoT: Stops host regulatory proteins by ribosylating them; ExoU: Destroys cell membranes by its phospholipase activity. Elastase, phospholipase. Alginate: capulse giving strains a mucoid appearance; blocks phagocytosis
|
|
|
Alginate
|
Capsule of P. aeruginosa that is produced in chronic infection. Block phagocytosis like capsules normally do.
|
|
|
This is the model organism for studying biofilms
|
Pseudomonas aeruginosa
|
|
|
Legionella pneumophila
|
Causes Legionaire's disease--a potentially fatal pneumonia. Identified recently in 1976.
|
|
|
This bacteria is most frequently found in the water of cooling towers, and resides within free-living amoeba
|
Legionella pneumophila
|
|
|
Gram negative, pleomorphic rod. Exhibits intracellular growth
|
Legionella pneumophila
|
|
|
Incubation period of Legionaire's disease
|
2-10 days
|
|
|
Transmission of Legionaire's disease
|
NOT person-to-person, but via the airborne route from environmental contamination
|
|
|
Legionaire's disease
|
Pneumonia, though most infections are probably clinically insignificant ("cold symptoms"). Other symptoms are fever, chills, and a dry or productive cough, diarrhea, muscle aches, etc. therefore it is difficult to distinguish from other types of pneumonia.
|
|
|
The reservoir for this bacteria includes stagnant water in air conditioning and heating units
|
Legionella pneumophila
|
|
|
Diagnosis of Legionaire's
|
Detection of bacteria in sputum; antigens in urine; or increased antigens against convalescent blood
|
|
|
These gram negative opportunists are lactose positive
|
E. coli, Klebsiella pneumonia, Enterbacter cloacae
|
|
|
Filters must have at least this size pore to sterilize against bacteria
|
0.2 microns
|
|
|
Cystic fibrosis patients are much more likely than normal individuals to be infected by this bacteria
|
Pseudomonas aeruginosa
|
|
|
This bacteria can multiply in phagocytic mononuclear cells where it is protected from antibodies
|
Salmonella typhi
|
|
|
This is thought to have a role in tissue tropism with respect to E. coli colonization and immune avoidance.
|
Phase variation
|
|
|
Diagnosis is by a serological test that depends on agglutination of Proteus
|
Primary endemic typhus
|
|
|
These bacteria grow well on chocolate agar in 5-10% CO2.
|
Neisseria
|
|
|
T/F: All Chlamydia share a common antigent
|
True
|
|
|
This is the most common cause of infectious arthritis in sexually active adults
|
Gonococcus
|
|
|
Inclusion bodies of this bacteria are caused by reticulate bodies
|
Chlamydia trachomatis
|
|
|
This bacteria principally infects vascular endothelial cells
|
Rickettsia typhi (cause of murine endemic typhus)
|
|
|
T/F: Pseudomonas aeruginosa is non-motile
|
True
|
|
|
T/F: C. psittact will not grow in blood agar
|
True
|
|
|
T/F: Pateurization disinfects but does not sterilize
|
True. It only kills pathogens but allows many organisms and spores to live.
|
|
|
Where staphylococcus aureus lives
|
Nose
|
