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59 Cards in this Set
- Front
- Back
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What are "diphtheroids"?
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Corynebacteria that are non-pathogenic commensal inhabitants of pharynx, nasopharynx, distal urethra and skin
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What are the 3 main disease causing corynebacterium?
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C. diphtheriae
C. ulcerans (mild disease) C. jeikeium ( nosocomial infection in immunosuppressd patients) |
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Characteristics of corynebacterium:
Gram stain ?? Growth conditions ?? Hemolysis ?? Catalase ? |
Gram + club-shaped bacillus
Aerobic Non-hemolytic Catalase + |
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What are clinical manifestation due to beta-phage encoded Diphtheria toxin (DT) in nasopharyngeal?
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Pharyngitis or tonsillitis
Membrane on tonsils, uvula made of fibrin, leukocytes & cell debris Respiratory obstruction --> death |
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What are some systemic effects of DT?
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Myocarditis
Nervous system involvement --> paralysis |
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What are some effects of cutaneous infection?
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Skin lesions with gray-brown pseudomembrane
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How is C. diphtheriae spread?
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Droplet spread (nasopharyngeal)
Direct contact (cutaneous) |
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How is C. diphtheriae maintained in the population?
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Asymptomatic carriers in oropharynx and skin of immune people
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Pathogenesis of C. diphtheriae is dependent on 3 things:
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1. Colonization of nasopharynx or skin
2. Production of PLP D to promote spread 3. Production of DT |
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What kind of toxin is DT?
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An exotoxin that is secreted by lysogenic strains of the beta-phage.
It is a simple A-B toxin. *It is lethal at 0.1 ug/kg! |
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How does DT kill sensitive cells?
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DT inactivates EF-2 by transfer of an ADP-ribosyl group from NAD to a modified His on EF-2
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Name some other A-B toxins whose A moieties also have ADP-ribosylating activity.
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P. aeruginosa - exotoxin A
Vibrio cholerae - cholera toxin E. coli - LT Bordatella pertuss - pertussis toxin |
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What are the steps required for DT to enter a cell?
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Toxin attaches to cell surface receptors via B moiety.
Complex is internalized into endosomes. Acidification = insertion of B into endosomal mem and transfer of A to cytosolic face. Reduction of disulfide bond releases A into cytosol. A inactivates EF-2 |
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How do you diagnosis diphtheria?
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Entirely clinical.
Can isolate C. diphtheriae from infected site and grow on Tellurite medium; catalase + |
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How do you demonstrate toxigenicity for C. diphtheriae?
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Elek immunodiffusion test.
Filter paper is impregnated with diphtheria antitoxin and embedded in culture medium. If toxin present it is secreted and reacts with the antitoxin to form lines of precipitin. |
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How do you treat diphtheria?
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1. Neutralize toxin by antitoxin therapy
2. Elimination of organism with penicillin & erythromycin |
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Why should it be possible to eradicate diphtheria?
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Humans are the only reservoir.
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What is the vaccine for diphtheria?
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A toxoid-DT that was treated with formaldehyde.
(Given as DPT = diphtheria, pertussis, tetanus) |
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What are the most common infections caused by Listeria moncytogenes?
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Meningitis and bacteremia (without obvious focus = Listerosis)
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What are the characteristic of L. monocytogenes?
Gram stain ?? Motility ?? Catalase ?? Hemolysis ?? |
Gram + rod (VERY SMALL - can be mistaken for diphtheroids)
Motile (UNLIKE corynebacterium!) Cat + Colonies are weakly hemolytic |
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Why is L. monocytogenes a serious infection in pregnant women?
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Vaginal colonization can cause abortion, still birth or premature birth.
May result in neonatal meningitis or bacteremia with high mortality. |
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True or false.
L. monocytogenes is the 5th most common cause of bacterial meningitis. |
TRUE
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How is L. monocytogenes transmitted?
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Foodborne transmission
Intrauterine transmission (infected mothers --> infants) |
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Where is the human reservoir for L. monocytogenes?
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Intestinal colonization
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What are U.S. periodic outbreaks of Listera associated with?
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Dairy products that are unpasteurized or contaminated after pasteurization.
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What are three things that pathogenesis of Listeria is dependent on?
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1. Penetration of host cells (epithelial cells, crypt cells, M cells)
2. Production of lysteriolysin O (LLO) 3. Production of phospholipases |
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L. monocytogenes multiplies extracellulary OR intracellularly in macrophages and epithelial cells?
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BOTH!
Extracellularly AND intracellularly |
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How do Listeria enter a host cell?
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Phagocytosis by macrophage
OR invasion of non-phagocytic cell mediated by bacterial protein called "internalin" |
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How does Listeria escape from the membrane-bound vacuole?
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LLO
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How does Listeria move through the membrane and penetrate neighboring host cells?
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Moves through cell via actin polymerization.
Phospholipase may also be used in penetration of neighboring cells. |
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How do you diagnose Listeria?
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Early = small coccoid gram positive rods in blood, CSF
If cultured, hemolysin is important marker and has characteristic tumbling motility at 25 C! |
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What is an appropriate treatment for Listeria?
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Penicillin, ampicillin
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Is there a vaccine for L. monocytogenes?
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NO vaccine. (cell-mediated immunity)
*Most adults have T-Ly primed specifically to Listeria antigens. **Increased incidence in immune-suppressed people |
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What type of infection does Bacillus cereus cause?
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Certain strains cause food poisoning.
Opportunistic infections are rare. |
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Characteristics of B. cereus
Gram ?? Motility ?? hemolysis ?? spore forming ?? |
Gram + rods
Motile Very hemolytic Spore forming |
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What are the 2 clinical manifestation of the disease?
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1. Diarrheal syndrome
2. Emetic syndrome |
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What kinds of toxins do certain strains of B. cereus produce?
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Heat-labile enterotoxin
Heat-stable entereotoxin |
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Which toxin causes diarrheal syndrome?
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Heat-labile
10-12 hour incubation <24 hour duration |
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Which toxin causes emetic syndrome?
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Heat-stable
1-5 hour incubation 1-5 hour duration |
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What is the ultimate reservoir for all Bacillus species?
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soil
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B. cereus food poisoning is often associated with ??
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Rice
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Is there any treatment/ prevention methods?
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No treatment for food poisoning.
No vaccine. Preventive measures include proper refrigeration, handling and re-heating of cooked foods. |
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Characteristics of B. anthracis:
Gram ?? Spores ?? Motility ?? |
Gram + rods
Spore-forming ** vegetative cells have distinctive "bamboo-like chains" NON-motile (vs. B. cereus is motile) |
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What happens when you grow B. anthracis in elevated CO2/bicarb environment?
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The vegetative cells will be encapsulated with a characteristic thick capsule that can be observed via India ink stain.
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Name 4 clinical manifestation of anthrax.
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1. Cutaneous anthrax
2. Inhalation anthrax 3. Intestinal anthrax 4. Oropharyngeal anthrax (rare) |
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What is the characteristic inflammed papule that blackens and is not very painful in cutaneous anthrax called ??
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"eschar"
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What are symptoms of inhalation anthrax or "woolsorter's disease"??
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hemorrhagic mediastinitis/meningitis
initially flu-like then rapidly progresses to high fever, chest pain and shock. |
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How is B. anthracis naturally aquired?
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Following contact with dead animals or their products by ingestion, inoculation or inhalation of Bacillus spores.
occupational exposure - such as farmers, vets, slaughterhouse workers |
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B. anthracis pathogenesis is dependent upon 2 things:
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1. secretion of anthrax toxin
2. synthesis of antiphagocytic capsule |
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What are the 3 proteins that make up the 2 exotoxins in anthrax toxin?
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PA = protective antigen
EF = edema factor LF = lethal factor *subunits alone are not toxic |
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What is the function of PA?
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PA is the "B" component of each exotoxin that mediates entry into the host cell
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What are the "A" components?
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LF = metalloprotease that cleaves MAP kinase; macrophage are very sensitive
EF = acts as an adenylyl cyclase (similar to pertussis toxin) |
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Where are virulence genes for B. anthracis located?
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They are located on 2 plasmids
(All 3 toxin genes are on one plasmid and genes for capsule biosynthesis are on the other plasmid) **Capsule is made of protein not carb. |
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What should you always do to diagnose anthrax?
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Take a blood culture.
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Why should you not worry about taking a sputum sample with inhalation anthrax?
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Anthrax sputum cultures are rarely positive because the spores do not germinate until they reach mediastinal lymph nodes.
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Which 2 main lab tests confirm the identification of B. anthracis?
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No hemolysis on blood agar.
Mucoid colonies (due to presence of capsule! - colonies are "medusa-shaped") |
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What are the choice antibiotics for anthrax treatment?
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Ciprofloxacin (quinolone) and
Deoxycycline (tetracycline) *Cutaneous is readily treatable; however inhalation is not very effective and has high mortality rate |
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What is required for protective immunity against B. anthracis?
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Requires antibodies against protective antigen (PA)
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Vaccines are given only in the case of outbreaks or to people at risk.
What is the difference between the human vaccine and the animal vaccine? |
Human vaccine consists primarily of the PA protein.
Animal vaccine is an attenuated strain that is non-capsulogenic. |
