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29 Cards in this Set

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corynebacterium diptheriae morphology
-gram positive pleomorphic(variation in size or shape) rods
-non-motile
-non-encapsulated
-non-spore forming
-normal flora: skin, and resp tract
corynebacterium diptheriae epidemiology
-cause of diptheria, an acute resp or cutaneous disease
-rare in US due to vaccination
-baceria found in the throat and nasopharynx of carriers and in patients w/ diptheria
-spread by resp droplets
-causes a local infection of throat or skin
corynebacterium diptheriae toxins
-exotoxin causes diptheria
-2 types: A subunit and B subunit
-A subunit: active, activates ADP-ribosylation of protein elongation factor-2 (EF-2) an inactive form, thus inhibiting protein synthesis
-subunit B: provides entry into cardiac and neural tissue
-once in the cell, the 2 subunits dissociate
corynebacterium diptheriae virulence
-resp form: produces a thick grayish adherent exudate called pseudomembrane producing a base where toxin can be secreted
-the pseudomembrane is composed of cell debris from mucous and inflammatory products
-can obstruct airway and cause resp arrest
-severe cases cause a bull neck appearance due to cervical adenitis(lymph node or gland inflammation) and edema
corynebacterium diptheriae transmission
-resp droplets from carrier
corynebacterium diptheriae metabolism
-catalase positive
-facultative anaerobe
corynebacterium diptheriae clinical
generalized symptoms:
-caused by absorption of toxins
-major clinical effects involve the heart and peripheral nerves
-complications include myocarditis leading to congestive heart failure and permanent heart damage
-rversible paralysis of soft palate, eye muscles, or other muscle groups due toxin absorption into circulation
-death can occur due to respiratory obstruction
-cutaneous diptheria can occur ranging from a simple pustule to a chronic non-healing ulcer
-disease resolves with formation of antitoxin antibody
corynebacterium diptheriae immunity
-antibody to the toxin is protective and neutralizes toxin
-clinical disease does not allways produce protective immunity
corynebacterium diptheriae prevention
-vaccine contains formalin treated toxin=toxoid, retains immunogenicity w/o toxicity, formalin inactivates the A fragment
-diptheria toxoid part of childhood immunizations; adults should be revaccinated every 10 yrs
-immunization does not prevent carrier state
corynebacterium diptheriae lab diagnosis
-definite diagnosis requires demonstration of toxin production
-culture in Loeffler's medium and stain with methylene blue. Reddish granules can be seen
tellurite culture: inhibits other flora, and shows dark black colonies
other corynebacterium
-normal flora=skin and pharynx

corynebacterium jeikeium
-most frequently isolated corynebacterium of clinical significance...neutropenic(neutrophil def) patients
-associated w/ wound infection, septicemia and endocarditis
-usually multi-resistant to antibiotics

corynebacterium urealyticum:
-causes chronic and recurrent UTIs
bacillus anthracis gram stain
-large, gram positive bacillus; boxcar, bamboo rod
-spore-forming
-usually grow in long chains
bacillus anthracis culture
-aerobic or facultative-can grow w/o oxygen
-colonies on blood agar
-large
-non-hemolytic-gamma
-gray to white
-flat to slight convex
-markedly tacky
-non-motile
bacillus anthracis virulence factors
-virulence factors expresed by the vegetative bacilli that result from germination of spores in body
-3 virulence factors:
capsule composed of poly-D-glutamic acid: high neg charge inhibiting phagocytosis
edema factor: active A subunit, causes in in cAMP, which impairs neutrophils and causes massive edema
lethal factor: zinc metalloprotease that inactivates protein kinase, stimulates release of TNF-alpha and IL-1beta which contribute to death
bacillus anthracis toxins
-releases 3 proteins which combine to form 2 binary exotoxins:
PA-protective antigen
EF-edema factor
LF-lethal factor
-PA is binding domain that mediates internalization of the other 2 proteins
bacillus anthracis edema toxin
-EF + PA=edema toxin (ET)
-increases intracellular cAMP resulting in a change in membrane permeability and is responsible for the overhwleming mediastinal edema seen in anthrax
-chest X-ray: reveals a widening of the mediastinum w/ pleural effusions w/o infiltrates
bacillus anthracis lethal toxin
-LF+PA=lethal toxin (LT)
-zinc dependent protease
-interferes w/ signaling pathways in major phagocytic cells, ie macrophages
-induces apoptosis and necrosis
-causes hemorrhagic necrosis in tissues
bacillus anthracis clinical
3 forms of anthrax
-cutaneous: 95% of naturally occuring cases, papule develops and evolves into a painless, black pustule=eschar; 20% mortality rate if untreated
-inhalation: incubation period 2-14 days
-GI: abdominal pain, vomitting and diarrhea
bacillus anthracis inhalation clinical features
-early prodromal: malaise, fatigue, myalgia, mild fever, non-productive cough, flu-like symptoms
-intermediate: positive blood cultures, mediastinal lymphadenopathy, hemorrhagic pleural effusions require repeated drainage, severe dyspnea, hypoxemia, cyanosis, tachycardia
-late fulminant: resp failure requiring intubation, meningitis and shock. High fatality rate
bacillus anthracis diagnosis
-gram stain and culture, PCR of skin biopsy, tissue, tissue immunoperoxidase
-cutaneous: swab of vesicle fluid, ulcer/eschar
-inhalational: blood
-meningeal involvement-CSF
-GI: feces, vomitus, blood
other bacillus species
-non-anthracis bacillus can cause opportunistic infections: lesions, infections of indwelling devices, IV catheters
-B. cereus produces a tissue destrcutive exotoxin and it also causes food poisoning
listeria monocytogenes morphology
-gram positive rods-looks like chinese characters
-sometimes looks like gram pos cocci in pairs
-non spore forming
-motile: tumbling motility is seen
listeria monocytogenes diagnostics
culture:
-gram positive rods
-on blood agar, produces narrow zone of beta-hemolysis; can be mistaken for group B strep. difference is listeria is catalase positive
-key characteristics=motility by tumbling
listeria monocytogenes epidemiology/trasnmission
-listeria monocytogenes only species of listeria that infects humans
-widespread amongst animals
-important in food-borne outbreaks-primarily unpasteurized dairy products
-grows well at low temp, so refrigeration does not slow growth
-types 1a,1b,and 4b most virulent in humans
listeria monocytogenes people w/ increased risk
-pregnant women 20% more likely, 1/3 of listeriosis happens during prgnancy
-newborns suffer the serious effects of infection, not the mom
-persons w/ weakened immune systems
-persons w/ cancer, diabetes, or kidney disease
-persons w/ AIDS
-glucocorticoid steroid med users
-elderly
listeria monocytogenes pathogenesis
-facultative intracellular parasite
-steps of infection:
1) phagocytosis
2) escapes phagolysosome due to listeriolysin O, membrane damaging toxin
3) listeria grows in cytosol, assembles an actin filament tail that propels organisms to the surface of the cell forming a pseudopod
4) organisms spread to adjacent cells: listeria produces 2 other lipases that hydrolyze cell membranes facilitating cell-to-cell spread and evasion of immune system
listeria monocytogenes clinical
-septicemia and meningitis most common
-granulomatous skin lesions-less common
-can colonize human intestine and vagina
-neonatal infections due to contact w/ organisms during birth-causes septicemia and meningitis
-maternal infection can result in abortion, preterm delivery
listeria monocytogenes lab
-culture of blood, CSF
erysipelothrix rhusiopathiae
-gram pos filamentous
-catalase neg
-causes rare skin infection called erysipeloid in people who handle animals: butchers, vetrinarians, and fisherpersons