Jungkind Bacterial Infections

Front 1

this bacteria found intracellularly in granulocytes

Back 1

s. aureus

Front 2

two enzymes that s. aureus has

test using of of these enzymes

Back 2

catalase and coagulase
coagulase test- s. aureus form clot in rabbit or human plasma.

Front 3

toxin produced by s.aureus - make pores and cause mammalian cell membrane to leak through.

other character

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alpha toxin

(low molecular weight, cause necrosis or death in animals)

Front 4

this chemical from this organism cause TSST-1 (toxic shock syndrome toxin 1)

mechanism.

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pyrogenic exotoxins from s. aureus

aborb toxic from local site--> cytokin storm--> directly toxic to endo thelial cells

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cause intercellular splitting of the epidermis bw s, spinosum and s. granulosum

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exfoliatin (exotoxin from s. aureus)

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exfoliatin from s. aureus (from infection site) --> this toxin travel in the blood stream--> epithelial desquamation at remote sites + erythema

this condition is called? s, aureus at the desquamation site?

Back 6

scalded skin syndrome, no- s,aureus can't be found at the desquamation site because the toxin traveled there by blood

Front 7

shape of s. aureus

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clusters of g+ cocci

Front 8

describe pattern of spreading of cellulitis by staph

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staph alternates b/w
walling off and rapid extension
spread fast, daily change

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s. aureus is the major cause of wound infection: name two strains ( by source)

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patients own, nosocomial strain by hospital workers

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Skin rash and strawberry tongue

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TSS - toxic shock syndrome ( s. aureus)

Front 11

which antibiotic for MRSA is least effective? oral, IM, IV

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oral least effective for MRSA--> lead to MRSA in outpatient and spread in the community

Front 12

what lead to VRSA

how to detect?
what happens when pt has VRSA?

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overuse of vancomycin

detect in normal vitro

pt with VRSA isolated, dedicated personnel, gov. involved

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VISA/hVISA compared to VRSA

detection, treatment, frequency

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harder to detect/treat
more common than VRSA

Front 14

coagulase -, but cause infection similar to s. aureus

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s. lugdunensis

-not resistant but difficult to treat

Front 15

coagulase negative staph are usually?

are they beta hemolytic?

Back 15

normal commensal ( in the skin, nose, ear, mocous membrane)

no, coagulase negative staphs are not beta hemolytic (except s. lugdunensis?)

Front 16

in what situations coag neg staph become pathogenic

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when you have a cut
opportunistic ( medical device of ill pts. , immunosuppressed, major surgery )

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coagulase negative organism
form biofilm, extracellular polysaccharide slime

how is biofilm advantageous?

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S. epidermidis

biofilm prevents phagocytosis, antibiotic effect, but still allow nutrition to s. epidermidis

"film on skin!!"

Front 18

how to collect sample to determine significance of Coagulase negative staph

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collect deep invasive samples ( difficult to determine because few in the superficial wound is normal)

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factors that increase/ decrease significance of coagulase negative staph

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increase sig: in multiple culture, 15 or more colonies on a plate, see intracellular g+ cocci,

decrease sig: organism in broth but not in the plate. reflect low#, not pathogenic

pathogenicity of coagulase negative strep depends on its quantity ( more present, more pathogenic)

Front 20

streph is normal flora in (3 parts)

what determines streph pathogenicity

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oral, GI, genital ( follow food...like strep)

location, location location!!!
(move to cut: pathogenic)
(nose, gi, genital tract: not pathogenic)

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gram stain of streph

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g+, in chain, (staph and strep always g+)

become gram variable as culture ages and cells die

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way to classify strep

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type of hemolysis

alpha- partial hemolysis ( green, viridian strep)
beta- complete hemolysis ( huge clearing of colony)
gamma- no hemolysis

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strep that form pus+ its classification

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pyogenic strep, beta hemolytic

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associated with dental caries

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strep. mutans

Front 25

cause endocarditis--> damage heart valve

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viridans strep.
abiotrophia sp.
group D

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detection and treatment of viridans strep

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blood culture & penicillin for weeks

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need nutrition, can't grow on ordinary blood agar

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abiotrophia

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worst enterococcus species:

E. Faecalis vs. E. Faecium

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Faecium is worse
("is"- is susceptible, "um"- ultra mean)
( Faecium is resistant to ampicillin and may be resistant to vancomycin, Faecalis is more common)

Front 29

after cephalosporin or gentamicin use ( broad spectrum)

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Enterococcus Disease- opportunistic infection

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coryne that cause skin infections

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c. ulcerans

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g+ rod, not acid fast
pleomorphic "chinese letters"

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corynebacterium
( c for chinese letters? coryne form is bizarre to the eyes)

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drug used to treat c. difficil

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vancomycin

Front 33

Cause endocarditis, UTI, wound infections in ICU

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Enterococcus ( group D)

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corynebacterium for nosocomial blood stream and wound infections

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c. jeikeium (jk)

Front 35

match
pathogen , none pathogen

in

c.diphtheriae, c. Diphtheroids

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c. diphtheriae is pathogen
c. diphtheroid is non-pathogen.

Front 36

true or false : C. diphtheriae is rarely fatal

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true

Front 37

fishermen, butcher, veterinarians- painful, slow spreading of skin infection

disease? microorg? treatment?

Back 37

erysipeloid
(e. rhusiopathiae infection)

treat with penicillin or erythromycin
"think red, painful hand infection"- ery, rhusio, path, erythromycin...etc

Front 38

cause impetigo like skin lesion, common in tropics, American indians

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c. diphtheriae

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toxin secreted by c. perfringens

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alpha, theta, enterotoxin