Staph Lange reading Flashcards
staph and strep belong to which genera
Gram positive cocci
staph aureus lab/culture findings
Coag + Catalase + protein A on surface beta hemolytic GRAPE LIKE CLUSTERS NON-MOTILE NON-SPORE FORMING
Strep pyogenes Lab/culture findings
Coag- Catalase - Beta Hemloytic Lancefield group A CHAINS NON-MOTILE NONSPORE FORMING
NAME THE COMUNITY ACQUIRED DISEASES STAPH CAN CAUSE
ABCESSES ENDOCARDITIS SEPTIC ARTHRITIS OSTEOMYELITIS FOOD POISONING SCALDED SKIN SYNDROME TOXIC SHOCK SYNDROME
NAME THE HOSPITAL RELATED DISEASES STAPH A. CAN CAUSE
HOSPITAL ACQUIRED PNEUMONIA
SEPTICEMIA
SURGICAL-WOUND INFECTION
NAME THE SKIN INFECTION STAPH A. CAN CAUSE
IMPETIGO
FOLLICULITIS
CELLULITIS
BACTERIAL CONJUNCTIVITIS (MOST COMMON CAUSE)
CLASSIC LESION CAUSED BY STAPH. A
ABCESSES
impetigo is caused by
either staph A or strep pyogenes
more commonly, endocarditis and septic arthritis is caused by
staph epi–> white colonies–> no staphyloxanthin (virulence much less than staph aureus)
what does catalase do
degrades h202–> o2 and h20
*important virulence factor because H2O2 is a microbicidal and its degredation limits neutrophils ability to kill
Staph aureus is distinguished by what
Coagulase production
what does coagulase do?
causes plasma to clot by activating prothrombin to thriombin–> thrombin catalyzes fibrinogen to fibrin forming a fibrin clot—>retards neutrophil migration ot infection site
why is staph aureus colonies golden
staphyloxanthin carotenoid
what does staphyloxanthin do?
incativate microbicidal effect of superoxides and other ROS within neutrophils
hemolytic profile of staph aureus
SA hemolyses RBCS and ferments mannitol–> epi and saprophyticus do not
*hemolysis provides the bacteria with enough iron for growth (used to make cytochrome enzymes to prduce energy)
required agent for any bacterial growht in host
iron
Staph aureus reistance profiles
90% resistance to beta lactamases (plasmid)
20% resistant to beta lactamase resistant antibiotics (Nafcillin and Methicillin)–> thanks to a antered PBB–mecA gene)
what percentage of strains of staph in hospital pt.’s are MRSA/NRSA
50%
most common being US300 strain
how do STaph become vanc resistant
cassette of genes substitutes D-LAC/D-LAC for DLAC/DALA
Function of Protein A
major cell wall protein
*binds to Fc portion fo IgG and inhibtis compliment activation on mirobial surface–> NO C3b is made…opsonization and phagosytosis of the bacteria is greatly reduced
Function of Teichoic acids
mediate adherance to mucosal membranes
Funciton of lipoteichoic acids
induce septic shock by inducing Il1 and TNF from macrophages
which serotypes of Staph A. cause 85% of infection
serotypes 5 and *–> there are 11 in all
describe polysaccharide capsule of Staph A.
thin…microcapsule..poorly immunogenic–> vaccine therefore difficult
Describe the peptidoglycan wal of Sta. Aureus
endotoxin-liek properties–> can stimulate macs to produce cytokines and activate the compliment and coag cascades–> leading to septic shock even without a TRUE ENDOTOXIN
Name the virulence factors for Staph Aureus
Protein A Hemolysis Teichoic Acids Lipoteichoic acids capsule peptidoglycan wall with endotoxin-like characteristics
main sites of colonization for Staph A
nose–> 30% are colonized
5% in the vagina–> predisposes to TSS
*skin of hospital personnel is a major reservoir
Fomites–> dirty towels
reduciton in transmission of Staph aureus
hand washing!!!
important predisposing factors to staph infection
sutures
catheters
family member with boils
low humoral immunity (t cells, compliment and antibodies)
chronic granulomatous disease (defective neutrophil killing of bacteria)
name the three clinically important toxins and enzymes produced by staph aureus
Enterotoxin–> food poisoning and Non-Bloody D
Toxic Shock Syndrome Toxin–> TSS
Exfoliatin–> Scalded Skin syndrome
Describe what enterotoxin does?
vomiting more prominent than diarrhea when Staph aureus is involved
IN the Gi tract-> acts as a superantigen to activate IL1 and IL2 from macs and T cells respectively–>
Vomiting-> cytokines released from lymphoid cells acting on enteric nervous system to activate Vomit center in brain
Enterotoxin-> heat resistant, type A-f, acid resistant
describe A super antigen
class of antigens that cause non-specific activation of T cells leadin to polyclonal T cell expansion and massive cytokine release *can activate 25% of t cell population and not bound to any specific eliciting antigen
who gets TSS
menstruating women with tampon use or individuals with wound infections, nasal packing
describe pathogenesis of TSS SUPERANTIGEN IN ppl who no dont have an antibody against TSST
Staph aures enter blood stream, causing toxemia BY REALEASING MASSIVE AMOUNT OF IL1 , TNF AND IL2–> BLOOD CULTURES WILL BE GEATIVE– IT IS THE SUPERANTIGEN CAUSING THE SYMPTOMS
how does exfolatin cause scalded skin syndrome
epidermolytic- acts as a protease that cleaves desmoglein in desmosomes–> leads to separation of the dermis epidermis at the GRANULAR LAYER
staph aureus has 2 exotoxins that can kill leukocytes (leukocidins) and can cause necorosis
Alpha toxin-necrosis and hemolysis (forms hols in cell membrane)
P-V leukocidin-pore forming toxin that kills cells, espcially WBCs
significance of P-V leukocidin
two subunits of toxin–> form a pore in the cell wall
->severe skin and soft tissue infection in MRSA and severe necrotizing pneumonia
2% of Staph aureus isolates cary this lysogenic phage
Staph epi and saprophyticus cause…
PYOGENIC INFECTIONS ONLY
no tss no exotoxins, no food poisoning
Epi- endocarditis and septic arthritis
Sap-cystitis and UTI
disseminated sepsis and endocarditis associated with IVDU is most likely caused by
Staph aureus fom IVDU
not epi
severe necrotizing and soft tissue infections with MRSA are caused by
community acquired strains that make the P-V leukocidin
*homeless an IVDU’s
of hospital acquired Staph infections
50% of the time are MRSA
right sided endocarditis in IV drug users–>
Staph Aureus
prosthetic valve endocarditis
Staph epi
most common cause of postsurgial wound infections
staph aureus
osteomyeltis in chilren
staph aureus
following a influenza URTI
Staph pneumonia and Pneumococcal pneumonia
- staph pneumonia- severe and necrotizing can be CA or HA
- empyema and abcesses
- in SOME HOSPITALS IT IS THE LEADING CAUSE OF VAP, BUT WE LEARNED P AERUGINOSA AND ACINETOBACTER
CONJUNCTIVITIS leading cause overall
tranfmitted from the eye by infected fingers
Staph aureus
Conjunctivitis leading cause in children
transmitted to the eye from infected fingers
strep penumo
then h flu
metastatic abcesses
occur via the spread of infection from the original site and can wind up in any organ (espcially the kidneys)
definition of TSS
hypotension
diffuse macular rash–> transition to desquamative
involing 3 or more: liver, kidney, GI, CNS, muscle, or blood
vasculitis involving small or medium blood vessels especially the coronary vasculature
KAWASAKI’S SYNDROMe
Describe scalded skin syndrome
CHILDREN–> fever, large bullae, erythematous macular rash–> desquamaive transition–> serous fluid exudates, and electrolyte imbalance occurs, hair and nails lost
*uaually resolves in 7-10 days
describe presentation of KS
high fever for 5 days bilateral non-purulent conjunctivitis STRAWBERRY TONGUE-->lesions of the lips/tongue/oral mucosa diffuse rash edema of the hands and feet leading TO HEART INVOLVEMENT
HEART INVOLVEMENT WITH KS
ANEURYSM OF CORONARY ARTERIES
MYOCARDITIS, ARRHYTMIAS, REGURGITAITON OF MITRAL OR AORTIC VALVES
WHO GETS KS
ASIAN KIDS UNDER 5–> MHC POLYMORPHISMS
TX FOR KS
IVIG
FEVER REDUCERS
SUPPORTIVE CARE
HOW TO DIFFERENTIATE STAPH EPI FROM SAPROPHITICUS
EPI-NOVOBIOCIN SENSITIVE
SAPROPHITICUS-NOVOBIOCIN RESISTANT
GOLD COLONIES ON MANNITOL SALT AGAR WITH BETA HEMOLYSIS
STAPH AUREUS
WHITE COLONIES ON MANNITOL-SALT AGAR WITH NO HEMOLYSIS
STAPH EPI
STAPH SAPROPHITICUS
SEROLOGIC OR skin test for acute staph infection
none
is a positive culture required for Dx of TSS
no
90% of US staph strains are resitant to
penicillin G–> most having a beta lactamase
tx for penicillin G staph strains
beta lactamase resistant penicillin (nafcillin, methicillin, cloxicillin)
some cephs
vancomycin
OR BETA LACTAMASE SENSITIVE PENICILLIN + BETA LACTAMSE INHIBITOR
(AUGMENTIN)
according to Derm website tx of MRSA OR NRSA=
- clindamycin
- bactrim (TMP/SMX)
- DOXYCYCLIN
- LINEZOLID
- VANCOMYCIN
20% OF STAPH STRAINS ARE…
METHICILLIN RESISTANT OR NAFCILLIN RESISTANT–> altered PBP’s
LANGE SAYS MRSA or NRSA tx is
Life threatening:
vancomycin (+ gentamicin)
daptomycin (cubicin)–> non pneumonia
NON-life threatening:
Bactrim
clindamycin
MRSA strains are resistant to almost all
beta lactam drugs including oenicllin and cephalosporins
first beta lactam capable of treating MRSA
ceftaroline
Tx of VISA an VRSA
also nafcillin and methicillin resistant too
daptomycin
quinipristin-dalfopristin
tx of tss
correction of shock with normal saline pressor drugs (alpha 1 agonist) intoropic agents naficllin (beta lactamase resistant penicillin) removal of tampon and debridement pooled serum antibodies against TSST
topical tx of STaph infections
murpirocin
also reduces nasal carriage
cornerstone of abcess tx
drainage either surgical or spontaneous
tx of faruncle (boil)
drainage–> no Ab’s required
staph epi tx
highly resistant
most produce beta lactamases but are susceptible to Nafcillin (beta lactamse resistant penicillin)
Vanc is MRSE due to altered PBP’s
tx of Staph saprophyticus
Bactrim or ciprofloxacin
