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103 Cards in this Set

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T/F: all of these pathogens cannot colonize asymptomatically.
F
are these pathogens primarily intra or extracellular?
extracellular
why is handwashing very important with S. aureus?
bc it can survive for a long time on dry surfaces (it exists virtually everywhere)
T/F: S. aureus can grow in high salt concentrations.
T. Salting foods will not prevent food poisoning from S. aureus
metabolically, how do you distinguish staph from strep?
staph is catalase positive
biochemically how do you differentiate between A. aureus and S. epidermis?
S. aureus is coagulase positive
most asymptomatic S. aureus colonizations are found where in the body?
in the nares, more likely if a health care worker
describe the two basic lesions caused by S. aureus.
an abscess is walled off bacs by fibrin (the bacs can break through via staphylokinase and cause bacteremia thus it is important to drain the absesses) or pyogenic exudate (pus)
define bacteremia.
presence of bacs in blood
define systemic inflammatory response syndrome (SIRS)
response of the body to systemic release of inflammatory mediators and must include at least two of the following: fever or hypothermia, tachypenia, leukocytosis or leukopenia
define sepsis, severe sepsis, and septic shock.
SIRS that is caused by a microbial etiology. sepsis with one or more signs of organ dysfunction. sepsis with hypotension.
describe multiorgan dysfunction syndrome.
SIRS with persistant hypotension leading to clotting, renal, hepatic, cardiac, or cognitive failure and acculmulation of products of metabolism that cannot be cleared
describe impetigo
pyogenic S. aureus infection superficial infection of the skin, primarily hits face and limbs, culture it bc Strep pyogenes can also cause it, and treat with antibiotics.
differentiate between foliculitis, furuncles, and carbuncles.
all from S. aureue and are pyogenic skin infections. Foliculitis is infection of hair folicle with a small pus pocket. furuncle are more severe extension of folliculitis and are large, painful with an underlying collection of dead/necrotic tissue. Carbuncles are furuncles that coalesce and extend into deeper tissue causing bacteremia and systemic symptoms
describe cellulitis.
nasty skin infection that can be due to staph aureus causing fever, severe pain, sometimes bacterema as the org penetrates
staph aureus wound infections usually occur when what?
after surgery, in immunocompromised, on foreign objects like dirt or suture in wound
differentiate between the types of pneumonia caused by staph aureus. What is the treatment for these diseases?
aspiration pneumonia develops after aspiration of oral sectretion, usually in young or CF, flu, or COPD pts, and has abscesses in the lung. Hematogenous pneumonia is common for pts with bacteremia. Necrotizing pneumonia is the most dangerous, is community aquired, can lead to septic shock, and has a high mortality rate. usually oxacillin or lactamase resistant antibiotic unless it is MRSA
in terms of staphyloccocal osteomyelitis, where does it normally effect adults and what are the treatment outcomes?
usually vertebral. with antibiotics and surgery it has good treatment outcomes
bacteremia of staph can lead to what mortal illness and what is the visible sign of this disease?
endocarditis seen with septic emboli which are occlusions of capillaries with micro colonies of staph aureus
septic arthritis usually occurs in tose who...
receive intrarticular injections
describe staphylococccal scladed skin syndrome AKA Ritter's disease.
caused by staph toxin, usually in neonates, redness and inflammation of mouth, blisters without orgs in the fluid, and finally desquamation of the epithelium. Rarely fatal
describe bullous impetigo.
a form of staphylococcal scalded skin syndrome that is localized and produced from toxins of S. aureus infected with a phage, but these blisters will have orgs in it unlike other forms of SSSS.
give facts about toxic shock syndrome.
Caused by TSST1 of staph aureus. causes fever, hypotension, and diffuse rash. complete desquaitization usually occurs. 90% of ppl have antibodies against TSST. 3-7% of menstruating women have vag staph. High risk of recurrence. ~50% of pts with TSS fail to develop antibody to TSST1 after
what causes staphylococcal food poisonoing? what are some characteristics of it?
the enterotoxins from staph, not the orgs themselves, thus you do not need infection, just the toxin. cannot reheat food bc the toxxin is very heat reresistant. Symptoms occur about 4 hours after ingestion, can only treat the symptoms
MRSA isolates can be categorized how?
heterogenous is a small fraction of the population while homogeneous is the entire pop is resistant
what are the treatments for MRSA?
vancomycin, is staph is just MSSA (sensitive) can use oxacillin. topical mupirocin can be used to decolonize nasal carriers. Also note that VRE has transferred its vanc resistance to some MRSA strains
T/F: a lot of staph and strep toxins are superantigens.
T
describe the virulence factors of staph aureus.
capsular polysaccharide inhibits neutrophil phag and chemotaxis. protein A binds the Fc portion of some IgG's thus neutralizing the ability of phagocytic cells to recognize it, but immuntiy to the bug can still develop. cytotxins a,b,d,g can kill various euk cells. panton valentine leukocidin lyses neutrophils and is responsible for necrotizing pneumonia. exofoliative toxins A and B are responsible for scalded skin syndrome. enterotoxins are responsible for food poisoning and are superantigens. TSST1 for toxic shock syndrome - massive cytokine release and thus shock and death, they are superantigens. peptidoglycan - like an endotoxin, stimulates pyrogens, activates complement, produces IL1, aggregates neutrophils (part of abscess formation. MSCRAMMs/adhesins which bind to the ECM and host cells
T/F staph epidermidis is normal flora?
T
what diseases does staph epidermidis cause?
infected catheters, or skin wounds it is almoust exclusively nocosomial
describe the bacteremia and sepsis caused by staph epidermidis
bacteremia can lead to seeding of damaged heart valves and subsequent endocarditis while sepsis can occur via the host's response to infection
describe the virulence factors of staph epidermidis.
capsular polysaccharides: slime that protects bacterium from antibiotics and immune cells and a glue (biofilm)
what special circumstances exist when culturing S. epidermidis
need multiple blood cultures in order not to contaminate with normal S. epi flora
treatment of S. epi?
vanc
what is the morphology of strep pneumoniae
diplococci
What are the alpha hemolytic strep? what does they look like on agar and what causes this effect?
S. pneumoniae and "viridans" strep. This is not actual RBC lysis, but is a greening of the agar due to H2O2 that is released from the bacs
what are the beta hemolytic strep species? what causes this?
S. pyogens and S. agalactiae. Exotoxins cause this via GAS in pyogenes and GBS in agalactiae
what surface antigens are associated with what strep species?
A is for pyogenes, B is for agalactiae and D is for enterococci. pneumniae is ungroupable
what is the key way to diagnose strep species?
by physiological means
what mode of respiration does S. pyogenes utilize?
facultative respiration
which protein is used for serotyping S. pyrogens and what can this protein do to evade the immune system?
M protein and it can undergo phase variation
what defense mechanism does S.pyogenes utilize to evade phagocytosis?
it is usually encapsulated
is S. pyogenes usually found intra or extracellularly?
extra
are strep orgs catalse + or -?
negative
where is S. pyogenes found in nature?
asymptomatically colonizes upper respiratory tract and skin of those with wounds or disease as well as those with poor hygeine
how is S. pyogenes spread?
it can survive on dry surfaces for a long period of time, can be spread through droplets, food, and water. It can also be spread via breaks in the skin after direct contact with the infected/colonized person, fomite, or arthropod vector
what strep species can cause disease in an otherwise healthy person?
S. pyogenes
what are the difficulties in diagnosing strep throat?
most pharyngitis cases are due to a virus and some ppl have an asymptomatic colonization of strep pyogenes. Thus lab tests show strep but the culprit is a virus this leading to the misuse of antibiotics
strep throat symptoms include what
sore throat, fever, malaise, headache
what types of complications may arise from untreated strep throat?
non suppurative and suppurative (pus producing). suppurative complications include otitis media, peritonsillar cellulitis, mastoiditis, peritonsillar or retropharyngeal abscesses. Non suppurative include acute rheumatic fever which involves inflammatory changes in heart, joints, blood vessels, and SQ tissues (includes carditis, polyarthritis, and chorea).
describe scarlet fever.
complication of S. pyogens infection of throat or skin. Strain of pyogenes is infected by bacteriophage which elaborate the exotoxins causing rash, high fever, strawberry tongue, eventual desquamation of the skin.
describe acute glomerulonephritis.
nonsupporative complication following pharyngitis or polyderma infection of S pyogenes. causes acute inflammation of renal glomeruli with edema, hypertension, hematuria, and proteinuria. mechanism of disease is unknown and can lead to loss of renal function in some adults whereas most younger patients recover with no problem
describe impetigo pyroderma.
very difficult to distinguish between streo and staph infection. Colonization occurs first and then infection at sight where skin integrity is compromised. red papules first and eventually to postules. spreads from original infection sight and is most common in young children; associated with poor hygeine and moist climate
describe erysipelas. cellultits.
local pain, inmflammation, fever, chills lymph node enlargement from S. pyogenes. cellulitis is another skin infection of pyogenes as well as staph aureus that occurs when the skin is compromised
what is the fatal progression of strep disease (pyogenes)
flu like symptoms, pneumonia, bacteremia, then fatal toxic shock. Note this pneumonia is different than S. pneumoniae in that it is more rapidly progressive
describe the process of streptococcal toxic shock syndrome.
GAS penetrates a skin lesion or introduced during surgery or due to pneumonia and dissemination into the blood stream. associated with strains that cause skin disease not pharyngitis. GAS multiply at site of infection and produce toxins (dif here bw staph and strep is strep has much more bacs at sight of infection). systemic symptoms then occur, the patient becomes bacteremic and many develop necrotizing fasciitis, hypotension, and impaired clotting
what are some differences between staph and strep toxic shock syndrome?
rash and desquamation are uncommon in strep. bacteremia is frequent in strep. mortality is much higher in strep
if a patient presents with infected skin lesion, SEVERE pain, and fever then think...
toxic shock syndrome
how do you treat strep toxic shock.
not penicillin bc the bacs are in stationary phase. use clindamycin and penicillin, may need surgical exploration and debridement of infected tissue if necrotizing fasciitis. IV fluids maybe needed
how does complement effect strep?
it cannot lyse it bc of thick peptidoglycan, but it can opsonize it (C3b) since it is extracellular
GAS means what?
group A strep toxin (S. pyogenes)
what are the major virulence factors of GAS M protein?
antiphagocytic against neutrophils, binds fibrinogen, sequesters C4b binding protein which decreases C3b deposition. sequesters Factor H which also decreases C3b deposition
what are S. pyogenes virulence factors?
capsule of hyaluronic acid (makes host think it is endogenous) that makes em antiphagocytic. DNAse which digests DNA in pus to allow the org to move around. Streptolysin S and O: lyses leukocytes, platelets, and erythrocytes. C5a peptidase: degrades complement component C5a thus impairing neutrophil chemotaxis. Superantigens that promote excesive T cells, cytokines and thus shock. Lipoteichoic acid acts synergistically with superantigen to promote shock
what kind of colony formation do hyperencapsulated strains of S. pyogenes have?
mucoid
what age group does strep pneumoniae usually effect?
very young, elderly or somehow immunocompromised
what are the key properties of S. pneumoniae?
gram pos diplococcus, facultative anaerobe, aerotolerant, virulent strains are encapsulated with dif polysaccharides than S. pyogenes. usually soluble in bile
can ppl have an asymptomatic colony of S pneumoniae?
yes about 1/3 of ppl have an asymptomatic colonization at some point in their lives, but it usually only effects those that are immunocompromised with an antecedent resp infection
what are the symptoms of pneumonia from S. pneumoniae?
shaking chills, productive cough, blood in sputum, chest pain, can become cyanotic due to damaged ciliated cells and lack of oxygen
what other diseases of S. pneumoniae are usually preceded by viral infection oof the upper resp tract?
otitis media and sinusitis
what are ways that S. pneumoniae can reach the CNS o cause meningitis?
bacteremia from pneumonia, infection of ear or sinus, trauma that causes communication bw subarachnoid space and nasopharynx
what are the symptoms of meningitis caused by S. pneumoniae?
fever, irritability, drowsiness, neck stiffness, seizure, coma... can lead to blindness, hearing loss, learning disabilities, paralysis, and death
what can cause S.pneumoniae to become bacteremic and what can this cause?
1/4 of pneumonia patients will become bacteremic, and 80%+ of meningitis patients will also. It usually does not occur in sinusitis/otitis media. it can result in endocarditis
what is the most useful tool against the S. pneumoniae capsule and how does the org fight back?
antibodies against the capsule, but the org can change the composition and antigenicity of the capsule
what org contains pneumolysin and what does it do?
S. pneumoniae and it is toxic for many cell types, activates complement, and suppresses oxidative bursts of phagoytes.
what bac uses teichoic acid and peptidoglycan fragments to activate complement and thus cause more damage to the infected tissues?
S. pneumoniae
what is the major contributor to damage of the host tissue in S. pneumoniae infections?
the host immune response that is illicited by the bug
what makes S. pneumoniae able to aquire drug resistance as well as new capsular polypeptide antigens?
it is naturally transformable
what are the treatment options for S. pneumoniae?
penicillin, but many strains are resistant now. Can use vanc. vaccine against the capsule is available but it is not very effective
how is S. pneumoniae spread?
by intensive close contact
what strep species is group B strep?
Strep agalactiae
describe the key properties of GBS.
gram pos, chain cocci, commensal as well as pathogenic, extracellular with a capsule that has different polysaccharides and is more effective than S. pneumoniae, usually infects elderly and immunocompromised
what is the resevoir for GBS?
normal member of GI flora as well as 10 to 30% of healthy vaginas
describe the early onset disease of GBS.
severly immunocompromised newborn (usually premie) gets it from asymptomatic mother. leads to sepsis and meningitis. all encapsulated serotypes can cause this
describe the late onset disease of GBS.
occurs after 7th day of childbirth. bacteremia, meningitis, bone/joint involvement, usually term baby with no risk factors, serotype III predominates. NOT PNEUMONIA, lung is npot sight of initial infection
what are the symptoms of early onset GBS disease?
lethargy, poor feeding, jaundice, hypotension... if meningitis, 1/2 have seizures, 5-10% mortality, as well as 25-50% chance of permanent neurologic sequelae from meningitis
how does a pre term baby aquire GBS?
mother has it in vagina, it then penetrates placental membranes, child aspirates large amounts of infected amniotic fluid, hits the lungs and causes pneumonia, then invades the pulmonary epithelial and endothelial cells to the blood stream and thus sepsis.
what are the risk factors used to determine if a baby is susceptable to GBS?
high inoculum of bacs, virulent strain, chorioamnionitis, gestation < 37 wks, ROM> 18 hours, lack of anti capsule antibodies from mom
what adults are susceptable to GBS infection?
pregnant - cesarean related wound infection. Immunocompromised or those with an underlying medical condition
what diseases can GBS cause in adults?
septic arthritis, meningitis, endocarditis, skin and soft tissue infection
how can an infant become infected with late onset GBS?
from mom or from another exogenous source
what is the mortality rate for adult GBS?
21-34%
what diseases can GBS cause in adults?
bacteremia is most common and if it does not kill you, it will reoccur usually. pneumonia, endocarditis, meningitis, arthritis and osteomyelitis, skin and soft tissue infections
what are the main virulence factors of GBS?
the capsule which inhibits phagocytosis and is antigenically variable bc of a terminal sialic acid, hemolysin which is toxic for many cell types, C5a peptidase
how is GBS controlled/treated?
pregnant women are tested 2 wks before birth and are given penicillin if needed.
what are the indications for intrapartum antibiotic prophylaxis for gbs?
previous infant with GBS, GBS bacteremia during pregnancy, positive GBS screenig culture, delivery at <37 wks, membrane rupture over 18 hrs, intrapartum temp > 100.4. NOTE this will only reduce early onset disease not late onset
how is GBS spread between asymptomatic carriers?
sexual contact (though it is not considered an STD), fecal oral route, some ppl have it asymptomatically in their throat
what antibiotics and vaccines are used for GBS?
penicillin or ampicillin, some resistance has been reported. for big time infections do ampicilin and aminoglycoside, vanc in pts allergic to penicillin. new vaccines being developed against the capsule and the surface proteins
what are key characteristics and properties of the enterococci?
gram pos coccus, in pairs or short chains, hardy on dry surfaces, microscopically indistinguishable from S. pneumoniae, facultative, often resistant to antibiotics (VRE), not as virulent as strep or staff, but can transfer resistance to other species! normal resident of healthy human colon as well as hands of health care workers
what can cause enteroccoci to become cause disease?
usually an opportunist, it becomes dangerous with prolonged hospitilization with long periods of antibiotic treatment, thus everything else is killed but it. It is 1st in causes of nosocomial bacteremia
describe the diseases caused by enterococci.
bacteremia can hit through urinary tract, pelvic sepsis, or wounds; it is usually transient but death rate is high bc pts usually have some other problem. Endocarditis usually in pt with underlying heart valve issue. UTI is most common in faecalis and usually associated with catheter that is contaminated. wound infection/pelvic infection/ intraab infection all usually found with other bacs, some can be septic.
how is enterococci spread?
thinking is now get an expgenous infection not endogenous normal flora. may be from hospital care workers
what are the control protocols of VRE?
isolate patient, all persons entering or leaving the room should wear gloves/gown, non critical items should remain in room, wash hands with antibac agent after contact, keep infected patient isolated until 3 stool cultures are negative
what are the antibiotics for enterococci?
1st try is aminoglycosides plus cell wall active antibiotic. If VRE do linezolid or quinupristin/Dalfopristen