Micro, Ass 4, Renee’s Questions – Flashcards

55.; Poly-gamma-DL-glutamic acid; antiphagocytic capsular material.

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It is found in the capsules of S. epi species which allows them to colonize skin and mucosal surfaces.

94.; Viridans Streptococci

Typically S. mutans

Methacillin-resistant Staph aureus

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A major problem!

MRSA have a unique penicillin binding protein that makes them resistant to methicillins, penicillins, and cephalosporins.

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For serious MRSA infections tx w IV vancomycin Daptomycin is also effective against MRSA and VRE (Vanc-R enterococci), depolarizes bacterial membranes.

Strep bovis,

Enterococcus faecalis,

Enterococcus faecium

Protein A is a major component of the bacterial cell wall.

It is also sloughed off of some bacteria and can be anti-phagocytic.

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In S. aureus protein A is a MSCRAMM. It is recgonized (along with clumping factors A and B) on the surface of S. aureus in Latex Aggulutination Tests.

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Protein A binds to the Fc portion of IgG and prevents activation of complement (anti-phagocytic property).

1) MSCRAMMs

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2) LPXTG Motif (a specific amino acid sequence that is cleaved by the enzyme sortase to attach the protien to uncrosslinked peptidoglycans to allow interaction with a host).

Staphlococcal infections.

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Granulomatous Dz pts do not make ROS used to kill many types of bacteria.

Staph species are catalase positive which means they are able to break down the minimal amounts of hydrogen peroxide in the phagcytes of these pts leaving their phagocytes helpless to fight infection.

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Strep infections do not present a problem to these pt because Strep is catalase negative.

Coagulase = Clumping Factor

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A MSCRAMM found in S. aureus species.

Thermonucleases are DNases.

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They are present in S. aureus but not in other forms of staph.

These leukocidis are capable of lysing PMNs and are found in most CA-MRSA.

These isolates cause particularily severe infections.

Both can grow on blood agar plates and both are beta-hemolytic.

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S. aureus produces golden-colored colonies while CoagNS typically produce white colonies.

Stahplococcal Scalded Skin Syndrome (SSSS),

Staphlococcal Scarlet Fever (which is a generalized form of SSSS),

Bullous Impetigo (blisters)

F.

Can be caused by Staph or Strep superantigens.

Specifically those of Staph aureus and Strep pyogenes.

M protein is the most significant, although there are others (M-like protein, F1/2, Epa)

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M protein is anti-phagocytic (either due to binding fibrinogen or C4b binding protien, either way inhbiting complement activation and thereby hindering phagocytosis).

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M protein is implicated in the development of acute rheumatic fever.

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anti-M abs are protective but there are multiple serotypes of M.

Fimbriae are a key mechanism of virulance for many species.

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In GAS, fimbriae are made up of M protein (a MSCRAMM) and Lipoteicholic Acids (LTA, pro-inflammatory adhesins).

Both of these components contribute to its virulence.

The rash and fever associated with Scarlet Fever.

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Streptococcal TSS

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Necrotizing fasciitis pathogenesis.

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Myositis

SLO and SLS (Streptolysin O and S) are hemolysins responsible for beta hemolysis on a blood agar plate.

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SLO is oxygen labile while SLS is oxygen stabile.

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SLO is used to dx ARF.

S. pyogenes is Bacitracin Sensitive.

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Bacitracin is used to distinguish Group A strep (BacitracinS) from Group B strep (Bacitracin R)

VIRUSES*

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If it is bacterial it is likely to be GAS but it is most likely viral.

(if it is GAS, tx with PenV)

A dz caused by SPE+ (Strep pyogenic exotoxin) strains of S. pyogenes.

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It is the toxin, rather than the strep itself which causes the symptoms (Strawbery tounge, red rash, sore throat, and fevers).

Can be a mono or polymicrobial infection!

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In either case GAS and/or S. pyogenes can be involved (as can other organisms).

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False.

GAS my follow strep throat but does not follow streptococcal skin infections.

May follow either a streptococcal pharyngitis OR a skin infection (unlike ARF).

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Associated with speficic M proteins which are siad to be nephritogenic.

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An immune complex dz

S. agalactiae (detectible by rapid group B carbohydrate latex agglutination test).

Beta-hemolytic, Bacitracin R, has multiple antiphagycitc cpasule types which contain sialic acid and are the major source of virulence for this GBS.

Normal flora of the GI and oropharynx but also colonize the vagina during pregnancy.

;Neonatial sepsis

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Mothers now screened.

E. coli and some G- enterics also imporant.

Causes septicemia, respiratory distress, early onset after birth.

Can lead to meningitis and respiratory disease.

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GBS can aslo cause infections, septicemia and endocarditis in immunocomprimised adults.

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It is considered an "honorary strep"

G(+) cocci

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All are Lancefield Group D (but some strep are also D)

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Bile esculin +

Salt tolorant

Some resistance to heat (overall hardy)

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Noraml folor of the skin, upper RT, GI and GU tracts.

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Most dz caused by this group is by E. faecalis and E. faecium is the strain most frequently VancR (VRE)

False.

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Enterococcus species are naturally resistant to Pen and to Cephalosporins with some strains being Vancomycin resistant (VRE).

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Some of the world's most resistant bacteria are in this group!

1. Nosocomial Infections (ex: UTI, septicemia, wound infection; Enterococci commonly involved in all)

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2. Subacute endocarditis (SBE), particularily involving the valves (Enterococci)

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3. Bacteremia: occurs when the colonic mucoas is disurpted by a tumor and S. bovis gets into to blood.

Is indication for a colonoscopy (intestinal cancer).

A glycopeptide abx which inhbits crosslinking of NAM and NAG in PG cell wall formation.

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Effective against G + species only.

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Used to treat potentially debilitating/fatal Dz:

MethR Staph infections (though there are Vanc alternatives here),

Pneumococcal meningitis (empirical tx, bf sensitivity profiles get back from the lab),

C. difficile infections/psudomembranous enterocolitis (again, alternative options are avail.)

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Always adjust tx when sensitivities are known.

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VRE: VancR Enterococcus, typically E. faecium

(the original VancR organism)

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VRSA: VancR S. aureus

(aquired resistance from Enterococcal species).

Linezolid is typically a first choice

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Synercid (a combo quinupristin/daflopristin) + Streptogramns

[Inhibition of bacterial protein synthesis]

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Daptomycin (lipoprotein that depoloarizes G+ bacterial cell walls causing bacterial cell death)

Viridans are a group of streptococci that excludes S. pneumo.

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Are non-typable by Lancefield groups.

Alpha-hemolytic

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Normal flora in the oral/pharyngeal cavities.

Important opportunists (SBE, bacteremia)

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Notable member of this group: S. mutans has a slimy capsule of sucrose which allows it to attach to teeth and cause dental carries.

S. mutans

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Viridans group strep (alpha hemolytic)

Non-typable alpha hemolytic strep that is not (for some unknown reason) considered a part of the Viridans group.

Can be normal flora of the pharynx.

Lancet-shaped

Diplococci*

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OptochinS

(used to identify it from other alpha-hemolytic strep species like S. viridans which are OptochinR)

Bile-soluble

(to distinguish from S. bovis and Enterococci which are not dissolved by bile).

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Capsule of S. pneumo=major virulence factor

(Anti-phagocytic, basis of pnumo vaccines, detectible by rapid agglutination tests).

Pnumolysin is a key virulence factor of Strep pneumo.

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Can lyse cells by binding to membrane cholesterol and forming a pore.

S. pneumo establishes infection (in RT, lungs, meninges, blood) by escaping host natural and adaptive immune responses and inducing inflammation (has C-substance which binds to C-reactive protein, inducing the release of acute phase reactants=inflammation).

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Ex: death from pneumonia is the result of an inflammatory response elading to excessive fluid accumulation in the lungs which causes suffocation.

Leading cause of bacterial pneumonia is Strep pneumo.

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Is most common in the elderly.

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Presents with a shaking chill (single rigor), rusty sputum (productive cough), pleuritic pain, and fever.

CXR shows lobar consolodation (due to fluid accumulation).

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Risk Factors: recent viral infection, chronic pulmonary dz, splenic disorders (SSA, DM, asplenia).

Variable resistance patterns make abx tx difficult.

Multiresistant Strep pneumo (MSRP) = problematic.

Sensitivies should be ordered for all isolates.

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If sensitivity allows, tx with Pen or ceftriaxone (3rd gen cephalosporin).

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In PenR strains, tx with a fluroquinone liek Levofloxacin (broad spectrum, high toxicity)

Prevent inflenza via flu vaccine!

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Viral illness predisposes to pneumonia!

URI

(otitis media, sinusistis, conjunctivitis)

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Septicemia

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Meningitis

(S. pneumo is the leading cause of bacterial meningitis in adults)

Causes: First weeks of life (GBS)

3 mo-18 yrs (Neisseria meningitis)

18-50+yrs (S. pneumo)

*Haemophilus, Listeria, E. coli are also causes.

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Symptoms:Stiff neck, Headache, photophobia, fever, vomiting, neuro dysfunction.

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CSF Findings: High opening pressure, large numbers of PMNs*, elevated protien levels.

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If bacterial meningitis is suspected a combination of Cephalosporin and Vancomycin is often used (tx S. pneumo-caused meningitis).

True

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Pneumovax is a non-conjugated vaccine for older people and those at high risk due to AIDS, asplenia, transplant.

Not effective in kids.

Protects against invasive pneumococcal dz.

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Prevnar is a new, expensive but safe, conjugated vaccine effective in children as young as 2 mo, creates a memory response.

G(-) *unique in this assessment material

Kidney-bean shaped

Diplococcal

Oxidase positive.

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The most common cause of bacterial menigitis in children (3 mo-18 yrs); can have very rapid dz progression leading to death.

Also a cause of bacteremia (Meningococcemia)

Throat (normal flora) ; Blood ; Meninges

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Virulence Factors: Pili, LPS, polysaccride capsule (distinguishes N. mengitidis from N. gonorrheae)

*Capsule is the basis for detection by rapid agglutination and for vaccine formulations.

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Risk Factors:Crowded populations and alcoholism, endemic in some areas.

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While rapid tx is vital, resistance is not a huge problem with N. meningitidis infections.

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Meningococcemia

(bacteremia caused by N. meningitidis)

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Is more rare than bacterial meningitis caused by N. meningitidis.

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While prompt tx is vital, resistance is not a huge problem with N. meningitidis.

True

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Ciprofloacin (floroquinalone abx which inhbits DNA synth) is given to those at high risk: colse contacts, medical personal etc...

;G- rod *unique in this assessment

Non-motile

Does not grow on BAP

(distinguishes from Strep/staph/enterococcus)

Does grow on Chocolate Agar Plate

(CAP, contains grwoth requirements for fussy bacteria)

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Since the vaccine, the incidence of H. flu caused bacterial meningitis has plumeted (only now occurs in partially/unvaccinated infants).

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Unencapsulated H. flu is a huge cause of otitis media in children (2nd behind S. pneumo)

Type b (the invasive type) has a capsule which allows it to cause severe systemic dz: meningitis, epiglottitis, cellulitis, osteomyelitis, pneumonia.

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Tx: Ceftriaxone typically used to tx H. flu infections

AmpR is common.

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Prevention: There is an effective conjugated type b vaccine that is part of standard vaccination series.

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G(+)

Club-shaped Rod

Motile over a ltd. temp range.

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A facultative intracellular parasite that infects mucoasl epi cells and non-immune macropahges.

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Sources: The environment (animals); human infection is typically food-borne (unpasturized cheeses, hot dogs, deli meat).

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Dz: Uncommon but serious food-borne illness with req hospitalization and high mortality.

Infections are flu-like in normal adults and more prevalent in pregnant women.

Can also cause bacteremia, meningitis in the immunocomrimised and neonates.

You suspect bacterial meningitis.

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1) Take blood/CSF cultures (send off for succeptibilites)

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2) Treat empirically

Cephtriaxone (broad spec abx, 3rd gen Cephalosporin)

+ Ampicillin (if listeria is suspected)

or + Vanc (if R S. pneumo is common in your area).

Bacterial: GAS, N. gonorrhoeae

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Many viral causes incl Rhinovirus/Coronovirus (common cold viruses) and Adnenovirus.

90% is caused by viruses and therefore should not be tx w/ Abx unless culture indicates.

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Viruses: Coronavirus, Rhinovirus, adenovirus (URT)

Influenza (LRT)

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Bacteria can cause more bronchitis in pt with underlying lung/respiratory problems*

S. pneumo, H. flu can cause in this case.

AOM: Amoxicillin

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Pneumonia: Amoxicillin or PenG (if PenS)

High dose Pen or Cephtriaxone (if Pen intermediate)

Fluroquinilone [Linezolid or Synercid] (if PenR)

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Meningitis: High dose PenG or Cephtriaxone (if PenS)

Vanc+Ceph (if PenR)

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All S. pneumo are B-lactam resistant due to altered penicillin binding proteins (PBP) not due to beta lactamases*

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All S. pneumo are VancS at this time.

Used to tell Group B strep and Enterococci apart from other Strep strains and from one another.

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GBS is the only type of strep that can grow in a high-salt medium.

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Enterococcal species can not only grow on this media but can convert bile esculin to a black breakdown product (distinguishing it from GBS).

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Thermonuclease Test

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S. aurueus (but not other staph, incl. epidermis) produces a heat-resistant DNase (a thermonuclease).

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Samples are boiled in blood broth culture and then inoculated on a thermonuclease plate.

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If S. aureus was present in the original culture its thermonucleases will have survived the boiling and will turn the blue agar pink.

Bile Solubility

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S. pneumo contain autolysins that are activated by bile salts. When bile salts are dropped onto a S. pneumo culture the entire culture will autolyse and disappear!

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Viridans and other species will persist.

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