Micro Streptococci

Front 1

Is Streptococci gram positive or negative?

Back 1

Positive

Front 2

Streptococci catalase negative or positive?

Back 2

Catalase negative.

Front 3

What are the three groups of strept. based on their hemolytic abilities?

Back 3

Alpha partially lyse RBCs, leaving greenish discoloration. Beta completely lyse RBCs, clearing a zone around itself in blood agar. Gamma are unable to lyse RBCs.

Front 4

Streptococcus pyogenes is AKA? And pyogenes means?

Back 4

Group A beta-hemolytic streptococci. Pus forming.

Front 5

Streptococcus pyogenes infection can cause?

Back 5

Pharyngitis ("strept throat"), folliculitis

Impetigo: confined to the epidermis, vesicular, blistered, eruption that becomes crusty and flaky, usually around the mouth. They have a characteristic yellow crust.

Erysipelas: Dermal lymphatics. Raised, bright red rash with sharp border that advances from the initial site of infection. Has "butterfly-wing" rash on the face. Fever and lymphadenopathy.

Pyoderma: is a pustule, usually on the extremity or face. Breaks down to a thick crust. Heals slowly and leaves depigmented area.

Cellulitis: deep infection of CT, producing red, swollen skin which is hot to the tough. Develops at sit of previous trauma.

Front 6

Streptococcus pygenes immune-mediated can cause?

Back 6

Glomerulonephritis and rheumatic fever.

Front 7

The toxin of streptococcus pyogenes can cause?

Back 7

Scarlet fever, toxic shock syndrome, and necrotizing fasciitis (flesh eating bacteria).

Necrotizing fasciitis and myositis: infections of deeper subcutaneous tissues, fascia, and muscle. Characterized by extensive, rapidly spreading necrosis and gangrene of the skin and surrounding structures.

Front 8

M protein of streptococcus pyogenes is?

Back 8

Major virulence, which inhibits complement and protective against phagocytosis; however, AB attack the M protein.

Note: >100 serotypes of M protein. Humoral immunity follows infection due to ONE M type.

Front 9

Streptolysin O on S. pyrogenes

Back 9

Oxygen labile, and is inactivated by oxygen. Destroys RBCs and WBCs and is the reason for the beta-hemolytic function. Can be measured as an ASO titer.

Is a potent pore-forming cytolysin.

Front 10

Streptolysin S on S. pyrogenes.

Back 10

Oxygen stabile. Beta-hemolytic, however, not antigenic.

Front 11

Pyrogenic exotoxin on S. pyogenes.

Back 11

Causes scarlet fever. ALSO, some strains are also superantigenic that are responsible for toxic shock syndrome.

Front 12

Additional enzymes for S. pyogenes?

Back 12

Streptokinase, hyaluronidase, and DNase.

Note: hyaluronidase breaks down CT that allows for its spread in the deeper layers of the skin.

Front 13

How do you diagnose S. pyrogenes?

Back 13

ASO+, Gram+ cocci, bacitracin sensitive, catalase negative

Front 14

How do you treat S. pyrogenes?

What about in necrotizing fasciitis?

Back 14

Penicillins.

Penicillin-allergic PTs, give erythromycin or clindamycin.

In Necrotizing fasciitis: penicillin G with clindamycin to reduce production of toxins.

Front 15

"Strep throat" AKA pharyngitis can lead to?

Back 15

Rheumatic fever, glomerulonephritis, scarlet fever, TSS, bacteremia, meningitis, otitis

Front 16

Valves damaged by Rheumatic fever are susceptible to?

Back 16

Colonization by Enterococci or Viridans Streptococci, causing subacute infective endocarditis.

Front 17

Streptococcus agalactiae AKA?

Back 17

Group B beta-hemolytic streptococci

Front 18

S. agalactiae is carried by? Because of this means of transport, what can result?

Back 18

Vaginally; therefore, can cause neonatal problems such as meningitis, pneumonia, and sepsis during pregnancy.

Front 19

Treatment of meningitis caused by S. agalactiae? Prophylaxis?

Back 19

Prior to obtaining results of LP, antibiotics must also cover E. coli, Listeria monocytogenes. Test mother prior to delivery.

Front 20

Streptococci viridans AKA

Back 20

Alpha hemolytic stretpococci

Front 21

Viridans stretpococci can cause?

Back 21

Dental caries (S. mutans), brain or abdominal abscesses (S. intermedius AKA Anginosus species group), and subacute bacterial endocarditis.

Front 22

Viridans stretpococci normally inhabits?

Back 22

Normal flora of the oropharynx epithelium. Therefore, dental extraction or vigorous tooth brushing can cause the bacteria to enter into the bloodstream.

Front 23

Treatment of viridans streptococci?

Back 23

Penicillin G

Front 24

Viridans Streptococci as well as enterococci can colonize?

Back 24

Previously damaged cardiac valves caused by Group A Streptococci; therefore, with a potential for embolism. This occurs because fibrin and platelets bind to the trauma (nonbacterial thrombotic endocarditis) and bacteremia then leads to seeding of lesions with adherent bacteria.

Front 25

Another name for group D streptococci?

Back 25

Enterococci and non-enterococci. These bacteria, use to be called streptococci, but they have their own genus now called enterococci and non-entercocci.

Front 26

Enterococcus faecalis and faecium, which is alpha or gamma hemolytic, can grow well in?

Back 26

40% bile or 6.5% NaCl

Front 27

Enterococcus faecalis and faecium can cause?

Back 27

UTIs, biliary tract infection, and subacute bacterial endocarditis.

Front 28

Enterococcus are the second to third most common?

Back 28

Nosocomial infections due to high resistance. They are a frequent complication of biliary/hepatic surgery.

Front 29

Treatment of enterococcus?

Back 29

Usually with treatment with ampicillin plus an aminoglycoside; however, with resistance, agents used have included dalfopristine/quinupristine.

Front 30

non-enterococci (streptococcus bovis and quinus) grows well in?

Back 30

40% bile, but not 6.5% NaCl

Front 31

What is an association with non-enterococci?

Back 31

Lives in the GI, and since it invades through GI lesions, S. Bovis oftentimes signals colonic carcinomas or inflammatory bowel disease.

Front 32

What streptococcus has no Lancefield antigen?

Back 32

Streptococcus pneumoniae

Front 33

Streptococcus pneumoniae can cause?

Back 33

Lobar pneumonia, otitis media (very common in children), and meningitis (S. pneumoniae is the most common cause in adults; second in children)

NOTE: Most common cause (MOPS)

Meningitis, Otitis media (in children), Pneumonia, Sinusitis)
AND
Most OPtochin Sensitive

Front 34

S. pneumoniae appear as what under the microscope?

Back 34

Diplococci

Front 35

What are two important lab test to identify S. pneumonococcus?

Back 35

Quellung reaction and Optochin sensitivity.

Front 36

What does optochin sensitivity differentiate?

Back 36

Between two alpha-hemolytic streptococcus. S. pneumoniae will not grow while S. viridans will continue to grow.

Front 37

S. Pneumoniae is the most common cause of what?

Back 37

MOPS: Meningitis (adults), Otitis media (children), Pneumonia (adults), Sinusitis

MOPS: Most, OPtochin Sensitive

Front 38

What is the treatment of S. pneumoniae?

Back 38

Penicillin and cephalosporins. Vancomycin for meningitis

Community-acquired pneumonia: empirical therapy includes a third-generation cephalosporin (cefotaxime or ceftriazone), plus a macrolide or a newer quinolone (levofloxacin or gatifloxiacin).

Front 39

What may be associated upon observation of the PT with S. pneumoniae?

Back 39

Rusty-colored or yellow-green phlegm.

Front 40

Bacterial endocarditis can be divided into what two categories and what are the differences?

Back 40

Acute bacterial endocarditis is usually caused by Staphylococcus aureus (PTs who are IV drug users), and less commonly with Strept. pyogenes and pneumoniae. There are large vegetations and occasionally abscesses.

Subacute bacterial endocarditis includes smaller vegetations on abnormal valves and has a more indolent course than acute does.

Front 41

What are two classification of subacute bacterial endocarditis?

Back 41

Native-valve endocarditis: viridans streptococci, enterococci, or HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) Usually from dental procedures.

Prosthetic valve endocarditis: (Staphylococcus epidermidis) PT may have a history of uneventful replacement of aortic valve with mechanical prosthesis due to severe aortic stenosis.

Front 42

What are the most common symptom of endocarditis?

Back 42

Janeway lesions (small erythematous lesions on palms or soles), Osler nodes (painful raised lesions on finger and toe pads), Roth spots (retinal lesions), and splinter hemorrhages on nail beds.

Fever, followed by malaise, night sweats, fatigue, weight loss, and arthralgias.

Front 43

What is commonly seen with subacute bacterial endocarditis?

Back 43

Elevated ESR and anemia.

PTs who are IV drug users, predominately have right-sided diseases caused by Staph. aureus involving the tricuspid valve.

Front 44

Treatment of viridans streptococci?

Back 44

Penicillin G with or without an aminoglycoside.

Front 45

Fibronectin-binding proteins and surface clumping factors do?

Back 45

Fibronectin-binding proteins on viridans streptococci facilitate adherence to thrombi. Surface clumping factors on more virulent S. aureus facilitate adherence to intact endothelium or exposed subendothelial tissue. Organisms become entrapped in the growing platelet-fibrin vegetation and proliferate forming microcolonies.

Front 46

What are community acquired pneumonia?

What are atypical pathogens?

Back 46

Community: S. pneumoniae, H. influenzae

Atypical: Chlamydia, Mycoplasma, and Legionella

Front 47

H. influenzae and M. catarrhalis are seen in?

K. pneumoniae is seen in?

S. aureus is likely to become pneumonia when?

S. pneumoniae occurs as?

Back 47

COPD

Alcoholics

Postinfluenza

Appears suddenly

Front 48

S. pneumoniae grows on what kind of agar?

Back 48

Sheep, yielding alpha-hemolytic colonies.

Front 49

Most common cause of community-acquired pneumonia?

Most commonly occurs with?

Back 49

S. pneumoniae via aerosolized droplets.

AIDS, asplenia, influenza, sickle cell, disease, multiple myeloma, alcoholism, smoking, diabetes, hypogammaglobulinemia, and nephrotic syndrome.

Front 50

What is the pathogenesis of S. pneumoniae?

Back 50

Upper airway colonization; aspiration into lower airways; failure of normal host defenses and inflammation.

Note: Those whose mucus and cilia functions are altered (e.g., smoking), facilitates this pathogen.

Front 51

S. pneumoniae generates?

What is another way that it can adhere?

Back 51

IgA protease, which degrades IgA AB and favors mucosal colonization.

It can bind to platelet activating factor receptors on epithelial cells; therefore, during inflammation, there is a stimulation production of PAF.

Front 52

What is unique about S. pneumoniae polysaccharide capsule?

Back 52

It has antiphagocytic properites.

Normally, bacteria would be opsonized by C3 and cleared via the alveolar macrophage C3b receptor.

Front 53

What is released during S. pneumoniae lysis?

Back 53

Hemolysin (AKA pneumolysin), which is pore forming and is cytotoxic.

Front 54

What is the pathology of pneumonia?--Congestion; red hepatization; gray hepatization; and resolution.

Back 54

Congestion: extensive serous exudation, vascular engorgement.

Red hepatization: airspaces are filled with PMNs, extravasation of RBCs causes reddish discoloration.

Gray hepatization: accumulation of fibrin, WBCs, alveolar spaces filled with exudates.

Resolution: resorption of exudate.

Front 55

Describe the airspace infection of S. pneumoniae.

What does TNF cause?

Back 55

Intra-alveolar exudates, spreading rapidly within a lobe through the pores of Kohn, until the entire lobe is consolidated.

Cytokines such as TNF, causes high fever, chills, myalgias and others.

Front 56

How do you prevent S. pneumoniae?

Back 56

Pneumococcal vaccine indicated for ppl older than 60 and at risk individuals; in children younger than 5 attending care centers.

Front 57

What is standard for diagnosing streptococcal pharyngitis?

Back 57

Throat culture and sheep blood agar for the medium

Front 58

What is the RADT, rapid (dipstick-based) test?

Back 58

Detects presence of cell-wall carbohydrate antigen in the throat swab, and positive test confirms S. pyogenes.

Front 59

Describe Scarlet fever

Back 59

Caused by S. pyogenes.

Rash appears on second day of pharyngitis; rash begins on trunk and spreads outward, sparing the palms and soles. Circumpolar pallor and red papillae on tongue (strawberry tongue)

Erythrogenic toxin causes the rash.

Front 60

Describe acute rheumatic fever.

Back 60

Caused by S. pyogenes.

Major manifestations: carditis, polyarthritis, chorea, erythema marginatum, and subcutaneous nodules.

Minor manifestations: fever, arthralgias, and elevated ESR.

Front 61

Describe rheumatic heart disease

Back 61

Recurrent strept infections.

Aschoff bodies (granuloma and giant cells) and Anitschkow cells (activated histiocytes).

Front 62

Describe the pathogenesis behind acute rheumatic fever and rheumatic heart disease.

Back 62

Note: Type II hypersensitivity due to molecular mimicry--M proteins are similar to cardiac antigens, but differ enough to evoke an immune response. This causes a complement (mm attack complex)-mediated damage (cytotoxicity) to heart valvess.

Diagnosis is based on preceding strept infection (e.g., elevated ASO)

Front 63

What is an oral beta-lactamase resistant penicillin?

Back 63

Cloxacillin and dicloxacillin.

Note: they have "clox" in their name.