Streptococcus & Enterococci

Front 1

Streptococcus genus organism properties

Back 1

gram +
cocci
chains
catalase -
Various alpha, beta, gamma hemolytic

Front 2

Pertinent Species streptococcus

Back 2

GAS (pyrogenes)
GBS (agalactlae)
Pneumoniae
Viridians
No longer enterrococci

Front 3

How can streptococcus be differentiated?

Back 3

Hemolysis when grown on blood agar
beta - pyrogenes or agalctiae
alpha - pneumoniae or viridians

Pneumoniae - have capsule with NO lancefield group ag

Rapid strep test - looks for Anti A antibodies. If negative confirm the negative with culture test.

Front 4

Enterrococcus

Back 4

This is simiilar to the streptococcus (gram + & Catalase - )
Group D ag
Gamma hemolysis

Front 5

Why is a culture required in pharyngitis?

Back 5

To much overlap from viral etiology and risk of post streptococcal sequelae.

Front 6

GAS organism properties

Back 6

chains, cocci, gram positive

Front 7

Describe Beta hemolysis, alpha hemolsys, gamma hemolysis.

Back 7

Performed on 5% SBC
Beta - Complete hemolysis of RBC, result in "clear" yellowish zone.
Alpha - partial hemolysis, greenish discoloration
Gamma - lack of hemolysis

Front 8

Describe catalase positive and negative. What is the reaction? What is streptococci? what are the 3 staph species?

Back 8

H2O2 --(catalse)--> H2O + O2

Strep - catalase (-)
Staph (3 species) - catalase (+)

Front 9

Describe Coagulase slide test. When is coagulase test used? Which one is +, which one are - ?

Back 9

Positive coagulase test shows clumping of suspension with in 10s.

Coagulase test is used to determine staph aureas from both the Staph epidermis & staph saprophyticus

+ coagulase = s. aureas
- coagulase = s. epidermis or s. saprophyticus

Front 10

Describe coagulase tube test? When is tube used compared to slide? What is the reaction occuring?

Back 10

When slide coagulase test has autoagglutination prior to adding plasma or on a negative slide test, it must be confirmed by the tube test. Reason is that s. aureas produces free coagulase that can dissociate away (opposed to bound coagulase)

Acts just like human thrombin
Fibrinogen --(Clumping factor0----> Fibrin clot

Front 11

Cytochrome Oxidase

Back 11

This enzyme is present as the bacterial ETC. The presence of enzyme will turn reagent purple in 5-10s

Oxidase + = Neisseria, P aeruginosa, Vibrio, Enterobacteriacae, Campylobacter or helicobacter

Front 12

How is pneumococci different from other streptococci?

Back 12

Capsule that varies and is a virulence factor (90 different serotypes)

Front 13

What is the crucial adherance structure for GAS? In nasopharynx? in Skin. What does it bind to on the epithelial cell? What adheres to langerhans cells?

Back 13

Fibronectin of the epithelial cells are bound differently in nasopharnyx (NP) & skin.

NP - M protein provides scaffold for LTA to bind

Skin - M protein binds to subcorneal keratinocytes

Protein F is important for binding langerhans cells

Lancefield antigens are contained inside the cell wall.

Front 14

Functions of M protein?

Back 14

Binds Fibrinogen, Serum factor H, and Ig.

Site for binding Ig is the variable region accounting for the 80 serotypes.

Suspect for etiology of Rheumatic fever induced Antibody.

Front 15

Extracellular Products of GAS?

Back 15

Streptolyin O - forms pores in lipid bilayer. Is antigenic and basis of ASO titer

StrepSAg - in about 10% GAS.

Front 16

Symptoms of Scarlet fever? What is etiology?

Back 16

Red face with circum-oral pallor, strawberry tongue (red papillae + yellow/white exudate), sandpaper rash upper chest to trunk + extremities.

Associated with GAS

Often these symptoms are superimposed on symptoms of STSS

Front 17

Describe pattern of rash in scarlet fever

Back 17

Sandpaper rash appears 2nd day of the fever and spreads from chest to the trunk & extremities.

Front 18

Describe the components of shock induced by Superantigens SAg?

What are symptoms of shock in general?

Back 18

Cytokine storm - shock, renal impairment, & diarrhea

Low BP, tachycardia, poor end organ perfusion.

Front 19

What is azotemia?

Back 19

This is renal failure. The name refers to the elevated Nitrogen. This results in an increase in BUN.

In the case of shock, prerenal azotemia is suspected and BUN:Cr should be >20.

Front 20

Progression of symptoms and lab findings of STSS?

Back 20

1. Begins with infection
2. vague myalgia, chills, severe pain at infection site
3. This leads to necrotizing fascitis & myonecrosis (tabloid flesh eating bacteria)
4. Continues with nausea, vomiting, diarrhea, hypotension, & organ failure
5. Lab findings are lymphocytosis, azotemia, & often bacteremia

Front 21

What is etiology of TSS, STSS?

Back 21

TSS - is staph aureas
STSS - is streptococcal (only GAS)

Front 22

Difference of Streptolysin O or S? and what test result they determine?

Back 22

Streptolysin O is oxygen labile and only lysis in anaerobic conditions.

Streptolysin S is oxygen stable and will lyse in both anaerobic/aerobic conditions.

Therefore it is important to incubate tests anaerobically.

Front 23

GAS transmission and what diseases is it associated with? What systemic effects can result?

Back 23

Group A streptococcal (GAS) disease overview. The primary sources of infection are respiratory droplets or direct contact with the skin. Impetigo results from minor trauma such as insect bites in skin transiently colonized with GAS. In streptococcal toxic shock, StrepSAgs producing GAS in a superficial lesion spread into the bloodstream. Note both toxin and bacteria are circulating

Front 24

Describe Erysipleas

Back 24

GAS of skin + subcutaneous tissues. Mostly the dermis is effected.

It has a rapidly spreading, well demarcated area of erythema & edema & pain.

Systemic symptoms include fever & lymphadenopathy.

Front 25

Describe entry and invasion by GAS

Back 25

Group A streptococcal disease, cellular view. The cellular events are similar to Staphylococcus aureus (see Figure 24–4). Streptolysin O is a pore-forming toxin (like -toxin), and there are many extracellular products. A difference is that although S aureus tends to be localized, group A streptococci (GAS) tend to spread diffusely, as shown in the cell on the right. This may be due to hyaluronidase (spreading factor) or resistance to phagocytosis. Below the cells, factor H binding is mediating GAS escaping the polymorphonuclear neutrophils (PMNs).

Front 26

What are Aschoff bodies?

Back 26

Aschoff nodule. Reacting lymphocytes and large mononuclear cells in myocardium demonstrate a cellular component to the immune reaction in rheumatic fever.

Front 27

Routes of entry and disease of Pneumococcus & GBS?

Back 27

GBS and pneumococcal disease overview. S pneumoniae is aspirated from the normal orophyaryngeal flora to the lung were it produces pneumonia. Bacteremic spread can infect other sites particularly the brain where meningitis is produced. GBS vaginal colonization during pregnancy leads to infection of the fetus either in the uterus or during childbirth.

Front 28

Risks of transmission GBS to neonate?

Back 28

Present in mother's vaginal flora
Ruptured membranes (>18H prior)
Premature birth

Disease will present in first few days of life or months later. 50% of the time sx are apparent at birth.

Front 29

Organism Pattern Streptococcus Pneumoniae

Back 29

Streptococcus pneumoniae in sputum of patient with pneumonia.

oval diplococci