Exam one: grpA strep, grpB strep, E. Faecali

Question 1

L10: where is strep pyogenes normally found

Answer 1

It is found in the skin nose and throat

Question 2

L10: what does group a strep bind to?

Answer 2

Group a strap finds to fibronectin 

Question 3

L10: how does group a strap bind to fibronectin?

Answer 3

It uses lipotechoic acid, protein, F, M protein, and M-like proteins 

Question 4

L10: what are some characteristics of and protein?

Answer 4

M protein is super coiled,
limits complement deactivation,
binds factor H, which enhances C3 converts, which is anti-phagocytic,
sequesters and neutralizes anti-microbial peptides that bind precursors
can mimic host proteins for immune evasion 

Question 5

L10: what do M like proteins do

Answer 5

They are non-op, sonic, immunoglobulin binding to decorate cell with host proteins

Question 6

L10: how does strep pyogenes evade the immune system?

Answer 6

It has a hyaluronic acid capsule, Hemolysin, C5a peptidase, and streptococcal pyrogenic exotoxins 

Question 7

L10: what is C5A peptidase and what does it do?

Answer 7

Inactivates major chemotactic factors, which inactivates C5a

Question 8

L10: what does SPEB do?

Answer 8

SPEB is surface bound cysteine protease. The adhesion binds host laminin, which causes signal cascade that triggers IL 1, IL 6 and TNF alpha 

Question 9

L10: what does SPEB produce, and what is its purpose?

Answer 9

It produces streptokinase, which activates host plasminogen to degrade fibrin

Question 10

L10: what is pharyngitis, who gets it, how do you treat it?

Answer 10

It is a strep throat, that school-aged kids get and you can use penicillin

Question 11

L10: What is acute rheumatic fever and what how was it caused?

Answer 11

It is an immunological complication of pharyngitis caused by coiled coil and protein that has a myosin hemology.
It is also caused by cross reactive antibodies that bind the sarcolemma membrane, and it is caused by enhanced T cell responses in heart valves that recognize strep antigens 

Question 12

L10: what is scarlet fever and how is it caused?

Answer 12

Scarlet fever is pharyngitis with a tongue rash that results from SPE intoxication

Question 13

L10: what is impetigo? How is it spread and what does it look like?

Answer 13

It is a transient skin colonization that is initiated by minor trauma and spread by direct contact. The superficial skin layer will form tiny pus, surrounded by redness. 

Question 14

L10: What is Erysipelas and cellulitis? How is it caused and what does it look like? 

Answer 14

It is a spreading of redness on the dermal tissue. It looks like advancing lesion with clear borders that spreads rapidly, and there’s accompanied by fever and lymphadenopathy. It is a facial infection, following pharyngitis that may cause necrotizing fasciitis if spread to the fascia. 

Question 15

L10: what is acute, glomerularnephritis, when does it occur, how does it occur?

Answer 15

It occurs one to four weeks post pharyngitis, 3 to 6 weeks after skin infection with elevated IgG levels. It is due to antibody antigen complexes that lead to complement activation and inflammation in kidneys. M proteins of some nephritic strains share antigenic similarity with glomerulus proteins. 

Question 16

L10: how is streptococcal, toxic shock caused and what does it look like?

Answer 16

It is due to SPE super antigenicity that leads to T cell activation in a non-specific way that stimulates IL1, IL6 and TNF alpha  it is a skin and soft tissue invasion that comes with nausea, vomiting, renal impairment, as well as muscle pain, chills, and pain at infection site. 

Question 17

L10: how do you culture strep pyogenes?

Answer 17

Anaerobic incubation on BA with hemolysis examination and identification of Lancefield group by latex gluten 

Question 18

L10: where is streptococcus agalactiae found

Answer 18

In the microbiota of the G.I. tract, vagina and glans penis 

Question 19

L10: how does strep agalactaie cause infection?

Answer 19

Via vertical ascent into amniotic fluid, and in the birth canal during delivery

Question 20

How does strep agalactiae attach to fibrinogen?

Answer 20

It uses BRAB, which is a bacterial surface, adhesion and SRR one and two, which are serine rich glycoproteins. It also uses pilli.

Question 21

How does streptococcus agile, lactate inhibit phagocytosis

Answer 21

It has 10 capsular types with sialic acid. Sialic acid binds serum factor H, which limits complement deposition. That in turn degrades C3 convertase and prevents phagocytosis and opsonization. 

Question 22

L10: how does strep, agile, lactic block inflammation

Answer 22

It has a hyaluronidase which degrades hyaluronic acid polymers into dimers instead of tetramers, the dimers block TLR2 and TLR4. That blocks inflammation.

Question 23

L10: how does streptococcus Aulac tie invade the cell epithelium

Answer 23

It uses Alpha C protein to bind a host extracellular matrix,
it has a hemolytic pigment that facilitates colonization that leads to pyroptosis and activation of IL1, IL 6 and TNF alpha. It also has a two component regulator of pigment production, which can increase colonization by increasing pH And it can regulate variance determinants 

Question 24

L10: what are the symptoms and risk factors of neonatal GBS disease? What is the protection for neonatal GBS? 

Answer 24

The symptoms are respiratory distress, fever, lethargy, hypotension, and it can evolve into pneumonia, meningitis or sepsis. The risk factors are premature birth and membrane rupture, and a neonate can gain protection by a transplacental, maternal IgG, that the new born can gain titer to when born. 

Question 25

L10: why is enterococcus Faecalis hard to culture?

Answer 25

It has an in vitro, high salt growth, can grow in bile, has a high pH and can grow in variable temperatures 

Question 26

L10: How is enterococcus usually spread?

Answer 26

Via hospital infections, and it has enhanced susceptibility when there is a disruption of normal functioning anatomy

Question 27

L10: what is special about the A1 subgrade of Anterra caucus?

Answer 27

It causes infection in humans, has multi drug resistant, has more virulence determinants, and increases mutation rate 

Question 28

L10: what is special about vancomycin resistant enterococcus strains?

Answer 28

It produces peptidoglycan precursors with terminal D- lactate that have a reduced binding affinity 

Question 29

L10: what is the Vancomyocin sensor receptor

Answer 29

The sensor is van S it is a histamine protein chase that is a sensor for glycopeptides and cell wall envelope alterations. Van is the response regulator that is activated by phosphorylation via Van S it turns on vancomycin resistant genes.

Question 30

L10: which genes are involved in being a type resistance and what do they do?

Answer 30

Van H is a dehydrogenase that produces D- lactate 
VA is a ligase that catalyzes D-ala D-ala
Van X is a DD dipeptidase that cleaves D-ala D-ala
Van Y is a carboxy peptidase that removes the terminal D- ala