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MICROBIOLOGY II > Lecture 2 - Streptococcal Infection > Flashcards

Lecture 2 - Streptococcal Infection Flashcards

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1
Q

Where are strep found

A

Everywhere

Gut, GI tract, mouth, URT

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2
Q

What is the classification of streptococcal

A

Streptococci

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3
Q

What is the pathogenic form of streptococcus

A

Strep pyogenes - Group A streptococcus

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4
Q

Who first described pyogenes infected patients with a ‘flesh eating disease’

A

Hippocrates

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5
Q

Who in 1874 designated the name strepto coccus

A

Theodore Billroth

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6
Q

Who in 1884 was the first person to recover and grow strep pyogenes from patients with puerperal sepsis (childbed fever)

A

Louis Pasteur

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7
Q

In 1884 which pioneer designated name streptococcus pyogenes

A

Anton rosenbach

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8
Q

Why is it called pyogenes

A

Pyo meaning inflammatory

Cause inflammation

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9
Q

Is strep pyogenes gram positive or gram negative

A

Gram positive

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10
Q

What is the size of strep pyogenes

A

0.5-1um

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11
Q

How do strep pyogenes gain energy E.g. Via oxygen or co2

A

FACULTATIVE ANAEROBES

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12
Q

What does capnophilic mean

A

Bacteria that live in high CO2

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13
Q

What temperate range does strep pyogenes fit into

A

18-40

Optimum 30

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14
Q

Is strep pyogenes positive or negative for catalase production

A

Catalase NEGATIVE

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15
Q

Where does S.salivarius live

A

MOUTH

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16
Q

What does S.agalactiae cause

A

Neonatal meningitis

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17
Q

Name 3 diseases caused by strep pyogenes

A

Tonsillitis, necrotising fasciitis (gangrene) and scarlet fever

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18
Q

What is a key factor of strep classification

A

Their haemolytic properties e,g, alpha, beta or gamma
And SURFACE ANTIGENS E.G. CHO antigens, classifies beta haemolytic strep into specific groups of carbohydrate surface antigen A,B,C,G,F

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19
Q

What enzymes are used in beta haemoyosis to break down our RBC

A

Streptolysin S and O

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20
Q

Who based classification on surface antigens

A

Rebecca lancefield

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21
Q

What strep species partake in partial haemolysis (alpha)

A

S. Pneumoniae and viridians strep

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22
Q

What does hydrogen peroxide produced by the alpha haemolytic species do the haemoglobin

A

Oxidises to green methaemoglobin

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23
Q

Which two species of strep partake in beta haemolysis

A

strep pyogenes and s,agalactiae

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24
Q

What do type II toxin do

A

Attack cholesterol in membrane

25
Q

Which streptolyosin is oxygen labile and which is oxygen stable

A

Labile - streptolysin O

Stable S - use oxygen

26
Q

Which species partake in gamma haemolysis

A

Enterococcus

27
Q

Rebecca lancefield identified two major surface antigens that could be used in classification of beta haemolytic strep. What are they?

A

M proteins

Group Antigen

28
Q

Surface antigen is a carbohydrate antigen incorporated into cell wall by strep. How do we extract it in the laboratory

A

Mix colony with nitrous acid and this brings the surface antigen away.

Also do a variety of agglutination tests using latex beads with antibodies against all group antigens e.g. Group A or B etc

29
Q

How many M proteins are there believed to be

A

Up to 18

30
Q

What is the group A antigen

A

NAG - rhamnose. Group A antigen surround cell wall particularly rhamnose

31
Q

What doesnt the antigen classification tell you and how do you resolve this

A

Species and genus
Use API - sugars and enzymes. If does ferment sugar get positive reaction. Add up scores and type into database give this info.

32
Q

What are three things needed to be pathogenic (general)

A

Colonisation - attachment
Evasion
Damage via toxins and invasins

33
Q

What do the surface proteins do

A

Allow colonisation of skin

34
Q

Apart from streptolysins and streptokinase what other enzyme is produced

A

Hyularonidase

35
Q

What are the toxins that lead to inflammation inducing temp

A

Streptococcal pyrogenic extoxins (SPE)

36
Q

What does F protein do

A

Recognise fibronectin on ECM.
Primary attachment to pharynx and skin
Facilitates internalisation to enter epithelial cells

37
Q

What is gas f protein process

A

Group A strep bound to f protein
This bind to fibronectin and get internalisaed
Can be phagocytosis/lysozyme
M protein then used to get tighter binding

38
Q

What do M proteins protrude in the form of

A

Fimbrae and pilli

39
Q

What must M protein go through to extrude as pili

A

Bound to cytoplasmic membrane, go through peptidoglycan and group antigen (polysaccharide)

40
Q

How many immunological types are there and is reinfectiuon hence common or rare

A

Excessing 80 types so common reinfection

41
Q

What is distinct about the structure of M proteins

A

Similar to some of our tissues, heart, kidney, muscle, skin

Risk of autoimmunity

42
Q

What key functions does m protein do

A

Attachment
Bind serum proteases - spread through tissue
Antiphagocytuc - prevent c3b binding complement

43
Q

How does it evade our immune system

A

Hyalurnic acid capsule - we have hyaluronic acd in our ECM so hides. Also bind CD44 which have a lot of in system. Can attach using CD44

Immunolglobulin binding protein - bind to fc region of IgA and IgG preventing opsonisation

C5a peptidase - inactivate c5a (reduce neutrophil recruitment)

44
Q

What virulence factors does it secrete

A

Strep o - MW 60,000. Lysis RBC, pore forming, type II toxin, highly antigenic (produce antibodies to it called streptolyosin o eaters can measure in patients)

DNAase - A,B,C,D (b mist common strep) - split DNA use to grow

Streptokinase - antigen secreted by strep combine with plasminogen to form plasmin - hydrolyse fibrin clot - spread

Hyalurondase - movement

SPE’s

45
Q

Which virulence factor used clinically and how

A

Streptokinase - catheter break down clot

46
Q

Where does streptococcal pyrogenic exotoxins bind

A

Membrane outer

47
Q

What is a superantigen

A

Antigen get massive cytokine release as doesn’t need to be digested and presented on MHC II - non specific binding so many more T cell binding so more TNFa

48
Q

What does immunologically mediated disease mean

A

Disease due to our antibodies attacking bacteria e.g. Rheumatic fever

49
Q

What are 4 types of disease strep and name infections for each

A

1- superficial - impetigo, vaginitis
2- deep - septicaemia , gangrene
3- toxin mediated - scarlet fever
4- immuno mediated - rheumatic fever

50
Q

Describe impetigo infection

A

Initial papulovesicular lesion surrounded by redness
Vesicles rapidly become purulent - covered thick honey coloured crust
- lesions mostly on face
- may resolve within 1-2 weeks but often spread to rest of body

Common preschool children, mental institution

51
Q

What is a predisposing factor to impetigo

A

Bad hygiene

52
Q

What other organism can cause impetigo and what is important vabout infection

A

Staph

Spread through cough and touch

53
Q

Where does gangrene occur

A

Subcutaneous tissue (fascia)

54
Q

Describe a gangrene infection

A

1- initial trauma
2- 48-72hr - skin purple and blisters containing yellow or haemorrhagic fluid appear
3- day 4 - gangrene present - sloughing of skin
4- day 7-10 - skin break down - necrosis subcutaneous tissue. Need surgical debridement to save life

55
Q

Describe first stage of scarlet fever (tonsillitis - strep throat)

A

Pain, erythema, temp, pus

Colonisation followed by inflamed throat ad release of pyrogenic exotoxins (A,B,C,F)

56
Q

Describe scarlet fever

A

If strep A tonsillitis not treated can get scarlet fever
Rash appear 12-72 hrs after fever

Spread via coughing, sneezing
Children - 5-15 years

Symptoms:
Sore throat, fever over 38 deg
Widespread rash - torso and arms and legs.

White strawberry tongue/ red strawberry tongue

57
Q

How many strep throats go to SF

A

10%

58
Q

Describe the autoimmune disease RF following strep infection

A

Antibodies produced to GAS M protein and nag cross react human myosin, tropomyosin, laminin and keratin

1-4 weeks post strep infection, associated with M types 1,3,5,6,18,24

Inflammation of joints, heart, CNS, skin

59
Q

Describe other immunologically mediated post strep disease

A

Glomerulonephritis - affect kidney
3 week post strep assocuiated M types (partiularly) 12, 4,2, 49

Symptoms ; swelling of face, haematuria, fluid balance irregularity

Pathogenesis: deposition immune complexes in glomeruli (basement membrane)

Cross reacting antibodies to GAS and glomerular antigens

MICROBIOLOGY II (9 decks)

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