Bacterial Virulence Flashcards

(55 cards)

1
Q

What do virulence factors contribute to?

A

The microbes ability to cause pathology

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2
Q

What is the function of adhesin?

A

Enables the binding of the organism to host tissue

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3
Q

What is the function of invasion?

A

Enables the organism to evade a host cell/tissue

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4
Q

What is the function of impedin?

A

Enables the organism to avoid host defence mechanism

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5
Q

What is the function of aggressin?

A

Causes damage to the host directly

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6
Q

What is the function of modulin?

A

Induces damage to the host indirectly

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7
Q

What are the factors responsible for the variation in virulence within and between species?

A

Adhesin
Impedin
Aggressin

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8
Q

What are the infections of the skin most commonly?

A

Gram +ve staphylococcus and streptocuccus

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9
Q

What differentiates staph aureus and staph epidermidis?

A

Coagulase test

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10
Q

Where is staph aureus common?

A

Anterior nares and perineum

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11
Q

Where is staph aureus contracted?

A

Nosocomial and community

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12
Q

What is MRSA defined by?

A

Flucloxacillin resistance

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13
Q

Who gets MRSA and where?

A
Nosocomial
Elderly and immunocompromised 
ICU
surgical patients
IV lines
Dialysis patients
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14
Q

Where is staph epidermidis common?

A

Skin and mucous membrane

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15
Q

Who gets staph epidermis?

A

Nosocomial infection in immunocompromised

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16
Q

What is staph epidermidis associated with?

A

Foreign devices e.g. catheters

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17
Q

What does superficial staph aureus look like?

A

Lesions- boils to abscesses

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18
Q

What is the toxinoses risk with S. aureus?

A

Toxic shock, scared skin syndrome

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19
Q

What is the role of fibrinogen binding protein in staph aureus?

A

Adhesin

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20
Q

What is the role of coagulase in staph aureus?

A

Clots plasma

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21
Q

What is the role of leukocidin (PVL) in staph aureus?

A

Kills leukocytes

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22
Q

What is the role of TSST-1 in staph aureus?

A

Shock, rash, desquamation

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23
Q

What is the progression and symptoms of TSST-1?

A

Rapid progression (48hrs)

High fever

vomiting

diarrhoea

sore throat

muscle pain

24
Q

What is the progression and symptoms of staphylococcal food poisoning?
enterotoxin SeA, SeB, SeC

A

intoxication
1-5hrs
vomiting diarrhoea

25
Describe SSS
>exfoliation toxins, often neonatal, face, axilla and groin | >ETA & ETB toxins target Desmoglein-1 (DG-1)
26
What is a super antigen?
activate 1 in 5 T cells (normally 1:10,000) Antigen is not processed by PMN and binds directly to MHCII complex outside of conventional binding groove
27
What is the result of super antigen activation?
Massive release of cytokines and inappropriate immune response
28
What are the diagnostic criteria for TSS?
-Fever >39 -Diffuse macular rash and desquamation (diffuse macular erythroderma- suburn) -hypotension =90mmHg in adults ->/=3 organ systems involved liver, muscular, blood, renal, mucous, GI , CNS
29
What are adhesins?
Extracellular matrix molecules are present on epithelial, endothelial surfaces as well as a component of blood clots
30
Name three adhesins
Fibrinogen binding (ClfA ClfB) Collagen binding (CNA) Elastin binding protein (EbpS)
31
What is Panton-Valentine Leukocidin?
PVL bicomponent toxin (lukS and lukF) Specifically toxic to leukocytes
32
What is PVL associated with?
Severe skin infections | e.g. recurrent furunculosis, sepsis/necrotizing fasciitis
33
What are PVL and alpha toxin linked to?
CA-MRSA responsible for necrotising pneumonia and contagious severe skin infections
34
What is necrotising pneunomia?
Preceding influenza like syndrome, neutralising haemorrhagic pneumonia
35
Describe the presentation of necrotising pneumonia?
Rapid progression ARDS Deterioration in pulmonary function Refractory hypoxaemia Multi-organ failure despite antibiotic therapy
36
Describe streptococcus pyogenes?
Gram +ve cocci in chains Catalase negative B haemolysis
37
What infections does streptococcus pyogenes cause?
Impetigo Cellulitis Necrotising faciitis
38
What is the lancefield system,?
Serotyping of cell wall carbohydrates
39
How many major lancefield serotypes are there?
A-H and K-V (20)
40
How are group a lancefield further divided?
M protein antigens - M1 & M3 major serotype - M3 & M18 severe invasive disease - emm typing and emm89 epidemic
41
What are the GAS skin diseases?
Impetigo Cellulitis Erysipelas
42
Describe impetigo
Highly contagious through contact with discharge on the face. infection immediately below surface (stratum corneum-keratin layers)
43
Describe cellulitis
deeper skin infections in the dermis not associated with necrosis
44
Describe erysipelas
Fever, riggers, nausea
45
What are the iGAS diseases?
Invasive group A streptococci - cellulitis - necrotising fasciitis
46
Describe necrotising fasciitis
>Type I, clostridia spp >invasive streptococcus A strains penetrate mucous membrane and develop in lesion >rapidly destroys connective tissue
47
What proteins are responsible for tissue/cell destruction?
Haemolysins | Streptolysin S
48
What is the role of SLS?
Pore forming cytolysis | Toxic to PMN, organelles, platelets, important in animal models
49
What are the virulence factors of Streptococcus pyogenes?
Superantigenic towns Haemolysins Capsule ``` M-protein binds; >factor M >fibrinonectin >fibrinogen >albumin ```
50
Describe TSLS (toxic shock like syndrome)
``` Pyogenic exotoxin -complication of invasive infections -30% mortality -hours to days hypotension to organ failure -SpeB, SpeC ```
51
What is a pyrogen
Agent that causes a raise in body tissue
52
Describe S.aureus toxic shock
- localised infection - no bacteraemia - menstrual TSST-1 - non-menstrual SEB or SEC - pyrogenic toxin
53
Describe S. pyogenes toxic shock
- invasive disease (pharyngitis - SpeA and SpeC most common toxin - pyrogenic toxin
54
What do S. aureus and s. pyogenes toxic shock have in common?
Virulence factor: Superantigen
55
What are the stages of horizontal gene transfer between bacteria?
a. bacterial transformation b. bacterial transduction c. bacterial conjugation