Gram positive organisms of clinical significance Flashcards

1
Q

List some G+ cocci

A
Staphylococci
Streptococci
Enterococci
Peptococci> anaerobic 
peptostreptococci> anaerobic
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2
Q

List some G+ rods

A

Clostridia> anaerobic
Corynebacteria (diphtheroids)
Listeria
Bacillus

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3
Q

What is the most common G+ organism of medical importance

A

Staphylococci

Streptococci

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4
Q

Characteristic of staphylococci

A
  • Catalase-positive: good at dealing with oxidative defensive processes
  • Hardy; survive well outside animal host
  • Many are normally harmless commensals
  • Infections can be relatively trivial or rapidly fatal
  • often resistant to natural penicillin
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5
Q

What does staphylococcus aureus look like

A

Golden colonies

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6
Q

Characteristic of Staphylococcus aureus

A

-Most virulent staphylococcus
-Carried by healthy people
+in patients and healthcare staff
-Simple colonisation is not infection but can lead to infection

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7
Q

What are the surface protein and toon staphylococcus aureus

A

1) Protein A(cell wall factor): bid to IgG
- anti-phagocytic affect
2) Fibronectin-binding protein/FnBP(cell wall factor)
- Promoted binding to mucosal cells and tissue matrices
3) Cytolytic exotoxins
- Haemotoxins: PVL is most significant (Panton-Valentine Leucocidin) Attack mammalian cell membranes
4) Super antigen exotoxins
- Stimulate enhanced T cell response
- toxic shock syndrome

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8
Q

What are the significant mild/moderate infection caused by SU

A

Impetigo

Localised to hair follicles, sweat/sebaceous glands, subcutaneous abscesses

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9
Q

What are the significant moderate/severe infection caused by SU

A
  • Localised skin infections (cellulitis)
  • Dermis / subcutaneous fat (lymph system possibly involved)
    - May respond to local therapy (if mild) but can lead to bacteraemia
    - More rigorous treatment for moderate/severe infection
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10
Q

Major infection caused by SU

A
-Septicaemia / bacteraemia
Often from starter lesion on skin wound, cannula, drain etc (ie often nosocomial)
-Endocarditis (heart valves) 
IV drug users, or after bacteraemia.  
Often quite rapidly damaging infection
-Pneumonia (often after ‘flu)
Can be severe
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11
Q

Toxic shock syndrome symptoms

A
  • Fever, rash, vomiting, diarrhoea, hypotension, multi-organ involvement
  • Rapid, severe, caused by “instant” activation of T cell response
  • Related to unremoved tampons, surgical dressings, nasal packs(much less common now that this has been recognised)
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12
Q

Major the clinically significant toxinoses cause by SU

A
  • Toxic shock syndrome -Major
  • Scalded skin syndrome- moderate
  • Gastroenteritis- moderate
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13
Q

Scalded skin syndrome

A
Result of specific toxins
Epithelial desquamation (skin peels)
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14
Q

Gastroenteritis

A

Ingestion of contaminated food

Nausea and vomiting

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15
Q

Treatment option for SU

A

Source control where possible: incision/drainage

Antibiotic: suppress toxin production as well as to kill

  • choices limited by resistance
  • beta- lactamase resistant lactams often used as first line
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16
Q

Hospital acquired MRSA

A

Has a PBP2a mutation so drugs are less effective

Vancomycin is the main antibiotic but VISA and VRSA exist

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17
Q

Characteristic of the coagulase-negative staphylococci (not S.aureus): Staphylococcus epidermidis

A

Part of normal flora
Lower virulence
Acquired drug resistance (b-lactams) is more common than in S. aureus
They are vancomycin resistive

18
Q

Characteristic of the coagulase-negative staphylococci (not S.aureus): Staphylococcus saprophyricus (digest waste/decay)

A
  • Part of the normal flora of female genital tract / perineum on both male/female
  • Cystitis (infection of the bladder)
  • especially in younger women(“honeymoon cystitis”) … within 24 h after intercourse
  • Sensitive to most antibiotics
19
Q

Describe the appearance of streptococci under the microscope

A

Long twisted chains

20
Q

What are the types of haemolysis caused by the streptococci

A

Gamma: No haemolysis so red blood cells are fine
beta: Total destruction of red blood cells
Alpha: Chemical modification of the haem group making it look green

21
Q

what is Haemolysin

A

it has a barrel like structure which can pass through red blood cells and cause it to lyse

It a a multimeric protein made of 7 subunits

22
Q

What are the different classifications of streptococci?

A

1- Haemolytic properties

2- Serologic grouping (Lancefield)

23
Q

What is serologic grouping

A

Antigen present in nearly all streptococcal cell walls in varying forms: antibodies can developed

Haemolytic streptococci fall into groups A-U so different antibodies will bind

Several fall outside the group including streptococci pneumonia

24
Q

What are the characteristic of Group A beta-haemolytic streptococci (GAS)

A
  • It is the most notable:
  • Mostly carried in the nasopharyngeal
  • Doesn’t survive well in environment
25
How is G.A.S passed?
By respiratory droplets
26
What are the major virulent features of GAS
-Capsules- Hyaluronic acid: Mimics that found in human CT a so hides from immune system -Cell wall fixed protein: =Avoids/reduce phagocytosis =help attachment to pharyneal epithelium -Extracellular products =Secretes a range of exotoxins
27
Minor clinical significance of GAS infections
Pharyngitis (strep throat) -Most common type of S. pyogenes infection -often mild, rarely progresses systemically but can cause Rheumatic fever, scarlet fever and renal damage Impetigo -Typically in children -Easily transmitted/extended by touch -Topical treatment is sufficient
28
Moderate to rapidly lethal clincially significant GAS infections
``` Cellulitis -Commonly S. aureus / GAS. -Deep structures of skin/soft tissue. -Often systemic symptoms and can --lead to invasive GAS disease Necrotising fasciitis -Deep, rapidly invasive, life-threatening invasion of the skin and underlying tissues -Mediated by multiple toxins -Often multibacterial but GAS common ```
29
Major clinically significant GAS infections
Acute rheumatic fever -Autoimmune disease -Cross reaction of heart and joint tissue and antigens bacterial protein -Fever, rash, arthritis, carditis Streptococcal toxic shock syndrome -Exotoxins mediate immune response (TNFα, cytokines, possibly direct T cell activation) -Treatment must be initiated quickly
30
Treatment for GAS infections
- penicillin G typically most effective but combinations used for invasive infection - penicillin G PLUS at least one of clindamycin or gentamicin for necrotising fasciitis and toxic shock
31
Group B beta haemolytic streptococci (G.B.S)
Streptococcus agalactiae (of no milk, mastitis in cows) Normal fluora of GI tract, vaginal tract, urethra Transmission - Mother to newborn - Adult to adult – rarely pathogenic Leading cause of meningitis and septicaemia in neonates - High mortality rate
32
Streptococcus pneumonia characteristics
NOT part of the Lancefield (group A/B/C … system) a-haemolytic – “usually” diplococcus (“chain” of two) nasopharyngeal carriage extremely sensitive to environment commonest bacterial cause of community-acquired lower respiratory tract infection
33
Virulence factors on streptococcus pneumonia
Capsule - Most important factor - Composed of polysaccharide - Antiphagocytic and antigenic
34
Major clinically significant streptococcus pneumonia infection
-Pneumonia Leading cause of C.A.P. (community-acquired pneumonia) -Otitis media Very common infection in children -Bacteraemia / sepsis No obvious focus of infection is common with pneumococcal bacteraemia (throat colonisation common) -Meningitis Relatively common organism High mortality rate even when treated
35
Treatment of Streptococcus pneumonia
Until the 1980s it was always sensitive to penicillin Resistance is increasing Mechanism = PBP changes High doses may overcome the raised MIC, except for meningitis (remember the difference between MIC and clinical breakpoints ?!) vancomycin or moxifloxacin
36
Vaccines used against SP
-Pneumococcal polysaccharide vaccine (PPSV) 23 serotypes 2 yrs and older Covers 80-90% of infections -Pneumococcal conjugate vaccine (was PCV7, now PCV13) 6 weeks – 5yrs pneumococcal antigens conjugated to “safe” diphtheria toxin
37
What infection is caused by Streptococcal endocarditis
Subacute endocarditis
38
How is streptococcus endocarditis grouped
In the Viridians group
39
Characteristic of streptococcus endocarditis
Relatively slow-growing valve lesions: (“vegetations” – organisms enmeshed in fibrin & platelets; hard to get immune cells or drugs to the site)
40
Treatment used against SE
synergistic” wall-active agent (penicillin) plus aminoglycoside