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Antimicrobial and chemotherapy > Gram positive organisms of clinical significance > Flashcards

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
Q

How is G.A.S passed?

A

By respiratory droplets

26
Q

What are the major virulent features of GAS

A

-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
Q

Minor clinical significance of GAS infections

A

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
Q

Moderate to rapidly lethal clincially significant GAS infections

A 
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
Q

Major clinically significant GAS infections

A

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
Q

Treatment for GAS infections

A
  • 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
Q

Group B beta haemolytic streptococci (G.B.S)

A

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
Q

Streptococcus pneumonia characteristics

A

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
Q

Virulence factors on streptococcus pneumonia

A

Capsule

  • Most important factor
  • Composed of polysaccharide
  • Antiphagocytic and antigenic
34
Q

Major clinically significant streptococcus pneumonia infection

A

-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
Q

Treatment of Streptococcus pneumonia

A

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
Q

Vaccines used against SP

A

-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
Q

What infection is caused by Streptococcal endocarditis

A

Subacute endocarditis

38
Q

How is streptococcus endocarditis grouped

A

In the Viridians group

39
Q

Characteristic of streptococcus endocarditis

A

Relatively slow-growing valve lesions: (“vegetations” – organisms enmeshed in fibrin & platelets; hard to get immune cells or drugs to the site)

40
Q

Treatment used against SE

A

synergistic” wall-active agent (penicillin) plus aminoglycoside

Antimicrobial and chemotherapy (4 decks)

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