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Infection and Immunity > Noscomial Infections > Flashcards

Noscomial Infections Flashcards

1
Q

How are hospital infections acquired?

A

Exogenous source
Cross infection
Endogenous source

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2
Q

What are exogenous sources?

A

E.g. other patients, medical staff, from hospital environment: food, air, dust, water, catheters, instruments and equipment

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3
Q

What are endogenous sources?

A

I.e. another site within the patient
Increased incidence when patients are elderly, immunocompromised, have undergone surgery or other invasive techniques such as catheterisation

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4
Q

How many individuals suffer a health care associated infection and where are most people usually situated in the hospital that are most vulnerable?

A

About 10% of patients suffer health care associated infections (rates between 6.9-25%)
More infection in intensive care units (high dependency units)

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5
Q

What are some examples o nosocomial (hospital-aquired) bacterial infections?

A 
Staphylococcus aureus
Clostridium difficle
Enterococcus faecalis
Pseudomonas aeruginosa
Staphylococcus epidermidis
Klebsiella pneumonia 
Norovirus- winter vomiting virus
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6
Q

In what ways could hospital infections be prevented?

A

By simple hygiene precautions; disinfection, especially hand-washing by staff; isolation of patients; use of sterile equipment; appropriate use of antibiotics

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7
Q

Roughly how many nosocomial infections are preventable?

A

15-30%

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8
Q

What are the risk factors in obtaining a nosocomial infection?

A 
Age 
Length of stay in hospital 
Immunocompromised status 
MRSA (added problem, anti-biotic resistance)
C. difficile- surpass gastric acidity
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9
Q

What is the cost of hospital acquired infection?

A

Increased length hospital stay
Increased number of admissions
Increased cost of drugs required to treat infections
Increased cost associated with surveillance and implementation of control measures
Infection control teams

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10
Q

What are the common infections seen within a hospital?

A

MRSA- Methicillin (Meticillin- drug to control) Resistant Staphylococcus aureus
Staphylococcus aureus

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11
Q

What is Staphylococcus aureus?

A 
Gram positive coccus
Grow in grape-like clusters
Golden colonies
Non-fastidious, facultative anerobe
Survives drying, salt-tolerant
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12
Q

What are the main ways Staphylococcus aureus is found and is spread by?

A

Commonly found in nose and on the skin of healthy humans

Spread by contact and airborne routes

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13
Q

What are some examples of diseases acquired in a hospital?

A

Food borne disease- caused by enterotoxin
Skin infections- pimples, boils, impetigo, scalded-skin
syndrome
Post-operative wound infections- catheter associated infection
Septicaemia- endocartisis (heart damage)
Osteomyelitis (bone infection)
Pneumonia

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14
Q

What are some of the toxins present in s. aureus infections?

A

Enterotoxins (vomiting, diarrhoea)
Toxic shock syndrome toxin (TSST)
‘Superantigens’, trigger cytokine release, cause ‘shock’

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15
Q

What are some of the cell-destroying enzymes and toxins present in s.aureus infections?

A

Alpha toxin
Leukocidin
Exfoliate toxin (scalded skin syndrome)
Panton-Valentine leukocidin

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16
Q

What are virulence factors?

A

Molecules produced by bacteria, fungi etc. that add to their effectiveness allowing them to colonise a host

17
Q

How do anti-chemotaxis allow the staphylococcus to enter the host?

A

Chemotaxis inhibitory protein of staphylococci (CHIPS)

Extracellular adhesion protein (Eap)

18
Q

How do anti-opsonic and anti-phagocytic allow staphylococcus to enter the host?

A

Staphylococcal complement inhibitor (SCIN)
Protein A (binds antibody wrong way round)
Capsule (formation of biofilms, adherence to plastic, hard to remove and treat)
Staphylokinase
Fibrinogen- binding proteins
Haemolysins and Leukocidins

19
Q

What virulence factors does Staphylococcus have?

A 
Anti-chemitaxis
Anti-opsonic and anti-phagocytic
Iron-uptake systems
Degradative enzymes
Toxins
Adherence
20
Q

How do degradative enzymes allow staphylococcus to enter the host?

A

DNAse
Lipases
Proteases
Hyaluronidase

21
Q

How do toxins allow staphylococcus to enter the host?

A

Exfoliative toxins
(scalded skin syndrome, leuocidin, alpha toxins)
Superantigens
(toxic shock toxins and enterotoxins)

22
Q

How does adherence allow staphylococcus to enter the host?

A

Fibronectin-binding protein
Other ECM binding proteins
MSCRAMMS- microbial surface components recognising adhesive matrix proteins- bind host proteins, may aid adherence to host tissues and serum-coated plastic

23
Q

What is the resistant strain of staphylococcus and when did it emerge?

A

Methicilin-resistance staphylococcus aureus (MRSA) emerged 30 years ago

24
Q

What gene gives staphylococcus resistant?

25
What does this mecA gene do?
Encodes mutant penicillin-binding protein (PBP2a) with lower affinity for beta-lactam antibiotics Replaces the ‘normal’ penicillin binding proteins (enzymes involved in the peptidoglycan synthesis) to which penicillin normally targets
26
How is staphylococcus prevented?
Vancomycin
27
What is Clostridium difficile?
Gram positive rod | Strict anaerobe, spore-forming
28
Where is C. difficile found?
In gut of: <1% of people outside hospitals 5-10% of hospital patients
29
What are the range of symptoms from C. difficile?
Mild, self-limiting diarrhoea Severe diarrhoea and abdominal pain Life-threatening pseudomembranous colitis • Extensive flammation and necrosis of the colonic mucosa
30
What are the steps that result in death from C. difficile?
``` Normal colon Reduction in major genera of anaerobes C. difficile grows to high numbers Production of exotoxins A and B Diarrhoea Ulceration of colon Death ```
31
What are the symptoms due to?
Toxin A (enterotoxin) cause hypersecretion of fluid (diarrhoea) Toxin B (cytotoxin) damage and destroy cells A negative and B positive cause clinical disease Both glucosyltransferases- affect actin cytoskeleton Damage powerful chemoatractant for neutrophils
32
What has ribotype 027 done?
Increased severity, mortality and relapses of C. difficile
33
What are the treatments of C. difficile?
Discontinuation of the implicated antibiotic | Specific therapy with metronidazole or vancomycin
34
Why do relapses often occur in c. difficile?
Can’t restore flora in time, treated by more antibiotics but now trying faecal transplantation
35
What vaccines are there for C. difficile?
Several currently in clinical trials
36
What are the problems with vaccines for C. difficile?
Problem elderly population to which they are targeted Impact on impact of the toxin within the gut Do not reduce colonisation
37
What control measures should be put in place once someone has been identified to have C. difficile?
Patient should be isolated Avoid cross-infection of others patients by use of disposables, hand washing (not with alcohol based gels- spores resistant) Use of chlorine-based disinfection- “deep cleaning”
38
Overall have cases of hospital acquired infection reduced?
Yes

Infection and Immunity (20 decks)

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