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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?

A

mecA gene

25
Q

What does this mecA gene do?

A

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
Q

How is staphylococcus prevented?

A

Vancomycin

27
Q

What is Clostridium difficile?

A

Gram positive rod

Strict anaerobe, spore-forming

28
Q

Where is C. difficile found?

A

In gut of:
<1% of people outside hospitals
5-10% of hospital patients

29
Q

What are the range of symptoms from C. difficile?

A

Mild, self-limiting diarrhoea
Severe diarrhoea and abdominal pain
Life-threatening pseudomembranous colitis
• Extensive flammation and necrosis of the colonic mucosa

30
Q

What are the steps that result in death from C. difficile?

A 
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
Q

What are the symptoms due to?

A

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
Q

What has ribotype 027 done?

A

Increased severity, mortality and relapses of C. difficile

33
Q

What are the treatments of C. difficile?

A

Discontinuation of the implicated antibiotic

Specific therapy with metronidazole or vancomycin

34
Q

Why do relapses often occur in c. difficile?

A

Can’t restore flora in time, treated by more antibiotics but now trying faecal transplantation

35
Q

What vaccines are there for C. difficile?

A

Several currently in clinical trials

36
Q

What are the problems with vaccines for C. difficile?

A

Problem elderly population to which they are targeted
Impact on impact of the toxin within the gut
Do not reduce colonisation

37
Q

What control measures should be put in place once someone has been identified to have C. difficile?

A

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
Q

Overall have cases of hospital acquired infection reduced?

A

Yes

Infection and Immunity (20 decks)

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