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Infection > Foundations of medicine > Flashcards

Foundations of medicine Flashcards

1
Q

5 Examples of different types of pathogen?

A

Bacteria, Viruses, Fungi, Protozoa, Helminths.

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2
Q

What are the features of a protozoa?

A

Eukaryotic, Unicellular and motile.

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3
Q

What’s an opportunistic pathogen?

A

A microbe that only causes disease if the host’s defences are compromised.

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4
Q

What is Virulence/Pathogenicity?

A

The degree to which a given organism is pathogenic.

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5
Q

What is Asymptomatic carriage?

A

When a pathogen is carried harmlessly at a tissue site where it causes no disease.

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6
Q

What is the definition of an immunocompromised host?

A

Alteration of the phagocytic or cellular immunity, or alterations of the skin or mucosal barriers that increases the risk of infection of opportunistic processes.

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7
Q

Definition of an opportunistic infection?

A

infection from a microorganisms that is not normally pathogenic but is in immunocompromised patients.

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8
Q

What is febrile neutropenia?

A

A defect in neutrophil function characterised by a neutrophil count of below 500/mm3

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9
Q

is their a difference in colonisation and infection?

A

Yes, colonisation does not necessarily mean infection.

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10
Q

List some bacterial infections of the skin and soft tissue, and where they affect.

A

impetigo - epidermis.

Erysipelas - intradermal infection.

Cellulitis - loose subcutaneous tissue.

Lymphangitis - the lymph vessels.

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11
Q

What are most common skin infections caused by?

A

Staphylococcus aureus, or streptococci (B-haemolytic group)

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12
Q

What is the treatment for most common skin infections? and in penicillin allergic patients?

A

Flucloxacillin and amoxicillin.

Erythromycin Clindamycin.

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13
Q

Mechanism of antibiotic action? (5)

Examples?

A

Interference with cell wall synthesis:

B-Lactams: e.g. penicillins, cephalosporins

Protein synthesis inhibition:

Bind to 50s ribosomal unit: clindamycin
Bind to 30s ribosomal unit:tetracyclines
Bind to bacterial isoleucyl tRNA synthesis: mupirocin

Interference with nucleic acid synthesis:

DNA synthesis: Fluoroquinolones
RNA synthesis: Rifampin

Inhibition with the metabolic pathway:

Sulfonamindes

Disruption of bacterial membrane structure:

Polymixins

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14
Q

Give three broad spectrum antibiotics?

A

Meropenem

Cefuroxime

Co-amoxiclav

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15
Q

Three ways in which antibiotic resistance has developed?

A

Genetic events: gene mutation, resistant gene acquisition

Selection: eradication of susceptible populations.

Dispersion: Spread of resistant isolates or genes

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16
Q

3 common mechanism of antibiotic resistance?

A

Antibiotic degrading enzyme e.g. B-lactamase.

Altered antibiotic target

Increased efflux

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17
Q

Common misuses of antibiotics? (6)

A

Unnecessary prescriptions

Delay in administration in critically ill patients.

Too narrow or too broad

Wrong dose

Duration too long or too short.

Failure to document and review antibiotic treatment

18
Q

What is virulence of a pathogen?

A

Relates to numbers of pathogen required to initiate infection and severity of symptoms.

19
Q

4 main routes of infection?

A

Respiratory tract

Via Gastric tract

By breaks in body defences (skin breaks)

Urinary/reproductive tract.

20
Q

The four main classifications of body defences?

A

Innate/acquired

Specific/non-specific

21
Q

The three steps of infection?

What happens if only the first step occurs?

A
  1. Colonisation - structures that allow pathogens to ‘stick’ to their hosts.
  2. invasion - pathogen can slip between close junction in epithelial cells, or destroy cells as they invade. symptoms result.

Colonisastion can occur and then the body can keep the colonisation ‘in check’ through the availability of nutrients and the hosts immune system.

  1. dissemination and disease - the pathogen can break down tissue, attack the immune system, and kill competing bacteria.
22
Q

Examples of specific host defence?

A

Antibodies and complement.

23
Q

Common routes to S. aureus infection?

A

Post operative wound
IV catheters
IV drug users

24
Q

What is septicaemia?

A

When the infection has spread to the blood stream

25
Q

Four of S. aureus’ virulence factors?

A

Gram-positive and resists lysis by antibody and complement.

Converts fibrinogen to fibrin (coagulase)

Haemolysins - protease and lipase enzymes destroy cell membranes.

B-lactamases - destroys penicillins

Catalase - breaks down H2O2 (stops neutrophils)

Leukocidin - Kills neutrophils

Protein A - prevents phagocytosis.

26
Q

Streptococcal pyogenes virulence factors?

A

Capsule

Protease

Nuclease

Streptokinase - liquifies pus (aiding it’s spread)

Hyaluronidase - destroys Ct aiding spread

27
Q

What is Clostridia?

A

An anaerobic spore, which will form a bacterium, found in soil and human/animal faeces.

28
Q

Three ways in which antibodies prevent infection?

A

aggulation

Complement mediated lysis

Direct inhibition of virulence factors

29
Q

What is a toxoid?

A

A toxin that has been converted into a harmless substance that can be used as a target in vaccination.

30
Q

What is an endotoxin?

A

An endogenous toxin, so one part of the structure of bacteria

Only one type of endotoxin - lipopolysaccharide, similar in all gram negative bacteria.

31
Q

Examples of the many actions of lipopolysaccharide?

A

Activation of complement and release of cytokines cause inflammation and fever.

Can lead to shock due to increased vascular permeability caused by damage to endothelial cells

Can cause blood coagulation leading to ischaemia.

32
Q

How does meningococcus use LPS (lipopolysaccharide) to cause septicaemia?

A

Releases LPS in outer membrane growths called blebs.

33
Q

What are exotoxins?

A

extracellular proteins secreted by many gram positive and some gram negative bacteria.

34
Q

What is the method by which the cholera exotoxin and the e. coli ETEC toxin cause pathogenesis

A

Through loss of bodily fluids a leading to severe dehydration.

35
Q

What are the problem with only capsule based immunisations?

A

No T-helper cell activity activated, so no ‘booster effect’, will activate short-lived IgM antibodies. Also will only be functional in non -immunogenic patients.

Will only produce short-term effects in healthy adults.

36
Q

How are Conjugate polysaccharide vaccines more effective than only capsule based ones?

A

Long lived IgG antibodies and t-cells are activated.

Can be given to infants and provide lasting immunity.

37
Q

Smallest virus?

A

Polio-virus

38
Q

Process of a gram-stain?

A

Stain with violet dye (crystal violet dye, sticks to peptidoglycan in gram-posistive organisms)

Fixed with iodine

Alcohol is added (this flushes out the stain from gram-negative organisms)

Counter staining with safranin

39
Q

Definition of sepsis?

A

Patient has symptoms consistent with infection.

40
Q

Septic shock causes?

A

Physiological changes to the body, e.g. hypotension.

41
Q

Differences in Gram-positive and Gram negative bacteria?

A

Gram-negative bacteria have three membranes, a cytoplasmic, inner and outer membrane with LPS extending from the outer membrane.

Gram-positive organisms have a thick peptidoglycan cell wall, with projections of LTS (also an endotoxin)

Infection (1 decks)

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