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Phase 2a > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Pathogen

A

Organism that causes or is capable of causing disease

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2
Q

Commensal

A

Organism that colonises the host but causes no disease in normal circumstances

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3
Q

Opportunistic Pathogen

A

Microbe that only causes disease if host defences are compromised

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4
Q

Virulence/Pathogenicity

A

The degree to which a given organism is pathogenic

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5
Q

Asymptomatic Carriage

A

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

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6
Q

Endotoxin

A

Lipopolysaccharide in gram negative bacteria

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7
Q

Exotoxin

A

Protein produced by gram negative and positive bacteria.

  • are able to produce a good immune response to them bc they’re protein
  • can become a toxoid
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8
Q

Protozoa

A

Single celled organisms - eukaryotes with definitive nucleus

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9
Q

Types of Protozoa

A

1) Flagellates
2) Amoebae
3) Sporozoa
4) Microsporadia
5) Cilliates

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10
Q

Flagellates (Mastigophora)

A
  • Reproduce by binary fission
  • Intestinal flagellates
  • Haemoflagellates
  • Other body sites
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11
Q

Intestinal Flagellates - Giardia lamblia (giardiasis)

A
  • Diarrhoea
  • Faeco-oral spread
  • Recent travel
  • Trophozoites/cysts in stool
    TREATMENT: metronidazole
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12
Q

Haemoflagellates - African Trypanosoma spp. (sleeping sickness)

A
  • Flu like symptoms
  • Chancre
  • Sleepiness, confusion, coma, death
  • Personality change
  • Irritable
  • Excessive weight loss
  • Transmitted by infected fly
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13
Q

Other sites: Trichomonas Vaginalis

A
  • Sexuall transmitted
  • Asymptomatic
  • Dysuria
  • Yellow, frothy discharge
    METRONIDAZOLE
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14
Q

Amoebae (Sarcodina)

A
  • Move by means of flowing cytoplasm & production of pseudopodia
  • Entamoeba histolytica
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15
Q

Entamoeba histolytica

A
  • Faeco-oral spread
  • Dysentry
  • Colitis
  • Lung and liver abscess
  • Trophozoites/cysts in stool
  • Poorly sanitary conditions
  • Gay sex
    METRONIDAZOLE
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16
Q

Sporozoans (Apicomplexa)

A
  • No locomotory extensions
  • All species are parasitic
  • Most are intracellular parasites
  • Reproduce by multiple fission
    e. g Malaria (Plasmodia spp.
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17
Q

Types of Malaria

A

1) Plasmodium. falciparum (most common)
2) P. ovale
3) P. viva
4) P. malariae
5) P. knowlesi

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18
Q

Increasing Incidence of Malaria

A
  • Increasing parasitic resistance to antimalarials
  • Increased resistance of mosquito to insecticides
  • Eco & climate changes - mosquitos found in more countries
  • Increased travel to endemic areas
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19
Q

The Malaria Vector

A

Female Anopheles mosquito

  • infection acquired during feeding from infected human
  • Mosquito gets infected for life
  • Life span = 3-4 weeks
  • Biting indoors & during nigh
  • Life cycle depends on water
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20
Q

Malaria Protozoon

A

Plasmodia lifecycle has stages in human & mosquito host

- lifecycle variation = different clinical manifestations

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21
Q

Pathogenesis of Malaria

A
  • Anaemia
  • Cytokine release
  • Widespread organ damage (due to impaired microcirculation)
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22
Q

Anaemia in Malaria

A

Due to:

  • haemolysis of infected RBC
  • haemolysis of non-infected RBC - results in dark urine if untreated
  • Splenomegaly
  • Folate depletion
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23
Q

P. falciparum Malaria

A

RBC contain schizonts - adhere to capillary lining in:
- brain
- kidney
- gut
- liver etc
Cause obstruction
Schizonts rupture - release toxins - stimulate cytokine release

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24
Q

Diagnosis of Malaria

A 
Blood film  - light microscopy
- can see trophozoite 
- can be thick or thin films (12 hours apart)
THICK FILM: 
- sensitive & low res
THIN FILM:
- identifies morphological features
- type & count of parasite
- identifes species
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25
Q

Clinical Features of Malaria

A
  • FEVER !!
  • chills & sweats
  • headache
  • myalgia
  • fatigue
  • nausea & vomiting
  • diarrhoea
  • abdo pain
  • hepatosplenomegaly
  • jaundice
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26
Q

Non-specific Features of Malaria

A
  • anaemia
  • low platelets
  • hyperbilirubinaemia
  • mildly raised transaminases
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27
Q

Treatment of Complicated P. falciparum

A
  • IV Artesunate

- IV Quinine

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28
Q

Treatment of Uncomplicated P. falciparum

A
  • Oral Riamet
  • Oral Quinine
    Add doxycycline as 2nd agent - to treat undiscovered/untreated malaria
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29
Q

Treatment of Non-falciparum Malaria

A

Oral Chloroquine

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30
Q

Treatment of P. vivax and P.ovale

A

Primaquine - hynozoite clearance

not suitable for pregnant women & G6PD deficiency

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31
Q

Genetic Immunity in Malaria

A

1) Sickle cell
2) G6PD deficiency (glucose-6-phosphate dehydrogenase deficiency)
- causes sudden RBC death
- leads to haemolytic anaemia
- malaria can’t survive in these RBC
3) Thalaessaemias

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32
Q

Acquired Immunity in Malaria

A

1) Recurrent infection - semi immunity within a couple of years
2) Maternal transmission of antibodies - decreases over time

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33
Q

Properties of a Virus

A
  • 20-220nm diameter
  • samples don’t need to be from sterile sites
  • only one type of nucleic acid (RNA or DNA)
  • No cell wall - have lipid envelope
  • Proteins on surface allow attachment
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34
Q

Stages of Virus Replication

A

1) Attachment
2) Cell entry
3) Interaction with host cells
4) Replication
5) Assembly
6) Release

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35
Q

Virus Replication: Attachment

A

Viral and cell receptors

e.g. gp120 on HIV and CD4 on T cell

36
Q

Virus Replication: Cell Entry

A

Only viral core & associated enzymatic proteins enter the host cell
- not the outer protein coat

37
Q

Virus Replication: Interaction with Host Cells

A

Uses cell materials for own replication

- subverts host cell defences

38
Q

Virus Replication: Replication

A

Production of progeny viral nucleic acid & viral proteins
- in nucleus and/or cytoplasm

39
Q

Virus Replication: Assembly

A

1) Can be in nucleus - herpes
2) Can be in cytoplasm - polio
3) Can be in cell membrane - influenza

40
Q

Virus Replication: Release

A
  • By lysis of cell (rhinovirus)
  • By exocytosis - ‘leaking’ (HIV and flu)
  • Few virus particles enter host but millions released due to replication
41
Q

How Viruses Cause Disease

A

1) Direct destruction of host cells
2) Damage by modification of host cell structure/function
3) Over-reactivity of host as a response to infection (immunopathological damage)
4) Cell proliferation & cell immortalisation (CANCER)
5) Evasion of EC and IC host defences

42
Q

Viral Evasion of EC & IC Host Defences

A

1) Virus persistance

2) Virus variability

43
Q

Mechanisms for Viral Evasion of Host Defences - Cellular Level

A

1) Persistence / Latency
- all herpes viruses
- VZV
- EBV
2) Cell to cell spread
- measles
- HIV

44
Q

Mechanisms for Viral Evasion of Host Defences - Molecular/Genetic Level

A

1) Antigenic variability
- Influenza A
- HIV
- Rhinovirus
2) Prevention of host cell apoptosis
- herpes
- HIV
3) Down regulation of interferon & other host defence proteins
4) Interference w. host cell antigen processing pathways
- HIV
- herpes
- measles

45
Q

Antibiotics

A

Agents produced by microorganism that kill/inhibit the growth of other microorganisms in high dilution
(nowadays they’re semi synthetic)

46
Q

What Antibiotics Are Used For

A
  • treatment
  • prophylaxis:
    > specific indications = endocarditis/ post-splenectomy
    > prevention of post-surgery infections
47
Q

Classes of Antibiotics

A

1) Beta-lactams
2) Glycopeptides
3) Macrolides
4) Lincosamides
5) Tetracyclines
6) Aminoglycosides
7) Oxacolidinones
8) Quinolones
9) Metronidazole
10) Trimethoprim

48
Q

Beta-Lactams (all target bacterial cell wall)

A

1) Penicillins
2) Cephalosporins
3) Carbapenems
4) Combo (B lactam inhibitor/B lactam)

  • contraindicated for penicillin allergies
  • caution if patient has no true IgE mediated/severe allergy
49
Q

Which virus is resistant to all beta-lactams?

A

MRSA - methicillin resistant S. Aureus

has flucloxacillin resistance so is resistant to all

50
Q

Penicillin Types

A

1) Benzylpenicillin/ Penicillin G (IV)
2) Phenoxymethylpenicillin/Pen V (Oral)
3) Amoxicillin (IV & Oral)
4) Flucloxacillin (IV & Oral)

51
Q

What would you use benzylpenicillin for?

> Streptococci

A

Skin and soft tissue infection

e.g endocarditis

52
Q

What would you use phenoxymethylpenicillin for?

A
  • Bacterial pharyngitis

- Splenectomy prophylaxis

53
Q

What would you use amoxicillin for?

> H. influenzae
Enterococci
Enterobactericae (E.coli, shigella)

A
  • Pneumonia
  • Skin and soft tissue infection
  • UTIs
54
Q

What would you use flucloxacillin for?

> S. aureus

A
  • Skin and wound infections

- Lung infections (pneumonia)

55
Q

Cephalosporins

A

1st generation: Cefalexin
2nd gen: Cefuroime
3rd gen: Ceftriaxone, Ceftoaxime

> earlier gens = more activity against gram +
newer gens = more activity against gram -

56
Q

What can cephalosporins be used to treat?

A
  • can be used for non-severe penicillin allergies
  • meningitis

C. difficile & enterococci are RESISTANT

57
Q

Carbapenems examples

A
  • meropenem
  • ertapenem
  • imipenem
58
Q

Use of carbapenems

> extended spectrum b-lactamases
AmpC b-lactamases

A
  • hospital acquired infection

- cover resistant gram - bacteria

59
Q

Disadvantages of carbapenems

A
  • expensive
  • C.diff risk
  • emerging resistance from production of carbapenemase by enterbactericae
60
Q

Function of beta-lactamase inhibitors

A
  • beta lactamases hydrolyse penicillin - make them resistant
  • inhibitor binds to b-lactamase - mimics b-lactam antibiotic
  • prevents degradation of antibiotic
61
Q

Examples of B-lactamase inhibitors

A
  • clavulanic acid
  • sulbactam
  • tazobactam
62
Q

Examples of Glycopeptide Antibiotics

> gram positive ONLY

A
  • vancomycin
  • teicoplanin

> target bacterial cell wall

63
Q

Use of Glycopeptides

A
  • MRSA & other serious infections

- penicillin allergies

64
Q

Risks of Glycopeptide Antibiotics

A
  • must monitor nephrotoxicity
  • some resistance possible

(mostly for vancomycin)

65
Q

Examples of Macrolides

> gram positive
group A streptococci

A
  • Clarithromycin
  • Erythromycin
  • inhibit protein synthesis
66
Q

Uses of Macrolides

A
  • severe/atypical pneumonia
  • penicillin allergic patients
  • MRSA
67
Q

Risk of Macrolides

A
  • C.diff

- Resistance

68
Q

Examples of Lincosamides

> gram positive

A

Clindamycin

  • inhibit protein synthesis
69
Q

Uses of Lincosamides

A
  • cellulitis (if allergic to penicillin)
  • necrotising fasciitis
  • MRSA
70
Q

Benefits/Risks of Lincosamides

A
  • good oral bioavailability

- C. diff risk

71
Q

Example of Tetracyclines

> broad spectrum activity

A

Doxycycline - oral

  • inhibits protein synthesis
72
Q

Uses of Tetracyclines

A
  • cellulitis (if allergic to penicillin)

- MRSA

73
Q

Example of Aminoglycosides

> broad spectrum activity
enterobacteriacae
staphylococci
synergistically used to treat strep

A
  • Gentamicin

- inhibits protein synthesis

74
Q

Uses of Aminoglycosides

A
  • UTIs

- infective endocarditis (synergistically)

75
Q

Benefits/Risks of Aminoglycosides

A
  • can be used against extended spectrum b-lactam & AmpC b-lactam
  • requires monitoring for nephrotoxicity
76
Q

Example of Oxazolidinones

> gram positive (MRSA & VRE)

A
  • Linezolid

- inhibits protein synthesis

77
Q

Uses of Oxazolidinones

A

serious/gram positive infections

e.g skin & soft tissue

78
Q

Benefits/Risks of Oxazolidinones

A
  • good oral bioavailability

- multiple side effects and interactions

79
Q

Quinolones

> gram negative more than +

A

Ciprofloxacin (IV & Oral)

80
Q

Uses of Quinolones

A
  • UTIs

- Penicillin allergy

81
Q

Benefits/Risks of Quinolones

A
  • good oral bioavailability
  • can be used against extended spectrum b-lactams
  • C.diff risk
82
Q

Metronidazole

> anaerobic bacteria

A

IV or Oral

  • inhibits nucleic acid
83
Q

Uses of Metronidazole

A

Intra-abdominal infection

84
Q

Benefits/Risks of Metronidazole

A
  • good oral bioavailability
  • cheap
  • emerging resistance
85
Q

Uses of Trimethoprim

> broad spectrum

A

UTIs

86
Q

Benefits/Risks of Trimethoprim

A
  • cheap

- increasing resistance

Phase 2a (7 decks)

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