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Phase 2a > Microbiology > Flashcards

Microbiology Flashcards

(86 cards)

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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
Clinical Features of Malaria
- FEVER !! - chills & sweats - headache - myalgia - fatigue - nausea & vomiting - diarrhoea - abdo pain - hepatosplenomegaly - jaundice
26
Non-specific Features of Malaria
- anaemia - low platelets - hyperbilirubinaemia - mildly raised transaminases
27
Treatment of Complicated P. falciparum
- IV Artesunate | - IV Quinine
28
Treatment of Uncomplicated P. falciparum
- Oral Riamet - Oral Quinine Add doxycycline as 2nd agent - to treat undiscovered/untreated malaria
29
Treatment of Non-falciparum Malaria
Oral Chloroquine
30
Treatment of P. vivax and P.ovale
Primaquine - hynozoite clearance | not suitable for pregnant women & G6PD deficiency
31
Genetic Immunity in Malaria
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
32
Acquired Immunity in Malaria
1) Recurrent infection - semi immunity within a couple of years 2) Maternal transmission of antibodies - decreases over time
33
Properties of a Virus
- 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
34
Stages of Virus Replication
1) Attachment 2) Cell entry 3) Interaction with host cells 4) Replication 5) Assembly 6) Release
35
Virus Replication: Attachment
Viral and cell receptors | e.g. gp120 on HIV and CD4 on T cell
36
Virus Replication: Cell Entry
Only viral core & associated enzymatic proteins enter the host cell - not the outer protein coat
37
Virus Replication: Interaction with Host Cells
Uses cell materials for own replication | - subverts host cell defences
38
Virus Replication: Replication
Production of progeny viral nucleic acid & viral proteins - in nucleus and/or cytoplasm
39
Virus Replication: Assembly
1) Can be in nucleus - herpes 2) Can be in cytoplasm - polio 3) Can be in cell membrane - influenza
40
Virus Replication: Release
- By lysis of cell (rhinovirus) - By exocytosis - 'leaking' (HIV and flu) - Few virus particles enter host but millions released due to replication
41
How Viruses Cause Disease
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
Viral Evasion of EC & IC Host Defences
1) Virus persistance | 2) Virus variability
43
Mechanisms for Viral Evasion of Host Defences - Cellular Level
1) Persistence / Latency - all herpes viruses - VZV - EBV 2) Cell to cell spread - measles - HIV
44
Mechanisms for Viral Evasion of Host Defences - Molecular/Genetic Level
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
Antibiotics
Agents produced by microorganism that kill/inhibit the growth of other microorganisms in high dilution (nowadays they're semi synthetic)
46
What Antibiotics Are Used For
- treatment - prophylaxis: > specific indications = endocarditis/ post-splenectomy > prevention of post-surgery infections
47
Classes of Antibiotics
1) Beta-lactams 2) Glycopeptides 3) Macrolides 4) Lincosamides 5) Tetracyclines 6) Aminoglycosides 7) Oxacolidinones 8) Quinolones 9) Metronidazole 10) Trimethoprim
48
Beta-Lactams (all target bacterial cell wall)
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
Which virus is resistant to all beta-lactams?
MRSA - methicillin resistant S. Aureus | has flucloxacillin resistance so is resistant to all
50
Penicillin Types
1) Benzylpenicillin/ Penicillin G (IV) 2) Phenoxymethylpenicillin/Pen V (Oral) 3) Amoxicillin (IV & Oral) 4) Flucloxacillin (IV & Oral)
51
What would you use benzylpenicillin for? >Streptococci
Skin and soft tissue infection | e.g endocarditis
52
What would you use phenoxymethylpenicillin for?
- Bacterial pharyngitis | - Splenectomy prophylaxis
53
What would you use amoxicillin for? > H. influenzae > Enterococci > Enterobactericae (E.coli, shigella)
- Pneumonia - Skin and soft tissue infection - UTIs
54
What would you use flucloxacillin for? > S. aureus
- Skin and wound infections | - Lung infections (pneumonia)
55
Cephalosporins
1st generation: Cefalexin 2nd gen: Cefuroime 3rd gen: Ceftriaxone, Ceftoaxime > earlier gens = more activity against gram + > newer gens = more activity against gram -
56
What can cephalosporins be used to treat?
- can be used for non-severe penicillin allergies - meningitis C. difficile & enterococci are RESISTANT
57
Carbapenems examples
- meropenem - ertapenem - imipenem
58
Use of carbapenems > extended spectrum b-lactamases > AmpC b-lactamases
- hospital acquired infection | - cover resistant gram - bacteria
59
Disadvantages of carbapenems
- expensive - C.diff risk - emerging resistance from production of carbapenemase by enterbactericae
60
Function of beta-lactamase inhibitors
- beta lactamases hydrolyse penicillin - make them resistant - inhibitor binds to b-lactamase - mimics b-lactam antibiotic - prevents degradation of antibiotic
61
Examples of B-lactamase inhibitors
- clavulanic acid - sulbactam - tazobactam
62
Examples of Glycopeptide Antibiotics > gram positive ONLY
- vancomycin - teicoplanin > target bacterial cell wall
63
Use of Glycopeptides
- MRSA & other serious infections | - penicillin allergies
64
Risks of Glycopeptide Antibiotics
- must monitor nephrotoxicity - some resistance possible (mostly for vancomycin)
65
Examples of Macrolides > gram positive > group A streptococci
- Clarithromycin - Erythromycin - inhibit protein synthesis
66
Uses of Macrolides
- severe/atypical pneumonia - penicillin allergic patients - MRSA
67
Risk of Macrolides
- C.diff | - Resistance
68
Examples of Lincosamides > gram positive
Clindamycin - inhibit protein synthesis
69
Uses of Lincosamides
- cellulitis (if allergic to penicillin) - necrotising fasciitis - MRSA
70
Benefits/Risks of Lincosamides
- good oral bioavailability | - C. diff risk
71
Example of Tetracyclines > broad spectrum activity
Doxycycline - oral - inhibits protein synthesis
72
Uses of Tetracyclines
- cellulitis (if allergic to penicillin) | - MRSA
73
Example of Aminoglycosides >broad spectrum activity > enterobacteriacae > staphylococci > synergistically used to treat strep
- Gentamicin | - inhibits protein synthesis
74
Uses of Aminoglycosides
- UTIs | - infective endocarditis (synergistically)
75
Benefits/Risks of Aminoglycosides
- can be used against extended spectrum b-lactam & AmpC b-lactam - requires monitoring for nephrotoxicity
76
Example of Oxazolidinones > gram positive (MRSA & VRE)
- Linezolid | - inhibits protein synthesis
77
Uses of Oxazolidinones
serious/gram positive infections | e.g skin & soft tissue
78
Benefits/Risks of Oxazolidinones
- good oral bioavailability | - multiple side effects and interactions
79
Quinolones > gram negative more than +
Ciprofloxacin (IV & Oral)
80
Uses of Quinolones
- UTIs | - Penicillin allergy
81
Benefits/Risks of Quinolones
- good oral bioavailability - can be used against extended spectrum b-lactams - C.diff risk
82
Metronidazole > anaerobic bacteria
IV or Oral - inhibits nucleic acid
83
Uses of Metronidazole
Intra-abdominal infection
84
Benefits/Risks of Metronidazole
- good oral bioavailability - cheap - emerging resistance
85
Uses of Trimethoprim > broad spectrum
UTIs
86
Benefits/Risks of Trimethoprim
- cheap | - increasing resistance

Phase 2a (7 decks)

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