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Clinical Pathology > 1 Core Microbiology > Flashcards

1 Core Microbiology Flashcards

1
Q

What are antibiotics?

A

Chemical products of microbes that inhibit or kill other organisms

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2
Q

What are antimicrobial agents?

A

drugs: antibacterial, antifungal or antiviral

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3
Q

What does bacteriastatic mean?

A

inhibits bacterial growth which enables them to be killed e.g. protein synthesis inhibitors

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4
Q

What does bactericidal mean?

A

kill bacteira

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5
Q

What is the MIC?

A

Minimum inhibitory concentration. minimum concentration of antibiotic at which visible growth is inhibited

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6
Q

What is synergism?

A

Activity of two anti-microbials given together is given together is greater than the sum of their activity if given separately e.g. combination of beta-lactam/aminoglycoside combination therapy of streptococcal endocarditis

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7
Q

What is antagonism?

A

one agent diminishes the activity of another

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8
Q

What is indifference?

A

Activity unaffected by the addition of another agent

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9
Q

How do antibacterials work?

A

inhibit critical processes in the cell

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10
Q

What are the 5 antibiotic targets?

A 
cell wall
protein synthesis on bacteria
DNA synthesis
RNA synthesis
Plasma membrane
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11
Q

What is targeted on the cell wall by antibiotics?

A

peptidoglycan: both gram negative and positive. It is a polymer of glucose derivatives: N-acetyl muramic acid (NAM) and N-acetyl glucosamine (NAG)

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12
Q

What are cell wall synthesis inhibitors and give examples?

A

B-lactams:
penicillins, cephalosporins, carbapenems, monobactams
Glycopeptidases:
vancomycin, teicoplanim

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13
Q

How do B lactams and glycopeptidases work on the cell wall?

A

interfere with transpeptidses which are involved in peptidoglycan cross linking

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14
Q

How is protein synthesis affected in bacteria?

A

translation of RNA is targeted

50S and 30S subunit form a 70S initiation complex on the mRNA

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15
Q

What are protein synthesis inhibitors?

A 
Aminoglycosides- gentamicin 
Macrolides (erythromycin), lincosamides, streptogramins (MLS)
Tetracyclines
Oxazolidinones (linezolid)
Mupirosin
Fusidic acid
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16
Q

What are DNA synthesis inhibitors?

A

Trimethoprim and sulfonamides (combines is co-trimoxazole)

Quinolones and fluoroquinolones

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17
Q

What is a RNA synthesis inhibitor and how does it work?

A

Rifampicin. It is an RNA polymerase inhibitor and prevents the synthesis of mRNA

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18
Q

What destroys the plasma membrane?

A

Colistin and daptomycin

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19
Q

What are adverse effects of aminoglycosides?

A

reversible renal impairment on accumulation

irreversible ototoxicity on accumulation

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20
Q

What are the adverse effects if B-lactams?

A

main problems: allergic reactions

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21
Q

What is the adverse effect of linezolid?

A

bone marrow depression if used for along period

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22
Q

What B lactam is safe to use in someone with a penicillin allergy?

A

a non-severe: cephalosporins and carbapenems

any allergy: aztreonam

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23
Q

What are the common precipitating antibiotics that cause Clostridium Difficile?

A

co-amoxiclav
cephalosporins
ciprofloxacin
clindamycin

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24
Q

What are 7 key antibiotic-bacteria combinations?

A

flucloxacillin- staphylococcus aureus (not MRSA)
benzylpenicillin- streptococcus pyogenes
cephalosporins- gram negative bacilli
metronidazole- anaerobes
vancomycin- gram positive (MRSA)
meropenem- most clinically-relevant bacteria
colistin- last option for multi-resistant gram negatives

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25
Q

What reasons are there for combining antibiotics?

A
  • increase efficacy
  • provide adequately broad spectrum
  • reduce resistance
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26
Q

What are the risks of empiric therapy?

A

risk of under treatment

risk of excessively broad spectrum

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27
Q

What are the disadvantages of targeted therapy?

A

alternative may be:
expensive - linezolid, tigecycline, daptomycin vs. flucloxacillin for MRSA
last line - meropenem vs. ciprofloxacin for multi-resistant enterobacteriaceae
toxic - colistin vs. meropem for NDM-1 producers

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28
Q

What is sensitivity testing and what are some of the advantages?

A

Culture of micro-organisms in the presence of antimicrobial agent: solid or liquid media
adv:
-enables targeted therapy over empiric
-explains treatment failures
-provides alternative antibiotics in case of treatment failure or intolerance/adverse effects
-provides alternative oral antibiotics if IV is not longer required

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29
Q

What are 6 resistance mechanisms?

A
  • no target
  • reduced permeability
  • altered target
  • over-expression of target
  • enzymatic degradation
  • efflux pump
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30
Q

Give 2 examples of reduced permeability?

A
  • gram negatives have an outer membrane that is impermeable to vancomycin
  • anaerobic organisms and gentamicin because uptake of aminoglycosides requires requires an O2 dependent active transport mechanism
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31
Q

Explain target alteration and give examples

A

target modified by single gene mutation so the antibiotic can’t interact with the target anymore
flucloxacillin: MRSA -altered penicillin-binding proetin (PBP2’ encoded by Mec A) does not bind B lactams
vancomycin: VRE- altered peptide sequence in gram pos peptodoglycan (D-ala D-ala to D-ala D-lac)
Trimethoprim: gram negative bacilli- mutations in dihydrofolate reductase gene

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32
Q

Explain enzymatic degradation and give examples

A

The drug is destroyed: the antibiotic gets into the cell but is attacked by an enzyme
penicillins and cephalosporins: B lactamases (includinging ESBLs and NDM-1)
gentamicin: aminoglycoside modifying enzymes
chlorampheniol: chloramphnicol acetyltransferae (CAT)

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33
Q

Where is resistance genes encoded in bacteria and how is it transferred?

A

resistance genes are encoded in plasmids

horizontal and vertical transfer

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34
Q

What is horizontal transfer of resistance?

A
  • enabled by transposons and integrons

- DNA sequences designed to be transferred from plasmid to plasmid or plasmid to chromosome

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35
Q

What is vertical transfer of resistance?

A

chromosomal or plasmid-born resistance gene transferred to daughter cells on bacterial cell-division

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36
Q

Which viral infections cause the child to present with a rash?

A
  • Parvovirus
  • Measles
  • Chickenpox
  • Rubella
  • Non-polio enterovirus infection
  • Glandular fever (more likely to get a rash if taken ampicillin. May think you’re allergic to penicillin)
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37
Q

What is the term for the measles virus?

A

Paramyxovirus

Enveloped single stranded RNA virus

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38
Q

What are the clinical features of measles?

A

Rash, Fever, Cough/coryza/conjunctivitis

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39
Q

What are the complications of measles?

A

Otitis Media: Inflamation of the ear (7-9%)
Pneumonia (1-6%)
Diarrhoea (8%)
Acute Encephalitis- rare but fatal (1 in 2000)

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40
Q

What is the treatment for measles?

A

Antibiotics for superinfection

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41
Q

How do you prevent measles?

A
  • Vacination with the live MMR before the age of 1
42
Q

What’s the name of the virus which causes chicken pox?

A

Varicella Zoster Virus or Herpes Virus

43
Q

What are the clinical features of chicken pox?

A
  • Fever
  • Malaise
  • Anorexia
  • Rash
44
Q

What are the complications of chicken pox?

A
  • Pnemonitis (especially in smokers)
  • CNS involvement
  • Thrombocytopenia Purpura
  • Foetal Varicella Syndrome
  • Congenital Varicella
  • Zoster
45
Q

What is the treatment for chicken pox?

A

It’s symptomatic in adults and immunocomprimised children

  • Aciclovir oral, IV in severe cases of the disease or neonates
  • Chloropheniramine can relieve itch in less that 1 year olds)
46
Q

How can you prevent chicken pox?

A
  • Expose when young

- Live vaccine, 2 doses (used in USA and Japan)

47
Q

Which virus causes Rubella?

A

Togavirus (an RNA virus)

48
Q

What are the clincal features of the Rubella Virus?

A
  • Prodrome (an early symptom or sign of disease)
  • Lymphadenopathy: post-auricular and sub-occipital
  • Very non specific rash: Transcient, erythematous, behind ears, face and neck
49
Q

What are the complications of rubella?

A
  • Thrombocytopenia
  • Post infectious encephalitis
  • Arthritis
50
Q

How is the child affected when you contract rubella in pregnancy?

A

Congenital Rubella Syndrome (CRS):
- Catarcts and other eye defects
- Deafness
- Cardiac abnormalities
- Microephaly
- Retardation of the intra-uterine growth
- Inflammatory lesions of the brain, liver, lungs and bone marrow
CRS is more severe when the infection is contracted earlier in pregnancy.
Foetal damage rare after 16 weeks. Deafness only reported up to 20 weeks

51
Q

What’s the treatment for rubella?

A

No treatment available.
Immunoglobulin given to exposed pregnant women.
Vaccine; part of the MMR. 2-3% of women of child bearing age remain susceptible

52
Q

What is the virus that cause Parvovirus?

A

B19 (a DNA virus)

53
Q

How is parvovirus transmitted?

A

Respiratory secretions or from mother to child

54
Q

What are the symptoms of parvovirus?

A
  • Asymptomatic in 20%
  • Risk of miscarriage in early pregnancy, but low risk
  • Foetal disease: Anaemia and hydrops (foetal transfusion)
  • Clinical disease: Minor respiratory illness, Rash (slapped cheek), Arthralgia, Aplastic anemia, Anaemia in the immunosuppresed (this may be prolonged)
55
Q

How do you treat parvovirus?

A
  • None if it’s a self limiting illness
  • Blood transfusion
  • Infection control: Difficult as infectious prior to the arrival of the rash.
56
Q

What is Respiratory Syncytial Virus (RSV)?

A

A form of Pneumovirus
Bronchilitis:
- Affects 0-24 month olds
- Annual winter epidemics, incubation 4-6 days
- It can be life threatening and reinfections are common

57
Q

What is Metapneumovirus?

A

Caused by the Paramyxovirus.
Causes respiratory illness similar to RSV.
It ranges from mild upper respiratory tract infection to pneumonia

58
Q

What is adenovirus?

A

Accounts for 10% of childhood respiratory infection

Clinical Disease: Mild URTI (occasionally Severe Pneumonia), Conjunctivitis and diarrhoea

59
Q

What is Parainfluenza?

A

Caused by the paramyxovirus
There are 4 types; 1 in winter and 3 in summer
It’s transmitted person to person
Clinical: Croup (Inflamation of the larynx), bronchiolitis and upper respiratory tract infection.

60
Q

What is Rhinovirus?

A

Also known as the common cold.
Found in 70% of children with mild upper respiratory tract symptoms.
Similar clincal features to adenovirus

61
Q

How do you diagnose and treat RSV?

A

Diagnosis- PCR on the secretions from nasopharyngeal aspirate
Treatment- O2, manage fever and fluid intake

62
Q

How do you diagnose and treat Metapneumovirus?

A

Diagnosis- PCR

Treatment- Supportive only

63
Q

How do you diagnose and treat Adenovirus?

A

Diagnosis- Respiratory panel PCR or eye swab PCR

Treatment- None or Cidofovir in immunocomprimised

64
Q

How do you diagnose and treat Parainfluenza?

A

Diagnosis- Multiplexed PCR

Treatment- None

65
Q

What is Rotavirus?

A

Reovirus (RNA virus)
Transmission: Foecal-oral and occasionally respiratory
Low infective dose
Incubation is only 1-2 days
Epidemiology: Seasonal in the UK (winter and spring) but worldwide
440000 deaths a year

66
Q

What are the clincal features of Rotavirus?

A
  • Diarrhoea and vomiting
  • It usually affects 6/12 months to 2 year old babies
  • It’s a severe disease if you’re 6 to 12 months old.
  • Increased mortality in poorer countries
67
Q

How do you diagnose, treat and prevent Rotavirus?

A

Diagnosis: PCR
Treatment: Oral rehydration
Prevention: Oral live vaccine- UK introduction in 2013. Given and 2 and 3 months of age.

68
Q

What is Norovirus?

A
  • Known as the winter vominting bug
  • Often outbreaks in nurseries, hospitals and cruise ships
  • It’s food-Borne
  • Transmitted by person to person transmission
  • High incidence of vomiting (more than 50%)
  • Short course: 12 to 60 hours
69
Q

How do you diagnose and treat Norovirus?

A

Diagnosis: PCR
Treatment: Oral rehydration

70
Q

Which virus causes mumps?

A

A member of the Paramyxoviridae family

71
Q

What is the current treatment for mumps?

A

The MMR.
In the pre-vaccine era 90% of infections were in under 14s and so more than 85% of adults were immune because of previous childhood infection

72
Q

What are the clinical features of mumps?

A
  • Prodrome
  • In the next 24 hours you develop earache and tenderness over the ipsilateral parotid
  • In the next 2-3 days you develop a gradually enlarging parotid with severe pain. It’s normally bilateral but can be unilateral in 25%
  • Pyrexia up the 40 degrees centigrade
  • Within a week the parotid gland returns to normal size
73
Q

Which viral infections cause the child to present with respiratory symptoms?

A 
repiratory syncytial virus (RSV)
metapnuemovirus
adenovirus
parainfluenza
rhinoviurs
74
Q

Which viral infections cause the child to be present with diarrhoea?

A

rota virus
norovirus
mumps

75
Q

What are good targets for anti-fungal agents?

A

beta-1-3-glucan present in fungal cell wall

ergosterol in the fungal cell membranes required for normal growth and function of the fungal cell wall

76
Q

What are beta-1-3-glucans?

A

large polymers of UDP glucose
major structural component of fungal cell wall
synthesized bu beta-1-3-glucan synthase

77
Q

Which anti-fungal drugs require therapeutic drug monitoring?

A

itraconazole (there is a minimum level at which it doesn;t work at)
5-flurocytosine (can’t go above a certain threshold)
voriconazole (high level cause liver toxicity and below a level it doesn’t work)

78
Q

What is aspergillosis?

A

a group of fungal conditions caused by aspergillus spp

79
Q

Describe the polyene anti fungal agents

A
  • joins with ergosterol, forms holes and causes death by the leakage of k+
  • amphotericin B and nyastatin
  • used against most fungi of medical importance
  • causes allergic reactions and nephrotoxicity
  • AmB not absorbed orally, administered parenterally and used for serious systemic infections
  • Nyastatin too toxic for systemic use so only used for superifical infections e.g. oral/vaginal candidiasis
80
Q

Describe the allylamines anti fungal agents

A
  • inhibits ergosterol (at first arrow)
  • terbinafine
  • has a broad spectrum of activity but only used for dermatophyte infections in practice
  • can cause liver toxicity
  • topical use: tinea, pedis, tinea corporis, tinea cruris
  • systemic use: tinea capitis, onychomycosis
81
Q

Describe azole anti fungal agents

A
  • inhibits ergosterol synthesis
  • has a 5 membered azole ring
  • imidazoles (clotrimazole) have 2 nitrogen atoms and are toxic so rarely used systemically
  • triazoles (fluconazole) have 3 nitrogen atoms and are less toxic
  • fluconazole cannot be used on Aspergillus soo
  • can cause hepato-toxicity and also have drug interactions : can inhibity cytochrome P450 enzymes
82
Q

Describe Echinocandins anti fungal agents

A
  • they inhibity beta-1.3-glucan synthase so there is construction of a severely abnormal cell wall
  • e.g. anidulafungin
  • used for aspergillus and candida but misses out certain moulds and crytococcus (causes meningitis in people with HIV)
  • has minimal adverse effects
83
Q

Describe 5 fluorocysteine anti fungal agents

A
  • enters cell using fungal cytosine permease, converts to 5FU (from 5FC) to inhibit DNA and RNA synthesis
  • only works on yeasts
  • can cause bone marrow suppressio
  • used to treat crytocoocal meningiitis in combination with AmB
84
Q

Describe Griseofluvin anti fungal agents

A
  • inhibit fungal mitosis

- works on dermatophytes e.g. kerion and onychomycosis

85
Q

What is a definitive host?

A

either harbours the adult stage of a parasie of where the parasite utilises the sexual method of reproduction

86
Q

What is an intermediate host?

A

harbours the larval or asexual stages of the parasite

87
Q

What is a paratenic host?

A

host where the parasite remains viable without any further development

88
Q

What are NRTI’s

A

nuceloside analogue reverse transcriptase inhibitors

  • they are activated by phosphorylation by cellular enzymes to the triphosphate form
  • inhibition of viral RNA-dependent DNA polymerase (reverse transcriptase) and chain terminaon of the viral RT reaction
89
Q

What are NNRTI’s?

A

non-nucleoside reverse transcriptase inhibitors

-non-competitive inhibitors of RT, they bind to hydrophobic pocket on RT, separate from the active site

90
Q

What are Protease Inhibitors?

A

binds to the protease active site and inhibits

91
Q

What mutation leads to reisistance to lamivudine?

A

M184V

92
Q

Name some anti-hepatitis C compounds

A
  • interferon alpha and pegylated interferon alpha

- ribavirin

93
Q

What is aciclovir used for?

A

treatment of herpes simplex virus and VZV

94
Q

What is ganciclovir used for?

A

cytomegalovirus (CMV)

95
Q

What is oseltamir and zanamavir used for?

A

they are neuraminidase inhibitors used for influenza

96
Q

What is ribavirin used for?

A

Hep C and Respiratory syncytical virus

97
Q

What are interferons used for?

A

hep B and hep C infections

98
Q

What is IgM?

A

produced in acute infections
short term
used to check for current illness
it is the primary repsonse which deveops in the few weeks following first exposure to antigen

99
Q

What is IgG?

A

it is long term immunity

used to check for past disease

100
Q

What is IgA?

A

it is found in breast milk and used in passive immunity

101
Q

What is IgE?

A

Used in allergy

102
Q

What is surveillance?

A

Process if gathering information to ensure that disease outbreaks are pre-empted or idenitified early

Clinical Pathology (1 decks)

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