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Phase 2a Stuff > ICS Microbiology > Flashcards

ICS Microbiology Flashcards

1
Q

Define Pathogen

A

Organism(s) that causes or have the potential to cause disease

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2
Q

Define Commensal Organism

A

Colonises the host but causes no disease in normal circumstances

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3
Q

Define Opportunist Pathogen

A

Microbe that only causes disease if host defences are compromised

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4
Q

Define Virulence/Pathogenicity

A

The degree to which a given organism is pathogenic

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5
Q

Define asymptomatic carriage

A

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

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6
Q

Describe the morphology of bacteria

A

Simple organisms. Coccus if round and bacillus if rod-shaped

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7
Q

What is a pair of cocci called?

A

Diplococcus

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8
Q

Results of a Gram stain

A 
Purple = Positive
Pink = Negative
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9
Q

Difference between gram positive and gram negative bacteria.

A

Gram positive have very thick peptidoglycan layer, this is very thin in gram negative bacteria. Gram negative bacteria have an extra outer membrane.

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10
Q

Describe exotoxins

A

Secreted proteins, produced mostly by gram +ve bacteria.
Specific actions with strong antigenicity.
Can be converted to toxoid.
Easily altered by heat.

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11
Q

Describe endotoxins

A

Component of the outer membrane of bacteria.
Lipopolysaccharide (LPS in gram -ve bacteria)
Non-specific action with weak antigenicity.
Cannot easily be converted to toxoid
Stable in different heats

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12
Q

What does the catalase test do?

A

Distinguishes staphylococci and streptococci (streptococci are positive)

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13
Q

Why do gram positive bacteria stain purple?

A

They have a thick layer of peptidoglycan which retains the colour of the crystal violet stain.

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14
Q

How are gram positive bacteria managed?

A

Antimicrobials and vaccination

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15
Q

What is the structure of staphylococci?

A

Clusters of cocci

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16
Q

What does the coagulase test differentiate?

A

Differentiates staph. aureus (positive) from the other staphylococci

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17
Q

What diseases does Staphylococci aureus cause?

A

Pyogenic infections (impetigo, wound infections, septicaemia, endocarditis)

Toxin-mediated problem (toxic shock syndrome, food poisoning, scalded skin syndrome)

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18
Q

Example of coagulase negative staphylococci

A

S. epidermidis

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19
Q

What is the structure of streptococci?

A

Chains of cocci

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20
Q

Different types of haemolysis of blood agar

A

Alpha - greening i.e. S. intermedius

Beta - complete lysis i.e. S. pyogenes

Gamma - no lysis i.e. some S. mutans

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21
Q

What diseases are caused by S. pyogenes?

A
  • Wound infections
  • Tonsillitis
  • Impetigo
  • Scarlet fever
  • Otitis media
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22
Q

Describe S. pneumoniae pathogenicity

A
  • Alpha haemolysis
  • Normal commensal in oro-pharynx
  • Causes pneumonia, meningitis, sinusitis or otitis media
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23
Q

Describe viridans group streptococci pathogenicity

A
  • Alpha haemolysis
  • Some cause dental caries and abscesses
  • Important in infective endocarditis
  • Cause deep organ abscesses
  • Examples include S. intermedius, S. anginosus etc.
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24
Q

What is Lancefield typing?

A

A method of grouping catalyse negative and coagulase negative bacteria based on bacterial carbohydrate cell-surface antigens

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25
Q

Examples of gram +ve bacilli

A
  • Listeria monocytogenes
  • Bacillus anthracis
  • Corynebacterium diphtheriae
  • Clostridia (tetani, botulism, difficile)
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26
Q

Describe the structure of gram -ve bacteria

A

Thin layer of peptidoglycan
Have a second outer double membrane.
Formed one side by phospholipids and other side by LPS (endotoxins)

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27
Q

Main groups of gram negative bacteria

A
  • Proteobacteria
  • Bacteroidetes
  • Chlamydiae
  • Spirochaetes
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28
Q

Main family of proteobacteria (of clinical importance)

A

Enterobacteria

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29
Q

Structure of enterobacteria

A

Rods, most are motile

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30
Q

Examples of enterobacteria

A

Shigella flexneri, Escherichia coli (E. coli), Salmonella enterica

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31
Q

What are serovars?

A

Distinct variations in antigenic structure between strains of the same species.

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32
Q

What are pathovars?

A

Strains or sets of strains with similar pathogenicity.

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33
Q

Why are some strains of E. coli commensal and some pathogenic?

A

There is a common core genome and pathogenicity genes can be acquired.

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34
Q

Examples of Shigella bacteria

A

S. dysenteriae, S. flexneri, S. boydii, S. sonnei.

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35
Q

What is shigellosis?

A

Pathology like that of entero-invasive E. coli but with Shiga toxin

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36
Q

Types of salmonella bacteria

A

S. enterica

S. bongori

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37
Q

The 3 forms of salmonellosis (caused by S. enterica)

A

Gastroenteritis (serovar Enteritidis and Typhimurium)

Enteric fever (serovar Typhi)

Bacteraemia

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38
Q

Describe Bacteroidetes

A

Non-motile rods
Strict anaerobes
Live as part of commensal flora of small intestine
Involved with opportunistic infections.

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39
Q

Which member of the Bacteroidetes is the most frequent cause of anaerobic infections?

A

B. fragilis

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40
Q

Groups of Chlamydiae

A

Chlamydia and Chlamydophila

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41
Q

Describe Chlamydiae

A

Very small, non-motile
Obligate intracellular parasites.
Many groups live asymptomatically.

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42
Q

Two types of bodies in the Chlamydiae

A

Elementary bodies

  • round
  • infectious
  • enter cell through endocytosis
  • prevent phagosome-lysosome fusion

Reticulate bodies

  • Pleiomorphic
  • Replicative
  • Non-infectious
  • Acquire nutrients from host cells
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43
Q

3 biovars of Chlamydia trachomatis

A

Trachoma biovar
Genital tract biovar
(LGV) biovar

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44
Q

Describe spirochaetes

A

Long, spiral shapes
Most non-pathogenic
Characterised by endoflagellum

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45
Q

Examples of spirochaetes

A

Borrelia burgdorferi
Leptospira interrogans
Treponema pallidum

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46
Q

Describe fungi?

A
  • Eukaryotic
  • Chitin cell wall
  • Heterotrophic
  • Move by growth or spores
  • Infections are opportunistic
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47
Q

Yeasts vs Moulds

A

Yeasts are small single celled organisms that divide by budding

Moulds form multicellular hyphae and spores

(some fungi are both - dimorphic)

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48
Q

Forms that fungal infections take

A

Skin infections
Wound infections
Mucosal infection
Invasive infections (life threatening)

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49
Q

What is the aim of antimicrobial drug therapy?

A

To achieve inhibitory levels of agent at the site of infection without damaging the cells too much

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50
Q

Microbiology of mycobacteria

A

Aerobic, non-spore forming, non-motile bacillus.

Cell wall contains high molecular weight lipids

SLOW reproduction
SLOW response to treatment
SLOW growing

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51
Q

What stain is used to identify organisms with wax-like thick cell walls?

A

Ziehl-Neelsen stain

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52
Q

How does the host aim to kill mycobacteria?

A

Microbicidal molecules and acidification acids digestion resulting in generation of antigens for presentation to T-cells

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53
Q

Characteristics of viruses

A
  • No membranes or cell organelles
  • Consist of outer protein coat and strand of nucleic acid
  • Come in variety of shapes
  • Cannot carry out metabolic reactions on their own
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54
Q

How do viruses replicate?

A
  1. Attachment: viral and cell receptors e.g. HIV
  2. Cell entry: only central viral core carrying the nucleic acid and some associated proteins enter host cells
  3. Interaction with host cells: use cell materials for their replication
  4. Replication: may localise in nucleus, cytoplasm or both
  5. Assembly: occurs in nucleus, in cytoplasm or at cell membrane
  6. Release: bursting open of cell, or by leaking from the cell over a period of time
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55
Q

How do viruses cause disease?

A
  • Damage by direct destruction of host cells e.g. HIV
  • Damage by modification of host cell structure or function e.g. rotaviruses
  • Damage involving over-reactivity of host as a response to infection e.g. hepatitis B
  • Damage through cell proliferation and cell immortalization e.g. HPVs
  • Evasion of both extracellular and intracellular host defences
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56
Q

Describe how Gram staining works.

A
  • Adding crystal violet dye to bacteria on a microscope slide (after bacteria is fixed by heating over a flame)
  • Washed off after a few seconds
  • Iodine added and then washed off after seconds
  • Decolourisation (with Gram’s alcohol)
  • Counterstain (fuchsin/safranin)
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57
Q

Appearance of colonies in blood agar of staphylococci

A

S. aureus is gold

All the rest are white

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58
Q

How to differentiate S. pneumoniae from other streptococci?

A

Optochin test (S/ pneumoniae is sensitive)

59
Q

Describe the oxidase test

A

Tests for the presence of cytochrome oxidase

Disk turns blue if positive

60
Q

What are the 5 major classes of protozoa?

A 
Flagellates
Amoebae
Sporozoans
Ciliates
Microsporidia
61
Q

Describe Protozoa

A

Single-celled eukaryotic organisms. Engulf food via phagocytosis and have important parasitic and symbiotic relationships.

62
Q

How do amoebae move?

A

By means of flowing cytoplasm and production of pseudopodia.

63
Q

Name a pathogenic amoeba

A

Entamoeba histolytica

64
Q

Describe the epidemiology of Entamoeba histolytica

A

Causes a severe dysenteric illness (amoebiasis)
More common in areas with poor water supply and contracted through faecal-oral contamination.
Combated through public health measures such as sanitation of water.

65
Q

Name 4 illnesses caused by flagellates.

A

Trypanosomiasis
Leishmaniasis
Giardiasis
Trichomonas Vaginalis

more info on each in notes

66
Q

Describe Sporozoans

A

Non-motile protozoa.

All species are parasitic and most are intracellular

67
Q

Three diseases caused by Sporozoans

A

Malaria
Cryptosporidiosis
Toxoplasmosis (toxoplasma gondii)

68
Q

5 species of Plasmodia sporozoan that cause human disease.

A 
P. Falciparum
P. Malariae
P. Ovale
P. Vivax
P. Knowlesi
69
Q

Vector of Malaria

A

Female Anopheles Mosquito

70
Q

3 stages of Malaria lifecycle

A

Human Liver Stage
Human Blood Stage
Mosquito Stage

(diagram in protozoa notes)

71
Q

Clinical features of malaria

A 
Fever
Chills and sweats
Headache
Myalgia
Fatigue
Nausea and Vomiting
Diarrhoea
72
Q

Which species causes severe malaria?

A

P. falciparum

73
Q

Complications of malaria

A
  • Cerebral malaria
  • ARDS
  • Renal failure
  • Bleeding
  • Shock
74
Q

Treatment of complicated malaria

A

IV Artesunate

75
Q

Treatment of uncomplicated malaria

A

Lots of options e.g. primaquine

76
Q

Define infectivity

A

The ability to become established in the host, can involve adherence and immune escape

77
Q

Define invasiveness

A

The capacity to penetrate mucosal surfaces to reach normally sterile sites

78
Q

What is antigenic drift?

A

Spontaneous mutations that occur gradually giving minor changes in haemagglutinin and neuraminidase

79
Q

What is antigenic shift?

A

Sudden emergence of a new subtype different to that of the preceding virus

80
Q

What is an antibiotic?

A

An agent produced by microorganisms that kill or inhibit the growth of other microorganisms in high-dilution.

81
Q

What does ‘antimicrobials’ include?

A 
Antifungal
Antibacterial
Anthelminthic
Antiprotozoal
Antiviral
82
Q

Main groups of Beta Lactams

A

Penicillin
Cephalosporins
Carbapenems
Monobactams

83
Q

How do Beta Lactams destroy bacteria?

A

Inhibit cell wall synthesis

84
Q

Which bacteria do Beta Lactams act on better

A

Gram positive bacteria

but still acts on some gram negative

85
Q

How does Rifampicin work?

A

Works against RNA polymerase and inhibits RNA synthesis

86
Q

What ‘accidental’ damages do antibiotics cause?

A 
Directly
Toxins
Indirect
- Inflammation
- Immune pathology
Diarrhoea
87
Q

What is the action of bacteriostatic antibodies?

A

Prevents growth of bacteria
Kills >90% in 18-24 hours
Inhibits protein synthesis, DNA replication or mitosis

88
Q

What is the action of bactericidal antibiotics?

A

Agent directly kills the bacteria (usually by inhibiting cell wall synthesis)
Kills >99.9% in 18-24 hours

89
Q

What are bactericidal antibiotics useful in treating?

A

Poor penetration (endocarditis)
Difficult to treat
Need to eradicate quickly (meningitis)

90
Q

What dose MIC stand for?

A

Minimum inhibitory concentration

91
Q

Examples of antibiotics who employ concentration-dependent killing.

A

Aminoglycosides

Quinolones

92
Q

Examples of antibiotics who employ time-dependent killing.

A

Beta lactams
Clindamycin
Macrolides
Oxazolidinones

93
Q

4 Reasons for antibiotics not working

A

Changes to binding site of antibiotic target
Destruction of antibiotic
Prevention of antibiotic access
Removal of antibiotic from bacteria

94
Q

How can bacteria develop resistance?

A

Natural innate
Spontaneous gene mutation
Horizontal gene transfer

95
Q

Factors important to consider when deciding if an antibiotic is safe to prescribe.

A
  • Intolerance, allergy and anaphylaxis
  • Side effects
  • Age
  • Renal and Liver functions
  • Pregnancy and breast feeding
  • Drug interactions
  • Risk of C. diff
96
Q

Examples of glycopeptides and what they do.

A

Vancomycin and Teicoplanin. (IV) Damage cell wall of gram positive bacteria.
Used when bacteria resistant to beta-lactams

97
Q

Example of Macrolides, what they do and mode of use

A

Clarithromycin and erythromycin
Inhibit protein synthesis
Oral (and IV if needed)

98
Q

When are macrolides used?

A

Gram positives and atypical pneumonia pathogen.

Use in penicillin allergy or severe pneumonia

99
Q

Example of Lincosamides, what they do and mode of use

A

Clindamycin
Inhibits protein synthesis
Oral (and IV)

100
Q

When are lincosamides used?

A

Gram positives, used in cellulitis or necrosing fasciitis

101
Q

Example of Tetracyclines, what they do and mode of use

A

Doxycycline
Inhibits protein synthesis
Oral

102
Q

When are tetracyclines used?

A

Mainly gram positive, used in pneumonia or cellulitis.

103
Q

Example of Aminoglycosides, what they do and mode of use

A

Gentamicin
Inhibit protein synthesis
IV only

104
Q

When are aminoglycosides used?

A

Gram negatives and staphs

Use in UTIs or infective endocarditis

105
Q

Example of Quinolones and what they do

A

Ciprofloxacin

Inhibits DNA synthesis

106
Q

When are Quinolones used?

A 
Gram negative (and positive sometimes) 
Use in penicillin allergy, UTIs and intra-abdominal infections. 
Risk of C. diff
107
Q

Other antibiotics used for UTIs

A

Trimethoprim

Nitrofurantoin (first line for lower UTIs)

108
Q

What does U=U mean in HIV?

A

UNDETECTABLE = UNTRANSMITTABLE

109
Q

What are the two things we look for in blood tests for HIV?

A
  • Low CD4 count (normal is 500 upwards)

- High HIV viral load

110
Q

First stage of HIV course

A

Acute primary infection. 2-4 weeks after exposure
Transient immunosuppression and fall in CD4 count (followed by gradual rise)
Acute rise in viral load then fall to ‘set point’

111
Q

What can happen in the primary HIV infection?

A

Abrupt onset of non-specific symptoms (can be mild or severe)

112
Q

What should be done in a patient with a fever, rash and non-specific symptoms?

A

Ask about sexual history

Consider HIV seroconversion

113
Q

What is the commonest opportunistic infection in HIV patients?

A

PCP

Pneumocystic pneumonia

114
Q

Second phase of HIV course

A 
Asymptomatic phase (clinical latency)
Progressive loss of CD4 cells and rise in viral load.
115
Q

When should we think about doing a HIV test?

A

Common problem in unexpected patient
No clear underlying cause to common problem
Recurring infections

116
Q

Third Stage of HIV course

A

Early symptomatic HIV

117
Q

Fourth stage of HIV course

A

AIDS

118
Q

What is AIDS?

A

Acquired immune deficiency syndrome

119
Q

Typical time from HIV infection to AIDS

A

5-10 years

120
Q

Factors causing more rapid progression from HIV to AIDS

A

Elderly and Children

High ‘set point’ viral load

121
Q

Is HIV clinically manageable using HAART?

A

YES!

With proper treatment even late-stage HIV has a good prognosis

122
Q

What are the 6 steps of HIV virus’s effect on host cells?

A
  1. Attachment
  2. Cell entry
  3. Interaction with host cell
  4. Replication
  5. Assembly
  6. Release
123
Q

What type of virus is HIV and therefore what enzyme does it contain?

A

HIV is a retrovirus so uses reverse transcriptase

124
Q

Describe the structure of the HIV genome

A

Small RNA virus, expresses just 10 genes. It is a retrovirus and a lentivirus.

125
Q

Which cells does HIV infect?

A

CD4+ cells (t-cells)

126
Q

What receptor protein on HIV binds with the CD4?

A

gp120

127
Q

Is it possible to be resistant to HIV?

A

YES! 1% of Caucasians are homozygous for a 32bp deletion in the CCR5 gene so they cannot be infected.

128
Q

Why does HIV mutate and evolve rapidly?

A

Error-prone replication
Rapid viral replication
Large population sizes

129
Q

Describe the majority of people currently with HIV

A

Living in sub-Saharan Africa

Heterosexual!

130
Q

What are the UNIAIDS 90/90/90 Goals?

A

By 2020:
90% of those living with HIV are diagnosed
90% of those diagnosed are on ART
90% viral suppression for those on ART

131
Q

Did we reach the UNIAIDS 90/90/90 goals?

A

Globally failed

In UK hit them in 2018

132
Q

What is defined as late diagnosis of HIV?

A

When someone is diagnosed, their CD4 count is less than 350

133
Q

Transmission routes of HIV

A

Blood
Sexual
Vertical (mum to baby)

134
Q

Main forms of HIV prevention

A

ART
PrEP
PEP
Behaivoural

135
Q

High risk groups for HIV

A

Men who have sex with men (MSM)
sub-Saharan African/Thailand
Multiple sexual partners
Rape in high prevalence localities

136
Q

HIV symptoms

A
  • Acute generalised rash
  • Glandular fever
  • Rash (involving palms)
  • Indicators of immune dysfunction
  • Unexplained weight loss or night sweats
  • Recurrent bacterial infections (including p. pneumonia)
137
Q

Who can offer a HIV test?

A

ANY healthcare professional

138
Q

Which diseases does VSV cause?

A

Chickenpox (primary infection)

Shingles (secondary reactivation)

139
Q

What is at the core of herpes viruses?

A

DNA genome

140
Q

Difference between distribution of Smallpox and Chickenpox rashes

A

Smallpox tends to be at the periphery.

Chickenpox tends to be on the trunk.

141
Q

Distributions of shingles rash

A

Dermatomal distribution. Most common in thoracic and ophthalmic divisions.

142
Q

Treatment of secondary syphilis

A

Penicillin

143
Q

Some rashes that effect the palms and soles of feet

A

HIV
Secondary syphilis
Hand, foot and mouth disease

144
Q

Presentation of primary CMV (cytomegalovirus)

A

Similar to Epstein-Barre
Atypical lymphocytes
‘Owls eye’ intranuclear inclusions

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