ICS Microbiology Flashcards
(144 cards)
1
Q
Define Pathogen
A
Organism(s) that causes or have the potential to cause disease
2
Q
Define Commensal Organism
A
Colonises the host but causes no disease in normal circumstances
3
Q
Define Opportunist Pathogen
A
Microbe that only causes disease if host defences are compromised
4
Q
Define Virulence/Pathogenicity
A
The degree to which a given organism is pathogenic
5
Q
Define asymptomatic carriage
A
When a pathogen is carried harmlessly at a tissue site where it causes no disease
6
Q
Describe the morphology of bacteria
A
Simple organisms. Coccus if round and bacillus if rod-shaped
7
Q
What is a pair of cocci called?
A
Diplococcus
8
Q
Results of a Gram stain
A
Purple = Positive Pink = Negative
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.
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.
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
12
Q
What does the catalase test do?
A
Distinguishes staphylococci and streptococci (streptococci are positive)
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.
14
Q
How are gram positive bacteria managed?
A
Antimicrobials and vaccination
15
Q
What is the structure of staphylococci?
A
Clusters of cocci
16
Q
What does the coagulase test differentiate?
A
Differentiates staph. aureus (positive) from the other staphylococci
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)
18
Q
Example of coagulase negative staphylococci
A
S. epidermidis
19
Q
What is the structure of streptococci?
A
Chains of cocci
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
21
Q
What diseases are caused by S. pyogenes?
A
- Wound infections
- Tonsillitis
- Impetigo
- Scarlet fever
- Otitis media
22
Q
Describe S. pneumoniae pathogenicity
A
- Alpha haemolysis
- Normal commensal in oro-pharynx
- Causes pneumonia, meningitis, sinusitis or otitis media
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.
24
Q
What is Lancefield typing?
A
A method of grouping catalyse negative and coagulase negative bacteria based on bacterial carbohydrate cell-surface antigens
25
Examples of gram +ve bacilli
- Listeria monocytogenes
- Bacillus anthracis
- Corynebacterium diphtheriae
- Clostridia (tetani, botulism, difficile)
26
Describe the structure of gram -ve bacteria
Thin layer of peptidoglycan
Have a second outer double membrane.
Formed one side by phospholipids and other side by LPS (endotoxins)
27
Main groups of gram negative bacteria
- Proteobacteria
- Bacteroidetes
- Chlamydiae
- Spirochaetes
28
Main family of proteobacteria (of clinical importance)
Enterobacteria
29
Structure of enterobacteria
Rods, most are motile
30
Examples of enterobacteria
Shigella flexneri, Escherichia coli (E. coli), Salmonella enterica
31
What are serovars?
Distinct variations in antigenic structure between strains of the same species.
32
What are pathovars?
Strains or sets of strains with similar pathogenicity.
33
Why are some strains of E. coli commensal and some pathogenic?
There is a common core genome and pathogenicity genes can be acquired.
34
Examples of Shigella bacteria
S. dysenteriae, S. flexneri, S. boydii, S. sonnei.
35
What is shigellosis?
Pathology like that of entero-invasive E. coli but with Shiga toxin
36
Types of salmonella bacteria
S. enterica
| S. bongori
37
The 3 forms of salmonellosis (caused by S. enterica)
Gastroenteritis (serovar Enteritidis and Typhimurium)
Enteric fever (serovar Typhi)
Bacteraemia
38
Describe Bacteroidetes
Non-motile rods
Strict anaerobes
Live as part of commensal flora of small intestine
Involved with opportunistic infections.
39
Which member of the Bacteroidetes is the most frequent cause of anaerobic infections?
B. fragilis
40
Groups of Chlamydiae
Chlamydia and Chlamydophila
41
Describe Chlamydiae
Very small, non-motile
Obligate intracellular parasites.
Many groups live asymptomatically.
42
Two types of bodies in the Chlamydiae
Elementary bodies
- round
- infectious
- enter cell through endocytosis
- prevent phagosome-lysosome fusion
Reticulate bodies
- Pleiomorphic
- Replicative
- Non-infectious
- Acquire nutrients from host cells
43
3 biovars of Chlamydia trachomatis
Trachoma biovar
Genital tract biovar
(LGV) biovar
44
Describe spirochaetes
Long, spiral shapes
Most non-pathogenic
Characterised by endoflagellum
45
Examples of spirochaetes
Borrelia burgdorferi
Leptospira interrogans
Treponema pallidum
46
Describe fungi?
- Eukaryotic
- Chitin cell wall
- Heterotrophic
- Move by growth or spores
- Infections are opportunistic
47
Yeasts vs Moulds
Yeasts are small single celled organisms that divide by budding
Moulds form multicellular hyphae and spores
(some fungi are both - dimorphic)
48
Forms that fungal infections take
Skin infections
Wound infections
Mucosal infection
Invasive infections (life threatening)
49
What is the aim of antimicrobial drug therapy?
To achieve inhibitory levels of agent at the site of infection without damaging the cells too much
50
Microbiology of mycobacteria
Aerobic, non-spore forming, non-motile bacillus.
Cell wall contains high molecular weight lipids
SLOW reproduction
SLOW response to treatment
SLOW growing
51
What stain is used to identify organisms with wax-like thick cell walls?
Ziehl-Neelsen stain
52
How does the host aim to kill mycobacteria?
Microbicidal molecules and acidification acids digestion resulting in generation of antigens for presentation to T-cells
53
Characteristics of viruses
- 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
54
How do viruses replicate?
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
55
How do viruses cause disease?
- 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
56
Describe how Gram staining works.
- 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)
57
Appearance of colonies in blood agar of staphylococci
S. aureus is gold
| All the rest are white
58
How to differentiate S. pneumoniae from other streptococci?
Optochin test (S/ pneumoniae is sensitive)
59
Describe the oxidase test
Tests for the presence of cytochrome oxidase
| Disk turns blue if positive
60
What are the 5 major classes of protozoa?
```
Flagellates
Amoebae
Sporozoans
Ciliates
Microsporidia
```
61
Describe Protozoa
Single-celled eukaryotic organisms. Engulf food via phagocytosis and have important parasitic and symbiotic relationships.
62
How do amoebae move?
By means of flowing cytoplasm and production of pseudopodia.
63
Name a pathogenic amoeba
Entamoeba histolytica
64
Describe the epidemiology of Entamoeba histolytica
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
Name 4 illnesses caused by flagellates.
Trypanosomiasis
Leishmaniasis
Giardiasis
Trichomonas Vaginalis
more info on each in notes
66
Describe Sporozoans
Non-motile protozoa.
| All species are parasitic and most are intracellular
67
Three diseases caused by Sporozoans
Malaria
Cryptosporidiosis
Toxoplasmosis (toxoplasma gondii)
68
5 species of Plasmodia sporozoan that cause human disease.
```
P. Falciparum
P. Malariae
P. Ovale
P. Vivax
P. Knowlesi
```
69
Vector of Malaria
Female Anopheles Mosquito
70
3 stages of Malaria lifecycle
Human Liver Stage
Human Blood Stage
Mosquito Stage
(diagram in protozoa notes)
71
Clinical features of malaria
```
Fever
Chills and sweats
Headache
Myalgia
Fatigue
Nausea and Vomiting
Diarrhoea
```
72
Which species causes severe malaria?
P. falciparum
73
Complications of malaria
- Cerebral malaria
- ARDS
- Renal failure
- Bleeding
- Shock
74
Treatment of complicated malaria
IV Artesunate
75
Treatment of uncomplicated malaria
Lots of options e.g. primaquine
76
Define infectivity
The ability to become established in the host, can involve adherence and immune escape
77
Define invasiveness
The capacity to penetrate mucosal surfaces to reach normally sterile sites
78
What is antigenic drift?
Spontaneous mutations that occur gradually giving minor changes in haemagglutinin and neuraminidase
79
What is antigenic shift?
Sudden emergence of a new subtype different to that of the preceding virus
80
What is an antibiotic?
An agent produced by microorganisms that kill or inhibit the growth of other microorganisms in high-dilution.
81
What does 'antimicrobials' include?
```
Antifungal
Antibacterial
Anthelminthic
Antiprotozoal
Antiviral
```
82
Main groups of Beta Lactams
Penicillin
Cephalosporins
Carbapenems
Monobactams
83
How do Beta Lactams destroy bacteria?
Inhibit cell wall synthesis
84
Which bacteria do Beta Lactams act on better
Gram positive bacteria
| but still acts on some gram negative
85
How does Rifampicin work?
Works against RNA polymerase and inhibits RNA synthesis
86
What 'accidental' damages do antibiotics cause?
```
Directly
Toxins
Indirect
- Inflammation
- Immune pathology
Diarrhoea
```
87
What is the action of bacteriostatic antibodies?
Prevents growth of bacteria
Kills >90% in 18-24 hours
Inhibits protein synthesis, DNA replication or mitosis
88
What is the action of bactericidal antibiotics?
Agent directly kills the bacteria (usually by inhibiting cell wall synthesis)
Kills >99.9% in 18-24 hours
89
What are bactericidal antibiotics useful in treating?
Poor penetration (endocarditis)
Difficult to treat
Need to eradicate quickly (meningitis)
90
What dose MIC stand for?
Minimum inhibitory concentration
91
Examples of antibiotics who employ concentration-dependent killing.
Aminoglycosides
| Quinolones
92
Examples of antibiotics who employ time-dependent killing.
Beta lactams
Clindamycin
Macrolides
Oxazolidinones
93
4 Reasons for antibiotics not working
Changes to binding site of antibiotic target
Destruction of antibiotic
Prevention of antibiotic access
Removal of antibiotic from bacteria
94
How can bacteria develop resistance?
Natural innate
Spontaneous gene mutation
Horizontal gene transfer
95
Factors important to consider when deciding if an antibiotic is safe to prescribe.
- Intolerance, allergy and anaphylaxis
- Side effects
- Age
- Renal and Liver functions
- Pregnancy and breast feeding
- Drug interactions
- Risk of C. diff
96
Examples of glycopeptides and what they do.
Vancomycin and Teicoplanin. (IV) Damage cell wall of gram positive bacteria.
Used when bacteria resistant to beta-lactams
97
Example of Macrolides, what they do and mode of use
Clarithromycin and erythromycin
Inhibit protein synthesis
Oral (and IV if needed)
98
When are macrolides used?
Gram positives and atypical pneumonia pathogen.
| Use in penicillin allergy or severe pneumonia
99
Example of Lincosamides, what they do and mode of use
Clindamycin
Inhibits protein synthesis
Oral (and IV)
100
When are lincosamides used?
Gram positives, used in cellulitis or necrosing fasciitis
101
Example of Tetracyclines, what they do and mode of use
Doxycycline
Inhibits protein synthesis
Oral
102
When are tetracyclines used?
Mainly gram positive, used in pneumonia or cellulitis.
103
Example of Aminoglycosides, what they do and mode of use
Gentamicin
Inhibit protein synthesis
IV only
104
When are aminoglycosides used?
Gram negatives and staphs
| Use in UTIs or infective endocarditis
105
Example of Quinolones and what they do
Ciprofloxacin
| Inhibits DNA synthesis
106
When are Quinolones used?
```
Gram negative (and positive sometimes)
Use in penicillin allergy, UTIs and intra-abdominal infections.
Risk of C. diff
```
107
Other antibiotics used for UTIs
Trimethoprim
| Nitrofurantoin (first line for lower UTIs)
108
What does U=U mean in HIV?
UNDETECTABLE = UNTRANSMITTABLE
109
What are the two things we look for in blood tests for HIV?
- Low CD4 count (normal is 500 upwards)
| - High HIV viral load
110
First stage of HIV course
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
What can happen in the primary HIV infection?
Abrupt onset of non-specific symptoms (can be mild or severe)
112
What should be done in a patient with a fever, rash and non-specific symptoms?
Ask about sexual history
| Consider HIV seroconversion
113
What is the commonest opportunistic infection in HIV patients?
PCP
| Pneumocystic pneumonia
114
Second phase of HIV course
```
Asymptomatic phase (clinical latency)
Progressive loss of CD4 cells and rise in viral load.
```
115
When should we think about doing a HIV test?
Common problem in unexpected patient
No clear underlying cause to common problem
Recurring infections
116
Third Stage of HIV course
Early symptomatic HIV
117
Fourth stage of HIV course
AIDS
118
What is AIDS?
Acquired immune deficiency syndrome
119
Typical time from HIV infection to AIDS
5-10 years
120
Factors causing more rapid progression from HIV to AIDS
Elderly and Children
| High 'set point' viral load
121
Is HIV clinically manageable using HAART?
YES!
| With proper treatment even late-stage HIV has a good prognosis
122
What are the 6 steps of HIV virus's effect on host cells?
1. Attachment
2. Cell entry
3. Interaction with host cell
4. Replication
5. Assembly
6. Release
123
What type of virus is HIV and therefore what enzyme does it contain?
HIV is a retrovirus so uses reverse transcriptase
124
Describe the structure of the HIV genome
Small RNA virus, expresses just 10 genes. It is a retrovirus and a lentivirus.
125
Which cells does HIV infect?
CD4+ cells (t-cells)
126
What receptor protein on HIV binds with the CD4?
gp120
127
Is it possible to be resistant to HIV?
YES! 1% of Caucasians are homozygous for a 32bp deletion in the CCR5 gene so they cannot be infected.
128
Why does HIV mutate and evolve rapidly?
Error-prone replication
Rapid viral replication
Large population sizes
129
Describe the majority of people currently with HIV
Living in sub-Saharan Africa
| Heterosexual!
130
What are the UNIAIDS 90/90/90 Goals?
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
Did we reach the UNIAIDS 90/90/90 goals?
Globally failed
| In UK hit them in 2018
132
What is defined as late diagnosis of HIV?
When someone is diagnosed, their CD4 count is less than 350
133
Transmission routes of HIV
Blood
Sexual
Vertical (mum to baby)
134
Main forms of HIV prevention
ART
PrEP
PEP
Behaivoural
135
High risk groups for HIV
Men who have sex with men (MSM)
sub-Saharan African/Thailand
Multiple sexual partners
Rape in high prevalence localities
136
HIV symptoms
- 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
Who can offer a HIV test?
ANY healthcare professional
138
Which diseases does VSV cause?
Chickenpox (primary infection)
| Shingles (secondary reactivation)
139
What is at the core of herpes viruses?
DNA genome
140
Difference between distribution of Smallpox and Chickenpox rashes
Smallpox tends to be at the periphery.
| Chickenpox tends to be on the trunk.
141
Distributions of shingles rash
Dermatomal distribution. Most common in thoracic and ophthalmic divisions.
142
Treatment of secondary syphilis
Penicillin
143
Some rashes that effect the palms and soles of feet
HIV
Secondary syphilis
Hand, foot and mouth disease
144
Presentation of primary CMV (cytomegalovirus)
Similar to Epstein-Barre
Atypical lymphocytes
'Owls eye' intranuclear inclusions
