Microbiology Flashcards
1
Q
Define pathogen.
A
An organism capable of causing disease.
2
Q
Define commensal.
A
An organism that colonises the host but causes no disease.
3
Q
Define opportunist pathogen.
A
An organism that only causes disease if host defences are compromised.
4
Q
Define virulence.
A
The degree to which a given organism is pathogenic.
5
Q
What would gram positive bacteria look like down the microscope?
A
Purple/blue.
6
Q
What would gram negative bacteria look like down the microscope?
A
Red/pink.
7
Q
What type of organism would you stain with Ziehl Neelsen?
A
Mycobacteria e.g. TB.
8
Q
How do you apply the gram stain?
A
Apply crystal violet to heat fixed bacteria. Treat with iodine. Decolourise the sample and then counterstain.
9
Q
Describe the characteristic features of gram positive bacteria?
A
- Single membrane.
2. Large peptidoglycan area.
10
Q
Describe the characteristic features of gram negative bacteria?
A
- Double membrane.
- Small peptidoglycan area.
- LPS (endotoxin area).
11
Q
Between what temperatures and what pH range can bacteria grow?
A
Between -80 to +80°C. And from a pH of 4 to 9.
12
Q
What are the 3 phases of bacterial growth?
A
- Lag phase.
- Exponential phase.
- Stationary phase.
13
Q
Give an example of a slow growing bacteria.
A
TB.
14
Q
Give an example of a fast growing bacteria.
A
E.coli and S.aureus.
15
Q
Give 2 functions of pili.
A
- Help adhere to cell surfaces.
2. Plasmid exchange.
16
Q
What is the primary function of flagelli?
A
Locomotion.
17
Q
What is the primary function of the polysaccharide capsule?
A
Protection; prevents MAC or opsonisation molecules attacking.
18
Q
What types of bacteria release endotoxin?
A
Gram negative.
19
Q
What types of bacteria release exotoxin?
A
Gram positive and gram negative.
20
Q
Describe endotoxins.
A
Endotoxin (LPS) is an outer membrane component released when bacteria are damaged. They are less specific and are toxic to the host. They are heat stable.
21
Q
Describe exotoxins.
A
Proteins secreted from gram positive and gram negative bacteria. They are specific and heat labile.
22
Q
What are endotoxins made from?
A
Lipopolysaccharides (LPS).
23
Q
What are exotoxins made from?
A
Proteins.
24
Q
What are plasmids?
A
Circular pieces of DNA that often carry genes for antibiotic resistance.
25
Give an example of a gram negative diplococci?
Neisseria e.g. N.meningitidis and N.gonorrhoeae.
26
Give an example of a gram positive cocci?
Staphylococcus and streptococcus.
27
What test can be done to distinguish between staphylococcus and streptococcus?
The catalase test; detects the presence of catalase enzyme using hydrogen peroxide. Staph = catalase + ve.
Strep = catalase - ve.
28
How would you describe the arrangement of staphylococci?
Clusters of cocci.
29
How would you describe the arrangement of streptococci?
Chains of cocci.
30
What test could be done to further distinguish between staphylococci bacteria.
Coagulase test; looks at whether a fibrin clot is produced.
31
What bacteria would be coagulase positive?
Staphylococci aureus.
32
What bacteria would be coagulase negative?
All others e.g. staphylococci epidermidis.
33
What test could be done to distinguish between different streptococci?
Blood agar haemolysis.
34
What further test can be done for those streptococci in the β haemolysis group?
Serogrouping; detecting surface antigens. e.g. lancefield grouping.
35
What would you see on the agar plate in α haemolysis and give an example of a bacteria in this group.
α haemolysis is partial erythrocyte lysis; you see a green colour. Streptococcus pneumoniae falls in this group.
36
What would you see on the agar plate in β haemolysis and give an example of a bacteria in this group.
β haemolysis is complete erythrocyte lysis; you see a clear area. Streptococcus pyogenes and streptococcus agalactiae fall in this group.
37
What would you see on the agar plate in γ haemolysis and give an example of a bacteria in this group.
γ haemolysis is when there is no haemolysis. Streptococcus bovis falls in this group.
38
Give examples of gram negative bacilli.
Shigella, salmonella, E.coli etc.
39
Give examples of gram positive bacilli.
Clostridium, bacillus, cornyebacterium etc.
40
What kind of bacteria is MacConkey agar used with?
Gram negative bacilli.
41
What is MacConkey agar?
MacConkey agar contains bile salts, lactose and pH indicator. If an organism ferments lactose, lactic acid will be produced and the agar will appear a red/pink colour.
42
Name 2 gram negative bacilli that will give a positive result with MacConkey agar.
1. E.Coli.
| 2. Klebsiella pneumoniae.
43
Where in the body might you find staphylococci?
Nose and skin.
44
How is staphylococcus aureus spread?
Aerosol and touch.
45
Give 4 virulence factors of staphylococci?
1. Toxins.
2. Proteases.
3. Toxic shock syndrome toxin.
4. Protein A.
46
How is c.diptheriae spread?
Droplet spread.
47
Does shigella have a H antigen?
Shigella is non motile and doesn't have flagellum. It therefore doesn't have a H antigen.
48
What category of bacteria does shigella fall under?
Gram negative bacilli.
49
Does shigella give a positive result with MacConkey agar?
No. Shigella does not ferment lactose and so gives a negative result.
50
Does salmonella have a H antigen?
Salmonella is motile and has a flagellum; it therefore does have a H antigen.
51
Does salmonella give a positive result with MacConkey agar?
No. Salmonella does not ferment lactose and so gives a negative result.
52
Does e.coli have a H antigen?
E.coli is motile and has a flagellum; it therefore does have a H antigen.
53
Does e.coli give a positive result with MacConkey agar?
Yes. E.coli does ferment lactose and so you would see a red/pink colour indicating a positive result.
54
How can you distinguish between gram negative bacilli (salmonella, shigella and e.coli)?
Use MacConkey agar and use serology to detect the presence of the H antigen.
55
Why are there pathogenic strains of e.coli?
Due to the acquisition of genes from other bacteria.
56
Which type of e.coli would you associate with causing travellers diarrhoea?
Enterotoxigenic e.coli (ETEC).
57
Describe the process by which enterotoxigenic e.coli (ETEC) causes traveller's diarrhoea?
Heat labile ETEC toxin modifies Gs protein, it is in a 'locked on' state. Adenylate cyclase is activated and there is increased production of cAMP. This leads to increased secretion of Cl- into the intestinal lumen, H2O follows this down an osmotic gradient and this subsequently results in traveller's diarrhoea.
58
What effect do enteropathogenic and enterohaemorrhagic e.coli (EPEC and EHEC) have on the mucosa?
They adhere to microvilli, rearrange actin, and lead to pedestal formation.
59
What are the symptoms of enteropathogenic e.coli infection?
Chronic watery diarrhoea.
60
What are the symptoms of enterohaemorrhagic e.coli infection?
Bloody diarrhoea.
61
What are the symptoms of shigella infection?
Severe bloody diarrhoea and frequent passage.
62
How is shigella passed on?
Via contaminated food/water or from person to person.
63
Shigella is acid tolerant. Why is this advantageous for shigella?
It means shigella can pass through the stomach without being destroyed by the low gastric pH. It can then move onto the intestine.
64
What is the action of shigella in the intestine?
In the intestine it induces self uptake and leads to macrophage apoptosis. Cytokines are released and neutrophils are attracted = inflammation. Shigella spread to adjacent cells.
65
What bacteria is responsible for salmonellosis?
S.enterica.
66
Name the 3 forms of salmonellosis.
1. Gastroenteritis.
2. Enteric fever.
3. Bacteraemia.
67
What is gastroenteritis?
Frequent cause of food poisoning, 24 hour incubation period. Highly infective dose.
68
What is enteric fever?
Enteric fever: typhoid fever. Systemic disease.
69
What are the symptoms of v.cholerae?
Huge volumes of watery stools (no blood or pus).
70
Why is v.cholerae so dangerous?
You're losing huge amounts of water which can result in hypovolemic shock and severe dehydration, this can lead to death.
71
Why is v.cholerae not killed if you have a fever?
It grows at 18 - 42°C.
72
Why would you need to be infected with a large amount of v.cholerae to show symptoms of the disease?
The optimum pH for v.cholerae growth is 8; alkaline. It is therefore very sensitive to the pH of the stomach.
73
How would you grow haemophilus influenzae?
On chocolate agar as it requires haem and NAD.
74
What diseases can haemophilus influenzae cause?
Meningitis and pneumonia.
75
Describe the pathogenesis of gastro-enteritis.
1. Endocytosis.
2. Chemokine release.
3. Neutrophil recruitment and migration.
4. Neutrophil induced tissue injury.
5. Fluid and electrolyte loss -> diarrhoea.
76
Describe the pathogenesis of enteric fever.
1. Endocytosis.
2. Migration to the basolateral membrane.
3. Survival in macrophage -> systemic spread.
77
Name the bacteria that can cause legionnaires disease?
Legionella.
78
Who might be susceptible to infection by legionella?
Immunocompromised individuals.
79
What type of bacteria are Neisseria?
Gram negative diplococci.
80
What are the two medically important species of neisseria?
N.meningitidis and N.gonorrhoeae.
81
How is N.meningitidis transmitted?
Aerosol transmission. High risk in colonised people e.g. university, Haj.
82
Describe the pathogenesis of N.meningitidis.
Crosses nasopharyngeal epithelium and enters blood stream. Can cause asymptomatic bacteraemia or septicaemia. If the bacteria crosses the BBB it can cause meningitis.
83
What are the virulence determinants of N.meningitidis?
1. Capsule; anti-phagocytic.
2. Pili; adherence to host cell.
3. LPS.
84
What are the consequences of N.gonorrhoeae infection?
STI - rectal, vaginal or oral inflammation.
85
Describe bacteroides.
Opportunistic, obligate anaerobes.
86
Can you grow chlamydia on agar?
No, chlamydia is an obligate intracellular parasite.
87
How can you detect chlamydia?
Serum antibodies or PCR.
88
What are the 2 developmental stages of chlamydia's unique growth cycle?
1. Elementary bodies (infective).
2. Reticulate bodies (intracellular multiplication).
- Reticulate bodies are converted back into elementary bodies and are released. The cycle continues.
89
What can c.trachomatis cause?
Chlamydia; the most common STI.
90
Name 2 bacteria in the chlamydophila genre.
1. C.pneumoniae - respiratory tract infection.
| 2. C.psittaci - associated with birds.
91
Describe the flagellum of a spirochaete.
Spirochaete's have an endoflagellum, it lies between the inner and outer membrane.
92
Name the spirochaete that is responsible for causing lyme disease.
B.burgdorferi.
93
Name the spirochaete that is responsible for causing syphilis.
T.pallidum.
94
Describe the three stages of syphilis.
1. Primary stage: localised infection.
2. Secondary stage: systemic - skin, lymph nodes etc.
3. Tertiary stage: CV syphilis and neuro syphilis.
95
Describe yeast.
Single celled organism. Asexual reproduction.
96
Describe mould.
Multicellular organism. Reproduce by spore formation.
97
What are dimorphic fungi?
Fungi that can exist as both yeast and mould; they are yeast in tissues but mould in vitro.
98
Give an example of a dimorphic fungi.
Coccidioides immitis.
99
Why are severe fungal infections rare?
Fungi are unable to grow at 37°C and are often killed by the innate and adaptive immune response.
100
Name 3 common fungal infections.
1. Nappy rash.
2. Tinea pedis.
3. Onychomycosis (fungal nail infection).
101
Name a drug that is good for treating onychomycosis.
Terbinafine - it reaches poorly perfused sites e.g. nails.
102
What is the fundamental principle behind antifungal treatments?
Selective toxicity!
103
What can antifungal treatments target?
1. Fungal cells walls; they contain polysaccharides and chitin.
2. Ergosterol containing plasma membrane.
104
Antifungal treatments: how does amphotericin work?
It targets ergosterol in the plasma membrane and causes pore formation, this leads to cell death.
105
Antifungal treatments: how do azoles work?
They affect the ergosterol synthetic pathway.
106
Give 4 disadvantages of azoles.
1. High first pass metabolism, bioavailability = 45%.
2. ADR's, can cause hepatitis.
3. Drug interactions due to CYP450.
4. Resistance can develop e.g. in candida.
107
What is candida?
A yeast. It grows in warm, moist areas and has high levels of β-D-Glucan.
108
What test can be done to identify fungal antigens?
β-D-Glucan test.
109
What fungal infection can often be a presenting factor for HIV?
Pneumocystis pneumonia; opportunistic infection, can cause lung infection in immunocompromised people.
110
Why is pneumocystis pneumonia not commonly found in the lungs of healthy people?
It is opportunistic and so can cause disease in immunocompromised individuals.
111
Give an example of a mould.
Aspergillus fumigatus.
| Aspergillus niger.
112
What are moulds composed of?
Branched filamentous filaments called hyphae.
113
Describe mycobacteria.
- Aerobic.
- Non-motile.
- Non spore forming.
- Bacilli.
114
Give an example of mycobacteria.
M.tuberculosis (TB).
| M.leprae (leprosy).
115
Why is it hard to use the gram stain on mycobacteria?
The cell wall is very thick and has a high lipid content.
116
Why is it hard to use therapeutic antibodies against mycobacteria?
Mycobacteria grow very slowly and so treatment with antibodies is difficult. (This also makes them hard to culture).
117
How would you stain mycobacteria?
Using Ziehl-Neelsen stain for acid fast bacili.
118
How could you detect whether an individual has had previous exposure to TB?
1. Tuberculin skin test (mantoux).
| 2. Interferon gamma release assays.
119
Name 6 sterile sites in the body.
1. Urinary tract.
2. CSF.
3. Pleural fluid.
4. Peritoneal cavity.
5. Blood.
6. Lower respiratory tract.
120
Where in the body would you find normal flora (commensals)?
1. Mouth.
2. Skin.
3. Vagina.
4. Urethra.
5. Large intestine.
121
Give an advantage and a disadvantage of the slide coagulase test as opposed to the tube test.
Advantage: quicker and easier.
Disadvantage: less sensitive as it only detects bound coagulase and not free coagulase too.
122
What colour do staphylococcus aureus colonies appear on blood agar?
Creamy/yellow.
123
Which Lancefield groups are associated with tonsilitis and skin infection?
A , C and G.
124
Which Lancefield groups are associated with neonatal sepsis and meningitis?
B.
125
Which Lancefield groups are associated with UTI's?
D.
126
What is the oxidase test?
Detects the presence of cytochrome oxidase in bacteria. A positive test is indicated by the disk turning blue.
127
Which group of streptococci can cause infective endocarditis?
Alpha haemolytic streptococci.
128
How can you differentiate streptococci pneumoniae from other streptococci?
The optochin test can differentiate streptococci pneumoniae from other streptococci. Pneumococci are sensitive and so a clear area would be seen.
129
Describe chocolate agar and explain why it might be used.
Chocolate agar is blood agar that has been heated so as to release nutrients. Chocolate agar is often used for growing fastidious bacteria.
130
What is the function of bile salts in MacConkey agar?
They inhibit gram positive bacteria growth.
131
What is CLED agar used for?
It is used to differentiate micro-organisms in urine and can classify lactose fermenters and non-lactose fermenters.
132
What is Gonococcus agar used for?
It contains growth factors to promote the growth of Neisseria. It also contains antibiotics and antifungal agents to inhibit growth of other organisms.
133
What is XLD agar used for?
It is a very selective growth medium used to isolate salmonella and shigella. Salmonella shows black dots.
134
What is Sabouraud's agar used for?
Used to culture fungi.
135
Why do bacteria produce coagulase?
They use it as a defence mechanism by clotting the areas of plasma around them, thereby resisting phagocytosis.
136
What are protozoa?
Single celled eukaryotic organisms.
137
What genus of parasitic protozoa is responsible for causing malaria?
Plasmodia spp.
138
How is malaria transmitted?
Via the bite of female mosquitos from dusk till dawn.
139
Why are there different clinical manifestations of malaria?
The difference in clinical manifestation can be due to variation in the plasmodia life cycle. The plasmodia life cycle has stages in the human and the mosquito.
140
What are the stages of the plasmodia life cycle in the human called?
Exo-erythrocytic and endo-erythrocytic stages.
141
What happens in the stages of the plasmodia life cycle that occur inside the human?
Exo-erythrocytic: Hepatcoytes become infected by sporozoites, the cells mature and develop and are released as tropozites.
Endo-erythrocytic: tropozites invade RBC's. Parasite numbers expand rapidly with a sustained cycling of the parasite population.
142
What 2 species of the plasmodia genus lie dormant and cause late relapse of malaria?
P.ovale and p.vivax.
143
What signs and symptoms might you see in someone who has been infected with malaria?
Fever, haemolysis, chills, sweats, headaches etc.
144
Describe the pathogenesis of p.falciparum?
Unique cerebral malaria, fatal infection. Parasites mature in RBC's, RBC's collect in small vessels and cause blockage of cerebro-microvasculature = hypoxia!
145
What are the clinical features of haemolysis?
Anaemia, jaundice (dark urine due to increased Hb).
146
Malaria diagnosis: what can thick and thin films tell you?
- Thick films: sensitive but low resolution, tell you if you have malaria.
- Thin films: tell you species and parasite count.
147
What genetic conditions can give immunity to malaria?
Someone with sickle cell anaemia or thalassaemias.
148
Can immunity to malaria be acquired?
Recurrent infection can lead to someone being 'semi-immune'. Antibodies could be transferred by maternal transmission.
149
Do viruses have a cell wall?
NO! Viruses have an outer protein coat that is sometimes surrounded by a lipid envelope but they do not have a cell wall.
150
How do viruses attach to a host cell?
Viruses have proteins on their surface that interact with receptors on host cell membranes.
151
What are the 6 stages of viral replication?
1. Attachment.
2. Cell entry.
3. Interaction with host cell.
4. Replication.
5. Assembly.
6. Release.
152
What part of the virus will enter the host cell?
Only the viral core carrying the nucleic acids will enter the host cell cytoplasm. Sometimes proteins that act as enzymes may enter too.
153
How do viruses interact with host cells?
Viruses use cell materials e.g. enzymes, amino acids and nucleotides, for their replication and they evade host defence mechanisms.
154
Where in a cell does viral replication occur?
In the nucleus, cytoplasm or both.
155
How can viruses be released from a cell?
1. Bursting open; lysis of cell.
| 2. 'Leaking' from the cell over a preiod of time; exocytosis
156
What are the 5 ways by which viruses can cause disease?
1. Damage by direct destruction: cell lysis.
2. Damage by modification of cell structure.
3. 'Over-reactivity' of the host as a response to infection: immuno-pathological damage.
4. Damage via cell proliferation and immortalisation.
5. Evasion of host defences.
157
Give an example of a virus that causes damage by direct destruction of host cells.
Poliovirus or HIV.
158
Give an example of a virus that causes damage by modification of cell structure.
1. Physical modification: Rotaviruses, HIV.
| 2. Functional modification: Rotaviruses, HIV.
159
Give an example of a virus that causes damage by triggering host cell 'over-reactivity' as a response to infection.
Hepatitis B and C viruses, HIV.
160
Give an example of a virus that causes damage via cell proliferation and immortalisation.
HPV's.
161
Give an example of a virus that everts host defences via virus persistence.
Herpesviruses, hep B and C viruses, measles virus.
162
Give an example of a virus that everts host defences via virus variability.
Influenza type A, HIV, hep B and C viruses, rhinoviruses.
163
Give an example of a virus that everts host defences via viral modulation of host defences.
Most viruses.
164
What are the 5 ways in which viruses can evert host defences.
1. Virus persistence or latency.
2. Down regulation of interferons.
3. Virus variability due to gene reassortment or mutation.
4. Prevention of host cell apoptosis.
5. Viral modulation of host defences.
165
Pathogenesis of rotavirus infection: How does rotavirus cause damage by modification of cell structure?
Rotaviruses infect the small intestine epithelial cells. There is vili atrophy and flattening of the epithelial cells. The patient suffers from malabsorption, this results in a hyper-osmotic effect causing diarrhoea.
166
Pathogenesis of hepatitis B infection: how does hepatitis B cause damage by triggering host cell 'over-reactivity'?
Hep B infection leads to an antibody and T cell response that destroys infected hepatocytes; this causes extensive liver damage.
167
Pathogenesis of cervical carcinoma: how does HPV cause damage via cell proliferation and immortalisation?
HPV types 16 and 18 infect the genital tract; there is viral replication. HPV genome integrates into host cell chromosome. p53 and Rb are inhibited and there is excessive cell growth and proliferation leading to cervical carcinoma.
168
Which HPV viral gene product controls viral gene expression?
E2.
169
Which HPV viral gene products inhibit p53 and Rb?
E6 and E7.
170
Give an example of a virus that prevents host cell apoptosis.
Herpesvirus, HIV.
171
What are the 3 main groups of helminths?
1. Nematodes (roundworms).
2. Trematodes (flatworms).
3. Cestodes (tapeworms).
172
Helminth infection: What is the pre-patent period?
The interval between infection and the appearance of eggs in the stool.
173
What type of blood cell would have a raised count in helminth infection?
Eosinophils. Eosinophils are associated with parasitic infection and helminth's are parasitic worms.
174
How are intestinal nematodes (roundworms) often diagnosed?
Stool microscopy looking for eggs.
175
How are intestinal nematodes spread?
Transmission is from human to human via eggs or larvae.
176
Intestinal nematodes: what are the signs and symptoms of ascaris lumbricoides infection?
- Loeffler's syndrome: larval migration to lungs results in cough, fever and wheeze.
- Often infection can be asymptomatic.
177
Intestinal nematodes: what are the signs and symptoms of hook worm infection?
Local dermatitis at the site of entry. Iron deficiency anaemia.
178
Intestinal nematodes: what are the signs and symptoms of threadworm infection?
Pruritus ani.
179
Intestinal nematodes: how would you diagnose threadworm infection?
Apply sellotape to the perianal area.
180
Intestinal nematodes: what are the signs and symptoms of strongyloides stercoralis infection?
Pruritus, pulmonary and gut symptoms, larva currens (skin rashes).
181
Intestinal nematodes: why can the symptoms of strongyloides stercoralis persist for years?
Strongyloides stercoralis is associated with auto-infection and an immunocompromised state.
182
Intestinal nematodes: what are the signs and symptoms of taenia saginatum infection?
Taenia saginatum is also known as beef tapeworm. Abdominal pain is a likely symptom.
183
Intestinal nematodes: what are the signs and symptoms of taenia solium infection?
Taenia solium is also known as pork tapeworm. Skin, muscle and the brain can be affected, the patient may suffer from fits.
184
What are 4 main problems that surround HIV treatment?
1. Mainly transmitted by sexual intercourse and so people don't like to talk about it - taboo.
2. Period of latency means someone may infect others unwittingly.
3. HIV leads to a weakened immune system and so there is increased risk of infection.
4. HIV mutates a lot and so drug treatment is difficult.
185
What enzyme copies HIV RNA into DNA?
Reverse transcriptase.
186
Why are mutations common in HIV?
HIV is a retrovirus and replicates via reverse transcription. This process is prone to errors and mutations.
187
Which genus does HIV belong to and what is the significance of this?
HIV belongs to the lentivirus genus. These viruses are characterised by having a long incubation period.
188
What did HIV arise from?
SIV - originally from chimpanzees.
189
What cells act as 'host cells' for HIV?
CD4+ cells. Macrophages and dendritic cells can also be invaded by HIV.
190
What is the affect of HIV infection on CD4 count?
HIV leads to uncontrolled CD4 activation and apoptosis. CD4 numbers decrease over time.
191
Which glycoproteins are on the surface of HIV?
GP41 and GP120.
192
How does HIV attach onto a host cell?
GP160 binds to CD4 receptors and also CCR5 co-receptors.
193
What part of HIV enters the host cell following attachment?
The viral caspid, enzymes and nucleic acids.
194
Briefly describe the mechanism of HIV replication.
1. GP160 binds to CD4 receptors.
2. Viral caspid, enzymes and nucleic acids are uncoated and released into the cell.
3. RNA is converted into DNA using reverse transcriptase.
4. Viral DNA is integrated into cellular DNA by intergrase.
5. Viral DNA is transcribed into viral proteins.
6. Splicing.
7. New HIV cells 'bud' from CD4.
195
Name 4 enzymes involved in HIV replication.
1. Reverse transcriptase.
2. Integrase.
3. RNA polymerase.
4. Proteases.
196
Which enzyme is responsible for integrating HIV DNA into cellular DNA?
Integrase.
197
What are the 10 main stages of HIV replication?
1. Attachment.
2. Cell entry.
3. Uncoating.
4. Reverse transcription.
5. Genome integration.
6. Transcription of viral DNA.
7. Splicing of mRNA.
8. Translation into proteins.
9. Assembly.
10. Budding.
198
How many genes are encoded in the HIV genome?
9.
199
What does Pol encode?
Enzymes e.g. reverse transcriptase, integrase etc.
200
Which gene encodes reverse transcriptase?
Pol.
201
Why might macrophages also be infected by HIV?
Macrophages also have CD4 and CCR5 receptors.
202
Describe what happens when someone is initially infected with HIV.
HIV enters via mucosa.
Macrophages ingest HIV and presents an epitope of HIV to a T cell. HIV then infects the T cell. Infection spills into the blood stream - viraemia.
203
HIV leads to immune dysfunction, how are the immune system cells affected?
1. CD4 cells are excessively and inappropriately activated.
2. There is impaired IL-2 production.
3. There is a decrease in the number and function of CD4 cells.
4. B cells produce fewer specific Ab's.
5. There are fewer NK cells, neutrophils and macrophages.
204
Name 4 'sanctuary sites' for HIV.
1. Genital tract.
2. GI tract.
3. CNS.
4. Bone marrow.
205
Define antibiotics.
Agents produced by micro-organisms that kill or inhibit the growth of other micro-organisms.
206
Where on the bacteria would penicillin bind?
Bacterial cell wall.
207
Define bacteriostatic.
Antibiotics that prevent bacterial growth by inhibiting DNA synthesis.
208
Define bactericidal.
Antibiotics that kill bacteria by inhibiting cell wall synthesis.
209
What is MIC?
The minimum inhibitory concentration: the lowest concentration of a chemical that prevents growth of a bacterium.
210
Does the lowest MIC mean the best antibiotic?
No. There are many other important factors that need to be considered e.g. the number of binding sites occupied and how long they're being occupied for.
211
What does a drug need to do to ensure it inhibits metabolic processes?
1. Occupy an adequate number of binding sites.
| 2. Occupy these binding sites for a sufficient period of time.
212
What is concentration dependent killing?
Antibiotics that eradicate pathogenic bacteria by achieving high concentrations at the site of binding: Peak conc/MIC ratio.
213
What is time dependent killing?
The time that serum concentrations remain above the MIC: t > MIC.
214
Give an example of a class of antibiotics that uses concentration dependent killing mechanisms?
Aminoglycosides e.g. gentamicin.
215
Give an example of a class of antibiotics that uses time dependent killing mechanisms?
Beta lactams e.g. penicillin.
216
What are 4 mechanisms of antibiotic resistance?
1. Change antibiotic target.
2. Destroy antibiotic.
3. Prevent antibiotic access.
4. Remove antibiotic from bacteria.
217
How can an antibiotic target change result in resistance?
Target site mutation can mean that the antibiotic can no longer attach to the bacteria. e.g. in MRSA.
218
Give an example of how an antibiotic is destroyed.
The beta lactam ring of penicillin can be hydrolysed. The ring is essential for the antibiotic and without it it is destroyed.
219
How can access to antibiotics be prevented?
Modification of membrane porin channel size, number and selectivity.
220
How can antibiotics be removed from bacteria?
Antibiotics can be removed via efflux pumps.
221
How does resistance develop?
1. Intrinsic: natural resistance.
2. Acquired:
- Spontaneous mutation.
- Horizontal gene transfer.
222
How can spontaneous mutation lead to antibiotic resistance?
- Change in AA sequence.
- Change to cell structure.
- Decrease affinity/activity of antibiotic.
- New nucleotide base pair.
223
Give 3 methods of horizontal gene transfer.
1. Conjugation.
2. Transduction.
3. Transformation.
224
What is a clinically important gram positive resistant bacteria?
MRSA - plasmid transfer resistance.
225
What is a clinically important gram negative resistant bacteria?
ESBL (extended spectrum b lactamase) - mutation at active site.
226
What are antibiotics used for?
- Treatment.
- Prophylaxis.
- Prevention of post-surgical infection.
227
What antibiotic might be used for the treatment of s.pneumoniae?
Amoxicillin.
228
When might you use penicillin?
For treatment of skin and soft tissue infections, endocarditis.
229
Give an advantage of penicillin.
It has a narrow spectrum and so there is a reduced chance of resistance.
230
What antibiotic might be used for the treatment of bacterial pharyngitis: 'strep throat'?
Phenoxymethylpenicillin.
231
How can amoxicillin be given?
Orally or intra-venously.
232
Amoxicillin can be given to people infected with which bacteria?
H.influenzae, enterococci, e.coli, shigella, streptococci etc.
233
What antibiotic would you give to someone infected with staph. aureus (MSSA)?
Flucloxacillin.
234
A person presents with cellulitis. What antibiotic might you give them?
Flucloxacillin - s.pyogenes and staph.aureus are often a cause of cellulitis.
235
What types of bacteria do monobactams work against?
Gram negative bacilli.
236
Why would you give someone monobactams?
If they have a penicillin allergy.
237
What types of bacteria does vancomyocin work against?
Gram positive only!
| Good for MRSA treatment.
238
A person presents with a UTI. What antibiotic might you give them?
Trimethoprin.
239
What are Carbapenemase producing enterobacteriaceae (CPEs)?
Gram negative bacteria that are resistant to broad spectrum antibiotics (carbapenems).
240
What is carbapenemase?
An enzyme that hydrolyses carbapenems and confers antibiotic resistance.
241
What virus can cause shingles?
Varicella Zoster Virus.
242
Where might you see a shingles rash?
Shingles rash can appear on various dermatomes but it is usually seen at areas associated with tight clothing.
243
What laboratory method can be used to detect viral pathogens?
PCR.
244
What is PCR?
PCR amplifies DNA to generate millions of copies of a particular DNA sequence. The specimen is mixed with nucleotides, primers and DNA polymerase.
245
Give some signs and symptoms of infective mononucleosis (glandular fever).
1. Reddening, swelling and white patches on the tonsils. 2. Swollen lymph nodes.
3. Spleen enlargement.
4. Chills, fever.
5. Cough.
6. Sore throat.
7. Fatigue, malaise, loss of appetite, headache.
246
What is the management/treatment of glandular fever?
Supportive therapy and advise the patient to avoid contact sport for 6 weeks in order to avoid splenic rupture.
247
What can qPCR detect?
1. The presence or absence of DNA/RNA.
| 2. It can quantify the level of virus in a tissue.
248
What are the consequences of influenza A infection?
Increased risk of ARDS and secondary bacterial pneumonia. The patient is also highly infective to others.
249
What are the markers for HIV in the blood?
Antigens, antibodies, HIV RNA.
250
If a HIV test comes back as negative in a high risk individual why should a second HIV test be done?
A second test should be done after the window period: the window period is the time between exposure to HIV infection and the point when the test will give an accurate result. During this time a person can be infected with HIV and be very infectious but still test HIV negative.
251
HIV: what is the 'window period'?
The time between potential exposure to HIV infection and the point when the test will give an accurate result. During this time a person can be infected with HIV and be very infectious but still test HIV negative.
252
HIV RNA can be detected using RT-PCR. What is this useful for?
It can quantify the amount of HIV RNA in the blood and so can indicate disease progression and how well the individual is responding to antiretroviral therapy.
253
Name 5 groups of people who are at high risk of HIV infection.
1. Homosexual men.
2. Heterosexual women.
3. Sex workers.
4. IV drug users.
5. Truck drivers.
254
What are the 3 stages of the HIV epidemic?
1. Nascent; <5% prevalence in risk groups.
2. Concentrated; >5% prevalence in one or more risk groups.
3. Generalised; >5% prevalence in the general population.
255
How can the impact of HIV be reduced?
1. Behaviour change; education, condom use, needle exchange.
2. Know your status; testing.
3. Specific interventions; PMTCT, PEP, VMCC, PrEP etc.
256
How can sexual transmission of HIV be reduced?
Condom use!
| Voluntary medical male circumcision.
257
Briefly explain why voluntary medical male circumcision can reduce sexual transmission of HIV.
Male circumcision leads to a change in mucosa. HIV is less able to penetrate due to an increase in keratinisation.
258
How can transmission of HIV among IV drug users be reduced?
Harm reduction measures e.g. needle exchange.
259
How can HIV among young children be eliminated?
To reduce MTCT; prevent breast feeding where possible; give lifelong antiretroviral treatments to the mother.
260
What are the problems with trying to ensure everyone living with HIV has access to antiretroviral treatments?
1. Lack of awareness.
2. Understaffed clinics.
3. Medication needs monitoring.
4. Cost.
5. Adherence.
261
How can awareness of HIV be increased?
TESTING! Ensure it is accurate, high quality and provides care, support and ultimately treatment.
262
What are the 4 main phases in the natural history of HIV?
1. Acute primary infection.
2. Asymptomatic phase.
3. Early symptomatic HIV.
4. AIDS.
263
What happens in the acute primary infection phase of HIV?
There is a transient fall in CD4+ count followed by a gradual rise. There is also an acute rise in viral load.
264
What signs and symptoms might you see when someone is in the acute primary infection phase of HIV?
Abrupt onset of non-specific symptoms e.g. fever, rash. Weight loss, lethargy and depression can also occur.
265
What happens in the asymptomatic phase of HIV?
There is a progressive loss of CD4+ cells. This is the latent phase and can last for years.
266
What signs and symptoms might you see when someone is in the asymptomatic phase of HIV?
This phase is the latent phase and so you will rarely see symptoms. However, you might sometimes see enlarged lymph nodes.
267
What is the CD4+ count when someone is diagnosed with having AIDS?
CD4+ <200.
268
Name 3 types of people who are likely to rapidly progress and develop AIDS.
1. Elderly people.
2. Children.
3. People with a high viral load.
269
Name 2 markers that are used for monitoring HIV.
1. CD4+ count.
2. HIV RNA copies (viral load).
- These markers are important in determining prognosis.
270
What is HIV seroconversion?
A period of time during which HIV antibodies develop and become detectable. Seroconversion generally takes place within a few weeks of initial infection.
271
Name 3 respiratory diseases associated with HIV.
1. Bacterial (pneumococcal) pneumonia.
2. TB.
3. Pneumocystis pneumonia (PCP).
272
What are the characteristic signs of pneumocystis pneumonia (PCP)?
Decreased CD4+ count.
Decreased O2 sats on exertion.
Decreased exercise tolerance.
273
Name 3 CNS diseases associated with HIV.
1. Mass lesions e.g. primary CNS lymphoma, cerebral toxoplasmosis.
2. Meningitis e.g. pneumococcal, cryptococcal.
3. Opthalmic lesions e.g. CMV, toxoplasmosis, choroidal tuberculosis etc.
274
What does HAART stand for?
Highly active anti-retroviral treatment.
275
What is HAART? What does it aim to do?
Anti-retroviral treatment where 3 drugs are taken together.
| The aim is to reduce viral load and increase CD4+ count. Good compliance = good prognosis.
276
Where in the cell can HIV drugs target?
1. Reverse transcriptase inhibitors.
2. Protease inhibitors.
3. Fusion inhibitors.
277
What is the UNAIDS goal by 2020?
90/90/90
- 90% diagnosed.
- 90% on anti-retroviral treatment.
- 90% viral suppression, undetectable viral load.
278
What behaviour modifications can be done in order to prevent HIV transmission?
Sex education, reduce frequency of changing sexual partners, reduce high risk sexual practices, consistent condom use!
279
Why is knowing your HIV status so important?
Knowing you HIV status will help to reduce MTCT and sexual transmission. It is good for public health and is cost effective.
280
What is targeted testing for HIV?
Clinician initiated diagnostic testing triggered by clinical indications e.g. immunosuppression.
281
Why is it bad to probe too deeply into a patients risk factors for HIV?
Patients may be unaware of their risk factors or may not want to admit to them. Asking about risk factors can lead to alienation and a decreased uptake of testing.
282
How would you define a 'late diagnosis' of HIV?
CD4+ count < 350.
283
Why is it bad to diagnose HIV late?
A late diagnosis is associated with a 10 fold increase in risk of death in the first year after diagnosis.
284
Chains of purple cocci are seen on a gram film. They show alpha haemolysis when grown on blood agar. They don’t grow near the optochin disc. What bacteria is likely to have caused this?
Streptococcus pneumonia.
285
Name a gram negative bacillus that is a lactose fermenter.
E.coli.
286
Name 4 diseases that haemophilus influenzae can cause.
1. Meningitis.
2. Otitis media.
3. Pharyngitis.
4. Exacerbations of COPD.
287
What does the HIV envelop contain?
RNA, caspid, reverse transcriptase.
288
What is ringworm?
A fungal infection that can cause an itchy, red, scaly, circular rash.
289
Is ringworm a helminth?
No! Ringworm is fungal.
290
True or False. Mycobacteria can withstand phagolysosome killing.
True. The bacterium has adapted to the intracellular environment can can withstand phagolysosome killing and escape to the cytosol.
291
Is pneumonia caused by pneumocystis jirovecii bacterial or fungal?
Fungal!
292
Give 3 defining features of systemic inflammatory response syndrome (SIRS).
- Temperature >38℃ or <36 ℃.
- Heart rate >90.
- White cell count >12.
- Hyperglycaemia.
293
Infection control. What are the five moments of hand hygiene?
1. Before patient contact.
2. Before aseptic procedure.
3. After bodily fluid exposure.
4. After touching a patient.
5. After touching patient surroundings.
294
Name 6 vaccine preventable diseases that are notifiable.
1. Diptheria.
2. Measles.
3. Mumps.
4. Rubella.
5. Tetanus.
6. Whooping cough.
295
Name 5 diseases that are notifiable.
1. Anthrax.
2. Cholera.
3. Rabies.
4. Smallpox.
5. Yellow fever.
6. Acute encephalitis.
7. Botulism.
8. Enteric fever.
9. Leprosy.
10. Malaria.
296
Why is it important to tell public health England about notifiable diseases?
It can aid disease surveillance: changes can be tracked. Interventions can be developed to protect the community.
297
What is passive immunisation?
Injecting immunoglobulins. Temporary increase in antibody levels.
298
Why might you use passive immunisation?
To protect immunocompromised children exposed to measles.
| To help people who have had exposure to hepatitis A.
299
What is active immunisation?
Vaccination that stimulates an immune response against toxoid.
300
What are the disadvantages of polysaccharide vaccines?
Protection is not long lasting and the response in children is poor.
301
How can polysaccharide vaccines be improved?
Conjugation can help improve immunogenicity.
302
How do live attenuated vaccines work?
The organism replicates in the host triggering an immune response. It is important to be aware of the risk of disease in immunocompromised individuals.
303
What is primary vaccine failure?
When a person doesn't develop immunity.
304
What is secondary vaccine failure?
When a person initially responds but protection wanes over time. Booster is required.
305
What does meningococcal infection usually present as?
Meningitis or septicaemia (blood poisoning).
306
How is Neisseria meningitidis transmitted?
Droplet transmission from person to person.
307
What kind of bacteria is Neisseria meningitidis?
Gram negative diplococci.
308
How can further cases of meningitis be prevented?
1. Notification.
2. Contact tracing.
3. Prophylaxis e.g. advice, medication, vaccination (serogroup dependent).
309
What is the percentage risk of MTCT of HIV for the following:
a) In a mother receiving anti-retroviral therapy and not breast feeding.
b) In a mother not receiving anti-retroviral therapy and is breast feeding.
a) < 1%.
| b) 35%.
310
CD4+ cells can differentiate into T helper 1 and T helper 2 cells. What is the function of TH1 cells?
TH1 produce interleukins that help coordinate the immune response. They activate macrophages and CD8+.
311
CD4+ cells can differentiate into T helper 1 and T helper 2 cells. What is the function of TH2 cells?
TH2 produce interleukins that help B cells produce immunoglobulins.
312
What interluekins do TH2 cells produce?
1. IL-4.
2. IL-6.
3. IL-13.
313
Name 1 staph and 1 strep that can cause impetigo.
1. Staphylococcus aureus.
| 2. Streptococcus pyogenes.
314
Give 2 examples of protozoa that can cause diarrhoea.
1. Cryptosporidium.
| 2. Giardia lamblia.
315
A patient has profuse vomiting after eating contaminated rice. What bacteria is responsible?
Bacillus cereus.
316
Define dysentery.
An inflammatory disorder of the GI tract associated with blood/pus in the faeces. It is usually due to large intestine disease.
317
A patient complaining of persistent watery diarrhoea is found to have been infected with cryptosporidium. What investigation has been done to reach this diagnosis?
Stool microscopy with Ziehl Neelsen stain can show cryptosporidium oocysts.
318
What empirical antibiotics should be started in someone with a ruptured appendix?
1. Co-amoxiclav.
| 2. Cefuroxime and metronidazole.
319
What antibiotic can be used to kill bacterioides?
Bacterioides are gram negative anaerobic bacilli. Metronidazole is the treatment of choice against anaerobes.
320
Name a bacteria that can cause ascending cholangitis.
Klebsiella pneumoniae.
321
Which people are at risk of cryptosporidium?
1. Children.
| 2. Immunocompromised e.g. HIV positive.
322
How can Salmonella be further classified?
Using the Kauffman White scheme.
323
What is the first line antibiotic for s.pyogenes?
IV benzylpenicillin.
324
What key additional tests need to be performed in someone with MRSA?
1. Echo - to rule out endocarditis.
| 2. Spinal MRI.
325
What is CLED agar?
A non-inhibitory growth medium used to grow common urinary organisms.
326
What colour do the colonies of lactose fermenting organisms e.g. e.coli appear on CLED agar?
Yellow.
327
What colour do the colonies of non-lactose fermenting organisms e.g. pseudomonas appear on CLED agar?
Blue.
328
CLED agar is electrolyte deficient. What is the advantage of this?
It prevents proteus bacteria from 'swarming' and covering the whole plate.
329
Describe the appearance of the meningococcal bacteria on microscopic
examination?
Gram negative diplococci.
(Neisseria meningitidis).
330
What is the first line treatment for meningitis?
Cefotaxime.
331
What would the CSF sample from someone with meningitis look like?
Purulent, cloudy.
Contains inflammatory cells = meningitis.
332
A 9 month child who has not had any vaccinations is found to have meningitis. His CSF is analysed and the gram film shows gram negative coccobacili. What organism has caused the meningitis?
H.influenzae.
Normally children are vaccinated against this.
333
A 1 day old baby is found to have a group B strep infection. What is the most likely source of this organism in this baby?
From the birth canal.
334
Describe the appearance of listeria monocytogenes on a gram film.
Gram positive bacili.
335
Name 3 groups of people who are at risk of listeria monocytogenes infection.
1. Immunocompromised.
2. The elderly.
3. Neonates.
336
Describe the antibiotic therapy for meningitis caused by listeria monocytogenes?
Cefotaxime and amoxicillin.
337
Who should be informed about a case of meningitis? And what other action should be taken?
Public health England should be informed of the case.
| Close contacts should be found and given prophylaxis.
338
What would the CSF cell count look like for viral meningitis?
- High lymphocytes.
- Normal/high protein.
- Normal glucose.
339
What would the CSF cell count look like for bacterial meningitis?
- Raised neutrophils.
- High protein.
- Low glucose.
340
What can cause encephalitis?
- Herpes simplex virus.
- Varicella zoster virus.
- HIV.
341
Name 2 bacteria that give a positive result with the oxidase test.
- Pseudomonas.
| - Neisseria.
342
What layer of the skin is affected in cellulitis?
The sub-cutaneous layer.
343
Name 2 bacteria that can cause cellulitis.
1. S.pyogenes.
| 2. S.aureus.
344
What disease is it important to rule out in someone with cellulits?
DVT!!
345
What is special about mycobacterium TB?
It grows intracellularly!
346
Name 3 species of the plasmodia genus that cause malaria.
1. P. falciparum.
2. P. ovale.
3. P. vivax.
4. P. malariae.
347
How would you test for malarial infection?
Thin (tells you species and parasite count) and thick (low resolution, tells you if you have malaria) blood films.
348
What is the treatment for malaria?
Chloroquine.
349
Name 3 species of the plasmodia genus that cause malaria.
1. P. falciparum.
2. P. ovale.
3. P. vivax.
4. P. malariae.
350
How would you test for malarial infection?
Thin (tells you species and parasite count) and thick (low resolution, tells you if you have malaria) blood films.
351
What is the treatment for malaria?
Chloroquine.
352
How does amoxicillin work?
Inhibits peptidoglycan cross-linking in bacterial cell wall formation.
353
Name an aminoglycoside antibiotic used only in hospitals that works by inhibiting ribosomal activity.
Gentamicin.
354
Name a fluoroquinolone antibiotic which works by inhibiting DNA gyrase. It is effective against intracellular bacteria and gram negative bacteria.
Ciprofloxacin.
355
Name 5 AIDS defining conditions.
1. Oesophageal candidiasis.
2. TB.
3. PCP (pneumocystis jirovecii pneumonia).
4. Recurrent bacterial pneumonia.
5. Kaposi's carcinoma.
6. Hodgkins and Non-Hodgkin's lymphoma.
7. HIV dementia.
356
A child is admitted to hospital with recurring meningitis. Bacterial cultures identify the causative organism as Neisseria meningitides. What is the most likely component associated with this immunodeficiency
Terminal complement deficiency e.g. unable to produce MAC is characterised by chronic neisserial infections - recurrent meningitis.
357
A 42-year-old man with Acquired Immunodeficiency Syndrome (AIDS) develops abdominal pain, bloody diarrhoea and a low grade pyrexia. Sigmoidoscopy shows a friable ulcerated rectal mucosa. Rectal biopsies show severe active chronic proctitis with ‘owls eye’ intranuclear inclusions in endothelial and epithelial cells. What virus is this man likely to be infected with?
Cytomegalovirus.
‘Owls eye’ inclusions are characteristic of CMV infections. The infection persists for life. In patients with HIV/AIDS, the latent virus becomes reactivated and can cause considerable morbidity e.g. colitis, retinitis, ulceration, pneumonitis and encephalitis.
358
What growth medium can be used to culture mycobacteria?
Lowenstein Jensen medium.
359
What organism can cause neonatal sepsis?
Group B streptococci.
