MICROBIOLOGY Flashcards
(382 cards)
1
Q
what is a commensal
A
organism which colonises the host but causes no disease in normal circumstances
2
Q
what is an opportunistic pathogen
A
a microbe which can only cause disease if the host defences are compromised
3
Q
What colour do gram positive bacteria stain
A
Purple
4
Q
What colour do gram negative bacteria stain
A
Pink
5
Q
what are the bacterial names for spheres or rods
A
coccus or bacillus
6
Q
what is the outer membrane of gram positive bacteria like
A
there is a inner membrane, surrounded by a large layer or peptidoglycan which is linked to the phospholipid membrane
7
Q
what is the outer membrane of gram negative bacteria like
A
There is two phospholipid membranes with a periplasmic space in-between containing a thin peptidoglycan layer
8
Q
what type of bacteria is lipopolysaccharide found on
A
found on gram negative bacteria
9
Q
what are the two types of bacterial toxins
A
Endotoxins - Component of the outer membrane of bacteria - LPS on gram negative bacteria
Exotoxins - secreted proteins of gram positive and gram negative bacteria
10
Q
how does bacteria gain genetic variation
A
- Mutation - base substitution, deletion, transfer
- Gene transfer - Transformation (plasmid), Transduction (phage), Conjugation
11
Q
what is the initial classification of bacteria
A
those that bay be cultured on artificial media, and obligate intracellular bacteria
12
Q
What are bacteria that may be cultured on artificial media split into
A
split into those with a cell and those without a cell wall
13
Q
what are the bacteria with a cell wall split into
A
those which grow as single cells and those that grow as filaments
14
Q
what are the bacteria that grow as single cells split into
A
Rods - ZN stain, Gram positive and gram negative
Cocci - Gram positive and gram negative
Spirochaetes
15
Q
what is the gram stain
A
it is where you apply a primary stain (such as crystal violet) to heat fixed bacteria. You then add iodide which binds to the crystal violet and fixes it to the cell wall. You then decolourise with ethanol or acetone and counterstain with safranin (pink)
16
Q
what is the coagulase test used for
A
distinguished S. aureus from other staphylococci (clustered gram positive cocci)
- it is coagulase positive
- if negative S. epidermidis (opportunistic factors)
17
Q
What bacteria would be gram positive cocci growing in
A. Chains
B. Clusters
A
A. Streptococcus
B. Staphylococcus
18
Q
what test do you do to distinguish between staphylococcus bacteria
A
the coagulase (or DNAse) test
- if positive then its S. aureus
19
Q
what test is done to distinguish streptococcus bacteria species
A
the haemolysis test
20
Q
what is seen in the haemolysis test for an alpha haemolytic strep
A
there is partial haemolysis of the blood agar, bacteria uses hydrogen peroxide to oxidise the haemoglobin and the agar appears green
21
Q
if the haemolysis test shows alpha haemolytic strep what other tests are then done
A
the optochin test
- if the bacteria is sensitive then it is S. Pneymoniae
- if the bacteria is resistant it is Viridans strep
22
Q
what bacteria are beta haemolytic strep
A
S. Pyogenes
23
Q
what is seen in the haemolysis test for beta haemolysis strep
A
there is complete lysis of the red blood cells causing the blood agar to appear clear
24
Q
what does gamma haemolysis for the haemolysis test imply
A
that no haemolysis was seen
25
what is the oxidase test
it tests if a microorganism contains a cytochrome oxidase which implies it is able to use oxygen as the terminal electron acceptor
- aerobic
26
why do gram positive bacteria stain purple
Because they retain the colour of the crystal violet stain because they have a thick peptidoglycan layer in their cell wall.
27
what are three ways to classify streptococci
1. Haemolysis
2. Lancefield typing
3. Biochemical properties
28
what is Lancefield grouping
where you group catalyze negative, coagulase negative bacteria, based on the bacterial carbohydrate cell surface antigens
29
what are the important gram positive bacteria to remember
1. S. aureus
2. S. epidermis
3. S. pyogenes
4. S. Pneumoniae
5. Viridans Streptococci
6. C. Diphtheriae
30
what is the main treatment for staphylococcus
flucloxacillin for 3 months
31
what is coagulase
it is an enzyme produced by bacteria that clots blood plasma
32
where is the normal habitat for staphylococci
the nose and skin
33
how is staphylococcus aureus spread
aerosol and touch
34
what are the virulence factors of staphylococcus aureus
Pore-forming toxins
Proteases
Toxic shock syndrome toxin
Protein A
35
what two types of infection can S. aureus produce
1. Pyogenic (pus)
2. Toxin mediated
36
what are two examples of coagulase negative staphylococci
1. S. epidermidis
2. S. saprophyticus
37
what is an example of a gamma haemolysis bacteria
S. mutans
38
what is antigenic sero-grouping used for
its used for beta haemolytic strep only and it looks at carbohydrate cell surface antigens. There are groups A-H and K-V.
- Group A - S. pyogenes
- Group B - S. agalactiae
39
how does the Lancefield microbead agglutination test work
- antibodies made that recognise each group
- these are tagged to tiny plastic beads
- added to suspension of bacteria
- antibodies bind to bacteria and beads clump
- this is visible to the naked eye
40
what are the S.pyogenes virulence factors
. Exported factors = enzymes: Streptokinase, hyaluronidase C5a peptidase
. Toxins = Streptolysins O&S, Erythrogenic toxin
. Surface factors = capsule, M protein
41
what are the tissue systems that S. pyogenes can infect
Respiratory, Skin and soft tissue
- can also cause scarlet fever and complications
42
what bacteria causes scarlet fever
S. pyogenes
43
what percentage of the population have S. pneumoniae as a commensal
about 30%
44
what factors can predispose you to catch S. pneumoniae
- impaired mucus trapping
- hypogammaglobulinemia - low serum immunoglobulin
- asplenia - absence of a spleen
- HIV
45
what are S. pneumoniae virulence factors
1. Capsule
2. Inflammatory wall constituents
3. Cytotoxin
46
what are examples of aerobic gram positive bacilli
1. Listeria monocytogenes
2. Bacillus anthracis
3. Corynebacterium diphtheriae
47
what are examples of anaerobic gram positive bacilli
Clostridia
1. C. tetani
2. C. botulinum
3. C. difficile
48
what are the four major groups of gram negative bacteria
1. Proteobacteria - rod shaped
2. Bacteroides - rod shaped
3. Chlamydia - round pleiomorphic
4. Spirochaetes - spiral/helical
49
what are the sterile sited of the body (should normally have no bacteria/pathogens)
1. Blood
2. CSF
3. Pleural fluid
4. Peritoneum
5. Joints
6. Urinary tract
7. Lower respiratory tract
50
what are pathogenicity determinants
any product or strategy which contributes to the pathogenicity or virulence
51
what are pathogenicity determinants of gram negative bacteria
1. colonisation factors: adhesins, invasins, nutrient acquisition, defence against host
2. Toxins
52
what is found in blood agar
sheep or horse blood
53
what is chocolate agar
blood agar which has been cooked for 5 minutes at 80oC to release some of the nutrients (allows more organisms to grow)
54
what is the function of CLED agar
it is cysteine lactose electrolyte deficient - used for urinary bacteria analysis
55
what is MacCONKEY agar
it contains natural red dye and lactose. Differentiates between lactose fermenting gram negative bacteria (E.Coli turns it pink)
and non lactose fermenters (salmonella, shigella)
56
what is gonococcus agar used for
for Neisseria culture
57
what is XLD agar used for
to differentiate between salmonella and shigella (salmonella red with black centres and shigella red only)
58
what is sabourard agar used for
for fungal culture
59
what bacteria would you be looking at down the microscope if its was purple and
A. in clusters
B. in chains
A. staphylococcus
B. Streptococcus
60
other than the coagulase test what's another was to differentiate S. aureus from other staphs
culture of blood agar, S. aureus colonies are gold while other staphs are colourless (white)
61
What are the mycobacteria of medical importance
- M. tuberculosis - tuberculosis
- M. leprae - leprosy
- M. avium - disseminated infection in AIDS
- M. kansasii - chronic lung infection
- M. marinum - fish tank granuloma
- M. ulcerans - buruli ulcer
- rapid growing myobacteria for skin and soft tissue infection
62
what are the features of mycobacteria
they are aerobic, non-spore forming, non motile bacilli
63
what do mycobacteria show on gram stain
weakly positive (or colourless)
64
can mycobacteria survive in harsh environments
yes, they can survive within macrophages even within a low pH environment
65
what is the reproduction time for mycobacteria
slow 0 M tuberculosis generation time is 15-20 hours. This means they are also slow growing and slow at responding to treatment
66
what stain can be used for mycobacteria which are resistant to gram stain
acid fast test - stain used to identify organisms with wax like thick cell walls
67
how are mycobacteria diagnosed
they are diagnosed using nucleic acid amplification such as PCR
68
are gram positive bacteria mostly cocci or bacilli
cocci
69
are gram negative bacteria mostly cocci or bacilli
bacilli
70
what patients might get opportunistic infections
those on immunosuppressant drugs, those with immunocompromise and those with a breakdown of host defences
71
what are the common spiral bacteria
vibrios, spirilla and spirochaetes
72
what is blood agar used for
commonly for streptococcus
73
what is chocolate agar used for
fastidious neisseria
74
what environment do gram positive bacteria prefer
dry, dusty environments. skin colonisers and spread by breathing in shed skin cells
75
what environment do gram negative bacteria prefer
wet, damp environments where the majority prefer to colonise mucous membranes
76
what is the catalase test used for
to differentiate between staphylococcus and streptococcus
77
what bacteria would it be if it was catalase positive
staphylococcus
78
what is the method for the catalase test
apply hydrogen peroxide to a small simple colony and if it bubbles then it is positive
79
what lancefield group is S. pyogenes
group A
80
how quickly do symptoms appear with CAP
they occur after LESS than 48 hours in the hospital
81
what is the common cause of CAP
S. Pneumoniae
82
what is treatment for CAP
amoxicillin first line, co-amoxiclav in unwell
83
how quickly do symptoms appear with HAP
symptoms occur after MORE than 48 hours in the hospital
84
who are the most likely to get HAP
People on ventilators, stroke, long stays, infection contact
85
what are the most likely causes of HAP
E. coli, Klebsiella pneumoniae, Enterobacter spp, pseudomonas aeruginosa, MRSA, streptococci
86
what is the treatment for HAP
guided by microbiology, often IV co-amoxiclav and gentamicin
87
what are the gram positive rods you need to know
- Anaerobic: Clostridium Spp (difficile and perfingens)
- aerobic: Bacillus spp and Corynebacterium
88
what are the medications for C. difficile
The 4 C's
- Clindamycin
- Cephalosporins
- Co - amoxiclav
- Ciprofloxacin
89
what are symptoms of C. difficile
diarrhoea, fever, abdominal pain, Hx of Ab
90
what is the pathological basis of meningitis
there is inflammation of the pia and arachnoid mater - microorganisms infect the CSF
91
what are symptoms of meningitis
stiffness of the neck, photophobia and severe headache.
infective: fever and malaise
Petechial rash associated with meningococcal meningitis
92
what is the treatment for meningitis
Bacterial: start on antibiotics before tests come back
- cephalosporins: IV cefotaxime/IV ceftriaxone
- if over 50 or immunocompromised add IV amoxicillin to cover listeria
- one oral dose of ciprofloxacin
Meningococcal septicemia: immediate IM benzylpenicillin in community and IV cefotaxime in hospital
Viral: supportive treatment
93
What are the oxidative positive gram negative rods
Indole negative: if its motile its pseudomonas aeruginosa
Indole positive: Haemophiles influenzae
94
what can pseudomonas aeruginosa cause
CF lung infection
Diabetic foot
burn infections
UTI
95
what can haemophilus influenzae cause
septic arthritis
CODP exacerbations
pneumonia
96
what are the oxidase negative gram negative rods
Bordetella pertussis (whooping cough)
Enterobacteria - non lactose fermenting and lactose fermenting
97
what are the non lactose fermenting enterobacteria
1. proteus mirabilis - UTI
2. Shigella spp - gastroenteritis
3. salmonella spp
4. S. typhi - typhoid fever
98
what are some lactose fermenting enterobacteria
1. indole positive E. coli - UTI, gastroenteritis, abdominal infection
2. Indole negative Klebsiella pneumoniae - UTI, abdominal infections, CF lungs
99
how can a UTI occur
certain bacteria and yeasts can enter the renal tract via the renal artery. Infection can also gain access via the urethra, with incompetence of the cysto-ureteric valves allows organisms to enter the upper urinary tract. organisms can then ascend the urethras to the kidneys
100
what are the symptoms of lower UTI
dysuria, urgency, frequency, cloudy or foul urine, haematuria, suprapubic tenderness
101
what are the symptoms of upper UTI
fever, confusion, loin tenderness
102
what are the common microorganisms that cause UTI
Klebsiella, E. coli, Enterococcus, proteus, S. saprophyticus
103
what is the most common cause of UTIs
85 - 90% of cases are E. coli
104
what is the treatment for UTIs
Oral nitrofurantoin or trimethoprim
in pregnancy give cefalexin
105
what are characteristics of viruses
Non - cellular structure
Consist of an outer protein coat and a strand of nucleic acid (DNA or RNA)
come in a variety of shapes
do not carry out metabolic reactions on their own
106
what is the process of viral replication
1. viral attachment: viral and cell receptors
2. cell entry; only central viral core carrying the nucleic acid and some associated proteins enter the host cell
3. Interaction with host cells: use cell materials (enzymes, amino acids, nucleotides) for their replication
4. Replication: may localize in nucleus, cytoplasm or both
Assembly: occurs in nucleus, in cytoplasm or at cell membrane
5. Release: bursting open of cell, or by leaking from the cell over a period of time
107
how do viruses cause disease
1. damage by direct destruction of host cells
2. damage by modification of host cell structure or function
3. damage involving over reactivity of the host cell as a response to infection
4. damage through cell proliferation and cell immortalization
5. evasion of both extracellular and intracellular host defences
108
what is the infectivity of a pathogen
the ability to become established in a host, can involve adherence and immune escape
109
what is a pathogens virulence
the ability to cause disease once established
110
what is required for a virus to infect someone
1, a rapid cell entry
2. correct receptors
3. evasion of immune cells
the ability to replicate and pass on
111
what is antigenic drift
spontaneous mutations, occur gradually giving minor changes in surface proteins such as haemaglutinin and neuraminidase in influenza. Epidemics
112
what is antigenic shift
sudden emergence of new subtype different to that of preceding virus. Pandemics
113
what are different ways bacteria can invade a host
respiratory tract
gastrointestinal tract
genitourinary tract
skin break
114
what immune responses are mounted against protozoan infection
depends on where the infection is
in blood there will be humoral immunity
in the tissues it will be cell mediated immunity
115
how is malaria spread
by the female anopheles mosquito bite
116
how do protozoa evade the immune system
1. surface antigen variation - different genes which can be switched on or off and mean that surface antigens can change
2. intracellular phase
3. outer coat sloughing - removed and replaced with a new one
117
what are features of helminth infection
1. they dont multiply in humans
2. they are not intracellular
3. few parasites carried
4. poor immune response - immune evasion
5. immune response not sufficient to kill
118
how to worms evade the immune response
decreased antigen expression by adults and they have a host derived glycolipid/glycoprotein coat
119
what is passive immunisation
where a preformed antibody is transferred
- transplacental
- colostrum
- injecting preformed antibody
120
what are the 5 major groups of protozoa
flagellates, amoebae, sporozoans, ciliates, microsporidia
121
what are features of flagellates
they have flagellum as the main way to move about, they usually reproduce by binary fission and they are found in intestine (can be elsewhere)
122
what are the features of amoeba
they move by means of flowing cytoplasm and production of pseudopodia
123
what are features of sporozoans
they have no locomotory extensions and are the most intracellular parasite. they reproduce by multiple fission
124
what is the most common sporozoan protozoa
malaria
125
what are features of ciliate protozoa
they have cilia that rhythmically beat at some stage so they can move. they have two types of nuclei, macro and micronucleus
126
what are features of microsporidia
they produce resistant spores, they have a unique polar filament which is coiled inside a spore
127
what are the 5 species of malaria
P. falciparum
P. orale
P. vivax
p. malariae
p. knowlesi
128
what is the most common type of malaria infection and the most deadly
P. falciparum
129
what are the clinical features of malaria
Very varied
Fever !!!!!!!!!!!!!!!!!!!!!!!!!
Other common;
Chills and sweats
Headache
Myalgia
Fatigue
Nausea and vomiting
Diarrhoea
These acute symptoms common to all 4 species
130
what is the lifecycle of malaria
1. mosquito has blood meal and takes in gametocytes of malaria (in gut of the mosquito)
2. sporozoites are released an migrates to salivary glands to mosquito
3. in its saliva it injects sporozoites into human host
4. migrates to liver cell and proliferates
5. bursts and ruptures into blood stream
6. in the blood stage the new trophocytes are made - infection of RBC, proliferating, bursting out
7. some become gametocytes to be taken up by another mosquito
131
what are symptoms of tuberculosis
night sweats, cough, hemoptysis, weight loss and malaise
132
what are treatments for tuberculosis
isoniazid, ethambutamol, rifampicin and pyrazinamide
133
what is the side effect of isoniazid
numb or tingly extremities
134
what is a side effect of ethambutamol
ocular side effects
135
what is a side effect of rifampicin
orange or red urine
136
what is a side effect of pyrazinamide
arthralgia
137
what types of bacteria CANT you use gram stain on
Mycobacteria, actinomycetes and parasite cryptosporidium as they have waxy lipid cell walls
138
what stain is used on bacteria that you cant gram stain
the Ziehl-Neelson stain
- heating the sample with strong dye (carbol fuchsin)
139
what are the two forms of fungi
yeast - single cells that divide by budding
moulds - multicellular hyphae or spores
140
what is the fungal cell wall made of
chitin and glucan
141
what is the treatment for fungal infection
antifungals - they tend to target the cell wall or the plasma membrane but they dont work incredibly well
- generally quite difficult to treat
142
what are features of fungus Candida albicans
it is the most pathogenic Candida spp
- vaginal and oral infections and cause sepsis (candidiasis)
- can also cause line or catheter infections
- can kill rapidly
143
What are the features of fungus Aspergillus fumigatus
it is the most pathogenic Asp. spp.
- predominantly causes lung infections and allergic disease
- poor prognosis but it kills slowly
144
what are the three subclasses of antibiotics
1. Cell wall synthesis
2. Nucleic acid synthesis
3. Protein synthesis
145
what are the different antibiotics which affect cell wall synthesis
1. Beta lactams - penicillins, cephalosporins, carbapenems, monobactams
2. Vancomycin
3. Bacitracin
4. cell membrane - polymyxins
146
what are the different antibiotics which affect nucleic acid synthesis
1. folate synthesis - sulfonamides, trimethoprim
2. DNA gyrase - quinolones
3. RNA polymerase - rifampin
147
What are different antibiotics which affect protein synthesis
1. 30S subunit affecting - tetracyclines, aminoglycosides
2. 50S subunit affecting - macrolides, clindamycin, linezolid, chloramphenicol, streptogramins
148
what is the cell wall affecting antibiotic mechanism of action
beta lactams bind covalently and irreversibly to the penicillin binding proteins. The cell lysis is disrupted and lysis occurs. this results in bacterial death
149
what is the most common cell wall affecting antibiotics
beta lactams
150
are gram negative or positive bacteria more susceptible to beta lactams
gram positive bacteria as they have thick walls making them more vulnerable
151
how do nucleic acid synthesis affecting antibiotics work
they prevent production of folic acid synthesis - cant make thymidine or purines
they affect the enzymes that are required for DNA replication
152
when are macrolides used (antibiotics affecting protein synthesis)
they will be used in respiratory infection, and when people are allergic to penicillin
153
what are the different antibiotic resistance mechanisms
1. efflux pumps
2. inactivating enzymes
3. alternative enzymes used
4. decreased uptake
5. target alterations - changes in gene/protein shape
154
what are the three specific examples of antibiotic resistance
1. Beta lactamase producing bacteria = resistant to penicillin derived Ab
2. MRSA carries mecA which is a unique transpeptidase that is not inhibited by beta lactams.
3. Efflux pumps
155
what is the minimum inhibitory concentration
the minimum antibiotic that will inhibit bacterial growth
156
what can be given for a toxin producing bacteria
you can use protein inhibitory antibiotics
157
how do you determine the minimum inhibitory concentration
Multiple tubes which contain the bacteria, tubes that have solution that promote growing and into these you add in different amounts of antibiotic
- from this you can work out at what concentration of antibiotic the bacteria cant grow
158
what two things are important for a drug to work
- concentration of the drug in use
- time
159
What is time dependent killing
key parameter is the time that serum concentrations remain above the MIC during dosing
160
what drugs use time dependent killing
- beta lactams
- clindamycin
- macrolides
- oxazolidinones
161
what is concentration dependent killing
the key parameter is how high the concentration is above the MIC
162
what drugs use concentration dependent killing
- aminoglycosides
- quinolones
163
whats important when considering distribution to the site of infection
some sites of infection dont have a blood supply
- pus doesnt have a blood supply and so it can go to the outside and will have to diffuse in
- heart valves
164
how do bacteria develop intrinsic resistance
this is where the bacteria is naturally resistant to something, all subpopulations are affected equally
165
how can bacteria acquire mutations
- spontaneous gene mutation - single point mutations
- conjugation
- transformation - free DNA taken up and integrated
- transduction - viruses (bacteriophage) move genes from one bacteria to another
166
what are the two resistance gram positive bacteria to be aware of
MRSA - mecA gene which confers resistance to beta lactams
VRE - plasmid mediated acquisition of gene preventing vancomycin binding
167
what are the 5 known hepatitis viruses that infect the liver
1. Hepatitis A - RNA
2. Hepatitis B - DNA
3. Hepatitis C - RNA
4. Hepatitis D - RNA
5. Hepatitis E - RNA
168
how is hepatitis A and E spread
fecal - oral transmission
169
How is hepatitis B, C and D spread
blood to blood transmission
170
what is acute viral hepatitis
when there is viral hepatitis which ends with complete resolution
171
what is chronic viral hepatitis
prolonged course of active disease or silent asymptomatic infection
172
what hepatitis viruses can cause chronic infection
HBV, HCV, HDV
173
what are features of acute viral hepatitis
- fatigue, fever, muscle or joint ache, cough, runny nose
- 1-2 weeks in you will develop jaundice bilirubin levels
- hepatic cell death
- liver function decreases (seen on LFT)
- can cause ALT and AST to elevate very high
174
what are the symptoms of Hep A
incubation 3 to 4 weeks
- fever, anorexia, nausea, vomiting and jaundice
- dark urine, pale feces, elevated transaminase levels
- most cases resolve in 2-4 weeks
175
how do you diagnose Hep A
- Liver function tests: high AST and ALT levels
- serology: detection of anti- HAV IgM and will remain positive for 3-6 months
176
What are the three main antigens for HBV
1. HBsAg - surface antigen
2. HBcAg - Core antigen
3. HbeAg -e antigen - indicator of transmissibility
177
what are the 3 clinical stages of HBV
1. acute hepatitis
2. fulminant hepatitis - severe acute hepatitis, rapid liver destruction
3. chronic hepatitis: asymptomatic carrier, chronic-persistent hepatitis and chronic active hepatitis
178
what does it mean if patient has HBsAg present
means that there is a LIVE virus and infection, either acute, chronic or carrier
179
what does the presence of high HBeAg suggest
high infectivity and active disease
180
what are the possible complications of Hep B
- HDV co-infection
- Hepatocellular carcinoma
- end stage liver disease/cirrhosis
181
how long is the incubation period of hepatitis C
6-12 weeks
182
what is the clinical features of Hep C
- often asymptomatic
- symptoms; malaise, nausea, upper right quadrant pain, fever, anorexia, nausea, vomiting and jaundice
- chronic carrier state occurs more often with HCV than HBV
- significant autoimmune reactions: vasculitis, arthralgias, purpura, glomerulonephritis
183
how is infection with HCV diagnosed
antiHCV antibodies
184
how is a positive HCV result confirmed
measured with HCV viral RNA
185
how do you treat HCV
peginterferon alfa decreases patients who become carriers
- Patients with chronic infection are advised to reduce alcohol consumption, and this is monitored with alpha fetoprotein levels
- most common HCV treatment is direct acting antivirals
186
what are the features of HDV
- it cant replicate by itself because it doesnt have the gene for its envelope protein, it can only replicate when the person is also infected with HBV
187
what is the difference between acute and chronic diarrhoea
- acute lasts less than two weeks
- chronic - persists more than four weeks
188
what is acute diarrhoea categorised as
1. noninflammatory (watery and non bloody)
2. inflammatory (bloody); dysentery
189
what are risk factors for developing diarrhoea
- patients taking PPI
- recent travel to developing countries
- antibiotic treatment
- immunosuppressed patients
190
what diarrhoea causing pathogens secrete exotoxins
staphylococcus aureus, bacillus cereus and clostridium perfringens
191
what pathogens cause non inflammatory acute diarrhoea by enterotoxin production
Enterotoxigenic Escherichia coli (ETEC)
Vibrio cholerae
192
what are pathogens that cause acute inflammatory diarrhoea
- Salmonella
- Shigella
- Campylobacter
- shiga toxin producing E. coli
- C. difficile
193
what bacteria can cause pseudomembranous colitis through antibiotic use
C. difficile
194
what does vomiting and diarrhoea indicate
suggests infection with S. aureus food poisoning or viral gastroenteritis
195
what bacteria cause acute non inflammatory diarrhoea
- staphylococcus aureus
- bacillus cereus
- ETEC
- listeria monocytogenes
- vibrio cholerae
- norovirus
- giardia lamblia
196
where are the most common sites for cellulitis to occur
legs, face and arms
197
what are risk factors for developing cellulitis
skin wounds, diabetes, bits, elderly, swollen legs, immunosuppression
198
what are the causative organisms of cellulitis
- beta hemolytic streptococci are common (S. pyogenes and streptococcus agalactiae)
- staphylococcus aureus
199
how does cellulitis present
- symptoms spread quickly
- erythema
- pain, swelling and warm to the touch
- associated wound such as an ulcer, bite or injection
- can have fever malaise and systemic signs
200
what is treatment for cellulitis
- elevate and mobilize limb
- washout wounds
- empiric treatment with IV flucloxacillin or clindamycin
- vancomycin, teicoplanin, linezolid or daptomycin are indicated for MRSA cellulitis
201
what is necrotizing fasciitis
it is a necrotizing infection of the deep structures of the skin including the underlying fascia
202
what are the causes of necrotizing fasciitis
break in the skin allows passage of the organism to deeper structures. Infection of the fascial layer results in thrombosis of the vascular supply and adjacent nerves. this manifests as necrosis and anaesthesia of more superficial layers
203
what pathogens can cause necrotizing fasciitis
- type 1: due to both aerobic and anaerobic organisms
- type 2: Usually due to streptococcus pyogenes. Others: V. vulnificus clostridium perfringens
204
how does necrotizing fasciitis present
- erythema, warmth and tenderness; pain out of proportion with findings
- skin changes often spread and progress quickly
- skin hypoperfusion, grey-blue colouring, loss of sensation
- signs and symptoms of systemic infection
- Fournier's gangrene if male
205
how is necrotizing fasciitis diagnosed
using surgery, confirmed by exploration and debridement
- microbiology; gram stain and culture
206
how do you treat necrotizing fasciitis
emergency surgery
empirical therapy: broad- piperacillin-tazobactam plus clindamycin
S. pyogenes causative; penicillin and clindamycin
207
what pathogens can cause appendicitis
1. normal colonic gut flora
2. Escherichia coli
3. Peptostreptococcus
4. Bacteroides fragilis
5. pseudomonas
208
how is appendicitis treated
surgery
management with antibiotics - metronidazole and cefoxitin
209
what is diverticulitis
it is inflammation of the diverticula (sac like protrusion of the colonic wall usually around the sigmoid colon)
210
what is acute diverticulitis
it is uncomplicated and common in the elderly and those with extensive disease
211
what is complicated diverticulitis
it is acute diverticulitis with one of the following:
1. abscess
2. colovesical or colovaginal fistula
3. perforation
4. obstruction
212
what pathogens can cause diverticulitis
bowel flora
- B. fragilis and E. coli are typically involved
213
how does diverticulitis present
dull aching pain in the lower left quadrant
low grade fever with nausea and vomiting
diarrhoea or constipation may be present
- if there has been perforation then there will be diffuse abdominal pain and shock
214
how do you treat diverticulitis
uncomplicated - co-amoxiclav, ciprofloxacin plus metronidazole
complicated; piperacillin-tazobactam
215
what is osteomyelitis
it is a bone or bone marrow infection with can occur in both adults and children. it can be acute or chronic
216
what pathogens can cause osteomyelitis
- most commonly caused by staphylococcus aureus
- IVD users; pseudomonas, E. coli
- Sickle cell patients; Salmonella
- hip of knee prosthesis: staphylococcus epidermis
217
how does osteomyelitis present
- pain around the infected region
- swelling, tenderness, warmth and erythema
- can be associated with systemic signs such as fever or tiredness
- chronic can have sinus tracts or within ulcers
218
how is osteomyelitis diagnosed
blood tests; raised white blood cell count and inflammatory markers
CT or MRI
X-ray after two weeks
bone or percutaneous biopsy
219
how do you treat osteomyelitis
surgery with antibiotics
- flucloxacillin and fusidic acid
- vancomycin and cefotaxime
220
what is septic arthritis
an infection of the joints
- organisms reach joint via blood
221
what are risk factors of septic arthritis
old age, diabetes mellitus, rheumatoid arthritis, prosthetic joint, recent joint surgery, skin infections or ulcers, intra-articular corticosteroid infection, injection drug use, alcoholism
222
what pathogens can cause septic arthritis
- most common cause is staphylococcus aureus
- young sexually active adults - Neisseria gonorrhoeae
- prosthetic hip or knee joints - s. epidermis
- IVD users; P. Aeruginosa
223
how does septic arthritis present
acute onset of an inflamed joint
fever is often present
- joint is red, warm, swollen, painful
224
how do you diagnose septic arthritis
- raised WBC and inflammatory markers
- ultrasound
CT/MRI
225
what is the treatment for septic arthritis
drainage of the joint urgently and removal or prosthetic if it is infected
- flucloxacillin or vancomycin
- vancomycin in staph aureus
- ceftriaxone in N. gonorrhoeae
226
what is the most common bacterial STI
Chlamydia
227
what is the pathogen that causes chlamydia
chlamydia trachomatis
228
what is the presentation of chlamydia in men
urethritis
testicular pain
- 50% of cases are asymptomatic
229
what is the presentation of chlamydia in women
vaginal discharge
post coital bleeding
intermenstrual bleeding
lower abdominal or pelvic pain
- 80% of cases asymptomatic
230
what are complications of chlamydia
Pelvic inflammatory disease
infertility
reactive arthritis
epididymo-orchitis
231
how id chlamydia diagnosed
NAAT - vaginal swabs, urethral swabs and first catch urine samples
232
how do you treat chlamydia
avoid sexual intercourse until treatment finished
screening for other STIs
antibiotics - doxycycline or azithromycin
alternatives: erythromycin or ofloxacin
in pregnancy doxycycline is contraindicated
- contact trace
233
what is the pathogen that causes Gonorrhoea
Neisseria gonorrhoea
234
how does ghonorrhoea present
- asymptomatic
in men: urethritis, purulent discharge and dysuria
in women: pelvic pain, vaginal discharge, itch, dysuria
235
how do you diagnose gonorrhoea
NAAT; first line screen
microscopy showing gram negative diplococci
236
what type of bacteria is Neisseria gonorrhoea
Gram negative diplococci
237
what is the treatment for gonorrhoea
antibiotics: ceftriaxone single dose plus azithromycin single dose
238
what pathogens cause viral meningitis
- enteroviruses (echoviruses, coxsackieviruses, polioviruses)
- herpes simplex virus
239
how does viral meningitis present
influenza like illness followed by meningism (stiff neck, headache, photophobia)
fever and non specific signs may also be present
240
how do you diagnose viral meningitis
lumbar puncture: CSF microscopy, PCR
- viral culture can be taken
241
what treatment is given for viral meningitis
no specific antiviral therapy
Supportive: analgesics, antipyretics, hydration
Acyclovir for herpes simplex virus
242
what bacteria causes bacterial meningitis
- Neisseria meningitidis
- Haemophilus influenzae
streptococcus pneumoniae - most common in young and old
243
how is neisseria meningitidis spread
spread by the respiratory route or via bloodstream
244
how does bacterial meningitis present
- usually rapid onset, headache, fever, meningism
- cerebral dysfunction
- seizures
- focal neurological deficits (cranial palsies)
- papilledema
- non blanching rash
245
how do you treat bacterial meningitis
- blood culture performed urgently
- lumbar puncture unless contraindicated (low glucose and increased protein
- physical examination
246
what is the treatment for bacterial meningitis
benzylpenicillin or cefotaxime/ceftriaxone
- vancomycin if resistant strep. is suspected
- steroids
247
what condition gives you protection against malaria
sickle cell trait (HbS) is protective
248
what pathogens cause malaria
1. P. falciparum: 80% of cases, highest mortality
2. P. vivax
3. P. ovale
4. P. malariae
5. P. knowlesi
249
how does malaria spread
humans acquire malaria from sporozoites transmitted by the bite of the female anopheles mosquito.
sporozoites travel through the bloodstream and hepatocytes
they mature into tissue schizonts which rupture and release merozoites into the bloodstream
they invade RBC and release more merozoites
some divide into sporozoites which can then be taken up by mosquito
250
how does malaria present
- fever and sweats; cyclical or continuous with spikes
- anemia; erythrocyte hemolysis
- hepatosplenomegaly
- complications; cerebral malaria, jaundice, kidney injury, acidosis
251
how do you diagnose malaria
- thick and thin blood smears; Field's or Giemsa stain
- lab findings; haemolytic anemia, thrombocytopenia, uremia, hyperbilirubinemia, abnormal LFTs, coagulopathy
252
what is the treatment for malaria
- quinoline derivatives (chloroquine, quinine)
- antifolates and ribosomal inhibitors - tetracycline, doxycycline
253
what is the cause of tuberculosis
mycobacterium tuberculosis
254
what is the pathogenesis of primary TB
- inhalation of M. tuberculosis results in mild reaction in lung
- alveolar macrophages phagocytose the pathogen
- some bacilli survive and multiply within the macrophages and are carried to the hilar lymph nodes
- the local lesion and lymph nodes are called the primary complex
- immune cells form a granuloma lesion
- in many individuals immune system kills the bacteria and the lesion becomes fibrotic and calcified
- in a small number of cases the TB isnt killed and is dormant
- in some patients TB spreads and invades the blood to other organisms - miliary TB
255
what is the pathogenesis of secondary TB
1. dormant TB reactivates often in those immunocompromised
2. a patient may become re-infected after further exposure
256
how does tuberculosis present
fever, night sweats
pleuritic chest pain and dyspnea
cough
fatigue, arthralgia, weight loss
257
how do you diagnose TB
sputum smear microscopy - acid fast bacilli
mycobacterial culture
chest x-ray and ultrasound
elevated ESR, SCR, anemia
tuberculin skin test shows latent TB
258
what is the treatment for tuberculosis
- for drug susceptible pulmonary TB; 2 month initiation phase with rifampicin, isoniazid, pyrazinamide, ethambutol, followed by 4 months of rifampicin and isoniazid
259
what are the 4 classifications of pneumonia
1. community acquired pneumonia
2. hospital acquired pneumonia
3. pneumonia in immunocompromised individuals
4. aspiration pneumonia
260
what are the risk factors for community acquired pneumonia
- extremes of age
- smoking
- COPD
- diabetes
- cardiovascular disease
- severe recurrent illness
- recent anesthetic or intubation
- immunosuppression
261
what pathogens cause CAP
- mycoplasma pneumoniae
- H. influenza
- strep. pneumoniae
- pneumocystis jiroveci in HIV/AIDS patients
- respiratory syncytial virus in young children
262
how does CAP present
sudden onset of chills, fever, cough, sputum, pleuritic chest pain, fatigue, anorexia and sweats. Tachypnoea, tachycardia and postural blood pressure may drop
- elderly may present as confused, with abdominal pain and nausea
263
how do you diagnose CAP
- sputum specimens for culture and microscopy
- blood cultures
- urine antigen detection for pneumococcal and legionella
- PCR for viral, mycoplasma, chlamydia and Coxiella infections
- bronchoalveolar lavage
- chest X-ray
- severity score of results
264
how do you treat CAP
- IV fluids and oxygen
- amoxicillin for non severe
- clarithromycin plus co-amoxiclav for severe
- once organism is identified you can give specific treatment
265
how do you treat S. pneumoniae CAP
amoxicillin or benzylpenicillin
266
how do you treat M. pneumoniae CAP
erythromycin or clarithromycin
267
how do you treat C. pneumoniae CAP
erythromycin or clarithromycin
268
how do you treat C. psittaci CAP
doxycycline
269
how do you treat C. burnetti CAP
doxycycline
270
how do you treat Legionella spp. CAP
clarithromycin (and rifampicin)
271
what is an antimicrobial agent
a substance with inhibitory properties against microorganisms, but with minimal effect on mammalian cells
272
what is an empirical therapy
it refers to the antimicrobial regimen used when a clinical diagnosis of infection has been made and delay in initiating therapy to await microbiological results would be inappropriate
273
what is pathogen susceptibility
the level of vulnerability of a microorganism to an antimicrobial
274
what are examples of beta lactams
penicillin, cephalosporins, monobactams, carbapenems
275
when are carbapenems used
they have broad spectrum activity and are generally used for treatment of severe infections of for infection caused by multiply resistant bacteria
276
what are glycopeptides
they are bactericidal for gram positive bacteria and have no activity against gram negative.
- vancomycin and teicoplanin
277
what is the mode of action of aminoglycosides
they inhibit protein synthesis via 30s ribosome inhibition
278
what problems can aminoglycosides cause
hypersensitivity, ototoxicity and nephrotoxicity
279
what are some side effects of vancomycin
can occasionally cause nephrotoxicity and ototoxicity
rapid infusion can cause erythematous rash
280
what is the action of tetracyclines
they inhibit the 30s ribosome subunit
- treat infections caused by Mycoplasma spp., rickettsia spp. coxiella burnetiid and chlamydia trachomatis
281
what are side effects of tetracycline
gastrointestinal intolerance
282
what is the mechanism of action for macrolides
they inhibit protein synthesis of the 50s subunit
- used for strep and staph soft tissue infections and resp infections including those caused by mycoplasma pneumoniae
283
what are examples of macrolides
clarithromycin, azithromycin and erythromycin
284
what is clindamycin useful against
anaerobes
285
what is the mechanism of action of clindamycin
it inhibits the 50s ribosome subunit
- associated with pseudomembranous colitis
286
what is fusidic acid used for
active against staphylococci (combine with flucloxacillin for serious staph infections0
- Inhibits protein synthesis
287
what are quinolones used for
inhibition of nucleic acid synthesis and function
- e.g ciprofloxacin, ofloxacin, norfloxacin
288
what are side effects of quinolones
gastrointestinal disturbances - photosensitivity, rashes, neurological disturbances
289
what is trimethoprim used for
- UTIs
inhibits folic acid synthesis
290
what is metronidazole used for
anaerobic infections - dysregulates DNA synthesis
291
what is nitrofurantoin used for
uncomplicated UTIs
292
what are the stages of the viral life cycle
1. attachment
2. entry
3. genome release
4. transcription
5. translation
6. genome replication
7. assembly
8. exit
293
what are the different ways viruses cause disease
1. direct destruction of host cells
2. modification of host cells
3. over reactivity of immune system
4. damage through cell proliferation
5. evasion of host defences
294
give an example of a virus that causes direct destruction of host cells
Polio virus causes host cell lysis and death after viral replication
the lysis of neuron cells leads to paralysis
HIV lyses CD4 t cells
295
give an example of a virus that causes modification of its host cell
rotavirus atrophies villi and flattens epithelial cells which means sugars cant be absorbed and hyperosmotic state leads to diarrhoea
296
give an example where a virus causes over reactivity of the immune system
the immune system response to HBV during chronic infection results in low level liver cell destruction leading to cirrhosis
297
give an example where a virus causes damage through cell proliferation
human papillomavirus integrated into cervical epithelial cells, expresses oncoproteins which can lead to the over proliferation of cells and cervical cancer
298
give an example where a virus evades host defences and causes disease
varicella zoster virus can lay dormant after chicken pox and can reactivate later as shingles
299
what are the different ways to diagnose viral infection
PCR, serology, histopathology
- less used is viral culture, light microscopy and electron microscopy
300
what type of virus is HIV
retrovirus
301
what type of cell does HIV infect
it infects CD4 T cells and macrophages
- transmits in bodily fluids
302
what is the treatment for HIV
Highly acting anti-retroviral therapies (HAART)
303
what are protozoa
microscopic unicellular eukaryotes
304
how are protozoa classified
classified on movement:
ameoboids, ciliates, sporozoan, flagellates
305
what type of malaria can go dormant in the liver causing relapse
P. vivax
P. ovale
306
what are the four major groups of gram negative bacteria
1. proteobacteria - all are rod shaped
2. bacteroids - rods shaped
3. chlamydia - round pleiomorphic
4. spirochaetes - spiral/helical
307
what are the direct ways one can diagnose bacterial infection
- gram stain
- acid fast stains
- wet film
- KOH (fungi)
- india ink
308
what are cultures you can do to diagnose bacterial infection
- solid media
- liquid culture
- blood culture
309
what is the difference between yeast and mould
yeasts are small single cell organisms that divide by budding
moulds form multicellular hyphae and spores
310
what are dimorphic fungi
where some fungi exist as both yeasts and moulds switching between the two when conditions suit them
311
how do you treat fungal disease
more difficult to treat fungi because they are eukaryotic cells
- the aim of antimicrobial therapy is to achieve inhibitory levels of agent at the sit of infection without host cell toxicity
312
what are the different classes of vaccine
inactivated - killed
attenuated
toxoid vaccines
proteins - components of pathogen
313
what are the key components of infection prevention and control
- infection prevention and control team
- ward teams
- microbiology/virology labs
- trust management
- estates
- domestic services
- pharmacy
314
what are the different infection control policies
MRSA policy
Tuberculosis policy
medical equipment management manual
single use items
outbreak control plan
315
when do you need to wash your hands in a hospital
- before and after handling patients/ clients
- after handling any item that is soiled
- after using the toilet
- before and after an aseptic procedure
- after removing protective clothing including gloves
316
when should use alcohol gel
- following hand washing, prior to a ward based invasive procedure
- following hand washing, when caring for a patient with barrier precautions
317
when would you were PPE
must be worn by all staff, whatever their role or grade, when there is a risk of contamination to the person or their clothing
318
what is an endogenous infection
infection of a patient by their own flora
- important in hospitalised patients, especially in those with invasive devices or surgical patients
319
how do you prevent endogenous hospital acquired infection
good nutrition and hydration
antisepsis/skin prep where indicated
control the underlying disease - drain pus, remove lines and catheters as soon as clinically possible, reduce antibiotic pressure as much as clinically possible
320
what are the different ways HIV can be transmitted
blood, sexual and vertical
321
what is the 90/90/90 rule
global target
- 90% of people living with HIV being diagnosed
- 90% diagnosed on ART (antiretroviral therapy)
- 90% viral suppression for those on ART
322
what is the benefits of knowing HIV status
- access to appropriate treatment and care
-reduction in morbidity and mortality
- reduction in vertical transmission
- reduction of sexual transmission
- public health
- cost effective - saving on social care, lost working days, benefits claims, costs associated with onward transmission
323
what are symptoms of HIV
- acute glandular fever rah
- glandular fever
- indicators of immune dysfunction
- unexplained weight loss or night sweats
- recurrent bacterial infections including pneumococcal pneumonia
324
what HIV receptors are needed for infection
HIV infects CD4 expressing cells (gp120 interacts). it also needs the accessory receptors CCR5 and CXCR4
325
what are the two markers that are used to monitor HIV infections
1. CD4 cell count
2. HIV viral load
326
what is the most common opportunistic infection in HIV
pneumocystis pneumonia (PCP)
327
good HIV drug adherence and avoidance drug interactions are key to what?
- suppression of HIV replication
- Avoidance of drug resistance
328
who is the most at risk of HIV
1. men who have sex with men
2. heterosexual women
3. injecting drug users
4. commercial sex workers
5. heterosexual men
329
what type of organisms would you stain with Ziehl Neelsen stain and why
Mycobacteria such as TB
because they dont stain with gram stain
330
what are the different appearances of coccus bacteria
diplococcus - pair
chain of cocci
clusters of cocci
331
what are the different appearances of bacillus bacteria
chains of rods
curved rods
spiral rods
332
what are the steps of a gram stain
come in and stain
- crystal violet
- iodine
- acetate/alcohol
- safranine counterstain
333
how do you perform a gram stain
apply crystal violet to heat fixed bacteria. treat with iodine. decolourise the sample and then counterstain
334
between what temperatures and what pH range can bacteria grow
between -80 and 80
between 4 to 9
335
what are the three phases of bacterial growth
1. lag phase
2. exponential phase
3. stationary phase
336
give an example of slow growing and fast growing bacteria
slow - TB doubling time is 2 weeks
fast - E.coli and S. aureus doubling time of 20-30 minutes
337
what are two functions of pili
1. adhere to cell surfaces
2. plasmid exchange
338
what is a nosocomial infection
a hospital acquired disease
339
give an example of a gram negative diplococci
neisseria
N. meningitidis and N. gonorrhoeae
340
how would you describe the arrangement of staphylococci
clusters of cocci
341
how would you describe the arrangement of streptococci
chains of cocci
342
what test can be done to distinguish between different streptococci
blood agar haemolysis
343
Name 2 gram negative bacilli that will give a positive result with MacConkey agar.
1. E.Coli.
2. Klebsiella pneumoniae
344
What gram negative bacteria are non-lactose fermenting and what colour would they appear on MacConkey agar?
Appear white.
Shigella
Salmonella
Pseudomonas
Proteus
345
Give examples of some conditions that S.aureus can cause
Pyogenic - wound infections
Impetigo
septicaemia
osteomyelitis
pneumonia
endocarditis
346
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
347
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.
348
What are the symptoms of enteropathogenic e.coli infection?
Chronic watery diarrhoea
349
What are the symptoms of enterohaemorrhagic e.coli infection?
Bloody diarrhoea.
350
what are the four species of shigella of medical importance
S.dysenteriae
S.flexneri
S.boydii
S.sonnei
351
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.
352
what bacteria is responsible for salmonellosis
S. enterica
353
what are the three conditions caused by salmonellosis
1. gastroenteritis
2. enteric fever
3. bacteraemia
354
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
355
Describe the pathogenesis of enteric fever.
1. Endocytosis.
2. Migration to the basolateral membrane.
3. Survival in macrophage -> systemic spread.
356
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.
357
Name the spirochaete that is responsible for causing lyme disease
Borrelia .burgdorferi.
358
name the spirochaete that is responsible for causing syphilis
T. pallidum
359
what are 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.
360
what are three common fungal infections
1. Nappy rash
2. Tinea pedis
3. Onychomycosis (fungal nail infection)
361
antifungal treatments: how does amphotericin work
targets ergosterol in the plasma membrane and causes pore formation and therefore cell death
362
antifungal treatment: how does azoles work
affect the ergosterol synthetic pathway
363
what are 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.
364
what are virulence factors of S. pyogenes
Streptokinase
Streptolysin O and S
Erythrogenic Toxin
M Toxin
365
which group of streptococci can cause infective endocarditis
alpha haemolytic strep
366
why do bacteria produce coagulase
defence mechanism to clot areas of plasma around them and thereby resisting phagocytosis
367
name 4 sanctuary sites for HIV
1. Genital tract
2. GI tract
3. CNS
4. Bone marrow
368
what is a clinically important gram negative bacteria
ESBL - extended spectrum b lactamase
- mutation at active site
369
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.
370
what is the CD4+ count of someone diagnosed with having AIDS
CD4+ <200
371
Name 3 respiratory diseases associated with HIV.
1. Bacterial (pneumococcal) pneumonia.
2. TB.
3. Pneumocystis pneumonia (PCP).
372
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.
373
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.
374
Give 3 defining features of systemic inflammatory response syndrome (SIRS)
- Temperature >38℃ or <36 ℃.
- Heart rate >90.
- White cell count >12.
- Hyperglycaemia.
375
Name 6 vaccine preventable diseases that are notifiable.
1. Diptheria.
2. Measles.
3. Mumps.
4. Rubella.
5. Tetanus.
6. Whooping cough.
376
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
377
What is primary vaccine failure?
When a person doesn't develop immunity.
378
what are disadvantages of polysaccharide vaccines and how can they be improved
protection is not long lasting and the response in children is poor
improved by conjugation to help improve immunogenicity
379
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.
380
What does C.botulinum do to the body?
Botulinum toxin blocks ACh release at the NMJ and therefore causes paralysis spreading from head to body.
(inverse of C.tetani)
381
Why should you not give a pregnant women trimethoprim?
Because it will inhibit folate acid synthesis which is required for neural tube closure and therefore could cause the child to have spina bifida or anencephaly
382
What qualities of P.falciparum make it more serious?
obstructs microcirculation to make complex malaria
Causes in situ rosetting of RBCs causing obstruction of vessels
