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Microbiology Flashcards

1
Q

Define pathogen

A

Organism that causes or is capable of causing disease

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2
Q

Define commensal

A

Organism which colonises the host but causes no disease in normal circumstances

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3
Q

Define opportunist pathogen

A

Microbe that only causes disease if the host defences are compromised

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4
Q

Define virulence/pathogenicity

A

Degree to which a given organism is pathogenic/any strategy to achieve this

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5
Q

Define Asymptomatic carriage

A

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

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6
Q

What is the name given to bacteria that have round morphology

A

Coccus

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7
Q

What is the name given to bacteria that have a rod shaped morphology

A

Bacillus

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8
Q

What does the gram stain determine?

A

If a bacteria has a single membrane or a double membrane

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9
Q

A gram positive bacteria will stain what colour on the gram stain q

A

Purple

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10
Q

A gram negative bacteria will stain what colour on the gram stain

A

pink

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11
Q

What is the term used to describe cocci that grow together

A

Diplococcus

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12
Q

What strain of bacteria can not be differentiated by the gram stain

A

Mycobacteria

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13
Q

What stain can be used to differentiate mycobacteria

A

Ziehl neelsen stain

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14
Q

What does the Ziehl Nielsen stain determine?

A

Whether a bacteria is an acid fast bacilli (Red) or a non-acid fast bacilli (Blue)

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15
Q

What does the catalase test involve

A

Adding H2O2 to bacteria and looking for bubbling which indicates a positive reaction

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16
Q

What is the catalase test used for

A

To differentiate between staphylococci and streptococci

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17
Q

Are staphylococci catalase positive or negative

A

Positive

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18
Q

Are streptococci catalase positive or negative

A

Negative

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19
Q

What is the coagulase test used for

A

Coagulase is an enzyme only produce by Staphylococcus aureus so test distinguishes staphylococcus aureus from other staphylococci

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20
Q

Which bacteria produces a positive result with the coagulase test and why is the result positive

A

Staphylococcus aureus because it is coagulase positive and will produce clumping - a negative result will not produce clumping

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21
Q

Describe the observed result for alpha haemolysis in the haemolysis test

A

An indistinct zone of partial destruction of red blood cells appears around the colony accompanied by a greenish to brownish discolouration of the medium

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22
Q

What bacteria is alpha haemolytic

A

Streptococcus pneumoniae

Streptococcus Intermedius

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23
Q

What is the haemolysis test useful for

A

Classifying streptococci

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24
Q

Describe the observed results for beta haemolysis in the harmolysis test

A

A clear colourless zone appears around the colonies in which red blood cells have undergone complete lysis

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25
Name bacteria that are beta haemolytic
Streptococci pyogenes Streptococci agalactiae Listeria monocytogenes
26
What test can be used to further differentiate Beta haemolytic bacteria
Lancefield grouping
27
What are the components of the bacterial wall
Capsule - protects the bacteria from the host immune system Cell wall - made of phospholipid membrane Do not have a nuclear membrane Contain one circular chromosome
28
Describe the cell envelope of a gram positive bacteria
Single cytoplasmic membrane Large amounts of peptidoglycan No endotoxin
29
Describe the cell envelope of a gram negative bacteria
``` Double membrane (inner and outer) Smaller amount of peptidoglycan Outer membrane has Lipopolysaccharide (endotoxin) ```
30
Which mucosal surfaces are areas open to bacterial colonisation
Nasal cavity Larynx Stomach Colon
31
Which areas need to be kept sterile from bacterial colonisation
Lungs Gall bladder Kidneys Eyes
32
What is the name given to a bacteria with a curved rod morphology
Vibrio
33
What is the name given to a bacteria with a spiral rod morphology
Spirochaete
34
What environment is required for bacterial growth
Temperature between -80 and +80 pH between 4 and 9 Water/desiccation - 2 hours to 3 months
35
What are the three phases of bacterial growth
Lag phase Exponential stage Stationary stage
36
Endotoxin is a component of what
The outer lipopolysaccharide membrane of gram negative bacteria
37
Exotoxin is a component of what
Protein Secreted by gram +ve and -ve bacteria that can interfere with the nervous system, de-regulate G proteins and stop macrophage phagocytosis of bacteria
38
Describe the DNA of a bacteria
Single chromosome of double stranded DNA that is converted to RNA polymerase by ribosome and then from mRNA to protein by the ribosome
39
Due to their rapid rates of multiplication, what sort of mutations would you expect to see in a bacteria?
Base substitution Deletion Insertion
40
How is genetic variation produced in bacteria
Mutations gene transfer Conjugation by the sex pillus
41
What are the two forms of gene transfer in bacteria
Transformation via a plasmid | Transduction via a phage
42
What is bacterial transformation
genetic alteration of a bacterial cell via the uptake of an exogenous substance via a plasmid
43
What is bacterial transduction
Process by which foreign DNA is introduced into a bacteria via vector or virus ie. bacteriophage
44
What is bacterial conjugation
Transfer of genetic material between bacterial cells by direct cell to cell contact ie. via the sex pillus
45
What is an obligate intracellular bacteria
Bacteria that cannot be cultured on an artificial media and needs to be grown on host cells
46
Give examples of the three genus of obligate intracellular bacteria
Rickettsia Chlamydia Coxiella
47
Give examples of bacteria with no cell wall
Mollicutes including Mycoplasma pneumoniae M. Hominis Ureaplasma Urealyticum
48
Name three genus of bacteria that grow as filaments
Anctinomyces Nocardia Streptomyces
49
Name the types of bacteria that grow as single cells
Rods Cocci Spirochaetes
50
What is an obligate anaerobe?
Microbe that can only grow in the absence of oxygen
51
What are the three main types of gram positive bacteria
Staphylococcus Streptococci Corynebacterium
52
Is S.aureus coagulase coagulase positive or negative
Coagulase positive
53
What is the normal habitat for staphylococcus
Found in the nose and the skin
54
How is staphylococcus aureus spread?
Aerosol and touch (Coughing and breathing)
55
What is MRSA
Methicillin resistant staphylococcus aureus
56
What is MRSA resistant to
B-lactam Gentamicin Erythromycin Tetracycline
57
What are the virulence factors of staph aureus
Pore-forming toxins (Haemolysin) Proteases (Exfoliatin) Toxic shock syndrome toxin (Stimulate cytokine release) Protein A (Surface protein which binds Ig's in wrong orientation so cant be recognised by immune system)
58
What are some S.aureus associated conditions
``` Wound infections (pyogenic) Absecesses (Pyogenic) Impetigo (Pyogenic) Pneumonia (Pyogenic) Osteomyelitis (Pyogenic) Scalded skin syndrome (Toxin mediated) Food poisoning (Toxin mediated) Endocarditis (Coagulase negative) ```
59
Name 2 types of coagulase negative staphylococci
S.Epidermis | S.Saprophyticus
60
What is Staphylococcus Epidermis
Opportunistic infection in prosthetic limb and catheters
61
Name three ways that streptococci can be classified
1. Haemolysis 2. Lancefield typing 3. Biochemical properties
62
What can be differentiated using lancefield typing
A method grouping catalase negative and coagulase negative bacteria based on the bacterial carbohydrate cell surface antigens
63
What are the two important groups of the lancefield typing
Group A - strep. pyogenes | Group B - Strep. agalactiae
64
What are the some of the infections caused by S.pyogenes
``` Wound infections - cellulitis Tonsilitis Pharyngitis Otitis Media Impetigo Scarlet fever Rheumatic fever Glomerular nephritis ```
65
What are the virulence factors of S.pyogenes
Hyaluronidase - enables spread Streptokinase - breaks clots C5a peptidase - reduces chemotaxis Streptolysins O and S - bind cholesterol Erythrogenic toxin Hyaluronic acid capsule - protection M surface protein - encourages complement degradation
66
What infections does streptococci pneumoniae cause
Pneumonia Otitis media Sinusitis Meningitis
67
What are the predisposing factors for streptococci pneumoniae
``` Impaired mucus trapping Hypogammaglobulinaemia Asplenia Diabetes Sickle cell Renal disease ```
68
What are the virulence factor for streptococci pneumoniae
1. Polysaccharide capsule is antiphagocytic 2. Teichoic acid in wall binds choline receptors on host cell to enable adhesion 3. Peptidoglycan in wall causes inflammatory reaction in host 4. Cytotoxin pneumolysin insets into host cell membrane, creating a pore for the cell to burst open
69
What are the results of viridians streptococci in the haemolysin test
Alpha or non-haemolytic
70
What does viridians streptococci cause
Dental caries and abscesses Infective endocarditis Milleri group
71
What is the common clinical presentation of corynebacterium diphtheriae
``` Child with sore throat Fever and malaise Lymphadenopathy in neck Rapid breathing Greyish membrane on tonsils ```
72
How does corynebacterium diphtheriae spread
Droplet spread
73
How is corynebacterium diphtheria spread?
Production of a toxin that inhibits protein synthesis
74
How do you prevent corynebacterium diphtheriae
Vaccination with toxoid (inactivated toxin)
75
What is the major difference between gram-negative and gram positive bacteria
Gram negative bacteria has lipopolysaccharide
76
What does the lipopolysaccharide endotoxin on the outer membrane of gram-negative membrane contain
Lipid A - toxic portion Core R antigen - short sugar chain Somatic O antigen - highly antigenic repeating chain of oligosaccharides
77
What are the three different cell surface antigens on enterobacteria
K (cell capsule) H (flagellum) O (LPS antigen)
78
What are enterobacteria?
Proteobacteria that are rod shaped facultatively anaerobic motile bacteria with flagella
79
What test is used to differentiated between lactose and non-lactose fermenting enterobacteria?
MacConkey Agar - if bacteria can use lactose it generates lactate and lowers pH producing red bumps
80
What are the three main types of enterobacteria
E.coli Shigella Salmonella
81
Which enterobacteria is lactose +ve
E.coli
82
Which enterobacteria Is lactose -ve
salmonella and Shigella
83
Is E.coli commensal and does it have a flagella?
Yes and Yes
84
What are infections caused by pathogenic E.coli
``` Wound infections UTIs Gastroenteritis Travellers diarrhoea Bacteraemia (Infection of abdominal organ) Infant meningitis ```
85
What are the virulence factors for E.coli
1. Entero-toxigenic (ETEC) 2. Entero-pathogenic (EPEC) 3. Entero-haemorrhagic (EHEC) 4. Entero-invasive (EIEC) 5. Entero-aggregative (EAEC) 6. Uro-pathogenic (UPEC)
86
How does entero-toxigenic E.coli work and what does It cause
Toxin and pilli | Acts in small intestine to cause secretory diarrhoea
87
How does entero-pathogenic E.coli work and what does it cause
Pedestal formation | Acts in small intestine to cause chronic watery diarrhoea
88
How does entero-haemorrhagic E.coli work and what does It cause
Pedestal formation and shiga-like toxin | Acts in the large intestine to form bloody diarrhoea
89
How does entero-invasive E.coli work and what does it cause
Invasins --> Inflammation and ulceration | Acts in the large intestine to cause bloody diarrhoea and dysentry
90
How does entero-aggregative E.coli work and what does it cause
Pilli + cytotoxin - shorter villi and mucus production | Acts I the large intestine to produce chronic diarrhoea
91
How does uro-pathogenic E.coli work and what does It cause
Haemolysin producing inflammation | occurs In the urinary tract to produce UTIs
92
Describe the pathogenicity of entero-toxigenic E.coli
1. Heat labile toxin enters epithelial cell and causes GPCR modification (Gs) 2. Transfers NAD ribose so GPCR becomes locked on with adenylate cyclase activated 3. Leads to increased cAMP 4. cAMP binds PKA which phosphorylates CFTR leading to loss of Cl- into intestinal lumen 5. This alters osmotic balance so Na+ also leaves followed by water leading to diarrhoea
93
Describe the pathogenicity of pedestal formation in EPEC and EHEC
1. Pathogen adheres to microvilli with pathogenic ili 2. T3SS acts like syringe and injects toxin into epithelial cells which rearranges actin and disrupts tight junctions 3. Microvilli reform in pedestals holding pathogen
94
What are the four species of shigella
S.dysenteriae S.Flexneri S.boydii S.sonnei
95
How does a shigella infection pass from person to person
Person to person contact or via contaminated water or food
96
Describe the pathogenesis of the shigella
1. Bacteria enter the gut mucosa and invade M cells in the gut associated lymphoid tissue 2. Bacteria are phagocytose and released during apoptosis resulting in inflammation and cell damage 3. Shiga toxin damages epithelium which enables the bacteria to infect adjacent cells and polymerise actin to make filaments that it uses to move through the cell
97
What are the symptoms associated with Shiga toxin
Bloody diarrhoea Small volume stools pain in straining Prostrating cramps
98
What are the complications associated with shiga toxin
Targets the kidneys leading to renal failure
99
What are the two main species of salmonella
Salmonella enterica | S.bongori
100
What is the name of the infection caused by salmonella enterica
Salmonellosis
101
What are the three types of salmonellosis caused by salmonella enterica
Gastroenteritis Enteric fever (Typhoid) Bacteraemia
102
Describe the pathogenesis of salmonellosis in gastroenteritis
1. Bacteria mediated endocytosis 2. Induction of chemokine release 3. Neutrophil recruitment and migration 4. Neutrophil induced tissue injury 5. Fluid and electrolyte loss causing diarrhoea Inflammation/necrosis of gut mucosa
103
Describe the pathogenesis of salmonellosis in enteric fever
1. Bacteria mediated endocytosis 2. Transcytosis to basolateral membrane 3. Survival in macrophages 4. Spreads systemically to the lymph nodes and enters the bloodstream and causes septicaemia 5. Spreads to the gall bladder from the liver where person can be a carrier for 1 year to rest of the their life
104
Name three other types of enterobacteria
Proteus Mirabilis Klebsiella pneumoniae Yersinia
105
What are the properties of proteus mirabilis and what is its virulence factor
Opportunistic infection that causes pyelonephritis and septicaemia Virulence factor = increased urease --> kidney stones
106
What are the properties of klebsiella pneumoniae
Environmental, opportunistic, nosocomial infection in neonates, elderly and immune compromised Colonises the GIT and oropharynx leading to UTIs, pneumonia, surgical wound infection and sepsis
107
What is the shape of vibrio cholerae
Curved rods with single polar flagellum
108
What is the pathogenesis of vibrio cholerae
1. Toxin binds ganglioside (Glycolipid receptor) 2. A subunit ADP ribosylates G protein (Gs) --> Locked ON state 3. Leads to uncontrolled cAMP production 4. Protein kinase becomes activated 5. CFTR activity becomes modified = loss of Cl- and Na+ which subsequent loss of H2O
109
What are the symptoms of vibrio cholerae
Rice water stools (high volume and watery) (No blood or pus) Can lose 20L fluid per day leading to dehydration and hypovolaemic shock
110
What is pseudomonas aeruginosa
opportunist Free-living aerobe that has a motile single poler flagellum
111
What acute infections does pseudomonas aeruginosa cause
Localised (Burns, surgery UTI and keratitis) Systemic (Bacteraemic) - sepsis ICU patients on ventilators leading to nosocomial pneumonia Chronic infections - cystic fibrosis
112
What are the virulence factors of pseudomonas aeruginosa
Twitching motility Pili Multiple toxins inhibit protein synthesis Interference with cell signalling (Exoenzyme S and U) Cell death and damage (Exotoxin A, elastase and phospholipase)
113
What is haemophilia influenza
Exclusively human parasite opportunistic infection carried mainly by nasopharyngeal Mainly seen in young children and adult smokers
114
What conditions are associated with haemophilia infleunzae
``` Meningitis Bronchopneumonia Sinusitis Epiglottis Bacteraemia Otitis media Pneumonia in CF, COPD and HIV patients ```
115
What are the virulence factors of haemophilia influenza
Pili (adherence) Invasive strains have a penetrating capsule that can penetrate the nasopharyngeal epithelium and are resistant to phagocytosis and the complement system
116
What disease does legionella pneumophila cause
Legionnaires disease in immunocompromised
117
Where might one obtain an legionala pneumophila infection
Aquatic environment, air conditioning, water towers, shower heads, humidifiers
118
What is the pathogenesis of Legionella pneumophila
1. Pathogen infects alveolar macrophages so it can avoid destruction and replicate 2. Release pro-inflammatory signals causing neutrophil influx into the lungs
119
What disease does bordetella pertussis cause?
Pertussis (Whooping cough)
120
How is bordetella transmitted>
Aerosol transmission
121
What are the virulence factors of bordetella pertussis?
1. Pertussis toxin | 2. Adenylate cyclase haemolysin toxin
122
What is the pathogenesis of the pertussis toxin?
1. S1 subunit ADP ribosylates G protein (Gi) causing it to be locked in an off state 2. Switching off of Gi prevents the inhibition of adenylate cyclase 3. Increased cAMP production
123
What is the pathogenesis of the adenylate cyclase haemolysin toxin
Increases cAMP levels in the affected cell which suppresses the innate immune function such as phagocytosis
124
Describe the characteristics of neisseria bacteria
Non flagellated Gram negative Diplococci Fastidious
125
What are the two main species neisseria bacteria?
N.Meningitidis | N.Gonorrhoea
126
How is N.menigitidis spread and where does it enter the body?
Person to person areosol transmission | Enters at the nasopharyngeal epithelium
127
What are the conditions caused by N.meningitidis
Meningitis Septicaemia Low level bacteraemia
128
What are the virulence factors of N.meningitidis
Anti-phagocytic capsule Pili (colonisation) LPS results in cytokine cascade and inflammatory response which can lead to sepsis
129
How is N.gonorrhoea spread
Person to person contact
130
What conditions can be caused by N.gonorrhoea
Salpingitis Proctitis Gingvitis Pharyngitis
131
What is the pathogenesis of N.gonorrhoea
Sexual transmission | rectal, vaginal and oral inflammation
132
What are the virulence factors of N.gonorrhoea
Twitching motility | LPS --> Inflammation
133
What are the two main types of campylobacter
Jejuni and coli
134
Describe the characteristics of campylobacter
Spiral rods with unipolar or bipolar flagella
135
What are the two most common causes of a campylobacter infection
Undercooked poultry | Unpasteurised milk
136
What are the symptoms of a campylobacter infection
Mild to severe diarrhoea often with blood - usually self-limiting within a week Campylobacter usually shed in the faeces for around 3 weeks
137
What are the virulence factors of campylobacter infection
Invasins invade the ideal and colonic epithelial cells resulting in acute inflammation Cytolethal distending toxin arrests cell cycle meaning target cells swell and lyse
138
What conditions are caused by helicobacter pylori
Gastritis Peptic ulcer disease Gastric adenocarcinoma
139
What is the virulence factor of helicobacter pylori
Urease hydrolyses urea to generate ammonia to act as a buffer to gastric acid
140
What are the two main chlamydiae
Chlamydia and chlamidophyl
141
What are the characteristics of chlamydiae
Very small and non-motile | Obligate intracellular parasites that cannot be cultured in media
142
What are the two stages in the development of chlamydia
1. Elementary bodies | 2. Reticulate bodies
143
Describe what happens during the elementary body stage of chlamydia development
Infectious stage where the chlamydia enters the cell through endocytosis and inhibits phagosome-lysosome function but Is dormant
144
Describe what happens during the reticulate body stage of chlamydia development
Replicative but not infectious stage where the bacteria acquires nutrients from the host cell and is metabolically active
145
What are the 4 main types of chlamydia
1. C. trachomatis = STD 2. C.Pneumoniae = respiratory tract 3. Atypical community acquired pneumonia pathogen 4. C. psittaci
146
What are the three biovars of C.trachomatis
1. Trachoma biovar (blindness) 2. Genital tract biovar (STD - infects epithelial cells of mucous membranes of urethra and vagina) 3. Lymph granuloma venereum biovar (Invasive urogenital or anorectal infection)
147
What are the three main types of spirochetes
1. Borrelia burgdoferi --> Lyme disease 2. Leptospira --> Zoonosis 3. Trepinema Pallidum --> Syphilis
148
What are the three stages of a syphilis infection
1. Primary - localised infection 2. Secondary - systemic infection (Skin, lymph and vessels) 3. Tertiary = granuloma of the soft tissue - cardio and neuro syphilis
149
Which gram -ve bacteria would you most commonly find in the respiratory tract
``` Bordetella pertussis Haemophilus influenzae Pseudomonas aeruginosa Legionella pneumophila Chlamydia pneumoniae ```
150
Which gram -ve bacteria would you most commonly find in the urinary tract
E.coli Klebsiella pneumoniae Proteus mirabilis
151
Which gram -ve bacteria would you most commonly find in the GIT
``` Vibrio cholera Shigella dysenteria Some E.coli Campylobacter jejuni Helicobacter pylori S. Enterica and S. typhimurium ```
152
Describe the structure of fungi
Eukaryotic with a nuclear membrane Chitinous cell wall Heterotrophic so get nutrients from what they are living on Move through growth or spore formation
153
What is a yeast
Small single celled organism that divides by budding (Asexual reproduction)
154
What is a mould
Multicellular hyphae with reproduction by spores
155
Why do very few fungi actually infect humans
Have an inability to grow at 37 degrees | Fungi cannot evade the adaptive/innate immune response
156
What fungal diseases might you see in an immunocompromised host?
Candida line infections Pneumocystis Invasive aspergillosis
157
What fungal diseases might you see in a post-surgical patient
Intra-abdominal infections
158
What fungal diseases might you see in a healthy individual
Fungal asthma | Travel associated fungal infections (Dimorphic fungi)
159
What are the three main genera of fungi
Ascomycota Basidiomycota Mucormycota
160
Give some examples of ascomycota
``` Aspergillus Pneumocystis Candida Fusarium Scedosporium ```
161
Give some examples of basidiomycota
Cryptococcus | Trichosporon
162
Give an example of mucormycota
Zygomycetes
163
What is the aim of selective toxicity antimicrobial drug therapy
Achieve inhibitory levels of the agent at the site of infection without host cell toxicity
164
What qualities are required in selecting an antimicrobial target
1. Target doesn't exist in humans 2. Target is significantly different to human analogue 3. Drug is concentrated in organism cell with respect to humans 4. Increased permeability to the compound 5. Modification of the compound in the organism or human cellular compartment 6. Human cells are rescued from toxicity by alternative metabolic pathways
165
Instead of cholesterol, the major component of a fungal plasma membrane Is what?
Ergosterol
166
Flucytosine targets what
Fungal DNA synthesis
167
Echinocandins target what?
Cell wall
168
Amphotericin, azole and terbinafine target what?
Ergosterol plasma membrane and causes pore formation leading to cell death
169
What molecules exist in fungal cells that do not exist in human cells that make them good antimicrobial targets
Ergosterol Mannoproteins Glucan Chitin
170
Amphotericin is what class of antimicrobial
Polyene
171
What is the mechanism of action of amphotericin
forms pores in the ergosterol component of the plasma membrane - fungicidal
172
What are some of the side effects of amphotericin
Nephrotoxicity | Distal renal tubule acidosis
173
Terbinafine is what class of antimicrobial
Allylamine
174
What is the mechanism of action of terbinafine
Fungicidal -causes reversible inhibition of squalene epoxidase which is required for the growth of the fungi
175
What is the mechanism of action of azoles
Dose dependent inhibitors of 14a-sterol demethylase which is an important intermediate in the ergosterol production pathway
176
Clotrimazole and ketoconazole are used against what
Candida
177
Fluconazole is used against what
Cryptococcus
178
Itraconazole is used against what
Aspergillus and fusarium
179
Voriconazole is used against what
Moulds! mainly invasive aspergillus
180
Posaconazole and isavuconazole are used against what?
Zygomycetes
181
What is the mechanism of action of echinocandins
Inhibit 1,3 B glucan synthesis
182
What are the echinocandins used against
Yeast and moulds
183
What are three methods of diagnosing fungal disease
Microscopy and histology Culture Molecular methods and serology
184
What is onychomycosis?
Fungal infection of the nail
185
What are the treatment options for onychomycosis
Topical amorolfine | Systemic itraconazole or terbinafine
186
what is the most common causative fungi of onychomycosis
Trichrophyton rubrum
187
Name the sorts of individuals that may be susceptible to infection with pneumocystis
Moderate to severe immunocompromised patients ie. HIV, steroids and transplant
188
What is the major difficulty with pneumocystis
Unable to culture it
189
What is the treatment for pneumocystis
Co-trimoxazole
190
Which gram -ve bacteria would you most commonly find to cause meningitis
Neisseria meningitidis Some E.coli Haemophilus influenza
191
Which gram -ve bacteria would you most commonly find in to cause sepsis
Neisseria meningitidis E.coli and K. pneumonia Pseudomonas aeruginosa
192
Which gram -ve bacteria would you most commonly find as STDs
Neisseria gonorrhoea Chlamydia trachomatis Treponema pallidum
193
Which gram -ve bacteria would you most commonly find in wound infections
E.coli Bacteroides fragilis Pseudomonas aeruginosa
194
What Is the morphology of proteobacteria
All rod shaped bacilli except neisseria (Diplococci) or campylobacter/helicbacter which are spiral
195
What is the morphology of bacteroides
Rod shaped bacilli
196
What is the morphology of chlamydia
Round (elementary bodies) | Pleimorphic (Reticulate bodies)
197
What is the morphology of spirochetes
Spiral/helical
198
Define a virus
An infectious obligate intracellular parasite comprising genetic material surrounded by a protein coat and or a membrane
199
What is the name given to a virus when it is not inside a cell and what does it consist of
``` Virion Genetic material (DNA and RNA) Protein Coat (Capsid) ```
200
What are the different shapes of virus nucleocapsid (Protein coat of virus and genetic material)
Helical Iscosahedral Complex
201
Give an example of a virus with a helical nucleocapsid
Influenza
202
Give an example of a virus with a icosahedral nucleocapsid
Adenovirus
203
What is the size range of human viruses
20-260nm in diameter
204
Do viruses have a cell wall
No
205
Do viruses have organelles
No
206
Are viruses dependent on the host cell
No
207
Are viruses living
No | They do not feed or respire and cannot reproduce independently
208
What are the 5 main stages of virus replication
1. Attachment - Attach to specific receptor 2. Cell entry - Virion uncoats outside the cell and only the core contains nucleic acids and replication enzymes are freed into host cell cytoplasm 3. Host cell interaction and replication - Migration of genome to cell nucleus where transcription to mRNA using host materials occurs - mRNA translated to produce structural proteins and viral genome 4. Assembly of virion - Occurs in different locations depending on the virus 5. Release of new virus particles - Either bursts out leading to cell death or undergoes a budding/exocytosis process
209
assembly of the herpes virion occurs where in the cell
Nucleus
210
Assembly of the poliovirus virion occurs where in the cell
Cytoplasm
211
Assembly of the influenza virus occurs where in the cell
Cell membrane
212
Name a disease that bursts out of the host cell causing cell death
Rhinovirus
213
Name a disease that releases new disease particles by budding/exocytosis
HIV or influenza
214
Name the 5 mechanism through which a virus can cause disease
1. Direct destruction of host cells 2. Modification of the host cell 3. Over-reactivity of the immune system 4. Damage through cell proliferation 5. Evasion of host defences
215
Name a virus that causes direct destruction of host cells
Poliovirus causes host cell lysis and death after viral replication period of 4 hours
216
Name a virus that modifies the host cell
Rotavirus - atrophies villi and flattens epithelial cells which decreases the small intestine surface area so nutrients aren't absorbed leading to. a hyperosmotic state and profuse diarrhoea
217
Name a virus that causes over-reactivity of the immune system
Hep B and C | HIV
218
Name a virus that causes damage through cell proliferation
Human papilloma virus ie. cervical cancer
219
Which virus evades host defences through latency
Herpesviridae - after primary disease the virus is not detectable but the viral DNA lies latent and can be reactivated at times of Lower immune control Hep B and C Measles virus
220
Which virus evades host defence via cell to cell spread
Measles and HIV Cell to cell spread avoids random release into the environment, increased the speed of spread and avoids the immune system
221
Which virus evades the host defence through antigenic variability
Influenza, HIV and Rhinovirus | - have ability to change the surface antigens in order to evade the hosts immune system
222
Which virus evades the host defence through prevention of host cell apoptosis
Herpesviridae - in response to viral infection, cells undergo apoptosis which reduces further viral spread - preventing host cell apoptosis allows virus to continue to replicate so more virus is produced
223
Which virus evades host defence by interfering with host cell antigen processing pathways
Herpesviridae Measles HIV
224
Why do viruses vary in the range of clinical syndromes they can cause
Different host cells and tissues they can infect Different method of interaction with the host cell
225
What are protozoa
Single cell eukaryotes
226
What are the 5 types of protozoa
``` Flagellates (Flagella) Sporozoans (Non-motile) Amoebae (Pseudopodia) Ciliates (Cilia) Microsporidia ```
227
Name 4 types of flagellate
Trypanosoma (Sleeping sickness) Trichromonas vaginalis (STI) Leishmania Spp Giardia lamblia
228
Name 3 types of sporozoans
Plasmodium (Malaria) Toxoplasma gondii (Toxoplasmosis) Cryptosporoidium
229
Name a type of Amoebae
Entamoeba histolytica
230
Name a type of ciliate
Balatidium coli
231
What are the two species of African trypanosomiasis
Trypanosoma brucei gambiense (Central/West Africa) Trypanosoma brucei rhodesiense (East Africa)
232
How is the African trypanosomiasis transmitted
By the bite of the Tsetse fly
233
What are the symptoms associated with African trypanosomiasis
Flu like symptoms followed by CNS involvement (Sleepiness, extreme fatigue, chancre, confusion, and personality changes) leading to coma and death
234
How do we diagnose African trypanosomiasis
Visualise trypomastigotes on microscopy of blood or CSF
235
What is American Trypanosomiasis known as
Chagas disease
236
What is the cause of American trypanosomiasis
Trypanosoma Cruzi
237
Where is American trypanosomiasis found mainly
Central and South America
238
How is American trypanosomiasis transmitted
Triatomine bug
239
What are the symptoms of American trypanosomiasis
Acute flu like syndrome (Romana's sign) Cardiomyopathy Megaoesophagus Megacolon
240
Leishmaniasis is spread by what
Bite of the sandfly
241
Where is leishmaniasis found
Disease of poverty in Africa, Asia and South America
242
How is leishmaniasis found
Diagnosed through biopsy and serology
243
What are the three clinical manifestations of Leishmaniasis
Cutaneous Mucocutaneous Visceral (Kala Azar)
244
What are the cutaneous manifestations of Leishmaniasis
Ulcers on the exposed parts of the body including face, arms and legs Creates issues with social rejection and scarring
245
What are the mucocutaneous manifestations of Leishmaniasis
Lesions that cause destruction to the mucous membranes of the nose, mouth and throat Can lead to pneumonias and sepsis
246
What are the visceral manifestations of Leishmaniasis
Affects the internal organs and is characterised by irregular bouts of fever, weigh loss, swelling of the spleen and liver and anaemia Has an incredibly high fatality rate if not treated
247
What are the symptoms of trichomonas vaginalis in women
Dysuria Yellow frothy discharge Abdominal pain Vulvar and cervical lesions
248
What are the symptoms of trichromonas vaginalis
Urethritis Epididymitis Prostatitis Can be asymptomatic in males though
249
What is the treatment for trichromonas vaginalis
Metronidazole
250
Giardiassis is caused by what
Giardia lamblia
251
How is giardiassis spread
Faeco-oral spread
252
What are the symptoms of giardiassis
``` Diarrhoea Cramps Bloating Flatulence Recent travel Childcare ```
253
How might we identify giardiassis
Trophozoites/cysts seen in the stool
254
What is the treatment for giardiassis
Treat with metronidazole and tinidazole
255
What is amoebiasis caused by
Entaemoeba histolytica
256
Where are entamoeba histolytic commonly found
In the gut
257
How is entamoeba histolytica spread>
Faeco-orally Ingestion of mature cysts faeceally contaminated water and food - cysts travel from the small intestine where they release trophozoites which travel to the large intestine where they invade the intestinal wall
258
What are the symptoms of entamoeba histolytica
Dysentry Colitis Liver and lung abscesses Trophozoites/cysts seen in stool
259
How do you treat entamoeba histolytica
Metronidazole
260
Which protozoa cause cryptosporidosis
Cryptosporidium
261
How is cryptosporidium spread
Waterborne - transmitted via contaminated food/water - ingestion of cysts
262
What are the symptoms of cryptosporidosis
``` Diarrhoea (watery with no blood) Vomiting Fever Weight loss Oocytes seen in the stool ```
263
How do we diagnose cryptosporidosis
Acid-fast staining | Immunofluorescent
264
How do we treat cryptosporidosis
Treat with hydration and replacement of electrolytes
265
What is the cause of toxoplasmosis
Toxoplasma gondii
266
How is toxoplasmosis spread
Ingestion of contaminated food (Meat and shellfish) and water/feline faeces
267
Toxoplasmosis can cause
Disseminated disease Toxoplasma encephalitis Chorioretinitis
268
What are the effects of toxoplasmosis
Severe consequences in pregnancy and immunodeficient patients
269
How can we identify toxoplasmosis
Produces ring enhancing lesions on the brain CT
270
Why is the prevalence of malaria increasing
1. Increasing resistance of parasite to antimalarials 2. Increasing resistance of mosquito to insecticides 3. Ecological and climate change 4. Increased travel to endemic areas
271
What are the 5 malaria causing plasmodium
``` Falciparum Ovale Vivax Malariae Knowlesi (Very rare) ```
272
What is the vector of malaria
Female anopheles mosquito around stagnant water
273
What is the life cycle of malaria
3-4 weeks
274
How do you diagnose malaria
Using a blood film and microscopy to identify trophozoite
275
Describe the life cycle of the mosquito
1. Exo-erythrocytic - Mosquito injects plasmodium (Sporozoites) into human from salivary gland - Sporozoites travel in blood to liver hepatocytes - Sporozoites replicate asexually in hepatocytes to form merozoites which replicate to form Schizont - Schizont ruptures and merozoites enter bloodstream and infect RBCs Plasmodium ovale and vivax can lie dormant in the hepatocytes and reactivate later (Hypnozoite stage) 2. Endo-Erythrocytic cycle - Merozoites infect RBC and mature to trophozoites which forms a Schizont which ruptures and releases merozoites (Causes clinical manifestations) - Some trophozoites become male and female gametocytes which are ingested by another unaffected mosquito during a meal 3. Mosquito Stage - Male and female gametocytes fuse to form a zygote which forms and ookinete and oocyst which ruptures and releases sporozoite which collects in the salivary gland
276
What are the clinical features of malaria
Fever, chills, sweats, headaches, myalgia, fatigue, nausea, diarrhoea, vomiting and abdominal pain
277
What are the signs of malaria
``` Anaemia Jaundice Hepatosplenomegaly Haemoglobinuria Monocytosis and lymphopenia Thrombocytopenia ```
278
Describe the pathology of malaria
1. Spleen kills damaged RBCs with macrophages phagocytosing infected RBCs 2. This can cause ANAEMIA and pro-inflammatory cytokine release (TNFa and IL-1B) 3. Macrophages release interferon gamma which affects blood vessels as parasites causes RBCs to express a surface protein and interferon gamma causes expression of adhesion molecules on endothelial cells 4. if infected RBC adheres to adhesion molecule it triggers coagulation and forms a ROSETTE causing tissue inflammation and obstruction leading to tissue hypoxia
279
How do you diagnose malaria
Anaemia Hyperbilirubinaemia Blood films Light microscopy
280
What are the affects of malaria in the brain
Rosettes blocks the brain circulation leading to tissue hypoxia Vascular occlusion and hypoglycaemia leads to raised intra-cranial pressure, seizures, coma, drowsiness and death = CEREBRAL MALARIA
281
What are the affects of malaria on the lungs
Vascular occlusion, anaemia, lactic acidosis and increased vascular permeability lead to shortness of breath, hypoxia and pulmonary oedema = ACUTE RESPIRATORY DISTRESS SYNDROME
282
What are the affects of malaria on the kidneys
Vascular occlusion, dehydration leads to decreased blood pressure, haemoglobinuria, proteinuria, fatigue = RENAL FAILURE and METABOLIC ACIDOSIS
283
Malaria induced thrombocytopenia causes what
Activation of coagulation cascade leads to disseminated intravascular coagulation, anaemia and bleeding
284
What are the clinical features of malaria in adults
``` Coma ARDs Hypoglycaemia Renal failure Shock ```
285
What are the clinical features of malaria in children
Tachypnoea Acidosis Anaemia Hypoglycaemia
286
Which malaria plasmodium causes complicated malaria
Plasmodium falciparum
287
What is the treatment for complicated falciparum malaria
IV artesunate (Quinine and doxycycline)
288
What is the treatment for normal falciparum malaria
Oral riamet or oral quinine and doxycycline
289
What is the treatment for non-falciparum malaria
Oral chloroquine
290
What is the treatment for vivax and ovale malaria
Primaquine for hypnozoite clearance to eliminate them from the liver
291
What treatment might be given to an individual suffering cerebral malaria induced seizures
Anti-epileptics
292
What treatment might be given to someone with malaria induced ARDs
Oxygen Diuretics Ventilation
293
What treatment might be given to someone with malaria induced renal failure
Fluids and dialysis
294
What treatment might be given to someone with malaria induced sepsis
Broad spectrum antibiotics
295
What is the treatment is given to someone with malaria induced anaemia
Blood products
296
What are the key attributes of a pathogen
1. Infectivity = ability of to become established in host which involves adherence and immune escape 2. Virulence = ability to cause disease once established 3. Invasiveness = capacity to penetrate mucosal surfaces to reach normal sterile sites
297
What does a primary pathogen do?
Causes disease in a proportion of exposed individuals irrespective of immunological status
298
Define microbiome
Describes the totality of micro-organisms, their genetic elements and their environmental interactions in an environment
299
What does a viral infection require to be effective?
Need rapid cell entrance to avoid the immune response as free virus in the blood stream is easily neutralised
300
What is the humoral response to a viral infection
IgA blocks viral binding so cant gain entry or inject genetic material into cells IgM aids agglutination Complement causes opsonisation, cell lysis and neutralise toxins
301
What is the cell mediated response to a viral infection
Interferon = prevents infection of non-infected cell through production of anti-viral protein DAI Cytotoxic T lymphocytes directly kill infected cells Natural Killer cells and macrophages activate the antibody dependent cell destruction
302
What are the virulence factors of viral infection
Direct cell cytotoxicity
303
Give some examples of viral infection direct cell cytotoxicity
``` Resp epithelium (Influenza) Skin (Shingles and varicella zoster virus) T cells (HIV) Yellow fever (liver cells) ```
304
Give some examples of how viral infections evade the host defence
Adenovirus and EBV block DAI HSV binds to C3b and inhibits classic and alternate complement Rhinovirus, HIV and Influenza cause antigenic variation HIV, MMR and EBV cause immune suppression
305
What are the two forms of antigenic variation
Antigenic Drift - spontaneous mutations occurs gradually producing changes in haemagglutinin and neuramidase (Epidemic) Antigenic Shift - sudden emergence of new subtype different to that of the preceding virus (Pandemic)
306
Where does a bacterial infection enter the host
GIT, GUT or wound
307
What is the response to low number of virulence factors
Phagocytes
308
What is the response to high number of factors
Cell mediated immunity
309
What is the response to extracellular bacteria
antibody response
310
What is the response to intracellular bacteria
Cellular response
311
What factors are important for colonisation
Adhesins and biofilms
312
How do bacteria compete with host cells
Sequestering nutrients using novel metabolic pathways Out competing other micro-organisms
313
What do adhesins do and what are some examples
Help bacteria bind to mucosal surfaces - Fimbriae and pili filamentous proteins - Non fibril proteins - lipids - glycosaminoglycans - Lectins of viruses and parasites
314
Whats a biofilm
bacteria can stick to a surface by secreting an extracellular polymeric substance of protein,polysaccharides and DNA Helps protect against antimicrobials
315
What is the immune response to bacterial infection
Antibodies to neutralise toxins, block host cell attachment (IgA) complement to cell lyse, opsonisation and proliferation prevention
316
How does Neisseria gonorrhoea evade the host defence
Secretes proteases that lyse IgA
317
How does B pertussis evade the host defence
Secretes adhesion molecules
318
How does S.pneumoniae evade the host defence
Polysaccharide capsule that prevents phagocytosis
319
How does streptococci pyogenes evade the host defence
Release M protein that inhibits phagocytosis
320
How does staphylococci evade the host defence
Produces coagulase that form fibrin close around organism thus protecting it
321
How does pseudomonas evade host defence
Secrete elastase that inhibit C3a and C5a which normally attract neutrophils to site of inflammation
322
How does mycobacterium evade the host defence
Escape from phagolysosome and live in cytoplasm
323
Protozoa in the blood triggers what
Humoral immunity
324
Protozoa in the tissue triggers what
Cell mediated immunity
325
How does protozoa evade defence
Surface antigen variability Intracellular phase Shed outer coat
326
Do worms multiple in humans
NO - form eggs
327
Is the immune response sufficient to kill worms
No
328
What is the immune response to killing worms
IgG and IgE produced IL5- eosinophil production IL3- Mast cell growth Eosinophilic basic protein toxic to worms
329
How do worms evade host defences
Adult worms demonstrate decreased antigen expression Glycolipid coat is host derived utilising host self-antigens so not perceived as foreign to the immune system
330
Describe results of inflammation
``` Up regulation of adhesion molecules Chemotaxis Degranulation Vascular permeability Vasodilation ```
331
Define antibiotic
Molecule that binds to bacteria target site and affects reactions critical to bacterial survival
332
What are the different types of antimicrobials
``` Antifungals Antibacterials Antihelminthic Antiprotozoal Antivirals ```
333
What do we use antibiotics for
Treatment Prophylaxis Prevention of post surgical infection
334
Name different types of beta-lactam
``` Penicillins Cephalosporins Carbapenems Glycopeptides Vancomycin Monobactams ```
335
What is the mode of action of beta lactams
Bind to peptidoglycan penicillin binding proteins which inhibits cell wall synthesis
336
What is the mode of action of metronidazole and rifampicin
Interfere with nucleic acid synthesis or function
337
What is the mode of action of fluroquinolones
Inhibit DNA gyrase (Essential for bacterial DNA replication)
338
What is mode of action of aminoglycosides, tetracyclines, macrolides and chloramphenicol
Inhibit ribosomal activity and protein synthesis
339
What is the mode of action of sulphonamides and trimethoprim
Inhibit folate synthesis - required for bacteria to grow since folic acid cannot cross the bacteria cell wall
340
What are the two different types of antibiotics
Bacteriostatic | Bactericidal
341
How do bacteriostatic bacteria work
Inhibit bacterial growth but don't necessarily kill - inhibits protein synthesis, DNA replication and metabolism
342
How do bactericidal bacteria work
Kill bacteria | Inhibit cell wall synthesis
343
When are bactericidal bacteria useful
Poor tissue penetration (Endocarditis) Difficult to treat infections (TB) Need to eradicate the infection quickly (Meningitis)
344
What are the two major determinant of anti-bacterial effects
Concentration of antibiotic | Time the antibiotic remains on these sites
345
What is concentration dependent killing and give an example
Knock out punch - eradicate pathogenic bacteria by acheiving high concentrations at site of binding How high the concentration is above the lowest minimal inhibitory concentration Aminoglycosides and Quinolones use this mechanism
346
What is time dependent killing and give some examples
Sustained killing Time that the serum concentration remains above the lowest minimal inhibitory concentration during the dosing interval Beta-lactams, clindamycin, macrolides, oxazolidinones
347
What considerations need to made to safely prescribe antibiotics to a patient
``` Intolerance, allergy and anaphylaxis Side effects Age Renal and liver function Pregnancy and breast feeding Drug interactions Risk of clostridium difficile ```
348
How do bacteria resist antibiotics
1. Change antibiotic target or mask it 2. Destroy antibiotic 3. Prevent antibiotic access 4. Remove antibiotic from bacteria
349
How do bacteria change antibiotic targets
change the molecular configuration of antibiotic site or mask it - Flucloxacillin no longer able to bind PBP of staphylococci (MRSA)
350
How do bacteria destroy antibiotics
Beta lactam ring of penicillins and cephalosporins can be hydrolysed by bacteria enzyme beta lactamase which means they are unable to bind penicillin binding proteins and inhibit cell wall synthesis
351
How do bacteria prevent antibiotic entry
Bacteria modify its bacterial membrane porin channel size, numbers or selectivity
352
How do bacteria remove antibiotic from bacterium
Proteins in the bacterial membrane can export or efflux so antibiotic pumped out the bacteria resulting in reduced levels so effect of antibiotic on bacteria is reduced
353
What are the two ways that bacterial antibiotic resistance develop
Intrinsic natural resistance Acquired resistance (2 types) - Spontaneous gene mutation - Horizontal gene transfer
354
Describe intrinsic natural resistance and give examples
All subpopulation of species will be equally resistant Aerobic bacteria are unable to reduce metronidazole to its active form so antibiotic is harmless Anaerobic bacteria lack oxidative metabolism required to uptake aminoglycosides Vancomycin is not taken up by gram negative bacteria because it is too large to penetrate the outer membrane
355
Describe acquired bacterial antibiotic resistance
A bacterium that was previously susceptible obtains the ability to resist the activity of a particular antibiotic
356
Describe the different types of spontaneous gene mutations that can cause bacterial resistance
New nucleotide base pair Change in AA sequence Change to enzyme or cell structure Reduced affinity or activity of antibiotic
357
What are the three different methods of horizontal gene transfer that can cause antibiotic resistance
1. Conjugation = sharing extra chromosomal DNA plasmids (bacterial sex) 2. Transduction = insertion of DNA by bacteriophage 3. Transformation = Picking up naked DNA
358
Name two different gram positive antibiotic resistant bacteria
Methicillin resistant staphylococcus Aureus (MRSA) Vancomycin resistant enterococci
359
Name three different gram negative antibiotic resistant bacteria
B-lactamases Extended Spectrum Beta Lactamase AmpC Carbapenems resistant enterobacteria
360
When are cephalosporins used
Penicillin allergies Resistant bugs Bacteria in hard to reach places (meningitis)
361
What antibiotics are used for gram positive bacteria
Beta lactams to target peptidoglycan
362
Skin infections caused by staphylococcus aureus and Group A, C and G strep need what antibiotic
Flucoxacillin
363
Chest infections caused by streptococcus are treated by what antibiotic
PO amoxicillin | IV Benzylpenicillin
364
Throat infections caused by group A, C and G streptococcus are caused by
PO penicillin V | IV Benzylpenicillin
365
Why are beta lactams less effective for gram negative bacteria
Gram negative have a thinner cell wall so therefore require a different weapon
366
Urine infections are caused by what bacteria
Escherichia coli Klebsiella Sp Proteus Sp
367
Gallbladder infections are caused by
Escherichia coli Klebsiella Sp Proteus Sp
368
Abdominal infections are caused by
Escherichia coli Klebsiella Sp Proteus Sp
369
Infectious diarrhoea is caused by
Shigella and salmonella
370
Vancomycin and teicoplanin are what type of antibiotic
Glycopeptides
371
When are glycopeptides required
Only gram + ve bacteria MRSA Penicillin allergies
372
What modes of action do antibiotics have
``` Inhibitors of cell wall synthesis Inhibitors of protein synthesis Inhibitors of nucleic acid synthesis Anti-metabolites Inhibitors of membrane function ```
373
Clarithromycin and erythromycin are what sort of antibiotic
Macrolides
374
When would you use a macrolide antibiotics
Gram +ve (S.aureus, B-haemolytic strep, atypical pneumonia) Penicillin allergies MRSA
375
Give an example of a lincosamide antibiotic
Clindamycin
376
When would you use a lincosamide antibiotic
``` Gram +ve Anaerobic cellulitis Penicillin Allergy Necrotising Fasciitis MRSA ```
377
Give an example of a tetracycline antibiotic
Doxycycline
378
When might you give a tetracycline antibiotic
Cellulitis Broad spectrum mainly used for gram +ve Penicillin allergy Chest infection (Pneumonia)
379
Give an example of a quinolone antibiotic
Ciprofloxacin
380
When might one give a quinolone antibiotic
``` Gram -ve specific Affects DNA synthesis UTIs Gall bladder Abdominal infections ```
381
Give one example of an aminoglycoside antibiotic
Gentamicin
382
When might one give an amino glycoside antibiotic
Gram -ve bacteria and staphs | used in UTIs and infective endocarditis
383
When might you give trimethoprim
Gram -ve bacteria Folate antagonist UTIs Broad spectrum
384
When might you give nitrofurantoin
Gram -ve and gram +ve | Used as frontline for UTIs
385
What are the mycobacteria of medical importance
``` M.Tuberculosis M.Leprae (Leprosy) M.Avium Complex (MAC) -disseminated infections in AIDs M.Kansasii (Chronic lung infection) M.Marinum (Fish tank granuloma) M.Ulcerans (Buruli ulcer) ```
386
Describe the microbiology of mycobacteria
``` Aerobic Non-motile Non-spore forming Slow growing Survive in macrophages even in low pH ```
387
What does the cell wall of mycobacteria contain
Mycolic acids Lipoarabinomannan Make up a strong waxy cell wall that is hard for the immune system to target/damage
388
Why are mycobacteria resistant to the gram stain
High lipid content within the cell wall makes mycobacteria resistant to the gram stain
389
What stain is used for Acid fast bacilli/rods
Ziehl-Neelsen stain
390
Describe the immunology of mycobacterial disease
1. Mycobacteria are phagocytosed and placed in a phagolysosome 2. Bacteria are adapted to intracellular environment and withstand phagolysosomal killings and escape to the cytosol 3. Host aims to kill the mycobacterium using microbial molecules 4. Acidification aids digestion by degradation by proteases of the mycobacteria which results in generation of antigens for presentation of T cells 5. CD4-T cells generate interferon gamma which activates intracellular killing by macrophages 6. IL-12 release by macrophages further stimulates generation of T helper cells and interferon gamma release
391
What increases susceptibility to mycobacterial infection
Genetic defects in interferon gamma or IL-12 receptors or elements of their signalling pathways
392
What are granulomas
Lesions that arise in a response that tries to contain mycobacteria
393
How do granulomas form in the case of mycobacteria
1. Highly stimulated macrophages become epithelioid cells 2. Some macrophages fuse with each other to form giant multinucleated cells (Langahans giant cells) 3. T Collins including CD8 T cells infiltrate mycobacterial lesion 4. Fibroblasts laid down around granuloma wall off 5. Central tissues may necrose an form a caseating granuloma
394
describe tuberculoid leprosy
TH1 response (IFN and TNF) --> Tissue hypersensitivity + granulomas = tissue damage
395
Describe Lepramatous leprosy
TH2 response (IL 4,5,10) --> Lesions full of bacilli + No granuloma --> Skin lesions
396
What are the treatments for mycobacterium
Isoniazid Rifampicin Pyrazinamide Ethambutol
397
What is the name of the skin test for tuberculosis
Tuberculin Skin Test (Mantoux test)
398
What occurs in primary tuberculosis
Bacilli settle in apex and granulomas forms Bacilli taken in lymphatics to hilarious lymph nodes in apex of lungs there is more air and less blood supply so fewer defending white cells to fight off infection Granuloma + Lymphatics + Lymph nodes = primary complex
399
What occurs in latent tuberculosis
Cell mediated immune response from T cells Primary infection is contained by CMI persists No clinical disease Detectable CMI to TB n tuberculin skin test
400
What occurs in pulmonary tuberculosis
Occurs immediately following primary disease or after latent reactivation Necrosis in the lesion TB may spread in lung causing other lesions
401
Where can TB spread beyond the lungs
``` TB meningitis Miliary TB (widespread dissemination an tiny spotted lesions all over the lungs) Pleural TB Bone and Joint TB Genitourinary TB ```
402
What type of organism would you stain with ziehl Nielsen
Mycobacteria ie. TB
403
How do you apply the gram stain
Apply crystal violet to heat fixed bacteria Treat with iodine Decolourise the sample and counterstain
404
Give an example of a slow growing bacteria
TB
405
Give an example of a fast growing bacteria
E.coli and S.aureus
406
Give two functions of pilli
1. Help adhere to cell surfaces | 2. Plasmid exchange
407
What is the primary function of flagella
Locomotion
408
What is the primary function of the polysaccharide capsule
Protection - prevents MAC or opsonisation molecules attacking
409
What types of bacteria release endotoxin
Gram -ve
410
What types of bacteria release exotoxin
Gram -ve and gram +ve
411
What are exotoxins made from
Proteins
412
How would you describe the arrangement of staphylococci
Clusters of cocci
413
How would describe the arrangement of streptococci
Chains of cocci
414
what test can be done to distinguish between different streptococci
Blood agar haemolysis
415
What further test can be done for streptococci in the B-haemolysis group
Serogrouping - detecting the surface antigens ie. Lancefield grouping
416
What would you see on the agar plate in gamma haemolysis and give an example of bacteria in this group
gamme haemolysis when there is no haemolysis | ie. Streptococcus Bovis falls in this group
417
What kind of bacteria is MacConkey agar used with
Gram negative bacilli
418
What is 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
419
Name two gram negative bacilli that will produce a positive result with MacConkey agar
E.coli | Klebsiella Pneumoniae
420
Where in the body might you find staphylococci
Nose and skin
421
How is staphylococcus aureus spread
Aerosol and touch
422
How is C.diptheriae spread
Droplet spread
423
Does shigella have a H antigen
Shigella is non motile and doesn't have flagellum - therefore doesn't have a H antigen
424
Does shigella produce a positive result with MacConkey agar
No - shigella does not ferment lactose and gives a negative result
425
Does salmonella have a H antigen
Salmonella is motile and has a flagellum - therefore does not give a H antigen
426
Does Salmonella give a positive result with MacConkey agar
No - does not ferment the lactose so gives a negative result
427
Does E.coli have a H antigen
E.coli Is motile nd has a flagellum so it does have a H antigen
428
Does E.coli give a positive result with MacConkey agar
Yes E.coli ferments lactose and so a red/pink colour would be seen giving a positive result
429
How can you distinguish between gram negative bacilli
Use MacConkey agar and then use serology to detect the presence of a H antigen
430
Shigella is acid tolerant - why is this advantageous for the shigella
Means shigella can pass through the stomach without being destroyed by low gastric pH - can then move into the intestine
431
How would you grow haemophilus influenzae
On chocolate agar as it requires haem and NAD
432
Who might be susceptible to infection by legionella
Immunocompromised patients
433
Describe the pathogenesis of N.meningitidis
crosses nasopharyngeal epithelium and enters the blood stream, can cause asymptomatic bacteraemia or septicaemia - if crosses the BBB can cause meningitis
434
Describe bacterioides
opportunistic, obligate anaerobes
435
Can you grow chlamydia on agar
No because it is an obligate intracellular parasite
436
How can you detect chlamydia
Serum antibodies and PCR
437
Describe the flagellum of a spirochete
Have an endoflagellum that lies between the inner and outer membrane
438
Name the spirochaete that is responsible for causing lyme disease
B. Burgdoferi
439
Name the spirochaete that is responsible for causing syphilis
T.pallidum
440
What are dimorphic fungi
Fungi that can exist both as yeast and as mould - they are yeast in tissues but mould in vitro
441
Give an example of a dimorphic fungi
Coccidioides Immitis
442
Name three common fungal infections
Nappy rash Tinea Pedis Onychomycosis
443
name a drug that is used in the treatment of onychomycosis
Terbinafine - good at reaching poorly perfused areas
444
What can antifungal treatments target
1. Fungal cell wall which contains polyssacharides and chitin 2. Ergosterol containing plasma membrane
445
Give 4 disadvantages of azoles
1. High first pass metabolism 2. ADRs - cause hepatitis 3. Drug interactions due to CYP450 4. Resistance can develop ie. in candida
446
What is candida
A yeast that grows in warm moist areas and has high levels of B-D-glucan
447
What test can be done to identify fungal antigens
B-D-glucan test
448
Give an example of a mould
Aspergillus fumigatus | Aspergillus Niger
449
What are moulds composed of
Branched filamentous filaments called hyphae
450
Why is it hard to use therapeutic antibodies against mycobacteria
Mycobacteria grow very slowly and so treatment with antibodies is difficult and it is hard to culture them
451
How can you detect whether an individual has had previous exposure to Tb
1. Tuberculin skin test (Mantoux) | 2. Interferon gamma release assay
452
Name 6 sterile sites in the body
``` Urinary tract CSF Pleural fluid Peritoneal cavity Blood Lower respiratory tract ```
453
Where in the body would you find normal flora (Commensals)
``` Mouth Skin Vagina Urethra Large intestine ```
454
Which lance field groups are associated with tonsillitis and skin infection
A, C and G
455
Which lance field groups are associated with neonatal sepsis and meningitis
B
456
Which lance field groups are associated with UTIs
D
457
What is the oxidase test
Detects the presence of cytochrome oxidase in bacteria - positive test is indicated by the disk turning blue
458
Which group of streptococci can cause infective endocarditis
Alpha haemolytic streptococci
459
How can you differentiate streptococci pneumoniae from other streptococci
Optochin test - Pneumococci are sensitive so clear area would be seen
460
What is the function of bile salts in MacConkey agar
inhibit the gram positive bacteria growth
461
What is CLED agar used for
It is used to differentiate micro-organisms in urine and can classify lactose fermenters and non-lactose fermenters
462
What is XLD agar used for
selective growth medium used to isolate salmonella and shigella
463
Why do bacteria produce coagulase
used it as a defence mechanism by clotting the areas of plasma around them thereby resisting phagocytosis
464
What two species of plasmodia genus lie dormant and cause late relapse of malaria
P.ovale and P.vivax
465
malaria diagnosis - what can thick and thin films tell you
Thick films - sensitive but low resolution - tell if you have malaria Thin films - tell you the malaria species and the parasite count
466
What genetic consditions can give immunity to malaria
Someone with sickle cell anaemia and thalassaemias
467
What part of the virus will enter the host cell
Only the viral core carrying nucleic acids will enter the host cell cytoplasm
468
How do viruses interact with host cells
Viruses used the cell materials for their replication and they evade host defence mechanisms
469
How can viruses by released from a cell
1. Bursting open = lysis | 2. Leaking from the cell over a period of time = exocytosis
470
What are the 5 was a virus can ever 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
471
Where on the bacteria would penicillin bind
Bacteria cell wall
472
What is MIC
Minimum inhibitory concentration - lowest concentration of a chemical that prevents bacterial growth
473
Does the lowest MIC mean the best antibiotic
No - other considerations are important such as number of binding sites occupied and how long they are occupied for
474
What does a drug need to do to ensure it inhibits metabolic processes
1. Occupy and adequate number of binding sites | 2. Occupy these binding sites for a sufficient period of time
475
Amoxiciilin can be given to people infected with which bacteria
H.influenzae, enterococci, e.coli, shigella, streptococci etc.
476
A person presents with cellulitis. What antibiotic might you give them?
Flucloxacillin - s.pyogenes and staph.aureus are often a cause of cellulitis.
477
What are Carbapenemase producing enterobacteriaceae (CPEs)?
Gram negative bacteria that are resistant to broad spectrum antibiotics (carbapenems).
478
What is carbapenemase?
An enzyme that hydrolyses carbapenems and confers antibiotic resistance.
479
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.
480
Is pneumonia caused by pneumocystis jirovecii bacterial or fungal?
Fungal!
481
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.
482
Name 6 vaccine preventable diseases that are notifiable.
1. Diptheria. 2. Measles. 3. Mumps. 4. Rubella. 5. Tetanus. 6. Whooping cough.
483
What are the disadvantages of polysaccharide vaccines?
Protection is not long lasting and the response in children is poor.
484
How can polysaccharide vaccines be improved?
Conjugation can help improve immunogenicity.
485
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.
486
What antibiotic can be used to kill bacterioides?
Bacterioides are gram negative anaerobic bacilli. Metronidazole is the treatment of choice against anaerobes.
487
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. These are probably 1. Streptococcus pneumoniae 2. Staphylococcus epidermidis 3. Viridans Streptococci 4. Group A streptococci (S. pyogenes) 5. Neisseria meningitidis
Streptococcus Pneumoniae
488
Which of these is a gram negative bacillus that ferments lactose? 1. Shigella sonnei 2. Listeria monocytogenes 3. Neisseria meningitidis 4. Eschericia coli 5. Streptococcus pyogenes
Eschericia Coli
489
Which is incorrect? Haemophilus influenzae is an important cause of 1. meningitis in pre-school children 2. Otitis media 3. Pharyngitis 4. Gastroenteritis 5. Exacerbations of Chronic Obstructive Pulmonary Disease (COPD)
Gastroenteritis
490
``` Which is a normally sterile site? The pharynx The urethra Cerebrospinal fluid The lung Skin ```
CSF
491
Which of these is NOT a means by which viruses cause disease? 1. direct destruction of host cells 2. cell proliferation and cell immortalisation 3. inducing immune system mediated damage 4. Endotoxin production 5. modification of host cell structure or function
Endotoxin Production
492
When diagnosing viral infections which is not true? 1. The sample must come from a sterile site 2. Electron microscopy is rarely used 3. Use a green swab not a black swab 4. PCR results take 1-2 days 5. A detectable IgM in serum may be diagnostic
The sample must come from a sterile site
493
Which is most accurate?The HIV virus envelope contains 1. RNA + capsid + DNA polymerase 2. DNA + capsid + Reverse transcriptase 3. DNA + p24 + protease 4. RNA + capsid + reverse transcriptase
RNA + Capsid + reverse transcriptase
494
Which pair is correct? 1. Pityriasis versicolor = bacterium 2. Ringworm = helminth 3. Aspergillus fumigatus = mycobacterium 4. Falciparum malariae = fungal 5. Giardia lamblia = protozoal
Giardia lamblia = Protozoal
495
Mycobacteria. Which is not a feature? 1. Resistance to destaining by acid and alcohol 2. Cell wall contains lipoarabinomannan 3. They only divide every 20 hours 4. They cannot withstand phagolysosomal killing 5. May cause meningitis
They cannot withstand phagolysosomal killing
496
Regarding antimicrobial resistance, which is true? 1. it is spread by plasmid mediate gene transfer 2. spontaneous gene mutations do not occur 3. MRSA refers to vancomycin resistant S. aureus 4. Only Mereopenem is effective against all gram negative bacteria
MRSA refers to vancomycin resistant S. aureus
497
Antimicrobials. Which paring is incorrect 1. S. pyogenes : can use penicillin 2. Meropenem : a carbapenem 3. Glycopeptides : use for MRSA 4. Co-amoxiclav : contains a Beta-lactamase inhibitor 5. Cefuroxime : a macrolide
Cefuroxime : a macrolide
498
A 21 year old complains of myalgia, sore throat and tiredness. He is febrile and has an enlarged spleen. Which is the best answer? 1. He has sepsis and needs broad spectrum antimicrobial therapy with cefotaxime 2. A charcoal throat swab will confirm the diagnosis Finding atypical lymphocytes on a blood film and a positive EBV IgM in serum would be consistent 3. PCR on a viral throat swab will confirm the diagnosis 4. This is a viral upper respiratory tract infection and doesn’t warrant investigation or antimicrobial therapy
Finding atypical lymphocytes on a blood film and a positive EBV IgM in serum would be consistent
499
A 34 year old gay man who has had prolonged diarrhoea now presents short of breath with a dry cough and hypoxia. Which is most accurate? 1. This is bacterial pneumonia caused by pneumocysitis jirovecii. 2. It is too early for a 4th generation HIV test to be positive 3. The CD4 T cell count will be between 500 and 750 4. Even if the HIV test is negative this man has AIDS 5. With appropriate therapy he has a good prognosis
With appropriate therapy he has a good prognosis
500
Which of these does NOT feature in the definition of Sepsis? 1. Temperature >38.3oC or <36oC 2. Heart rate >90 3. Systolic blood pressure >130 4. White Cell count >12 5. Hypoxia
Systolic blood pressure >130
501
What are retroviruses?
Enveloped viruses
502
Describe the genetic component of a retrovirus
Viral genetic material is RNA which is copied into DNA by reverse transcriptase and incorporated into the host cell to allow gene transcription
503
What is the origin of HIV 1 lentivirus
Originates from the simian immunodeficiency viruses chimpanzees
504
What is the origin of HIV2 lentivirus
Simian immunodeficiency virus sooty mangabey
505
Describe the structure of HIV
Enveloped with GP120 and GP41 Matrix with P17 protein Protein capsid with p24 protein housing the core enzymes Viral RNA, reverse transcriptase and integrase
506
What does HIV result in?
The death of CD4+ T lymphocytes - replication of the virus within the CD4 T cells leads to their death
507
Describe the pathophysiology of HIV
1. Attachment and entry - gp120 attaches to CD4 receptor and CCR5 co-receptor 2. Uncoating - Viral capsid enters cell and nucleic acids and enzymes released 3. Reverse transcriptase - converts RNA to double stranded DNA 4. Integration - viral integrase integrates viral DNA into host DNA 5. Transcription - when the cell divides, the viral DNA is transcribed and proteins are produced 6. Virion assembly - viral RNA and proteins are reassembled to form a new virus 7. Budding - immature virus leaves the cell through exocytosis and breaks free to undergo more maturation
508
What are the main CD4 T cells affected
Memory CD45RO are infected preferentially early on Naive CD45R cells infected later on
509
What are the main CD4 T cells affected
Memory CD45RO are infected preferentially early on Naive CD45R cells infected later on
510
Describe how the HIV infection works
1. Virus enters the body through mucosa and becomes established in mucosal macrophages or dendritic cells and spreads to other cells 2. HIV APC's migrate to the lymph nodes and present to T cells - T cell infection 3. Infected T cells enter bloodstream = exponential T cell infection rise = viremia
511
What are the mucosal surfaces that viruses infect
Vagina/rectal and intestinal
512
Describe the humoral HIV immune response
Low numbers of neutralising antibodies due to viral genetic variability
513
Describe the cell mediated HIV immune response
CD8 Cytotoxic T lymphocytes cause early reduction in HIV numbers but the immune response is incomplete due to virus escape due to mutations CD4 lymphocyte numbers are reduced due to the HIV infection - no proliferation
514
What characterises the HIV infection
A progressive decline in the number and function of CD4T lymphocytes leading to a susceptibility of disease
515
Name the mechanisms by which CD4 lymphocytes are depleted by the HIV infection
1. CD4 cell death - direct cytotoxicity and premature apoptosis 2. Decreased T cell production due to infected bone marrow progenitors 3. Activation induced death 4. Redistribution 5. Bystander killing
516
Describe the mechanisms of HIV immune dysfunction
1. CD4 depletion mechanisms 2. Excessive and innapropriate activation of immune system 3. Decreased proliferation in response to antigens 4. Increased activation of CD8 lymphocytes but decreased cytolytic function 5. Increased B cell activation and decreased proliferation resulting in increased non-specific antibody production but decreased specific antibody production 6. Decreased function of NK, macrophage and neutrophils
517
Where are the HIV reservoir sites
Genital/GIT CNS Bone Macrophages and microglia
518
What is the UNAIDs 90/90/90 principle
90% of people with HIV should be diagnosed 90% of diagnosed patients should be on ART 90% of patients on ART should have viral suppressants by 2020
519
Define a late diagnosis of HIV
CD4 count below 350 = 10 fold increased in the risk of death in the first year of diagnosis
520
Which groups of people are most likely to be diagnosed late with HIV
Women Older age groups (50+) Black African ethnicity
521
How Is HIV transmitted
Blood Sexually Vertically (Mother to child)
522
How can we prevent HIV
``` Circumcision Pre/post-exposure prophylaxis of HIV Behaviour (Sex ed, safe sex) Antiretroviral treatment STI control Vaccines Microbicides HIV diagnosis/partner notification Screen blood products Needle exchange ```
523
What is the U=U campaign
Undetectable = untrabnsmittable signifies that those who receive effective antiviral therapy and have achieved and maintained an undetectable viral load cannot transmit the virus to a sexual partner
524
What are the effects of the U=U campaign
Remove the fear of sexual transmission Dismantle HIV stigma Encourage people with HIV to start and stay on treatment Encourage people to get tested
525
What are the benefits of knowing your HIV status
``` Access to care Reduce vertical transmission Reduce sexual transmission Public health Reduction in morbidity and mortality Cost effect ie. - Saving on social care - prevent lost working days - Prevent benefit claims - Prevent costs associated with further onward transmission ```
526
Who gets screened for HIV
Clinician triggered tests (Symptoms) High risk groups Patient requests Antenatal screening
527
What are the risk factor for HIV
Sexual contact with high risk groups ie. Iv drug users Multiple sexual partners Rape in high risk areas Mother to child transmission
528
What are the general symptoms of HIV
``` Lymphadenopathy Acute rash Immune dysfunction Glandular fever Prolonged episodes of herpes Persistent recurrent candidiasis unexplained weight loss or night sweats Persistent diarrhoea Increasing shortness of breath and dry cough Recurrent bacterial infections (Pneumoccocal pneumonia) ```
529
How do you test someone for HIV
1. Venous blood sample - detectable 4 weeks after infection | 2. HIV point of care tests - pinprick of blood
530
What are the advantages of point of care testing
Outreach into community settings Increase patient choice Increased access to testing and case detection Earlier diagnosis in non-healthcare seeking individualls Reduce risk of complications Reduce transmission
531
Why do doctors not test for hIV
1. Don't think of HIV 2. Underestimate the risk of HIV in their patients 3. Failure to recognise HIV as modifiable prognostic indicator 4. Misconception they need pre-test counselling 5. Misunderstanding of the implications for insurance 6. Fear of offending the patient
532
Describe what happens to the CD4 count in stages during a HIV infection
Acute primary infection = transient immunosuppression where there is a fall then a rise in CD4 Asymptomatic phase where there is progressive loss of CD4+ T cells = poor immunity Early symptomatic phase - manifestations of clinical features AIDS
533
Define AIDS
CD4 T cell count <200 leading to immune deficiency symptoms and opportunistic infections Normally takes 5-10 years to reach AIDs status and faster/elderly children with high viral loads
534
Patient with a fever, rash and non-specific symptoms should be test for what?
HIV
535
What are the primary HIV infection symptoms
``` 2-4 weeks between infection and symptoms Abrupt onset of non-specific symptoms Weight loss Lethargy Fever Rash ```
536
A patient with recurrent shingles and candidiasis should be tested for what condition
HIV
537
What conditions occur in association or are more frequent with HIV
Oral/vaginal candidiasis Oral hairy leukoplakia Varicella zooster virus
538
Name some AIDs respiratory conditions
Pneumocystis pneumonia Bacterial pneumonia (Pneumoccocal, H.influenza, S.aureus) TB Fungal infections - candidiasis, pneumocystis jiroveci pneumonia (PCP)
539
Name some AIDS CNS conditions
CNS lesions = cerebral toxoplasmosis, tuberculoma (Space occupying lesion), primary CNS lesion Ophthalmic lesions = cytomegalovirus retinitis, choroidal tuberculosis, toxoplasmosis chorioretinitis Meningitis = cryptococcal, tuberculous, pneumococcal
540
Name some neoplasms associated with AIDS
Lymphoma - CD4 count under 100 = non-hodgkins lymphoma or primary CNS lymphoma Kaposis sarcoma Cervical Neoplasia
541
What are the treatment options for HIV
Reverse transcriptase inhibitors Protease inhibitors - cant repackage new virus Fusion inhibitors HAART
542
Which individuals are most at risk of HIV
``` Men how have sex with men Heterosexual women Injecting drug users Commercial sex workers Heterosexual men Truck drivers Migrant workers ```
543
Which age group is most affected by HIV
15-24 year olds
544
What are the difficulties in delivering ART in developing countries
``` Awareness Procurment/delivery Clinical services (Staff, clinics, testing) Cost/choice of drugs Adherence Efficacy Co-morbidities ```
545
What virus can cause shingles
Varicella zooster virus
546
Where might one see a shingles rash
May appear on the dermatomes but associated with area of tight clothing
547
What laboratory tests may be used to detect viral pathogens
PCR
548
Give some signs and symptoms of infective mononucleosis (Glandular fever)
1. reddening, swelling and white patches on tonsils 2. Swollen lymph nodes 3. Spleen enlargement 4. Chills and fever 5. Cough 6. Sore throat 7. Fatigue, malaise, loss of appetite and headache
549
What is the management/treatment of glandular fever
Supportive therapy and advise patient to avoid contact sport for 6 weeks in order to avoid splenic rupture
550
What can qPCR detect
Presence/absence of DNA/RNA Can quantify the level of virus in a tissue
551
What are the consequences of infleunza A infection
Increased risk of ARDs and secondary bacterial pneumonia - patient will be highly infective
552
What are the markers for HIV in the blood
Antigens Antibodies HIV RNA
553
If a HIV test comes back as negative in a high risk individual, why should a second HIV test be done
Second test after the window period - window period is time between exposure to HIV infection and the point when the test will give and accurate result - during this time a person can be infected with hIV and be very infectious but still test HIV negative
554
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 ART
555
What are the three 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
556
How does circumcision reduce the sexual transmission of HIV
Change in the mucosa - HIV is less able to penetrate due to an increase in keratinisation
557
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
558
What are the two markers that are used for monitoring HIV
1. CD4+ count | 2. HIV RNA copies (Viral load)
559
What is HIV seroconversion
A period of time during which HIV antibodies develop and become detectable - usually takes place within a few weeks of initial infection
560
What are the characteristic signs of pneumocystis pneumonia
Decreased CD4+ count Decreased O2 sats on exertion Decreased exercise tolerance
561
What is HAART and what does it aim to do?
Anti-viral treatment where 3 drugs are taken together - aim is to reduce viral load and increase CD4+ count
562
Chicken pox is caused by what virus
Varicella zoster virus
563
What is the primary infection with varicella zoster virus
chicken pox
564
What is the second infection with varicella zoster virus
Shingles
565
How does the varicella zoster virus enter the body
Mucous membranes or if you touch a lesion
566
How long is the symptomatic incubation period for varicella zoster virus
7-21 days
567
What are the high risk groups for varicella zoster infection
``` immunocompromised Adults Infants pregnancy Smokers ```
568
Describe the stages of lesion formation process in chickenpox
``` Macule (Flat, can see but cant feel) Papule (See and feel) Vesicle (Fluid filled) Pustule (WBC filled) Crust ```
569
What are the complications of varicella zoster viral infection
``` Dehydration Haemorrhagic change Cerebellar ataxia Encephalitis Chicken pox pneumonitis Skin and soft tissue infections Varicella pneumonia ```
570
Where does the chicken pox virus lie dormant
dorsal root or cerebral ganglion for years
571
Describe the pathophysiology of shingles
Primary infection moves down sensory neurones - lies dormant in dorsal root Reduced immune system - localised reactivation affects the dermatome
572
What does parvovirus do
Attaches to immature red precursor cells which prevents their maturation and increases the risk of the individual developing anaemia
573
What treatment is used for herpes
Acyclovir

Phase 2 (16 decks)

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