Medical microbiology! Flashcards
(198 cards)
1
Q
What is a key epidemiology marker?
A
Death/mortality.
2
Q
What is epidemology?
A
Diagnose, treat, prevent
epi = of demos = the people
- study of disease
3
Q
Why is infection important in epidemiology?
A
It was and still is a major killer.
1.7 million people in 20th century
4
Q
2 major bacterial diseases? one respiratory, one diarrhoeal
A
Respiratory - mycobacterium tuberculosis
Diarrhoea - vibrio cholerae
5
Q
Which infectious diseases were major killers in the last century?
A
Measles, HIV/AIDS, Hepatitis, Influenza, Respiratory viruses, Smallpox (eradicated).
6
Q
Which infectious diseases are of current and future concern?
A
HIV/AIDS, Influenza, SARS and Ebola, COVID, parasitic diseases, bacterial diseases.
7
Q
What threats are projected to increase global deaths?
A
Antimicrobial resistance, COVID, and another pandemic.
8
Q
What is an obligate pathogen?
A
A pathogen that can only reproduce inside a host.
- causes damage and infection
9
Q
Give an example of an obligate pathogen.
A
Mycobacterium tuberculosis.
10
Q
What disease does Mycobacterium tuberculosis cause?
A
Tuberculosis.
11
Q
What are the characteristics of Mycobacterium tuberculosis?
A
Obligate pathogen, gram +ve, aerobe, actinobacteria.
12
Q
What is a facultative pathogen?
A
A pathogen that can cause disease in a host but can also live and reproduce in a non-pathogenic manner.
A facultative pathogen is a microorganism that can cause disease but doesn’t necessarily require a host to survive. It can replicate in an environmental reservoir, like water or soil, and only infects a host if it encounters one
- only causes disease in one part of its lifecycle or if in a specific host
13
Q
Give an example of a facultative pathogen.
A
Vibrio cholerae.
14
Q
What disease does Vibrio cholerae cause?
A
Cholera.
15
Q
What are the characteristics of Vibrio cholerae?
A
Gram -ve, facultative anaerobe, proteobacteria.
16
Q
What is an opportunistic pathogen?
A
A pathogen that causes disease in a compromised host (e.g., weakened immune system).
17
Q
Give an example of an opportunistic pathogen that is gram -ve.
A
Pseudomonas aeruginosa.
18
Q
What does Pseudomonas aeruginosa cause?
A
Wound, blood, burn, and lung infections.
19
Q
What are the characteristics of Pseudomonas aeruginosa?
A
Gram -ve, proteobacteria.
20
Q
Give an example of an opportunistic pathogen that is gram +ve.
A
Staphylococcus aureus.
21
Q
What does Staphylococcus aureus cause?
A
Skin, wound, blood infections and endocarditis.
22
Q
What are the characteristics of Staphylococcus aureus?
A
Gram +ve, firmicutes phylum, bacilli class.
23
Q
What is a commensal pathogen?
A
Bacteria that live on the body surface or mucosa without harming human health but may elicit an immune response.
24
Q
Give examples of commensal gut bacteria.
A
Lactobacillus and Acidophilus.
25
What are the characteristics of Lactobacillus and Acidophilus?
Gram +ve, firmicutes, bacilli; promote health and are part of the normal gut microbiota.
26
What is pneumonia?
Swelling (inflammation) of tissue in one or both lungs.
27
What is bronchitis?
Infection of the main airways of the lungs (bronchi), causing irritation and inflammation.
28
Why are lower respiratory infections (LRI) significant?
They are the leading cause of death due to infectious disease in the world.
29
What were the global LRI stats in 2019?
2.5 million deaths, 672,000 children under 5, 1.23 million adults over 70.
30
Name 4 major pathogens involved in LRI.
Streptococcus pneumoniae, Haemophilus influenzae type B, Influenza virus, Respiratory syncytial virus.
31
What are the features of Streptococcus pneumoniae?
Gram +ve, cocci, opportunistic pathogen, extracellular bacteria. becoming more resistant due to colonisation.
32
Where are most cases of S. pneumonie found?
In children
33
What is bacterial carriage?
The harbouring of a potentially disease-causing organism without contracting the disease.
34
Is S. pneumoniae an obligate human host?
Yes.
35
How is S. pneumoniae transmitted?
Contact with secretions (saliva and mucus).
36
What percentage of invasive S. pneumoniae infections are fatal?
5%.
37
What are the treatment options for S. pneumoniae?
Oral B-lactams; IV: ceftriaxone, cefotaxime, or amoxicillin-clavulanic acid.
38
What vaccines are used for S. pneumoniae?
PCV7, PCV13 (babies), PPSV23 (adults over 65).
39
How does S. pneumoniae evolve genetically?
Transformation - through uptake and incorporation of exogenous DNA via natural competence.
40
What are the features of Haemophilus influenzae?
Gram -ve, pleomorphic coccobacillus (variable shape), extracellular, opportunistic pathogen.
41
What divides typeable and non-typeable strains of H. influenzae?
Presence or absence of a polysaccharide capsule.
42
What is the colonisation rate of H. influenzae?
20% infants <1, 50% aged 5–6, 75% adults.
43
How is H. influenzae transmitted?
Airborne droplets and secretions.
44
What diseases do NTHi strains cause?
Bronchitis (children), pneumonia (adults with lung disease).
NTHi means no polysaccharide capsule
45
What antibiotics are used to treat H. influenzae?
B-lactams, cephalosporins, amoxicillin-clavulanic acid, TMP-SMX, tetracyclines, quinolones, macrolides.
46
What vaccine covers H. influenzae?
The 6-in-1 vaccine (3 doses at 8, 12, and 16 weeks).
- covers tetanus and Hep B too
47
What are the four influenza genuses and what's the family?
- Family: Orthomyxoviridae
Genuses: (geni??)
Influenza A, B, C, D
48
What animals can influenza A infect?
Humans, pigs, horses, poultry, and wild migratory birds.
49
Which influenza strains affect humans?
Influenza A and B.
50
What does influenza B infect?
Humans only
51
How many influenza seasons are there per year?
2 - northern and southern hemisphere
one in winter for us and then one for winter in Australia ect
52
What are the main transmitters of influenza?
Children
53
What is the influenza incubation period?
1–4 days.
54
What is the annual global burden of influenza?
~1 billion infections, 3–5 million severe cases, 300,000–500,000 deaths.
55
What is the death rate of influenza?
0.1%
56
What type of virus is influenza?
Negative-sense, single-stranded RNA virus with 8 segments.
- RNA strand is complementary to mRNA and require RNA polymerases (can't make themselves)
57
What do segments 1–3 of influenza RNA code for in the host cell?
RNA-dependent RNA polymerases.
58
What does segment 4 code for?
HA (haemagglutinin) – binds to sialic acid receptors on human cells.
59
What does segment 5 code for?
NP (nucleoprotein) – binds viral RNA genome.
60
What does segment 6 code for?
NA (neuraminidase) – helps viral release and spread.
61
What is antigenic drift?
Gradual accumulation of mutations = minor changes in surface proteins.
- escapes vaccine
62
What is antigenic shift?
Sudden major change when viral strains combine to form a new subtype (e.g., COVID).
63
Why is antigenic shift dangerous?
It can cause pandemics due to little to no population immunity.
64
What are post-influenza bacterial superinfections?
Flu weakens immune system, leading to secondary infections (e.g., S. pneumoniae, H. influenzae).
65
How is the flu vaccine produced?
Egg-based takes 6 months; cell-based takes 3 months.
66
What is herd immunity?
When enough people are vaccinated, disease transmission becomes difficult.
67
What is the incubation period of SARS-CoV-2?
2–14 days.
68
What is the infection rate in the population?
131 per 100,000 people.
69
What is R0 for COVID-19?
3.28 – average number of secondary infections per primary case.
70
How big can the corona virus be?
Up to 32kbps
71
What type of virus is SARS-CoV-2?
+ve single-stranded RNA virus.
72
How many coding regions are predicted in corona virus RNA?
12
73
What does the 1ab region encode?
Replicase proteins with proofreading activity.
74
What does the S gene encode?
Spike protein – binds to cell receptors.
75
What does the E gene encode?
Envelope protein – morphogenesis, assembly, budding.
76
What does the M gene encode?
Membrane glycoprotein.
77
What does the N gene encode?
Nucleocapsid protein – binds RNA genome in a beads on a string fashion.
78
What animal has the highest similarity to SARS-CoV-2?
RaTG13 bat coronavirus (96.2% similarity).
79
What pangolin virus shares key features with SARS-CoV-2?
MP789 – shares 5 amino acids for ACE2 binding in the S.
80
What is diarrhea?
The passage of unusually loose or watery stools at least three times in 24 hours.
81
What are the four main types of diarrhea?
Acute watery
Acute bloody (dysentery)
Persistent (14+ days)
Diarrhoea with severe malnutrition.
82
What are the 2 types of acute watery diarrhoea?
Osmotic
Secretory
83
What causes osmotic diarrhea?
Presence of non-absorbable solutes in the intestine.
84
What causes secretory diarrhea?
Excessive secretion of electrolytes and water into the gut.
85
What characterizes acute bloody diarrhea?
Presence of mucus and blood in stools.
86
What is persistent diarrhea?
Diarrhea lasting 14 days or longer.
87
What is diarrhea with severe malnutrition?
Diarrhea associated with Marasmus or Kwashiorkor.
88
How common are diarrheal diseases in children?
1.7 billion cases per year globally.
89
How often do adults experience diarrhea?
On average once every two years.
90
Why is diarrhea dangerous in children?
It is a leading cause of malnutrition in children under 5 and is a vicious cycle of malnutrition leading to diarrhoea but diarrhoea leading to malnutrition too
91
What is the leading viral cause of childhood diarrhea?
Rotavirus.
92
What impact did rotavirus vaccination have in Rwanda?
61-70% reduction in rotavirus cases.
93
Name 3 key bacterial causes of diarrhea.
Shigella, Salmonella, Campylobacter.
94
What are the 4 Shigella species?
S. flexneri, S. sonnei, S. boydii, S. dysenteriae.
95
What is the most common cause of food poisoning in the U.S. & Europe?
Campylobacter jejuni.
96
List types of diarrheagenic E. coli strains.
EPEC, EHEC/STEC, ETEC, DAEC, EAEC, EIEC.
97
Can E.coli be commensal?
Yes 10^21 cells are commensal
98
What type of diarrhoea does E.coli cause?
Blood diarrhoea
99
How many E. coli are there?
6
- and no vaccines!
100
What does EPEC stand for?
Enteropathogenic E. coli.
101
What does EHEC/STEC stand for?
Enterohemorrhagic / Shiga-toxin-producing E. coli.
102
What does ETEC stand for?
Enterotoxigenic E. coli.
103
What does DAEC stand for?
Diffusely adherent E. coli.
104
What does EAEC stand for?
Enteroaggregative E. coli.
105
What does EIEC stand for?
Enteroinvasive E. coli.
106
What bacteria causes cholera?
Vibrio cholerae.
107
What bacteria is linked to antibiotic-associated diarrhea?
Clostridium difficile.
108
What pathogen produces enterotoxins?
Toxigenic Staphylococcus aureus.
- food poisoning but only sick because of the toxin it produces
109
What are the main organs of the digestive system?
Stomach, duodenum, jejunum, ileum, colon, rectum.
110
What are 3 functions of the digestive system?
Digestion, absorption, elimination of waste.
111
Where does Hep B target?
Liver
112
Where does cholera target?
Jejunum (pathogens go into the bottom of the villi) and ileum and appendix
113
Where does clostridium difficile target?
Colon (pathogens mostly stay at the top of the villi)
114
Where does salmonella target?
Gallbladder
115
What are some host defenses in the gut?
Mucus layer, microbiota, antimicrobial proteins like IgA, virulence factors to target bacteria
116
What enzymes do the GI tract have?
Brush border enzymes
- some pathogens destroy the brush border so cells can't digest the food and get a large influx of water - osmotic diarrhoea
117
What enzyme breaks sucrose into glucose and fructose?
Sucrase-isomaltase.
118
What happens if sucrose isomaltase is destroyed?
Sucrose concentration increases so osmotic pressure increases
119
What enzyme breaks lactose into glucose and galactose?
Lactase.
120
What enzyme breaks maltose into glucose?
Maltase.
121
What is secretory diarrhoea caused by?
Toxins
122
What causes secretory diarrhea in cholera?
Cholera toxin increases cAMP → chloride secretion via CFTR channels which are then constantly open when cholera binds.
- H20 follows the Cl- so lots of water moves in
123
How much fluid can be lost per hour in cholera?
Up to 1L per hour.
124
What are 3 major sources of diarrheal disease transmission?
Water, food, human contact (fecal-oral).
- sewage into water - wash hands and food
125
Which vegetables were linked to ETEC?
Parsley.
126
Which vegetables were linked to EAEC?
Bean sprouts.
127
Which vegetables were linked to EHEC?
Radish sprouts, alfalfa sprouts, romaine lettuce.
128
What % of UK motorway users claimed to wash hands?
99%.
129
What % of men actually washed hands?
32%.
130
What % of women actually washed hands?
64%.
131
Where was fecal bacteria found in the UK study?
26% of hands, 16% of phones, 14% of banknotes, 10% of credit cards.
132
What % of people wash hands before eating?
Only 39%.
133
Name 3 key prevention strategies for diarrheal disease.
Safe water, sanitation, exclusive breastfeeding (to pass on immunoglobulins).
134
What hygiene measure can reduce diarrheal cases by 23-40%?
Hand washing with soap.
135
How much can handwashing reduce diarrhea in immunocompromised individuals?
By 58%.
136
How much does handwashing reduce school absenteeism?
By 29–57%.
137
What is ORS and what does it contain?
Oral rehydration salts; water, salt, and sugar.
138
Why is ORS effective?
Absorbed in small intestine and replaces lost fluids.
- makes osmotic diarrhoea worse in children tho
139
When is IV fluid needed?
Severe dehydration or shock.
140
What is a caution when using ORS?
Watch for osmotic diarrhea patients.
141
How does zinc help treat diarrhea?
Reduces duration by 25% and increases stool volume by 30%. Helps immune system respond faster
142
Why are nutrient-rich foods important?
Prevent malnutrition but may worsen osmotic diarrhea.
143
When is loperamide used?
For symptom relief; use with caution as it slows gut motility - block stools leaving and bacteria build up
144
Are antibiotics always used?
No, only for specific infections; avoided in EHEC to prevent HUS.
- can be lethal if used for blood diarrhoea as toxins build up
145
What are the 6 key concepts to know?
Definition/types, mechanisms, epidemiology, pathogens, prevention, treatment.
146
What is an antibiotic?
A chemical compound produced by a microbe that kills or inhibits other microbes, specifically bacteria, with a single mode of action.
147
What is an antimicrobial?
Any compound that kills or inhibits microbes (bacteria, viruses, fungi), not limited to bacteria.
148
Who discovered the first antibiotic, and what was it?
Alexander Fleming in 1928; Penicillin from Penicillium notatum - a fungi that inhibited staphylococcus aureus
149
What was the first antibiotic produced (not discovered)?
A sulphonamide
150
What are the three types of antimicrobial action?
Bacteriostatic (inhibit growth), Bactericidal (kill cells, no lysis), Bacteriolytic (kill and lyse cells).
151
What is the difference between narrow-spectrum and broad-spectrum antibiotics?
Narrow-spectrum targets specific bacteria; broad-spectrum targets many bacteria.
152
What are the advantages of narrow spectrum activity?
Limits spread of resistance and less detrimental on microbiome
153
Challenges to narrow spectrum activity?
Requires rapid, accurate and sensitive diagnostic assays for identification of bacteria
154
Advantages of broad spectrum activity?
Can be used quickly before formal identification of causative bacteria
155
Challenges to broad spectrum activity?
Selection for and spread of resistance
156
Give an example of a narrow-spectrum antibiotic.
Azithromycin (Macrolide to treat pneumonia).
157
Give an example of a broad-spectrum antibiotic.
Amoxicillin.
158
What do beta-lactams target?
Bacterial wall synthesis
159
What do sulphonamides and fluoroquinolones target?
DNA synthesis
160
What do macrocodes, tetracyclines and ahminoglycosides target?
Protein synthesis
161
Which classes of antibiotics target the bacterial cell wall?
β-Lactams - bactericidal - kill but not lyse, broad spectrum
162
Which classes of antibiotics inhibit protein synthesis by binding the 50S ribosome?
Macrolides.
163
Which classes of antibiotics inhibit protein synthesis by binding the 30S ribosome?
Tetracyclines and Aminoglycosides.
164
Which class of antibiotics inhibits DNA synthesis by targeting topoisomerases II and IV?
Fluoroquinolones.
165
Name a key side effect of β-Lactams.
Allergic reactions.
166
Name a key side effect of Sulfonamides.
Hypersensitivity, anemia, insomnia.
167
What type of antibiotic are sulphonamides?
Bacteriostatic (stops growth but not death)
Broad spectrum
Targets DNA synthesis
Competitive inhibitors of folate synthesis (needed for purines)
168
Name a key side effect of Fluoroquinolones.
Tendinopathy, hyperglycemia/hypoglycemia.
169
What type of antibiotic are fluoroquinolones?
Bactericidial (kills but doesn't lyse)
Broad spectrum
Targets DNA synthesis by inhibiting topoisomerases - lowers transcription and replication
170
Name a key side effect of Macrolides.
Heart arrhythmias, hepatotoxicity.
171
What type of antibiotics are macrolides?
Bacteriostatic
Broad spectrum
Targets protein synthesis
Targets 50S ribosomal subunit
172
Name a key side effect of Tetracyclines.
Discoloration of teeth, photosensitivity, hepatotoxicity.
173
What type of antibiotics are tetracyclines?
Bacteriostatic
Broad spectrum
Targets 30S subunit of ribosome to stop protein synthesis
Never given to children
174
Name a key side effect of Aminoglycosides.
Nephrotoxicity, ototoxicity, neuromuscular blockage
175
What type of antibiotic are aminoglycosides?
Bacteriacidal
Broad spectrum
Targets 30S ribosome unit
Can't be absorbed so has to be injected IV
176
Why can’t antibiotics treat viral infections?
Viruses lack cellular structures like cell walls or ribosomes, which antibiotics target.
177
When are antibiotics used for viral infections?
For secondary bacterial infections (e.g., pneumonia after influenza).
178
Why are antibiotics used in agriculture?
For disease prevention, growth promotion, and improved feed efficiency.
179
What drives antibiotic resistance (AMR)?
Misuse/overuse in medicine and farming, patients not finishing prescriptions, poor infection control, lack of diagnostics.
180
Why has Big Pharma abandoned antibiotic research?
Low profits, high R&D costs, strict pricing regulations.
181
Name two future strategies for antibiotics.
Antimicrobial peptides, bacteriophage therapy, antivirulence therapies, combination therapies.
182
What are antimicrobial peptides (AMPs)?
Small proteins that attack bacterial membranes, broad-spectrum but may cause toxicity.
183
What are bacteriophages?
Viruses that kill bacteria, requiring personalized matching to patient-specific pathogens.
184
What is the main challenge with bacteriophage therapy/ antivirulence strategies?
Narrow host range and the need for personalized phage matching.
185
What is combination therapy?
Beta lactamase inhibitor and beta lactam
186
Name three WHO priority Gram-negative pathogens.
Acinetobacter baumannii, Pseudomonas aeruginosa, Escherichia coli (EHEC, ETEC).
187
What is the mechanism of action of β-Lactams?
Inhibit bacterial cell wall synthesis.
188
What is the mechanism of action of Sulfonamides?
Inhibit folate synthesis by blocking DHPS enzyme.
189
What is the mechanism of action of Fluoroquinolones?
Inhibit DNA topoisomerases II and IV.
190
What is the mechanism of action of Macrolides?
Bind the 50S ribosomal subunit to stop protein synthesis.
191
What is the mechanism of action of Tetracyclines?
Bind the 30S ribosomal subunit to stop protein synthesis.
192
What is the mechanism of action of Aminoglycosides?
Bind the 30S ribosomal subunit to stop protein synthesis.
193
What is a key challenge of broad-spectrum antibiotics?
Risk of selecting for resistance in many bacterial species.
194
What is a key advantage of narrow-spectrum antibiotics?
Less impact on host microbiome, lower risk of widespread resistance.
195
Why is combination therapy used in antibiotics?
To overcome resistance, e.g., β-lactam + β-lactamase inhibitor.
196
What is the target of antivirulence therapies?
Bacterial virulence factors (e.g., adhesins, toxins).
197
What is a major future challenge for antibiotic therapy?
Developing new drugs while balancing resistance risk and profitability.
198
Why is rapid diagnostics important in antibiotic use?
To quickly identify pathogens and reduce inappropriate antibiotic use.
