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Medical Microbiology Flashcards

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1
Q

What is the emphasis of medical microbiology compared to general microbiology?

A

Medical microbiology focuses on the prevention, diagnosis, and treatment of infectious diseases caused by microorganisms.

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2
Q

Why are strong microbiology laboratory systems crucial for infectious disease control?

A

Microbiology laboratories provide timely and reliable information on pathogen detection and characterization, essential for effective disease prevention and treatment, especially during epidemic threats.

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3
Q

What is the regional burden of infectious diseases, particularly in sub-Saharan Africa?

A

Sub-Saharan Africa bears a significant burden of infectious diseases, including tuberculosis, malaria, and antimicrobial resistance-related deaths.

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4
Q

Why is antimicrobial resistance (AMR) a global health threat?

A

AMR poses a critical threat to public health globally, potentially causing 10 million deaths annually and incurring a cumulative cost of $100 trillion by 2050 if unchecked.

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5
Q

Explain the clinical relevance of the Gram stain in microbiology.

A

The Gram stain helps classify bacteria based on their cell wall properties, informing diagnosis and treatment strategies. It distinguishes between Gram-positive and Gram-negative bacteria.

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6
Q

What are the key learning objectives in studying medical microbiology?

A

Understanding infectious disease syndromes, identifying causative microorganisms, grasping their pathogenesis, clinical features, diagnosis, treatment, and prevention methods.

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7
Q

Why is it essential to differentiate between broad-spectrum and directed antibiotic therapy?

A

Broad-spectrum antibiotics are used for empiric therapy but contribute to antimicrobial resistance. Directed therapy targets specific pathogens, optimizing treatment and reducing unnecessary antibiotic use.

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8
Q

ist major medically important bacteria and their classifications.

A

Gram-positive cocci, Gram-positive bacilli, Gram-negative cocci, Gram-negative bacilli, Spirochaetes, Anaerobes, and Mycobacteria.

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9
Q

What are the major infectious syndromes discussed in medical microbiology?

A

Respiratory tract infections, urinary tract infections, sepsis, intra-abdominal infections, cardiovascular infections, central nervous system infections, skin and soft tissue infections, gastrointestinal infections, bone and joint infections, and reproductive organ infections.

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10
Q

Name significant medically important fungi and parasites.

A

Fungal infections: Candida spp., Aspergillus spp., etc.
Protozoal infections: Malaria, E. histolytica, etc.
Helminth infections: Nematodes, Cestodes, Trematodes.

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11
Q

Meaning of pathogenicity

A

this refers to the capacity of a pathogenic agent to cause a disease in the host.

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12
Q

meaning of virulence

A

this is a measure of “pathogenicity” or the likelihood that a microorganism will cause a disease after infecting someone

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13
Q

Compare and contrast principle pathogens with opportunistic pathogens

A

Principle pathogens are highly virulent meaning that they may cause disease in hosts with an intact immune system. opportunistic pathogens cause disease in hosts with compromised immune system meaning that they are less virulent.

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14
Q

give the types of principal pathogens and an example of each

A

2 types, obligate pathogens e.g. salmonella typhi and Occasional pathogens e.g. staphylococcus aureus.

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15
Q

give types of opportunistic disease and an example of each

A

2 types, Classic opportunistic e.g. Pneumocytis jirovecii and Rare opportunistic e.g Proplonibacterium

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16
Q

how are mutations on the bacterial chromosome acquired

A

this are acquired by horizontal gene transfer

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17
Q

Give 3 different types of ways that horizontal gene transfer can occur

A

Bacterial transformation, Bacterial transduction, Bacterial conjugation

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18
Q

what are environmental non-pathogenic strains

A

Infected by a bacteriophage (a bacteriophage is a virus which infects bacteria) called “Vibrio Pathogenicity Island - VPIΦ”
VPIΦ encodes the ‘Toxin Co-regulated Pilus (TCP)’ which mediates attachment to mucosal receptors
Vibrio cholerae uses the TCP to wriggle through the mucus layer overlying gut cells
Does not invade, but lives attached to the gut mucosa

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19
Q

write a response for the interaction of TCP with CTX0

A

TCP acts as a receptor for a second bacteriophage called CTX0

CTX0 has genes for cholera toxin
increase in cAMP in gut cells
increase in the secretion of chloride
leading to massive fluid outpouring

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20
Q

Ways un which M.tuberculosis can spread.

A

Aerosol spread and droplet spread

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21
Q

what phagocytoses the small droplet of nuclei that enters terminal airspaces?

A

alveolar macrophage

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22
Q

how does M.tuberculosis survive within macrophages

A

inhibits phagosomal maturation
Inhibiting MHC Class II expression and Ag presentation

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23
Q

name intervention control

A

vaccine
anti-toxin
antibiotic
IPC
vector control

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24
Q

Treatment and prevention of cholera

A

Treatment
Rapid fluid replacement
Antibiotics only for severe disease
Prevention
Oral vaccines about 80% effective
Infection prevention and control
Water and food hygiene
sanitation

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25
M. tuberculosis: treatment and prevention
Treatment Effective, but emergence of MDR- and XDR-TB Multi-drug required due to high rate of spontaneous drug resistant mutants Prevention BCG-vaccine Probably only prevents children from severe disease, not adults IPC Prevent hospital acquired transmission Prevent household and community transmission.
26
Give the type of therapeutics that are requires by the following classes of microbes Bacteria? Fungi? Parasites? Viruses?
Antibiotics Antifungals Anti-parasitic agents Antivirals
27
Another name for Adjunct therapeutics
non-antimicrobial
28
What are the indications for antibiotic therapy
A bacterial infection that: .is severe .unlikely to resolve spontaneously .may be followed by severe complications -When viral infections are associated with bacterial superinfection that requires antibiotics.
29
Indication foe antibiotics
When Group A streptococcal sore leads to rheumatic heart disease
30
Mode of action of antibiotics
-Inhibit core metabolic processes in bacteria e.g. biochemical pathways
31
differentiate between Broad spectrum and Narrow spectrum of antibiotics
Broad spectrum- active against both gram negative and gram positive and useful for empiric therapy Narrow spectrum- active against few families of bacteria and useful for direct therapy
32
between the 2, broad spectrum and narrow spectrum which is most likely to lead to formation of multi resistant bacteria
Broad spectrum
33
How does resistance spread in a bacterial population?
A bunch of bacteria including a resistant variety get bathed in antibiotics. most of the normal bacteria die. the resistant bacteria multiply and become more common. Eventually the entire infection evolves into a resistant strain.
34
35
name the different types of vaccine.
Inactivated Attenuated Toxoid subunit Conjugate Heterotypic/Jennerian
36
define an inactivated Vaccine
this is the type of vaccine where the whole micro-organism is destroyed by heat chemicals, radiation or antibiotics
37
define attenuated vaccine
live organism are modified to be less deadly or closely-related microorganism which induce the immunity
38
Define Toxoid Vaciine
this is when inactivated toxic substance is used
39
Define subunit vaccine
a protein component of the microorganism is used
40
Define conjugate vaccine
Polysaccharides on bacterial outer coats that poorly stimulate the immune system paired with a protein that is highly immunogenic
41
define heterotypic/Jennerian
pathogen that infect other animals but do not cause disease or cause mild disease in human like cowpox
42
differentiate between a monovalent vs multivalent vaccine
A monovalent vaccine is a vaccine which immunise against a single strain of microorganism. a multivalent vaccine is a type of vaccine which immunise against multiple antigens, strains or microorganisms.
43
How do vaccines work
They elicit an adaptive immune response with memory
44
Define Bactericidal
Antibiotic actually kills organism
45
Define Bacteriostatic
Antibiotic prevents growth of bacteria without killing them
46
Define intrinsic(primary) resistance
This is natural resistance and is present before exposure to antibiotics
47
Define acquired resistance
This refers to genetic change after exposure to an antimicrobial.
48
Give the three types of Horizontal gene transfer
Transduction Conjugation Transformation
49
Explain the concept of selective toxicity, and how it is achieved.
This refers to the concept of being toxic to the bacteria but not to the host. It is achieved by exploiting the differences in structure and metabolism of the bacteria(prokaryotic cells) and human cells(eukaryotic cells).
50
Target sites for antimicrobial agents: MOA?
Cell wall synthesis Protein synthesis Nucleic acid synthesis Cell membrane function Metabolic pathways
51
Mechanisms of resistance.
1. Enzymatic inactivation or modification of the antibiotic.(bacteria degrading the antibiotic) 2. Alteration of target site of antibiotic(The structure of target site might be altered) 3.Decreased entry of antibiotic into bacteria wall. 4. Increased efflux of antibiotic from bacterial cell. 5.Developmennt of alternative? bypass metabolic pathways by bacteria.
52
Explain the mechanisms of Beta-lactams
They inhibits enzymes involved in the formation and cross-linking of peptidoglycan cell wall. i.e. they inhibit cell wall synthesis
53
Give the main groups of beta-lactams and an example of each.
Penicillins, e.g. amoxicillin Cephalosporins e.g. ceftriaxone Cerbapenems e.g. ertapenem
54
Give different types of mechanisms of resistance to beta-lactams.
.Target site modification(most common in gram positive organisms, e.g. Pneumococcal resistance to penicillin) .Enzymatic inactivation of antibiotic(most common in gram negative organisms, e.g. Carbapenem resistance in Gram-negative enterobacterales) .
55
Explain the MOA of glycoproteins and then give an example of the gylcopeptides.
This bind the building blocks that make peptidoglycan(a substance that forms the cell wall of many bacteria cell walls) e.g. vancomycin
56
Explain resistant to Glycopeptides
Decreased entry into cells Gram negatives are inherently resistant to vancomycin Target-modification Vancomycin resistant enterococci
57
Name to microorganism involve in cell wall stnthesis
Beta-lactims Glycopeptides
58
Explain the mechanism of Aminoglycosides when they act on bacterial ribosomes and give examples.
Firstly they bind on the 30S subunit and then cause a misreading of the genetic code on mRNA. e.g. Gentamicin, Amikacin. this are used for Gram negative infections
59
Explain the mechanism of Macrolides when they act on bacterial ribosome and give examples.
firstly they bind on the on the 50S subunit and then prevent chain elongation. e.g. Erythromycin, Azithromycin active against garam positive bacteria
60
explain the mechanism of resistance for aminoglycosides
-Enzymatic modification of antibiotic
61
Explain the mechanisms of resistance for Macrolides.
Target site modification on the ribosome Efflux pumps
62
Explain the mechanism of Fluoroquinolones
It binds to two nuclear enzymes, inhibiting DNA replication. It does this by inhibiting DNA gyrase and topoisomerase IV.
63
Explain the mechanism of resistance.
Target site modification
64
Explain the mechanism of resistance for inhibitors of metabolic pathways
They develop alternative metabolic pathways.
65
Give examples of inhibitors of metabolic pathways
.Cotrimoxazole .Tetrahydrofolic acid(THFA)
66
Give an example of inhibitors of cell membrane.
Polymyxins
67

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