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POM 4: Immunity and Infection > 1: Microbial Infection and Antimicrobial Therapies > Flashcards

1: Microbial Infection and Antimicrobial Therapies Flashcards

1
Q

5 main types of infectious agents

A

Viruses
Bacteria
Fungi
Protozoa
Helminths

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2
Q

Viruses

A

obligate intracellular parasites

contain RNA/DNA
Replicate using host cell machinery : Budding, Cytolysis
specific to host cell
e.g HIV retrovirus

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3
Q

4 routes of viral infection

A

Faecal-oral
Airborne
Insect vectors
Blood borne

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4
Q

Bacteria

A

prokaryotes - no internal cell surface membrane
single circular chromosome - haploid
poorly defined cytoskeleton
cell wall - peptidoglycan
Binary fission

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5
Q

Examples of Bacteria

A

Shigella - GI tract , faecal-oral transmission

Neisseria Meningitidis - Commensal > pathogen, community acquired, can cause septicaemia, meningitis and septic shock

C.Difficile & MRSA - hospital acquired infection

mycobacterium tuberculosis - TB= top infectious killer

Helicobacter pylori - peptic ulcer, Gastric cancer

Pathogenic e.coli - faecal-oral route

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6
Q

Why do bacteria have high mutation rates?

A

smaller generation times - quick replication
haploid, so only one gene needs to be mutated to have a phenotypic effect

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7
Q

Fungi

A

eukaryotic - unicellular or multicellular
exist as yeasts, filaments or both
yeast spread by budding
filaments have hyphae which have cross walls/septa

causes mycoses:
cutaneous - skin
mucosal - inner lining
systemic - whole body

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8
Q

Protozoa

A

unicellular eukaryotic
intestinal, blood or tissue parasites
Binary fission or formation of trophozoites
often two hosts - infection acquired by ingestion or through vector

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9
Q

Protozoa examples

A

malaria
leshmania species e.g leshmaniasis

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10
Q

Malaria

A

Plasmodium species e.g malaria
- blood and tissue parasites
- acquired via mosquito vector
- spread by forming trophoziotes inside cell

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11
Q

Leshmaniasis

A

leshmania species
- blood and tissue parasites
- acquired via sandfly vector
- spreads by forming trophoziotes inside cell
- causes cutaneous and visceral diseases

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12
Q

Helminths

A

macroscopic multi-cellular eukaryotes
life cycle outside human host
replicate sexually - eggs: some hermaphroditic
e.g roundworms, flatworms, tapeworms
faecal-oral transmission

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13
Q

Antibiotic

A

antimicrobial agent produced by microorganism that kills or inhibits other microorganisms

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14
Q

Antimicrobial

A

chemical that selectively kills or inhibits microbes

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15
Q

Bactericidal

A

kills bacteria

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16
Q

Bacteriostatic

A

stops bacterial growth

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17
Q

Antiseptic

A

chemical that kills/inhibits microbes, often used topically

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18
Q

Minimum inhibitory concentration (MIC)

A

lowest [AB] needed to inhibit growth of bacteria

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19
Q

Protonsil

A

first sulphonamide antibiotic
acts only on Gram +ve bacteria
Bacteriostatic and synthetic
Treats ; UTIs, RTIs, bacteraemia & given as prophylaxis for HIV
some toxicity, but used due to resistance to other ABs

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20
Q

Gram positive bacteria

A

peptidoglycan wall
one membrane

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21
Q

Gram negative bacteria

A

two membranes
thin peptidoglycan wall

22
Q

(class) Beta-Lactams

A

Penicillin, methicillin
Binds to PBPs; inhibit peptidoglycan wall synthesis
inhibit gram +ve bacteria

23
Q

(class) Aminoglycosides

A

Gentamycin, Streptomycin
Bactericidal, target 30s ribosome subunit, prevent PS; damage cell membrane
Host toxicity but used more due to other AB resistance, inhibit both gram +/- bacteria

24
Q

(class) Macrolides

A

Erythromycin, azithromycin
Targets 50s ribosomal subunit preventing amino-acyl transfer and truncation of polypeptides
Gram +ve and some gram -ve

25
(class) Quinolones
Bactericidal; synthetic, broad spectrum; targets DNA gyrase in Gram -ve and topoisomerase in Gram +ve
26
Rifampicin
Bactericidal, target RpoB subunit of RNA polymerase spontaneous resistance common; red excretions, inhibits both gram +/-
27
(class) Sulphonamides
prontosil, trimethoprim, sulpha-methoxazole Bacteriostatic, synthetic host toxicity but used more due to other AB resistance
28
Vancomycin
Bactericidal; inhibits cell wall biosynthesis and prevents cross-linking between peptidoglycan units used more due to other AB resistance (MRSA), Inhibits gram +, administered by IV
29
Linezolid
Bacteriostatic, inhibits protein synth. by binding to 50s rRNA subunit gram +ve given orally
30
Daptomycin
Bactericidal; targets bacterial cell membrane gram +ve only toxicity so low dose
31
Ab target sites
Inhibition of cell wall synthesis Inhibition of nucleic acid replication and trasncription Injury to plasma membrane Inhibition of synthesis of essential metabolites Inhibition of protein synthesis
32
Examples of Gram-negative bacteria
Pseudomonas aeruginosa - CF, burn wound infections, survives on abiotic surfaces E. Coli (ESBL) - Gi infections, neonatal meningitis, septicaemia, UTI E. Coli, Klebisiella spp (Carbapenase producing) Salmonella spp. (MDR) - GI infection, typhoid fever Acinetobacter baumannii (MDRAB) - opportunistic, wounds, UTI, pneumonia (VAP) Neisseria gonorrhoeae - Gonorrhoea Haemophilus influenzae - fever and malaise
33
Examples of gram positive bacteria
Staphylococcus aureus (MRSA, VISA)- wound and skin infect. pneumonia, septicaemia, infective endocarditis Streptococcus pneumoniae - pneumonia, septicaemia Clostridium difficile - pseudomembranous colitis, antibiotic-associated diarrhoea Enterococcus spp (VRE) - UTI, bacteraemia, infective endocarditis Mycobacterium tuberculosis (MDRTB, XDRTB) - TB
34
How has Antibiotic resistance evolved through natural selection
Diverse bacterial population with some Ab resistance due to DNA mutations Selective pressure --> resistant strains survive and multiply No selection pressure --> low prevalence of Ab resistance
35
Ab resistance genes are found in
Plasmids Transposons Naked DNA - DNA from dead bacteria released into environment
36
resistance genes in plasmids
extra-chromosomal circular DNA, often multiple copy Often carry multiple AB resistance genes- selection for one maintains resistance to all
37
resistance genes in transposons
integrate into chromosomal DNA Allow transfer of genes from plasmid to chromosome and vice versa
38
Which 3 ways can bacteria transfer Ab resistance genes?
Transformation - uptake from extracellular DNA Conjugation - DNA transfer Transduction -phage-mediated DNA transfer
39
4 mechanisms of antibiotic resistance
Altered target site: alternative gene which codes for different/modified Ab target site (MRSA, Strep pneumoni) Inactivaton of Ab- gene that degrades Ab e.g Beta-lactamase Altered metabolism - bacteria switch to other metabolic pathways to synthesis a certain substance Decreased drug accumulation - reduced penetration of Ab into bacteria, increased efflux of Ab
40
How does Ab resistance lead to increased mortality, morbidity and cost?
STATE (the effects) Second choice- use of less effective Abs Time - increased time to effective therapy Additional approaches - e.g surgery Toxic drug use - more toxic drugs used Expensive- newer drugs = costly
41
Why might treatment with antibiotics fail?
inappropriate choice for organism poor penetration of AB into target site inappropriate dosage (issues with half-life) inappropriate administration commensal flora are Ab resistant
42
Common Hospital Acquired Infections
MRSA - methicillin resistant S. aureus VISA - Vancomycin-insensitive S. aureus Clostridium difficle E. Coli
43
Why do HAIs arise
many ill people with high AB dosage crowded wards different pathogens broken skin staff transmission intubation
44
Commensal flora
Harmless bacteria already present within the body can be impaired by Ab therapy
45
How can Abs affect commensal flora
broad spectrum ABs attack commensal flora AB resistant pathogen now has no competition pathogen produces toxins and damages host
46
How can we prevent the emergence of drug resistant bacteria?
BE SICK Broad spectrum reduction Existing medication alteration Strategies of prescription Identifying resistant strains quickly Combination of Abs and inhibitors Knowledge of local strains/patterns
47
Streptococcus pyogenes is
species of Gram-positive extracellular bacteria that spreads through airborne droplets, shared food and drinks, and direct contact with infected carriers. A Streptococcus pyogenes infection manifests as: Rheumatic fever Scarlet fever Streptococcal pharyngitis
48
Rheumatic fever
inflammatory disease involving the heart, joints, and skin, typically developing a few weeks after a streptococcal throat infection. This occurs due to cross reactive antibodies being produced by the host towards the bacterial antigens that mimic host antigens. Antibodies produced may target cardiac tissue, such as heart valves, resulting in rheumatic heart disease.
49
Scarlet fever
characterised by a red rash on the tongue, as well as a sore throat, fever, and swollen lymph nodes. The bacteria produce pyrogenic exotoxin which causes the disease in patients without antitoxin antibodies
50
Streptococcal pharyngitis
symptoms include fever, sore throat, enlarged and red tonsils and lymph nodes. This is caused by group A streptococcus.
51
Staphylococcus aureus
gram +ve bacteria releases superantigens that interfere with T-cell function = massive cytokine release (cytokine storm), causes high fever, nausea, fatigue and can lead to coma Aureus also releases leukocidins which directly lead to neutrophil cell death
52

POM 4: Immunity and Infection (9 decks)

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