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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
Q

(class) Quinolones

A

Bactericidal; synthetic, broad spectrum; targets DNA gyrase in Gram -ve and topoisomerase in Gram +ve

26
Q

Rifampicin

A

Bactericidal, target RpoB subunit of RNA polymerase
spontaneous resistance common; red excretions, inhibits both gram +/-

27
Q

(class) Sulphonamides

A

prontosil, trimethoprim, sulpha-methoxazole
Bacteriostatic, synthetic
host toxicity but used more due to other AB resistance

28
Q

Vancomycin

A

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
Q

Linezolid

A

Bacteriostatic, inhibits protein synth. by binding to 50s rRNA subunit
gram +ve
given orally

30
Q

Daptomycin

A

Bactericidal; targets bacterial cell membrane
gram +ve only
toxicity so low dose

31
Q

Ab target sites

A

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
Q

Examples of Gram-negative bacteria

A

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
Q

Examples of gram positive bacteria

A

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
Q

How has Antibiotic resistance evolved through natural selection

A

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
Q

Ab resistance genes are found in

A

Plasmids
Transposons
Naked DNA - DNA from dead bacteria released into environment

36
Q

resistance genes in plasmids

A

extra-chromosomal circular DNA, often multiple copy
Often carry multiple AB resistance genes- selection for one maintains resistance to all

37
Q

resistance genes in transposons

A

integrate into chromosomal DNA
Allow transfer of genes from plasmid to chromosome and vice versa

38
Q

Which 3 ways can bacteria transfer Ab resistance genes?

A

Transformation - uptake from extracellular DNA
Conjugation - DNA transfer
Transduction -phage-mediated DNA transfer

39
Q

4 mechanisms of antibiotic resistance

A

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
Q

How does Ab resistance lead to increased mortality, morbidity and cost?

A

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
Q

Why might treatment with antibiotics fail?

A

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
Q

Common Hospital Acquired Infections

A

MRSA - methicillin resistant S. aureus
VISA - Vancomycin-insensitive S. aureus
Clostridium difficle
E. Coli

43
Q

Why do HAIs arise

A

many ill people with high AB dosage
crowded wards
different pathogens
broken skin
staff transmission
intubation

44
Q

Commensal flora

A

Harmless bacteria already present within the body
can be impaired by Ab therapy

45
Q

How can Abs affect commensal flora

A

broad spectrum ABs attack commensal flora
AB resistant pathogen now has no competition
pathogen produces toxins and damages host

46
Q

How can we prevent the emergence of drug resistant bacteria?

A

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
Q

Streptococcus pyogenes is

A

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
Q

Rheumatic fever

A

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
Q

Scarlet fever

A

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
Q

Streptococcal pharyngitis

A

symptoms include fever, sore throat, enlarged and red tonsils and lymph nodes. This is caused by group A streptococcus.

51
Q

Staphylococcus aureus

A

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
Q
A

POM 4: Immunity and Infection (9 decks)

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