Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Veterinary Science and One Health 23/24 > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

Name 5 bacteriostatic drugs.

A

Sulphonamides
Trimethoprim
Tetracyclines
Chloramphenicol
Linocomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name 6 bactericidal drugs.

A

Penicillins
Cephalosporins
Fluoroquinolones
Aminoglycosides
Metronidazole
Sulphonamides + trimethoprim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a concentration dependent drug?

A

Will be static (lower) or cidal (higher) depending on concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name a concentration dependent drug.

A

Erythromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How can bactericidal drugs be further classified?

A

Time or concentration dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How are time dependent drugs given?

A

Work slowly so given over a period of days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is characteristic about time dependent drugs?

A

Plasma levels should be above minimum inhibitory concentration for as long as possible in each 24 hour period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some examples of time dependent drugs?

A

Penicllins
Cephalosporins
Sulphonamide + trimethoprim combinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is characteristic about concentration dependent drugs?

A

The peak concentration determines how effective the drug will be

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some examples of concentration dependent drugs?

A

Aminoglycosides
Fluoroquinolones
Metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do beta-lactam drugs work?

A

Inhibitors of peptidoglycan synthesis by preventing the cross-linking peptides from binding to the tetrapeptide side-chains.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are 2 examples of beta-lactam drugs?

A

Penicillins
Cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is beta-lactamase?

A

Diverse group of enzymes produced by different bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the beta lacatamase produced by staphylococcus?

A

Penicillinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does beta-lactamase work?

A

Breaks beta-lactam ring and the drug can no longer bind. Method of drug inactivation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is clavulanic acid?

A

A beta lactamase inhibitor and has no anti-bacterial effect alone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is Synulox?

A

1:1 mix of amoxicillin and clavulanic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does the acid stability of a drug mean?

A

Acid stability being poor means it cannot be given orally/breaks down in stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the pharmacokinetics of penicillins.

A

Oral availability varies depending on acid stability. Widely distributed but do not cross BBB and eliminated at kidney.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the pharmacokinetics of cephalosporins.

A

Some can be orally administered, most parenterally. Widely distributed, some cross the BBB and eliminated by the kidney.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the effect of impaired kidney function of drugs?

A

Will increase half-life of some drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is gastrointestinal superinfection as an adverse effect of antibacterial drugs?

A

Death of susceptible gut flora allows proliferation of non-susceptible bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is the mycobacterial cell wall different to other bacteria?

A

Have mycolic acids in cell membrane and different enzymes responsible for synthesising the cell wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is a mycobacterial infection in cats treated?

A

Difficult to treat so need a combination for 6 months:

  • Fluoroquinolone – inhibits DNA gyrase
  • Clarithromycin – a macrolide that inhibits protein synthesis
  • Rifampicin – inhibits RNA synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Name 4 antibacterial drugs that inhibit bacterial protein synthesis.

A

Aminoglycosides
Macrolides
Tetracyclines
Chloramphenicol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How do aminoglycosides work?

A

Produce misreading in translation, so wrong tRNA binds to ribosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Name 2 examples of aminoglycosides.

A

Gentamicin
Neomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the spectrum of activity for aminoglycosides?

A
  • Generally gram negative bacteria
  • Some have broader spectrum of activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Why are aminoglycosides more effective against aerobic bacteria?

A

Must be transported across outer membrane, as they cannot easily pass through, so is a partly energy dependent process. This process is more efficient if energy aerobically generated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the pharmacokinetics of aminoglycosides.

A

Poor gut absorption, renal excretion, IV, SC, intramammary injections, topical eye/ear drops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the adverse reactions of aminoglycosides?

A

Nephrotoxicity - fine for short period, long period will result in kidney damage.

Ototoxicity is irreversible but has genetic component and does not occur every time these drugs are given.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe nephrotoxicity.

A
  • Drugs bind to proximal tubule cells
  • Get taken up into cells
  • Accumulate in intracellular compartments and cause changes in cell structure and function
  • Reduce glomerular filtration rate
  • Kidney damage usually reversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How does macrolides work?

A

Bind to P site and prevent translocation/moving along mRNA. May also inhibit transpeptidation, causing premature release of ribosome complex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Name 2 examples of macrolides.

A

Tylosin
Erythromycin,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the activity spectrum of macrolides?

A

Gram positive bacteria. Bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the pharmacokinetics of macrolides?

A

Wide distribution, oral bioavailability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the adverse reactions of macrolides?

A

GI upset/diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How do tetracycline work?

A

Bind to the A site on the ribosome complex and prevent tRNA binding. Also have other effects on protein synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Name examples of tetracyclines.

A

Tetracycline
Oxytetracycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the activity spectrum of tetracyclines?

A

Wide spectrum against aerobic and anaerobic gram positive and gram negative bacteria. So was widely used, as it affects lots of bacteria, but this has encourages lots of resistance. Bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the pharmacokinetics of tetracyclines?

A

Oral bioavailability varies by drug, absorption impaired by calcium and milk products, widely distributed in the body, including CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the main resistance mechanism bacteria have against tetracyclines?

A

Can be pumped out of bacterial cells by efflux pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Why must tetracyclines not be administered to ruminants?

A

GI disturbances due to superinfection by fungi, yeasts and resistant bacteria possible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How must oral doxycycline be administered?

A

Can cause oesophageal ulceration in cats so give with a syringe of water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What can rapid IV injection of tetracyclines cause?

A

Hypotension and collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How does tetracyclines adversely affect the teeth?

A

Tetracycline chelate/bind to calcium so affects development of enamel, as calcium can’t be taken up into the body. Protective layer of teeth is compromised, causing hypersensitivity, increased wear and risk of fracture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the affect of tetracyclines on bones?

A

Can also slow bone development, and at high concentrations, can inhibit bone repair.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How does chloramphenicol work?

A

Inhibit peptide bond formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is an example of a chloramphenicol?

A

Florfenicol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Can chloramphenicols be used in food animals?

A

No, may enter food chain. But florfenicol can

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the spectrum of activity for chloramphenicol?

A

Wide spectrum of activity
Bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the pharmacokinetics of chloramphenicol?

A

Well absorbed after oral dosing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the adverse reactions of chloramphenicol?

A

Anaemia by suppression of bone marrow, so can interfere with antibody formation, metabolism in cats is poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How do sulphonamides work?

A

Competitive inhibitors of DHPS. Bacteria use DHPS to produce folate, most eukaryotes take up folate from environment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is an example of sulphonamide?

A

Sulfadiazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the spectrum of activity of sulphonamides?

A

Wide spectrum against gram negative and positive bacteria. Bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the pharmacokinetics of sulphonamides?

A

Well absorbed from gut (Can be given orally), widely distributed in the body, renal excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the adverse reactions of sulphonamides?

A

Hypersensitivity reactions, immune mediated reactions (keratoconjunctivitis sicca and polyarthritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How does trimethoprim work?

A

Inhibits DHFR (prevents DNA synthesis in both human and bacterial cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the spectrum of activity of trimethoprim?

A

Always co-administered with sulphonamide – referred to as potentiated sulphonamide. Bactericidal combination due to bigger effect on folate metabolism. Still not a great antibacterial effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How do fluoroquinolones work?

A

Fluoroquinolones inhibit supercoiling by interfering with the actions of DNA gyrase (topoisomerase II).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Name some examples of fluoroquinolones.

A

Enrofloxacin
Marbofloxacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the spectrum of activity of fluoroquinolones?

A

Wide spectrum activity for a wide range of gram negative and number of gram positive aerobes. Bactericidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the pharmacokinetics of fluoroquinolones?

A

Well absorbed from gut, good distribution to all tissues, renal and hepatic excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the adverse reactions of fluoroquinolones?

A

Inhibition of cartilage growth in young animals
Retinal degeneration in cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How should fluoroquinolones be used?

A

Should not be used as a first line treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are 2 examples of metronidazole?

A

Clostridium
Helicobacter

68
Q

What is the spectrum of activity of metronidazole?

A

Only works in obligate anaerobic bacteria as they can only activate the pro-drug. So activity is only for obligate anaerobes, can be found in the stomach and wounds. Also effective against some protozoal infections

69
Q

What does metronidazole cause?

A

Causes DNA fragmentation

70
Q

What are the pharmacokinetics of metronidazole?

A

Well absorbed from gut, good distribution to all tissues, renal and hepatic excretion

71
Q

What are the adverse reactions of metronidazole?

A

Rare and usually mild: vomiting, nausea, dry mouth. Can see neuro side effects such as ataxia, head tilt and convulsions but these are very rare. May cause cats to salivate. May be teratogenic.

72
Q

What are 5 biochemical mechanisms of antibiotic resistance?

A
  • Inactivation of the antibacterial drug – most clinically relevant
  • Alteration of the target site
  • Decrease drug accumulation in the bacterium
  • Upregulate synthesis of target
  • Alter metabolic pathway
73
Q

What do MRSA and VRE stand for?

A

MRSA – methicillin-resistant Staphylcoccus aureus

VRE – vancomycin-resistant Enterococci

74
Q

What is MRSA resistant to?

A

MRSA also resistant to ampicillin and other penicillins, erythromycin, tetracyclines. Can only be treated by vancomycin

75
Q

What are the ways that helminths are controlled?

A
  • Ecological – change environment to favour their resilience against parasitic infestation, co-infection or predatory species (fungi)
  • Genetic – can selectively breed animals that are more resistant to parasitic infestation.
  • Immunological – vaccines
  • Chemical – pharmacological
76
Q

What must an anthelmintic do?

A
  • Reach the site of action in suitable quantity
  • Interrupt the normal function of the parasite allowing clearance
  • Not be toxic to the host
77
Q

What are the properties of the ideal anthelmintic?

A
  • Selective toxicity/wide therapeutic index
  • Favourable pharmacokinetics
  • Broad spectrum of activity
  • Economical
  • Robust to developing drug resistance
78
Q

Why is there lots of opportunity for selective toxicity when treating helminths?

A
  • Helminths and mammals are very far apart
  • Many anthelmintics interact with targets which are simply not present in their host
  • Inhibit metabolic processes vital to parasite but not host
79
Q

What are the mechanisms of selective aggregation in parasite?

A
  • Integrity of parasite cells
  • Neuromuscular coordination
  • Protective mechanisms from host immunity
  • Interfering with energy generation
80
Q

How do anthelmintics enter the different helminths?

A
  • Predominantly oral ingestion = trematodes
  • Passive diffusion, except for high plasma binding drugs = nematodes
  • Predominantly passive diffusion = cestodes
81
Q

How does helminth epidermis anatomy affect anthelmintic drugs?

A

Epidermis of nematodes is not a static barrier and is several layers thick with a large lipid component. So only suitably lipophilic drugs will be able to diffuse across the external layer. Another factor of nematodes is that they have a certain layer and compartment within their epidermis which contains buffered liquid, so relatively basic drugs will protonate and suddenly be a lot more polar and unable to cross through the lipophilic layers of the epidermis, particularly relevant for Benzimidazoles.

82
Q

Why are helminths resistant to anthelmintic drugs?

A

Short generation time
Large populations
Lots of random mutations

83
Q

Which species of helminths are more likely to develop anthelmintic resistance?

A

Haemonchus
Teladorsagia
Trichostrongylus

84
Q

Distinguish broad and narrow spectrum anthelmintics.

A

Broad spectrum anthelmintics often refer to drugs with high efficacy for the major species of parasitic nematodes.

Narrow spectrum anthelmintics often refer to drugs which are effective on trematodes and blood-sucking nematodes.

85
Q

What are the mechanisms of action of anthelmintic drugs?

A
  • Integrity of parasite cells
  • Neuromuscular coordination
  • Protective mechanisms from host immunity
  • Interfering with energy generation
86
Q

Name 10 anthelmintic drugs.

A

Benzimidazoles
Levamisole
Macrolytic lactones
Amino-acetonitrile derivatives
Spiroindoles
Piperazine
Emodepside
Praziquantel
Salicylanilides
Benzenesulphonamides

87
Q

What are benzimidazoles effective against?

A
  • More effective on nematodes than cestodes and trematodes
  • High therapeutic index
88
Q

How do benzimidazoles work?

A
  • Bind to beta-tubulin
  • Inhibits polymerisation resulting in depolymerisation
89
Q

How is benzimidazole efficacy correlated with their solubility

A

More solubility = poor absorption = low potency. Less lipid solubility = less likely to cross membranes = high potency. Can tailor these properties via pro-drugs.

90
Q

What are the factors affecting benzimidazole bioavailability?

A
  • Ruminant oesophageal groove closure
  • Reduced GI flow rate
  • Type of diet
  • Nutritional status and degree of parasitic infection
91
Q

What is levamisole effective against?

A

Effective against nematodes in the lungs and GI tract

92
Q

What are the pharmacological properties of levamisole?

A
  • Lower therapeutic index
  • Rapidly absorbed and excreted
93
Q

What is the mechanism of action of levamisole?

A

Nicotinic acetylcholine receptor agonist, induces prolonged activation of nAChR in body wall leading to spastic muscle paralysis.

94
Q

What are pyrantel and morantel?

A

Specific nemotodicide with more narrow spectrum of action than levamisole. Poor absorption in ruminants – particularly useful for horses

95
Q

What are macrolytic lactones effective against?

A

Effective on nematodes but not cestodes and trematodes

96
Q

What is the mechanism of action of macrolytic lactones?

A

Glutamate-gated chloride channel agonists and to a lesser extent GABA channels. Influx of chloride ions inhibits the activation of the neuromuscular junction and causes flaccid paralysis and death by starvation.

97
Q

What are amino-acetonitrile derivatives effective against?

A
  • Effective against all GI nematode species including those resistant to treatment
  • Not ovicidal
98
Q

What is the mechanism of action of amino-acetonitrile derivatives?

A

Activates nematode-specific nAChR subtype. Depolarisation of muscle cells leads to irreversible paralysis and rapid expulsion from host.

99
Q

What is piperazine effective against?

A

Specific GI nematode species – limited action in common ruminant parasites

100
Q

What are the pharmacological properties of piperazine?

A
  • Low toxicity
  • Oral bioavailability so quickly metabolised
101
Q

What is the mechanism of action of piperazine?

A

Activates GABA chloride channels via hyperpolarisation and flaccid paralysis. Paralyses but worms may be passed alive. May also make worms more sensitive to immune attack.

102
Q

What is emodepside?

A

A complex peptide derived from a protein found in the black widow spider

103
Q

What is emodepside effective against?

A
  • Active on triple resistant nematodes in sheep
  • No ovicidal and causes death of parasite
104
Q

What is the mechanism of action of emodepside?

A

Not fully understood. Binds to a latrophilin-like receptor causing a signal cascade that leads to hyper-polarisation of the post synapse at the neuromuscular junction, leading to flaccid paralysis.

105
Q

What is praziquantel effective against?

A

All tapeworms, as well as schistosomes and some nematodes

106
Q

What is the mechanism of action of praziquantel?

A

Neuromuscular coordination and integrity of parasite cells. Exact mechanism unclear. Increases the permeability of cell membranes to calcium ions, leads to sustained paralytic muscle contraction and segmental disruption and loss of homeostasis.

107
Q

What is salicylanilides effective against?

A

Liver fluke

108
Q

What is the mechanism of action of salicylanilides?

A

Interfering with energy generation and neuromuscular coordination. Disrupts mitochondrial function reducing ATP production decreased segmental pH inducing spastic paralysis.

109
Q

What are benzenesulphonamides effective against?

A

Highly effective against adult and late stages of common liver fluke. Almost only available in combination with ivermectin

110
Q

What is the mechanism of action of benzenesulphonamides?

A

Interfering with energy generation. Inhibits glycolytic enzymes. Fluke unable to obtain energy from glucose depleting ATP levels.

111
Q

How does resistance develop in a population of worms?

A
  1. Resistant parasites survive drug treatment
  2. Reproduce/spread passing on resistant genes
  3. Resistant population accumulates
  4. Treatment failure
112
Q

Why may treatment failure of worms be due to drug inefficiency rather than resistance?

A
  • Incorrect diagnosis/inappropriate drug
  • Incorrect dose
  • Drug interactions
  • Pathophysiological state of host
  • Out of date or poorly stored product
  • Compliance failure
  • Reinfection and/or multiple concurrent infection when treated and healthy animals are mixed
113
Q

What are the human factors that contribute to anthelmintic resistance?

A
  • Under-dosing/too frequent dosing
  • Unnecessary dosing – use of combinations
  • Administration to low-level egg shedders
  • Misdiagnosis and use of inappropriate drugs
  • Long tail with long half-life formulations
114
Q

What are the evolved adaptative factors of helminths that contribute to resistance?

A
  • Adaptions effecting accumulation of drug at site of action
  • Increased activity of enzymatic systems
  • Changes to receptors for drugs
  • Amplification of target genes
115
Q

How is resistance to benzoimidazoles developed?

A
  • Resistance due to Modification of β-tubulin
  • F200Y substitution in β-tubulin though mutation at amino acid residue 167
  • BZDs no longer bind with high affinity
116
Q

How is resistance to levamisole developed?

A
  • Changes to nAChRs
  • Altered drug binding due to mutation of receptor
  • Lower number of active receptors
  • Change from excitatory to inhibitory channel in some parasites
117
Q

How does resistance to macrolytic lactones develop?

A
  • Subunits of Glutamate-gated Cl- channels
  • P-glycoprotein (drug transporters)
  • GABA-gated Cl- channels
  • β-tubulin
118
Q

What are triple resistant infections?

A

Resistance to groups 1, 2 and 3 (BZDs, levamisole and macrocyclic lactones).

119
Q

What are the treatment aspects of minimising resistance?

A
  • Minimise exposure of parasite to drug
  • Limit treatment to significant infestation
  • Limit frequency of treatments
  • Seasonal drug alternation
  • Ensure effective dose rates
120
Q

How can combination products minimise resistance?

A
  • Broad spectrum of target helminths increase duration/efficacy of single dose make dosing routines easier
  • Utilise synergistic effects of each agent
121
Q

What is startect?

A

A combination product: Startect = abamectin and derquantel

122
Q

Describe the individual and combined effects of abamectin and derquantel.

A

Abermectin – glutamate receptor agonist. Paralysis of pharynx prevents feeding

Derquantel – blocks function of Acetylcholine. Paralysis of body wall muscles – paralysis and death

Synergy – similar PK but different molecular targets. Potential potentiation effect

123
Q

What are the alternatives to manage anthelmintic resistance (other than chemically)?

A
  • Culling programme
  • Protein intake - abolishment of periparturient egg rise as immunity closely linked to protein repletion
  • Ecological/animal management
124
Q

How can animal management be used to manage anthelmintic resistance?

A
  • Intermediate host control where relevant
  • Prevent faecal cross-contamination
  • Pasture management for herbivores
  • Quarantining of incoming animals
125
Q

Why have anthelmintic vaccines not be successful?

A
  • Limited by knowledge of host-parasite relationship, immune molecules involved, or host pathways involved
  • Translation from in vivo laboratory models to host has not been successful
  • Only 3
126
Q

What are the 3 vaccines available for anthelmintic control?

A
  • For bovine lung worm, for treatment of D viviparus - complete, L3 can’t develop to adult
  • For haemonchus contortus - antigen based, harvested from infected sheep
  • Telodorsagia circumcinta for treatment of brown stomach worm in sheep - recombinant antigens
127
Q

What are the general properties of anticoccidials?

A
  • Mostly used prophylactically (due to diagnosis only in late infection)
  • Generally coccidiostatic not coccidiocidal
  • Oral
128
Q

What does Eimeria cause in poultry?

A

Inflammation of intestine
Diarrhoea (with/without blood)
Lower growth rates
Increased mortality
Resistance with low level infections

129
Q

Describe Eimeria vaccines.

A
  • Mix of low levels of various Eimeria species
  • Administered once by addition to feed or drinking water or by spraying onto birds so important that animals are not exposed to other anticoccidials as this will decrease the effectiveness of the vaccine
130
Q

Name 8 antiprotozoals.

A

Ionophores
Amprolium
Sulphonamides
4-Hydroxyquinolines
Toltrazuril
Imidocarb
Clindamycin
Metronidazole

131
Q

What are ionophores?

A

Prophylactic. Most common used group of coccidiostatic drug in poultry. Growth promotor in cattle as it removes protozoal growth from gut which will promote growth of cattle.

132
Q

What is the mechanism of action of ionophores?

A
  • Make cell membranes permeable to inorganic cations
  • Equal action on mammalian, avian and protozoal cell membranes
  • Form a complex with inorganic cations
  • Affect ion distribution and pH
  • Disrupt metabolic functions
  • Minimal drug resistance problems as it is just moving ions across membranes
133
Q

Which species are ionophores toxic to?

A

Horses, as they are 10-100x more sensitive than cattle

134
Q

What does thiamine deficiency lead to?

A

Required for carbohydrate (CHO) metabolism. Deficiency leads to suppression of coccidial infection

135
Q

What is the mechanism of the thiamine analogue, amprolium?

A
  • Blocks thiamine transporter
  • Prevents thiamine entry into protozoa
  • Protozoa more sensitive than host animal
136
Q

What is the spectrum of activity of amprolium?

A
  • Eimeria species
  • Mediocre efficacy, but little resistance development
  • Commonly used with sulphonamides
137
Q

What is the spectrum of activity of sulphonamides?

A
  • Antibacterial
  • Dose-dependent effect: coccidiostatic to coccidiocidal
138
Q

What is the antiprotozoal mechanism of action of sulphonamide?

A

Competitively inhibits dihydropteroate synthase (DHPS) and blocks folate synthesis

139
Q

Why do sulphonamides only work in prokaryotes?

A

Sulphonamides do not work on mammalian cells as dihydropteroate synthetase is not used to make folate in mammals as they take it up from the environment.

140
Q

What is the spectrum of activity of 4-hydroxyquinolines?

A
  • Activity primarily limited to Eimeria and Babesia
  • Effective coccidiostat
  • Little toxicity – in part due to low rate of absorption from gut
141
Q

What is the mechanism of action of 4-hydroxyquinolines?

A
  • Target Cytochrome b, which is used in electron transport chain in mitochondria
  • Antagonist
  • Potent inhibitor of protozoal NADH- or succinate-induced mitochondrial respiration
  • No effect on mammalian or avian mitochondria
142
Q

Which species are 4-hydroxyquinolines used in?

A

Used prophylactically in poultry – no withdrawal period

Used prophylactically and for treatment in sheep and cattle – no withdrawal period for meat, not permitted in animals producing milk for human consumption

143
Q

Which species is toltrazuril used in?

A

Coccidiostat in variety of species: poultry, pigs, sheep, cattle. Used for outbreaks

144
Q

What is the mechanism of action of toltrazuril?

A

Induces changes in coccidian developmental stages, due to swelling of organelles, and disturbances in mitosis in coccidia

145
Q

What are some side effects of antiprotozoals?

A

Acute – diarrhoea, vomiting

Chronic – renal and/or hepatic dysfunction/damage)

More rarely – CNS or CVS responses

146
Q

What are the properties of the ideal ectoparasitide?

A
  • Destroy all parasites at all stages of their lifecycle
  • Be rapid in action
  • Be non-toxic to the host
  • Provide a minimum residue in the host and be rapidly detoxified in the environment
  • Resistance in parasites should be slow to develop
147
Q

How are ectoparasiticides classified?

A

Drugs that act upon the insect nervous system - affecting acetylcholine neurotransmission, axonal sodium channels, octopamine system, chloride channels

Drugs which act as insect growth regulators - juvenile hormone analogues just in insects so mammals not affected, chitin synthesis inhibitors

148
Q

Name 10 ectoparasiticides.

A

Organophosphates
Carbamates
Imidacloprid
Pyrethroids
Amidines
Fipronil
Avermectins
Isoxazolines
Juvenile hormone analogues
Benzoyl ureas/chitin synthesis inhibitors

149
Q

Which ectoparasiticides inhibit acetylcholinesterase?

A

Organophosphates
Carbamates

150
Q

What is the effect of ectoparasiticide inhibition of acetylcholinesterase?

A

Accumulation of acetylcholine leads to flaccid paralysis

151
Q

Distinguish the actions of organophosphates and carbamates.

A

Organophosphates are irreversible inhibitors. Carbamates are reversible inhibitors

Administration of organophosphates by all routes, absorbed systemically by host, parasite takes drug in by feeding on host. Carbamates administered topically

152
Q

What is the mechanism of action of imidacloprid?

A
  • Patrial agonist at nicotinic Ach receptors in insect CNS, blocks transmission by disrupting nAchR signalling.
  • Causes depolarising block, leading to flaccid paralysis and death
  • Highly selective for insect over mammalian nicotinic receptors
153
Q

What are 4 drug examples of pyrethroids?

A

Cypermethrin
Deltamethrin
Permethrin
Fenvalerate

154
Q

What is the mechanism of action of pyrethroids?

A

Cause a prolonged depolarising afterpotential causes hypersensitivity so that the whole nervous system locks up

155
Q

What does feline permethrin toxicity present as?

A

Acute symptoms of muscle tremors and seizures.

156
Q

What are 3 factors of selective toxicity or pyrethroids?

A
  • Potency increases with decreasing temperature. The body temperature of insects is 10˚C lower than that of mammals.
  • Insects metabolise the pyrethroids slower than mammals
  • Small size - insects will have less chance to metabolise the insecticide before it reaches its target organ
157
Q

What is octopamine?

A

The invertebrate equivalent of noradrenaline. Octopamine receptors are the only non-peptide receptors present exclusively in invertebrates

158
Q

What is the mechanism of action of amitraz?

A

Amidines such as Amitraz are specific agonists of the octopamine receptor. Causes CNS hyperexcitability in parasite = death

159
Q

What is the mechanism of action of fipronil?

A

Receptors, causing hyperexcitation in the CNS and periphery, causing convulsions and rapid death

160
Q

When is fipronil used?

A
  • Protects from reinfection for up to 3 months in dogs and 2 months in cats
  • Not to be used on puppies or kittens less than 2 days old, or on rabbits
161
Q

What is the toxicity and adverse effects of fipronil?

A
  • It is highly selective for insect over mammalian GABA receptors, so toxicity is minimal
  • Adverse effect is a transient hypersalivation if the animal licks the area immediately after treatment
162
Q

What is the mechanism of action of avermectins?

A

Activate GABA receptor, inhibiting neurotransmission

163
Q

When are avermectins used?

A

Used in most domesticated species to treat Arthropod ectoparasites such as fleas, sarcoptic mange, mites, lice and more

164
Q

What are isoxazolines used for?

A

Effective against fleas and ticks

165
Q

What is the mechanism of action of insect growth regulators?

A

Exhibit greater selectivity of action than conventional ectoparasiticides. Interfere with growth, development, metamorphosis or reproduction. Either juvenile hormone analogues or chitin synthesis inhibitors.

166
Q

What is the mechanism of action of juvenile hormone analogues?

A

Prevents metamorphosis until the larva is fully grown. Cause the development of abnormal pupae, and prevent emergence of viable adults.

167
Q

What is the mechanism of action of chitin synthesis inhibitors/benzoyl ureas?

A
  • It does not kill flea but affects the development of its offspring, thus the reduction in flea count is not seen for two weeks
  • It accumulates in host adipose tissue thus maintains therapeutic plasma concentration for up to 1 month after 1 oral dose

Clinical Veterinary Science and One Health 23/24 (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions