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*B33VPI - Pharmacology & Therapeutics > Ectoparasites; Arachnida (Ticks & Mites) > Flashcards

Ectoparasites; Arachnida (Ticks & Mites) Flashcards

1
Q

What are the generic signs and symptoms of ectoparasite infestation?

A
  • Itching
  • Scratching
  • Bites
  • Soreness/raised red skin
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2
Q

Ectoparasite infestation is not life threatening. Why bother?

A
  • Mild to severe discomfort
  • Secondary infection from scratching
  • Public issues, contagious
  • Social stigma
  • Parasites hosts for transmitted pathogens and diseases
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3
Q

What phylum do ticks, mites, fleas and lice belong to?

A

Arthropoda (insects/spiders/crabs)

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4
Q

What Class do fleas and lice belong to, and what are their characteristics?

A
  • Class: Insecta
  • 6 legs
  • Wingless
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5
Q

What Class do ticks and mites belong to, and what are their characteristics?

A
  • Class: Arachnida
  • 8 legs
  • Spiders, scorpions
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6
Q

What do fleas and lice, ticks and mites all do in common?

A
  • All blood-sucking parasites
  • Live on skin (ectoparasites)
  • Host specific e.g. human (unlikely from pet)

> > > Lice most prevalent in UK, others have greater socioeconomic impact.

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7
Q

What is the latin name for ticks? How are they typically transmitted?

A
  • Ixodes ricinus ‘hard tick’
  • Climb tall grass and scrubs “questing”
    »> Playing in long grass/hiking
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8
Q

What is the three host life cycle for Ixodes ricinus (ticks)?

A

1) Adult females drop off third host to lay eggs (after feeding)
2) Eggs hatch into 6-legged larvae, overwinter in larvae stage.
3) Larvae attach and to first host in spring (small rodent)
4) Engorged larvae leave first host in summer
5) And molt into nymphs, in the fall, overwintering.
6) Nymphs attach and feed on second host at following spring (rodent/lagomorph - rabbit)
7) Nymphs drop off late in summer, molt into adults (late summer/fall) and overwinter.
8) Next spring, adults attach to 3rd host; large herbivore (cow), carnivore, human. Adults feed and mate on third host during summer, before females drop off and restart cycle.
»> Humans may serve as hosts at any point, one host could be all three hosts.
> Life cycle spans 3 years

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9
Q

Where do ticks like to frequent (geographically and on the body)

A
  • Mainly on the coast; warm and damp
  • Or common around deer
    »> Inspect skin after long grass/hiking; warm sweaty places (pits/groin/nape)
    > Tick migrates up body
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10
Q

What are the signs of tick (Ixodes ricinus)

A
  • Move up body
  • Exposed limbs (top of arms/legs)
  • Neck
  • Visual examination is the ONLY way to detect (rice/frozen pea size)
    »> Do NOT itch
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11
Q

How are ticks removed/treated?

A
  • No pharmacological treatment

- Physical removal; use of tweezers

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12
Q

What are the counselling points for tick removal?

A
  • Do NOT squeeze or crush body; do not want tick to regurgitate blood back into the body (pathogenic)
  • Do NOT leave head behind
  • Do NOT try to burn off, or other noxious means
  • Keep tick for positive identification (GP?)
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13
Q

What are the possible complications of tick infestation?

A
  • Tick-Borne encephalitis (virus)

- Lymes disease (bacteria)

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14
Q

What is Tick-Borne encephalitis? (Symptoms?)

A
  • Viral disease carried by tick
  • Flavivirus; infects the brain (encephalitis = inflammation of brain)

Symptoms;
- Malaise, weakness (IgM/IgG levels increased)
- Can lead to meningitis/high fever
- 2% mortality (death within 7 days of neurological symptoms)
»> Seek clinical help

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15
Q

What is Lymes disease? (Symptoms? Incubation?)

A
  • Bacterial disease caused by tick
  • Spirochetes Borrelia burgdorferi

Symptoms:

  • Bulls eye rash (characteristic; dartboard red/white circles)
  • Flu like symptoms (malaise)
  • Tired and general malaise
  • Seek clinical help (antibiotic treatment)

Incubation:
- 2-100 days (symptoms can take 3 months to manifest after being bitten)

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16
Q

What types of mites are there?

A
  • Bed mites

- Scabies

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17
Q

What is the life cycle for a mite?

A

1) Female bed mite lays 5 eggs daily (in ‘sheltered’ location e.g. seams, spaces under floorboards)
2) Eggs hatch in 4-12 days to instar nymph
3) First nymphal instar takes a blood meal from warm-blooded host, molts to second nymphal instar.
4) 5) 6) Five nymphal stages in total, each requiring a blood meal between to molt to the next
7) Before the 5th stage becomes an adult.

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18
Q

What are the signs & symptoms of bed mite infestation?

A

Itchy bites (unlike ticks)

  • Allergic reaction (not all; mite saliva?)
  • Bites in straight lines (not random like mosquitos or fleas)
  • Red spots on sheets; crushes mites in sleep
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19
Q

What is the treatment for bed mite infestation?

A
  • No pharmacological treatment
  • Minimal, symptomatic treatment
  • Empirical treatment for bite reactions
    > Antibiotics; if infection
    > Antihistamines; itching/irritation/inflammation
    > Topical/oral corticosteroids; if really bad
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20
Q

How can bed mite infestation be prevented?

A
  • Can survive 6-12 months without a blood feed
    > Hot linen wash, drying 60 Degrees C, ironing
    > Airing bedclothes
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21
Q

What is the latin name for bed bugs? Do they carry human disease?

A
  • Cimex lectularius
  • Were suspected carriers of HIV, Hep B etc.
    »> Little evidence to support
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22
Q

What are Scabies? (Latin name? Signs and symptoms?)

A

Sarcoptes scabiei (to scratch incessantly)

Signs and symptoms:

  • Epidermal skin infestation
  • Feed in tissue and fluids (NOT blood)
  • Characterised by superficial burrow and pruritus (intense itching)
  • 300 million cases worldwide

Scabere = to scratch

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23
Q

Where do Sarcoptes scabiei (Scabies) like to inhabit?

A
  • Skin folds (sweaty places)

- Fingers, buttock, breast creases

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24
Q

What is the life cycle of Sarcoptes scabiei?

A

All in skin:

  • Eggs laid in stratum corneum
  • Mature to larvae (3 pairs of legs); migrate to skin surface, burrow into stratum corneum to form molting pouches
  • Which mature to nymph (greater size, 4 pairs of legs)
  • Mature to Adult Male/Female
  • Female is larger, mating takes place once and female remains fertile forever, and lays eggs (2-3 per day)
25
Q

What are the signs and symptoms of Scabies infestation?

A
  • Intense pruritus

Visual signs:

  • Ensure no impetigo or eczema
  • Burrow markings (raised lumps)
  • Ink test; ink penetrates and leaves coloured lines
  • Skin biopsy; scabies mites (moderate/greater infection)
26
Q

Why is there such intense pruritus w/scabies infestation?

A

Delayed type IV-sensitivity reaction to:

  • Mite
  • Saliva
  • Eggs
  • Excrement
27
Q

What is SMIPP, and how does it aid infection by mite?

A

Scabies Mite Inactivated Protease Paralogue

  • In saliva
  • Protein w/no enzyme activity
  • Antagonist to PAR-2 (protease-activated receptor) on keratinocytes
  • Inhibits inflammatory response; thus aiding infestation.
28
Q

Can immunity be acquired to Scabies?

A

Yes:

  • Secondary infestations have reduced parasite burden
  • Can eliminate second infection (antibodies)
29
Q

How is Scabies spread? How contagious is it?

A

Spread directly:

  • Scratching, picking up mites under the fingernails
  • Touching infested person’s skin

Spread indirectly (fomites; objects):

  • Keyboards, toilets, clothing, towels, bedding, furniture
  • Anything that the mite could be rubbed off to

> > > V. contagious; 1/1000 see GP per month in the UK.

30
Q

How long can Sarcoptes scabiei survive away from a host?

A
  • Survive up to 14 days away from host

- BUT; less than 36 hours devoid of human skin.

31
Q

When do symptoms develop following Sarcoptes scabiei infestation?

A

3 - 4 weeks (delayed inflammatory action; due to SMIPP antagonising PAR-2 on keratinocytes.

32
Q

How common is Sarcoptes scabiei infestation?

A

Mainly south of equator, where there is poor hygiene, high densities of people, dogs, immunosuppression:

  • Africa
  • Central and South America
  • Caribbean Islands
  • India
  • SE Asia
33
Q

Who are more at risk from Sarcoptes scabiei infestation?

A

Institutional settings:

  • Elderly people (nursing homes)
  • Children (schools/nurseries)

> Young mothers; close contact w/infected children
Sexually active people (considered STD)

34
Q

How is Sarcoptes scabiei infestation treated? Who needs to be treated?

A
  • Resistant to soap and water, including scrubbing
  • Can be infected indefinitely (if don’t treat); life cycle
  • Family and sexual partners need to be treated; prevent reinfection
    »> Insecticides: acaricides
35
Q

What is the insecticide class acaricides effective against? Give examples.

A

Effective against Arachnid subclass Acari; ticks and mites:

  • Permethrin cream
  • Malathion lotion
  • Ivermectin
  • Benzyl benzoate; though less effective than above (and unknown action)
36
Q

What are the first and second line treatments respectively for treating Sarcoptes scabiei infestation?

A

1) Permethrin cream 5% (Lyclear); whole body
2) Malathion lotion 0.5% (Derbac-M)
> If Permethrin ineffective

37
Q

Why is Permethrin cream 5% (Lyclear) first line for Sarcoptes scabiei infestation?

A

More effective than topical crotamiton 10%, or oral Ivermectin (Cochrane review 2007)

38
Q

How is the pruritus from Sarcoptes scabiei treated?

A
  • Crotamiton (Eurax)

- Sedating antihistamine (oral)

39
Q

How does Permethrin work?

A

Synthetic pyrethroid:

  • Similar to natural pyrethrins from Chrysanthemum
  • Ion channel agonist
  • Acts on nervous system of animal

Neurological toxin:

  • Binds to NaV-gated channels in Sarcoptes scabiei
  • Prolongs Na+-channel activation; prevents inactivation and deactivation
  • Paralyses animal function, leading to death.
  • Permethrin prevents inactivation gate closing; repeated APs = repeated depolarisation of muscle
40
Q

If Permethrin is a neurological toxin; an agonist of sodium-gated ion channels, why are humans unaffected?

A
  • Humans have diff. AA sequence of activation gate

- Thus humans have no sensitivity to permethrin

41
Q

How do Sarcoptes scabiei develop resistance to pyrethroids (e.g. Permethrin)?

A
  • Methionine AA at position 918 is substituted for a Threonine
  • Mutation means the ion channel looks more like mammalian NaV
  • Thus resistance (no sensitivity)
42
Q

What is it regarding the M918T mutation of insects (e.g. Sarcoptes scabiei) that renders the mite now resistant to pyrethroids (e.g. Permethrin)?

A
  • Mutation at Domain II’s S4-5 linker
  • Originally Methionine sulfur (hydrophobic) side chain at activation gate; thioester (S) interacted w/aromatic groups of pyrethroids (pi e- interaction) = toxicity
  • But mutation leads to Threonine; a polar uncharged, chiral side chain instead (which does not interact w/pyrethroid aromatic side chains)
  • Which is much closer to Isoleucine; the mammalian AA component at the DIIS4-5 linker, which has a non polar, branched chiral side chain.
    »> Thus Threonine does not bind Permethrin (as Isoleucine doesn’t in mammalian NaV)
43
Q

What are the contraindications of Permethrin/pyrethroid use?

A

None really:

  • Absorption of topical cream is minimal
  • In breast feeding; no evidence of risk, but just remove cream before feed.
44
Q

Why may itching persist up to 3 weeks post-treatment of Sarcoptes scabiei with permethrin/pyrethroids?

A
  • Animal material and faees may remain in the skin

- Symptomatic treatment; antihistamine cream

45
Q

How does treatment failure present of Permethrin therapy to treat Sarcoptes scabiei infestation?

A
  • If itching persists > 6 weeks

- New burrows appear

46
Q

Why is Permethrin treatment of Sarcoptes scabiei repeated one week after the initial treatment? Who else is treated?

A
  • Initial overnight complete coverage
  • Repeating one week later makes sure all remaining eggs are killed, after all live organisms are killed the first time
  • Personal close contacts treated too; prevent reinfestation (especially sexuak partners)
47
Q

What is the course of action in suspected resistance to Permethrin?

A
  • Skin biopsy; determine genotype of animal

- Recommend Malathion lotion (second line)

48
Q

How does Malathion work?

A

Anticholinesterase:
- Organophosphorus compound

Neurological toxin:

  • Acts on nervous system of animal
  • Irreversibly binds to and blocks cholinesterase (preventing NT [ACh] breakdown/recycling to acetate + choline)
  • Promotes all cholinergic transmission (xs ACh in synaptic cleft)
  • Postganglionic neuron excitation (prolonged post-synaptic stimulation)
  • Continuous muscle excitation and contraction
49
Q

Humans have cholinesterase too. Why is Malathion safe to use?

A

Malathion of low toxicity to humans:

  • Only with repeated exposure; overdosage
  • Ingestion and metabolism to malaoxon far more toxic
  • Chlorination of water promotes oxidation
50
Q

What would occur if anticholinesterase (Malathion) was ingested in humans?

A

Anticholinesterase in man:

  • Parasympathomimetic, promotes muscarinic transmission
  • Promotes neuromuscular nicotinic transmission at SkM
  • Promotes central cholinergic neurotransmission (brain)
51
Q

What are the muscarinic effects of Malathion/Malaoxon poisoning?

A

Parasympathomimetic, promotes muscarinic transmission:

  • Miosis
  • Salivation
  • Sweating
  • Bradycardia
52
Q

What are the nicotinic effects of Malathion/Malaoxon poisoning?

A

Promotes neuromuscular nicotinic transmission at SkM:

  • Fasciculation (twitching of SkM; spontaneous release of ACh)
  • Paralysis; depolarising neuromuscular block
53
Q

What are the CNS symptoms of Malathion/Malaoxon poisoning?

A

Promotes central cholinergic neurotransmission (brain):

  • Anxiety
  • Restlessness
  • Dizziness
  • Depression
54
Q

How does Ivermectin work?

A

Macrocyclic lactone

  • Derived from Streptomyces bacterium
  • Ion channel agonist
  • Acts on nervous system of Sarcoptes scabiei/animal

Neurological toxin

  • Binds to and activates GluCl; Glutamate gated Cl channels (stays open; Ivermectin takes Glu’s place, binds almost irreversibly)
  • Member of Cys-loop ligand-gated ion channel family; GABAaRs in brain and nACHRs in vertebrates (post-synapatic SkM)
  • GluCl are invertebrate specific; muscle and neuron
  • Paralyses animal function; hyperpolarization of chloride channel, cell is negative af, less excitable
55
Q

Why is Ivermectin safe for PO administration in humans, given GluCl is of the same ion channel family (Cys-loop) as GABAaR and nACHR?

A
  • In humans, ivermectin modulates nAChR and GABAaR, NOT activates
  • Does not cross BBB; P-glypcoprotein allows efflux of drug, as does MDR1 (multi-drug resistance) gene
56
Q

What are the contraindications for Ivermectin PO?

A
  • Children U5
  • Body weight < 15 kg
  • Breastfeeding
  • Hepatic and/or renal distress; affects distribution/pharmacokinetics
57
Q

What are the potential complications of scabies, Sarcoptes scabiei?

A

Secondary infection (from pruritus)

  • Staphylococcus (need antibiotics)
  • Impetigo

Social stigma
- Psychological harm; ‘guilt and shame’

Crusted scabies:
- Extreme infestation (thousands to millions)
- Does not itch
- Thick, warty crusts
- Immunocompromised; very young, elderly, HIV, chemotherapy
»> Treat w/Ivermectin 200 micrograms/kg PO (ivermectin is first line for crusted scabies)

58
Q

What prophylactic/preventative measures can be taken with Sarcoptes scabiei infestation?

A
  • Avoid sharing of: clothing, towels, bed linen.
  • Avoid dirty hotels and accommodation
  • General hygiene

*B33VPI - Pharmacology & Therapeutics (3 decks)

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