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Flashcards in Richard Wall Deck (32):
1

What 5 things are considered when evaluating disease risk due to arthropod ectoparasites?

1 vectorial potential - biting rate, dispersal rate, vector abundance
2. Intervention - driven by clinical signs, reservior populations, awareness of public
3. new vetors - arrival, spread and establishment
4. distribution - spatial and temporal phenology
5. arthropod abundance - birthrate, dev rate, dath rate.

2

how are arthropod ectoparasites damaging?

1. directly -chorioptic mange, acariasis
2. causes - inflammation, allergic responses, pruritus, excoriation and alopecia.
3. May be blood feeding - fleas, Tabanids - blood feeding flies.
4. Can be zoonotic - sarcoptes scabei causes scarcoptic mange
5. pathogenic effects are related to abundance.

3

what is the pre patent period?

extrinsic incubation time
after this, the vector is infectious.

to understand infectivity, must know the pre patent duration, and vector survival rate, eg mosquitoes have high mortality during ppp, so low proportion of mosquitoes are actually infectious.

4

what are 4 characteristics of a mechanical vector?

1. Interrupted feeds
2.Short re-feeding interval
3. High fly mobility
4. High survival of pathogens on insect
Mechanical vector = passive transfer of pathogen btw hosts, often on feet or mouthparts

5

define prevalence and incidence

Prevalence - is the proportion of the population affected by a particular disease
Incidence - probability of occurrence of a given disease in a population within a specified period of time

It is important to distinguish real underlying changes from changes in perception and awareness.

6

characteristics of co-evolved ectoparasites, eg lice, mites.

Highly host specific,
obligate,
permanent,
low dispersal ability,
relatively low pathogenicity

7

characteristics of pre-adapted ectoparasites
eg flies

Mobile,
long off-host survival,
intermittent,
facultative,
relatively high pathogenicity
recently became parasitic.

8

what recent changes could potentially cause unstability in interactions betweenhosts and parasites?how has intensification facilitated instability between ectoparasites and host?

1. domestication
2. Intensification
3. Insecticide resistance - head lice now resistant to most treatments.
4. Increased global movement of humans, domestic animals and arthropod parasites and
vectors.
5. Anthropogenic environmental change
6. Climate warming
7. Novel pathogen emergence/resurgence

9

how has increased global movement affected ectoparasite prevalence?

Increased global movement of humans, domestic animals and arthropod parasites and vectors. Airport hubs are huge areas of disease. Asian tiger mosquito - Aedes albopictis, spread through small pools of water, eg in tyres and lucky bamboo trade. vector of dengue, massive increase in reportedcases of dengue globally since 1950s risen to approx 960,000 annually, from 1 to nearly 60 countries.

Gatherings of Nomadic people - Cure Salee gathering, causes outbreaks of Rift Valley fever in Niger 2016, 2m cattle infected, increased infection in W africa.

10

how has domestication affected ectoparasite prevalence/incidence?

domestication - eg breeding sheep for woolly undercoat is also beneficial for parasites.
Mouflon - not domesticates has thin layer of fur, bred to produce domesticated sheep - Ovis aries. Similarly rabbits bred for floppy ears.

11

how has anthropogenic environmental change affected ectoparasites?

increased puddles of water from agricultural irrigation and wetland conservation - increased breeding ground for vectors.

12

how has climate warming affected ectoparasites?

more rain and increased distribution of mosquitoes.

13

how has novel pathogen emergence or resurgence affected ectoparasites?

not enough knowledge about this.
eg Schmallenberg virus - cattle - fever, severe diarrhoea, loss of appetite and body condition, reduced milk yield
Goats and seep - still births and birth defects. probably transmitted by blood feeding culicoides midges.

14

5 points about culicoides midges.

- scotland/scandinavia
- bite humans and other animals
- cause hypersensitivity in horses - sweet itch
- possibly a vector of Schmallenberg virus.
- known vector of BTV

15

what is BTV?
what species does it affect?

Blue tounge Virus
Orbivirus, 26 serotypes recognised.
all ruminants are host, severe disease in sheep and deer.
mild disease in cattle, goats, wild ruminants and camelids.

16

symptoms of BTV

swollen lips and tounge
lack of oxygen to tounge - blue.
trouble breathing and swallowing.in africa no mortality in local breeds but imported breeds 90% mortality.

17

transmission cycle of BTV

in host: incubation period of 5-20 days. short viraemia, 30-60 days
in vector: no transovarian development, short adult midge lifespan.
needs continual trandmission but adult midges diw over winter in N europe so only are sporadic outbreaks.

18

transmission cycle of BTV

in host: incubation period of 5-20 days. short viraemia, 30-60 days
in vector: no transovarian development, short adult midge lifespan.
needs continual transmission are sporadic outbreaks.

19

why is it unexpected that BTV occurs in Europe?

adult midges die over winter in N europe so only are sporadic outbreaks.
primary vector Culicoides imicola limited to N africa and mediteranean.
Genetic analyses has shown 6 serotypes have entered Europe since 1998, 4 routes of entry: through portugal,
greece, Baleric islands, italy.

20

BTV in netherlands, belgium, germany, france

August 2006-January 2007
gene sequence data - origin of BTV8 in sub saharan africa.
unsure why SO widespread and persistent, all aspects of biology say it shouldnt.possibly due to unexpected ability of culicoides obsoletus and pulicaris to transmit disease.
Spreadto UK in 2007

21

How can BTV survive overwinter in temperate regions? 3

1. A few infected adult Culicoides midges may survive mild winters.
2. BTV can cause a chronic or latent infection in some individuals animals.
3. Can be transmitted to fetus if infection occurs in mid pregnancy, = chromic infection lingering until a few months after birth, then spreads to other animals.

22

describe adaptations of hard ticks

Ixodidae -
hard dorsal scutum, chelicerates - use chelicerae to cut holes in host. hypostome ventral to chelicerae to suck up blood.
backward pointing teeth to hold into host.

23

lifecycle of ixodidae

3 hosts
larvae in vegetation, attach to small mammal host eg mouse, by questing behaviour.
nymphs grab onto larger mammal eg rabbit
adults on deer/sheep. females gorge on blood, grow to 200x size. lays eggs and then adult drops off host and dies.

24

pathology of ticks

cause blood loss, anaemia
inflammation
lesions
restlessness
reduced body condition
carry more pathogens than any other arthropod group.

25

why are ticks effective vectors?

1. Long lived - 3 yrs
2. Attach securely to host/Large blood meals (increases risk of infection)
3. High fecundity/high density - 2000 eggs at once
4. Relatively non-host specific
5. Difficult to control off the host - bury into the ground when off host. only on host for 3-4 weeks
6. Trans-stadial transmission - host passes infection to next stage in mouth.
7. Trans-ovarial transmission
8. SAT (salivary assisted transmission) - pool of blood forms under skin with many ticks probing it, sharing pathogens

26

what i sone well known disease transmitted by ticks?

Lyme borreliosis
Bacterium: Borrelia burgdorferi complex
Vector: Ixodes ricinus
Humans - bulls eye rash in 70% cases, fever, headache, depression, joint pains. difficult to diagnose. treated with antibiotics.

27

describe the distribution of lymes disease

found wherever there are ticks.
2-3000 clinically confirmed cases per year, but actual cases assumed 10x higher.
concerns of climate change increasing epidemics.

28

how many pets move in and out of uK?

in 2012, estimated 300,000 pets travelling to and from UK.
in 2012 removed the compulsory tick treatment upon re entry.

29

What tickis associated with dogs and is worrying atm?

Rhipicephalus sanguineus
Adapted to warmer temperatures and low humidity
Found in heated kennels and houses
Rapid development - life-cycle completed in 3 months
Will diapause for up to 1 year in cold environments
Not in UK (yet) – Mediterranean - but may be moving north.
Transmits: Babesia vogeli, Hepatozoon canis, Ehrlichia,

30

how is conservation and deer populations affecting tick abundance?

deer conservation programs increasing rapidly. red and roe deer. main host for ticks, so tick pop is strongly correlated w deer pop, and higher incidence of tick bourne disease.

31

another tick bourne disease concerning the CNS

Tick bourne encephalitis - TBE
viral
Far Eastern form (20% mortality) or European form (1-2% mortality).
Clinical signs: fever, headache, anorexia, nausea, vomiting and photophobia.
Followed by a stiff neck, sensory changes, visual disturbances and other neurological deficits.
No specific drug therapy.

32

what affects spread off tick bourne disease such as TBE and lymes disease?

tick abundance is spreading north due to climate change, but changes in incidence of TBE and lymes disease dont always correlate with tick abundance.
incidence driven by exposure, due to good weather and economic hardship causing people to forage for berries and mushrooms. varies with cultural practice and economic constraint.