Arthropod-Borne Diseases
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- Created by: fionnualamaire94
- Created on: 09-01-17 19:18
Leishmania infantum
- protist - eukaryotic non-animal/plant/fungus
- amastigote - located within macrophages, passes large nucleus, rod-shaped kinetoplast, rudimentary flagellum
- promastigote - developmental stages - sand fly vector, elongated, centrally positioned nucleus, kinetoplast at anterior end with flagellum, replication via binary fission
- indirect life cycle
- definitive host - mammal - amastigote
- intermediate host - sand fly vector - promastigote
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Leishmania infantum - Epidemiology/Pathology
- high prevalence of subclinical infection
- bimodal disease <3 >8
- dogs - can be either visceral or cutaneous
- usually chronic with low mortality, can manifest as acute, rapidly fatal form
- recovery - cell-mediated immunity - Th1
- Th2 - active lesions persist - chronic enlargement of spleen/liver/lymph nodes
- cutaneous - shallow skin ulcers - often on lip/eyelid
- visceral - 'lunettes' - depilation of hair around eyes, generalised loss of body hair, eczema, intermittent fever, anaemia, cachexia, generalised lymphadenopathy, periods of remission
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Leishmania infantum - Diagnosis/Treatment
- amastigotes - using direct methods, cytology, direct immunofluorescence
- antibodies - indirect methods, ELISA, dipstick tests
- leishmania DNA - DNA in tissues, PCR - sensitive and specific
- treatment- remission of clinical signs over infection clearance
- pentavalent antimonials
- meglumine antimonite
- allopurinol
- amphotericin B
- pentamidine
- aminoside
- ketoconazole
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Leishmania infantum - Control
- sand fly population reduced as a result of mosquito control - leishmaniosis incidence reduced
- general chemical control of sand fly vectors has very limited success
- insecticides and repellents (collar/spot-on) give some protection
- vaccine available in some southern European countries e.g. Italy - protection against disease rather than infection - vets divided on efficacy and limiting capacity to spread infection
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Babesia (Babesia divergens) - Life cycle
- protozoa
- indirect life cycle
- definitive host - tick
- intermediate host - mouse, cattle, humans, sheep, cat
- multiplication in vertebrate host - binary fission in RBC > merozoites
- liberated RBC to invade others - indefinite cycle
- ingestion by adult tick - vermiform - ovary/eggs - round up and divide to form small round organisms
- larval ticks moult and parasites enter salivary glands, binary fission, vermiform, break to lumen of gland - mammalian host infected when tick sucks blood
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Babesia (Babesia divergens) - Epidemiology
- B. bigemina and B. bovis - highly pathogenic - tropics/sub-tropics
- B. divergens - relatively pathogenic - northern Europe
- age of host - young animals are less susceptible
- immune status of host - endemic areas - colostrum gives passive immunity - transient infections with mild clinical signs - sufficient to trigger active immunity
- level of tick challenge - endemic areas - many infected ticks - immunity of host is maintained - overt disease is rare; few ticks - immune status of population low if ticks increase suddenly clinical cases rise sharply
- stress - endemic areas, occasional outbreak of clinical disease esp. adult animals
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Babesia (Babesia divergens) - Pathogenesis/Treatme
- rapid destruction of the erythrocytes - haemoglobinaemia, fever, anorexia, fever, slight jaundice
- acute disease occurs 1-2 weeks after tick feeding - death or weight loss, decreased milk production and diarrhoea - followed by constipation
- diagnosed by blood films stained with Glemsa
- treatment
- amicarbilide
- diminazene aceturate
- imidocarb
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Dirofilaria immitis - 'heartworm'
- nematode
- definitive host - mostly dog
- intermediate host - mosquito
- right ventricle, right atrium, pulmonary artery, posterior vena cava
- females release microfilariae directly into blood stream
- ingested by female mosquitos - L3 development takes 2 weeks
- larvae present in mosquito mouthparts
- dog - L3 migrates to subcutaneous or subserosal tissues - 2 moults
- PPP = 6 months minimum - up to 5 yr patency
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Dirofilaria immitis - Epidemiology
- infects dogs >1yo
- host factors - high density of dogs, lengthy patent period, lack of effective immune response
- vector factors - ubiquity of mosquito host, capacity for rapid population increase, short development period from microfilariae to L3s at optimal temp
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Dirofilaria immitis - Pathogenesis
- adult parasites
- circulatory distress only occurs in heavy chronic infections, chronic right-sided heart failure, mass of active worms - endocarditis in heart valves, dead or dying worms mat cause pulmonary embolism
- worms may lodge in posterior vena cava - acute, fatal, vena caval syndrome
- cats - pulmonary hypertension, right-sided heart failure
- heavily infected dogs - listless, gradual loss of condition, exercise intolerance
- lightly infected dogs - poor performance
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Dirofilaria immitis - Treatment/Control
- drugs are complex
- first treated IV with thiacetarsamide twice daily over 2-day-period
- OR IM melarsamide over 2 days - remove adult worms, toxic reactions not uncommon
- activity restricted for 2-6 weeks
- THEN dithiazanine iodide, levamisole, avermectins or milbemycin - 6 weeks later to remove microfilariae
- mosquito control is difficult
- prophylaxis = medication - diethylcarbamazine - orally to pups from 2-3 months of age, kills developing larvae, tropical areas all year around, temperate zones - 1 month prior to mosq. season, 2 months after end (ivermectin/milbemycin)
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