Arthropod-Borne Diseases

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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