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214 Cards in this Set
- Front
- Back
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protozoan classes
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-mastigophera
-coccidia -piroplasmidia |
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mastigophera
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-leishmania
-trypanosoma -trichomonas -giardia |
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coccidia
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-eimeria
-isospera -cryptosporidium -toxoplasma, neospora |
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piroplasmidia
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-babesia
-theileria |
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eimeria (general)
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-parasites of epithelial cells in which sexual & asexual reproduction take place
-intracellular for large part of life cycle -many species infecting wide range of hosts (esp. poultry but also ruminants & rabbits) -pathology dependent on level of infection -species are host specific but several species can infect a single host |
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eimeria in poultry
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-intracellular
-infects gut epithelium -transmission: faecal-oral -major pathogen of intensely reared chickens |
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eimeria (life cycle)
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-3 phases: sporulation (in environ), infection & schizogany (asexual), gametogony (sexual)
1. sporulated OOCYST (contains 4 sporocysts ea. with 2 sporozoites) ingested 2. oocyst partially digested to release SPOROZOITES: colonizes gut epithelial cells (becomes TROPHOZOITE) 3. divides by fision and develops into SCHIZONT 4. schizont releases MEROZOITES which colonize new epithelial cells 5. merizoites give rise to MICROGAMETOCYTE (male) & MACROGAMETOCYTE (female - unicellular) 6. microgametocyte release MICROGAMETES (flagellated): penetrates MACROGAMETOCYTE to form OOCYST (zygote) |
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eimeria (oocyst sporulation)
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under correct temp & humidity, oocyst (in faeces) develops 4 sporcysts --> ea. containing 2 sporozoites (bananna shaped)
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eimeria (sporozoite)
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-emerges from sporulated oocyst (ruptures) & infects enteric epithelial cell
-will divide (fission) and develop into a schizont |
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eimeria (schizont)
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-sporozoite divides (fission) and develops into schizont
-schizont will rupture will rupture and release merozoites that will infect another gut epithelial cell |
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eimeria (merozoite)
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-emerges from a schizont (ruptures epithelial cell) and infects another epithelial cell
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eimeria (microgametocyte)
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-merozoites emerge from epithelial cell (schizogony) and forms gametocytes to begin sexual cycle
-microgametocyte = male: containts many microgametes -microgametes will release to fertilize the macrogametocyte (female) to form zygote (oocyst) |
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macrogametocyte
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-merozoites emerge from epithelial cells (schizogony) to form gametocytes (male or female)
-macrogametocyte = female: will be fertilized by microgametes (from microgametocyte) to form zygote (oocyst) |
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eimeria in chickens (highly pathogenic species)
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-E. tenella: mainly in the caeca; fast devel. (young: 3-7wks); diahrrea & blood in faeces
-E. brunetti: terminal SI (sometimes rectum & caeca); slower (older birds); haemorrhage in SI -E. necatrix: mid SI (some caeca); like brunetti |
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eimeria (pathogenesis)
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-destruction of gut epithelial cells
-villous atrophy -blood loss (some species) -malabsorption of nutrients: limited weight gain, loss of egg production -death if severe -1 oocyst = 8 sprozoites = 160 merozoties x 3 asexual cycles = 6600 merozoites = 6600 epithelial cells destroyed |
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eimeria (diagnosis)
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-bloody/water faeces
-failure to thrive -ID of schizonts & oocysts |
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eimeria (epidemiology: broilers & breeders)
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-housing: deep litter/warm/humid/crowded
-transmission: oral-faecal -intro: infected chick or farmers boots -disease: high # of oocysts (high repro rate) -layers & free range: limited contact with faeces so little problem |
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eimeria (control)
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1. management: litter changes & stacking (piles will ferment & heat will kill oocysts), ventilation (decr. humidity), design of water troughts
-chemotherapy: coccidostats in feed/water (concern about resistance) -vaccines: low dose live oocyst (overdose = disease), attentuated live -vaccine issue: b/c broilers grow so fast, by time immunity develops (several weeks) will have already been challenged |
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eimeria life cycle (ruminants)
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-similar to poultry
-oocysts --> sporozoites --> invade gut epithelium --> schizonts --> merozoites --> macro & micro-gametes --> oocysts |
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eimeria bovis & zuerni (cattle)
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-low level of oocysts on bedding & pasture: many animals infected
-adults immune but shed oocysts -overcrowded, unsanitary conditions promote infection -young calves become infected & disease occurs: due to oocyst numbers |
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sheep coccidiosis
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-life cycle similar to poultry eimeria
-ingestion of sporulated oocysts from pasture/bedding -many animals infected but disease primarily in lambs -species (11): eimeria ovinoidalis, E. crandallis -bloody, watery diarrhea; failure to thrive; inappetance, dehydration, anaemia, death |
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coccidiosis (sheep: epidemiology)
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-unweaned twin or triplet lambs (generally 4-8wk)
-lowland farms with high stocking rates -source of infection: ewe (immune) & lambs -stress, poor nutrients, severe weather, concurrent infections all predispose |
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isospera
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-class: coccidia
-life cycle similar to eimeria but unlimited rounds of asexual repro (unlike 2-4 rounds in eimeria) -cat & dog species can cause diarrhea & haemorrhage in young animals species (4 of vet significance): 1. isospera suis: pig (most prevalent) 2. i. felis: cat 3 i. revolta: cat 4. i. canis: dog |
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isospera suis
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1. clinical significance:
-affects nursling piglets (15-20% diarrhea) -adults immune but shed oocysts 2. clinical signs & pathogenesis: -yelowish/gray faeces (mortality < 20%) -villous atrophy & necrotic enteritis -failure to thrive 3. epidemiology -sows produce few oocysts -oocysts left on farrowing crates -not transmitted by milk or faeces |
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cyrtosproridium
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-class: coccidia
-only 1 species of vet significance: cryptosporidium parvum -wide host range, zoonosis -typical coccidial life cycle: infects gut epithelial cells -villous atrophy & epithelial cell distruction -malabsorption & diarrhea -transmission: faecal-oral & water/food born |
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cryptosporidium (life cycle)
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1. oocyst ingested
2. excystation --> sporozoite --> trophozoite --> 1st gen meront (like schizont) 3. emergence of reinfection of epithelial cell --> 2nd gen meront 4. emergence of merozoite --> macrogametocyte + microgametocyte --> oocyst (zygote) |
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cryptosporidiosis diagnosis (cattle)
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-concentrate faecal samples: best way to detect aysmptomatic infections
-oocyst detected by ziehl-neelsen stain -antigens can be detected by ELISA |
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cryptosporidium parvum(importance)
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-acute diarrhea in young livestock
-failure to thrive -zoonotic: similar problem in humans -highly prevanlent in UK |
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cryptosporidium parvum (epidemiology)
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oocysts autosporulate: infection can build up rapidly
-adults become immune but sill shed oocysts -crowded, unsanitary conditions -can be water or feed born -oocysts v. resistant to disinfectants & environ -human: contact with infected animals, water/food, contaminated swimming pools & rivers (all routes faecal-oral) |
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toxoplasma gondii (final host)
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-final host: cat ingests IMH (bird, mouse, etc) with encysted bradyzoit in tissues
-cyst wall digested: release bradyzoits which invade intestinal epithelium -asexual repro (several rounds): schizonts produce merozoites --> reinvade epithelial cells) -sexual phase: microgametes & macrogamete fuse --> oocyst (shed in faeces) -also infection from igestion of tissue containing tachyzoites -can get extra-intestinal generation of tachyzoites & bradyzoites in cat |
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toxoplasm gondii (IMH)
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-any mammal/birds-sheep/goats and humans (often birds & mice)
-oocyst sporulates in 1-5d (2 sporocysts/4 sporozoites) & are ingested -sporozoites released in gut: invade intestinal cells --> form tachyzoites (crescent shape) -tachyzoites multiply & released (destroy host cell): can reinvade any nucleated cell --> spread throughout body (by blood/lymphatics) -immune system controls tachyzoites: encysts --> bradyzoite (divide slowly w/in cyst) -bradyzoites usually in tissue of brain, liver, lung, muscle -IMH infected either by ingestion of sporulated oocyst or another IMH containing bradyzoites or tachyzoites |
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toxoplasma gondii (epidemiology)
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-ingestion of sporulated oocyst via contaminated food or hands
-ingestion of infected tissue via encysted bradyzoite (eg. undercookd lamb/ork) -ingestion of infected tissue via tachyzoite (rare) -can get transplacental passage of tachyzoite (only if 1st time, acute infection) -cat is central to spread to sheep: direct contaminatin of feed -vertical transmission in mice: resevoir -oocysts only shed for 1-2wk (kittens) before immunity (no longer shed oocysts) |
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toxoplasma gondii (pathology)
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-related to extra-intestinal phase of infection:
1. acute: caused by multiplying tachyzoites resulting in necrosis of vital organs 2. healthy host (transient - often undiagnosed): pyrexia & lymphadenopathy (glandular fever) 3. immuno-compromised host (eg. AIDS): hepatitis, hepatosplenomegaly, encephalitis, death |
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toxoplasmosis (cats)
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-clinical disease is rare
-fever, enteritis, pneumonia, ocular lesions (retinochoroiditis/uveitis) -congenital toxoplasmosis is uncommon; can result in severe & fatal disease in kittens: anorexia, hypothermia, lethargy, sudden death |
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family: sarcosystidae
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-class: coccidia
-genera: 1. toxoplasma 2. sarcocystis 3. neospora |
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family: eimeridae
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-class: coccidia
-genera: 1. eimeria 2. isospera 3. cryptosporidia |
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toxoplasma gondii (ovine abortion & perinatal mortality)
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-infection w/in 1st 50/55d: death, expulsion of small foetus or resorption (rates of bareness higher than expected)
-infection 50-120d: premature birth of stillborn/weak lambs + chocolate brown mummified foetus a few days before term -infection late: infected but normal lambs (immune to reinfection) |
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toxoplasma gondii (diagnosis)
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-placental cotyledons: bright to dark red w/ small white foci of necrosis
-Ab in foetal fluids & precolostral lamb serum -innoculation of mice with test tissue (slow & expensive) -immunohistochemistry or immunofluorescence -PCR (placental tissue) |
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toxoplasma gondii (control)
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1. prevent infection in cats: dispose of infected material, no raw meat fed
2. prevent infection of sheep -cover feed & prevent access to cats -retain immune animals (eg. previously infected) -removed aborted material: prevent exposure to pregnant -decoquinate to feed -vaccinate: attenuated tachyzoites (can't produce bradyzoites) |
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toxoplasma gondii (behavioral changes)
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-rats: less fear of open space & cat urine --> more predation by cats
-humans: |
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sarcocystis
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-class: coccidia (family: sarcocystidae)
-IMH: ruminants, pigs, horses -final host: carnivores (dogs) -species: sarcocystis bovi canis, eg. (bovine = IMH & canis = final) -sarcocysts commonly found in heart & skeletal muscle (cysts in direction of muscle fibres) of sheep (UK): S. ovi canis -not as important as toxplasma gondii -loss of productivity & condemnation of carcass |
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sarcocystis (life cycle)
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1. final host infected by ingestion of muscle containing sarcocyst: bradyzoites released
2. bradyzoites infect epithelial cells of SI: directly form macro & micro gametes --> fuse to form oocyst 3. sporulation in gut: sporulated oocyst released in faeces 4. IMH ingests: sporocytes released in SI & invade endothelial cells of mesenteric arteries 5. divide asexual --> form schizonts (1st asexual): merozoites produced & released from cell (2nd asexual) 6. free merozoites invade mononuclear leukocytes --> schizonts (3rd asexual) formed & produce merozoites: released (3rd gen merozoites) 7. merozoites invade muscle cell --> form bradyzoites within a sarcocyst (2-3mo) |
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sarcocystis (pathogenesis)
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-significant disease only in IMH (no cysts in final host - some diarrhea)
-disease assoc. with replication of 2nd stage schizont -acute infection: death & abortion, haemorrhages, myeloencephalitis, myositis, inflammatory response -chronic disease: emaciation/premature growth cessation, reduced milk yield, condemnation of carcass |
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sarcocystis (clinical signs & diagnosis)
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-fever & increased metabolism
-anaemia (haemorrhage), submandibular oedema -shivering, inappetence, weight loss -muscle wasting, recumbency, lethargy -some sheep: death of recently lambed ewes, vague neuro disease, hind limb paralysis (dog sitting posture) -PM: petechial haemorrhages & lymphadenopathy -histo: schizonts in endothelial cells, developing sarcocysts |
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neospora
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-class: coccidia (family: sarcocystidae)
-parasite infectino of cattle (abortion) & dogs -life cycle similar to toxoplasma but dog is final host & cow is IMH -bradyzoites & tachyzoites (asexual stage) -oocysts (sexual stage) |
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neospora (asexual life cycle in IMH)
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-ingestion of infected tissue or oocysts: produce tachyzoites
-form bradyzoites in tissue cysts -pregnancy can reactivate bradyzoites --> release tachyzoites: cross placenta --> abortion (foetus recognized as foreign body) |
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neospora (sexual cycle in final host: dog)
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1. ingestion of infected tissue: bradyzoites from offal or tachyzoites/bradyzoites from aborted foetus
2. invasion of gut epithelial cells --> generation of gametes 3. oocysts shed in faeces: contamination of feed & infection of IMH by sporozoites (oocyst contains 2 sporozoites) |
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neospora (transmission scenario)
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1. infected dog on farm --> shed oocysts on feed: calves become infected
2. in gut: oocysts liberate sporozoites --> infect gut cells --> cycles of multiplication (tachyzoites) in other tissues 3. immune response --> bradyzoites encyst in tissues 4. adult services --> bradyzoites reactivate (drop in immunity) 5. tachyzoites repliate & cross placenta to foetus --> 3 possible outcomes: abortion*, infected, or neuro signs |
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neospora (pathogenesis: cattle)
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3 possible outcomes (depends on time of bradyzoite activation)
1. early: infected foetus aborts (necrosis of neural tissue) 2. mid: calf born with neuro symptoms (rare) 3. late: no visible signs but infected NOTE: no abortion if oocyst infection during pregnancy --> requires horizontal transmission (not vertical) |
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neospora (pathogenesis: dogs)
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-hind limb ataxia & paralysis (adults & pups)
-behavioral changes -lesions around eye & mouth (rare) -no abortion -bitch infected for life (in brain or other tissues) |
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bovine neosporosis (summary)
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-neospora caninum infects cattle worldwide
-epidemic: cluster of abortions ("abortion storm") or sporadic, endemic abortions (from infected dog) -key issues for control is transplacental transmission |
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canine neosporosis (summarY)
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-sexual cycle leads to oocysts & bovine infection
-asexual cycle leads to disease transmitted directly or transplacentally -as with cattle, seropositive bitches will give rise to infected pups with neuro signs -difficult to treat |
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neospora (control)
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-no effective or licensed drugs
-no vaccine -infection remains in herd b/c transplacental transmission -difficult to treat b/c immune cows show no signs -ask farmer: neuro signs? new dog? -test tissue sample from aborted foetus - |
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mastigophera
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protozoa:
-leishmania -trypansosoma -trichomonas -giardia |
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mastigophera of vet importance
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-flagellate protozoa (primarily extracellular)
1. trichomonas foetus (cattle): vagina/penis 2. giardia lambia (man/domestics): gut 3. histomonas meleagridis (turkey/chicken): liver 4. leishmania infantum & L. chagasi (dog/man): blood/tissues 5. trypanosoma spp (cattle/camels/man): blood/tissues |
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trichomonas foetus
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-class: mastigophera
-replicates (binary fission) in the preputial cavity, vagina & uterus -causes low grade endometreitis --> abortion -indications: early abortion & apparent infertility -bull: no real symptoms -transmitted at coitus -immune response (inflammation) in vagina -diagnosis: agglutinating antibodies |
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trichomonas foetus (structure)
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-single nucleus
-free flagellae -undulating membranes -very motile -axostyle: cyto-skeletal structure |
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trichomonas foetus (life cycle)
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-replicates soley by binary fission
-bull transmits to cow at coitus |
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trichomonas foetus (importance)
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-reduced reproductive efficiency
-decreased pregnancy -increased abortion -no drug or vaccine: must cull bull; cows will become immune |
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giardia lamblia
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-gut parasite: diarrhea
-low host specificity: zoonotic -transmitted by water contamination of directly via faecal-oral route |
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giardia lamblia (life cycle)
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-transmission: foecal-oral
-ingestion of dormant cysts -trophozoites released: browse on gut epithelium (motile) --> malabsorption -trophozoites multiply by fission --> encyst -both trophozoites and cysts passed in faeces but only cysts can survive in environment |
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giardia lamblia (structure)
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-2 nuclei (as opposed to 1 in trichomonas)
-sucker pad: adhesion to gut epithelium -free flagella -undulating membranes |
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giardia lamblia (consequences)
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-malabsorption
-loss of weight gain -villous atrophy -diarrhea -zoonosis |
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histomonas meleagridis
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-disease of turkeys
-heterakis is vector -virtually absent in UK: industrial rearing has lead to its disappearance |
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leishmania
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-infects blood/tissues
-vector: sandflies -disese: cutaneous & visceral form -species: 1. Leishmania tropica 2. L. braziliensis (man/dog): S. America 3. L. donovani (man) 4. L. chagasi/infantum (dog/rodent/man) |
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leishmania (life cycle)
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1. metacyclic enters blood stream
2. invades macrophages --> becomes amastigote 3. amastigote replicates (binary fission) 4. amastigotes burst host cell & reinvade uninfected macrophages 5. infected macrophage taken up by sandfly 6. transform to promastigote & divides 7. migrates to proboscis & attach to epithelial cells |
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leishmania (disease)
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1. cutaneous form:
-L. braziliensis (S. America), L. tropica (Africa/Asia) -skin lesions & destruction of nasal & buccal tissue (man - also dog but rare) 2. visceral: -L. donovani/infantum/chagasi (N. Africa/S. Europe) -liver & spleen ulceration, enlargment (man) -loss of hair, skin ulceration, wasting (dog) -L. infantum seen in UK & USA |
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leismania (diagnosis)
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-clinical signs: not totally specific
-detection of parasites in lesions/lymph nodes/bone marrow biopsies -ELISA: antibodies (low sensitivity) -PCR -long PPP: antibodies appear late |
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leishmania (importance)
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1. endemic regions:
-zoonosis -dogs act as resevoir & suffer disease -AIDS patients infected in S. Europe 2. UK: -PETS: return from holiday w/o quarantine --> increased movement 3. N. America: only found in foxhounds & hunting dogs (eastern & southern states) |
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trypanosoma
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-transmitted by tsetse fly
-many species of flagellate protozoa infecting wide range of animals -pathogenic species: tropical regions -major restraint on cattle rearing in Africa & S. America -most species multiply in blood & tissues -important for human nutrition & livelihood |
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trypanosoma (structure)
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-flagellum: full length of parasite
-single nucleus -kinetoplast (posterior): mitochondrial DNA (stains with giemsa) -covered by surface protein coat: antigenic variation |
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trypanosoma (species)
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-T. brucei (Africa): tsetse
-T. congolense (Africa): tsetse -T. vivax(Africa/S.America/Asia)): tsetse + biting flies -T. evansi (Africa/S.America/Asia): tsetse + biting flies -T. eqiperdum (horse - all tropical regions): coitus |
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trypanosoma species (morphological differences)
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-T. congolense: kinetoplast set to 1 side; flagellum does not extend beyond body
-T. brucei: kinetoplast centered; flagellum extends beyond body (long tail) -T. vivax: short tail |
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trypanosoma (life cycle: L. brucei & L. congolensis)
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1. tsetse ingests during blood meal: short stumpy (SS) form
2. procyclic division: gut of tsetse (binary fission) 3. epimastigote division: sailvary gland (T. brucei) or proboscis (T. congolense) of tsetse (binary fission) 4. blood meal: inject metacyclic stage into host -L. vivax: both procyclic & epimastigote in proboscis |
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trypanosoma (antigenic variation)
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-glycoprotein coat covers surface
-1000 genes encode different code proteins: many possible combos -as immune response develops to one coat & eliminate the parasite, others change thir coat by expressing a different gene -preculdes developing a vaccine -race between immune system and antigenic variation |
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trypanosoma (pathogenesis)
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-cellular infiltration of muscle tissue
-degeneration of muscle tissue (oedema & wasting) -mycarditis -anaemia, low PCV -splenomegaly -inflammation -LN enlargment -loss of meat & milk production -death if not treated |
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trypanosoma (clinical signs)
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-anaemia
-lymph node enlargment -stunted growth & muscle wasting -splenomegaly |
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trypanosoma (diagnosis)
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-thick blood film: microscopy
-giemsa stained blood smear -PCR (research) |
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trypanosoma (control & treatment)
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1. trypanocydal drugs (eg. samorin, berenil)
2. control of tsetse fly -insecticides (screens, pour ons, sprays): lack of specificity & potential resistance -traps -sterile male release (female stores sperm & doesn't re-mate): localized --> will move in from other areas 3. breeding trypanotolerant cattle (n'dama): not highly productive (milk or meat) |
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trapanosoma brucei (zoonosis)
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-causes sleeping sickness
-crosses blood-brain barrier -3 subspecies: T. b. gambiense, T. b. rhodesiense, T. b. brucei |
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arachnids
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-4 pair of legs
-abdomen & cephalo-thorax (2 segments) -extensively modified mouth parts: imp't for life cycle & disease transmission -arachnids do not have antennae or wings |
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tick families
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1. ixodidae (hard ticks): rigid chitinous plate (scutum) on dorsal surface
2. argasidae (soft ticks): no scutum |
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hard tick (morphological characteristics)
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-scutum: rigid plate covering dorsal surface of male (partial on female)
-eyes on outer margin of scutum -festoons: rows of notches on posterior margin of body -ornate (enamel like areas or patterns) or inornate |
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ixodes (hard ticks)
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1. ixodes canisuga: british dog tick
2. ixodes hexagonus: hedgehog tick (cats) 3. ixodes ricinus* (most important): European sheep tick (+ dogs ruminants & dogs) --> ectoparasite of all mammals & birds |
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ixodes (species ID)
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-ixodes ricinus: overlapping spur on 1st coxa
-ixodes canisuga: no overlapping spur (vestigial) -ixodes hexagonus: has spur but does not overlap |
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ixodes (preferred sites)
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-face
-ears -axilla -inguinal region |
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ixodes ricinus (life cycle)
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3 host tick (only 26-28d on host: temporary parasite): cycle takes 3yr
1. male & female mate on host: female complete large blood meal over 14d 2. females drop to ground & lay eggs (1k-2k) 3. eggs hatch into larvae (3 pair of legs): quest for host, attach & feed for 6d (1st host) 4. larvae drop to ground & moult into nymphs (resemble small adult: 4 pair of legs) 5. nymphs quest for host, attach & feed for 6-8d (2nd host) 6. nymphs drop to ground & moult into adults --> quest & mate (3rd host) |
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ioxedes ricinus is 3 host tick
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3 host tick:
-larvae feed on host A -nymphs feed on host B -adults feed on host C 2 host tick: -larvae & nymphs feed on host A -adults feed on host B 1 host tick: larvae, nymphs, & adults feed on host A |
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ixodes ricinus (epidemiology)
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-requires high humidity: largely confined to deciduous woodland, rough grazing or moorland in wetter parts of UK
-peak feeders: April & May -spring feeders: moult in autumn & overwinter unengorged -autumn feeders: overwinter engorged & moult following summer -where high rainfall feed August to November |
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ixodes ricinus (feeding mechanism)
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-chelicarae: cutting action makes initial lesion
-hypostome then pushed through -dorsal groove in hypostome channels for saliva into host (anti-coagulant, cement, hyaluronidase) -blood back into tick via dorsal groove |
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ixodes ricinus (pathogenic significance)
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-heavy infection: anaemia
-lesions result in inflammation, irritation, loss of production, hide condemnation -secondary infections: blow fly strike (attracted by tick lesion), tick pyaemia in sheep (staphylococcus: septicaemia/abcess) |
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ixodes ricinus (disease transmission)
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1. red water: babesia divergens (fever/anaemia/haemaglobinuria)
2. tick-borne fever (sheep, cattle, goats, dogs): anaplasma (fever/abortion) 3. louping ill (sheep, cattle, grouse): flavivirus (encephalitis/abnormal gait) 4. lyme disease (horses, cattle, dogs): borelia burgdorferi (persistent fever/arthritis/lameness) |
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ticks (other genera)
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1. haemaphysalis punctata:
-3 host tick: S. England & Wales -transmits protozoan parasites: Babesia major (cattle) & Babesia motasi (sheep) 2. Dermacentor reticulatus -3 host (ornate) tick: S.England & Wales -can transmit babesia to horses & dogs (mainland Europe) |
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hard ticks (genus ID)
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-ixodes: anal groove is anterior
-haemaphysalis: anal groove is posterior -dermacentor: anal groove is absent |
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family: argasidae (soft ticks)
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-mouth parts NOT visible from above
-adults & nymphs feed repeatedly -mating takes place off the host -drough resistant -Argas pericus (fowl tick): restlessness, loss of productivity, anaemia |
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tick borne diseases
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1. protozoan parasites (class = piroplasmidia): babesia & theileria
2. rickettsia: anaplasma & cowdria |
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babesia
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-class: piroplasmidia
-intraerythrocitic parasite -hosts: cattle, sheep hosrses, pigs, dogs -vectors: ixodes (hard) tick -worldwide distribution |
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babesia (morphology)
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-small babesia (1-2.5 microns): more pathogenic & more resistant to drugs
-large babesia (2.5-5 microns): less pathogenic & less resistant to drugs |
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equine babesiosis
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-babesia equi: small pathogenic
-vector: dermacentor reticulatus (hard tick) -mainland Europe |
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canine babesiosis
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-babesia canis: large, pathogenic
-babesia gibsoni: small, pathogenic -vectors: rhipicephalus sanguineus & dermacentor reticulatus -common: B. gibsoni in US (29 states); UK threat b/c PETS -vaccine available |
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bovine babesiosis (N. Europe & UK)
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1. babesia divergens: small, pathogenic
-vector: ixodes ricinus (hard tick) -N. Europe & UK 2. babesia major: large, mildly pathogenic -vector: haemaphysalis punctata -S. England & parts of Wales |
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babesia (species & vector)
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-B. equi (horse): small, pathogenic --> dermacentor reticulatis
-B. canis (dog): large, pathogenic --> rhipicephalus sanguineaus/dermacentor reticulatus -B. gibsoni (dog): small, pathogenic --> rhipicephalus sanguineaus/dermacentor reticulatus -B. divergens (bovine): small, pathogenic --> ixodes ricinus babesia -B. major (bovine): large, mildly pathogenic --> haemaphysalis punctata -B. bovis (bovine): small --> boophilus (tropical) -B. bigemina (bovine): large --> boophilus (tropical) |
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bovine bebesiosis (tropical)
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-B. bovis (small) & B. bigemina (large)
-transmitted by ticks w/in genera Boophilus: ornate 1 host tick -600 million cattle at risk |
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babesia divergens (life cycle)
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1. sporozoites inoculate by feeding tick: directly invade RBCs
2. form piroplasm & divide (binary fission) into 2-4 merozoites -merozoites released as RBC ruptures --> invade more RBCs & divide: parisitaemia rises 3. merozoites eventually form gametocytes inside RBCs: tick infected by uptake of RBCs with gametocytes 4. gametocytes released & form gametes --> fuse to form zygote 5. zygote invades tick gut cell --> sexual division --> forms multiple vermicules 6. vermicules released & invade tick tissues (esp. ovary & then egg) 7. egg hatches: larvae infected --> takes blood meal --> vermicules migrate to salivary gland & form sporozoites --> into cow |
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babesia (transmission)
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1. transovarian: infection acquired by adult tick & transmitted through egg to larvae, nymphs or aults of next generation
2. transtadial: infection acquired by one stage of tick then transferred to next (eg. larvae acquire & nymphs transmit or nymphs acquire & adults transmit) -B. divergens: transovarian is normal route of transmission (transtadial occasionally) |
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bovine babesiosis (pathogenesis: general)
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-destruction of erythrocytes & release of vasoactive substances
-significant anaemia & organ damage through tissue anoxia |
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bovine babesiosis (pathogenesis: B. divergens & B. bigemina)
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-classical haemolytic anaemia
-parasites multiply in RBCs up to 40% parasitaemia -marked fall in PCV (<20%) -up to 75% of RBC can be destroyed: 1. through mechanical disruption by parasite 2. increased osmotic fragility & phagocytosis of infected & uninfected RBCs |
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bovine babesiosis (pathogenesis: B. bovis)
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-fall in PCV when parasitaemia is low (<1%)
-release of substances that activate plasma components: increase vascular permeability, vasodilation & intravascular coagulation -consequences: circulatory stasis & shock + RBC destruction & tissue anoxia |
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babesiosis (epidemiology)
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-can be acute, severe, or mild
-dependent on age & immune status of host 1. endemic regions: -calves challenged early & develop innate resistance -disease mild & transient -constant challenge but balance by herd immunity: enzootic stability 2. non-endemic regions: -challenge is light & sporadic: calves do not become immune -infection of naive adults: acute outbreaks -enzootic instability |
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babesiosis (clinical signs)
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-"redwater fever"
-incubation 1-2wk -initially fever + anaemia (pale mucus membranes), diarrhea, incr. respiratory/heart rate -haemoglobinuria -anaemia advances, constipation, dehydration, heart beat audible, red water stops, temp falls -terminal cases: weak pulse, recumbent, death -if survives: convalescence is prolonged (loss of weight & decr. milk yield) -subclinical infections: low parasitaemia, mild fever, anorexia |
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babesiosis (control)
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-prevent tick challenge
-prophylaxis: imidocarb over 1st month -acaracides: dips (may lead to resistance) -vaccine for B. bovis & B. bigemia -vaccine against ticks: TickGARD (gut antigen) |
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theileria
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-protozoan parasite (class = piroplasmidia)
1. T. annulata (cattle): S. Europe, N. Africa, Mid East, Asia 2. T. parva (cattle): E. & Central Africa 3. T. hirci (sheep/goats): S. Europe, N. Europe, Mid East, Africa |
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theileria parva
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-protozoan parasite (class = piroplasmidia)
-disease: East Coast Fever (near 100% mortality in cattle) -vector: rhipicephalus appendiculatus (brown ear tick - 3 host) -transmission by trans-stadial route: larvae acquire & nymph transmits or nymph acquires & adult transmits -only south of Sahara |
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theileria annulata
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-protozoan parasite (class = piroplasmidia)
-disease: Tropical Theileriosis (cattle - near 70% mortality in exotics) -vector: hyalomma ticks (2 host) -mild to moderate pathogenicity in indigenous breeds (reduced productivity) -transmission is trans-stadial: larva/nymphs acquire --> adults transmit |
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theileria (life cycle)
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1. sporozoites innoculated by feeding tick --> invade leukocytes
2. forms macroschizont --> stimulates leukocyte division (parasite divides with it by attaching to mitotic spindle) 3. eventually division slows & macroschizont enlarges --> forms merozoites 4. leukocyte ruptures & releases merozoites --> invades RBCs & forms gametocytes 5. gametocyte infected RBCs taken up by feeding tick --> gametocytes released & fuse to form zygote 6. zygote infects tick gut epithelial cells --> becomes kinete 7. after tick moult kinete moves to salivary gland --> tick feeds & induces sporozoite formation (sporozoites inoculate) |
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theileria parva (clinical pathology)
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-"East Coast Fever"
-leucopenia, severe damage to & disorganization of lymphoid system A. incubatin period ~1wk B. lymph node hyperplasia, followed by fever & systemic infection C. lymphodepletion due to lymphocytolysis & depressed leucopoesis: death w/in 18-26d -clinical signs: enlarged lymph nodes, fever, respiratory distress (pulmonary oedema), and blood tinged diarrhea |
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theileria annula
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-"Tropical Theileriosis"
-lymph node enlargment then fever -marked anaemia: pale mucus membranes (may be jaundiced), diarrhea, blood stained faeces -sub acute/chronic cases: intermittent fever, anaemia & jaundice -poor condition & convalescence is protracted |
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theileria (diagnosis & control)
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-ID parasite: giemsa stain, immunofluorescence, PCR
-chemotherapy: buparvaquone -acaracides: dipping (up to 2x/wk) -vaccination: T. parva (sporozoite) & T. annulata (attenuated macroschizont) |
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anaplasma
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-Rickettsia (not protozoan)
-anaplasma marginale/centrale -cattle in tropical regions -causes bovine anaplasmosis -transmission: trans-stadial & transovarian (20 tick species) -bovine transplacental transmission can occur |
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anaplasma marginale
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-inclusion body at edge of RBC: 1 inclusion body contains up to 8 initial bodies
-RBC lyses: initial bodies release --> infect new RBCs -severe haemolytic anaemia: 70% of RBC can be destroyed -rising fever, pale mucus membranes, loss of coordination, abortion, death -no haemoglobinuria -control: vaccination (attenuated or A. centrale) |
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cowdria ruminantium
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-Rickettsia (not protozoan)
-Heartwater disase -severe febrile illness of calves/lambs in caribbean & subsharan African -transmission: Amblyomma tick (3 host ornate tick) --> normally trans-stadial -multiplies in vascular endothelial cells: circulates in neutrophils -acute: sudden onset of fever followed by nervous signs, constant lip chewing & licking, circling with high stepping gait -eventually recumbency: animals die while undergoing massive convulsions --> brain oedema |
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tick borne diseases (control)
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1. extensive dipping with acaricides: resistance
2. pasture control: burning/spelling 3. cross breed for resistance: bos indicus x bos taurus 4. vaccination: anaplasma, babesia, cowdria, theileria 5. vaccination against ticks: reduces tick fertility 6. enzootic stability: promote immunity (protect naive animals) 7. enzootic instability: eradicate using extensive control measures |
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arthropods (classes)
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1. insecta: flies, lice, fleas
2. archnida: mites & ticks |
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class: insecta
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-3 pairs of legs
-body divided into head, thorax & abdomen -single pair of antennae -families: midges (sweet itch), blackflies (vector of onchocerca), sandflies (vectors of leishmaniasis), mosquitos (malaria & dog heartworm), also horseflies -significance: fly worry (loss of grazing & growth), disease vectors, parasitic in own right |
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culicoides: biting midge
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1. vectors of:
-filarial parasites of man -onchocerca cervicalis -blue tongue virus -african horse sickness 2. cause of sweet itch (horses): seasonal puritic skin disease |
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muscidae (outright parasitic flies)
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1. warbles & bots: oestridae
2. blow flies: calliphoridae 3. keds & forest flies: hippoboscidae 4. flesh flies (feed on dead): sarcophagidae |
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muscidae (nuisance flies & vectors)
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1. non-biting:
-house & face fly: musca domestica/autumnalis -head fly: hydrotea irritans 2. biting: -stable fly: stomoxys calcitrans -horn fly: haematobia irritans -tsetse fly: glossina spp |
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flies (general life cycle)
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1. adults mate
2. female lays eggs: on or off host 3. larvae hatch on/off host (3 stages: L1,L2,L3): segmented, mobile, oral hooks (feed) 4. pupation (usually off host): develop hard outer casing 5. pupae develop into adults |
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musca domestica (specialized mouthparts for feeding)
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-labella with pseudotrachea: like large sponge --> go around eye & suck up nutrients (or on dung heap & back to eye)
-palps: feelers |
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hydrotea (head fly)
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-feeds on wound secretions (eg. fighting wounds): often to dung heap & back to wound (infection)
-interrupted grazing if high numbers: "fly worry" -transmission of bacteria & viruses (mastitis & conjuctivitis) -intense irritation of horned sheep: target area around horns -control: reduce breeding sites in manure & soiled straw, insecticide sprayed on byre walls or impregnated ear tags, dips/pour ons |
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non-biting flies
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1. house & face fly: musca domestica/autumnalis
2. head fly: hydrotea irritans |
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biting flies
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1. stable fly: stomoxys calcitrans
2. horn fly: haematobia irritans 3. tsetse fly: glossina spp |
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stomoxys calcitrans (stable fly)
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-painful bites: multiple bites due to interupted feeding
-vector: habronema, T. evansi, T. vivax -mouthparts (parts of proboscis): 1. labella with teeth: skin penetration 2. labium 3. labrum 4. hypopharynx: inserts once finds capillary |
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haematobia (horn fly)
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-biting, blood sucking fly
-feeds on cattle: around base of horns -may be multiple bites from interrupted grazing -transmission of stephanofilaria -adults on host (most of time, except egg laying): 1000s per animal |
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tsetse fly
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-biting
-vector of trypanosomiasis: man, cattle, game -subsaharan africa |
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tsetse fly (ID)
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1. wings folded over (as opposed to haematobia)
2. brown, size of house fly 3. hatchet 'cell' on wing 4. larvae white 5. pupae brown & barrel shaped: characteristic polypneustic lobe |
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tsetse fly (life cycle)
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-mating on host
-female stores sperm & releases single egg -larvae develop in utero -deposited in soil & burrows beneath surface -pupates & 30-60d later adult emerges |
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oestridae (warbles & bots)
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-obligate myiasis: larvae devleop w/in host
-larvae are parasitic & host specific -adults have non-functional mouth parts -large hairy flies -3 genera of importance: 1. hypoderma: warble fly (bee like) 2. oestrus: sheep bot 3. gastrophilus: horse bot |
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oestrus ovis (sheep bot)
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-dark grey fly
-viviparous: develop to larvae w/in female -female squirts larvae into nostrils of sheep -larvae migrate to sinuses & mature: ingest contents of nose/sinuses -larvae sneezed out onto ground --> pupate on ground -2 to 3 generations/yr -L2 can overwinter insunuses |
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oestrus ovis (consequences)
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-nasal discharge: parasitic rhinitis
-grazing disruption due to adult attempting to deposit larvae (main problem): sheep bury nose in ground to avoid -loss of weight gain if fly in high numbers -larvae can penetrate brain: false gid (rare - true gid from cestodes) -low prevalance in N. Europe, high in S. Europe |
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hypoderma bovis & lineatum (warble fly)
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-host: cattle, rarely man, horse or sheep
-hairy, bee like fly: no mouthparts (do not feed) -distribution: N. Europe (up to 80% of herds), eliminated from UK (compulsary dipping) |
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hypoderma (warble fly life cycle)
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1. adult females cement eggs to hairs: eggs hatch & larvae migrate through hair follicles (obligate myiasis)
2. larvae migrate through flesh to spinal canal (LI) --> migrate under skin on back & develop to L3 (warble = L3 under skin) 3. L3 penetrate hide to breath --> pre-pupae forces its way through hole & drops to ground to pupate |
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warble & larval tracks
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-L3 of hypoderma under skin on back of cattle
-larval migrate by secreting digestive enzymes & mascerating tissue with oral hooks -creates track of gelatinous material: "butchers jelly --> reduces value of meat |
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warble (significance)
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-animals panic on sound of fly: 'gad'
-reduced grazing: loss of weight gain -hide damage due to perforation: loss of value of leather -butchers jelly reduces carcass value -life cycle ~3wk: treat w/ ivermectin but NOT if in spinal canal (immune response) |
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gasterophilus (horse bot)
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-larvae develop in stomach
-adults: hairy pointed abdomen -larvae: reddish orange -no mouthparts -3 species: 1. G. intestinalis 2. G. nasalis 3. G. haemorhoidalis |
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gasterophilus (horse bot: life cycle)
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1. adults mate: 1 generation/yr
2. eggs attach to hairs, hatch & transferred to mouth by licking 3. penetrate tongue & buccal mucosa (sometimes tongue ulceration) 4. attach to stomach (oral hooks) 5. develop for several months & passed in faces (red larvae alarm owners) 6. larvae pupate & adults hatch (1-2mo) |
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gasterophilus (pathogenesis & importance)
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-fly worry from adult laying eggs
-rarely tongue ulceration -may cause stomach ulceration -owners concern about red bots in faeces (though may not be a health concern): so treat (ivermectin) -G. intestinalis most common (30-50% of horses in N. Europe) |
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oestridae (warbles & bots)
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-obligate myiasis: larvae devleop w/in host
-larvae are parasitic & host specific -adults have non-functional mouth parts -large hairy flies -3 genera of importance: 1. hypoderma: warble fly (bee like) 2. oestrus: sheep bot 3. gastrophilus: horse bot |
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oestrus ovis (sheep bot)
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-dark grey fly
-viviparous: develop to larvae w/in female -female squirts larvae into nostrils of sheep -larvae migrate to sinuses & mature: ingest contents of nose/sinuses -larvae sneezed out onto ground --> pupate on ground -2 to 3 generations/yr -L2 can overwinter insunuses |
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oestrus ovis (consequences)
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-nasal discharge: parasitic rhinitis
-grazing disruption due to adult attempting to deposit larvae (main problem): sheep bury nose in ground to avoid -loss of weight gain if fly in high numbers -larvae can penetrate brain: false gid (rare - true gid from cestodes) -low prevalance in N. Europe, high in S. Europe |
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hypoderma bovis & lineatum (warble fly)
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-host: cattle, rarely man, horse or sheep
-hairy, bee like fly: no mouthparts (do not feed) -distribution: N. Europe (up to 80% of herds), eliminated from UK (compulsary dipping) |
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hypoderma (warble fly life cycle)
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1. adult females cement eggs to hairs: eggs hatch & larvae migrate through hair follicles (obligate myiasis)
2. larvae migrate through flesh to spinal canal (LI) --> migrate under skin on back & develop to L3 (warble = L3 under skin) 3. L3 penetrate hide to breath --> pre-pupae forces its way through hole & drops to ground to pupate |
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calliphoridae (blow flies)
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-mainly affect sheep but also rabbits
-myiasis is facultative (NOT obligate) -blow fly strike: 'blow' = laying of eggs, 'strike' = larval development -2 types of strike: primary flies can penetrate skin; secondary cannot penetrate but will enter a wound or follow path of primary -3 species in UK: 1. lucilla sericata*: greenbottle (primary strike) 2. phormia terra nova: blackbottle (secondary strike) 3. calliphora spp: bluebottle (secondary strike) |
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calliphoridae (blow fly: life cycle)
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1. adults mate & female deposits eggs on fleece (200 eggs)
2. larvae hatch & develop: oral hooks & enzymes macerate & digest tissue (3-10d) 3. larvae drop to ground & pupate (3-7d) --> can overwinter on ground 4. fly emerges & feeds (5-6 generations per summer) |
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blow fly (types of strike)
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defined by region of body where strike occurs: depends on rot or soiling (odor)
1. body (common in UK) 2. breech (back end): eg. lamb scour 3. penile sheath (pizzle rot) 4. tail 5. poll |
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blow fly (pathogenesis)
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-very irritating lesions --> interrupted grazing & loss of condition
-secondary bacterial infection can lead to septicaemia -prevalence (UK): 80% of sheep farmers report cases of strike (only 1.5% of sheep affected) |
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blow fly strike in pat rabbits
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-primarily lucillia sericata (greenbot)
-struck in breech -dirty conditions, diarrhea, long haired breeds -significan mortality |
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blow fly (epidemiology)
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1. temp (late spring): overwintered pupae develop & adults emerge (life cycle in 10d) --> rapid increase in numbers --> slow in autumn
2. climate/rain: rain wets wool & in warm spring creates wool rot --> odor attracts fly & eggs laid (body strike) 3. breed: fine wool breeds --> wool rot (body), wrinkled breeds (merin) --> accumulation of faeces (breech), narrow penile sheath --> accumulation of urine 4. diarrhea: infection with helminths or protozoa --> tail & breech; non-docked tail --> faeces (tail) 5. wounds: fighting or injuries due to barbed wire --> poll & body |
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blow fly (control)
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-prophylactic insecticides: pour ons
-prevention of diarrhea: anthelmintics -tail docking -remove carcasses (limit populatoin) -clip wool around lesion -pick larvae off -dress strike wound with cream containing insecticide |
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hippoboscidae (keds & forest flies)
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1. sheep ked: melphagus ovinus
-permanant ectoparasite: mating, larvae & pupae all on host -blood sucking -anaemia & fleece damage 2. forest fly: hippobosca equina (horses & cattle) -blood sucking: attach with claws (cluster around perineum & hind legs) -remain on host except to deposit larvae in soil -acute irritation |
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mites
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-burrowing or non-burrowing
-permanant ectoparasites: complete life on host -transmission by contact -populations can build from single mite (w/in weeks to months) |
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burrowing mites
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-2 families:
1. sarcoptidae -sarcoptes (dogs) -notoedres (cats) -knemidocoptes (birds) 2. demodicidae: demodex (dogs) |
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sarcoptes scabei
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-sarcoptic mange: severe pruritis
-identify from other mites by: transverse ridges, spines & scales on dorsal surface |
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sarcoptes (life cycle)
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1. fertilized female burrows into surface layers of skin: generates winding tunnel (lays 1-3 eggs/day over 2mo)
2. eggs hatch into larvae (3-5d) --> go to skin surface & form moulting pockets 3. moult to form nymph & adult stages --> adult male seeks female on surface or in pocket (cycle takes 2-3wk) |
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sarcoptic mange (dogs)
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-highly contagious
-usually sparsely haired areas: ears, face, muzzle, elbows --> intense pruritis & obsessive scratching -pathogenesis: assoc. with burrowing/feeding (pierce skin to feed on exudate from inflamm. response) -erythema, papules, excoriation, alopecia, crust, progressive weakness (stop eating b/c obsessed w/ scratching) -exacerbated by hypersensitivity rxn to mite allergens -dog strain most common source for man (tho not most severe) |
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sarcoptic mange (dogs: treatment)
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-bath weakly in acaricide (amitraz) for 4wk or longer
-selemectin: spot on -isolate cases & treat all dogs in group -corticosteroid treatment |
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sarcoptic mange (cattle)
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-mite prefers neck & tail region
-usually mild but potentially severe -mild: scaly skin with little hair loss (can be confused with lice infestation) -severe: marked alopecia, thickened skin, crusts --> loss of production & hide damage |
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sarcoptic mange (pigs)
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-common (often asymptomatic)
-transmission oduring suckling -red papules erythema: eyes, snout, ears* -pruritis: continuous scratching (lose condition) -excoriation & scab formation -wrinkled, thickened skin covered with crusty lesions -treat with doramectin |
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notoedres cati
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-cats only: lesions on ear edge --> spreads over ears, face, neck
-dry encrusted lesions/thickened leathery skin -intense pruritis & severe excoriation -occurs in nests (groups of females): highly contagious (all kittens in a litter) -distinguish from sarcoptes by: 1. smaller size (~1/2) 2. lack of projecting spines/scales 3. thumb print striations |
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knemidocoptes
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-burrowing mites of domestic birds:
1. K. gallinae (poultry): depluming itch (burrows into feather shaft) 2. K. pillae (caged birds): scaly face, beak, head, neck, feet (if crosses beak & spreads to face can be fatal) 3. K. mutants (poultry): scaly leg (attacks skin below scales which rise up) --> lame |
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demodex
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-commensals in skin of most animals
-live in sebaceous glands & hair follicles: quite deep in dermis (need deep skin scraping to capillary to diagnosis) -morphology: cigar shape with 4 pair of stumpy legs -named for definitive host (eg. demodex canis or felis) |
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demodectic mange (dogs)
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-transmission requires prolonged contact
-most commonly mild (localized): slight hair loss & acanthosis -not usually pruritic: may resolve spontaeneously & not need treatment |
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generalized demodecosis
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-genetically inherited immunodeficiency or immunosuppression
-2 types 1. squamous (less severe): alopecia, desquamation & skin thickening 2. pustular (more severe): -bacterial invasion of lesions (eg. secondary staph infection) -acanthosis & small pustules -ooze serum, pus, blood, erythema -hyperpigmentation: 'red mange' -severe disfigurement |
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pustual demodecosis (treatment)
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-difficult to treat
-can be fatal: animals may be euthanized -repeated treatment with acaracide (amitraz) + antibiotic (for pyoderma) -takes at least 3 months: remission not guaranteed -if get in a litter --> spay bitch |
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non-burrowing mites
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3 families
1. psoroptidae: -psoroptes: p. ovis (sheep scab), p. equi -chorioptes: C. bovis -otodectes: O. cynotis (otitis externa in cats) 2. chyletidae: -cheyletiella: C. yasguri (dgos), C. blakei (cats), C. parasitivorax (rabbits) 3. dermanyssidae: dermanyssus gallinae (red mite of poultry) |
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sporoptidae
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non-burrowing mites
1. psoroptes ovis: sheep (sheep scab) & cattle 2. sporoptes equi: horses 3. psoroptes cuniculi: horses & rabbits |
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psoroptes ovis (sheep scab: pathogenesis)
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-allergic reactio to mite antigens (type I hypersensitivity)
-inflammation & serous exudate (mites feed on) -exudate dries to form scab surrounded by moist border & inflamed skin -mites active in scab border: population expands & scab extends (75% of body) -pruritis --> excess rubbing, loss of wool, excoriation |
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psoroptes ovis (sheep scab: clinical signs & diagnosis)
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-lighter wool is 1st visible sign (usually over shoulders)
-restlessness, rubbing, scratching: wool becomes ragged & stained -large area of wool loss + open bleeding wounds & acanthosis -loss of condition: stop eating -part wool & look for crusty lesion of scab -skin scraping from edge of lesion (in 10% KOH) -ID: oval body, legs project from body margin (unlike short stumpy legso of burrowing mtie), funnel shaped suckers, long 3 jointed stalk (pedicel) attach sucker to legs |
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psoroptes ovis (life cycle)
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1. female lays eggs (1-5/d)
2. larvae hatch 3. 2 nymph stages: protonymph & deutonymph 4. male & female attach: before maturity 5. adults: cycle takes 11-14d |
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psoroptes (epidemiology)
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-rapid spread (rapid life cycle)
-disease of late autumn/winter: egg laying increases (inverse relationship b'twn egg laying & temp b/c incr. fleece growth causes incr. humidity) -summer: latent phase (resevoir in axilla, eyes, ears) -contact transmission: around water troughs, clipping shears, movement, etc -short survival time off host: premises vacant for >3wk deemed free of scab |
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psoroptes ovis (sheep scab: treatment)
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-plunge dipping: autumn
-dips contain: organophophates (long residual effect) &/or synthetic pyrethroids (suspended 2006) -sheep in dop at least 60sec (head immersed twice) |
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bovine psoroptic mange
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-assoc. with intensive husbandry
-lesions on abdomen, tail head, ecutcheon, prepuce -pruritis, thickened skin wiht crusty lesions, feed intake reduced |
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chorioptes
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-family: psoroptidae (related to psoroptes but more mild)
-C. bovis: feeds on skin surface (less pruritis & hypersensitivity) -cattle: mild w/ localized lesions & economic loss -sheep: lower leg & scrotum (can result in stirility) -horses: below knees (crusty lesions, irritation, leg injury) |
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otodectes cynotis
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-family: psoroptidae
-otitis externa in cats & dogs -waxy exudate which becomes crusty -purulent otitis -scratching & head shaking: may cause haematoma |
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otodectes cynotis (diagnosis)
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-ear scratchin & head shaking
-dark brown waxy deposit in ear canal of dog -remove deposits & look for mites -ID: closed apodemes adjacent to leg pairs 1 & 2 -control: ear drops containing acaricide, antibiotics, fugicides & steroids (selamectin) |
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cheyletiella
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-mange contagious but mild
-mites in hair/fur: visit skin to feed -look for shed skin scales, dandruff in coat along back: "walking dandruff" b/c mites moving -ID: clawed palps + legs terminate w/ combs (instead of suckers) -species: 1. C. yasguri (dogs) 2. C. blakei (cats) 3. C. parasitivorax (rabbits) |
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dermanyssus gallinae
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-red mite of poultry
-obligate blood feeder: heavy infestion causes severe anaemia -only on birds during feeding: irritation, restlessness, debility -resevoir population in empty poultry houses: can live off host for several months -rapid life cycle: 7-8d -control: treat birds with acaracide + clean & treat habitat |
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guide to differential features of psoroptes ovis & chorioptes bovis
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1. size:
-psoroptes = .75mm -choriopes = .3mm 2. pedicels -psoroptes: long, 3 joint with sucker funnel -chorioptes: short, unjointed with sucker cup 3. mouthparts: -psoroptes: pointed -chorioptes: round 4. tubercles (males): -psoroptes: round -chorioptes: truncate (blunted) |
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fleas as disease vectors
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1. parasites:
-IMH of dipylidium caninum: ctenocephalides & pulex (tapeworm control linked to flea control) 2. viral pathogens: -myxomatosis: spillopsyllus cuniculi (rabbit flea) 3. zoonotic diseases -bubonic plague (pasteurella pestis): xenopsylla cheopis (rat flea) -murine typhus (rickettsia typhi): xenopsylla cheopis rat flea) & ctenocephalides felis (cat flea) 4. suspected role -cat scratch fever (bartonella henseleae: ctenocephalides felis (cat flea)? -feline infectious anaemia (haemoplasma spp): ctenocephalides felis (cat flea)? |
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fleas (general)
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-not completely host specific (host preference): will feed on humans but not infest
-most of life cycle off host: important for control -single most important cause of skin disease in sm. animal practice -rare in horses & ruminants |
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fleas (species found on cats & dogs)
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-ctenocephalides felis: accounts for 90+% of cases in cats & dogs
-ctenocephalides canis -pulex irritans (human) -spilopsyllus cuniculi: rabbit flea (pinna of ear) -echidnophaga gallinacea: avian -archaeopsylla erinacei: hedgehog |
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ctenocephalides flea (morphology)
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-dark brown & laterally flattened
-genal comb: 'mouth' area -pronatal comb: 'neck' region |
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fleas (life cycle)
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-adult lays eggs on host
-eggs brushed off into environment & hatch (1-6d) in environ: 3 stages of larvae -larvae pupate (8-32d) -exit pupae (1wk-1yr): stimulus is temp & vibration |
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flea allergic dermatitis
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-most common skin disease of dogs & cats: major cause of miliar dermatitis in cats
-allergens present in flea saliva -hypersensitivity reactions (types I & IV) -can have large flea burdens with minimal signs if not hypersensitive: problem not necessarily assoc. with # of fleas |
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flea allergic dermatitis (clinical signs)
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1. papular pruritic dermatitis: licking & scratching
2. secondary changes (assoc. with self trauma): -mainly dorsal lumbosacral region, caudomedial thighs, flanks, ventral abdomen -chronic: crusting, alopecia, hyperpigmentation, lichenification -sometimes pyotraumatic dermatitis (wet eczema) -cats: miliary dermatitis & eosinophilic granuloma associated |
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fleas (epidemiology)
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-pick up new infections from environment
-direct transfer between hosts in uncommon -adults fleas spend majority of time off host -feed soon after arriving on new host |
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fleas (role of pupae)
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-delayed emergence of adults from pupae: mass hatching in response to vibration (& warmth)
-pre emerged adults resistant to dessication: can remain in pupae for up to 1yr |
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fleas (control)
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-need to preent flea bites in hypersensitive animals:
1. remove adult fleas from animal: initiation of control 2. remove immature stages from environment (critical): maintenance of control -modern approach: "host-targeted therapy" to achieve both |
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lice
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-2 types: sucking (haematopinus) & biting
-less important than other ectoparasites -usually mild clinical effects -usually problem with husbandry or secondary to othe disease -pediculosis = louse infestation -strong host specificity -only survive 1-2d off host: life cycle entirely on host -transmission: direct contact |
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lice (life cycle)
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-adult life span: ~1mo
-eggs white & glued to hairs (nits) -eggs hatch & nymph emerges: smaller version of adult (no metamorphosis) -3 moults to adult -life cycle take 2-3wk |
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sucking lice
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-genera: haematopinus, linognathus, solenoptes
-large (up to 5mm) -small pointed heads -1 large claw per leg -piercing mouthparts: suck blood -pruritis & aneamia in heavy burdens |
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biting lice
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-genera: damalinia (farm), felicola (cat), trichodectes (dog)
-smaller -large rounded head -small claws -feed on skin surface/debris -intense prurits (not anaemia) |
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sucking lice (ID)
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1. haematopinus:
-all claws large -abdominal ridges prominent 2. linognathus: -1st claw small -abdominal ridges not prominent |
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sheep lice
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-bovicola ovis: chewing louse
-mild dermatitis & fleece derangment -heavy infestations are welfare problem & cause some production loss (not like sheep scab) -rare in UK |
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differential diagnosis of louse infestation & sheep scab
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1. severity:
-lice: chronic -psoroptes: acute 2. wool -lice: damage -psoroptes: loss 3. irritation: -lice: mild/moderate -psoroptes: severe 4. moratlity: -lice: no -psoroptes: common 5. scab: -lice: diffuse, scaly -psoroptes: definite crusty scab 6. point of origin -lice: not obvious -psoroptes: obvious |
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lice (epidemiology)
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-poorer body condition = more lice
-seasonal: highest in winter (fleece length) -husbandry |
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lice (treatment & control)
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-macrocyclic lactones: not effective
-pour ons: not 100% effective in longwool sheep -plunge dipping with OPs & synthetic pyrethroids: effective |
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cattle lice (species)
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1. biting lice:
-bovicoa (damalinia) bovis: top of head, back of shoulders & rump 2. sucking lice: -linognathus vituli & solenopotes capillatus: head, neck, rump -haematopinus eurystemus: poll, base of horns, ears, eyes, nostrils |
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cattle lice (clinical signs)
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-mild/moderate infestation common: clinically insignificant
-heavy infestation often sign of other problem (disese, neglect) -heavy: intense pruritis (esp. Bovicola), rubbing, hair loss, self inflicted trauma, hide damage, loss of condition -lice visible next to skin (eggs on hairs give powder appearance) -moderate infections can cause hide damage: financial loss to leather industry |
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cattle lice (epidemiology)
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-survive 1-2d off host
-transmission by direct bodily contact -housed animals or gatherins (eg. sale yards) -highest numbers in winter: coat thickest & skin coolest -numbers fall in summer: coat thinner, increase skin temp, direct sunlight |
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cattle lice (control)
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-parental ivermectic, doramectin: effective against sucking lice but only partially against biting lice
-most insecticides will work |
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lice (species in dogs & cats)
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1. dogs (head, neck, ears)
-lignognathus setosus: sucking -trichodectes canis: biting 2. cats (around ears) -felicola subrostratus: biting |
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lice (clinical signs in dogs & cats)
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-most heavy infestations in young animals
-often sign of neglect or underlying disease 1. dogs: -trichodectes is more harmful: v. active causing intense pruritis (self trauma, hair loss, "wet eczema") -heavy infections with linognathus: anaemia -very heavy combined infections: fatalities in pups 2. cats: -felicola: intense pruritis |
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pediculosis (louse treatment in dogs & cats)
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-treat all in contact
-clip out long haired breeds (esp. mats) -most insecticides effective: eg. selamectin against biting & sucking lice (not in animals <6wk) -3 treatments at 10d intervals kill new crops of hatched lice -thorough cleaning of bedding & grooming instruments |
