Week 10 Flashcards
Coccidia related vector borne agents
Agent, disease, IH, and DH
Life Cycle of Coccidia related vector borne agents
* iatrogenic- blood transfusions
* transovarial transmission in ticks for Babesia spp. only
* Sporozoite is infective phase–> injected into blood stream_-> merogony phase 1 & 2–> etc.
** Asexual phase is the pathogenic phase, remain in RBCs as macro and microgametes
Significance of Piroplasmosis
In Australia, what are the 3 main tick vectors that impact cattle and dogs?
Haemaphysalis (Bush tick), Rhipicephalus microplus (Cattle tick), Rhipicephalus sanguineus (Brown dog tick)
Distribution of Rhipicephalus microplus (cattle tick)
Global distribution of malignant theileriosis
Distribution of benign theileriosis- T. orientalis group
* compared to malignant forms it has mild pathogenecity (lucky for Australia!)- not always the case as it depends on immunity
Pathogenecity of coccidia vector borne?
* Haemolytic anaemia (hypoxia, organ damage)
- direct RBC destruction- merogony
- indirect- anti-RBC anti-bodies- splenomegaly
* Thrombocytopaenia
- splenic sequestration of platelets
- auto anti-platelet antibodies
- consumptive coagulopathy- DIC, shock
* Cytoadhesion of RBC to capillaries of brain
- cerebral babesiosis in Babesia bovis and Babesia caballi (horses)
What is unique about Theileria pathogenesis?
* Lymphadenopathy because body is trying to replace leukocytes
* Species and strain dependent on how pathogenic
* B. gibsoni would come between B. canis & B. vogeli
Immunity to piroplasms
* why in endemic areas you wouldn’t see Babesiosis- the main issue comes from naive animals exposed to ticks from introduction to a naive herd
Babesiosis in cattle
Canine babesiosis – name, vector, geography, and how pathogenic?
Babesiosis in dogs (Australasia)– what are the two genera? IHs? Clinical signs? Who?
Theileriosis in cattle- genera? What does it cause?
* cows in late pregnancy, early calving- cows are most susceptible to clinical forms
* might just see slight production loss, subclinical
Ante-mortem diagnosis of piroplasmosis
Has this dog always been in QLD?
* Cattle: Any new introductions to the herd? (especially in a tick free zone) OR have the cattle moved?
Post mortem diagnosis of B. bovis?
Impression smear of the brain due to massive numbers- capillaries of the brain are predilection site
Lymph node aspirate Schizont of T. annulata with merozoites in monocyte
Blood smear of cow infected with T. annulata
Babesia bigemina
Brain capillaries packed with infected erythrocytes parasitised by B. bovis
Normal capillary impression smear
Babesiosis
Differentials: Toxins (hepatotoxicity), Babesia bovis, Theileria orientalis complex, Babesia bigemini, Anaplasma (2 genera)
Live Samples: Whole blood- CBC, smear, stain, serology for exposure for Babesia, urine sample, rule out Theileria by FNA of lymph nodes, clotting times- blood that fails to clot
Dead samples: capillary impression smear of the brain, clotting times- blood that fails to clot
Findings: Regenerative anaemia - 0.14- 0.22- haemoglobinaemia
Found schizonts
How does Imidocarb dipropionate work? What does it treat?
Imidocarb dipropionate treats Babesiosis
* renders animal immune for 4 weeks- as it wears off slowly- ticks bite the animal and the animal gains exposure related immunity
Treatment of Theileriosis in Australia?
Controlling Tick Fever in Australia
Malaria (plasmodium) significance
Malaria (Plasmodium) Life Cycle
What species of Plasmodium has dormant forms? How does this impact host? What species is the malignant form?
* Immunosuppressed impacted by P. vivax if lay dormant
* P. falciparum- malignant, cerebral form
* black water- aka haemoglobinuria
Malaria (Plasmodium) Control
* Wolbachia Sterile male release- makes the females infertile
Haemosporidians in birds
* Malaria like
What phylum are Flagellates in?
For flagellates, what are cysts? Trophozoite? Promastoigote? Amastigote?
Life Cycle of Giardia
What is the most likely source?
* Ingest a cyst–> trophozoites come out–> divide by binary fission–> colon–> form cyst wall
** most likely source– person to person OR between kid and dog OR contaminated food and water
Significance of Giardiosis
Endemic * Adults- subclinical carriers– kids as well
Naive –> end up with full blown acute diarrhoea, if you’re not treated you become a subclinical carrier too
Species of Giardia
Only one we need to know
What are the two genotypes of G. duodenalis that infect humans?
Pathogenesis of Giardia
* literally physically preventing nutrients from entering the blood stream- “carpet”
Typical presentation of Giardia
Fatty, Floaty, Flatulence
Diagnosis of Giardia, Dog in the house?
Treat the dog- 3 days of febantel (drontal)
* fresh faeces- fresh faecal smear
* in house SNAP test
* research purposes always use PCR- because most sensitive
Treatment and control of Giardia
Trichomonads Features
* Simple direct life cycle– faecal oral (close contact, wet environment), venereal transmission (not very enviornmentally resistant)
* no cysts- just live in trophozoite form
* 3-6 Flagella– one of which forms an undulating membrane
* Single nucleus
Trichomoniosis– in humans, cattle, cats, and pigeons, doves, fowl and other birds
Feline intestinal trichomoniosis
Relatively new pathogen of cats
* Agent- Tritrichomonas foetus
Typically:
* Large bowel diarrhoea (mucoid, tenesmus)
* Waxes and wanes
* Chronic diarrhoea (weeks) cats up to 2 years of age
* Cattery outbreaks
* Asymptomatic shedding common
Diagnosis and treatment of feline tritrichomoniosis
What’s the difference between giardia and tritrichomoniosis in faecal smear?
** in faeces: Giardia– looks like a falling leaf motion VS. Tritichomoniosis- goes in a straight line
Bovine tritrichomoniosis
* Agent: Tritrichomonas foetus
* Venereal disease- STD- mating/ coitus +/- iatrogenic
* Infertility and early embryonic death
* costs to endemic herd- culling, replacement herd, vet fees
* endemic in the NT extensive cattle farming- uncontrolled mating
Tritrichomoniosis Presentation in a bull
Tritrichomoniosis Presentation in a cow
Tritrichomoniosis presentation in a herd
Diagnosis in Trichomoniosis
Control of tritrichomoniosis in bulls
* you don’t treat bulls, you cull!
* with replacement heifers, they take a few months to get over infection 3-4 months– retain cows if they continue to test negative- if they continue to test positive– cull them too
* notifiable!!
** vaccine only increases fertility, does not cure
Avian Trichomoniosis- signficance
Avian Trichomoniosis Transmission, who is normally affected?
** direct route- not faecal oral, mother to baby
Avian Trichomoniasis- Presentation
Diagnosis, Treatment and control of Avian Trichomoniosis
Histomoniosis significance in birds– what does it cause? Who? morbidity and mortality?
Life cycle of Blackhead (Histomonas meleagridis+ co infection with E. coli)
* Blackhead Stored in cecal worm egg–> earthworm eats eggs–> chickens eat earthworms–> flagellated trophozoites get in they quickly invade cecal muscosa, lose tail, become amastigote forms–> some enter circulation enter liver or other organs–> bird can become a carrier or get sick and die
** Cloacal drinking is another means of transmission: birds sitting in wet litter sucking it up
Presenation of Histomoniosis in a bird
Diagnosis of Histomoniosis
Control of Histomoniosis diagnosis
