Protozoa Flashcards

A. true coccidia
- cystiospora
- cryptosporidium
- toxoplasmosis
B. piroplasms
- babesia
- thelieria
C. Haemosporidia
- plasmodium
- haemoproteus
D. Ciliates
E. Flagellates/ Hemoflagellates
F. Amoeba
what mechanisms do apicomplexa use to move around?
- flagella - whip like
- pseudopodia - temporary extensions (false feet)
- cilia - hair-like extensions of cell membrane
- undulating - tiny undulating waves gliding motion
What is the infective form of an apicomplexa?
‘zoite” w/ apical complex (microtubules allow movement & rhoptries secreted)
What is the function of the apical complex (apicomplexa)?
- cytoskeltal & secretory funx
- central to cell penetration & invasion
-
parasitophorus vacuole
- communicates w host cell through secretions
- look for the halo
Apicomplexan life cycle?
unsporulated oocyst in environment in poo from DH - non infective
- sporogony - over 3-4d (asexual mitotic)
Sporulated oocyst w sporocysts & sporozoites
- ingestion of sporozoites
Pentrate intestinal epithelium > asexual = merogony (multigeneration)
- merozoites w/parasitophorus vacuole = meront/schizont
- burst release merozoites into lumen & invade next cell
- exponential amplification
- merogony # determines pathogenicity > # gametes
-
gametogony = union of gamets
- macrogamete = female
- microgamete = male
- zygote > fertilzation intracellularly then excreted into lumen and pass in feces as an unsporulated oocyst
What is merogony starting stage > process > product?
Start
- zoite
Process
- asexual replication of merozoites -intracell
Product
- gamont/gamete
What is gametogony starting stage > process > product?
Starting
- gamete
Process
- macro& microgametes fuse to produce zygote - intracell
Product
- unsporulated oocyst
What is sporogony starting stage > process > product?
Start
- unsporulated oocyst
Process
- sporulation of the oocyst external environement or w/in the host lumen to the “infective unit” - extracell
Product
- sporulated oocyst (contain sporozoites)
What is the sporulated OOCYST morphology

A. Eimeria
B. (cyst)isopora
C. Sarcocystis
D. Cryptoporidium
What are examples of coccidia & what is the nature of their LC?
Direct LC & rapid
- eimeria - birds, ruminants, lagomorphs
- cystisospora - carnivores, omnivores, birds
- cryptosporidium - broad range
What are examples of cyst - forming coccidia & what is the nature of their LC?
Indirect LC - slow
- toxoplasma
- IH tissues- mammals (sheep, humans, cats) birds
- DH - intestine - felids
- neospora
- IH tissues - cattle, dog
- DH intestine - canids
- sarcocystis
- IH tissues- herb, omn
- DH intestine - carnivore
What are some examples of vector borne apicomplexa
mosquito
- plasmodium (malaria)
ticks
- piroplasms
- babesia
- theileria
Are emeria & cystisospora zoonotic?
no
the definitive host develops species specific immunity w. exposure or scours +/- dxa (mostly weaners- immunity, dose & virulence) - what eucoccidia is this and what are important husbandry risk factors?
Eimeria & Cystisospora
- overcrowding, stress, climate, poor hygiene, poor nutrition
Eimeria - DH? economic significance? clin signs?
DH
- birds, ruminants, lagomorphs
- HIGHLY host specific & site specific
Significance
- 90% subclin
- production loss, reduced growth rate
- increase in susceptibility to secondary infections - colibacilosis
Pathogenic -symptomatic
- watery hemorrhagic dxa, mortality
Eimeria LC
- direct- rapid
- PPP= 3-21d
- sporulation 1-3d (21-30* C humid optimal)
- vary in virulence
What are the main predisposing factors of coccidiosis in livestock?
Host
- susceptibility/age
- stress -weaning, change diet, shipping, crowding
- immune status
- exposure
Parasite
- number
- type
- dispersion
Environment
- conditions for sporulation (T, O2, humidity)
- mgmt
- hygiene
- feed & drinking hygiene
- climate
What are the 3 main anti-coccidial agents
Ionophore Antibiotics
- cell membranes (Na2 influx)
- static - extracellular stages only
- monensin
- chicken, cattle, sheep, goats, turkyes
- lasalocid
- sheep cattle & off label cats/dogs
- salinomycin - chickens
Toltrazuril
- affect plastid-like organelles
- cidal (all stages)
- long acting - single prophylaxis & multi trx
- long WHP for meat
- poultry, dogs, cattle, sheep, pigs
Sulfonamides
- cidal
- interfere w folate & DNA production
- birds, dogs, cats, pigs
Why would you use a coccidiostatic drug?
dont want to clear too quickly otherwise reduce future immunity
Can you treat layers with eimeria?
no bc of WHP - problem in non caged layers
What are the 4 main causes of coccidiosis in poutry?
- E. tenella (most path)
- E. necatrix
- E. maxima
- E. acervulina
What are the main symptoms and predilection sites of E. tenella, E. necatrix, E. maxima & E. acervulina
E. tenella (most path)
- ceca - bloody droppings & high mortality
E. necatrix
- upper SI - dropped weight & egg production
E. maxima
- lower SI - dxa
E. acervulina
- upper SI - drop in egg, chronic, +/- dxa
How can you diagnose coccidiosis due to Eimeria?
Post mortem
- gross observation -predilection & path
- sample
- mucosal smears/scraping + fixed gut sections for histo
- schizonts w merozoites
- gametes
- mucosal smears/scraping + fixed gut sections for histo
Ante mortem
- fecal float
- unsporulated oocyst
Feed Sample- check dosage of coccidiostats
How do you control coccidiosis in poultry?
Vaccine
- live & live attenuated vaccine (put into eye > nasolacrimal duct > swallowed)
- sporulated oocysts, species specific immunity, inoculate chick or hatchery
Hygiene
- resistant oocysts
- ammonia based disinfectant (bleach helps sporulation!)
- quaranitine
- on farm biosecurity
- too clean– immunity?
What causes hepatic coccidiosis in rabbits - merogony in bile duct epithelium >> jaundice & dxa w. mortality in weanlings? What are the necropsy findings?
Eimeria stiedai - focal white yellow nodules or cords in liver along bile ducts (cholangitis)
How does coccidiosis present in cattle? What are the species involved?
E. zuernii & E. bovis
- 1-2 mo <1 yr
- calf dxa/bloody scours
- 2* colibacillosis
- subclin - production loss
What can predispose calves to coccidiosis?
overcrowding, weaning to pasture/feedlots, stress/ low immunity
How can you prevent coccidiosis in calves?
- coccidiostats in milk replacer, feed (monensin, lasalocid) or single drench (toltazuril) before weaning
how does coccidiosis present in lambs? what are the species involved?
E. crandallis & E. ovinoidalis
- lambs 1-5 mo
What are the risk factors of coccidiosis in lambs? Prevention?
Risk
- lambing pens (ewe can infect neonate), weaning, introduction to feedlots
Prevent
- coccidiostats in feed
- late gestation in ewe (21d prior to lambing)
- prior to weaning lambs

E. ovinoidalis - small intestinal polyps & large intesinal mucosa w. meronts
How can you diagnose coccidiosis in sheep?
- necropsy
- incubate feces (3d)
- sporulation in 2% potassium dichromate soln
- mcmaster for oocyst counts & ID
Case study: You are called to a free-range poultry facility –Clinically approximately 35% of chickens have bloody faeces, ruffled feathers and pale mucous membranes History? Differentials? Diagnostic samples? Tests? Treatment? Prevention?
NEXT: perform necropsy- note distribution of lesion
- (if a pet then do a fecal float and check for eimeria oocysts)
Check feces regardless
- if you DO NOT find oocysts on fecal float —> you cannot rule out acute coccidiosis (no oocysts bc gametogony hasn’t occurred- only merogony)
Primary differential: eimeria tenella (Cecum) : not zoonotic but can get salmonella and campylobacter 2*
Confirm diagnosis : submit fixed intestinal sections for hstopath and non affected gut and perform fresh mucosal scrapings for cytology (may find zoites)
What is the life cyce of isospora (cystisospora)
unsporulated oocyst passed in feces >> sporulation 3-4d
- 2 sporocysts each w. 4 sporozoites
PH ingestion (rodent/livestock)
- tachyzoites (quick replication = inflam) >> bradyzoites (slow asexual rep = min inflam) in tissue (extra epithelial cells - brain, lung, muscle)
DH ingest PH or sporulated oocyst (dog, cat, pig, human) -FO
- intestinal epithelial cells
- asexual - merogony
- sexual - gametogony
PPP= 4-11d
What are the risk factors associated w cystisospora? immunity? Diagnosis?

Risk
- overcrowding
- dogs - breeders feed raw beef/lamb
- other risks - campy & slamonella
strong acquired immunity +/- dxa (not bloody)
diagnosis - oocyst 1:2:4
- rare to find in older dogs
- if you have bloody dxa look for other causes
- dont need to sporulate/ just treat
What are the species of cystisospora associated w. dog, cat, & pig?
dog
- C. canis
- C. ohioensis complex
cat
- C. felis
- C. rivolta
pig
- C. suis
How would you treat cystisospora in domestic animals? Prevention?
Treat
- supportive care
- sulphonamides for 1-2 wks
- toltazuril for 1-3d
Prevent
- mass treat all animals (bitch & queen incl)
- also bathe bitch before whelping & during lactation
- clean environment w/ ammonium based compounds
- prevent predation / feeding of raw meat
Case study: 10 day old confinement reared piglets suddenly developed scours and appear to have lost body condition, some vomiting milk…diagnostics below (stunted vili & nothing in fecal float) necropsy ok >> diagnosis? Control?

Coccidiosis
Control
- hygiene, biosecurity, all in all out system
- medicate sow feed w anticoccidial drugs (static?)
- piglets
- single dose = toltazuril (baycox) @ 3-5d
- long acting = sulphonamide inj @ 6do
What is the common host of the zoonotic cryptosporidium? What is the common zoonotic spp?
cattle - Cryptosporidium parvum
How would you describe the positioning of cryptoporidium? What types of tissue can you find it?

- epicellular position - intracellular but extracytoplasmic
- gastric or intestinal
- respiratory epithelium in poultry
What is the lifecycle of Cryptosporidium?
Direct - fecal oral route
- sporogony w/in host
- infective immediately
- hard to control in environment
- thick walled oocysts passed in feces
-
thin walled oocysts - autoinfection
- esp if immunocompromised
What is the pathogenesis of cypto infection
villous atrophy
- parasite destruction
- t cell apoptosis
epithelial mucosa release cytokines
- increased H20 & chloride
watery dxa & malabsorption
What is the significance of crypto infections?
- neonatal/post weaning dxa
- livestock, foals, pigs, pups, kittens
- poor colostrum intake
- immunocompromised
- zoonosis
- C.parvum - calves
- direct & waterborne - incl healthy humans
- C. hominus - human to human
- C. meleagridis, C. canis & C. felis
- direct
- young children or immunocompromised
- no cure!!
- C.parvum - calves
Apart from being zoonotic, what is the public health significance of cryptosporidiosis?
- major water born pathogen
-
oocysts resistant in chlorine (C. hominus most likely)
- sinking -
- spreader +
-
oocysts resistant in chlorine (C. hominus most likely)
- self limiting dxa (2-4 w in healthy)
- chronic life threatening dxa in HIV/AIDS
How does crypto present in calves?
- calves <4 wks have C. parvum
- high intensity of oocysts excretion
- Low infectious dose (5-10 oocysts)
How do you diagnose crypto?
- zinc or sucrose floats (SG 1.12- 1.18)
- oocysts small
- immunoflourescence - oocyst wall protein
- Zn smear, acid fast
- ELISA or immunochromatography
- PCR
how do you treat crypto?
no curative treatment
supportive care > fluids & electrolytes
hyper-immune bovine colostrum (cattle infected w. crypto)
halofuginone - reduce oocyst output
nitazoxanide (anti-protozoal) & paromomycin/azithromycin > humans
How do you control crypto infections?
- hygiene (heat . 70* C - steam, dry, ammonia)
- doesnt survive long in dry clean environment
- biosecurity/quarantine
- adequate colostrum
Toxoplasma gondii - LC in cats
DH - feline - intestinal merogony & gametogony (sexual development and oocyte formation)
- ingestion of sporulated oocysts in fresh or undercooked meat w/ viable zoites or transplacentally
- primary infection = naive kittens oocyst excretion (20 mill over 10-21d)
- long lived immunity
- oocysts not found on coat likely due to fecal burying & grooming behaviour
DH - feline extraintestinal
- zoites mulitply w.in tissue tachyzoites & bradyzoites in tissue of cat
Toxoplasma gondii - LC
DH : feline > excreted in feces > oocysts sporulated over 2-4d
PH : sheep, chickens, humans, rodents > ingest sporulated oocysts or infected meat or gardening
- zoites multiply in issue tachyzoites & bradyzoites in tissue
how is toxoplasma transmitted?
oral
- ingestion of oocysts
- resistant up to 18 mo - cool/ wet
- ingestion of tissue cysts
- raw, undercooked meat, unpasturised milk
vertical
- to kittens
- humans- only if infected for first time during pregnancy
When are cats immune to toxoplasma? When is there a high shed?
- intestinal phase
- kittens shed millions for 10-21d
- adult cats rarely shed - lower burdens
- long lasting immunity by premunition in all hosts
- due to extra-intestinal stages (tissue cysts)
- bradyzoites slowly replicate, may burst and get rise in Ab
- except immunocompromised (HIVAIDS, FIP, FeLV, FCoV)
- due to extra-intestinal stages (tissue cysts)
What is the pathogenesis of toxoplasma infeciton in the tissue stages?
- acute infection in naive host - primary exposure
- reactivate latent infection - immunocompromised
- tachyzoites multiply destroying tissue - multisystemic signs
What is the significance of a toxoplasma infection?
- abortion in ewes - economic
- abortion & congenital deformities in humans
- primary infection during gestation
- multisystemic disease in warm blooded mammals
- cats, marsupials, dogs, humans
What is the presentation of toxoplasmosis in cats?
intestinal - mild self limiting dxa (v young kitten)
extra intestinal
-
systemic disease- increased liver enzymes = jaundice
- CNS signs, hepatic necrosis, uveitis, interstitial pneumonia
- immunocompromised - kitten or underlying FIV, FeLV, FIP
- corticosteroirds, cyclosporin trx
- similar presentation in dogs
What is the public health significance of toxoplasmosis?
- majority asymptomatic - mild flu (bradyzoites in tissues)
- acute outbreak (high infectious dose)
- chorioretinitis - waterborne outbreak
- peeps camping drinking lake water - cougar poo
- chorioretinitis - waterborne outbreak
- HIV-AIDS/organ transplant patients
- 10-30% fatality from latent (90%) or newly acquired infection
- encephalitis, pneumonia, ocular dz
How does toxoplasma pose a risk to preg women?
- life long immunity once exposed
- protects against vert transplacental transmission
- unless immunocompromised
- clindamycin can prevent vert trans
- if infection first contracted during pregnancy - infection may be vertically transmitted to fetus
What is the likelihood of transmitting toxoplasma to fetus during 1st trimester? What is the out come? third trimester?
1st
- low 5-10%
- severe outcome - abort, neuro abnormalities (hydrocephalus)
3rd
- high 70-80%
- milk outcome - asymptomatic (95%), chorioretinitis
how can you diagnose toxoplasma infections?
-eggs are 10um rare to find in cat fecal float
T. gondii Ab titers (IgM or paired IgG)
detect tachyzoites
- cytology or PCR > CSF, aqueous humor, amniotic, peritoneal or pleural fluid
post mortem -histopath (tachyzoite will have inflam & necrosis)
CBC & Biochem
- change consistent w organ specific dz (hepatitis - incr liver enz)
Xray/ US
What drugs suppress tachyzoite replication (toxoplasma)
- Pyrimethamine
- Clindamycin
- Sulfonamides
- Azithromycin
- clin improvement in 24-48 h (unless organ necrosis)
how can you prevent toxoplasma infection?
- cook meat thoroughly
- wash/cook raw foods thoroughly
- cat
- dont allow to hunt (keep indoors)
- dont feed raw meat
- clean litter tray DAILY wearing gloves
- hygiene
- wash hands
- avoid gardening
- oocysts can survive for 1.5 yr in soil
- toxovax in maiden ewes - 6 wks prior to mating
- life long protection
- increases lambing %
What is the life cycle of neospora caninum
DH - dog
- intestinal: eating raw meat
- extraintestinal - tachy/bradyzoites in tissue
- placental transmission (breeders shouldnt feed raw meat)
- excretion - rare to find oocysts in poo
IH/PH - tachy/bradyzoites in tissue - cattle, sheep, poutry, rodents
- oocyts on pasture ingested
- abortion in cattle or calf born normally and continually passes oocytes
What is the significance of Neospora caninum infection in Cattle vs Dogs?
Cattle
- abortions - 5-7m
- congenitally abnormal calf
- asymptomatic carrier calf = persistently infected cattle
- may need replacement heifers
Dogs
- paralysis in pups - polyradiculoneuritis
- LMN proprioceptic deficits
- arthrogryposis - dorsal root nerves inflamed
- multisystemic in older immunocompromised in dogs
- can present like toxoplasmosis
- NOT zoonotic
What is the best course of action for congenital neosporosis?
- stop breeding - ovariohysterectomy
- test other pups in litter - treat if not showing clinical signs (progessive LMN once showing clin signs - decreased proprioception - rubs on tops of paws)
- could treat but if no improvement in 2-3d then euthanasia
How can you diagnose and treat neospora infections?
- Ab Titer
- fecal float unrewarding
- treat
- Clindamycin, pyrimethamine,
sulphonamides or combinations
- Clindamycin, pyrimethamine,
- prognosis
- early case: good
- mm contracture of hind limb - poor
Compare Toxoplasma gondii & Neospora caninum
What is the sarcocystis LC?
- MANY host specific species
- DH = canids, felids, humans
- gametogony & sporogony
- IH = herb, omn
- merogony - tissue cysts
- HIGHLY host specific
>> human eats undercooked meat containing mature sarcocysts > SI gamete> unsporulated oocyst> sporulated oocyst > sporocyst passed in feces > ingested by pig or cow > mature sarcocyst in mm
Significance of sarcocystis infection (cattle, acute infection, etc)
condemnation of carcases - sheep & cattle
- microscopic & macroscopic (granuloma)
Acute infection - merogony in vascular endothelial cells > vasculitis
- abortion & still birth in cattle
- (neospora & sarcocystis - abortion in cattle)
- (toxoplasma - abortion in sheep)
- multisystemic dz
- equine protozoal myeloencephalitis
What would infected DH fecal sample contain? What diagnostics do you perform? What are some differentials?

-naked sporocysts in feces = Sarcocystis
Diagnostics - histopath, PCR tissue
DDX
- hydatid
- taenia saginata
- calcified sarcocystis
What are some examples of coccidia-related vector borne agents? What type of life style do they have?
indirect LC
- babesia
- theileria
- plasmodium
What are the main LC differences bw babesia/theileria and plasmodium?
B/T
- IH= mammals
- DH= ticks
P
- IH= vertebrates (humans, birds)
- DH= mosquitoes
What is the piroplasm general LC?
Tick (DH) bites mammalian host (IH) > introduction of sporozoites > merogony phase 1 - ring form
- babesia - rbc
- theileria - lymphocytes
- plasmodium - hepatocytes
Merogony phase 2 - merozoite > gamete
- all rbc
tick takes a blood meal and ingests gametes > gametogony in tick gut > ookinete enters salivary gland > sporogony > sporozoite
apart from being bitten by a tick, what are other ways piroplasms can be intoduced to mammals?
- iatrogenicaly - bood transfusions
- transovarial transmission in ticks for babesia spp only
what is the significance of piroplasmosis?
- hemolytic anemia
- cattle, dogs, horses & other wild & domestic animals
- significant economic cost to cattle industry
- impact on small farms (asia & africa)
- production loss & abortion
- mortalities
- zoonosis (invade habitats & climate change)
What ticks cause piroplasmosis in australia?
- haemaphysalis longicornis
- Rhipicephalus australis
- R. sanguineous
Where is tick fever most common? what are the agents of tick fever?
babesia bovis, B bigemina & anaplasma spp
- warm humid tropical and subtropical conditions (central & south america, SE asia and N. aus)
What is the vector for tropical theileriosis (in asia) (malignant theriosis)
Hyalomma spp ticks
What is the vector for east coast fever (africa) (malignant theriosis)
R. appendiculatus
What is the distribution of benign theriosis - T. orientalis?
- humid coastal areas, sub tropical/ temperate conditions (haemaphysalis longicornis SE QLD & NSW) - also in parts of europe, RU, asia, NZ, pacific islands & hawaii
What is the mechanism of hemolytic anemia in piroplasmosis?
- hypoxia, organ damge
- direct RBC destruction - merogony
- indrect anti RBC antibodies - splenomegally
What is the mechanism of thrombocytopenia in piroplasmosis?
- splenic sequestration of platelets
- auto antiplatelet antibodies
- consumptive coagulopathy - DIC, shock
- increased bleeding w petechiation
What is the consequence of cytoadhesion of RBC to capillaries in the brain in piroplasmosis?
cerebral babesiosis in Babesia bovis & babesia caballi (horse)
- RBC surface is sticky and stick to endothelium of the brain
Where is Theileria during merogony phase 1? What is the pathogenicity?
Leukocytes - thmphadenopathy, lympgoid depletion and leukopenia
What is the most pathogenic babesia spp of cattle
B. bovis
What is the most pathogenic babesia spp of dogs
B. rossi > B. canis > B. gibsoni > B. vogeli
What is the most pathogenic species of theileria
T. parva > T. annulata > T. orientalis complex
Regarding immunity to piroplasmosis- what is enzootic stability vs enzootic instability?
- Maternal ab transfer = temp immunity (pups & calves) to babesiosis
- bos indicus more resisitant (same with indigenous wild dogs)
- Enzootic stability - no clinical dz in herd
- continous presence of piroplasmosis in both animals and ticks
- Enzootic instability - clin dz may be apparent
- not all animals are exposed while young - eg tick control, drought (when it rains the ticks come out)
- intro naive animal to herd
- cows in calf, stressed cattle
What are sublinical & acute signs of babesiosis in cattle
Subclinical
- weight loss, decreased milk production
- poor calving rates, loss of bull fertility
Acute
- fever
- abortion
- ill thrift
- pale mm, jaundice
- hemoglobinuria
- agression/neuro - usually B. bovis
- coagulopathy
- death
What are the 2 spp of babesia in AU that can infect dogs- what are their vectors and how pathogenic are they?
babesia vogeli - mild path - Rhipicephalus sanguineous
Babesia gibsoni - mod path - Haemaphysalis longicornis
What babesia spp are able to be transmitted directly from dog to dog via fighting or vertical transmission?
B. gibsoni & B. vulpes (eu & usa)
What are the 4 routes of transmission of canine babesia
- direct
- transplacental (vertical)
- blood transfusion
- tick bite
primary differentials?

- polychromasia (reticulocytes - indicative of regeneration), ansiocytosis
- regenerative anemia after hemolytic anemia?
- echinocytes, spherocytes > spleen eats up bc ab on RBC
- splenomegally?
- TEST of vector borne dz before immunosupression
- endemic tick area? history of tick prevention?
- if serious - hemoglobinuria & jaundice
- thrombocytopenia could be subclin > corticosteroids could kill
- splenectomy - could die from babesia
3 mo pup from the tropics (QLD) - found a brown dog tick (R. sanguineous) under the collar & the dog is pyrexic, icteric & has a large spleen & hemoglobinuria..what is the most likely diagnosis? How can this be complicated iatrogenically?
Babesia vogeli - can be confused with immune mediated hemolytic anemia (steroid use) & can be a problem in splenectomised dogs
What canine babesia species is transmitted by dog fighting, vertically and Haemaphysalis longicornis ticks - what kinds of dogs is this most common in?
B. gibsoni - adults (esp pitbull terriers or dogs w history of fighting/agression) and pups
What are the different (4) presentations of theileriosis in cattle?
- asymptomatic - enzootic stability
- sublicincal - production loss
- hemolytic anemia (except T. parva)
- severe pyrexia, lymphadenopathy, lymphoid depletion > death
- T. parva (severe) & T. annulata
- LN aspirate to diagnose
when is theileriosis mostly seen in cattle?
late preg, calving & early lactation
How can you diagnose piroplasmosis ante-mortem?
- history & clin signs
- stained capillary smears - ticks feed & form aggragate
- stained LN (theileria) aspirate
- EDTA blood - CBC/ PCR detection
- serum biochem
- PCR on whole blood
How can you diagnose piroplasmosis post-mortem?
- brain (grey matter) capillary impression smear - B. bovis
- histopath - LN, brain, kidneys, liver, spleen
blood smear cattle

T. annulata
LN aspirate

T. annulata
L vs R - what is the level of parastiemia

L - Babesia bigemina
- high parasitemia - 10-30%
- parasite pair forms an acute angle
R- Babesia bovis
- low parasitemia - < 1 %
- parasite pair forms obtuse angle
What is the most likely diagnosis

babesiosis (b. bovis - distension of capillaries of brain)
What supportive care and anti-protozoal agents can be given to treat babesiosis?
Supportive care - blood transfusion, iron, vit B12
Antiprotozoals
-
Imidocarb dipropionate (drug of choice)
- SQ/IM
- off label for dogs
- sterilization of infected animals moving to non endemic areas
- meat & milk WHP
How can you treat B. gibsoni in dogs?
- challenging - relapses common
- macrolid ab + antiprotozoal (off label)
- atovaquone (anti malarial) & azithromycin
What are the effective drugs used to treeat theileriosis?
- Buparvaquone (drug of choice)
- primaquine
- currently not registered in aus
IN AUS - imidocarb dipropionate (not great efficacy - tick control and quarantine best)
What is the best treatment & control of piraplasmosis in cattle?
Annual Vaccination w/ trivalent tick fever vax (anaplasma, B. bovis & B. bigemina)
- most effective - calves 3-9 mo
- vax all introduced cattle 4 wks prior to moving to endemic area
Tick control
- acaricide resistance & reducing endemic stability –> VAX
Risk assessment
- avoid transport across endemic/ non-endemic zones
- NO VAX for theileriosis
what is the significance of malaria (plasmodium)? What is the vector & distribution?
- tropics & subtropics > anopheles mosquito (not in AUS but vector present in north - endemic in PNG & SE asia)
- most significant parasite in humans (> 1 mil deaths per yr)
- affects birds, primates, reptiles & rodents
What is the avian hemoprotozoa? Where does merogony occur? where are the gametes? Vectors?

Haemoproteus spp
Merogony - tissue
Gametes - RBC - highly endemic in wild birds
Rare mortality
Vector - Hippoboscids & culicoides midges
What are the clinical signs? What vectors?

- Leucocytozoon
- Anemia, emaciation, death, multifocal signs (block of capillaries of lungs, brain, kidney)
- young newly hatched or newly introduced birds most suceptible
Vectors - black flies (simulium) & midges (culicoides)
What are the clinical signs? Vectors?

Plasmodium spp
Anemia, emaciation, death, multifocal signs (block of capillaries of lungs, brain, kidney)
Vectors - Culex, aedes mosquitoes
Case study : Presented with a 11 week old pup that was purchased from a breeder on Gumtree a month ago. The dog saw you for its 8 week vaccinations and deworming. Pup is lethargic, pale, has enlarged lymph nodes and is pyretic. CBC findings reveal moderate regenerative anemia and mild thrombocytopenia. ID the organism in the blood smear. What is the most likely source? How do you treat?

Babesia vogeli - from brown dog tick (R. sanguineous) - treat w. imidocarb dipropionate inj now & 2 wks (off label)
Define flagellate terms: Cyst, Trophozoite, Promastigote, Amastigote
Cyst: resistant to unfavorable environmental conditions outside host
Trophozoite: active, feeding, motile stage
Promastigote: single anterior flagellum
Amastigote: non-flagellated intracellular stage
What is the life cycle of Giardia?
- flagellated protozoan of SI
- infects wide range of mammals & birds & reptiles
- cyst transmitted by fecal oral route
- direct or contaminated food/water
- trophozoites divide by binary fission (asexual)
What is the significance of Giardiosis?
- neglected tropical dz (WHO)
- chronic subclinical infection in developing regions
- stunted growth
- reduced cognitive development
- chronic subclinical infection in developing regions
- Dxa - humans & animals
- mostly young (immunity follows - chronic carriers)
- kennels
- day care centers
- farms - calves (prod loss)
- waterborne outbreak (zoonosis)
What is the species of giardia that infects a wide range of hosts? humans, cats, dogs, cattle, horses, etc
G. duodenalis
What 3 giardia spp infect dogs?
G. duodenalis, G enterica, G. canis
What giardia spp infect cats
G. duodenalis, G. enterica, G. cati
What giardia spp infect cattle
G. duodenalis, G. bovis
Is giardia zoonotic?
Yes - only G. duodenalis & G. enterica (even if immunocomp wont see infection w/ G. canis - crypto has a wider infective range)
What is the pathogenesis of giardia?
-
Extracellular
- attach via ventral adhesive or sucking disc to small intestinal mucosa
- villous atrophy & malabsorption > fatty floating dxa malodorous
- most subclinical infections
- strong exposure related immunity but not absolute
- older humans/animals > asympt shedding
What is the typical presentation of giardiosis? Where is it most common in AUS?
- watery or steatorrheic dxa
- flatulance
- vomitting
- young animal or traveller
- chronic malabsorption
- asymptomatic shedding (majority - not treated)
in aus- most common in pet dogs & children day care centers
motile binucleated trophozoites in fresh fecal smear from a severly diarrheic animal.. diagnosis? what solution do you use to visualize cysts? What other diagnostics?

Giardia spp
visualize cysts: zinc sulfate (SG 1.2) w. floatation soln of choice
other diagnostics > coproantigen test, qPCR
(DXA panel = giardia, crypto, tritrichomonas in cats)
When are you most likely going to see giardia trophozoites in a fecal smear?
w/ severe watery dxa bc transit time so fash there isnt enough time to estabilsh cyst (falling leaf motion in floatation)
Why is drontal (for 3 d) used to treat giardiosis?
- drontal = febantal, pyrantal, praziquantel
- febantal is metabolised to high concentrations of fenbendazole in the serum and slowly released
How do you control/ prevent giardiosis?
hygiene, reduce over crowding & stress - change bedding, pick up dog poo, wash dog, kids wash hands
What drugs can you use off label to treat giardiosis?
fenbendazole for 5 d
metronidazole for 5-7d
What are the main features of the trichomonads LC
- Simple direct LC
- FO - close contact, wet environment - & venereal
- NO cysts - trophozoites only
What are the morphological features of trichomonads?
- 3-6 flagella anterior (one forms an undulating membrane)
SINGLE nucleus (giardia has 2)
Trichomonad of humans - type of disease caused
Trichomonas vaginalis - veneral
Trichomonad of cattle - type of disease caused
Tritrichomonas foetus - venereal
Trichomonad of cats - type of dz caused
Tritrichomonas blagburni - intestinal colitis
Trichomonad of pigeons and other birds - type of dz caused
Trichomonas gallinae- upper digestive tract - invasive/systemic forms
What are the clinical features of Feline intestinal trichomoniosis? What is the agent? What are differential diagnoses?
Tritrichomonas blagburni = agent
Presentation
- lg bowel dxa
- wax & wane - straining w. mucoid dxa (tenesmus)
- chronic dxa (wks) in cats up to 2 yr
- cattery outbreaks
- asympt shedding common
DDX
- urinary bladder obstruction?
How do you diagnose feline tritrichomoniosis
-
fresh fecal smear for motile (forward motion) trophozoites
- cat will be pooing frequently so rectum likely empty
- saline enema
- fecal culture (In-pouch TF) - 12d
- qPCR
How do you treat feline tritrichomoniosis
-
off label ronidazole 30 mg/ kg once daily for 14d + probiotic
- registered in birds
- variable sucess - relapse common
- caution = neurotoxicity
What is the signficance of Tritrichomonas foetus infection? How is it transmitted and what is the host?
Cattle - venereal dz (mating or iatrogenic - test before mating & CULL ++)
impact
- cost to endemic herd
- culing, replacement herd, vet fees
- endemic in NT - extensive farming = uncontrolled mating
How does Bovine tritrichomoniosis present in cows? Immunity? Why is it endemic in NT?
- self limiting infection - cows become clear a few mo of sexual rest > COW SUSCEPTIBLE TO REINFECTION (poor immunity)
- mild vaginitis +/- discharge, metritis, salpingitis
-
embryonic death & absorption
- return to service
- aborted/retained fetus @ 2-4 mo
- not checking cattle as frequenly in NT - v free range
How does Bovine tritrichomoniosis present in bulls?
asymptomatic - live in crypts of penis and prepuce (crypts get bigger as they get older - increase risk)
*perm carriers
How can you diagnose bovine tritrichomoniosis?
- bull sheath wash
- 1x week > 3 sucessive negs at lease 2 wks after last service
- allow buildup of organisms = better Se
- 1x week > 3 sucessive negs at lease 2 wks after last service
- cow cervical wash following abortion
- direct microscopy
- culture (in -pouch)
- qPCR
there is no effective, approved treatment or vaccine in AU for Bovine tritrichomoniosis - how do you control?
- notifiable dz - test & cull bulls
- rest positive cows
- replacement w/ virgin heifers & bulls
- pre-entry test bulls
- AI
- good fencing
- Vax (NOT IN AU) - trichGuard only reduces severity
What are ddx for abortion in cattle
- BVD
- Trichomonas
- Sarcocystis
- Neospora
- Babesia bovis & Theileria = pyrexia & anemia
What is the significance of Avian trichomoniosis? What birds are affected?
- “CANKER” in pigeons “FROUNCE” in falcons
- Trichomonas gallinae
- upper digestive tract
- nasal cavity
- Affects pigeons, budgerigars,backyard poultry and raptorial birds
How is Avian trichomoniosis transmitted?
- ingestion
- infected parent feeding young “pigeon milk”
- contaminated drinking water - esp shared domestic/wild water sources
- pigeons asymptomatic
- prey for another bird (raptorsmost common)
- young immunocomp birds
- PBFD - circovirus
- poor hygiene, overcrowding, stress
What is the typical presentation of Avian Trichomoniasis (clin signs and lesions)? What does SQUABS mean?
SQUABS = symptomatic = usually youngest
- stop feeding, lose weight, rufflyed and dull, dysponea, difficulty swallowing
-
circumscibed caseous plaques
- oropharynx, esophagus, crop, proventriculus
- ulceration, abscessation
- oropharynx, esophagus, crop, proventriculus
- localised & systemic (invasive)
How can you diagnose Avian Trichomoniasis?
scrape/crop flush >> microscopy, PCR or culture (In Pouch TF)
What are the best treatment and control methods for Avian Trichomoniasis?
- quarantine - test new comers & cross react w. qPCR (tritrichomonas in cats)
- sx removal of caseous plaques
- ronidazole, metronidazole (doesnt completely get rid)
- cull carriers
What is enterohepatitis or Black head? What is the pathogenesis? Who is most vulnerable?

Histomonas meleagridis + colibacilosis
Pathogenesis
- turkeys > chickens (asymt carriers) > phesants
Outbreaks lead to high morbidity & mortaility
Young turkeys are most vulnerable and severely affected (up to 14w)
What is the lifecycle of blackhead in poutry?
trophozoites of Histomonas infect ovaries of Heterakis > stored in egg of cecal worm > Heterakis egg eaten by earth worm > poutry eat earthworm > flagellated promastigotes (trophozoites) invade> lose flagella> amastigote > multiply in ceca> enter vessels to migrate to liver > liver failure or enteritis or resistant asymp carriers shed heterakis
* turkeys get infected from cloacal drinking
What is the presentation of Histomonas meleagridis in chickens
asymp reservoir
What is the presentation in turkeys?

Histomonas meleagridis
- localised (ceca) = necrotising typhlitis
- mustard dxa
- thick & caseous exudate
- +/- peritonitis
- systemic = enter circulation > liver, spleen, lung
- target lesion - focal necrosis > peripheral extension
How do you contol Histomonas meleagridis in a poultry flock?
- never mix chix & turkeys
- farm biosecurity (quarantine, intensive vs free range)
- Anthelmintic for heterakis cecal worm
- only home farm treat (not approved for commercial flock)
- nitroimidazoles - ronidazole, ipronidazole
liver of a bird - diagnosis?

Histomonas meleagridis (black arrows are amastigotes w/in hepatocytes)
Purple v red

Purple = kinetoplast
Red = nucleus
What is a kinetoplast?
dense area of mitochondrial DNA arranged in interlocking rings
Define : trypomastigote, Amastigote, Epimastigote, Promastigote
Trypomastigote : motile, extracellular, flagellum attached via undulating membrane. Kinetoplast posterior to nucleus
Amastogote : intracellular, no flagella, asexual binary fission. kinetoplast anterior to nucleus
Epimastigote : extracellular, motile. Kinetoplast central just anterior to nucleus, flagellum
Promastigote : extracellular motile. Kinetoplast anterior to nucleus, flagellum
What is the significance of Trypanosomiasis- distribution?
- all vector borne
- significant mortaility, morbidity and economic losses
- sub saharan Africa, S. america & parts of asia
- disease = surra
What is the trypanosome that infects a range of domestic animals, causes surra and transmitted by tabanid flies?
Trypanosoma evansi (in africa)
What is the LC of African Trypanosomiasis?
- tsetse fly takes blood meal > injects trypomastigotes
- other flies can be mechanical vectors as well as reusing needles
- trypomastigotes carried to other sites > multiply by binary fission in blood, lymph and spinal fluid
- circulating trypomastigotes in blood during acute stage (undetectable in latent phase)
- tsetse fly takes blood meal > trypomastigotes multiply via binary fission in midgut
- trypomastigotes leave and transform in epimastigotes
- epimastigotes multiply in salivary gland > transfor into trypomastigotes
Cattle and wild ungulates = reservoirs
What is the pathogenesis of trypanosomiasis? Hemolymphatic vs encephalitic stage?
Early (hemolymphatic) stage - febrile illness
- trypanosomes injected into bloodstream = chancre formation
- extracellular multiplication in lymph & blood & formation of variant surface protein (VSPs) = B cell activtion & Ab production against VSP > phagoctosis by RES
- anemia, thrombocytopenia
- hyperglobulinemia (high IgG response)
- RES hyperplasia, lymphadenopathy
- immune complex formation
- pancytopenia (splenomegally & bone marrow over produce)
Late (encephalitic stage)
- coma (sleeping sickness), delirium, narcolepsy, severe organ failure & eventually death = parasites cross BBB
What is the presentation of trypanosomiasis in animals? differentials?
- Fever (cyclical)
- Lymph node enlargement
- Splenomegaly
- Anaemia,
- lethargy
- Oedema
- Uveitis (esp dogs & corneal edema > almost always fatal)
- Wasting
- Meningoencephalitis
- Death
DDX
- hemonchus, babesia, theileria
What diagnostics do you run?

Trypanosomiasis
- detection of parasite in chancre, blood or csf (chronic forms may be a parasitaemic)
- thin & thick blood smears - capillary
- concentration tests
- detection of Ab in ELISA, card agglutination test (IgM)
- PCR
- boil blood then shine UV > infective are fluorescent
How do you treat and control trypanosomiasis?
- release sterile male flies
- trypano-tolerant cattle (african cattle that have coevolved)
- test & treat (before BB crossed)
- drugs
- arsenicals, anti neoplastics
- diminazine, isometamidium chloride, homidium bromide, suramin, melasoprol etc
- highly carcinogenic
- vector treatment more effective
What is the Leishmania LC?
- Promastigotes injected into host during feeding (common around face/mouth) - into definitive host (human, dog)
- Promastigotes phagocytosed by macrophages (langerhans in skin) > amastigotes in macrophages/RES multiply > promastigote > invade another cell
- Female sandfly takes blood meal w/ infected macrophages = intermediate host (sandfly- phlebotomid)
- amastigotes multiply to form promastigotes w.in sandfly > promastigotes injected into DH
What is are the 2 major forms of Leishmaniasis?
- visceral (leishmania donovani - india & L. infantum - S.america & africa, mediter)
- mucocutaneous/ cutaneous (L tropica, L braziliensis)
- all zoonotic except leishmania donovani
What is the presentation of Visceral leishmaniasis - in healthy populations vs immunocomp populations?
- healthy
- asymptomatic or mild infection
- young, old, immunosuppressed
- 85% fatality rate w/o treatment (esp HIVAIDS)
- 0-50% fatality rate w/ trx
In visceral leishmaniasis, amastigotes multiply in RES- what clinical signs do you expect to see?
- fever, hepto-splenomegally & pancytopenia
- liver failure, bleeding, anemia, secondary infections
What is the presentation of cutaneous leishmaniasis?
- localised nodulo-ulcerative lesion
- 1.5 mil new cases annually
- affects all age groups
- if left untreated may become diffuse w. invasion of mucosa & cartilage
What is the presentation of Infantile leishmaniasis? what is the agent and primary reservoir? Distribution?

Leishmania infantum
- dogs = primary reservoirs
- prevalence up to 15% in mediterranean/ middle east? s. America
- onyl 10-15% display overt dz
- non specific dermatitis - patchy alopecia
- signs of visceral dz
- anemia, wasting, bleeding disorders, protein losing nephropathy
- long fast growing nails that are splitting
How do you diagnose?

Leishmania
- detection of amastigotes in RES cells
- blood smear - buffy coat
- LN aspirate
- impression smear of lesion
- PCR on conjunctival swab, blood, lesion
- serology most reliable

How do you control Leishmania infections?
- vector control & reservoir control
- treatment supresses clinical dz but doesnt eliminate parasite
- carrier w/ relapse common
- repellents
- impreg collars on spot on - synthetic pyrethroids
- bed nets
- commercial canine vax
- blocks transmission to other hosts
Route of transmission? where do the trophozoites invade in humans? Balantindiasis

Balantindiasis - ingestion from contaminated food/ water - trophozoites in wall of colon
What are the typical hosts of Balantidium coli? How do you treat? Clinical signs?

- pigs humans primates - zoonotic
- immunocomp humans
- may be invasive (colon)
- dysenteric syndrome
- prevalent in commercial piggeries (50-100%)
- dxa in weaners or asymptomatic
- immunocomp humans
- treat w. nitroimidazoles
- similar to giardia trx (metronidazole)
What agent causes Amoebic dysentry? significance? Distinguishing featues? LC?
Entamoeba histolytica
- Humans - only pathogenic species
- tropics, subtrop, poverty
- 50-100,000 deaths pa
- morphologically indistinguishable from other species
transmission
- FO w. simple direct LC (ingest mature cysts & pass cysts and trophozoites)
- colonic pathogen
Possible clinical signs : Asymptomatic
>mild – diarrhoea, colitis, cramp
>moderate - dysentery
>severe - extra-intestinal - invades the liver and forms necrotic abscess, other tissues (CNS, lungs)
May rupture, fistulas
What is the likely cause?

Amoebiasis
What is the best treatment of Amoebiasis? Control? Differentials?
Treat
- drain abscess
- Nitroimidazoles (e.g. metronidazole) ± paromomycin
Control
- basic sanitation
- Indoor defaecation
- Ban use of night soil
- Wash fresh fruit and vegetables
- Water treatment
- boil water for 10 min
- avoid raw veg if not clean water
DDX
- ETEC - 24h dxa
- longer dxa - campy, salmonella, amoeba
What are the differences bw Naegleria flowleri & Acanthamoeba/Balamuthia mandrillaris? They both cause Amoebic meningoencephalitis and their main pathology is necrosis.
Naegleria flowleri
- cysts free living & trophozoites & flagellated forms (I) in natural bodies of water (sumemr lakes, hot springs)
- neti pots, diving
- enter through olfactory neuroepithelium causing 1* amebic menigoencephalitis in healthy individuals
- trophozoites in CSF & tissue
- flagellated forms in CSF
Acanthamoeba/Balamuthia mandrillaris
- enter through LRT or ulcerated broken skin causing granulomatous amebic encephalitis in immunocomp individuals
- gardening, older people
- can have systemic infection
- cysts & trophozoites in tissue
- not necessarily infected from water - soil more common
What clinical signs would you expect?

- 1* neuological - Amoebic meningoencephalitis
- granulomatous amebic encephalitis (Acanthamoeba/Balamuthia mandrillaris)
- +/- multisystemic spread
- individual may may immunosupressed but not always
- lesions of necrossis & hemorrhage
How do you treat Amoebic meningoencephalitis?
> 90% fatal
Miltefosine recently approved for amebic ME (registered for visceral leishmaniosis) >> analogue of eukaryotic membrane phospholipid - antineoplastic drug