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Parasitology > Protozoa > Flashcards

Protozoa Flashcards

1
Q
A

A. true coccidia

  • cystiospora
  • cryptosporidium
  • toxoplasmosis

B. piroplasms

  • babesia
  • thelieria

C. Haemosporidia

  • plasmodium
  • haemoproteus

D. Ciliates

E. Flagellates/ Hemoflagellates

F. Amoeba

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2
Q

what mechanisms do apicomplexa use to move around?

A
  • flagella - whip like
  • pseudopodia - temporary extensions (false feet)
  • cilia - hair-like extensions of cell membrane
  • undulating - tiny undulating waves gliding motion
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3
Q

What is the infective form of an apicomplexa?

A

‘zoite” w/ apical complex (microtubules allow movement & rhoptries secreted)

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4
Q

What is the function of the apical complex (apicomplexa)?

A
  • cytoskeltal & secretory funx
  • central to cell penetration & invasion
  • parasitophorus vacuole
    • communicates w host cell through secretions
    • look for the halo
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5
Q

Apicomplexan life cycle?

A

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
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6
Q

What is merogony starting stage > process > product?

A

Start

  • zoite

Process

  • asexual replication of merozoites -intracell

Product

  • gamont/gamete
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7
Q

What is gametogony starting stage > process > product?

A

Starting

  • gamete

Process

  • macro& microgametes fuse to produce zygote - intracell

Product

  • unsporulated oocyst
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8
Q

What is sporogony starting stage > process > product?

A

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)
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9
Q

What is the sporulated OOCYST morphology

A

A. Eimeria

B. (cyst)isopora

C. Sarcocystis

D. Cryptoporidium

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10
Q

What are examples of coccidia & what is the nature of their LC?

A

Direct LC & rapid

  • eimeria - birds, ruminants, lagomorphs
  • cystisospora - carnivores, omnivores, birds
  • cryptosporidium - broad range
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11
Q

What are examples of cyst - forming coccidia & what is the nature of their LC?

A

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
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12
Q

What are some examples of vector borne apicomplexa

A

mosquito

  • plasmodium (malaria)

ticks

  • piroplasms
    • babesia
    • theileria
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13
Q

Are emeria & cystisospora zoonotic?

A

no

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14
Q

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?

A

Eimeria & Cystisospora

  • overcrowding, stress, climate, poor hygiene, poor nutrition
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15
Q

Eimeria - DH? economic significance? clin signs?

A

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
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16
Q

Eimeria LC

A
  • direct- rapid
  • PPP= 3-21d
  • sporulation 1-3d (21-30* C humid optimal)
  • vary in virulence
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17
Q

What are the main predisposing factors of coccidiosis in livestock?

A

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
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18
Q

What are the 3 main anti-coccidial agents

A

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
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19
Q

Why would you use a coccidiostatic drug?

A

dont want to clear too quickly otherwise reduce future immunity

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20
Q

Can you treat layers with eimeria?

A

no bc of WHP - problem in non caged layers

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21
Q

What are the 4 main causes of coccidiosis in poutry?

A
  1. E. tenella (most path)
  2. E. necatrix
  3. E. maxima
  4. E. acervulina
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22
Q

What are the main symptoms and predilection sites of E. tenella, E. necatrix, E. maxima & E. acervulina

A

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
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23
Q

How can you diagnose coccidiosis due to Eimeria?

A

Post mortem

  • gross observation -predilection & path
  • sample
    • mucosal smears/scraping + fixed gut sections for histo
      • schizonts w merozoites
      • gametes

Ante mortem

  • fecal float
  • unsporulated oocyst

Feed Sample- check dosage of coccidiostats

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24
Q

How do you control coccidiosis in poultry?

A

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?
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25
Q

What causes hepatic coccidiosis in rabbits - merogony in bile duct epithelium >> jaundice & dxa w. mortality in weanlings? What are the necropsy findings?

A

Eimeria stiedai - focal white yellow nodules or cords in liver along bile ducts (cholangitis)

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26
Q

How does coccidiosis present in cattle? What are the species involved?

A

E. zuernii & E. bovis

  • 1-2 mo <1 yr
  • calf dxa/bloody scours
    • 2* colibacillosis
  • subclin - production loss
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27
Q

What can predispose calves to coccidiosis?

A

overcrowding, weaning to pasture/feedlots, stress/ low immunity

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28
Q

How can you prevent coccidiosis in calves?

A
  • coccidiostats in milk replacer, feed (monensin, lasalocid) or single drench (toltazuril) before weaning
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29
Q

how does coccidiosis present in lambs? what are the species involved?

A

E. crandallis & E. ovinoidalis

  • lambs 1-5 mo
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30
Q

What are the risk factors of coccidiosis in lambs? Prevention?

A

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
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31
Q
A

E. ovinoidalis - small intestinal polyps & large intesinal mucosa w. meronts

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32
Q

How can you diagnose coccidiosis in sheep?

A
  • necropsy
  • incubate feces (3d)
    • sporulation in 2% potassium dichromate soln
    • mcmaster for oocyst counts & ID
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33
Q

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?

A

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)

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34
Q

What is the life cyce of isospora (cystisospora)

A

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

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35
Q

What are the risk factors associated w cystisospora? immunity? Diagnosis?

A

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
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36
Q

What are the species of cystisospora associated w. dog, cat, & pig?

A

dog

  • C. canis
  • C. ohioensis complex

cat

  • C. felis
  • C. rivolta

pig

  • C. suis
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37
Q

How would you treat cystisospora in domestic animals? Prevention?

A

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
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38
Q

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?

A

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
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39
Q

What is the common host of the zoonotic cryptosporidium? What is the common zoonotic spp?

A

cattle - Cryptosporidium parvum

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40
Q

How would you describe the positioning of cryptoporidium? What types of tissue can you find it?

A
  • epicellular position - intracellular but extracytoplasmic
  • gastric or intestinal
  • respiratory epithelium in poultry
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41
Q

What is the lifecycle of Cryptosporidium?

A

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
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42
Q

What is the pathogenesis of cypto infection

A

villous atrophy

  • parasite destruction
  • t cell apoptosis

epithelial mucosa release cytokines

  • increased H20 & chloride

watery dxa & malabsorption

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43
Q

What is the significance of crypto infections?

A
  • 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!!
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44
Q

Apart from being zoonotic, what is the public health significance of cryptosporidiosis?

A
  • major water born pathogen
    • oocysts resistant in chlorine (C. hominus most likely)
      • ​sinking -
      • spreader +
  • self limiting dxa (2-4 w in healthy)
  • chronic life threatening dxa in HIV/AIDS
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45
Q

How does crypto present in calves?

A
  • calves <4 wks have C. parvum
  • high intensity of oocysts excretion
  • Low infectious dose (5-10 oocysts)
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46
Q

How do you diagnose crypto?

A
  • zinc or sucrose floats (SG 1.12- 1.18)
    • oocysts small
    • immunoflourescence - oocyst wall protein
  • Zn smear, acid fast
  • ELISA or immunochromatography
  • PCR
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47
Q

how do you treat crypto?

A

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

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48
Q

How do you control crypto infections?

A
  • hygiene (heat . 70* C - steam, dry, ammonia)
    • doesnt survive long in dry clean environment
  • biosecurity/quarantine
  • adequate colostrum
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49
Q

Toxoplasma gondii - LC in cats

A

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
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50
Q

Toxoplasma gondii - LC

A

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
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51
Q

how is toxoplasma transmitted?

A

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
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52
Q

When are cats immune to toxoplasma? When is there a high shed?

A
  • 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)
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53
Q

What is the pathogenesis of toxoplasma infeciton in the tissue stages?

A
  • acute infection in naive host - primary exposure
  • reactivate latent infection - immunocompromised
  • tachyzoites multiply destroying tissue - multisystemic signs
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54
Q

What is the significance of a toxoplasma infection?

A
  • abortion in ewes - economic
  • abortion & congenital deformities in humans
    • primary infection during gestation
  • multisystemic disease in warm blooded mammals
    • cats, marsupials, dogs, humans
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55
Q

What is the presentation of toxoplasmosis in cats?

A

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
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56
Q

What is the public health significance of toxoplasmosis?

A
  • majority asymptomatic - mild flu (bradyzoites in tissues)
  • acute outbreak (high infectious dose)
    • chorioretinitis - waterborne outbreak
      • peeps camping drinking lake water - cougar poo
  • HIV-AIDS/organ transplant patients
    • 10-30% fatality from latent (90%) or newly acquired infection
    • encephalitis, pneumonia, ocular dz
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57
Q

How does toxoplasma pose a risk to preg women?

A
  • 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
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58
Q

What is the likelihood of transmitting toxoplasma to fetus during 1st trimester? What is the out come? third trimester?

A

1st

  • low 5-10%
  • severe outcome - abort, neuro abnormalities (hydrocephalus)

3rd

  • high 70-80%
  • milk outcome - asymptomatic (95%), chorioretinitis
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59
Q

how can you diagnose toxoplasma infections?

A

-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

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60
Q

What drugs suppress tachyzoite replication (toxoplasma)

A
  • Pyrimethamine
  • Clindamycin
  • Sulfonamides
  • Azithromycin
  • clin improvement in 24-48 h (unless organ necrosis)
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61
Q

how can you prevent toxoplasma infection?

A
  • 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 %
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62
Q

What is the life cycle of neospora caninum

A

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
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63
Q

What is the significance of Neospora caninum infection in Cattle vs Dogs?

A

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
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64
Q

What is the best course of action for congenital neosporosis?

A
  • 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
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65
Q

How can you diagnose and treat neospora infections?

A
  • Ab Titer
  • fecal float unrewarding
  • treat
    • Clindamycin, pyrimethamine,
      sulphonamides or combinations
  • prognosis
    • early case: good
    • mm contracture of hind limb - poor
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66
Q

Compare Toxoplasma gondii & Neospora caninum

A
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67
Q

What is the sarcocystis LC?

A
  • 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

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68
Q

Significance of sarcocystis infection (cattle, acute infection, etc)

A

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
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69
Q

What would infected DH fecal sample contain? What diagnostics do you perform? What are some differentials?

A

-naked sporocysts in feces = Sarcocystis

Diagnostics - histopath, PCR tissue

DDX

  • hydatid
  • taenia saginata
  • calcified sarcocystis
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70
Q

What are some examples of coccidia-related vector borne agents? What type of life style do they have?

A

indirect LC

  • babesia
  • theileria
  • plasmodium
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71
Q

What are the main LC differences bw babesia/theileria and plasmodium?

A

B/T

  • IH= mammals
  • DH= ticks

P

  • IH= vertebrates (humans, birds)
  • DH= mosquitoes
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72
Q

What is the piroplasm general LC?

A

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

73
Q

apart from being bitten by a tick, what are other ways piroplasms can be intoduced to mammals?

A
  • iatrogenicaly - bood transfusions
  • transovarial transmission in ticks for babesia spp only
74
Q

what is the significance of piroplasmosis?

A
  • 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)
75
Q

What ticks cause piroplasmosis in australia?

A
  • haemaphysalis longicornis
  • Rhipicephalus australis
  • R. sanguineous
76
Q

Where is tick fever most common? what are the agents of tick fever?

A

babesia bovis, B bigemina & anaplasma spp

  • warm humid tropical and subtropical conditions (central & south america, SE asia and N. aus)
77
Q

What is the vector for tropical theileriosis (in asia) (malignant theriosis)

A

Hyalomma spp ticks

78
Q

What is the vector for east coast fever (africa) (malignant theriosis)

A

R. appendiculatus

79
Q

What is the distribution of benign theriosis - T. orientalis?

A
  • humid coastal areas, sub tropical/ temperate conditions (haemaphysalis longicornis SE QLD & NSW) - also in parts of europe, RU, asia, NZ, pacific islands & hawaii
80
Q

What is the mechanism of hemolytic anemia in piroplasmosis?

A
  • hypoxia, organ damge
  • direct RBC destruction - merogony
  • indrect anti RBC antibodies - splenomegally
81
Q

What is the mechanism of thrombocytopenia in piroplasmosis?

A
  • splenic sequestration of platelets
  • auto antiplatelet antibodies
  • consumptive coagulopathy - DIC, shock
  • increased bleeding w petechiation
82
Q

What is the consequence of cytoadhesion of RBC to capillaries in the brain in piroplasmosis?

A

cerebral babesiosis in Babesia bovis & babesia caballi (horse)

  • RBC surface is sticky and stick to endothelium of the brain
83
Q

Where is Theileria during merogony phase 1? What is the pathogenicity?

A

Leukocytes - thmphadenopathy, lympgoid depletion and leukopenia

84
Q

What is the most pathogenic babesia spp of cattle

85
Q

What is the most pathogenic babesia spp of dogs

A

B. rossi > B. canis > B. gibsoni > B. vogeli

86
Q

What is the most pathogenic species of theileria

A

T. parva > T. annulata > T. orientalis complex

87
Q

Regarding immunity to piroplasmosis- what is enzootic stability vs enzootic instability?

A
  • 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
88
Q

What are sublinical & acute signs of babesiosis in cattle

A

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
89
Q

What are the 2 spp of babesia in AU that can infect dogs- what are their vectors and how pathogenic are they?

A

babesia vogeli - mild path - Rhipicephalus sanguineous

Babesia gibsoni - mod path - Haemaphysalis longicornis

90
Q

What babesia spp are able to be transmitted directly from dog to dog via fighting or vertical transmission?

A

B. gibsoni & B. vulpes (eu & usa)

91
Q

What are the 4 routes of transmission of canine babesia

A
  • direct
  • transplacental (vertical)
  • blood transfusion
  • tick bite
92
Q

primary differentials?

A
  • 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
93
Q

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?

A

Babesia vogeli - can be confused with immune mediated hemolytic anemia (steroid use) & can be a problem in splenectomised dogs

94
Q

What canine babesia species is transmitted by dog fighting, vertically and Haemaphysalis longicornis ticks - what kinds of dogs is this most common in?

A

B. gibsoni - adults (esp pitbull terriers or dogs w history of fighting/agression) and pups

95
Q

What are the different (4) presentations of theileriosis in cattle?

A
  • 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
96
Q

when is theileriosis mostly seen in cattle?

A

late preg, calving & early lactation

97
Q

How can you diagnose piroplasmosis ante-mortem?

A
  • 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
98
Q

How can you diagnose piroplasmosis post-mortem?

A
  • brain (grey matter) capillary impression smear - B. bovis
  • histopath - LN, brain, kidneys, liver, spleen
99
Q

blood smear cattle

A

T. annulata

100
Q

LN aspirate

A

T. annulata

101
Q

L vs R - what is the level of parastiemia

A

L - Babesia bigemina

  • high parasitemia - 10-30%
  • parasite pair forms an acute angle

R- Babesia bovis

  • low parasitemia - < 1 %
  • parasite pair forms obtuse angle
102
Q

What is the most likely diagnosis

A

babesiosis (b. bovis - distension of capillaries of brain)

103
Q

What supportive care and anti-protozoal agents can be given to treat babesiosis?

A

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
104
Q

How can you treat B. gibsoni in dogs?

A
  • challenging - relapses common
  • macrolid ab + antiprotozoal (off label)
  • atovaquone (anti malarial) & azithromycin
105
Q

What are the effective drugs used to treeat theileriosis?

A
  • Buparvaquone (drug of choice)
  • primaquine
  • currently not registered in aus

IN AUS - imidocarb dipropionate (not great efficacy - tick control and quarantine best)

106
Q

What is the best treatment & control of piraplasmosis in cattle?

A

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
107
Q

what is the significance of malaria (plasmodium)? What is the vector & distribution?

A
  • 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
108
Q

What is the avian hemoprotozoa? Where does merogony occur? where are the gametes? Vectors?

A

Haemoproteus spp

Merogony - tissue

Gametes - RBC - highly endemic in wild birds

Rare mortality

Vector - Hippoboscids & culicoides midges

109
Q

What are the clinical signs? What vectors?

A
  • 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)

110
Q

What are the clinical signs? Vectors?

A

Plasmodium spp

Anemia, emaciation, death, multifocal signs (block of capillaries of lungs, brain, kidney)

Vectors - Culex, aedes mosquitoes

111
Q

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?

A

Babesia vogeli - from brown dog tick (R. sanguineous) - treat w. imidocarb dipropionate inj now & 2 wks (off label)

112
Q

Define flagellate terms: Cyst, Trophozoite, Promastigote, Amastigote

A

Cyst: resistant to unfavorable environmental conditions outside host

Trophozoite: active, feeding, motile stage

Promastigote: single anterior flagellum

Amastigote: non-flagellated intracellular stage

113
Q

What is the life cycle of Giardia?

A
  • 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)
114
Q

What is the significance of Giardiosis?

A
  • neglected tropical dz (WHO)
    • chronic subclinical infection in developing regions
      • stunted growth
      • reduced cognitive development
  • Dxa - humans & animals
    • mostly young (immunity follows - chronic carriers)
    • kennels
    • day care centers
    • farms - calves (prod loss)
    • waterborne outbreak (zoonosis)
115
Q

What is the species of giardia that infects a wide range of hosts? humans, cats, dogs, cattle, horses, etc

A

G. duodenalis

116
Q

What 3 giardia spp infect dogs?

A

G. duodenalis, G enterica, G. canis

117
Q

What giardia spp infect cats

A

G. duodenalis, G. enterica, G. cati

118
Q

What giardia spp infect cattle

A

G. duodenalis, G. bovis

119
Q

Is giardia zoonotic?

A

Yes - only G. duodenalis & G. enterica (even if immunocomp wont see infection w/ G. canis - crypto has a wider infective range)

120
Q

What is the pathogenesis of giardia?

A
  • 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
121
Q

What is the typical presentation of giardiosis? Where is it most common in AUS?

A
  • 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

122
Q

motile binucleated trophozoites in fresh fecal smear from a severly diarrheic animal.. diagnosis? what solution do you use to visualize cysts? What other diagnostics?

A

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)

123
Q

When are you most likely going to see giardia trophozoites in a fecal smear?

A

w/ severe watery dxa bc transit time so fash there isnt enough time to estabilsh cyst (falling leaf motion in floatation)

124
Q

Why is drontal (for 3 d) used to treat giardiosis?

A
  • drontal = febantal, pyrantal, praziquantel
  • febantal is metabolised to high concentrations of fenbendazole in the serum and slowly released
125
Q

How do you control/ prevent giardiosis?

A

hygiene, reduce over crowding & stress - change bedding, pick up dog poo, wash dog, kids wash hands

126
Q

What drugs can you use off label to treat giardiosis?

A

fenbendazole for 5 d

metronidazole for 5-7d

127
Q

What are the main features of the trichomonads LC

A
  • Simple direct LC
  • FO - close contact, wet environment - & venereal
  • NO cysts - trophozoites only
128
Q

What are the morphological features of trichomonads?

A
  • 3-6 flagella anterior (one forms an undulating membrane)

SINGLE nucleus (giardia has 2)

129
Q

Trichomonad of humans - type of disease caused

A

Trichomonas vaginalis - veneral

130
Q

Trichomonad of cattle - type of disease caused

A

Tritrichomonas foetus - venereal

131
Q

Trichomonad of cats - type of dz caused

A

Tritrichomonas blagburni - intestinal colitis

132
Q

Trichomonad of pigeons and other birds - type of dz caused

A

Trichomonas gallinae- upper digestive tract - invasive/systemic forms

133
Q

What are the clinical features of Feline intestinal trichomoniosis? What is the agent? What are differential diagnoses?

A

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?
134
Q

How do you diagnose feline tritrichomoniosis

A
  • 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
135
Q

How do you treat feline tritrichomoniosis

A
  • off label ronidazole 30 mg/ kg once daily for 14d + probiotic
    • registered in birds
  • variable sucess - relapse common
  • caution = neurotoxicity
136
Q

What is the signficance of Tritrichomonas foetus infection? How is it transmitted and what is the host?

A

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
137
Q

How does Bovine tritrichomoniosis present in cows? Immunity? Why is it endemic in NT?

A
  • 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
138
Q

How does Bovine tritrichomoniosis present in bulls?

A

asymptomatic - live in crypts of penis and prepuce (crypts get bigger as they get older - increase risk)

*perm carriers

139
Q

How can you diagnose bovine tritrichomoniosis?

A
  • bull sheath wash
    • 1x week > 3 sucessive negs at lease 2 wks after last service
      • allow buildup of organisms = better Se
  • cow cervical wash following abortion
  • direct microscopy
  • culture (in -pouch)
  • qPCR
140
Q

there is no effective, approved treatment or vaccine in AU for Bovine tritrichomoniosis - how do you control?

A
  • 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
141
Q

What are ddx for abortion in cattle

A
  • BVD
  • Trichomonas
  • Sarcocystis
  • Neospora
  • Babesia bovis & Theileria = pyrexia & anemia
142
Q

What is the significance of Avian trichomoniosis? What birds are affected?

A
  • “CANKER” in pigeons “FROUNCE” in falcons
    • Trichomonas gallinae
    • upper digestive tract
    • nasal cavity
  • Affects pigeons, budgerigars,backyard poultry and raptorial birds
143
Q

How is Avian trichomoniosis transmitted?

A
  • 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
144
Q

What is the typical presentation of Avian Trichomoniasis (clin signs and lesions)? What does SQUABS mean?

A

SQUABS = symptomatic = usually youngest

  • stop feeding, lose weight, rufflyed and dull, dysponea, difficulty swallowing
  • circumscibed caseous plaques
    • oropharynx, esophagus, crop, proventriculus
      • ulceration, abscessation
  • localised & systemic (invasive)
145
Q

How can you diagnose Avian Trichomoniasis?

A

scrape/crop flush >> microscopy, PCR or culture (In Pouch TF)

146
Q

What are the best treatment and control methods for Avian Trichomoniasis?

A
  • quarantine - test new comers & cross react w. qPCR (tritrichomonas in cats)
  • sx removal of caseous plaques
  • ronidazole, metronidazole (doesnt completely get rid)
  • cull carriers
147
Q

What is enterohepatitis or Black head? What is the pathogenesis? Who is most vulnerable?

A

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)

148
Q

What is the lifecycle of blackhead in poutry?

A

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

149
Q

What is the presentation of Histomonas meleagridis in chickens

A

asymp reservoir

150
Q

What is the presentation in turkeys?

A

Histomonas meleagridis

  • localised (ceca) = necrotising typhlitis
    • mustard dxa
    • thick & caseous exudate
    • +/- peritonitis
  • systemic = enter circulation > liver, spleen, lung
    • target lesion - focal necrosis > peripheral extension
151
Q

How do you contol Histomonas meleagridis in a poultry flock?

A
  • 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
152
Q

liver of a bird - diagnosis?

A

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

153
Q

Purple v red

A

Purple = kinetoplast

Red = nucleus

154
Q

What is a kinetoplast?

A

dense area of mitochondrial DNA arranged in interlocking rings

155
Q

Define : trypomastigote, Amastigote, Epimastigote, Promastigote

A

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

156
Q

What is the significance of Trypanosomiasis- distribution?

A
  • all vector borne
  • significant mortaility, morbidity and economic losses
  • sub saharan Africa, S. america & parts of asia
  • disease = surra
157
Q

What is the trypanosome that infects a range of domestic animals, causes surra and transmitted by tabanid flies?

A

Trypanosoma evansi (in africa)

158
Q

What is the LC of African Trypanosomiasis?

A
  1. tsetse fly takes blood meal > injects trypomastigotes
    1. other flies can be mechanical vectors as well as reusing needles
  2. trypomastigotes carried to other sites > multiply by binary fission in blood, lymph and spinal fluid
  3. circulating trypomastigotes in blood during acute stage (undetectable in latent phase)
  4. tsetse fly takes blood meal > trypomastigotes multiply via binary fission in midgut
  5. trypomastigotes leave and transform in epimastigotes
  6. epimastigotes multiply in salivary gland > transfor into trypomastigotes

Cattle and wild ungulates = reservoirs

159
Q

What is the pathogenesis of trypanosomiasis? Hemolymphatic vs encephalitic stage?

A

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
160
Q

What is the presentation of trypanosomiasis in animals? differentials?

A
  • Fever (cyclical)
  • Lymph node enlargement
  • Splenomegaly
  • Anaemia,
  • lethargy
  • Oedema
  • Uveitis (esp dogs & corneal edema > almost always fatal)
  • Wasting
  • Meningoencephalitis
  • Death

DDX

  • hemonchus, babesia, theileria
161
Q

What diagnostics do you run?

A

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
162
Q

How do you treat and control trypanosomiasis?

A
  • 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
163
Q

What is the Leishmania LC?

A
  • 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
164
Q

What is are the 2 major forms of Leishmaniasis?

A
  • visceral (leishmania donovani - india & L. infantum - S.america & africa, mediter)
  • mucocutaneous/ cutaneous (L tropica, L braziliensis)
  • all zoonotic except leishmania donovani
165
Q

What is the presentation of Visceral leishmaniasis - in healthy populations vs immunocomp populations?

A
  • healthy
    • asymptomatic or mild infection
  • young, old, immunosuppressed
    • 85% fatality rate w/o treatment (esp HIVAIDS)
    • 0-50% fatality rate w/ trx
166
Q

In visceral leishmaniasis, amastigotes multiply in RES- what clinical signs do you expect to see?

A
  • fever, hepto-splenomegally & pancytopenia
  • liver failure, bleeding, anemia, secondary infections
167
Q

What is the presentation of cutaneous leishmaniasis?

A
  • 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
168
Q

What is the presentation of Infantile leishmaniasis? what is the agent and primary reservoir? Distribution?

A

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
169
Q

How do you diagnose?

A

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
170
Q

How do you control Leishmania infections?

A
  • 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
171
Q

Route of transmission? where do the trophozoites invade in humans? Balantindiasis

A

Balantindiasis - ingestion from contaminated food/ water - trophozoites in wall of colon

172
Q

What are the typical hosts of Balantidium coli? How do you treat? Clinical signs?

A
  • pigs humans primates - zoonotic
    • immunocomp humans
      • may be invasive (colon)
      • dysenteric syndrome
    • prevalent in commercial piggeries (50-100%)
      • dxa in weaners or asymptomatic
  • treat w. nitroimidazoles
    • similar to giardia trx (metronidazole)
173
Q

What agent causes Amoebic dysentry? significance? Distinguishing featues? LC?

A

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
174
Q

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?

A

Amoebiasis

175
Q

What is the best treatment of Amoebiasis? Control? Differentials?

A

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
176
Q

What are the differences bw Naegleria flowleri & Acanthamoeba/Balamuthia mandrillaris? They both cause Amoebic meningoencephalitis and their main pathology is necrosis.

A

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
177
Q

What clinical signs would you expect?

A
  • 1* neuological - Amoebic meningoencephalitis
  • granulomatous amebic encephalitis (Acanthamoeba/Balamuthia mandrillaris)
    • +/- multisystemic spread
    • individual may may immunosupressed but not always
  • lesions of necrossis & hemorrhage
178
Q

How do you treat Amoebic meningoencephalitis?

A

> 90% fatal

Miltefosine recently approved for amebic ME (registered for visceral leishmaniosis) >> analogue of eukaryotic membrane phospholipid - antineoplastic drug

Parasitology (5 decks)

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