Protozoans

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Indirect Lifecycle

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Requires definitive host AND intermediate host OR paratinic host

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Direct Lifecycle

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Only required definitive host. No intermediate host required for completion of lifecycle

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Definitve Host

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Every parasite has at least 1 definitive host. Both direct and indirect lifecycles. The definitive host harbors the adult or sexual stages of the parasite. Immature forms may also exist

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Intermediate host

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For indirect lifecycles. Intermediate host harbors the pre-adult/asexual stages of the parasite. Parasite development occurs within the host. REQUIRED for completion of the lifecycle.

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Paratenic host

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AKA transport host. Can have an indirect lifecycle with a paratenic host. Harbors the pre-adult/asexual stages of the parasite. Little to no development occurs within the host but is capable to survive. NOT required for the completion of the lifecycle

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Reservoir host

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All parasites have a reservoir host. Host in which the organism (parasite) occurs in nature and is the source of infection for other hosts.

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3 types of protozoans

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Sarcomastigophora (flagellates and amoebae), ciliophora (ciliates) and apicomplexans

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Flagellates have tails in what stage?

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Trophozoite

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Apicomplexan lifecycle type and reproduction

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Obilgate intracellular parasites. Multiply through strict sequence of asexual and sexual repro. May have direct or indirect lifecycles

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Eimeria spp. host specificity

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High degree of host specificity, a few can cross species.

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Eimeria life cycle

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Direct. Each cycle has seeral asexual generations and 1 sexual generation.
-Oocysts sporulate in environment; ingested by next host
-Sporozoites excyst; invad intestinal cells. 8 sporzoites, each one will infect a different intestinal cell
-Asexual repro -->numerous merozoites; burst from cell and invades new cells
-1-2 addl rounds of asexual repro followed by 1 round of sexual repro
-Fertilization results in zygote; oocyst wall laid down; UNSPORULATED oocyst passed in feces (not infective until sporulated)

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Eimeria pre patent period

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The time it takes from when the host ingest the infectious stage ntil the diagnostic stage can be found in the host. 4-30 days

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Eimeria pathogenesis

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Can be self limiting. In heavy infestations, death may result. Immunity is species specific and incomplete.
-Destruction of host cells during asexual and sexual repro and during release of oocysts is primary pathogenic mechanism.
-In ruminants severity is influence by location within the intestinal tract. SI has less effect bc it is so large
-Destruction happens during PPP so hard to dx
-Long term negative effects on growth rate

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Clinical signs of eimeria in cattle

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-Infection is common, dz is sporatic. Usually in claves <1yr.
-Light infections cause watery feces and reduced wt gain
-Heavy infection cause projectile bloody D w mucus, rectal tenesmus, inappetence, dehydration and wt loss.
-Signs last ~ 1 wk

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Pathogenic eimieria spp of cattle

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-E. zuernii, E. bovis and possible E. alabamensis

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Eimeria zuernii

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Pathogenic eimeria of cattle

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Eimeria bovis

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pathogenic eimeria of cattle

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Pathogenic eimeria of sheep

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E. crandallis, E. ovinoidalis

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Eimeria ovinoidalis

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Pathogenic eimeria of sheep

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Eimeria crandallis

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Pathogenic eimeria of sheep

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Clinical signs of eimeria in sheep

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Lamns less than 6 months diarrhea, usually lasts a week, no blood or tenesmus

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Clinical signs of eimeria in goats

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Kids 2-3 weeks after weaning
-pasty watery D
-Deydration

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Pathogenic spp of eimeria in goats

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E. ninakohlyakimovae, E. caprina, E. chritenseni

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Eimeria ninaholyakimovae

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Pathogenic eimeria of goats

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Eimeria caprina

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pathogenic eimeria of goats

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Eimeria christenseni

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pathogenic eimeria of goats

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Eimeria macusaniensis

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Pathogenic eimeria of camelids

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Eimeria leuckarti

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Eimeria of horses, infections usually not noticed

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Eimeria in chickens

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-Major production loss
-severe d in 3-6 week chicks
-poor growoth, mucoid D +/- blood
-recovery in 1-2 weeks or death
-many pathogenic spp

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Coccidiosis

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Name of the disease causeed by eimeria protozoa

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Eimeria in pigs

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Does not cause coccidosis

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Coccidiosis in carnivores

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caused by cystoisopora

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Cystoisospora host specificity

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Very specific

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Cystoisospora life cycle

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-Direct or indirect with paratenic host
-Sporulation of oocysts passed in feces-->Ea oocyst contains 2 sporoblasts-->oocyst w/ 2 sporocysts (4 sporozoites ea)-->ingestion-->1 sporozoite from ea mature oocyst infects 1 cell (8 sporozoites in ea oocyst)-->ea host cell release 4 merozoites when ruptures-->reinfects cells for sexual repro-->oocyst passed in feces

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Cystoisospora canis and felis

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-oocysts ingested by mice and birds
-sporozoites penetrate SI and migrate to various organs
-Enlarge and encysts (called hypnozoite)
-Dog/cat eats paratenic host and becomes infected

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Coccidiosis in pigs

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cystoisospora suis

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Clinical signs of Cystoisospora in carnivores

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-Often inapparent
-D, Abdominal pain, dehyration, anorexia, wt loss
-Can have very heavy infestations

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Clinical signs of Cystoisospora in Pigs

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-Neonatal procin coccidiosis
-Pale, watery, fetid D and decreased growth in piglets 5-15 days old
-High morbidity, low mortality

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Detection of Cystoisospora

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-Unsporulated oocysts MAY be found on fecal flotations.
-Presence or absence of oocysts does not necessary correlate with dz.
-Diagnosis can be made based on hx

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Control of Cystoisospora

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Minimize stress
-Clean, dry housing, not crowded
-Dog and cat tx are off label use

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Sarcocystis spp type of life cycle

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-Indirect
-Intermediate host is herbivore
-Definitive host is carnivore/omnivore

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Sarcocystis neruona

-Who is effected and where is it prevalent?

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-Horses (dead end host)
-MOST COMMON CAUSE OF EQUINE PROTOZOAL MYELOECEPHALITIS (EPM)
-Western hemisphere

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Definitve host and Intermediate hosts of Sarcocystis neurona

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-DH: Opossums (sarcosysts [tissue] containg bradyzoites)
-IH: Amadillos, domestic cat, raccoon (sporulated occyst)

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Life cycle of Sarcocystis neurona

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-Sporozoites leave sprotocysts/oocyst in gut
-Penetrate and migrate to other areas of the body; w/in tissue cysts
-undergo asexual repro becoming tachyzoites
-leave tissue cysts, enter new tissue and multiply asexually
-CNS signs within 1 week of infection

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Diagnosis of EPM

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-3 As
-Asymmetry
-Ataxia
-Atrophy (head or butt)
WESTERN BLOT; antibodies in serum and CSF

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Neospora caninum type of life cycle and hosts

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-Indirect life cycle
DH: Dogs
IH: dogs, cattle, sheep, goats

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Neospora caninum life cycle

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-Unsporulated oocysts in feces
-Sporuylates in water, food, or soil
-Ingested by IH
-IH, passes it in feces or host eaten by dog
-IH feces ingested by another IH. Transplacental transmission via tachyzoites

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Most common mode of transmission of Neospora caninum in dogs

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-Congential
-Insufficent to maintain endemicity

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Pathogenesis of neospora caninum in adult dogs

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-Can be fatal in adult dogs
-BAR with abnormalities of hind limbs
-Inflammation of mm and nn roots
-progressive hind limb paresis, mm atrophy, loss of reflexes
-Pyognaulomatous dermatitis (immunodeficiency)

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Pathogenesis of Neospora caninum in puppies

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-Dz most severe in congenitally infected pups (meningoencephalities/CNS signs)
-Multiple organ involvment
-Myocarditis
-Jaw paralysis, mm flaccidity or atrophy

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Pathogenesis of Neospora caninum in cattle

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-LOSS OF CALF, resorption of embryo. abortion/still birth
-Usually mid gestation
-Infection acquired PRIOR to pregnancy can do this
-Tachyzoites enter fetal blood stream
-Clinical signs only reported in calves < 2 months
-Reduced milk production

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Diagnosis of Neospora caninum in dogs

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IFAT
CSF antibody titer
Tissue PCR (problem with false negatives)
IHC

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Diagnosis of Neospora caninum in cattle

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-Serology Indicates exposure only in aborting cow
-Histology: fetal brain, heart, liver, placenta
-Remember, IgG does not cross placenta in cows

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Treatment of Neospora caninum

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-Prevent vertical transmission in cows via embryo transfer or cullins
-Clindamycin tx for dogs, prevent scavenging

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Toxoplasma gondii type of life cycle and hosts

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-Indirect or direct life cycle
-DH is only felids
-IH are very widespread

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Toxoplasma gondii life cycle

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-unsporulated oocysts passed in feces
-Sporulate within 24-96 hours (contains 2 sporocysts ea with 4 sporozoites
-In IH sporozoites invade intestinal cells and assoc. lymphnodes to become rapidly dividing tachyzointes
-Ruptures cell, spreads throughout body, bradyzoites develope into tissue cysts
-IH can also be infected by igesting bradyzoites in tissue cysts
-Dam must be infected DURING pregnancy for transplacental transmission to occur
-Tachyzoites migrate to fetus, congenital infections important for humans, sheep and goats

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Pathogenesis of Toxplasma gondii in cats, sheep, goats, pigs, dogs and humans

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Cats: Usually inapparent, may be assoc w/pneumonia, ocular lestions
Sheep/Goats: Abortion. Can be fatal in adult goats
Pigs: Usually inapparent, abortion or fever, encephalitis, myocarditis & pneumonia in piglets
Humans: Undercooked meat or oocysts. Chorioretinitis, hydrocephalus, mental retardation and jaundice

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Diagnosis of T. gondii in felids

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-Fecal flotation
-Serology with pair Igm/IgG titers
-IH: lymph node bx
-Post mortem

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Cryptosporidium Life cycle

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-Direct
-Sporulated oocysts passed in feces and ingested
-Sporozoites invade microvilli in lower SI, bile duct or respiratory tract and lie in a vacuole just beneath host cell membrane
-Asexual then sexual repro
-Oocysts in 72 hours
-Thin walled break and reinfect host, thick walled are passed in feces
-ppp is little as 3 days
-Very stable in environment and resistant to chemicals

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Cryptosporidum parvum

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-Self limiting
-Usually lasts 1-3 weeks
-Nutritional plane influences resolution of D, hydration and growth
-Exacerbated by other pathogens (i.e.: Rotovirus in cattle)

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Cryptosporidum andersoni

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-Infects abomasum
-Clinically mild
-Potential for lack of gain and mild production
-Typically in older cattle

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Cryptosporidium canis

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-Puppies
-Older dogs are usually asymptomatic shedders

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Cryptosporidum felis

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-Usually kittens
-Almost exclusively immunosuppressed cats

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Cryptosporiduim serpentis

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-Mature snakes
-Hyperplasia of gastric glands/atrophy of granular cells
-Edema of submucoa, lamina propria and inflammation of gastric mucosa
-Regurgitation, mid body swelling, lethary, death
-Not self-limiting

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Cryptosporidum baileyi

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-Chicks or old birds
-Bursa of fabricus, cloaca and respiratory tract
-Exacerbated by other pathogens

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Cryptosporidium melegridis

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-Turkey ileum
-Severe D

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Detection of Cryptosporidum

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-Fecal float (sugar)
-Fecal smear
-ELISA/RID
-Immunofluoresence
-PCR
-Necropsy, SI

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Is Cryptosporidum zoonotic?

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-Yes, but not very common
-Most human infections are from other humans (C. hominis)
-C. parvum, from calves
-Rare from companion animals

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Cytauxzoon felis type of life cycle and hosts

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-Indirect
-DH: dermacentor variabliis and amnlyomma americanum
IH: cats
-Natural reservoir host: Bobcat

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Cytauxzoon felis transmission

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-Transtadial NO transovarial
-From amblyomma americanum and dermacentor variabilis
-Sporozoites from tick bite to IH, invades mononuclear cells lining venules of lungs, liver, spleen
-Grow into large meronts; merozoites penetrate RBCs

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Cytauxzoon felis pathogenesis

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-Monocytes enlarge & become adherent as parasite reproduces
-Diapedesis is reduced and accumulation of monoytes obsruct small veins in lungs, spleen lymph nodes
-Monocytes release vasoactive mediators-->congestion and hemorrhage
-Monocytes act as thrombi, cytotoxic effects-->shock
-Non regenerative anemia-->icterus and cholestatis
-Likely fatal
-Usually happens during autumn

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Cytauxzoon felis diagnosis

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-Clinical signs and lab findings, look @ monocytes

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Hepatozoon americanum type of life cycle & hosts

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-Indirect life cycle
-DH: Amblyomma maculatum
-IH: dogs
-Paratenic host: rabbit or mouse
-dog INGESTS tick and asexual repro in mm

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Hepatozoon americanum pathogenesis

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-Occurs in skeletal and cardiac mm
-Intense inflammatory response
-Periostal prolifereation of long bones
-Non regenerative anemia w/PROFOUND LEUKOCYTOSIS
-Lethargic and painful
-Untreated dogs die in <12mo., relapses in treated dogs

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Hepatozoon americanum diagnosis

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-MM bx (onion lesion)
-Neutrophilic leukocytosis, non regenerative anemia
-Osteoproliferative lesions of long bones
-Blood smears are not acurate

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Hepatozoon canis type of life cycle and hosts

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-Indirect
-DH: Rhipicephalus sanguineus and amblyomma (in other areas, not known in US)
-IH: Canids
-Reservoir host: Red fox

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Hepatozoon canis pathogeneis and diagnosis

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-Clinically normal unless co-infection or high parasitemia
-Fever, lethargy, emaciation (usually mild)
-Blood smear diagnostic
-PCR
-Normal bones on Xray
-Tx is difficult

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Babesia type of life cycle

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-Indirect
-DH: Ixodes ticks

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Types of canine Babesiosis

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-B. canis vogeli
-B. gibsoni
-B. conradae
-Babesia sp (small babesia)

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Babesia canis vogeli

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-Transmission my Rhipicephalus sanguineus
-Transovarial and transtadial transmission
-Most common in greyhounds
-Puppies more severely infected (respond well to tx)
-Adults have subclinical or chronic issues
-Depression, weakness, anorexia, regenerative anemia, thrombocytopenia, splenomegaly

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Babesia gibsoni

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-Most commonly diagnosed cause of K9 babesiosis
-Most common in pit bull
-Tick vector unknown
-MIsdiagnosed as idiopathic or IMHA

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Babesia conradae

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-Mixed breeds
-Common in CA
-Tick vector unknown

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Babesia sp

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-AKA small babesia
-Tick vector unknown
-Very little known

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Pathology and clinical signs of babesia

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-Hemolytic anemia: RBC damage, hemolysis, anemia, ischemic tissue injury
-Hypotensive shock syndrome, fluid shift from interstitial to intravascular compartments
-"Sick dog syndrome", fever, lethargy, anorexia, pale
-Icterus, lymphadenomegaly, splenomegaly
-THROMBOCYTOPENIA

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Babeia detection

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-Blood smear (won't help you determine which species)
-PCR (method of choice)

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Treatment outcomes of babesia

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-Complete cure
-Subclinical carrier
-Partial recovery
-Relapse

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Types of Babesia that can be transmitted transtadially

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All but B. bovis

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Babesia transovarial transmission within the tick

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-B. bigemina
-B. bovis
-B. canis vogeli
-B. caballi

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Bovine babesiosis species of importance and hosts

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B. bigemina
B. bovis
texas cattle fever, Redwater
Rhicephalus annulatus and microplus

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Clinical signs of Bovine Babesiosis

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-Acute dz 3-7 days
-High fever more likely with B. bovis
-Anorexia, depression, rough coat, rumen atony, dyspnea, tachypnea, anemia, ictuerus, hemoglobinuria (B. bigemina)

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Detection of Bovine Babesiosis

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-Appropriate ticks on animals
-Infected erythrocytes on blood or brain smears
-Piriform, round, ring shaped, pear bodies joined at acute angles
REPORTABLE

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Causes of Equine piroplasmosis

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-In Texas: amblyomma cajennense (dermacentor nitens)
-Outside of Texas: Iatrogenic from blood transfusions
-Also, but less frequently: dermacentor variablilis and Rhicepalus microplus

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Types of Equine piroplasmosis

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-B. caballi
-B. equi
(both have transtadial transmission)
Both considered eradicated in US

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Transovarial transmission of Equine Piroplasmosis

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-B. caballi

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Testing for Equine piroplasmosis

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-Need a negative test for racetrack: Any vet lab
-Clinical signs present: Ames, IA NVSL
-Serology
-Positive horse quarantined or euthanized

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Equine piroplasmosis clinical signs

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-Destruction of RBCs, anemia
-Fever
-Icterus
-Splenomegaly

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Giardia life cycle

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Reproduces in brush border of jejunum-->Ea trophozoite lays down cell wall-->divides in 2 (binary fission)-->cyst w/2 in feces-->ingested (from water or feed)-->2 trophozoite come out of cysts and go through repro.-->sit on top of epith cells-->some can come out in feces, but won't survive w/o cyst
-PPP 5-16 days

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Giardia pathogenesis and clinical signs

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-Villus atrophy and crypt hyperplasia-->decreased absorpitve area for water, glucose, sodium
-Does not invade cells
-Signs may be absent in ruminants
-Diarrhea, Wt loss
-Dogs may have acute or chronic intermittent foul smelling fatty diarrhea, dehydration and anorexia

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Giardia detection

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-Wet, direct smear within 20 min
-Trophozoines detected in unstained prep
-Lugol's iodine kills organism, but it stains better
-Fecal centrifugation with zinc sulfate
for cyst
-ELISA (antigen in feces)
-Immunoflourescence
-PCRs
-False negatives are common with all of these

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Host associated giardia types

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A/B: Humans, dogs, cats
C/D: Dogs (rarely in humans)
E: Ruminants and pigs
F: Cats (rare in humans)
G: Rodents
H: Marine mammals

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Tritrichomonas foetus

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Worldwide distribution
-Cattle (venereal dz)
-Swine (nasal sinuses GI tract)
-Cats (waxing and waning large bowel D)