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305 Cards in this Set

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Disease is associated with what in Hepatozoonosis

With infection by Haemogregarine parasiotes in genus Hepatozoon

Hepatozoons host range

is broad among vertebrates (~46 species)

Largest distribution of species is in reptiles ( over 120 species in snakes!)

Hepatozoon disease results from?

ASEXUAL replication of the parasite in leukocytes in bone marrow, spleen, and to a lesser extent the liver of the intermediate host

What is the DH for hepatozoons?

Ticks are the DH

This is where sexual reproduction occurs

How are dogs infected by hapatozoons generally?

Ingestion of ticks with mature oocysts in the hemocel

What are the intestinal coccidia species?






What are the blood coccidia species?




Hepatozoon canis

One World Hepatozoonosis

In general

-Long term host association: world wide distribution

- disease in infected dogs is milder compared with H. americanum

Is there any immunity with hepatozoon canis?

What are the signs of disease in natural infections?

-Age associated immunity:

>4-6 months old apper resistant to experimental infections

-naturally infected dogs in US are generally asymptomatic

How do dogs obtain Hepatozoon canis

and what is the typical lifecycle?

Ingestion of oocysts in infected Rhicephalus sanguinensis

Meronts replicate asexually in bone marrow

ticks infected by ingestion of gamon ts in circulating neutrophils by 3 weeks post infection

What are the signs of Hepatozoon canis in xperimentally infected dogs?

transient fever, skeletal pain, and recumbency

But, there were low levels of parasitemia except in severe cases with 100% of neutrophils infected

Hepatozoon americanum is?

a distinct species confirmed b y PCR sequence analysis

How are dogs infected by Hepatozoon americanum?

Ingestion of infected Amblyomma maculatum

transmission by paratenic host

How is the disease of Hepatozoon americanum in comparison to Hepatozoon canis?

It has a relatively recent history with dogs

previous association with unknown vertebrate host

disease is more severe compared to H. canis

Where do Hepatozoon americanum Meronts replicate

Asexually replicate in host cells in striated muscle

-developing organisms (merogony) are protected from host immunity while in cyst

-free merozoites elicit a pyogranulomatous inflammatory response

Clinical Disease of Hepatozoon americanum

-Fever, lethargy, mucopurluent ocular discharge

-neutrophilic leukocytosis and non-regenerative anemia

-Stiff gait, ascending progr3essive muscle weakness and atrophy of head muscles

Periosteal lesion and proliferation

Treatment of Hepatozoonosis

Lifeliong infection in dogs, so treatment is for control of disease and is not curative

Remission of clinical disease by combination therapy in 14 day regimen with TCP




Relapse with Hepatozoonosuis

Commin within 2-6 months

daily treatment with decoquinate protected against relapse in a 2 year study

Prevention of Hepatozoonosis

Avoidance of tick exposure and predation of paratenic hosts

Are Hapatozoons zoonotic?


General features of Bloodstream Coccidia Haemosporidia:

Disease, DH, IH transmission

Disease is associated with asexual replication in tissues and blood cells of mammalian intermediate hosts

Ticks are the definitive host where sexual reproduction occurs

Sporozoites transferred to IHs by the tick DH during the obligate blood meal

What are Piroplasms?

Pyriform, round, amoeboid or rod-shaped parasite stages seen in blood are termed "Piroplasms"

Bloodstream Coccidia Haemosporidia: 3 species



Cytauxzoon felis

Babesia: brief overview

Disease associated wirh non-regressive anemia from destruction of RBCs

Unlimited asexuaal replication

World-wide distribution with at least 18 species

Theileria: brief overview

Primarily African and Mediterranean distribution

East Coast Fever, Egyptian Fever, Etc

Disease associated with livestock

Cytauxzoon felis: Brief overview

Formerly known as Theileria felis

Disease associated with asexual replication in macrophages in the spleen and hepatic tissues

clog blood vessels and obstruct blood flow

almost universally fatal in domestic cats

Babesia is a _______ and occurs where and in what?

Babesia is a protozoan species occurring in the red blood cells of various vertebrate hosts

Babesia species in the dog

-B. canis

-B. gibsoni

-B. conradae (more pathogenic in the dog- may be zoonotic and associated with wildlife)

Babesia species in the cow

B. bigemina

B. bovis

Babesia species in the horse

B. caballi

Babesia species in the human

B. microti

B. conradae

-Ixodes scapularis, co-incident with Lyme Disease

Babesia is an etiologic agent of?

Texas Cattle Fever

-Controlled by dipping the "one-host" tick Rhipcephalus microplus

How are ticks infected with Babesia?

Ingesting the merozoites in the RBS of the vertebrate IH

What occurs inside the tick with babesia?

sexual reproduction occurs in the tick tissue with stages transovarially infecting tick offspring

How are the IH infected by Babesia?

Ticks during their obligate blood meal

Canine Babesiosis: B. canis

-Piroplasms are much larger

-4-5 micrometers and pear shaped

-world wide

-Rhipcephalus sanguinensis in US

-Associated with Greyhounds in florida (46% seroprevalence)

-relatively non-pathogenic except in puppies

Canine Babesiosis: B. gibsoni

-Piroplasm is smaller

-~3micrometers and round/oval

-Signet ring form is common

-US distribution

-Rhipcephalus sanguinensis

-Direct transmission from fighting

-dogs with fighting scars are 5x more likely to be positive

-subclinical to acutely fata

What causes disease with Babesia?

unlimited asexual multiplication of the parasite and its destruction of RBCs in the vertebrate host

-contrast with asexual disease process from intestinal coccidia infections

Babesia Disease in cattle






Babesia Disease in Dogs








Is Babesia zoonotic?

Potentially in dogs, wildlife, and people

Diagnosis of babesia

-demonstration of piroplasms in blood smear (host, site, morphology)

-Serology for IgG antibodies

-PCR testing and matching gene sequence data

Treatment of Babesia

-Previously Imidiocarb

-Recently, 10 day regimen of Azithromycin and Atovaquone

-Remission of clinical signs and removes parasites from blood

-Animals are asymptomatic carrier for life!

Babesia infected animals should avoid

splenectomy and immunosuppressive therapies

and avoid using them as a blood donor

Prevention of babesia

tick control

quick tick removal

avoid contact fighting with known carriers....or fighting in general?

What is Cytauxzoon felis?

An Intracellular Haemoprotozoan parasite in wild and domestic Felidae

When and where was Cytauxzoon felis first reported?

in domestic cats from MO in 1979

Where is Cytauxzoon felis distributed?

Throughout the central, south-central and south eastern US

What is the disease cause by in Cytauxzoon felis

Disease in domestic cats associated with asexual replication (schizogony) in macrophages in spleen and hepatic tissues

What do the blood cells do in Cytauxzoon felis

Engorged leukocytes adhere to the walls in the lumen of veins in various organs

-obstruction of blood flow

-tissue ischemia

What do Schizonts do in Cytauxzoon felis

They develop into merozoites and rupture host cells to infect RBCs

How is Cytauxzoon felis prasitemia detectable?

It is detectable in stained blood smear

late stage disease with eminent death

What are natural asymptomatic hosts for Cytauxzoon felis?

Bobcats (Lynx rufus)

Intermediate Host role in Cytauxzoon felis

Rick implied from direct SQ inoculation of infected bobcat blood into domestic cat

What is odd about Cytauxzoon felis

Nonfatal persistent parasitemia without schizogony 6 months post infection

What is a competent vector for transmission of Cytauxzoon felis?

Amblyomma americanum

Dermacenter varriabilis in Cytauxzoon felis

demonstrated experimentally as host for transmission to domestic cats

nymphs fed on infected bobcats, allowed to molt, adult ticks fed on domestic cats, produced clinical signs at 13-17 days post tick engorgement

Clinical signs show up around ___________ days with Cytauxzoon felis disease


What is only found in wild Amblyomma americanum

Cytauxzoon felis

Cats infected with Cytauxzoon felis often:

exhibit non-specific signs of disease: acute lethargy, depression, anorexia

-icteric with pale MM, dehydrated, polydipsi

-have recent history of disappearance from residence

Advancedd cases of Cytauxzoon felis may be:

dyspenic with radiographic evidence of severe bronchointerstitial pulmonary disease

Less frequently observed: splenomegaly and hepatomegaly

What is often coincident with parasitemia of Cytauxzoon felis?

Pyrexia (103-107)

Signs of terminal disease with Cytauxzoon felis





immediately prior to death

Cytauxzoon felis Diagnosis methods


Clinical Chemistry

Parasites detected in host cells

Cytauxzoon felis: Hematology

leukopenia with left shift and toxic change of neutrophils


normocytic, normochromic, non-regenerative anemia (immune-mediated destruction of parasitized RBCs

Cytauxzoon felis: Clinical Chemistry





elevated ALT activity

Cytauxzoon felis: parasites detected in host

piroplasms in RBCs

Schizonts in macrophages

Cytauxzoon felis: Tickborne parasitic disease

obligate relationship with ticks and the bobcat reservoir

Cytauxzoon felis: prognosis and treatment

used to be considered 100% fatal

mixed results with imidocarb and diminazene

some cats are surviving with atovaquone and azithromycin

Successful treatment of Cytauxzoon felis is related to

initiation "when in the disease process"

goal is to shut down asexual reproduction

tx initiated in early tsages of disease has greater likelihood of successed

When should treatment be initiated with Cytauxzoon felis

for any cat with outdoor access presenting with acute lethargy and other classical signs from march to october

submit blood for confirmation

Cytauxzoon felis prevention

Prevention has more promise than cure

tick control in cats

keep cats indoors and be observant of acute disease between march and october

hepatozoon americanum

hepatozoon americanum in canine muscle

Hepatozoon americanum

classic onion peel cyst containing the merozoite stage

hepatozoon americanum in WBC

hepatozoon americanum in blood


Babesia canis

pear shaped and larger

Babesia gibsoni

oval/round, smaller, and signet ring formation


Cytauxzoon felis

Cytauxzoon felis

Cytauxzoon felis in blood cells

Cat demonstrating Cytauxzoon felis

Cytauxzoon felis

Cytauxzoon felis in blood

What is neospora caninum

intercellular parasite of dogs, domestic livestock, and grazing wildlife

What is the DH for Neospora caninum

Domestic and wild dogs

only host with sexual multiplication

Shed oocysts sporadically, small number per gram of feces

Where do Neospora caninum oocysts live

in the DH's small intestinal epithelium

What stages of Neospora caninum are found in the tissues of the IH and DH

Tachyzoites and Bradyzoites

Neospora caninum is morphologically similar to what?

T. gondii

BUT different!

How is Neospora caninum different?



-predominantly indirect lifecycle

- ingestion of tissue cysts in IH


-Not zoonotic

-Significant in cattle production

What does Neospora caninum use as an IH and what routes of infection does it use?

Domestic livestock, grazing wildlife, and dogs

-only competent IH

-viable parasites capable of in vivo passage

-infected by oocysts

-vertical transmission

Symptoms of disease in Neospora caninum

Neuromuscular disease in canines

-congenital infection

-asymptomatic at birth with clinical disease after 3 weeks

-posterior paresis

Serologic prevalence of neospora caninum

Pet dogs: 3%

Stray dogs: 23%

Farm dogs: 51%

exposure to cattle


Neospora caninum's significance in cattle

reproductive disease

-history of abortion? cow is 2x more likely to be seropositive

-Disease of placenta/fetus

-primary infection in dam

-recrudescence of chronic infection

-neuromuscular disease in congenitally infected calves

Cattle management with Neospora caninum

Dairy cattle are 3 times more likely to be seropositive than beef cattle

Dairy heifer x 8.59 compared to beef heifer

Stocking density

- 0.8 head/hectare (Beef)

- 1.5 head/hectare (Dairy)

Neospora caninum: economic impact

-Primarily Reproduction

-Epidemic "abortion storms" most devastating

-Culling and replacement of breeding stock

-Weight gain/Milk yield do not show clear cut association (production losses when cows miss entire lactation cycle

Neospora caninum tissue cyst in fetal cow brain

Neospora caninum

Neospora caninum Tachyzoites in cattle tissue by IFA

Treatment of Neospora caninum in dogs

No FDA approved curative Tx

Mortality in dogs with and without Tx



Prevention of Neospora caninum in dogs

do not allow access to fetal or placental tissues

do not feed raw meat

do not breed females previously diagnosed with clinical disease or whelped litters with affected puppies

avoid immunosuppressive therapies in seropositive dogs

Treatment of Neospora caninum in cattle

No FDA approved Tx


- vaccine withdrawn from market

Prevention of Neospora caninum in cattle

- restrict dog access to cattle feed and facilities

-be especially observant for signs of reproductive loss in herd

- keep records on herd productivity

-remove fetal/placental tissues promptly dispose in biosecure manner

make an effort to keep a close herd

cull seropositive cows (controversial)

Serological assessment if outbreak is suspected

Neospora caninum's lifecycle

Obligate indirect

-oocyst transmission to DH appears insignificant

-Viable tissue cysts in narrow range of IHs (grazing hoof stock)

Is Neospora caninum zoonotic?


Neospora infected animals have a lifelong risk of?

Lifetime risk of congenital infection

-vertical transmission to offspring important for maintenance of parasite lifecycle

What type of lifecycle do Sarcocystis sp. have?

Obligate indirect lifecycle

-ingestion of tissue cysts in specific intermediate hosts

Sheep: dog

Cow: dog


Sarcocystis sexual replication

Dogs and cats (domestic and wild)

-only host where sexual multiplication occurs

-sexual reproduction occurs in the small intestine

-sporocysts with 4 sporozoites on fecal flotation

Sarcocystis treatment in cats and dogs

no clinical signs, so no treatment necessary

Other animal's roles in Sarcocystis sp.

-Domestic livestock, birds, grazing wildlife, birds

-IH with asexual replication in striated muscle or endothelial cells, disease only in IH

-Production losses may be associated with infection

-Equines accidental host for S. neurona (EPM)

Opossum and other various warm blooded mammals ( natural IH)

Sarcocystis cruzi:

lifecycle, DH, and IH

Obligate indirect lifecycle

Dogs: DH

Cattle: IH

Sarcocystis cruzi: route of infection

Dogs ingest tissue cysts in cattle, sporocysts in feces ~2 weeks post infection

Cattle: infected by sporocysts while grazing

2 generations of asexual replication


- vascular endothelia of mesenteric arterioles and lymph nodes

-endothelial tissues of organs

-development of infective stage "sarcocysts" in striated muscle fibers

Sarcocystis: Adverse health effects

-Most infections are asymptomatic

-Adverse health effects

* abortion, still birth, eosinophilic myositis

* necrotic encephalitis in 2 heifers

* Fever, anorexia, diarrhea, muscle

spasm, loss of tail hair, hyperexcitability

* Cachexia, weakness, decreased milk yield (cows)

-Calves that survive acute infection fail to thrive, premature death in cachectic state


Sarcocystis cruzi: Treatment

Treatment of infected hoof stock and not economically practical


Sarcocystis cruzi: Prevention

Risk mitigation by excluding dogs from production facilities, keep ration covered to prevent fecal contamination

Periodic fecal examination of dogs to monitor sporocyst shedding

Equine Protozoaa Myloencephalitis is caused by?

Primary etiologic agent is Sarcocystis neurona

What other species are involved, in a minor degree, with Equine Protozoa Myloencephalitis

Neospora hughesi

Sarcocystis fayeri

What is the DH of Sarcocytis neurona?


with sporocytes in feces

What are the IHs of Sarcocystis neurona?

Select mammals

isolate tissue cysts for in vivo passage to other hosts

Who are the accidental/aberrant hosts of Sarocystis neurona?


tissue cysts are not viable

Infection by ingestion of sporocytes in contaminated feed/pasture

Equine Protozoa Myloencephalitis: Sarcocystis neurona: Clinical Signs

Neurologic disease

-stumbling, ataxia, incoordination, lameness

-paresis, muscle atrophy, recumbency

-diaphoresis, urinary incontinence, constipaation

Equine Protozoa Myloencephalitis: Sarcocystis neurona: Diagnosis


-IgG antibodies

-IFA testing to distinguish EPM caused by S. neurona or N. hughesi

Equine Protozoa Myloencephalitis: Sarcocystis neurona: Seropositivity

does NOT equate to disease

-infection widespread

-Disease, EPM, is rare

-May be an indication of risk to subsequently developing disease

Equine Protozoa Myloencephalitis: Sarcocystis neurona: Distribution

EPM and distribution of S. neurona endemic to N and S America (follows range of Opossum DH)

Occurrence in Europe, Asia, Africa traced back to American origin horses

Seroprevalence in 30-50% of tested horses via USDA stats

Equine Protozoa Myloencephalitis: Sarcocystis neurona: Likelihood of clinical disease

EPM is sporadic with less than 1% of infected horses developing clinical disease

it is rare to have outbreaks involving multiple horses on the same farn

Equine Protozoa Myloencephalitis: Sarcocystis neurona: Serology

Serologic phenotypes are associated with disease potential and response to treatment

-SAG 1 ~93% of neurovirulent isolates, non responsive to Tx

-SAG 5 ~7% neurovirulent, non responsive

- SAG 6 neurovirulent in sea otters, ataxic horses respond to Tx

Equine Protozoa Myloencephalitis: Sarcocystis neurona: Treatment Goals

Recognition of phenotypes and response to Tx is promising

Goal is to contain parasite replication and isnt curative

prophylactic drug use is questionable and expensive

Equine Protozoa Myloencephalitis: Sarcocystis neurona: Treatment Drugs

Ponazuril: targets mitochondria to disrupt amin acid synthesis and energy metabolism, crosses blood-brain barrier into CSF

Sulfadiazine/Pyrimethamine: interferes with the parasite's ability to make folic acid and inhibits energy metabolism. It is possible to have a toxicity with the drug after long term use: anemia and bone marrow suppression. You must replace folic acid deficiency in host with supplements

Tissue Cyst forming Coccidia of Minor Importance: Hammondia spp

Hammondia spp

-H. heydorni (dogs)

-H. hammondi (cats)

~10 micrometer oocysts indistinguishable from Neospora caninum or T. gondii

Obligate 2 host llifecycle with TRUE IH

Tissue Cyst forming Coccidia of Minor Importance: Besnoitia

Cats are DH for various species

Oocysts resemble T. gondii

Tissue cysts in various IH, disease produced by asexual replication

B. bennetti important sounrce of disease in donkeys

What parasitic disease is this horse displaying?

What parasitic disease is this horse displaying?

Equine Protozoa Myloencephalitis from Sarcoystis neurona

Cross Section of spinal cord with focal necrosis from Sarcoystis neurona

Sarcoystis neurona

Spinal cord with infected neuron; small dots are merozoites

Sarcoystis neurona

Sarcoystis neurona

High magnification view of meronts

Sarcoystis neurona

Experimentally infected mouse brain with antibody stained meronts

Sarcoystis neurona

Schizonts in cell culture

Sarcoystis neurona

Mature sarcocyst in tissue

Sarcoystis neurona

Sarcocyst in tissue

Sarcoystis neurona

Live, unstained sarcocyst

Two sporocysts from Sarcoystis neurona

General features of Protozoans

-Single celled organisms

-microscopic and small

-Parasitic in ALL vertebrate hosts

-Variable lifecycles (direct, Ob indirect, Fac indirect

What is a Trophozoite?

The living, motile form of a protozoan

What is a cyst/oocyst?

The environmental transmissible form of a protozoan

What is reproduction in protozoans based on?

Like what methods can they utilize?

Asexual- simple division

Sexual- genetic recombination

Combination/alteration involving both modes

Newly defined- allelic sequence heterogeneity

How do Ameoba's cause disease?


They feed on solid tissues directly or after liquefying them (amoebas)

How does Giardia cause disease?


Compete with the host for ingested food: absorb nutrients through the body wall and block absorptive capacity of the host's GI tract

How do coccidia and malaria cause disease?


Destroy hosts cells by growing in them

Other methods of causing disease with protozoans

production of various toxic substances that aid in their ability to enter host tissues, feed, or reproduce: hemolysis, histolysins, anticoagulants

cause various host reactions such as allergic, inflammatory, hyperplasia, and thrombocytopenia

Reduce host resistance to other disease and parasites

What are the Major Protozoan Groups

Flagellates and Coccidia (class: Sporozoa)

What are the 2 protozoan flagellates


Tritrichomonas foetis

They are intestinal

What are the intestinal Coccidia protozoans





What are the blood Coccidia protozoans



What is Giardia primarily associated with?

-Waterborne outbreaks

(swimming pools, water slides, sewage)

-Daycare centers

-Occupational Risk

-Outdoor recreation

-Travel outside of US

Describe Giardia's lifecycle

Direct lifecycle

trophozoites multiply by binary fission in lumen of proximal small intestine, they live freely (extracellularly) or attach by their ventral sucking disk

Host infection via fecal-oral contamination and ingestion of cysts

How long does it take to start shedding Giardia cysts?

Cysts passed in the feces following a 7 to 14 day inocubation period

The two types of Giardia infection:

Symptomatic and Asymptomatic

Symptomatic Giardia infections: Signs

In dogs and cats:

Watery diarrhea in acute phase (~5 days post infection)

Voluminous, malodorous stools with mushy consistency


*Cysts appear in stools 7-14 days post infection

How long do clinical signs last with Symptomatic Giardia infections

They may persist for 2-6 weeks before resolution in immunocompetent animalls

source for infection to other suseptible pets or animals in the household

Symptomatic Giardia infections: Human Symptoims

Voluminous watery diarrhea

gas, greasy stools that float

abdominal discomfort, anorexia, nausea, vomiting, weight loss, fatigue

Symptoms appear 7-14 days PI

Illness duration is 2-6 weeks (may be self limiting if immunocompetent

Giardia Genotype Assemblage A: Host range






guinea pigs

slow loris

Giardia Genotype Assemblage B: Host range


Slow loris






Other Giardia Genotypes and hosts

Assemblage C and D: DOGS, not in humans in the US

E: livestock cattle, goats, pigs, sheep, alpaca

F: Cats

Where can Giardia be found?


Widespread in the US

States with over 20 cases/100,000 population in every region

estimated incidence is difficult to establish (passive survelliance)

Who is at risk for Giardia?

Prevalence in daycare children and their parents

daycare workers, backpackers, people who drink from shallow wells, and veterinary personnel

Animals in shelters, boarding kennels, multi-animal situations facilitate spread from infected asymptomatic animals to susceptible hosts

How do you Diagnose Giardia?

Diagnosis by ZnSO₄

take fecal samples on 3 consecutive days (reveals 90% of all infections)

Giardia SNAP in combo with flotation may help

Direct smear is only useful for samples with diarrhea


Treatment of Giardia

Supportive care

Restore electrolyte balance

Ensure nutrition



Bathe a pet at beginning of treatment protocol to remove immediately infective cysts

How does one disinfect after Giardia has been around?

Disinfection of pet residential environment

-Chlorine bleach at high concentration (1:16) effective

Lysol at 2-5%

Quaternary ammonia compounds also effective when diluted )1:320) and with lower contact time

Giardia: Immunoassay

GSA- 85 in feces

ID ~60% of cyst negative stools

Micro-plate and cassette formats

Sensitivity > 95% overall

What is Tritrichomonas blagburni

Flagellate protozoan parasite in large intestines of cats

-formerly known as T. foetus (in cattle)

-molecular genetics confirm identity as distinct species

What does Tritrichomonas blagburni cause?

Chronic diarrhea

-long duration (weeks, months, years)

otherwise the cat is healthy

fecal incontinence is cause for owner surrender and euthanasia

Lymphoplasmacytic/neutrophilic colitis, crypt abcess, increased mucous production, generalized erosion of colonic mucosa

Tritrichomonas blagburni: suspected risk factors

Residence in cattery

Coccidiosis as adult cat

smaller square footage of housing per cat

Tritrichomonas blagburni: Diagnosis

Microscopically by direct smear ( Must differentiate from Giardia)

PCR specific assay to identify organism isolated from infected animals

Fecal culture and isolation in commercially available media will increase sensitivity

Tritrichomonas blagburni: Treatment

No FDA approved therapy



Reversible neurotoxicity with both drugs has been reported

Impairment of DNA function by strand breakage and loss of helical function

Tritrichomonas blagburni: Prevention

Suspected transmission between hosts by fecal-oral route

No environmentally resistant cyst stage

Trophozoites may survive out of host for variable times (Water:30-60 min, Urine over 180 min, Canned cat food up to 180 min)

Segregate infected cats, separate litter bozes, etc

Tritrichomonas blagburni: Is it Zoonotic?

It is not known to be

Humans/Dogs may share closely related Pentatrichomonas hominis

Tritrichomonas foetus: What is it?

A flagellate protozoan parasite in the reproduction tract of cattle

Tritrichomonas foetus: What is it morphologically indistinguishable from?

T. blagburni and other Trichomonad protozoa

What does Tritrichomonas foetus cause?

Bovine genital trichomoniasis


-Spontaneous abortion in 1st trimester

-Generalized reproductive tract infection

Tritrichomonas foetus: Who are responsible for herd infection?

Culls are generally asmyptomatic and responsible for herd-level infections

-Prevalence has decreased with use of artificial insemination

-Breeding bulls entering TN must have certificate of Veterinary inspection

How do you diagnose Tritrichomonas foetus

PCR and culture methods

Tissue and blood flagellates are broadly classified as?

What do its relatives cause?


family members well known for causing African Sleeping Sickness

Trypanosomes: Flagellate trophozoite stage circulating in blood/lymph is known as


-infective for the vertebrate host

-other stages are developmental in the arthropod IH

Trypanosomes: Classification by Modes of Transmission

Anterior Station, Salivarian: bite of infected "Teste Fly"

Posterior Station, Sectorian: feeding Rejuvidae bugs defecate and pass parasites

How are Arthropods infected with Trypanosomes

They become infected during a blood meal

What happens within the Arthropod IH ith Trypanosomes

Epimastigotes divide and multiply in IH


develop into Trypomastigoates

Where do Trypanosomes replicate?

within the human or animal host

African Trypanosomiasis

Different species involved

live in blood, invade lymph nodes and intercellular spaces

Generally produce anemia from immune-mediated processes and mechanisms (depressed erythropoiesis, hyperplasia in bone marrow and spleen, erythrophagocytosis because trypanosome antigens attach to RBCs)

Animal production is limited to areas where disease is not prevalent

Trypanosoma cruzi: What does it cause?

Chaga's Disease


American Trypanosomiasis

Trypanosoma cruzi: Naturally endemic where?

Central and South America

Recent cases in US

-border region, TX, OK, LA, TN

-Hunting dogs in VA

Trypanosoma cruzi: Obligate IH

Triatomin/Reduviid bugs

Other animals playing a reservoir role with Trypanosoma cruzi?

Opossums, Raccoons, and Armadillos

Trypanosoma cruzi: Romana's sign

Edema and inflammatory response resulting from trypomastigotes that have defected on host and it has been rubbed into the eye

Trypanosoma cruzi: Proliferation and severity

Trypomastigotes proliferate asexually in histocytes as amastigote stage organisms

Spread by the lymphatics and enter tissues and continue to proliferative

Disease process may be acute with death 2-4 weeks post infection

Trypanosoma cruzi: Chronic infection

Myocardial disease



Trypanosoma cruzi: Acute Disease Signs in Dogs



pale MM



Trypanosoma cruzi:: Diagnosis

Serology and PCR

Trypanosoma cruzi: Treatment

No effective therapeutic intervention

Leishmania sp. infect what?

They are parasites infecting macrophages of vertebrate hosts

Leishmania sp: Stage importance

how is it transmitted and where does it undergo development

Amastigote stages only!

-developmental stages occur in the Sand Fly

-Transmitted by fly bite

Which Leishmania species are associated with visceral disease?

L. donovoni

L. infantum

-amastigotes proliferate in macrophages and tissues, typically fatal

Which Leishmania specie is associated with muco-cutaneous disease?

L. mexicana (New World)

Which Leishmania specie is associated with cutaneous disease?

L. tropica (old world)

Leishmania species that effect dogs

Dogs are significant hosts for the parasite in endemic localities

Mediterranean (L. infantum)

Brazil (L. chagasi)

Leishmania: Disease in the dog

Severe cutaneous manifestation of disease

proliferation in visceral tissue in advanced cases

Leishmania: Treatment in dog

Antimony therapy pursued in Europe, must be long term to prevent relapse

Brazil has not attempted treatment due to public health concerns (significant reservoir for human infection, control based on culling)

Leishmania: Dog outbreaks in US

1st reported in Oklahoma in the 19802

Ohio in 1988

New York Hunt Club in 1999

Va Tech developed diagnostic PCR based protocol for additional investigations (suspected prenatal transmission based on experimental infection, Direct contact with cutaneous lesions also possible)

Leishmania: Possible dog prevention

Spot-on/ permethrin flea control products have repellent properties for flies

overall low prevalence of infection raises issue of actual risk in US

Leishmania must be differentials for T. cruiz

T. cruiz

presenting with symptoms of cardiac disease and infection including




-hepato/spleno megaly

Residence and travel history that includes centrl and south america

outdoor residence with hunting dogs

association with kissing bugs

Leishmania infection should be on the differential diagnosis for dogs that are

presenting with symptoms of dermatologic disease and infection including:


-hepato/spleno megaly

Residence and travel history that includes central and south america, europe, particularly the mediterranean region

How does one confirm a diagnosis of Leishmania?


isolation of organism by biopsy

Eimeria sp: Lifecycle, route of infection

Direct lifecycle

ingestion of sporulated oocysts

4 sporocysts each with 2 sporozoites

Eimeria: DH

Domestic livestock, birds, grazing wildlife

Eimeria: Replication type and site

Asexual replication in small intestine

Sexual reproduction in fresh uninfected cells of large intestine

Eimeria: How does it cause diarrhea?

Diarrhea is associated with destruction of enterocytes (2-3 asexual cycles)

Eimeria: What is the disease associated with?

Asexual replication in hosts tissues

Eimeria: Can an animal have negative fecal samples and still be sick?

Yes, large numbers of oocysts are common in fecal samples of healthy animals

Herd-wide prevalence can be as high as 50% without overt clinical disease

Eimeria Coccidiosis is a function of






Gestation status


Eimeria: Host immunity?

Host immunity with age and exposure

-premuntion (periodic challange of host)

-Generally species specific immunity

Eimeria: Risk of disease

Risk of disease is a function of environmental contamination, moderate levels of infection, and stress in the host population

Eimeria: Control

Environmental hygiene

-removal of manure, keeing surfaces dry and clean

-no practical form of disinfection because oocysts are hardy and resistant

-dehydration and direct sunlight

Eimeria: Treatment


-Targets the asexual stage of replication

-variety of drugs with different MOAs

All Tx decisions need to be based on holistic assessment of environmental contamination, health status of herd, risk of exxposure to susceptible hosts, and production goals

What type of coccidia is Cystoisopora?


Cystoisopora: Lifecycle and route of infection

Faculative Direct/Indirect lifecycle

-ingestion of sporulated oocysts

-2 sporocytes each with 4 sporozoites

Cystoisopora: DH




Some birds

Cystoisopora: Paratenic hosts




Cystoisopora: Where does replication occur?

Asexual/Sexual replication occurs in the small intestine

Cystoisopora: What is the diarrhea associated with?

Destruction of enterocytes (3 asexual cycles)

Cystoisopora: Prepatent Period

6-12 days

Cystoisopora is AKA


Cystoisopora species in dogs

C. canis

-teardrop shaped

40 x 30 micrometers

C. ohioenis


~25 micrometers in diameter

Cystoisopora species in cats

C. felis

-Teardrop shaped

40x 30 micrometers

C. rivolta


~25 micrometers in diameter

How do you diagnose Intestinal Coccidia infections

Diagnosis by either centrifugal ZnSO4 or Sucrose Flotation

Fecal on samples taken 3 consecutive days reveals 90% of all infections

Treatment type of Intestinal Coccidia infections

Supportive care, especially in young animals

Pharmacological Intestinal Coccidia Treatment in Dogs and Cats

Dogs: Albon

Cats: Trimethoprim Sulfadiazine

Both: Ponazuril

bathe at beginning of treatment and remove feces daily

Cryptosporidium spp. is associated with?


Waterborne activies, daycare centers, foodborne (homemade natural unpasturized apple cider/bottle water for pediatric colic), farm visits by school children, occupational risks

Cryptosporidium spp.: How many recognized species are there that are capable of infection

At least 15 different species capable of infecting over 115 mammalian hosts recognized from molecular taxonomic study

Cryptosporidium spp: host specificity

is variable

C. parvum most widespread readily infects humans, cattle, cats, dogs, deer, rabbits, etc

Cryptosporidium spp: tranmission

transmissibility of dog/cat/other species is poorly understood and could be dose dependent, rely on the host's immune status, etc

Cryptosporidium spp. Oocyst: When are they infective?

Oocysts of ALL species are passed in feces and are immediately infective and morphologically indistinguishable

Plus, they are able to survive in the environment and water treated by chlorine. Ew for public pools.

Cryptosporidium spp:

lifecycle, route of transmission, and types of infections

Direct lifecycle

-sexual and asexual replication occur in the small intestinal epithelium (inter-cellular)

-oocysts passed in the feces following 3 to 5 day incubation period

-host infection via fecal-oral route via contamination and ingestion of occysts

-infectious dose with as few as 9 oocysts

Asymptomatic and Symptomatic infections


Types of oocysts

1. Thick wall

2. Thin wall: never leaves host, moves down ailmentery tract and follow the autoinfection cycle

Causing a BAD disease in a SHORT amount of time

Cryptosporidium spp. Clinical Features of Symptomatic infections

Voluminous watery diarrhea

mucous present, rarel blood/leykocytes

abdominal discomfort, anorexia, nausea, vomiting, wt. loss, fatigue, fever

Mean illness duration 12 days (2-26)

may be self limiting if immunocompetent

IgA antibodies

19% of patients had positive stools for ~6.9 days following cessation of symptoms











Trypanosoma cruzi

From Trypanosoma cruzi

What is this bug and what is it associated with?

What is this bug and what is it associated with?

Reduviid bug


What parasitic infection could this woman be suffering from? What is this symptom called/.

What parasitic infection could this woman be suffering from? What is this symptom called/.

Romana's sign

from Trypanosoma cruzi


Leishmania, Human Disease

Leishmania: Dog Disease

Leishmania: In the dog

Eimeria bovis schizont (asxexual stages) in intestinal epithelial cell

Eimeria developing oocysts in goat intestinal epithelium


in goat


Eimeria oocysts

Eimeria mascusaniensis


Sporulated Eimeria oocyst

Sporulated Eimeria oocyst







Cryptosporidium oocysts are TINY

What is the treatment for Cryptosporidium?

In Adults: there are no consistently effective drugs

In pediatrics 1-11yrs: Nitazoxanide

it interferes with anaerobic energy metabolism

Crptosporidum spp.: Disinfection

Chlorine at swimming pool concentration levels are NOT effective

Ammonia compounds, ethylene oxide, methyl bromide, and ozone appear most effective

Hydrogen peroxide and formaldehyde containing compounds show promise with increased contact times

oocysts in milk and water killed by commercial pasteurization @ 71.7 degrees C for 5 seconds (NOT from the animal, but from other sources)

Toxoplasma gondii: Lifecycle

Faculative Direct/Indirect

Ingestion of sporulated oocysts

2 sporocysts with 4 sporozoites

Ingestion of tissue cysts

Toxoplasma gondii: DH

Cats (domestic and wild)

Only host where sexual replication occurs, and it happens in the small intestine

They shed oocysts only once

Infected for life, just only a one time shedding

Toxoplasma gondii: IH

Domestic livestock, birds, grazing wildlife, dogs, people all harbor it

Asexual replication in CNS (where disease occurs) and edible tissues

Toxoplasma gondii: Phases

Intestinal and Tissue (asexual) phases

Toxoplasma gondii: Intestinal phase clinical signs in the cat

Behaves like other coccidia

oocysts in stool

Diarrhea, soft stool, no real clinical signs

Toxoplasma gondii: Tissue phase clinical signs in the cat

Asexual replication causing

Respiratory disease: sneezing, light cough from intercellular replication of tachyzoites in lungs

Lymphadenopathy: Tachyzoites in lymph nodes and macrophages

Toxoplasma gondi oocysts

measuring ~12 micrometers on a cat fecal

Toxoplasma gondii

Tachyzoites in lymph node aspirate

Toxoplasma gondii

Bradyzoites in brain of an infected mouse

How can one diagnose Toxoplasma gondii? (4 main methods)

Fecal Exam: oocysts

Serologic testing: IFA, ELISA, MAT


Specimens: Serum, Fluids (CSF, Aqueous Humor, Amniotic), Tissue cysts (Biopsy and necropsy)

You can diagnose by tissue biopsy

LN aspirate in early stages

By the time it is in the chronic stage you may not see it,

Then necropsy become is the gold standard

Toxoplasma gondii: Zoonotic?

Yes, unequivocal zoonotic parasite

domestic and wild felidae are the primary sources for all infections

infectious oocysts are passed in the feces

Hiow does one become infected with toxoplasma gondii?

People and other intermediate hosts infected by oocysts or tissue stages

50% of cases are foodborne

Toxoplasma gondii: Public Health Significance

Congenital birth defects or abortion to fetus when mother acquires primary infection during pregnancy

Major cause of mortality for HIV and other immunocompromised persons

Toxoplasma and HIV

Toxoplasmic encephalitis and HIV: occurrence almost always causeed by reactivation of a chronic infection

Risk of TE decreased with introduction of primary prophylaxis against T. gondii and effective antiretroviral therapy

What is the congenital infection with T. gondii called



90% of infected babies appear normal at birth

between 55 and 85% develop problems months to years later (eye infections, hearing loss, learning disabilities)

Often asymptomatic until the second or third decade of life, when lesions develop in the eye.

What is also thought to be responsible for Congenital Toxoplasmosis

Food borne illness is mother is thought to be responsible for 2,000 of the 9,500 infants born in the US with congenital toxoplasmosis

How do you diagnose Toxoplasmosis?

-Serologic testing for IgG and IgM antibodies

-Observation of parasites in patient specimens (tissue biopsy and amniotic fluid) may be enhanced with immunohistochemical staining

-Isolation of parasites from blood or other body fluids by intraperitoneal inoculation into mice or tissue culture

-PCR for cogenital infections in utero

Treating Toxoplasmosis

Treatment should not be based on likelihood of cat exposure (ownership has not shown increase of risk)

Tx may or may not be indicated based on presence of active v. chronic disease, immune status, and site of infection

prevention of exposure and infection is most important way to mitigate disease potential for serologically negative pregnant women and immunocompromised.

Toxoplasma Recommendations

women should be testing prior to pregnancy

seronegative women to be tested regularly during prenatal exams

Positive IgM titers during preg need confirmation by additional PCR-AF test

Adverse health effects can be mitigated with appropriate therapy by early detection of infection

Household cats should be tested for Toxoplasma, but which cat is more problematic? Seronegative or positive


Cat litter boxes and Toxoplasma

should be dumped daily by a non-preg member of household

Pregnant women should avoid?

How should meat be prepared?

Veggies and fruits?

meat that is cooked less that well done

wash all fruits and vegetables

avoid gardening

Concerninbg Toxoplasmna and meat

Eat well cooked meat, esp. pork

do not sample before meat is well cooked

freeze meat for several days before cooking to reduce chance of infection