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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?

-Eimeria


-Cystoisospora


-Toxoplasma


-Neospora


-Sarcocystis

What are the blood coccidia species?

Heaptazoon


Babesia


Cytauxzoon

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


-Trimethoprin-sulfadiazine


-Clindamycin


-Pyrimethamine

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?

No

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

Babesia


Theileria


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

Pyrexia


hemoglobinuria


anemia


icterus


splenomegaly

Babesia Disease in Dogs

pyrexiaanemia


thrombocytopenia


splenomegaly


lymphadenomegaly


dysorexia


vomiting


lethargy

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

13ish

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

hypothermia


recumbent


comatose


vocalization



immediately prior to death



Cytauxzoon felis Diagnosis methods

Hematology


Clinical Chemistry


Parasites detected in host cells

Cytauxzoon felis: Hematology

leukopenia with left shift and toxic change of neutrophils



thrombocytopenia



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

Cytauxzoon felis: Clinical Chemistry

HypERbilirubinemia


hypERglycemia



hypOalbuminemia


hypOkalemia



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

Babesia canis



pear shaped and larger

Babesia gibsoni



oval/round, smaller, and signet ring formation

Babesia

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?

Immunologically


Biologically:


-predominantly indirect lifecycle


- ingestion of tissue cysts in IH


Epidemiologically


-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


-fetuses/placenta

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


-clindamycin


-trimethoprim

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


-toltrazuril


- 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?

No

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


etc

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


(schizogony)


- 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


-amprolium


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?

Opossum


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?

Horses!



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

Serology



-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?



Protozoan

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





How does Giardia cause disease?



Protozoan

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?



Protozoan

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

Giardia


Tritrichomonas foetis



They are intestinal

What are the intestinal Coccidia protozoans

Eimeria


Isospora


Toxoplasma


Sarcocystis

What are the blood Coccidia protozoans

Babesia


Cytauxzoon

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


Flatulence



*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

Humans


livestock


dogs


cats


beavers


guinea pigs


slow loris

Giardia Genotype Assemblage B: Host range

Humans


Slow loris


chinchillas


dogs


beavers


rats


siamang

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?

Everywhere


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



Immunoassay

Treatment of Giardia

Supportive care


Restore electrolyte balance


Ensure nutrition


Panacur


Metronidazole



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


Ronidazole


Metronidazole



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


-Infertility


-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?

Trypanosomes



family members well known for causing African Sleeping Sickness

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

Trypomastigoate


-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


then


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



OR



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


mega-esophagus


meg-colon

Trypanosoma cruzi: Acute Disease Signs in Dogs

Lymphadenopathy


myocarditis


pale MM


tachycardia


splenomegaly

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


-lymphadenopathy


-tachycardia


-ascites


-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:


-lymphadenopathy


-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?

Serology/PCR


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

Age


Nutrition


Stress


Sex


Season


Gestation status


etc

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

Chemoprophylaxis


-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?

Intestinal

Cystoisopora: Lifecycle and route of infection

Faculative Direct/Indirect lifecycle


-ingestion of sporulated oocysts


-2 sporocytes each with 4 sporozoites

Cystoisopora: DH

Cats


Dogs


Pigs


Some birds


Cystoisopora: Paratenic hosts

Mice


Birds


Rodents

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

Isospora

Cystoisopora species in dogs

C. canis


-teardrop shaped


40 x 30 micrometers



C. ohioenis


-round


~25 micrometers in diameter

Cystoisopora species in cats

C. felis


-Teardrop shaped


40x 30 micrometers



C. rivolta


-Round


~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?

NOTICE the DIFFERENCES from GIARDIA!



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

Giardia

Giardia

Giardia

Giardia

Giardia

Tritrichomonas

Tritrichomonas

Tritrichomonas


Trypanosome

Trypanosome

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



Trypanosoma

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

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

Eimeria



in goat

Eimeria

Eimeria oocysts

Eimeria mascusaniensis



llama

Sporulated Eimeria oocyst

Sporulated Eimeria oocyst

Cystoisopora

Cystoisopora

Cystoisopora

Cystoisopora

Cryptosporidium

Cryptosporidium

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



PCR



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

Toxoplasmosis

Toxoplasmosis

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

Seronegative

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