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305 Cards in this Set
- Front
- Back
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Disease is associated with what in Hepatozoonosis |
With infection by Haemogregarine parasiotes in genus Hepatozoon
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Hepatozoons host range |
is broad among vertebrates (~46 species) Largest distribution of species is in reptiles ( over 120 species in snakes!) |
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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 |
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What is the DH for hepatozoons? |
Ticks are the DH This is where sexual reproduction occurs |
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How are dogs infected by hapatozoons generally? |
Ingestion of ticks with mature oocysts in the hemocel |
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What are the intestinal coccidia species? |
-Eimeria -Cystoisospora -Toxoplasma -Neospora -Sarcocystis |
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What are the blood coccidia species? |
Heaptazoon Babesia Cytauxzoon |
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Hepatozoon canis One World Hepatozoonosis In general
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-Long term host association: world wide distribution
- disease in infected dogs is milder compared with H. americanum
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Is there any immunity with hepatozoon canis? What are the signs of disease in natural infections?
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-Age associated immunity:
>4-6 months old apper resistant to experimental infections
-naturally infected dogs in US are generally asymptomatic
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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 |
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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
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Hepatozoon americanum is? |
a distinct species confirmed b y PCR sequence analysis |
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How are dogs infected by Hepatozoon americanum? |
Ingestion of infected Amblyomma maculatum
transmission by paratenic host |
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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 |
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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 |
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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 |
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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 |
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Relapse with Hepatozoonosuis |
Commin within 2-6 months
daily treatment with decoquinate protected against relapse in a 2 year study
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Prevention of Hepatozoonosis |
Avoidance of tick exposure and predation of paratenic hosts
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Are Hapatozoons zoonotic? |
No |
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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
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What are Piroplasms? |
Pyriform, round, amoeboid or rod-shaped parasite stages seen in blood are termed "Piroplasms" |
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Bloodstream Coccidia Haemosporidia: 3 species |
Babesia Theileria Cytauxzoon felis |
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Babesia: brief overview |
Disease associated wirh non-regressive anemia from destruction of RBCs
Unlimited asexuaal replication
World-wide distribution with at least 18 species |
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Theileria: brief overview |
Primarily African and Mediterranean distribution
East Coast Fever, Egyptian Fever, Etc
Disease associated with livestock |
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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 |
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Babesia is a _______ and occurs where and in what? |
Babesia is a protozoan species occurring in the red blood cells of various vertebrate hosts |
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Babesia species in the dog |
-B. canis
-B. gibsoni
-B. conradae (more pathogenic in the dog- may be zoonotic and associated with wildlife) |
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Babesia species in the cow |
B. bigemina B. bovis |
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Babesia species in the horse |
B. caballi |
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Babesia species in the human |
B. microti B. conradae -Ixodes scapularis, co-incident with Lyme Disease |
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Babesia is an etiologic agent of? |
Texas Cattle Fever -Controlled by dipping the "one-host" tick Rhipcephalus microplus |
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How are ticks infected with Babesia? |
Ingesting the merozoites in the RBS of the vertebrate IH |
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What occurs inside the tick with babesia? |
sexual reproduction occurs in the tick tissue with stages transovarially infecting tick offspring |
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How are the IH infected by Babesia? |
Ticks during their obligate blood meal |
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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 |
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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 |
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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 |
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Babesia Disease in cattle |
Pyrexia hemoglobinuria anemia icterus splenomegaly |
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Babesia Disease in Dogs |
pyrexiaanemia thrombocytopenia splenomegaly lymphadenomegaly dysorexia vomiting lethargy |
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Is Babesia zoonotic? |
Potentially in dogs, wildlife, and people |
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Diagnosis of babesia |
-demonstration of piroplasms in blood smear (host, site, morphology)
-Serology for IgG antibodies
-PCR testing and matching gene sequence data |
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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! |
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Babesia infected animals should avoid |
splenectomy and immunosuppressive therapies
and avoid using them as a blood donor |
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Prevention of babesia |
tick control quick tick removal avoid contact fighting with known carriers....or fighting in general? |
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What is Cytauxzoon felis? |
An Intracellular Haemoprotozoan parasite in wild and domestic Felidae |
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When and where was Cytauxzoon felis first reported? |
in domestic cats from MO in 1979 |
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Where is Cytauxzoon felis distributed? |
Throughout the central, south-central and south eastern US |
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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 |
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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 |
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What do Schizonts do in Cytauxzoon felis |
They develop into merozoites and rupture host cells to infect RBCs |
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How is Cytauxzoon felis prasitemia detectable? |
It is detectable in stained blood smear late stage disease with eminent death |
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What are natural asymptomatic hosts for Cytauxzoon felis? |
Bobcats (Lynx rufus) |
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Intermediate Host role in Cytauxzoon felis |
Rick implied from direct SQ inoculation of infected bobcat blood into domestic cat |
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What is odd about Cytauxzoon felis |
Nonfatal persistent parasitemia without schizogony 6 months post infection |
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What is a competent vector for transmission of Cytauxzoon felis? |
Amblyomma americanum |
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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 |
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Clinical signs show up around ___________ days with Cytauxzoon felis disease |
13ish |
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What is only found in wild Amblyomma americanum |
Cytauxzoon felis |
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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 |
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Advancedd cases of Cytauxzoon felis may be: |
dyspenic with radiographic evidence of severe bronchointerstitial pulmonary disease
Less frequently observed: splenomegaly and hepatomegaly |
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What is often coincident with parasitemia of Cytauxzoon felis? |
Pyrexia (103-107) |
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Signs of terminal disease with Cytauxzoon felis |
hypothermia recumbent comatose vocalization
immediately prior to death
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Cytauxzoon felis Diagnosis methods |
Hematology Clinical Chemistry Parasites detected in host cells |
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Cytauxzoon felis: Hematology |
leukopenia with left shift and toxic change of neutrophils
thrombocytopenia
normocytic, normochromic, non-regenerative anemia (immune-mediated destruction of parasitized RBCs |
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Cytauxzoon felis: Clinical Chemistry |
HypERbilirubinemia hypERglycemia
hypOalbuminemia hypOkalemia
elevated ALT activity |
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Cytauxzoon felis: parasites detected in host |
piroplasms in RBCs Schizonts in macrophages |
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Cytauxzoon felis: Tickborne parasitic disease |
obligate relationship with ticks and the bobcat reservoir |
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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 |
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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 |
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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 |
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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
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hepatozoon americanum |
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hepatozoon americanum in canine muscle |
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Hepatozoon americanum
classic onion peel cyst containing the merozoite stage |
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hepatozoon americanum in WBC |
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hepatozoon americanum in blood |
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Babesia |
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Babesia canis
pear shaped and larger |
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Babesia gibsoni
oval/round, smaller, and signet ring formation |
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Babesia |
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Cytauxzoon felis |
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Cytauxzoon felis |
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Cytauxzoon felis in blood cells |
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Cat demonstrating Cytauxzoon felis |
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Cytauxzoon felis |
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Cytauxzoon felis in blood |
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What is neospora caninum |
intercellular parasite of dogs, domestic livestock, and grazing wildlife |
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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 |
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Where do Neospora caninum oocysts live |
in the DH's small intestinal epithelium |
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What stages of Neospora caninum are found in the tissues of the IH and DH |
Tachyzoites and Bradyzoites |
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Neospora caninum is morphologically similar to what? |
T. gondii
BUT different! |
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How is Neospora caninum different? |
Immunologically Biologically: -predominantly indirect lifecycle - ingestion of tissue cysts in IH Epidemiologically -Not zoonotic -Significant in cattle production |
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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 |
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Symptoms of disease in Neospora caninum |
Neuromuscular disease in canines -congenital infection -asymptomatic at birth with clinical disease after 3 weeks -posterior paresis |
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Serologic prevalence of neospora caninum |
Pet dogs: 3% Stray dogs: 23% Farm dogs: 51%
exposure to cattle -fetuses/placenta |
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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 |
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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) |
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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 |
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Neospora caninum tissue cyst in fetal cow brain |
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Neospora caninum |
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Neospora caninum Tachyzoites in cattle tissue by IFA |
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Treatment of Neospora caninum in dogs |
No FDA approved curative Tx
Mortality in dogs with and without Tx -clindamycin -trimethoprim |
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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 |
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Treatment of Neospora caninum in cattle |
No FDA approved Tx -toltrazuril - vaccine withdrawn from market |
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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 |
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Neospora caninum's lifecycle |
Obligate indirect
-oocyst transmission to DH appears insignificant -Viable tissue cysts in narrow range of IHs (grazing hoof stock) |
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Is Neospora caninum zoonotic? |
No |
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Neospora infected animals have a lifelong risk of? |
Lifetime risk of congenital infection
-vertical transmission to offspring important for maintenance of parasite lifecycle |
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What type of lifecycle do Sarcocystis sp. have? |
Obligate indirect lifecycle -ingestion of tissue cysts in specific intermediate hosts Sheep: dog Cow: dog etc |
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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
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Sarcocystis treatment in cats and dogs |
no clinical signs, so no treatment necessary |
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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) |
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Sarcocystis cruzi: lifecycle, DH, and IH |
Obligate indirect lifecycle
Dogs: DH Cattle: IH |
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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
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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 - |
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Sarcocystis cruzi: Treatment |
Treatment of infected hoof stock and not economically practical -amprolium
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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 |
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Equine Protozoaa Myloencephalitis is caused by? |
Primary etiologic agent is Sarcocystis neurona |
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What other species are involved, in a minor degree, with Equine Protozoa Myloencephalitis |
Neospora hughesi Sarcocystis fayeri |
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What is the DH of Sarcocytis neurona? |
Opossum with sporocytes in feces |
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What are the IHs of Sarcocystis neurona? |
Select mammals isolate tissue cysts for in vivo passage to other hosts |
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Who are the accidental/aberrant hosts of Sarocystis neurona? |
Horses!
tissue cysts are not viable
Infection by ingestion of sporocytes in contaminated feed/pasture |
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Equine Protozoa Myloencephalitis: Sarcocystis neurona: Clinical Signs |
Neurologic disease -stumbling, ataxia, incoordination, lameness -paresis, muscle atrophy, recumbency -diaphoresis, urinary incontinence, constipaation |
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Equine Protozoa Myloencephalitis: Sarcocystis neurona: Diagnosis |
Serology
-IgG antibodies -IFA testing to distinguish EPM caused by S. neurona or N. hughesi |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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What parasitic disease is this horse displaying? |
Equine Protozoa Myloencephalitis from Sarcoystis neurona |
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Cross Section of spinal cord with focal necrosis from Sarcoystis neurona |
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Sarcoystis neurona
Spinal cord with infected neuron; small dots are merozoites |
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Sarcoystis neurona |
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Sarcoystis neurona
High magnification view of meronts |
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Sarcoystis neurona
Experimentally infected mouse brain with antibody stained meronts |
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Sarcoystis neurona
Schizonts in cell culture |
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Sarcoystis neurona
Mature sarcocyst in tissue |
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Sarcoystis neurona
Sarcocyst in tissue |
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Sarcoystis neurona
Live, unstained sarcocyst |
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Two sporocysts from Sarcoystis neurona |
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General features of Protozoans |
-Single celled organisms -microscopic and small -Parasitic in ALL vertebrate hosts -Variable lifecycles (direct, Ob indirect, Fac indirect |
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What is a Trophozoite? |
The living, motile form of a protozoan |
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What is a cyst/oocyst? |
The environmental transmissible form of a protozoan |
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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 |
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How do Ameoba's cause disease?
Protozoan |
They feed on solid tissues directly or after liquefying them (amoebas)
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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 |
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How do coccidia and malaria cause disease?
Protozoan |
Destroy hosts cells by growing in them |
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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 |
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What are the Major Protozoan Groups |
Flagellates and Coccidia (class: Sporozoa) |
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What are the 2 protozoan flagellates |
Giardia Tritrichomonas foetis
They are intestinal |
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What are the intestinal Coccidia protozoans |
Eimeria Isospora Toxoplasma Sarcocystis |
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What are the blood Coccidia protozoans |
Babesia Cytauxzoon |
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What is Giardia primarily associated with? |
-Waterborne outbreaks (swimming pools, water slides, sewage) -Daycare centers -Occupational Risk -Outdoor recreation -Travel outside of US |
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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 |
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How long does it take to start shedding Giardia cysts? |
Cysts passed in the feces following a 7 to 14 day inocubation period |
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The two types of Giardia infection: |
Symptomatic and Asymptomatic |
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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 |
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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 |
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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 |
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Giardia Genotype Assemblage A: Host range |
Humans livestock dogs cats beavers guinea pigs slow loris |
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Giardia Genotype Assemblage B: Host range |
Humans Slow loris chinchillas dogs beavers rats siamang |
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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
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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) |
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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 |
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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 |
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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 |
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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 |
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Giardia: Immunoassay |
GSA- 85 in feces ID ~60% of cyst negative stools Micro-plate and cassette formats Sensitivity > 95% overall |
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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 |
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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 |
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Tritrichomonas blagburni: suspected risk factors |
Residence in cattery Coccidiosis as adult cat smaller square footage of housing per cat |
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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 |
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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 |
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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 |
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Tritrichomonas blagburni: Is it Zoonotic? |
It is not known to be Humans/Dogs may share closely related Pentatrichomonas hominis |
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Tritrichomonas foetus: What is it? |
A flagellate protozoan parasite in the reproduction tract of cattle
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Tritrichomonas foetus: What is it morphologically indistinguishable from? |
T. blagburni and other Trichomonad protozoa |
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What does Tritrichomonas foetus cause? |
Bovine genital trichomoniasis -Infertility -Spontaneous abortion in 1st trimester -Generalized reproductive tract infection |
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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 |
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How do you diagnose Tritrichomonas foetus |
PCR and culture methods |
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Tissue and blood flagellates are broadly classified as?
What do its relatives cause? |
Trypanosomes
family members well known for causing African Sleeping Sickness |
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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 |
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Trypanosomes: Classification by Modes of Transmission |
Anterior Station, Salivarian: bite of infected "Teste Fly"
Posterior Station, Sectorian: feeding Rejuvidae bugs defecate and pass parasites |
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How are Arthropods infected with Trypanosomes |
They become infected during a blood meal |
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What happens within the Arthropod IH ith Trypanosomes |
Epimastigotes divide and multiply in IH then develop into Trypomastigoates |
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Where do Trypanosomes replicate? |
within the human or animal host |
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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 |
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Trypanosoma cruzi: What does it cause? |
Chaga's Disease
OR
American Trypanosomiasis |
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Trypanosoma cruzi: Naturally endemic where? |
Central and South America
Recent cases in US -border region, TX, OK, LA, TN -Hunting dogs in VA |
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Trypanosoma cruzi: Obligate IH |
Triatomin/Reduviid bugs |
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Other animals playing a reservoir role with Trypanosoma cruzi? |
Opossums, Raccoons, and Armadillos |
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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 |
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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 |
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Trypanosoma cruzi: Chronic infection |
Myocardial disease mega-esophagus meg-colon |
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Trypanosoma cruzi: Acute Disease Signs in Dogs |
Lymphadenopathy myocarditis pale MM tachycardia splenomegaly |
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Trypanosoma cruzi:: Diagnosis |
Serology and PCR |
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Trypanosoma cruzi: Treatment |
No effective therapeutic intervention |
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Leishmania sp. infect what? |
They are parasites infecting macrophages of vertebrate hosts |
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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 |
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Which Leishmania species are associated with visceral disease? |
L. donovoni L. infantum
-amastigotes proliferate in macrophages and tissues, typically fatal |
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Which Leishmania specie is associated with muco-cutaneous disease? |
L. mexicana (New World) |
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Which Leishmania specie is associated with cutaneous disease? |
L. tropica (old world) |
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Leishmania species that effect dogs |
Dogs are significant hosts for the parasite in endemic localities
Mediterranean (L. infantum) Brazil (L. chagasi) |
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Leishmania: Disease in the dog |
Severe cutaneous manifestation of disease
proliferation in visceral tissue in advanced cases
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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) |
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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) |
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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 |
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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 |
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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 |
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How does one confirm a diagnosis of Leishmania? |
Serology/PCR isolation of organism by biopsy |
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Eimeria sp: Lifecycle, route of infection |
Direct lifecycle
ingestion of sporulated oocysts
4 sporocysts each with 2 sporozoites |
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Eimeria: DH |
Domestic livestock, birds, grazing wildlife |
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Eimeria: Replication type and site |
Asexual replication in small intestine
Sexual reproduction in fresh uninfected cells of large intestine |
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Eimeria: How does it cause diarrhea? |
Diarrhea is associated with destruction of enterocytes (2-3 asexual cycles) |
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Eimeria: What is the disease associated with? |
Asexual replication in hosts tissues |
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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 |
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Eimeria Coccidiosis is a function of |
Age Nutrition Stress Sex Season Gestation status etc |
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Eimeria: Host immunity? |
Host immunity with age and exposure -premuntion (periodic challange of host) -Generally species specific immunity |
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Eimeria: Risk of disease |
Risk of disease is a function of environmental contamination, moderate levels of infection, and stress in the host population |
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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 |
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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 |
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What type of coccidia is Cystoisopora? |
Intestinal |
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Cystoisopora: Lifecycle and route of infection |
Faculative Direct/Indirect lifecycle -ingestion of sporulated oocysts -2 sporocytes each with 4 sporozoites |
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Cystoisopora: DH |
Cats Dogs Pigs Some birds
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Cystoisopora: Paratenic hosts |
Mice Birds Rodents |
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Cystoisopora: Where does replication occur? |
Asexual/Sexual replication occurs in the small intestine |
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Cystoisopora: What is the diarrhea associated with? |
Destruction of enterocytes (3 asexual cycles) |
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Cystoisopora: Prepatent Period |
6-12 days |
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Cystoisopora is AKA |
Isospora |
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Cystoisopora species in dogs |
C. canis -teardrop shaped 40 x 30 micrometers
C. ohioenis -round ~25 micrometers in diameter |
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Cystoisopora species in cats |
C. felis -Teardrop shaped 40x 30 micrometers
C. rivolta -Round ~25 micrometers in diameter |
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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 |
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Treatment type of Intestinal Coccidia infections |
Supportive care, especially in young animals |
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Pharmacological Intestinal Coccidia Treatment in Dogs and Cats |
Dogs: Albon Cats: Trimethoprim Sulfadiazine
Both: Ponazuril
bathe at beginning of treatment and remove feces daily |
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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 |
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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 |
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Cryptosporidium spp: host specificity |
is variable
C. parvum most widespread readily infects humans, cattle, cats, dogs, deer, rabbits, etc |
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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 |
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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. |
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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 - |
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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 |
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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 |
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Giardia |
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Giardia |
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Giardia |
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Giardia |
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Giardia |
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Tritrichomonas |
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Tritrichomonas |
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Tritrichomonas
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Trypanosome |
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Trypanosome |
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Trypanosoma cruzi |
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From Trypanosoma cruzi |
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What is this bug and what is it associated with? |
Reduviid bug
Trypanosoma |
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What parasitic infection could this woman be suffering from? What is this symptom called/. |
Romana's sign from Trypanosoma cruzi |
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Leishmania |
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Leishmania, Human Disease |
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Leishmania: Dog Disease |
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Leishmania: In the dog |
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Eimeria bovis schizont (asxexual stages) in intestinal epithelial cell |
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Eimeria developing oocysts in goat intestinal epithelium |
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Eimeria
in goat |
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Eimeria |
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Eimeria oocysts |
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Eimeria mascusaniensis
llama |
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Sporulated Eimeria oocyst |
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Sporulated Eimeria oocyst |
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Cystoisopora |
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Cystoisopora |
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Cystoisopora |
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Cystoisopora |
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Cryptosporidium |
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Cryptosporidium |
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Cryptosporidium oocysts are TINY |
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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 |
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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) |
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Toxoplasma gondii: Lifecycle |
Faculative Direct/Indirect Ingestion of sporulated oocysts
2 sporocysts with 4 sporozoites Ingestion of tissue cysts |
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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 |
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Toxoplasma gondii: IH |
Domestic livestock, birds, grazing wildlife, dogs, people all harbor it
Asexual replication in CNS (where disease occurs) and edible tissues |
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Toxoplasma gondii: Phases |
Intestinal and Tissue (asexual) phases |
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Toxoplasma gondii: Intestinal phase clinical signs in the cat |
Behaves like other coccidia
oocysts in stool
Diarrhea, soft stool, no real clinical signs |
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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 |
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Toxoplasma gondi oocysts
measuring ~12 micrometers on a cat fecal |
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Toxoplasma gondii
Tachyzoites in lymph node aspirate |
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Toxoplasma gondii
Bradyzoites in brain of an infected mouse |
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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 |
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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
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Hiow does one become infected with toxoplasma gondii? |
People and other intermediate hosts infected by oocysts or tissue stages
50% of cases are foodborne |
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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 |
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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 |
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What is the congenital infection with T. gondii called |
Toxoplasmosis |
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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. |
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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 |
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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 |
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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. |
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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
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Household cats should be tested for Toxoplasma, but which cat is more problematic? Seronegative or positive |
Seronegative |
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Cat litter boxes and Toxoplasma |
should be dumped daily by a non-preg member of household |
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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
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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 |
