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parasitology exam 2 > horse protozoa > Flashcards

horse protozoa Flashcards

1
Q

Sarcocystis fayeri:

A

-causes tissue cyst
-dog DH, Horse IH
▪ Sarcocysts are
incidental finding in
muscle biopsy or
histopathology
▪ Rarely cause
eosinophilic
myositis

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2
Q

Cryptosporidium
parvum clinical

A
  • Often asymptomatic
  • Prevalence in horses in Canada ~17%
  • Most common in foals
  • Villous atrophy and epithelial
    sloughing
  • Malabsorptive diarrhea
  • Life threatening in
    immunocompromised (SCID foals)
    -zoonotic
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3
Q

Cryptosporidium
in horses diagnosis and tx.

A
  • Dx: IFAT on feces, acid fast stain
  • Tx: supportive, ELDU
    paromomycin, tylosin,
    azithromycin
  • Environmental decontamination
    difficult
  • ZOONOTIC potential
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4
Q

Equine Protozoal
Myeloencephalitis (EPM) causes

A

-Sarcocystis neurona* (most common)
-Neospora hughesi
* Only in North and South America
* Seroprevalence: in many horses hard diagnosis, asymptomatic
– S. neurona ranges from 15-89% (USA) –
N. hughesi much lower (<10%)
* Young (<5 yrs) and old (>13 yrs)
* Usually sporadic, only 1 horse/farm
* Stress trigger (heavy exercise, transport,
injury, surgery, birth and lactation)

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5
Q

Sarcocystis neurona

A

▪ * Definitive host: opossum
▪ * Intermediate hosts (IH): skunks,
raccoons, armadillos, cats, birds…
▪ * Horse is ABERRANT IH –
Sarcocysts seldom develop
▪ – Pathology associated with
merozoites (asexual reproduction)
▪ – Vertical transmission considered rare in horses
-asexual repro merogony in aberrant IH or cats then sporogony in possums DH.

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6
Q

Neospora hughesi

A

-helps cause EMP
-DH is unknown, horses are IH they develop tissue cytsts with bradiyzoites
* Tissue cysts with bradyzoites associated with pathology in horses
* Transplacental transmission important, occurs in multiple pregnancies. could be in placenta or aborted feces.
* Only ~1/10 positive horses develop EPM

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7
Q

Diagnosis of
EPM in horses

A

Can be asymptomatic, highly variable
– Dysphagia, lameness, seizures, muscle wasting,
ataxia
* Most consistent: asymmetric gaitand focal
muscle atrophy
1) Neurological exam
2) Rule out other causes (non febrile, no
pain)
3) Definitive antemortem diagnosis is a high
CSF: serum antibody ratio
– Many horses are seropositive for antibodies
to S. neurona
– Seropositivity for N. hughesi more useful to
dx EPM
* Definitive PM diagnosis: – IHC or PCR on
CNS

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8
Q

Management of EPM in horses:

A

▪ * Do Treat! (10 times more likely to improve)
▪ * Sulfadiazine and pyrimethamine (coccidiostatic)
▪ * Ponazuril, diclazuril (coccidiocidal) -BETTER
* Duration 6-8weeks, longer if still improving
* May relapse

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9
Q

Haemosporidia

A

Babesia caballi
▪ Theileria equi *, T. haneyi (more pathogenic)
▪ Equine piroplasmosis
▪ Foreign Animal Disease in Canada
Reportable disease (CFIA)
Sporadic outbreaks in USA

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10
Q

Haemosporidia indirect life cycle

A

-goes between an animal and blood feeder (tick is DH) and mammel is IH.
-asexual repro in mammal, sporogony in salivary glands, sexual repro in the tick gut. transfered through blood feeds.

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11
Q

Haemosporidia clinical

A

▪ Animals may be asymptomatic, but infective
▪ Symptoms range from mild weight loss/fever to
anemia, splenomegaly, hepatomegaly, abortions,
death
▪ 50% mortality
▪ May be acute- horses found dead
-impacts, animal losses, sports performance, travel restrictions, cost of treatment.

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12
Q

Human-assisted
transmission of Haemosporidia

A

-If coming from endemic country (Asia, South Europe, Central/south America, Africa), require negative test
▪ To transport horse from Canada to USA, only need 30-day health/negative EIA
▪ If travelling for sport, no testing required (and known positives can
enter the country)
▪ Horses traveling to endemic areas are not tested upon re-entry
-very very contagious 1 case 400 effected.

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13
Q

Diagnostics/Prevention of Haemosporidia

A
  1. trophozoites or merozoites on peripheral blood smear (ear
    nick)
  2. – History, clinical signs, serology (IFA, ELISA – done at
    CFIA), PCR
    ▪ Prevention: tick control, movement controls, avoid illegal
    doping (or at least use a clean needle)
    ▪ high doses of
    imidocarbdipriopionate until
    seronegative (1-2 years) or euthinasia
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14
Q

Chagas disease/American
Trypanosomiasis

A
  • Chagas disease is caused by the hemoflagellate protozoan parasite, Trypanosoma cruzi.
  • T. cruzi is primarily transmitted to humans and animals via the feces of
    the triatomine bug\
    -in USA, mexico, southamerica.
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15
Q

typonosoma cruizi chages disease life cycle

A
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16
Q

Chagas disease - transmission

A
  • ~ 150 species of triatomine bugs all with
    varying levels of vector competence.
  • Feces rubbed into wound, mouth, eyes,
    feeding site, eating the bug, blood transfusion, contaminated food, etc.
  • Dogs can become infected from eating infected kissing bugs for consuming
    infected tissue from other animals
17
Q

Chagas disease – clinical manifestations

A
  • The clinical signs in humans and dogs are largely the same.
  • The clinical signs in dogs are variable and non-
    specific: lethargy, decreased appetite, and weight loss.
  • More severe and explicit clinical signs could be fainting, exercise intolerance,
    vomiting, and diarrhea
  • CHARACTERISTIC Chagas disease signs – cardiomegaly, heart failure, arrythmias,
    organomegaly (spleen, liver), sudden death.
18
Q

chages disease 3 stages

A
  • Acute: Usually no clinical signs, or nonspecific. Occasionally lymph
    nodes and spleen will be enlarged, pale gums.
  • Indeterminate/latent: Dog enters this stage after seroconversion
    (~1 month) asymptomatic, amastigotes present in tissue. Dog may stay in this stage for life and not develop symptoms.
  • Chronic: If the dog presents with symptoms, they now enter the the chronic stage. As amastigotes continue to replicate in (most commonly heart tissue) the dog will develop signs of heart failure
  • Sudden death can occur in any stage
19
Q

chages disease diagnosis

A

-diagnosis uncommon in acute no signs until chronic, use PCR on blood.
-when intermidiate they seroconvert so they can use serological ELISA, IFA.
-chronic: usually cardiomegaly, and organomegaly and ECG.

20
Q

epidemiology of chages disease

A
  • Remember the importance of epidemiology. If you are treating a dog for with cardiomegaly from the
    Canada that has never travelled, it is not Chagas disease, but if the dog was born in or has
    travelled to the southern United States, Mexico, Central America, or South America than it is possible.
    -Be cognizant of the dog’s breed and diet. Doberman Pinscher’s, Great Dane’s, Boxer’s, and
    Cocker Spaniel’s are more susceptible to dilated cardiomyopathy (not chages)
21
Q

chages disease treatment

A
  • Treatment options are poor for humans and dogs
  • Benznidazole & Nifurtimox are used in humans
  • Benznidazole, Ravuconazole, and Albaconazole can be used in treatment of dogs
    -works best in acute stage
    -usually just symptom treatment for dogs ex. antiarrythmics.
22
Q

chages disease public health importance

A
  • 65-120 million people live in at-risk areas
    for infection
  • 6-12 million people are estimated to be
    infected
  • 10-50,000 deaths in humans annually
  • No vaccine and poor treatment options
  • It is estimated that ~99% of CD cases in
    humans are undiagnosed
23
Q

Leishmaniasis

A
  • Leishmania is caused by an intracellular protozoa
  • 3 main forms of leishmaniases
  • 30 leishmania species infect mammals (21 in humans)
  • Most important species in dogs is Leishmania infantum (also called L. chagasi in Latin America)
  • Major zoonotic disease in >89 countries
  • Much larger geographic range than Chagas disease
  • *41 cases of leishmaniasis in humans in Texas since 2007
24
Q

Leishmania lifecycle

A

-mammelian host amastigote in tissues
-insect vector host: procyclic and metaclylic promastigote.

25
Q

Leishmaniasis –
geographical distribution

A

1.The Americas
2.Southern Europe
3.Africa
4.The Middle east
5.Asia (not SE Asia

26
Q

Leishmaniasis - transmission

A

-transmitted via sandflies
* (Over 90 species of Sandfly)
* When the sand fly takes its blood meal it injects
promastigotes into the skin
* Leishmania can be passed vertically (mother to
offspring) and by blood transfusions
* Leishmaniasis is endemic in foxhound populations in the south-east and eastern US

27
Q

leshmanaisis transmission dogs, humans ect.

A
  • Direct dog-to-dog transmission
    “may” be possible through an
    infected wound rubbing up against an uninfected dog or through blood transmission from fighting.
  • Humans, dogs, coyotes, foxes,
    rodents and occasionally cats, and horses can be infected
  • Not all infected animals present with
    disease, but all are important to transmission
    -seen in eastern USA then canada from foxhounds in hunt clubs.
  • Seroprevalence in domestic dogs from
    southern Europe can be upwards of 30%
    -warming climate has led to more sandflies leading to larger endemic region (europe)
28
Q

Leishmaniasis – clinical
manifestations

A
  • 3 main types – cutaneous, mucocutaneous
    (often grouped just as cutaneous) and
    visceral
    -humans get cutaneous
    -cats get musculocutanoues.
    -dogs viseral and musculocutanos
    -dogs: open lesions on muzzle and footpads, nodules, dull coat
    -viseral: lack of appetite, weakness, weight loss, vommiting, LN enlarged. FATAL IS 95% IN HUMANS IF UNTREATED. also fatal in dogs.
29
Q

Leishmaniasis - diagnosis

A
  • Diagnosis is often made via serology, with quantitative serologic tests such as
    immunofluorescence assays or ELISA as confirmation
  • PCR using blood or tissue
30
Q

Leishmaniasis - treatment

A

-glutanatime 2-6 weeks up to 6-12 months
-allopurinol for 4+ months
mitefosine
-$$$
-dog may remain carrier, vaccines for dogs. only 1 yr of protection. not in CAD.

31
Q

Leishmaniasis – Public health importance

A
  • An estimated 700,000 – 1 million new cases of CL annually and
    100,000-400,000 of VL annually in humans
  • 12 million people infected, 20-30,000 deaths a year
  • Is a serious public health problem, because dogs are the most
    important reservoir that leads to human infection
  • Perfect storm = obsolete treatments, absence of effective
    vaccines and fast drug-resistance emergence

parasitology exam 2 (2 decks)

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