Tick-Borne Protozoa Flashcards

1
Q

Hepatozoon infects more than _______ species worldwide

A

300 vertebrates

- amphibians, reptiles, birds, marsupials, mammals

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2
Q

Canine Hepatozoon spp

A

Hepatozoon americanum
- ACH: american canine hepatozoonosis
Hepatozoon canis

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3
Q

Hepatozoon americanum hosts

A

Southern US, South and Central America

  • DH: tick vector (Amblyomma maculatum)
  • IH: canids
  • PH: rodents, rabbits
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4
Q

How do dogs become infected with H. americanum?

A

My ingesting the tick, or by ingesting affected paratenic hosts
- tick does NOT bite the dog!

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5
Q

H. americanum has a(n) _______ life cycle

A

Indirect

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6
Q

What is a requirement for a tick-bite infection?

A

Sporozoites must be in the salivary glands of the tick

- with H. americanum they are in the body of the tick

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7
Q

H. americanum infective stages

A
  • tick vector (DH): ingests canine leukocytes with gamont
  • dog (IH): ingests tick with oocysts or PH with cystozoites
  • -> transplacental not confirmed
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8
Q

H. americanum sites of infection

A
  • tick vector (DH): mature oocysts in hemocoel
  • dog (IH): gamonts in leukocytes, meronts in skeletal muscle and cardiac tissue
  • PH: cystozoites in skeletal and cardiac muscle, kidney, lung
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9
Q

American canine hepatozoonosis - pathology

A
  • neutrophilic leukocystosis (moderate anemia)
  • periosteal bone proliferation (primarily long bones of younger dogs)
  • tissue lesions (onion skin cyst): pyogranulomas occur when merozoites come out of meronts
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10
Q

ACH - clinical signs

A

Occur 4-5 weeks post-infection

  • fever
  • weakness
  • chronic weight loss
  • depression
  • muscle atrophy, pain, gait abnormalities
  • mucopurulent ocular discharge
  • frequent relapses, death 12-24 mos post-infection if untreated*
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11
Q

ACH - presumptive diagnosis

A
  • profound neutrophilia
  • periosteal bone lesions
  • clinical signs, history
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12
Q

ACH - definitive diagnosis

A
  • gamonts in leukocytes
  • muscle biopsy (most likely to find cysts, most invasive)
  • PCR
  • ELISA
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13
Q

Where are gamonts found in ACH?

A

Rarely found, occurrence in less than 0.1% of WBC

- look at buffy coat

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14
Q

Pyogranulomas

A

Rupture of cyst with mature meront –> merozoites released, inflammatory cell infiltration

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15
Q

ACH treatment

A

No effective treatment in eliminating parasites!
Acute cases:
- ponazuril (2 weeks), or combination therapy for 2 weeks plus supportive therapy
Chronic cases:
- decoquinate daily for 2 years
Relapses can occur, sylvatic cycle is efficient

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16
Q

What drugs comprise combination therapy for ACH?

A
  • Trimethoprim-sulfadiazine
  • Clindamycin
  • Pyrimethamine
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17
Q

ACH control

A

Reduce risk of exposure

- tick prevention

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18
Q

Hepatozoon canis

A

Old World only

  • usually subclinical, genetic diversity
  • DH: tick vector (Rhipicephalus sanguineus)
  • IH: canids
  • PH: rodents
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19
Q

How does H. canis differ from H. americanum?

A
  • higher number of WBCs infected
  • meronts are in lymph nodes, bone marrow, spleen
  • meronts look like wheel spoke
  • dogs asymptomatic unless immunocompromised
  • good prognosis with treatment (Imidocarb)
  • PH has monozoic cyst
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20
Q

How does hematology differ with H. canis?

A

Gamonts are commonly found (1005)

- neutrophilia is rare

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21
Q

Histopathology of H. canis

A

Hepatitis, splenitis, pneumonia

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22
Q

Hepatozoon spp. in cats

A

Life cycle poorly understood

  • cysts with meronts in muscle, cardiac tissue
  • 1% of WBC infected (hard to detect)
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23
Q

Cytauxzoon felis

A

North America (southeastern, south central, mid atlantic)

  • DH: tick vector –> Amblyomma americanum, and to a lesser extent Dermacentor variabilis
  • IH: felids
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24
Q

Who is the reservoir for C. felis?

A

Bobcat (Lynx rufus)

- asymptomatic

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25
Q

C. felis has a(n) _______ life cycle

A

Indirect

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26
Q

C. felis infective stages

A
  • tick vector (DH): merozoite from infected (feline) RBCs

- cat (IH): sporozoite from infected tick or from blood transfusion

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27
Q

C. felis sites of infection

A

Cat (IH)

  • merozoites in RBCs
  • schizonts in macrophages associated with endothelium of lung, liver, lymph node, spleen, bone marrow
  • multisystemic clinical signs
28
Q

Cytauxzoonosis pathology

A
  • leukopenia, thrombocytopenia, non-regenerative anemia, elevated liver enzymes
  • progressive illness: multiple organ failure
29
Q

What are the 2 phases of cytauxzoonosis?

A
  • leukocytic (schizont): primary cause of severe clinical disease
  • erythrocytic (merozoites): RBC hemolysis
30
Q

Cytauxzoonosis clinical signs

A
  • lethargy/depression
  • icterus
  • high fever then subnormal
  • splenomegaly, hepatomegaly
  • death within 1st week after clinical signs
31
Q

What happens to survivors of cytauxzoonosis?

A

They become carriers

- rare, 1-2 week recovery

32
Q

When do clinical signs occur with cytauxzoonosis?

A

1-3 weeks post-infection

- several weeks after tick is gone

33
Q

Cytauxzoonosis diagnosis

A
  • clinical signs
  • history
  • merozoites in stained blood smears (round to oval ring, or safety pin in RBC)
34
Q

Schizonts of cytauxzoonosis occur in ______

A

Macrophages

  • bone marrow, lymph node, spleen aspirates
  • impression smears, biopsy material
35
Q

Cytauxzoonosis treatment

A

No efficacious treatment, poor prognosis

  • combo of atovaquone + azithromycin (60% survival)
  • imidocarb dipropionate following pretreatment with atropine or glycopyrrolate
36
Q

Cytauxzoonosis control

A
  • reduce risk exposure
  • routine on animal tick control
  • remove ticks immediately!!
  • -> 2-3 day window?
37
Q

Do cats become infected with cytauxzoon by tick bits or tick ingestion?

A

Tick bites

38
Q

Babesia hosts

A
  • DH: tick vector (wide range of tick species)
  • IH: wild and domestic animals (canids), humans
  • -> piroplasms in RBCs
39
Q

How does infected tick transmit sporozoites in Babesia?

A

Transmit sporozoites to vertebrate host via tick saliva

- sporozoites invade RBCs –> develop and asexually replicate –> merozoites

40
Q

How does the tick become infected with Babesia?

A

By biting infected vertebrate

  • ingests RBCS
  • gamogony –> sporogony –> sporozoites in salivary glands
41
Q

Babesia canis vogeli

A

Enzootic in US (esp south)
- greyhound kennels
DH: tick vector
- Rhipicephalus sanguineus, D. variabilis

42
Q

Babesia gibsoni

A

US - seen in American Staffordshire and pit bull terriers (mainly mechanical via dog fighting)
DH: tick vector
- R. sanguineus throughout the world, not confirmed in US

43
Q

Babesia conradae

A

No breed predilection, California

- DH: tick vector is currently unknown

44
Q

Canine babesiosis: transmission to canids in US

A

Bite from infected tick vector

  • Rhipicephalus sanguineus
  • B. canis vogeli
  • B. gibsoni (outside US)
  • B conradae: tick unknown
45
Q

Canine babesiosis direct

A

Animal to animal

  • dog fights (wounds): B. gibsoni
  • iatrogenic: B. canis, B. gibsoni
  • transfusions: B. canis, B. gibsoni
  • transplacental: B. canis, B. gibsoni?
46
Q

Canine babesiosis - transmission to DH

A

Blood meal from dog or transovarial transmission

47
Q

Canine babesiosis - pathology

A
  • hemolytic anemia
  • thrombocytopenia
  • hemoglobinuria
  • hemoglobinemia
48
Q

____ Babesia is more pathogenic than _____ Babesia spp

A

Small; large

  • B gibsoni > B canis vogeli
  • co-infections complicate disease
49
Q

Canine babesiosis - clinical signs

A

Can be subclinical

  • lethargy, fever, pallor, jaundice
  • splenomegaly
50
Q

Canine babesiosis diagnosis

A
  • blood smears: fresh, capillary source
  • antibody testing: negative in acute infection, detects exposure not infection
  • PCR: useful in early infection, interpret with caution
51
Q

Babesia gibsoni characteristics

A

Small babesia

  • single
  • pleiomorphic: oval, ring form, maltese cross
52
Q

Babesia canis vogeli characteristics

A

Large babesia

  • pyriform
  • often in pairs
53
Q

Babesia conradae is similar to _______

A

B. gibsoni

54
Q

Canine babesiosis treatment

A

Reduce parasitemia!

  • small babesia is more difficult to treat
  • reservoirs for parasite transmission –> chronic carriers/recrudesce (+ blood donors)
55
Q

Canine babesiosis control

A
  • decrease tick exposure
  • routine on animal tick control
  • remove ticks
56
Q

Bovine babesiosis

A

DH: tick vectors
- Rhipicephalus microplus
- Rhipicephalus annulatus
IH: cattle, other ruminants

57
Q

Is bovine babesiosis eradicated?

A

Yes, eradicated from US in 1943 via Tick Fever Eradication Program
- reportable!

58
Q

Bovine Babesiosis pathology

A

Disease characterized by fever, hemolytic anemia and severe multisystemic signs
- piriform or round parasites seen in RBCs on blood or brain smears

59
Q

Equine piroplasmosis

A

Babesia caballi and Theileria equi

  • DH: tick vector (dermacentor, hyalomma, rhipicephalus)
  • IH: equids (mules, donkeys, horses, zebras)
  • –> iatrogenic and vertical transmission is possible
60
Q

Is equine piroplasmosis reportable?

A

Yes

- eradicated in US in 1980, until outbreak in 2008

61
Q

Equine piroplasmosis clinical signs

A

Theileria equi more severe –> infects both WBC and RBC

  • acute: fever, inappetence, labored breathing, anemia, jaundice, hemoglobinuria, hemorrhage on conjunctiva, abortion
  • chronic: subtle signs of chronic infection, splenomegaly
62
Q

Equine piroplasmosis diagnosis

A

Challenging

  • antibody testing
  • PCR
63
Q

Are parasites detectible with chronic Theileria equi?

A

No

- acute stage you see small pyriform bodies (maltese cross)

64
Q

Feline babesiosis

A

Worldwide occurance

  • IH: panthers, cougars
  • -> no cases in domestic cats
  • DH: tick species (unknown)
65
Q

Feline babesiosis disease in domestic cats outside US

A

Anemia, depression, weight loss, GI signs, cardiac pathology
- 15-20% mortality, relapses

66
Q

Human babesiosis in US

A

Babesia microti

  • DH: tick vector (Ixodes scapularis)
  • IH: rodent (reservoir), humans are accidental
67
Q

Human babesiosis clinical signs

A

Asymptomatic or fever, chills, hemolytic anemia, myalgias, hepatomegaly

  • incubation 1-4 weeks
  • transfusion transmission