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VETM 424 Parasitology > Lecture 2 > Flashcards

Lecture 2 Flashcards

1
Q

What are some key features of apicomplexa

A
  • Apical cone that allows them to penetrate host cell
  • Apicoplast: remnant of chloroplast – common drug target
  • Include piroplasmidia and coccidia
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2
Q

Features of Piroplasmidia

A
  • Infect/replicate in blood cell = cause pale mucus membranes
  • Zoites: parasite life stages that affect erythrocytes (large or small)W
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3
Q

What are the types of hosts of Piroplasmidia

A
  • Vector transmitted protozoa
    o Vertebrate host = intermediate host
    o Invertebrate (ticks) = definitive host (sexual reproduction)
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4
Q

3 types of babesia affecting cows

A
  • B. bigemina: tropical/subtropical
  • B. bovis: tropical/subtropical
  • B. divergens
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5
Q

3 types of babesia affecting dogs

A
  • B. canis
  • B. gibsoni
  • B. vulpes
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6
Q

2 types of babesia affecting horses

A
  • B. caballi
  • B. equi
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7
Q

Explain the pathogenesis of Babesia

A

Pathogenesis
* Destroy RBC and release vasoactive substances
* Autoantibodies directed against host = anemia/hypoxia
1. Sporozoite infect RBC
2. Turn into trophozoite
3. Turn into merozoite
4. Turn into gametocyte – can transmit to ticks
5. Form gametes in ticks and turn into zygotes and infect their gut
6. Move to salivary glands and ovarian cells of ticks
a. Trans-ovarian infection – Female ticks can pass to offspring
b. Trans-stadial infection – maintain infection in tick at it moves through life stages
c. Can pass to hosts via saliva

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8
Q

What are the 3 ways babesia can be transmitted

A

a. Trans-ovarian infection – Female ticks can pass to offspring
b. Trans-stadial infection – maintain infection in tick at it moves through life stages
c. Can pass to hosts via saliva

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9
Q

What is the cause of Cattle/redwater/Texas fever

A
  • B. bigemina + B. bovis
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10
Q

What are the vectors for cattle babesia

A
  • Vectors: Rihpicephalus annulatus + Phiphicephalus microplus
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11
Q

How does babesia clinically affect cattle? What is the tx?

A
  • Clinically: anemia, icterus, hemoglobinuria, splenomegaly (40% mortality in outbreaks)
  • Tx: imidocarb
  • Survivors can be carriers
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12
Q

What is endemic stability? How does it relate to babesia

A

o Endemic stability: epidemiological concept, low clinical disease with high infection

In relation to babesia:
Low clinical risk when infection occurs in young animals. If there is high amounts of infection in the population there can be low risk. Outbreak occurs in naive older animals

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13
Q

What are key characteristics of B. canis? vector? host?

A
  • B. canis: large paired piroplasms
    o Many subspecies: B. canis vogeli (most common)
    o Tick vector: Rhipicephalus sanguinous (transstadial and transovarian)
    o Commonly affect greyhound
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14
Q

What are key characteristics of B. gibsonii? vector? host?

A
  • B. gibsoni: small pleiomorphic piroplasms
    o Most common cause of canine babesiosis
    o Commonly affect pit bulls and Staffordshire terriers
     Transmit via contact with blood (transfusion/fight) or vertical transmission
    o Tick vector: Rhipicephalus sanguineous + Dermacentor variabilis
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15
Q

What are the clinical signs, diagnosis, and treatment of canine babesiosis?

A
  • Clinically: lethargy, fever, splenomegaly, pale mucus membrane, discoloured urine, jaundice
    o can be subclinical
  • Diagnosis: blood smear, tick ID, PCR
    o Co-infections common
  • Treatment
    o B. canis/vogeli: imidocarb + dipropionate
    o B. gibsoni; azithromycin + atovaquone
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16
Q

Geography of theileria

A
  • Geography: Africa and Asia
17
Q

Lifecycle of theileria

A
  • Life cycle: inifects leukocyttess and RBC (minimal parasite dividion iin RBC – differentiates from Babesia
18
Q

Clinical signs of theileria

A
  • Clinically: fever, lympomegaly, anorexia, weight loss, nasal discharge, (pulmonary edema/mucosal hemorrhage if severe
19
Q

Agent (s) causing theileria? and associated location

A
  • Agent:
    o T. annuulata: Europe/N. Africa/Asia
     Vector: Rhipicephalus/Hyalomma
    o T. parva: Africa
     Vector: Rhipicephalus/Hyalomma
    o T. orientalis: E. Asia/USA
     Vector: Rhipicephalus/Haemaphysalis longicornis
20
Q

How to treat or prevent theileria

A
  • Can vaccinate – but strain specific (not always feasible)
  • Tx: parvaquone
21
Q

Most common agent for cytauxzoon

A

C. felis

22
Q

Vectors and hosts for cytauxzoon

A
  • Vectors: Amblyomma Americanum (found in AB recently) + Dermacentor variabilis
  • Host: wild felines (bobcats/cougars)
23
Q

Clinical signs of cytauxzoon

A
  • Clinically: asymptomatic for wild
    o Fever/lethargy/dehydration/jaundice/icterus/pale mucus membrane/dyspnea/low WBC+platelet/normocytic normochromic anemia
  • Fatal for domestic cats if untreated
24
Q

Describe the lifecycle of cytauxzoon

A
  • Life cycle:
    1. Sporozoites invade macrophages
    2. Asexually reproduce in macrophages
    3. Rupture and release merozoites causing tissue damage
    4. Merozoites invade RBC and do binary fission and form gametocyte – infect ticks
25
Q

What is the pathogenesis of cytauxzoon

A

o Schizont-filled macrophages occlude capillaries in organs = organ fail
 Brain/heart/lung/intestine/spleen/lymph node/kidney
o Causes DIC

26
Q

What is the diagnostics used and treatment for cytauxzoon

A
  • Diagnosis: identify piroplasms on blood smear (uncommon)
    o Usually FNA spleen/kidney/liver
    o PCR
  • Tx: atovaquone + azithromycin
    o May become carriers
27
Q

What is a common tick born coccidia

A

Hapatozoon

28
Q

Haptazoon vector and agent

A
  • Agent: H. Americanum (severe/emerging) + H. canis (mild/widespread)
  • Vector: tick
29
Q

Describe the haptazoon lifecycle

A
  • Life cycle:
    1. Gametogenesis/fertilization – sexual reproduction in tick
    2. Mature oocyst forms (contains infectious zoites)
    3. Paratenic host ingests tick (or directly ingested by dog host)
    4. Become a cystozoite in paratenic host
    5. Paratenic host eaten by dog
    6. Cystozoites develop tto sporozoites and go to GI
    7. Migrate to skeletal muscle and form onion-skin cysts in phagocytes
    8. Merozoites form in cysts/meronts and it will rupture
    9. pyogranuloma forms
    10. Gamonts enter circulation (leukocytes) and infect ticks
30
Q

What are the clinical signs of haptazoon infection

A
  • Clinical signs: fever, ocular discharge, pain, atrophy, weight loss, weakness
    o proliferative lesions in muscle and bone, locomotor abnormalities, inflammatory response to meront rupture
    o similar radiographs to hypertrophic osteopathy
31
Q

How to diagnose haptazoon infection

A
  • Diagnosis
    o Leukocytosis
    o Identify gamont (Giemsa stain blood smear) – must blood smear immediately (parasite will exit blood cells if blood is flowing)
    o Parasitaemia
    o Skeletal muscle biopsy
    o PCR (not as available)
32
Q

How to treat a haptazoon infection

A
  • Tx: trimethlprimsulphadiazine, clindamycin, pyrimethamine
    o Not a cure

VETM 424 Parasitology (12 decks)

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