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Parasitology > Lecture 2 > Flashcards

Lecture 2 Flashcards

1
Q

What is tick fever in australia

A

Tick transmitted disease of cattle caused by either

  • B.bovis
  • B. bigemia
  • A. marginale
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2
Q

Why is B.bovis so important

A

Causes 80% of outbreaks and even higer % of death

VERY PATHOGENIC

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3
Q

Where are B.Bovis outbreaks most likely

A

Bos taurus cattle

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4
Q

How do animals get infected with Babesia

A

Female ticks get infected after feeding on a parasitemic host. Then the infection is transmitted by next generation of ticks

  • Larvae for B.bovis
  • Nymph and adults for B.bigemia
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5
Q

Where do transovarial transmission need to get

A

Salivary glands -> divide and change to sporozoites -> babesia leave

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6
Q
A
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7
Q

Generatio time of babesia

A

8 hours

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8
Q

When can your see parasitemia

A
  • B.bovis - 6-12 day
  • B.bigemia: 12-18 days
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9
Q

Susceptibity of babsia depends on

A
  • Age - under 9 monts develop mild or inapparent signs
  • Breed - bos indicus more resistance
  • Condition of host
  • Immunity - recovery is followed by strong resistance
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10
Q

What is the source of infection of babsia

A
  • Infected animals
  • Ticks
    • Single tick can transmit
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11
Q

How do ticks get infected with babsia

A

Tick bite

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12
Q

Where is outbreak of babsia frequent

A
  • Animlas 1-3 years
  • Animlas introduced in endemic areas
  • South QLD: most cases in autumn
  • North QLD: most cases winter or spring
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13
Q

What is endemic stability

A

The presence of infection with babsia and their vectors in a cattle population without measurable economic losses or clinical disease

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14
Q

What does pathogenisi depend on wih B. bovis

A
  • Species
  • Strain
  • Condition of host
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15
Q

What does B.Bovis cause

A
  • Hypotensive shock syndrome
  • Blocking of capillaries by RBC
    • Stasis
      • Hypotension
      • Extravation of plasma fluid
      • Activation of the coagulation system -> increased fibrin concentration that adhere to RBC -> RBC becomes sticky
      • Local proliferation of the parasites -> increased local parasitemia
    • Sequestration
      • Ridges develop on the surface of infected RBC
    • Changes in the structure of RBC
      • Increased viscosity
      • Decreased deformability
  • Hamolysis
    • Cause increased osmotic ability causing damage to the blood cells
      • Infected blood cells increase
      • Damages organs
      • Intravascular haemolysis -> free hamoglobin released from rbc is excreted in urine -> haemoglobinuria
      • Phagocytosis of infected/damaged rbc in liver and spleen -> enlargement of these organs
  • The imune response tin the pathogenesis of the disease
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16
Q

Importance of immune response

A
  • Species specific
  • Immunity develops 3-4 weeks after vaccination
  • Most animals recover from disease will have a strong and long immunity
  • Babesa persist in blood for wile
  • Maternal Ab in calves protects them for 2 mntsh
  • Calves are protected up to 9 montsh
  • Primary infections depends on macrophages and Nk cells
  • Persistent infections depend on CD$+ cells and antbodies
17
Q

What is the significance of increased adherence and sequestration?

A
  • Immune evasion
  • The parasites invade cells in vicinity
  • In the brain -> cerebral babesiosis
  • In the lungs -> sequestration of RBC and neutrophils -> increased permeability -> oedema -> death
18
Q

Clinical signs of B.Bovis

A
  • Appear 6-12 days after begin to feed
  • Fever
  • Inappetence, depression, weakness, muscle tremor
  • Death within one week of fever
  • Anaemia, haemoglobinuria, jaundice
  • Diarrhoea
  • Cerebral babesiosos: hyperaesthesia, agression, coma, convulsion, paralysis
19
Q
A
20
Q

Pathogenesis of B.bigemia

A

Entirely related to the intravascular haemolysis

RBC count reduced

Increased levels of hemoglobin in serum

Proteinuria

21
Q

Pathology of babesia bovis

A
  • Acute infection most organs are swollen and congested, prolonged causes may show anaemia and jaundice
  • Blood is thin
  • The spleen is enlarged with dark red pulp
  • The liver is enlarged and brown/yello, the gall bladder contains large amounts of thick granular bile
  • Kidneys congested and enlarged
  • The lungs may be haemorrhagic with odema
  • In cerebral babesiosis the grey matter in the brain has a characteristic pink colour
  • Capillaries int he brain are dilated and filled with closely packed rbc, most which are parasitized
22
Q

How to diagnose babsia

A
  • History
  • Clinical signs
  • Thin and thick blood dilms stained by Giemsa - capillaries from tail and ear becasue there is a high chnage of finding the infection here
  • Serology: ELISIA, IFAT
  • PCR
23
Q

Diagnosis in animals with a PM

A
  • Pathology
  • Histopathology
  • Films from peripheral and general circulation and impression smears from cerebral cortex, spleen, liver, kidney and bone marrow
24
Q

Treatment of Babsia

A
  • Imidocarb dipropionate (Imizol, Imidox)
    • 1.2mg/kg - treatment
    • 3mg/kg - prevention
    • D not give to lactating dairy cows
    • Remove animals from infeted area and treat for ticks
25
Q

How to control babesia

A
  • Tick control
  • Vaccination - live, attenuated strains: trivalent/bivalent tick fever vaccine
  • Animal genetics
26
Q

Distribution of anaplasma marginale

A

Cattle tick area

27
Q

Transmission of anaplasma marginale

A

Transfer of infected larvae, nymphs or adult ticks from infected cattle to susceptible cattle - males very important

No transovarian transmission

28
Q

Clinical signs are shown ? anaplasma marginale

A

4 weeks

Fever, anorexia, drepression

29
Q

anaplasma marginale: treatment

A

Oxytetracyclines

Imidocarb

Parasitology (9 decks)

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