Chapter 31: Respiratory Flashcards

1
Q

Rhodococcus equi bacteria characteristics

A

Gram-positive, aerobic, facultative intracellular bacteria

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2
Q

What age range does R equi affect?

A

3 weeks to 5 months

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3
Q

Can this affect people?

A

People immunocompromised by HIV can contract R equi.

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4
Q

What are the R equi specific virulence-associated protein (Vap) families?

A

VapA, VapC, VapD, VapE, VapG, Vape (full length).

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5
Q

Which is the necessary virulence factor?

A

VapA. It is necessary, not sufficient.

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6
Q

Which virulence factors are required for intracellular growth in macrophages and virulence?

A

virR and virS

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7
Q

What are the clinic forms of R equi?

A
  1. Pulmonary
  2. Extrapulmonary
  3. Adult
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8
Q

Which is the most common clinical form of R equi?

A

Pulmonary form.

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9
Q

What lesions are seen in the pulmonary form of R equi?

A

Chronic suppurative bronchopneumonia & extensive abscessation.

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10
Q

What clinical signs are seen in the pulmonary form of R equi?

A

Cough, fever, lethargy, increased respiratory rate/effort.
Subacute form: respiratory distress.
Subclinical form: ultrasonographic evidence of peripheral pulmonary consolidation +/- abscessation without clinical signs.

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11
Q

Which is the second most common clinical form of R equi?

A

Extrapulmonary form. Lower survival due to poorer response to treatment compared to the pulmonary form.

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12
Q

What lesions are seen with the extrapulmonary form of R equi?

A
  1. Multifocal ulcerative enterocolitis +/- typhlitis - granulomatous/ suppurative lesions in colonnic and mesenteric lymph nodes - Peyer’s patches affected.
  2. Polysinovitis - 25 - 30% of cases - Ab-Ag complex deposition in the synovium.
  3. Uveitis
  4. Osteomyelitis
  5. Immune-mediated anaemia, thrombocytopenia, telogen effluvium
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13
Q

What is the rarest clinical form of R equi?

A

Adult infections.
1. Lungs
2. Abdominal lymph nodes
3. Wound infection

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14
Q

R equi pathogenesis?

A

On endemic farms, infection occurs at a younger age (incubation period ~ 2-4 weeks). At a younger age foals have a higher susceptibility to develop clinical disease.
1. Inhalation/ Ingestion
2. Receptor-mediated (CR3/Mac1) phagocytosis into the alveolar macrophages.
3. Immune response
a) increased NO results in iron sequestration and prevention of R equi replication. TNFa and IFNy cytokine action result in reduced growth of R equi.
b) uncontrolled intracellular R equi replication - macrophage necrosis

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15
Q

At what age are foals usually diagnosed with R equi?

A

35-50 days old

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16
Q

Main diagnostics used for R equi?

A

CBC: chronic inflammatory leukogram. hyperfibrinogenaemia
Ultrasound: pulmonary consolidation
Thoracic radiographs: alveolar pattern +/- abscesses

17
Q

What are the immune reponse to R equi?

A
  1. Antibody-mediated: IgGa, IgGb and IgG(T)
  2. Cell-mediated (very important): functional Th (CD4+) - cytokine secretion and cytotoxicity.
    Type 1 response - increased IFNy - sufficient to clear the pulmonary form. Young foals, deficient IFNy production.
    Type 2 response - increased IL-4 - detrimental.