microbiology workshop Flashcards

1
Q

What are the most common clinical signs of foot and mouth disease in the species it infects? Do these differ between species?

A
  • Pyrexia, inappetence, lethargy, drooling
  • Oral and foot lesions (vesicles/bullae then erosions).
  • Foot lesions more common in pigs
  • Oral lesions more common in cattle
  • Signs less obvious in sheep (or deer etc)
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2
Q

how is foot and mouth disease spread between animals and farms

A

Massive secretion of viruses from lesions when they rupture (and other aerosols). Direct contact most important means of spread (or via fomites). Airborne spread can result in long distance spread of the virus.

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3
Q

what type of virus is foot and mouth disease and which features does the virus have

A

Picornavirus family; apthovirus.
Positive sense single stranded RNA virus
Non-enveloped, icosahedral capsid

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4
Q

How is foot and mouth disease controlled in the UK?
What factors might determine whether the outbreak becomes widespread – list three in order of importance.

A

Notifiable disease in the UK, controlled by enforced cull of infected and in contact animals; movement restrictions etc.
1. Speed of diagnosis and subsequent control
2. Species affected (pigs shed more virus than cattle)
3. Spread to wild animals (e.g. deer)
4. Failure of containment (animals are moved to new farms)
5. Infected animals are slaughtered before diagnosis (virus in meat etc)

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5
Q

what organism causes johne’s disease

A

mycobacterium avium subspecies paratuberculosis

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6
Q

what are the steps of infection of johne’s disease and how does the granuloma form

A

Macrophages (Histiocytes) fail to clear foreign agent and become chronically infected. Activated macrophages constantly secrete TNF-α and other proinflammatory cytokines which promote the influx of T-cells and other cells, T-cell activation and inhibit regulatory T-cells and T-cell apoptosis. Removing TNF-α causes breakdown of the granuloma. T cells around the periphery secrete IFN-γ (Th1 response) which promotes chronic reactivity of macrophages. T-cell and macrophages stimulate fibroblasts promoting fibrosis which can lead to organ damage

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7
Q

What are the pros and cons of granuloma formation

A

Pros:
- Granuloma form a focal killing point and prevents dissemination
Cons:
- Chronic infiltrations lead to thickened gut wall and poor absorption.
- Break-down of a granuloma can have serious effects since the bacteria disseminate. Granuloma may cause severe tissue necrosis and affect organ function.

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8
Q

How can Johne’s disease be controlled on a farm?

A
  • Biosecurity plans and monitor
  • Improved farm management (IFM)
  • Strategic IMF with Testing segregation and culling (on high prevalence farm)
  • IFM testing segregation and culling (on low prevalence farm)
  • Breeding to terminal sire
  • Fire break vaccination
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9
Q

How can Johne’s disease be screened for?

A

-The main test used to diagnose is a blood test to look for the antibodies produced in response to infection with Mycobacterium avium subspecies paratuberculosis (MAP).
- Note tuberculin test can interfere so need minimum 3-month gap.
- Other tests milk ELISA for antibodies in milk.
- Faecal shedding test (PCR rapid) culture slow.

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10
Q

What are the clinical signs of Johne’s disease?(in cattle)

A
  • The disease progressively damages the intestines of affected animals,
  • First signs may be reduced productivity such as reduced milk yields.
  • As progresses to more severe disease can result in profuse and persistent diarrhoea, severe weight loss, loss of condition and infertility. Affected animals eventually and inevitably die.
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11
Q

How does Salmonella invade the mucosa?

A
  • Interaction with M cells, intestinal epithelial cells.
  • Type three mediated invasion of cells.
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12
Q

Salmonella stimulates the innate response through a few mechanisms. what are they

A
  • Some effectors injected by the TTSS stimulate cytokine production (part of the enteropathogenic response)
  • Extracellular bacterial components interact with Toll Like receptors (TLRs)
  • Intracellular bacterial components can interact with NOD receptors (Similar to TLRs but inside cells)
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13
Q

The host generates an antibody response to the Salmonella.

How are different antigens and pathogens are sampled and processed by the gut.?

A
  • Particulate antigens (e.g. bacteria) are sampled via M-cells and dendritic cells. Soluble antigens via epithelium.
  • Antigen presented to T cells in situ or in regional lymph nodes.
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14
Q

Describe the development of immune response to salmonella in the gut

A

Dendritic cells present antigens and co-stimulatory signal to T cells. Activated T cells travel (homing) from regional lymph nodes via blood to GALT. In GALT T cells secrete cytokines which promote proliferation and differentiation of B cells into plasma cells and T cells not CTLs. Plasma cells secrete first IgM followed by IgA which interferes with pathogen binding to epithelial cells. IgG is produced into the circulation to reduce or eliminate pathogen via opsonisation and neutralises bacterial toxins.

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15
Q

Is canine coronavirus the same as the virus that caused the covid pandemic in 2020?

A

No. Though both are beta coronaviruses and the canine virus is fairly similar to the human seasonal coronavirus OC43. The canine virus cannot infect humans.

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16
Q

How is canine coronavirus transmitted?

A

Enteric virus transmitted via the faecal-oral route
Note that other strains can cause respiratory infection and occasional more severe viruses arise by mutations.

17
Q

How is the canine coronavirus spread?

A

through feces. virus can be shed in apparently healthy dogs

18
Q

How can enteric viruses cause diarrhoea in the host?

A

Viruses cause lysis of enterocytes following infection, associated with inflammation, loss of tight cell junctions, decrease in absorptive surface area, reduced enzymes etc.
Four main mechanisms:
- Increased secretion (Cl-).
- Increased cell permeability (cells “leaky”)
- Decreased absorption
- Altered gut motility