4. Mycobacteria and Corynebacteria Flashcards
- Why are mycobacteria and corynebacteria difficult to grow?
- What phylum are corynebacteria and mycobacteria both members of?
- Strong waxy coat.
- Actinobacteria.
- What species does mycobacterium tuberculosis affect?
- M. tuberculosis subdivisions?
- Humans, bovids and many more.
- Major pathogens of animals (opportunistic and obligate), saprophytes (rarely progress to disease) (atypical).
- What bacteria type are mycobacteria?
- Motility – why?
- Sporing? – Why?
- Purpose of high-lipid waxy surface? – Trade off?
- Action on sugars?
- Gram +ve rods (in culture – fine rods, in tissue – plump rods or clumps due to being waxy and sticking together).
- Non-motile due to waxy surface.
- Non-sporing – due to waxy surface.
- Protection from immune system – slow progression.
- Oxidative
Mycobacteria staining.
Ziehl-Neelsen stain.
Heat required to melt wax and drive carbol fuchsin through lipid content of cell wall and into bacteria.
Cool and rewax.
Attempt to destain with just acid.
Any normal bacteria destains with acid (acid-fast) but mycobacteria does not.
Then attempt destain with acid-alcohol which can work through lipid coat of saprophytic mycobacteria (acid-alcohol fast) but not the very thick lipid contents of cell walls of pathogenic mycobacteria.
- What mycobacterial infections are closely related and what species do they affect and rarely affect?
- What mycobacterial infection affects poultry and what other species can it affect?
- Mycobacterial infection found in voles?
- Mycobacterial infection found in fish?
- M. tuberculosis – humans and primates, rarely affect dogs, caged birds, pigs and cattle.
M. bovis – cattle, rarely affect other farm animals, cats, deer, badgers and humans. - M. avium complex – Can affect most avian spp but not psittacines and very rarely affects pigs and cattle.
- M. microti.
- M. marinum.
- Pathogenesis of bovine TB?
- Inhalation or ingestion of mycobacterium.
Mycobacterium takes over macrophages and use it as a place to hide.
Mycobacterium causes the macrophages to move to the local LNs and start to aggregate.
Moves to lungs, liver or spleen dept on route of infection.
Miliary TB is caused – microscopic foci of infection.
Crunchy lesions (patient will be subclinical but will be shedding disease).
Infected macrophages start to aggregate and move together. They are surrounded by T cells, new macrophages. Then formation of epithelioid cells and giant cells (multinucleate bodies due to multiple cells merging to form one giant cell).
The necrosis and calcification, caseous cheese-like pus surrounding, surrounded by fibroblasts and thus a granuloma is formed.
- What can happen after granuloma formation?
2 Why is coughing seen in TB patients?
- Continuous activity – growth of tubercle which pops, risk of spread (around the body and via shedding).
or
Latent TB – subclinical
- Patient trying to clear airways of obstructions.
- Cause of M. tuberculosis?
- Cause of M. avium? – testing for this?
- Inhalation causing lesions in the lung and at local LNs.
- Faecal-oral spread (in gut rather than lungs), 1 year incubation, lesions of the intestine/liver/spleen/bone marrow.
Causes patient to be weak, listless, lame, wing droop.
– Possible to tuberculin test in wattle.
Treatment and prevention of mycobacterial infections?
No antibiotics given to animals, 3-4 antibiotics given for years – have been directly observed therapy.
Vaccination in humans (BCG vac).
No vac for animals.
Animals can be culled.
- What is Johne’s disease?
- What spp can also be affected?
- Where are these infections most prevalent?
- Spread?
- What does Johne’s disease cause?
- M. avium (paratuberculosis).
- Cattle, sheep, goats, deer.
- Worldwide in temperate areas.
- Faecal-oral spread.
Calves affected in first year of life by close contact.
Can survive for months in environment in the faeces.
Lives in macrophages at level of the ileum, colon and local LNs. - Appears like IBD as causes thickening of epithelium, slow burning inflammatory disease. Suggested could possibly be the cause of human IBD but no proof.
Get lesions in a few months and there is spread and progression down the gut. Becomes clinical after 1-2 years.
Clinical: D+ (lots in cattle, sometimes in sheep).
Wasting of the patient.
Death at approx. 2-3 years.
- Control of Johne’s disease?
- Testing?
- No eradication scheme.
- Johnin test (75% false positives).
Rectal smear with ZN stain (75% false negatives as very few of the mycobacteria are shed).
Other immunological assays and PCR.
Better to use culture:
Test faeces/rectal smears in cattle >2yrs biannually.
Cull infected animals.
Clean premises.
Buy Johnin negative cattle.
Vaccination.
Rabbit control.
- Corynebacteria seen in humans?
- C. diptheria.
- What are corynebacteria known as as a group?
- Where are they found?
- What type of infection do they cause?
- Diptheroids.
- Found widespread in the environment, in plants as pathogens and in animals as both commensals and facultative pathogens.
- Pyogenic – lots of pus.
- Major subdivisions of corynebacteria?
- C. renale, C. pseudotuberculosis, Rhodococcus equi.
Identification of corynebacteria.
With light microscopy of organisms in a clinical sample.
- See gram +ve rods that are non-motile and non-sporing.
- Pleomorphic – come in different forms e.g. almost cocci/slender rods/filamentouus, some clump together and stick to one another.
On culture.
- Corynebacteria = dry and crumbly, white-cream-yellow, non-haemolytic, very small (need 48-72hrs).
- BUT C. pseudotuberculosis = waxy flakes, haemolytic.
- Rhodococcus equi = 24hr – shiny colonies,
>24hr – mucoid + pink tinge.
