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Bacteriology > 5.3 Gram positive rods, Mycobacterium, Rhodococcus > Flashcards

5.3 Gram positive rods, Mycobacterium, Rhodococcus Flashcards

1
Q

how many species of mycobacterium? what general classification?

A

> 170 spp.
1. Mycobacterium tuberculosis complex
2. Non-tuberculosis
3. Leprosy-causing

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2
Q

important mycobacterium in cattle

A
  • M. bovis
  • M. avium subsp. paratuberculosis > ruminants
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3
Q

what species can mycobacterium bovis infect?

A
  • M. bovis > cattle, many others (incl. humans)
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4
Q

what is an important mycobacterium that can affect birds?

A

M. avium

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5
Q

mycobacterium characteristics:air stats, morphology, environment, growth, reproduction, lesions, weaknesses, gram stain, etc?

A
  • Strict aerobe, non-spore forming, rods
  • Very fastidious, slow growth rate
  • Saprophytes (multiply environment)
  • Some species are opportunistic or obligate pathogens
  • Survive inside macrophages
  • Cause chronic and granulomatous lesions
  • Persists in the environment, resistant to disinfectants
  • Susceptible to heat treatment (pasteurization)
  • Grampositive
  • Cell wall: rich in lipids, especially mycolic acid (virulence factor)
  • Ziehl Neelsen stain: Alcohol Acid Resistant or Acid-Fast bacterium
  • Resist the acid and/or ethanol-based decolorization procedures
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6
Q

difference between mycobacterium and other gram positive bacteria for staining?

A

mycobacteria have mycolic acid outer layer
-for mycobacteria, use Ziehl Neelsen stain: Alcohol Acid Resistant or Acid-Fast bacterium

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6
Q

difference between mycobacterium and other gram positive bacteria for staining?

A

mycobacteria have mycolic acid outer layer
-for mycobacteria, use Ziehl Neelsen stain: Alcohol Acid Resistant or Acid-Fast bacterium

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7
Q

does canada have bovine TB? is it reportable?

A
  • Canada is considered officially free of bovine TB
  • Isolated cases may occur
  • TB is a reportable disease and all cases must be reported to CFIA
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7
Q

does canada have bovine TB? is it reportable?

A
  • Canada is considered officially free of bovine TB
  • Isolated cases may occur
  • TB is a reportable disease and all cases must be reported to CFIA
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8
Q

mainteneace hosts of bovine TB

A

– Cattle
– Bison, elk and deer (USA and Canada) – Opossums, ferrets (New Zealand)
– Badgers (Europe)
– Buffalo (Africa)

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9
Q

how does transmission of bovine TB occur?

A
  • Inhalation (most common)
  • Ingestion (unpasteurized milk, calves)
  • Cutaneous, genital, congenital (rare)
  • Exposure to infected respiratory secretions, milk, saliva, urine
  • Exposure to infected free-ranging wildlife
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10
Q

pathogenesis of bovine TB

A

aerosol infection
>innate control
>containment in macrophages
>latency
>reactivation (<10%)
>disease/transmission

> > inhaled into lungs
infects macrophages
granuloma forms out of macrophages
granuloma bursts, releasing bacteria

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11
Q

what lesions are associated with M. bovis?

A
  • Granulomas (tubercles)
  • Yellow, caseous, calcified, may resemble abscesses
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12
Q

virulence factors of M. bovis?

A
  • Capability to escape killing by macrophages
  • Mycolic acid - protection against cationic proteins, lysozyme and oxygen radicals of phagocytosis
  • Iron capturing ability – required for survival inside macrophages
  • Sulfolipids – prevent phagosome-lysosome fusion (important for survival inside macrophages)
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13
Q

bovine TB clinical signs

A
  • Develop over months
  • May become dormant, reactivate (stress, old age)
  • Early stage may be asymptomatic
  • Late stage
    – Progressive emaciation
    – Fever, weakness, inappetence
    – Moist cough
    – Enlarged, draining lymph nodes
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13
Q

bovine TB clinical signs

A
  • Develop over months
  • May become dormant, reactivate (stress, old age)
  • Early stage may be asymptomatic
  • Late stage
    – Progressive emaciation
    – Fever, weakness, inappetence
    – Moist cough
    – Enlarged, draining lymph nodes
14
Q

Post-Mortem Diagnosis of bovine TB:

A

-Granulomas in the lymph nodes
-Lung granuloma
-Pleura granuloma
-Intestinal granulomas

> It affects many other organs depending on the portal of entry of the infection

15
Q

diagnostics for bovine TB in live cattle

A

Tuberculin skin test
-Purified protein derivative (PPD) tuberculin
- Caudal fold: Preliminary screening of cattle
- Comparative cervical: Re-testing of reactors

Blood-based test (ELISA): interferon gamma assay
- Identifies animals at an early stage of infection
- Used in conjunction with the tuberculin test

The basis of tuberculin testing is the induction of delayed-type hypersensitivity reaction to the intradermal injection of antigenic substances derived from a laboratory strain of Mycobacterium bovis (M. bovis). The hypersensitivity response results in the accumulation of cells and fluid in the dermis which creates swelling at the injection site. In test positive animals, the intradermal skin reaction develops within 24 hours post-injection, reaching a maximum by 48-72 hours, characterized by erythema and swelling, but rarely to the point of induration or ulceration.

16
Q

lab diagnostics of bovine TB

A

Specimens: lymph nodes, tissue lesion, aspirates, tracheobronchial wash

  • Agar: Löwenstein-Jensen + pyruvate (M. bovis 3-8 weeks)
  • Acid Fast (Ziehl Neelsen stain)
    Polymerase Chain Reaction (PCR)
    > Identify specific genes from Mycobacterium (heat shock protein and 16S rRNA genes)
17
Q

how can we control M bovis? what are issues we need to consider?

A

Wildlife reservoirs of M. bovis
– Complicate eradication efforts
– Culling
– Barriers to prevent wildlife access

Bovine TB vaccines are not commercially available

Treatment not advised (long term, shedding organism)
– Test-and-slaughter

Note:
Atypical mycobacteria in other animals? YES, there is
treatment!
Fluoroquinolones, macrolides, minocycline

18
Q

types of avian tuberculosis that cause disease? what kind of disease? how do they enter? how do we control?

A
  • M. avium-intracellulare complex, M. avium subsp. avium
  • Chronic infection
  • Often entry by intestine => dissemination
  • Control as bovine TB
19
Q

what disease is consistent with this clinical case?

  • Geraldine a four-year-old Guernsey
  • Top milker but started declining in last lactation
  • Started losing weight after calving, developed watery diarrhea
  • Eventually pregnant and kept until calved, although emaciated and seriously ill
A

Geraldine has paratuberculosis (Johne’s disease)

Agent: Mycobacterium avium subsp. paratuberculosis

20
Q

Lesions associated with Johne’s disease?

A

Granulomatous proliferation of ileo-caecal mucosa (presence also in local lymph nodes)

21
Q

what causes Johne’s disease? what species are affected and what are the symptoms?

A
  • Agent: Mycobacterium avium subsp.
    paratuberculosis
  • Intestinal infection of ruminants (occasionally other species)
  • Very slow growth (8-12 weeks)
  • Numerous asymptomatic shedders (feces,
    sometimes milk); “iceberg infection”
  • Infected herd: 35% immune, 60% asymptomatic shedders, 2-5% develop clinical disease
22
Q

what causes Johne’s disease? what species are affected and what are the symptoms?

A
  • Agent: Mycobacterium avium subsp.
    paratuberculosis
  • Intestinal infection of ruminants (occasionally other species)
  • Very slow growth (8-12 weeks)
  • Numerous asymptomatic shedders (feces,
    sometimes milk); “iceberg infection”
  • Infected herd: 35% immune, 60% asymptomatic shedders, 2-5% develop clinical disease
23
Q

what is the ‘life cycle’ of Johne’s disease?

A

-calves <6 mo. generally infected via fecal-oral transmission
>often latent
>2-6 years old, early subclinical MAP: appear healthy, mostly test neg
> could progress to advanced subclinical MAP: milk production drops, mostly test pos
> 2-8 years can see clinical disease
>stresses can trigger onset of clinical signs, high MAP shedding
>diarhhea, ill-thrift, wasting, death

23
Q

what is the ‘life cycle’ of Johne’s disease?

A

-calves <6 mo. generally infected via fecal-oral transmission
>often latent
>2-6 years old, early subclinical MAP: appear healthy, mostly test neg
> could progress to advanced subclinical MAP: milk production drops, mostly test pos
> 2-8 years can see clinical disease
>stresses can trigger onset of clinical signs, high MAP shedding
>diarhhea, ill-thrift, wasting, death

24
Q

Paratuberculosis (Johne’s disease) diagnosis

A

– Serology (ELISA, milk, serum; whole blood gamma
interferon)
– Acid-fast stain (biopsy, scraping, lymph node)
– Culture (biopsy, scraping, lymph node, feces)
– Real-time PCR similar to culture in sensitivity

25
Q

treatment of paratuberculosis (Johne’s)

A
  • Treatment: Culling affected or strongly seropositive animals
26
Q

prevention of Johne’s

A

– Culling sick animals, detect and culling of shedders
– Separate calves at birth from mother
– Pasture rotation (survives in the soil)
– Vaccination?

27
Q

Rhodococcus equi aka Prescottella equi characteristics: morphology, environment, lesions

A
  • Gram-positive coccobacilli-rods
  • Aerobic, slightly acid-fast
  • Saprophyte (soil with manure)
  • Foal, pig and cattle isolates have distinct species-specific virulence plasmids
  • Facultative intracellular pathogen
28
Q

what disease does rhodococcus equi cause? what animals and lesions? what is the mode of transmission?

A
  • Foals (1-2 months)
  • Pyogranulomatous bronchopneumonia
  • Foals swallow sputum laden with R. equi, which replicates in their intestinal tract (abscesses)
  • Rare other animal species (pigs and cattle “tuberculous” cervical lymphadenitis)
29
Q

epidemiology of rhodococcus equi in foals?

A

Epidemiology in foals:
– Heavy contamination of soil on pasture, in foaling and rearing
areas (fecal) > dust inhalation > infection by virulent strains
– Most frequent around fading period of maternal antibodies
– Antimicrobial resistance emerging due to prophylactic treatment

30
Q

Rhodococcus equi treatment

A

– Rifampicin + macrolide (Clarithromycin )=>penetrate cells
– 3-8 weeks

31
Q

prevention of rhodococcus equi?

A

– Colostrum; hyperimmune plasma
– Dust control
– No vaccine yet?? Challenging problem
– Prophylactic antibiotics?

Bacteriology (15 decks)

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