Mycobacterium Flashcards

1
Q

What family is Myocobacterium in?

A

Mycobacteriaceae

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2
Q

What are some characteristics of mycobacterium?

A

Gram positive, acid fast + bacteria, human and animal pathogen, mycolic acid and UNIQUE PEPTIDOGLYCAN

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3
Q

What are some characteristics of mycolic acids?

A

Lipid compounds, fatty acids in the cell wall, carbon chain length varies by genus, rapid growing (shortest chain), slow growing (longest chain), virulence factor.

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4
Q

Which bacterium has the shortest chain? Which bacterium has the longest chain?
Corynebacterium, nocardia, mycobacterium

A

Corynebacterium - longest
Mycobacterium - shortest
Nocardia - middle

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5
Q

T/F. Mycobacterium are resistant to some drugs, chemicals, and environmental factors.

A

True

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6
Q

What stain is used to stain mycobacterium? What are the steps? What are some examples of the stain?

A

Acid fast staining (uses a lipid permeabilizing first step (with heat or chemical solvent).
1. Primary stain
2. An acidic alcohol decolorizing step
3. A counter stain (Carbon fuscin > decolorizer > methylene blue)
Ziehl-Neelsen, Kinyons, Auramine Rhodamine (fluorescent based stain - sensitive)

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7
Q

T/F. Myocobacterium has immunomodulating activities and prevent phagocytic killing

A

True

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8
Q

What are obligate pathogens of mycobacterium? Can they survive a long time in a contaminated environment?

A

M. tuberculosis complex, M. avium subsp. paratuberculosis, M. leprae, M. lepraemurium.
YES!!

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9
Q

T/F. All mycobacterium are obligate pathogens.

A

False.

Some are opportunistic pathogens (soil/water saprophytes)

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10
Q

What are the two big virulence factors of mycobacterium?

A

Mycolic acid containing cell wall lipids, Cell protein antigens

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11
Q

What are the advantages of having mycolic acid containing cell wall lipids?

A
  1. Facilitate survival in macrophages (facultative intracellular)
  2. Stimulate cytokine production
  3. Enhance adjuvant/immunomodulating effects
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12
Q

T/F. Cell protein antigens (exotoxins and extracellular enzymes) of mycobacterium play a prominent role in disease pathogenesis.

A

False.
DO NOT PLAY A ROLE!
EXCEPT: M. ulcerans (mycolactone/macrolide toxin)

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13
Q

What are diseases that are caused by mycobacterium spp?

A

Mammalian tuberculosis: M. tuberculosis, M. bovis
Avian tuberculosis: M. avian subsp. Avium (serotypes 1-3)
Leprosy: M. leprae (humans), M. lepraemurium (cat)
Johne’s disease: M. avium subsp. paratuberculosis

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14
Q

This specie of mycobacterium is important to humans (maintain inside lungs). A serious disease causing agent in HIV/AID infected patients. An emerging zoonosis and artrozoonosis in animals. Elephant to human transmission is possible. Endemic infection in some wild life populations.

A

M. Tuberculosis

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15
Q

T/F. M. tuberculosis includes multidrug resistant TB (MDR-TB) and extensively drug resistant TB (XDR).

A

True

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16
Q

T/F. Treat Tuberculosis with heat and antibiotics.

A

False.

THERE IS NO TREATMENT FOR TUBERCULOSIS!

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17
Q

What is the route of entry for M. bovis?

A

Ingestion (common), inhalation, contact with mucous membranes and broken skin.
GI tract MAIN portal of entry (esp for CATS)
Basically can enter ANY SITE!

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18
Q

T/F. M. bovis has a narrow range of hosts and affect certain geographic regions.

A

False.

WIDE host range and geographic distribution.

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19
Q

Who is the primary host for M. bovis? Which regions are affected?

A

Bovine (infect several wildlife species).

Badgers in UK, Feral Brush tail possums in New Zealand.

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20
Q

T/F. Because M. Bovis is infective, it can survive for a long time outside of the host.

A

False. ONLY for a few WEEKS!

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21
Q

T/F. M. Bovis is distinguishable from M. Tuberculosis distinguishable in humans.

A

False. NOPE not distinguishable

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22
Q

What are some characteristics of BOVINE TUBERCULOSIS? How is in seen in livestock animals when they’re affected?

A

Chronic, progressive and latent infections (dormant in the body without progression).
Seldom until the disease is advanced (months).
Livestock: no evidence until slaughter (carcass is condemned).

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23
Q

Where are the lesions of Bovine Tuberculosis? How do lesions look? What do early lesions look like? What do later lesions look like?

A

Lesions in any organ (main lesion: GRANULOMA)
Early lesions: abscess-like
Late lesions: firm, nodular lesions in organs and associated with lymph nodes of lungs, head, GI.

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24
Q

T/F. M. bovis is shed in milk.

A

True.

Pasteurization is important for humans.

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25
Q

What is the initial pathogenesis of M. bovis?

A

Bacilli phagocytosed by macrophages > secrete TNF-alpha and IL-12 > T-helper lymphocytes activity > secretion of INF-gamma and IL-2 > cell mediated immunity and destruction of bacilli

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26
Q

What is the pathogenesis of M. bovis after it survives cell mediated immunity?

A

Infected macrophages killed after releasing cytotoxins and enzymes (type IV hypersensitivity) > tissue destruction and CASEIOUS NECROSIS
Advanced stage: Enzymatic action > liquefaction and cavity form > rupture > dissemination.

27
Q

What are “tubercles” caused by M. bovis?

A

Due to CELL MEDIATED IMMUNITY!
Granulomas with epithelioid macrophages or caseous necrosis in center surrounded by multinucleated giant cells (Langerhan’s cells).
Can be seen with acid fast.

28
Q

What are the elements of Tuberculosis lesions?

A

Granuloma, macrophages/epithelioid cells, coagulative/caseous necrosis, fibrosis, mineralization (liquefaction).

29
Q

What are diagnostic tests for M. bovis (Bovine Tuberculosis)?

A

Tuberculin hypersensitivity skin tests, In vitro whole blood tests (cell-mediated immunity), post-moretem/histopath, imaging, direct exam of tissues, culture.

30
Q

How do you perform Tuberculin hypersensitivity skin tests?

A

Screening test: caudal tail fold with SINGLE-strength dose of M. bovis PPD. Suspect reactors in screening > paired cervical tests with DOUBLE strength M. bovis PPD and M. avium PPD in separate areas of neck.
READ REACTION AT INJECTION SITE AFTER 72 HRS.
Low sensitivity in some species.

31
Q

What are some whole blood tests for cell-mediated immunity (INF release assays) for M. bovis?

A

Bovigam (bovine only - contains PPD), QuantiFERON-TB Gold (humans/primates - contain mixtures of synthetic peptides), Lymphocyte proliferation assays (zoo and wild type species)

32
Q

What are methods to perform direct exam of tissues?

A

Acid fast stained smear: sensitivity may be low due to low numbers.
Nucleic acid detection: PCR on fresh or fixed LN tissues.
Fatty acid methyl ester (FAME): detection by HPLC (rarely used).

33
Q

Which medium is used to culture M. bovis?

A

Lowenstein Jensen

Conventional tube medial slants, liquid media used with automated, continuously monitored incubators.

34
Q

T/F. ALWAYS use combinations of anti-tubercular drugs to treat active tuberculosis.

A

True.

35
Q

T/F. Treatment of bovine TB has >95% success, whereas optimum human treatment is not practical or efficacious.

A

False.
Bovine TB: not practical or efficacious.
Human; >95% success.

36
Q

What are the problems of Bovine TB in humans?

A

Single drug activity limited (bacT. is at different stages or different places), multiple drug resistance (prolonged treatment needed), lesions are walled off (poor drug distribution: reactivation).

37
Q

What are the most important factor for eradication of bovine TB/Preventon?

A

Tracing the potential source of infection (prevention)

USDA-APHIS accredited-Free status (eradication)

38
Q

Are there vaccines for cattle? humans? What is the disadvantage of vaccines? Are vaccines used in the US?

A

No vaccine for bovine (use INTRADERMAL test: false positive), human vaccine (BCG) used in high prevalence areas, interferes with diagnostic tests, not used in US.

39
Q

What is the main disease that is caused by M. Leprae?

A

Leprosy or Hansen’s disease

40
Q

How is M. Leprae transmitted?

A

Shedding (not from skin).

41
Q

What is the reservoir for M. Leprae? Is it zoonotic?

A

Nine banded Armadillo (southern US)

ZOONOTIC!

42
Q

Describe the lesions of Leprosy or Hansen’s disease caused by M. Leprae.

A

Chronic granulomatous debilitating disease.

Anaesthetic skin lesions, peripheral neuropathy, and nerve thickening.

43
Q

What do lesions caused by M.Leprae look like?

A

Tuberculoid lepropsy (paucibacillary)
AFB lepromatous lepropsy (multibacillary)
No cell mediated response, severe disease with AFB.

44
Q

What is the diagnostic testing for M. Leprae?

A

NONE.

45
Q

T/F. M. Leprae, M. Lepraemurium, M. Avium complex are all zoonotic.

A

True

46
Q

What disease does M. Lepraemurium cause? What an important characteristic of M. Lepraemurium?

A

Feline and Murine Leprosy.

Very fastidious organisms (hard to culture)

47
Q

How do lesions of Feline and Murine Leprosy caused M. Lepraemurium look like?

A

Solitary/multiple nodules or ulcerated lesions.

Granulomatous dermatitis panniculitis (inflammation of subcue tissue)

48
Q

What are some diagnostic testings for M. Lepraemurium?

A
Direct staining (Geimsa or Acid fast/neg. stained)
Culture, biopsy and histopath (best choice!), PCR.
49
Q

What is the most important subspecies within M. Avium Complex (MAC)? What does it cause?

A

M. Avium subsp. Prartuberculosis

Johne’s disease

50
Q

What are the characteristics of M. Avium Complex?

A

Wide spread in soil and water (including treated municipal tap water) > low pH and high temp. tolerance.
Phenotypically indistinguishable members.

51
Q

What are the characteristics of Johne’s disease caused by M. avium subsp. Paratuberculosis?

A

Chronic, progressive granulomatous enteritis: thicken ileal mucosa > no absorption > D+, bottle-jaw.

52
Q

Who is the primary host for Johne’s disease caused by M. avium subsp. paratuberculosis?

A

Ruminants (cattle), young.
Sheep, goat, illama, alpacas, deer can be infected.
Symptom appear 2 years after IP

53
Q

How is M. avium subsp. paratuberculosis transmitted? What is the possible etiology in humans?

A

Milk (resistance to pasteurization), ingestion

Crohn’s Disease

54
Q

What is the ICEBERG effect caused by M. avium subsp. paratuberculosis?

A

Clinical infected animals > other animal under different stages of the infection.

55
Q

What the diagnostic testings for M. avian subsp. paratuberculosis?

A

Cultures on Herrold’s egg yolk (GOLD STANDARD), Decontamination, Culture + PCR, biopsy/necropsy from ileal-cecal region, INF release assay/lymphblast Stimulation Assay Serology.

56
Q

T/F. M. avium subsp. paratuberculosis has mycobactin dependency for different from other species.

A

True

57
Q

T/F. The most sensitive test is a herd with a prior confirmed cases.

A

FALSE

A herd with no prior confirmed cases.

58
Q

Why do you get FALSE NEGATIVE from INF release assay/lymphoblast Stimulation Assay Serology?

A

Advanced stages of disease: anergy (no response)

59
Q

What is the treatment for M. Leprae?

A

Combination therapy (or else develop resistance)

60
Q

What is the treatment for M. Lepraemurium?

A
Combination therapy (long term therapy)
Dog: Doxy can be effective
61
Q

What are treatments/controls and eradications of M. avian complex?

A

Diagnosis and removal of infected animals, management programs, antimicrobial, ISOLATE/SLAUGHTER, purchase from negative herds, separate calf rearing area, prevent contamination of calf material, apply lime to contaminated pasture.
May interfere with M. bovis.

62
Q

What are the characteristics of other saprophytic mycobacterial species?

A

Rapid/slow growing species, Granulomatous to pyogranulomatous host response, Chronic, non-healing cutaneous lesions and lack of response to antibacterial treatments.
Lesions: multibacillary or paucibacillary (Depending on immunity.

63
Q

How do you diagnose Johne’s disease?

A

Hypersensitivity skin test
Serology
Nucleic acid detection