Lecture 6: Myobacteriae Flashcards

(75 cards)

1
Q

What is the family and genus of Myobacteriae?

A

Family: Mycobacteriaceae
Genus: Myobacterium
-more than 100 species

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2
Q

Define what Myobacteriae are?

A

Slow-growing, rod-shaped, non-spore forming, nonmotile

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3
Q

What is the main way to identify Myobacteriae?

A

Acid-fast staining (Ziehl-Neelsen stain)

  • Myobacteriae have cell walls with high lipid contents (25%) that are able to absorb the dye
  • once stained they cannot be decolorized with acid solutions
  • you’ll see a bunch of pink spots if it is a Zihel-Neelsen stain*
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4
Q

Define M. Tuberculosis

A
  • disease of humans transmitted by respiratory droplets
  • human host with person-to-person transmission
  • presents like cancer because of non-specific symptoms and hemoptysis
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5
Q

Which animals can be incidentally infected by M. Tuberculosis?

A
  • apes
  • elephants
  • dogs
  • cattle
  • pigs
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6
Q

What is the transmission of TB from humans to animals called?

A

Reverse zoonosis

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7
Q

When was reverse zoonosis of TB discovered?

A
  • exotic animal farm in Illinois in 1996 where elephant handlers may have transmitted disease to elephants
  • otherwise not typically found in the wild
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8
Q

What are specific clinical symptoms associated with MTB?

A
  • coughing that lasts three or more weeks
  • coughing up blood
  • chest pain, pain with breathing or coughing
  • unintentional weight loss
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9
Q

What are non-specific clinical symptoms of MTB?

A
  • fatigue
  • fever
  • night sweats
  • chills
  • loss of appetite
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10
Q

What is NTM?

A

Non-tuberculosis Myobacterium

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11
Q

What is the pathogenesis of NTM?

A
  • present in environment but rarely cause disease in comparison to MTB and M. leprae which are obligate pathogens (need to cause disease in order to be transmitted)
  • host susceptibility determines infection
  • share common properties with MTB: acid fastness, ability to cause pulmonary and extrapulmonary granulomatous disorders
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12
Q

What host susceptibility factors determine infection of NTM?

A
  • deficiencies of IFN-gamma receptor or IL-12 receptor
  • acquired deficiency of cell-mediated immunity (HIV)
  • diabetes
  • preexisting lung disease
  • body habitus in postmenopausal women (pectus excavatum, scoliosis, mitral valve prolapse)
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13
Q

What is the prevalence of NTM?

A

largely unknown because it’s not actually a reportable disease since its not transmissible from person-to-person
-rates increasing from 90s but this may be because of improved detection methods

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14
Q

What are recent trends that have sparked interest in NTM?

A
  • increasing NTM infections in AIDS patients
  • increasing NTM lung disease in HIV negative population (caucasian women over age of 50 who have had children are at higher risk of disease but they don’t know why)
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15
Q

Have rates of TB been decreasing in relation to NTM last 10 years?

A

NO, we have just gotten better at detecting NTM and distinguishing it from TB

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16
Q

What are the 4 clinical syndromes that NTM causes in humans?

A
  1. pulmonary disease (most common)
  2. superficial lymphadenitis
  3. Disseminated disease (MAC-myobacterium avium complex in HIV)
  4. skin and soft tissue infection due to direct inoculation
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17
Q

What are the 4 main methods to diagnose NTM?

A
  1. acid-fast microscopy with fluorochrome stains
    - but it has unreliable sensitivity
    - environmental contamination rarely positive on smear
  2. Gastric lavage fluid/Bronchoscopy if poor sputum production
  3. Nucleic Acid Amplification Tests (NAA): provides fast differentiation of TB from NTM
    - MTB-PCR identifies species
  4. Sputum culture = GOLD STANDARD but it takes forever
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18
Q

What are the 4 clinical syndromes that NTM causes in humans?

A
  1. pulmonary disease (most common)
  2. superficial lymphadenitis
  3. Disseminated disease (MAC-myobacterium avium complex in HIV)
  4. skin and soft tissue infection due to direct inoculation
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19
Q

What are the 4 main methods to diagnose NTM?

A
  1. acid-fast microscopy with fluorochrome stains
    - but it has unreliable sensitivity
    - environmental contamination rarely positive on smear
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20
Q

What is M. Bovis?

A
  • causes less than 1.4% of pulmonary TB
  • spread to humans from inhalation of infectious droplet nuclei and ingestion of raw milk
  • animal host: cattle
  • strictly pathogenic in humans but very rare in US
  • human-to-human transmission is rare
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21
Q

How is M. Bovis controlled in transmission from cattle to humans?

A

Pasteurization

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22
Q

What are the two main ways M. Bovis is transmitted to humans?

A
  1. direct contact with infected bodily secretions (i.e. inhalation of infected droplets)
  2. consumption of infected animal products (i.e. milk)
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23
Q

What is the largest impact that M. Bovis has?

A

constraint in international trade of animals and their products –> results in major economic losses

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24
Q

What is the main route of cattle-to-cattle transmission of M. Bovis?

A

respiratory excretion and inhalation (cattle show respiratory disease at slaughter)

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25
What does consumption of M. Bovis infected milk cause?
extrapulmonary TB-like symptoms = Bovine TB
26
Does M. Bovis only exist in cattle?
NO; cattle are natural and main host but also exists among bears, cheetahs, possums, deer, pigs, leopards, lions etc.
27
What is treatment for M. Bovis?
RIPE without the P: Rifampin, Isoniazid, Ethambutol - 2 months isoniazid, rifampin and ethambutol - followed by 7 months of isoniazid and rifampin * * all three because it is resistant to pyrazinamide**
28
Do you have a special risk of acquiring M. Bovis if you are immunocompromised?
NO
29
In Kruger National Park which animals were spreading TB and how?
- high prevalence of tb in buffalo populations - contaminate the environment through saliva and nasal secretions - warthogs were drinking from same watering holes and grazing same areas
30
What is a spillover species?
animals that can move pathogens between natural areas and surrounding human settlements and agricultural areas
31
What was the spillover species in Kruger National park?
Warthog - comingled with other animals - breached fences and barriers surrounding wild areas - found in farms, golf courses, gardens, trash bins, and rest camps where tourists stay
32
What is the biggest threat of TB in Kruger National Park?
Ecosystem Collapse
33
How did they resolve M. Bovis outbreak in KNP?
- tagged warthogs and tried to give them M. Bovis therapies | - helped decrease transmission a lot
34
Where is the highest prevalence of M. Bovis in California?
desert areas in the lower, southern areas
35
What is M. Simiae?
- isolated in humans in Europe, USA, Asia (mostly in immunocompromised hosts i.e. HIV patients) - first isolated in healthy Macacus rhesus monkeys imported from India - Transmission: animal-to-animal between animals in captivity; animals to humans - primates do not PRESENT with disease
36
What is M. Avium Complex (MAC)?
- multiple subspecies that cause human disease (M. avium & M. intracellulare) - acquired from environment - unknown prevalence b.c not mandatory to report
37
What are the main three risk factors for MAC Exposure?
aerosolized water, soil exposure, showerheads
38
What are the 4 subspecies for M. Avium?
1. ssp. avium 2. ssp. paratuberculosis 3. ssp. silvaticum 4. ssp. hominissuis
39
What are the three ways MAC displays?
1. Disseminated MAC in immunocompromised hosts 2. Cervical lymphadenitis in children (causes lymph node enlargement) 3. Pulmonary (most common) also reported to infect bones, joints, urinary tract, skin
40
Can MAC cause a latent infection?
NO: this is how you can distinguish MAC from TB (TB does have latent infection)
41
What is the primary reservoir for MAC for human disease?
Birds: secrete large amounts in their feces
42
Are protozoa and insects involved in spreading MAC?
Yes; specifically M. avium ssp. avium and ssp. paratuberculosis
43
What other animals play host to MAC?
-rabbits, deer, bison, elk, boar, birds, kangaroo
44
Who is at the highest risk of acquiring MAC?
immunocompromised patients
45
How do birds spread MAC?
They excrete bacilli in large amounts in their feces, bacteria can persist in the soil or in water for long periods afterwards
46
How does MAC manifest in immunocompetent patients?
- Most people never develop clinical disease, indicating that the normal immune system can control the organism - If it does develop infection it is primarily pulmonary
47
What are the symptoms of pulmonary MAC?
``` Presents the same way TB does -chronic cough -fevers -chills -night sweats -dyspnea hemoptysis -weight loss ```
48
How does pulmonary MAC show up in a high resolution CT?
-shows infiltrates without cavitation in upper lobes
49
Which two groups show pulmonary MAC?
1. those with underlying lung disease | 2. those without underlying lung disease, particularly women over the age of 50 who do not smoke
50
What is disseminated MAC?
Opportunistic infection typically seen in HIV patients - associated with more rapid progression of HIV because it activates lymphocytes * disseminated MAC is huge risk for people who have uncontrolled HIV*
51
What are symptoms of disseminated MAC?
Fever, drenching sweats, anorexia, diarrhea, abdominal pain
52
What diagnosis Disseminated MAC?
1. Median CD4 cell count of less than 50 2. Anemia or Elevated alkaline phosphatase 3. Blood cultures growing Acid-fast bacilli
53
What is the main treatment for MAC?
- daily clarithromycin or azithromycin paired with rifampin or rifabutin and ethambutol - could add streptomycin 2-3x a week for 2 months - check sputum monthly for AFB smear and culture - need to treat for at least one year after culture is negative
54
What is required in order to start long treatment period for MAC?
-have at least 2 sputum culture or deep bronchoscopy/levage along with displayed symptomatology
55
Who takes MAC prophylaxis?
HIV-infected patients with CD4 count less than 50
56
What is taken for MAC prophylaxis?
1200 mg azithromycin weekly
57
When do you discontinue MAC prophylaxis?
When patients respond to HAART therapy and have a CD4 count >100 for more than 3 months
58
What is Myobacterium marinum?
- "swimming pool granuloma"/ "fish tank granuloma" - free living bacterium found in fish - cutaneous disease is acquired after trauma to skin in contaminated nonchlorinated fresh or salt water
59
What are the symptoms of M. Marinum?
- papulonodular lesions that ulcerate - abscess formation - nodules along lymphatics
60
What activities are most closely associated with acquiring M. Marinum?
- cleaning an aquarium | - diving activities
61
What causes Leprosy?
Myobacterium leprae
62
What are characteristics of M. Leprae?
- aerobic acid fast bacilli - obligate intracellular pathogen - waxy coating of mycolic acid
63
How is M. Leprae transmitted?
Unclear, suspected to be through prolonged close contact and transmission via nasal droplets
64
Who is at risk for Leprosy?
- small percentage that has cell-mediated immunity defects | - 95% are resistant
65
Which countries have been worst hit with Leprosy?
- Brazil - India, Nepal - Tanzania, Mozambique
66
How prevalent is Leprosy in the United States?
- Fewer than 100 cases annually - California, Louisiana, Massachusetts, NY, Texas and Hawaii affected - most patients acquired it abroad
67
What is the Pathogenesis of Leprosy?
-M. Leprae prefers infection of skin and Schwann cells, causes skin lesions and neuropathy in cold, peripheral locations (fingers, toes, testicles, ears, nose)
68
What are symptoms of Leprosy?
- nerve demyelination - loss of sensation/vision - loss of fingers and toes (from injury and infection) - skin dryness - muscle weakness - severe pain
69
What are two types of Leprosy presentation?
1. Tuberculoid Leprosy | 2. Lepromatous Leprosy
70
What is Tuberculoid Leprosy?
Cell-mediated immune response predominates (T cells)
71
What is Lepromatous Leprosy
Humoral immune response predominates (B cells) - poorly controlled with high bacterial load which makes it highly infectious - "classical" picture of leprosy
72
How do you diagnose Leprosy?
- Lepromatous Form: observe acid-fast bacilli microscopically - Histopathologic Forms: use skin testing to inject inactivated antigen and test for hypersensitivity reaction
73
What is the treatment for Leprosy?
Lepromatous Form: Rifampin, Dapsone, or Clofazimine for a year Tuberculoid Form: Rifampin and Dapsone for 6 months
74
Main impacts Leprosy has on quality of life?
1. physical deformities including loss of sensation and loss of motor function 2. lost income/disability 3. stigma
75
What is the main host for Leprosy?
Armadillos