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Bugs and Drugs > Acid-Fast Bacilli and Filamentous Bacteria > Flashcards

Acid-Fast Bacilli and Filamentous Bacteria Flashcards

1
Q

What are Koch’s Postulates?

A
  1. The microorganism must be present in all cases of the disease
  2. The pathogen can be isolated and grown in pure culture
  3. The pathogen can be inoculated into a healthy, susceptible host and cause disease
  4. The pathogen can be reisolated from the new host and shown to be the same as the original inoculated pathogen
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2
Q

What is unique about the growth of mycobacteria and filamentous bacteria?

A

They are extremely slow growing and resemble fungi on plates

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3
Q

What is the oxygen dependence of mycobacterium?

A

They are aerobic

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4
Q

What is the generation time for mycobacterium?

A

Over 24 hours (extremely slow growing)

E. coli generates in 20 minutes

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5
Q

Do mycobacterium more closely resemble gram positive or gram negative bacteria?

A

Gram positive because they lack LPS (however, they do NOT gram stain)

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6
Q

What is the waxy coat of mycobacterium made of?

A

Mycolic acid

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7
Q

What are the layers of the mycobacterial cell wall?

A
  1. cell membrane
  2. peptidoglycan
  3. arabinogalactan
  4. mycolic acid
  5. superficial lipids (cord factor)
  6. stretching from cell membrane to cell surface = LAM
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8
Q

What is LAM?

A

Lipoarabinomannan which is a glycolipid found in numerous subspecies of mycobacteria.
It is a virulence factor that modulates macrophage function and scavenges oxygen radicals

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9
Q

What is the major virulence factor of mycobacteria and how does it work?

A

LAM modulates macrophage function and scavenges oxygen radicals

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10
Q

What makes mycobacteria waxy, and difficult to stain via gram stain?

A

Mycolic acids which are very long chain fatty acids. They are in mycobacteria, nocardia and corynebacteria

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11
Q

What three bacterial species have mycolic acids?

A

Mycobacteria
Corynebacteria
Nocardia

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12
Q

What is Wax D?

A

it is mycolic acid, peptidoglycan and arabinogalactan (the layers of the mycobacterial cell wall below the superficial lipids)

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13
Q

What pathogenesis is associated with Wax D?

A
  1. granuloma formation

2. caseous necrosis

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14
Q

What is Freund’s adjuvant?

A

It is mineral oil and killed Mycobacteria bovis which can be used as an immunopotentiator (booster)

Killed M bovis serves as an antigen to stimulate and immune response and make Ab

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15
Q

What is trehalose dimycolate?

A

Cord factor associated with mycobacteria.

It forms serpentine cords in culture and is toxic to PMN, damages mitochondria and causes granuloma formation

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16
Q

What is cord factor?

A

Trehalose dimycolate of mycobacteria

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17
Q

What three pathogenic responses are associated with cord factor?

A
  1. granuloma formation
  2. PMN toxicity
  3. Damaged mitochondria
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18
Q

Acid fastness is a property of what two bacteria?

A

Mycobacteria and nocardia

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19
Q

Describe the process of acid-fast staining.,

A
  1. boiling carbol fuschin (red basic dye)
  2. acid wash with alcohol and hydrochloric acid
  3. Methylene blue counter stain
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20
Q

What is the original stain used in acid-fast staining? Why must it be boiling?

A

Boiling carbol fuschin (basic red dye) is used. It must be boiling to penetrate the waxy layer

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21
Q

How many species of mycobacterium tuberculosis exist? Which causes most disease in humans?

A
  1. M. tuberculosis
  2. M. bovis (disease with ingestion of raw dairy, BCG vaccine)
  3. M. africanum
  4. M. canetti
  5. M. microti
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22
Q

Which mycobacteria tuberculosis species is the basis for the BCG vaccine against TB?
How else is this bacteria acquired?

A

M. bovis

It can also be acquired by ingesting raw dairy

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23
Q

What percent of the world’s population is a reservoir for M. tuberculosis?

A

1/3

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24
Q

How does transmission of M. tuberculosis occur?

A

person-to-person (inhalation, ingestion), although they can survive on inanimate objects that are out of direct light

Inhalation- 1 to 5 micron droplets that go to alveoli
Ingestion- raw dairy from infected cattle

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25
Q

When M. tuberculosis is in a host, what happens?

A
  1. it gets ingested by macrophages and inhibits phagolysosomal fusion so it is not killed by inactivated macrophages
  2. Drain to hilar and mediastinal nodes and multiply locally
  3. bacteremic spread to other organs
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26
Q

Why is M. tuberculosis not killed when it is ingested by macrophages?

A

It prevents the fusion of the phagolysosome so it is able to survive in the inactivated macrophage

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27
Q

What two factors does control of initial M. tuberculosis infection depend on?

A
  1. inoculum size (number of organisms)

2. Resistance of the host (IL-12, IFNg, TNF, immunosuppression HIV, malnutrition)

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28
Q

Resistance of the host to M. tuberculosis can be affected by genetics or acquired factors. What three genetic factors play the largest role in resistance?

A

IL-12. IFNg, TNF

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29
Q

What are the two types of TB lesions?

A
  1. Exudative- acute, edema, PMN, macrophages
  2. Granulomatous- later, central zone with giant cells, midzone epithelioid cells, outer fibroblasts, monocytes, lymphocytes
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30
Q

What are the three zones of granulomatous TB lesions?

A

central zone- giant cells
midzone- epithelioid cells
Outer zone - fibroblasts, monocytes, lymphocytes

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31
Q

What are the three phases of TB disease?

A
  1. Primary disease
  2. Progressive primary disease (or Latent)
  3. Reactivation disease
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32
Q

Describe primary disease of TB.

A

Most are asymptomatic or have mild respiratory infection that may present as pneumonia

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33
Q

Describe progressive primary disease of TB.

A

This occurs in elderly and immunocompromised and is a progressive pneumonia

34
Q

What is reactivation disease of TB?
How long does it take for reactivation symptoms to develop?
Where does reactivation most frequently occur?

A

4% per year in the first two years of the infection get reactivated pneumonia along with:
fever, night sweats, malaise, fatigue and weight loss

It takes months for symptoms to develop and they usually occur at the apices of the lungs because it requires high O2 tension

35
Q

What are the 5 ways to test for TB?

A
  1. skin testing - PPD, Tuberculin
  2. Quantiferon
  3. Staining (acid-fast)
  4. Culturing
  5. Molucular techniques (PCR, molecular probes)
36
Q

What is the “gold standard” of TB testing?

A

culturing the bacteria

37
Q

What is the Quantiferon test?

A

It is a TB test that uses IFNg release assays

38
Q

Describe the treatment requirements for TB.

A

They require multiple drugs over extended time

Typical = 4 drugs for 2 months, 2 drugs for 4 months

39
Q

What does it mean if a TB strain is MDR?

A

Multi-drug resistant meaning that it is not treated by 2 of the first line drugs

40
Q

What does it mean if TB is XDR?

A

extremely drug resistant meaning that it is resistant to the first line drugs (isoniazid, rifampin, fluoroquinolone) and resistnat to at least one second line drug (kanamycin, amikacin, capreomycin)

41
Q

Non-tuberculosis mycobacteria are also called ______________. They are organized with the _______________ classification system.

A

Atypical mycobacteria.

They are classified by the Runyon Classification

42
Q

What are the 4 Runyon Classification groups for atypical mycobacteria?

Which are slow-growing?

A

1- photochromogens- produce pigment in light

  1. Scotochromogens- make pigment in light or dark
  2. nonchromogens- no pigment
  3. rapid growers

Groups 1,2,3 are slow growing

43
Q

What are the three group 1 mycobacteria?

A

Theses are the photochromogens that make pigment in the light.
M. Kansaii- TB-like syndrome
M. Marinum- skin/soft tissue infection with water
M. ulcerans- buruli ulcer from water/soil organism

44
Q

What is the pigment characteristics of group 2 atypical mycobacteria?
What is an example of this bacteria?
What is the pathogenesis?

A

Scotochromogens= pigment in light or dark

M. scrofulaceum causes cervical adenitis in kids

45
Q

What are examples of group 4 mycobacteria? How do they differ from the other mycobacteria?

What pathogenesis do they cause?

A

They are rapid growers
M. abscessu/chelonae

They usually are just contaminants in culture but occassionally cause infection when a foreign object is left post surgery

46
Q

What is group 3 Runyon’s mycobacteria?

What are the two strains, and which causes most disease in human

A

They do not produce pigment and are:
M. avium - most infections in humans
M. intracellulare

47
Q

What is the environment of type 3 mycobacteria?

A

ubiquitous in water at a temperature of 41 degrees celcius (like campylobacter)

48
Q

What are the two major disease syndromes of M. Avium (type 3 runyons)

A
  1. lung disease- usually in patients with preexisting lung disease (smokers, COPD)
  2. HIV infections- causes nonfocal fever in patients with HIV and CD4 below 100
49
Q

M. avium causes nonfocal fever syndrome in patients that have ____________ and a CD4 count below _________.

A

HIV, below 100

50
Q

What percent of adults have tattoos?

A

21%

51
Q

What mycobacteria is associated with bad tattoo ink?

A

M. chelonae a type 4 rapid-grower

52
Q

M. Leprae is associated with what disease?

A

Hansen’s disease (leprosy)

53
Q

How many cases of leprosy are noted worldwide? In the US?

A

10 million worldwide

100 in the US

54
Q

M. leprae is morphologically identical to what other bacteria?

A

M. tuberculosis

55
Q

M. leprae cannot be cultured in vitro but must be grown on what?

A

The footpads of mice and 9 banded armadillos

56
Q

How is M. leprae spread?

A

Respiratory or direct contact but transmission is difficult

57
Q

What is the incubation time of M. leprae?

A

2-10 years

58
Q

What are the two classification systems of M. leprae?

A
  1. WHO by number of bacteria (paucibacillary or multibacillary)
  2. Ridley-Jopling- lepromatous to tuberculoid
59
Q

What are the 4 associations of tuberculoid M. leprae?

A

stronger T-cell response
fewer skin lesions
localized skin reaction
few bacteria (paucibacillary)

60
Q

What are the 4 associations of lepromatous M. leprae?

A
  1. weak/no T cell response
  2. nodular lesions
  3. abundant bacteria (multibacillary)
  4. progressive clinical course
61
Q

How do you diagnose M. leprae?

A
  1. acid-fast staining

2. lepromin

62
Q

What is the mainstay treatment of M. leprae?

A

Dapsone

rifampin and clofazimine too

63
Q

How do nocardia stain with a gram stain?

A

Gram positive

64
Q

What is the oxygen consumption of nocardia?

A

Aerobic- has catalase and SOD

65
Q

Describe the shape of nocardia.

A

Filamentous bacteria that has a branching morphology like fungus

66
Q

What is the minimum number of days needed to culture and grow nocardia?

A

3-5

67
Q

What bacteria is classified as “weakly acid fast”?

Why is it only weakly acid fast?

A

Nocardia is weakly acid fast because instead of very long chain mycolic acid lipids, they have short mycolic acid

68
Q

Where are nocardia found?

A

In soil- an opportunistic infection

69
Q

What nocardia strain is in the US and who does it infect?

A

N. asteroides and it infects immunocompromised patients

70
Q

What are the 3 clinical syndromes associated with nocardia?

A
  1. subacute pneumonia
  2. brain dissemination
  3. Skin disease
71
Q

What is the mode of transmission if someone gets skin disease from nocardia?
What is the strain?

A 
Direct implantation (skin trauma) usually in the tropics
Nocardia Brasiliensis which usually forms granules
72
Q

What is the drug of choice for nocardia infections?

How long should it be given?

A

Trimethoprim-sulfamethoxazole given for 6 to 12 months

73
Q

Describe the structure of Actinomyces.

A

They are “ray-fungi” that are filamentous branching gram positive rods
They do NOT stain with acid fast

74
Q

How do you stain actinomyces?

A

with gram stain.

They do NOT stain with acid fast because they lack mycolic acid

75
Q

What is the oxygen consumption of actinomyces?

A

microaerophiles or anaerobic

76
Q

How long does it take for actinomyces to grow?

A

Over 2 weeks

77
Q

What actinomyces strain is the primary human pathogen?

A

A. israelii

78
Q

Where are actinomyces found?

A

Part of normal flora (mouth, GI, GU)

79
Q

Who does actinomyces infect?

A

Immunocompromised patients typically following trauma or procedures where foreign objects are introduced

80
Q

Actinomyces present with chronic __________ noted by the presence of _________ granules.

A

Chronic draining sinuses associated with sulfur granules

81
Q

What are the 3 syndromes associated with actinomyces?

A
  1. orocervicofacial- lumpy jaw and bad dentition
  2. thoracic- descending infection
  3. Abdominopelvic- after surgery
82
Q

How long is therapy for actinomyces infections? What is the drug of choice?

A

4-12 months and we use penecillin

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