Microbiology - Acid-Fast Bacteria And Bacteria Without Cell Walls

Front 1

What are the two species of Mycobacterium?

Back 1

Mycobacterium tuberculosis
Mycobacterium leprae

Front 2

What makes the Mycobacteria acid-fast on staining?
What other species are acid-fast?
What color do they stain?

Back 2

Mycobacterium are thin rods with lipid-laden cell walls. This high lipid content makes them acid-fast on staining.

Only Mycobacterium and Nocardia are acid-fast.

Acid-fast organisms stain red.

Front 3

What is Mycobacterium tuberculosis?

Where does it most commonly infect?

Back 3

Mycobacterium tuberculosis is an acid-fast bacillus (rod) that is an obligate aerobe.

It most commonly infects the lungs, where oxygen is abundant.

Front 4

What are the mycosides of Mycobacterium tuberculosis?

Back 4

1) Mycolic acid
2) Mycoside: mycolic acid bound to a carbohydrate, forming glycolipid
3) Cord factor: formed by the union of 2 mycolic acids
4) Sulfatides: resemble cord factor with sulfates attached to the disaccharide
5) Wax D

Front 5

What are the functions of the cord factor, sulfatides, and Wax D mycosides?

Back 5

Cord factor: found only in virulent strains of Mycobacterium tuberculosis, its presence results in parallel growth of the bacteria, so they appear as cords. Cord factor inhibits neutrophil migration and damages mitochondria. Cord factor may also contribute to the weight loss found in TB patients.

Sulfatides: inhibit the phagosome from fusing with the lysosome that contains bacteriocidal enzymes.

Wax D: acts as an adjuvant (enhances antibody formation to an antigen) and may be the part of Mycobacterium tuberculosis that activates the protective cellular immune system.

Front 6

What is the pathogenesis of Tuberculosis?

Back 6

1) Facultative intracellular growth: inhaled bacteria cause local infiltration of neutrophils and macrophages. Phagocytosed bacteria are not destroyed because of the sulfatides. They multiply and survive in the macrophages. The bacteria cruise through the lymphatics and blood to set up camp in distant sites.

2) Cell-mediates immunity: Some of the macrophages succeed in phagocytosing and breaking up the invading bacteria. These macrophages then run toward a local lymph node and present parts of the bacteria to T-helper cells, which multiply and enter circulation. When T-cells encounter their antigenic target, they release lymphokines that serve to attract and activate macrophages, which can now destroy bacteria.

Macrophage attack usually results in local destruction and necrosis of the lung tissue. The necrosed tissue looks like a granular creamy cheese, called caseous necrosis.

Front 7

Why might you get a patient with a false positive PPD test?

Back 7

Some people from other countries have had the BCG (bacillus Calmette-Guerin) vaccine for tuberculosis.

Front 8

Which patients might present with a false negative PPD test?
How do you confirm the test?

Back 8

Patients that are usually anergic, lacking a normal immune response due to steroid use, malnutrition, AIDS, etc.

A second injection (either with Candida or mumps antigen) is given. Most people have been exposed to these antigens, so only individuals who are anergic.

Front 9

Mycobacterium tuberculosis is transmitted via aerosolized droplet nuclei. Where do these inspired droplets land in the lungs?

Back 9

The inspired droplets land in the areas of the lung that receive the highest air flow: the middle and lower lung zones.

Front 10

What is a Ghon focus? Ghon complex?

Back 10

Ghon focus: a calcified tubercle in the middle or lower lung zone
Ghon complex: a Ghon focus accompanied by perihilar lymph node calcified granulomas

Front 11

Which groups are susceptible to symptomatic tuberculosis?

Back 11

Children, the elderly, and the immunocompromised (especially HIV infected persons).

Front 12

What are the types of infections that are caused by tuberculosis?

Back 12

1) Pulmonary tuberculosis
2) Pleural and pericardial infection
3) Lymph node infection
4) Kidney
5) Skeletal
6) Joints
7) Central nervous system
8) Miliary tuberculosis

Front 13

What is the most common site of reactivation tuberculosis?

Back 13

The apical areas of the lungs around the clavicles, where the oxygen tension is the highest.

Front 14

What is the most common extrapulmonary manifestation of tuberculosis?

Back 14

Scrofula, AKA Lymph node infection: the cervical lymph nodes are usually involved. They become swollen, mat together, and drain.

Front 15

What is miliary tuberculosis?

Back 15

Tiny millet-seed-sized tubercles (granulomas) are disseminated all over the body like a shotgun blast. The kidneys, liver, lungs, and other organs are riddled with the tubercles.

Front 16

What are the tools for diagnosis of tuberculosis?

Back 16

1) PPD skin test: screening test indicates an exposure sometime in the past
2) Chest X-ray: May show an isolated granuloma, Ghon focus, Ghon complex, old scarring in the upper lobes, or active tuberculosis pnemonia
3) Sputum acid-fast stain and culture: when this is positive, it indicates an active pulmonary infection

Front 17

What is the Tuberculosis "Rule of Fives"

Back 17

- Droplet nuclei are 5 micrometers and contain 5 Mycobacterium tuberculosis bacilli
- Patients infected with Mycobacterium tuberculosis have a 5% risk of reactivation in the first 2 years and then a 5% lifetime risk.
- Patients with "high five" HIV will have a 5 + 5% risk of reactivation per year

Front 18

What are some examples of atypical Mycobacterium?

Back 18

Mycobacterium avium-intracellulare: in AIDS patients, causes disseminated infection with fever, weight loss, hepatitis, bone marrow suppression, and chronic water diarrhea. In normal hosts (rare), it causes pulmonary tuberculosis and cervical lymphadenitis

Mycobacterium kansaii: causes pulmonary tuberculosis

Front 19

Where does Mycobacterium leprae usually infect?

Back 19

Mycobacterium leprae infection involves the cooler areas of the body (skin, superficial nerves, eyes, nose, and testes).

Front 20

What are the two forms of leprosy? Which one is more severe?

Back 20

1) Lepromatous leprosy (Most severe)
2) Tuberculoid leprosy

Front 21

What is the pathogenesis of lepromatous leprosy?

Back 21

Defective T-suppressor cells (T-8 cells) block the T-helper cell's response to the antigens. Patients cannot mount a delayed hypersensitivity reaction.

Front 22

What is the pathogenesis of tuberculoid leprosy?

Back 22

Delayed hypersensitivity reaction is intact, so macrophages are able to destroy the bacterium. Patient demonstrates localized superficial, unilateral skin and nerve involvement. Patients are non-infectious and spontaneously recover.

Front 23

What is the lepromin skin test? Which patients would have a positive result?

Back 23

It measures the ability of the host to mount a delayed hypersensitivity reaction against antigens of Mycobacterium laprae.
Patients with tuberculoid leprosy will have a positive result.

Front 24

What is unique about Mycoplasmataceae?

Back 24

They are unique bacteria because they lack a peptidoglycan cell wall. Their only protective layer is a cell membrane, which is packed with sterols (like cholesterol) to help shield their organelles from the exterior environment.

Front 25

What are the 2 pathogenic species of Mycoplasmataceae?

Back 25

Mycoplasma pneumoniae
Ureaplasma urealyticum

Front 26

What antibiotics are effective or ineffective against Mycoplasmataceae species?

Back 26

Erythromycin and Tetracycline are effective
Penicillin and Cephalosporins are ineffective because of the lack of cell wall.

Front 27

What does Mycoplasma pneumoniae cause?

Back 27

1. Tracheobronchitis
2. Walking (atypical) Pneumonia: Fever with a dry, nonproductive hacking cough

Front 28

What is the virulence factor of Mycoplasma pneumoniae?

Back 28

Protein P1 (an adhesin) that helps the organism attach to respiratory epithelium.

Front 29

What is a diagnostic test for Mycoplasma pneumoniae? How does it work?

Back 29

Cold agglutinins: Certain antigens present on human RBCs are identical to antigens of the Mycoplasma pneumoniae membrane glycolipids. Antibodies to these bacterial antigens crossreact with RBC antigens and agglutinate the RBCs at 4 C.

Front 30

Where might you find Ureaplasma urealyticum?

Back 30

Ureaplasma loves swimming in urine and produces urease to break down urea.
Ureaplasma urealyticum is part of the normal flora in 60% of healthy sexually active women and commonly infects the lower urinary tract, causing urethritis.