Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

micro unit 4 > mycobacteria I and II > Flashcards

mycobacteria I and II Flashcards

1
Q

mycobacteria gram stain

A

poor. acid fast stain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

do mycobacteria grow in vitro?

A

yes, buit very slowly and need special nutrients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what kind of metabolism do they have?

A

obligate aerobic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the important structural components of the mycobacteria

A

mycolic acid (acid fastness), wax D: adjuvant, phosphatides for caseating necrosis. cord factor gives it serpentine appearance. phtiocerol dimycocerosate lung pathogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

are mycobacteria oxen producing?

A

no.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what else in the environment are they resistant to?

A

alkali and acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

TB resistance to antibiotics?

A

yes. they are chromosomal resistant. it is a large health emergency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the reservoir for TB?

A

humans.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how is TB transmitted?

A

human to human through respiratory droplets.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what happens after inhalation of the TB

A

it resides in macrophages where it inhibits the fusion of the phagosome with the lysosome and the bacteria proliferate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is a TB exudative lesion?

A

in the lung, at the initial site of infection. it gives an acute inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is a ghon complex? where is it located

A

it is the exudative lung lesion and its draining lymph node. it is usually present in the lower lobe.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

granulomatous lesion from TB

A

central area of infected langerhan’s giant cells surrounded by a zone of epithelioid cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

tubercule of TB infections

A

older granuloma surrounded by fibrosis and calcification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what can happen to tubercules

A

they can erode and empty contents. directly it can infect new lung lung parenchyma. if coughed up it can infect GI or be inhaled and infect new lungs. if it gets into the blood stream it can infect new organs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

TB reactivation lesions occur where?

A

they can happen in the apices, lower lobes, kidneys, brain, bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how is TB infection usually controlled?

A

by the CMI (CD4+, TH-1 cells) macrophages and gamma interferon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what cell and protein is specifically important?

A

macrophage with protein NRAMP isa critical. mutations lead to more severe infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

why is the TB infections hard to clear?

A

can be intracellular. caseous material is hard to penetrate. and because it multiplies slowly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

can TB carriers by contagious with negative sputum?

A

yes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what demographics are predisposed to TB

A

poverty, poor health and diet, elderly men, native Americans and african americans.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

TB infection findings on exam? constitutional

A

fever, fatigue, night sweats, weight loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what clinical features of pulmonary TB

A

cough, hemoptysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is scrofula

A

it is cervical adenitis caused by either TB or M. scrofulaceum infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is common in primary TB infections?

A

erythema nodosum. nodules on the skin of the legs. immunogenic response from CMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is miliary TB

A

multiple disseminated lesions forming millet seed appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what can disseminated TB cause?

A

meningitis, osteomyelitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

most common site of TB osteomyelitits?

A

vertebral spine. Potts disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

GI TB symptoms and cause?

A

diarrhea, abdominal pain, obstruction and hemorrhage in the ileocecal region. maybe caused by TB or M. bovis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

oropharyngeal TB

A

usually painless ulcer with local adenopathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

renal TB

A

usually presents as sterile pyuria. dysuria, flank pain, hematuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are the symptoms of most mycobacterial infections

A

they are usually asymptomatic. the CMI holds them back.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

AIDS + TB

A

this is very dangerous. rapid decline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

mycobacteria and remicade?

A

this may reactivate latent infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

PPD skin test for TB?

A

PPD injected and the diameter of the erythema/induration from the HSR is measured. this is a response to the tuberculin. positivity is subjective.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

15mm PPD?

A

positive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

10mm PPD

A

positive with risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

5mm PPD

A

positive if deficient CMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what must be considered if the test is misleading, such as <15mm

A

positives may result from past disease or vaccination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

when are there misleading negatives for PPD

A

when the infection is new (<5weeks) or if connected with measles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how long does culturing TB take?

A

2 weeks.

42
Q

is there a PCR for TB?

A

yes, but not sensitive.

43
Q

treatment for pulmonary TB?

A

isoniazid 6mon + rifampin 6 month, + pyrazinamide 6 mon.

44
Q

treatment if disseminated and likely immunocompromised or resistant TB?

A

9-12 months isoniazid+ rifampin+ pyrazinamide + ethambutol

45
Q

treatment for asympt or latent TB infections

A

isoniazid for 6 mon

46
Q

prophylaxis for TB exposed children

A

6 mon of isoniazid

47
Q

treatment for resistant TB

A

use rifampin for prophylaxis if the resistance was isoniazid

48
Q

for MDR strains of TB

A

use cipro + amikacin + ethionamide + cycloserine/

49
Q

XDR strains of TB

A

contact the CDC.

50
Q

what must we monitor TB treated patients for?

A

for hepatitis, drug-induced.

51
Q

how long before patient loses TB infectivity

A

3 weeks

52
Q

is there a vaccine for TB?

A

yes. based on bacillus calmette guerin a live attenuated M. bovis. its is only semi affective. prevents 70% of infectious cases, but not latent ones.

53
Q

what are the atypical mycobacters?

A

photochromagens. scotochromagens, nonchromagens, rapidly growing

54
Q

photochromagens characteristics

A

produce pigment in the light. do not kill guinea pigs.

55
Q

what are the two types of photochromagens

A

M. kansaii, and M. marinum

56
Q

M. kansaii

A

environmental with an unknown reservoir. found in midwest and texas

57
Q

what does kansaii cause?

A

it causes a lung disease similar to TB. treated with some antibiotics.

58
Q

M. marinum

A

found in fresh and salt water.

59
Q

what does Marinum cause?

A

forms granuloma, ulcerating lesions on abrasions exposed to swimming water or aquariums. t

60
Q

what to treat marinum with?

A

tetracyclines

61
Q

scrotochromagens characteristics and organism

A

produces pigment in the dark. doesn’t kill guinea pigs. M. scrofula.

62
Q

what does M. scrofula cause?

A

it causes scrofulas like TB, actually more common cause than TB for pediatric scrofula.

63
Q

what is the reservoir for M scrofula?

A

water.

64
Q

how do we treat scrofula infections?

A

surgically excise the infected nodes.

65
Q

nonchromogens characteristics and organisms

A

no pigment. doesn’t kill guinea pigs. M. avium/M. intracellularae hard to distinguish. they are highly drug resistant.

66
Q

what do the nonchromogens causes?

A

they cause a pulmonary disease indistinguishable from TB in severely immunocompromised patients.

67
Q

where do we find nonchromogens?

A

they are environmental found in soil and water.

68
Q

how do we treat the nonchromogens

A

highly drug resistant so we need clarithromycin with ethambutol, rifabutin or cipro.

69
Q

rapidly growing mycobacteria characteristics and organmis

A

no pigment doesn’t kill guinea pigs, culturable in about 1 week. M. fortuitum/M. chelonei. very difficult to distinguish. M. abscessus M. smegmatis

70
Q

where do we find M. fortuitum/M. chelonei

A

in soil and water

71
Q

who gets infected with the M. fortuitum/M. chelonei?

A

prosthetic hips. indwelling catheters, immunocompromised, puncture wounds.

72
Q

how do we treat M. fortuitum/M. chelonei

A

amikacin + doxy + surgical excision.

73
Q

where do we find M. abscessus?

A

environment.

74
Q

what does abscessus causes?

A

lung infections, skin, bone and joints. highly antibiotic resistant.

75
Q

where we find M. smegmatis

A

normal flora under the foreskin of the penis

76
Q

M. leprae characteristics

A

slowest growing human pathogen. 14 day doubling time

77
Q

what temperature does M. leprae like?

A

30 C. thats why its found on the periphery

78
Q

what are the reservoirs for M. leprae

A

humans and armadillos

79
Q

how is M. leprae transmitted?

A

by prolonged contact with an infected patient. spread by nasal secretions and skin lesions.

80
Q

where is M. leprae found?

A

worldwide. seen in the US: TX, LA, CA, HA.

81
Q

what percentage exposed is actually infected?

A

only 10%. 90% + clear the infection.

82
Q

what happens when infected?

A

the bacteria replicates within the skin histiocytes, endothelial cells, and schwann cells.

83
Q

is there nerve damage in M. leprae infection?

A

yes, both by bacterial infection and by immunological response.

84
Q

why do the symptoms range on a scale?

A

because the of CMI response.

85
Q

tuberculoid leprosy characteristics

A

strong CMI response! CD4+ and Th1 cells. Th1 secretes gamma interferon, IL-2, 12. granulomas containing giant cells form.

86
Q

how many bacteria are seen with tuberculoid leprosy?

A

few bacilli seen in this form

87
Q

what is the lepromatin skin test in tuberculoid form?

A

the test will be positive due to strong response.

88
Q

lepromatous leprosy characteristics

A

poor CMI response! there is useless Th2 response that forms non protective antibodies. anergic. foamy histiocytes form

89
Q

what causes nerve damage in tuberculoid leprosy

A

the immunological response.

90
Q

what causes the nerve damage in lepromatous leprosy

A

the bacterial infection in schwann cells.

91
Q

how many bacteria are seen in the lepromatous form

A

there are a ton of bacilli present.

92
Q

what is the lepromatin skin test show in lepromatous

A

it will be negative due to lack of immunity

93
Q

what does the tuberculoid form look like?

A

hypopigmented macular or plaque-like skin lesions, thickened superficial nerves, anesthesia of the skin lesions

94
Q

what does lepromatous form look like?

A

multiple nodular skin lesions, leonine facies,

95
Q

labs for tuberculoid

A

they will be negative, diagnose on the exam

96
Q

labs for the lepromatous

A

acid-fast stain of the skin lesions or nasal scrapings, lipid-laden macrophages full of acid-fast. VDRL and RPR +
PCR also +

97
Q

treatment for tuberculoid?

A

dapsone + rifampin for 2 years

98
Q

treatment for lepromatous

A

dapsone + rifampin + clofazimine for 2 yrs or until the lesions clear.

99
Q

what is a common complication of the treatment?

A

severe erythema nodosum.

100
Q

how do we control the EN from therapy?

A

treat with thalidomide.

101
Q

why do we bother distinguishing between the mycobacteria?

A

because some are highly contagious and others are not.

micro unit 4 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions