Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

micro unit 4 > mycobacteria I and II > Flashcards

mycobacteria I and II Flashcards

(101 cards)

Start Studying
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
what is common in primary TB infections?
erythema nodosum. nodules on the skin of the legs. immunogenic response from CMI
26
what is miliary TB
multiple disseminated lesions forming millet seed appearance
27
what can disseminated TB cause?
meningitis, osteomyelitis.
28
most common site of TB osteomyelitits?
vertebral spine. Potts disease.
29
GI TB symptoms and cause?
diarrhea, abdominal pain, obstruction and hemorrhage in the ileocecal region. maybe caused by TB or M. bovis.
30
oropharyngeal TB
usually painless ulcer with local adenopathy.
31
renal TB
usually presents as sterile pyuria. dysuria, flank pain, hematuria
32
what are the symptoms of most mycobacterial infections
they are usually asymptomatic. the CMI holds them back.
33
AIDS + TB
this is very dangerous. rapid decline.
34
mycobacteria and remicade?
this may reactivate latent infections.
35
PPD skin test for TB?
PPD injected and the diameter of the erythema/induration from the HSR is measured. this is a response to the tuberculin. positivity is subjective.
36
15mm PPD?
positive.
37
10mm PPD
positive with risk factors
38
5mm PPD
positive if deficient CMI
39
what must be considered if the test is misleading, such as <15mm
positives may result from past disease or vaccination
40
when are there misleading negatives for PPD
when the infection is new (<5weeks) or if connected with measles.
41
how long does culturing TB take?
2 weeks.
42
is there a PCR for TB?
yes, but not sensitive.
43
treatment for pulmonary TB?
isoniazid 6mon + rifampin 6 month, + pyrazinamide 6 mon.
44
treatment if disseminated and likely immunocompromised or resistant TB?
9-12 months isoniazid+ rifampin+ pyrazinamide + ethambutol
45
treatment for asympt or latent TB infections
isoniazid for 6 mon
46
prophylaxis for TB exposed children
6 mon of isoniazid
47
treatment for resistant TB
use rifampin for prophylaxis if the resistance was isoniazid
48
for MDR strains of TB
use cipro + amikacin + ethionamide + cycloserine/
49
XDR strains of TB
contact the CDC.
50
what must we monitor TB treated patients for?
for hepatitis, drug-induced.
51
how long before patient loses TB infectivity
3 weeks
52
is there a vaccine for TB?
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
what are the atypical mycobacters?
photochromagens. scotochromagens, nonchromagens, rapidly growing
54
photochromagens characteristics
produce pigment in the light. do not kill guinea pigs.
55
what are the two types of photochromagens
M. kansaii, and M. marinum
56
M. kansaii
environmental with an unknown reservoir. found in midwest and texas
57
what does kansaii cause?
it causes a lung disease similar to TB. treated with some antibiotics.
58
M. marinum
found in fresh and salt water.
59
what does Marinum cause?
forms granuloma, ulcerating lesions on abrasions exposed to swimming water or aquariums. t
60
what to treat marinum with?
tetracyclines
61
scrotochromagens characteristics and organism
produces pigment in the dark. doesn't kill guinea pigs. M. scrofula.
62
what does M. scrofula cause?
it causes scrofulas like TB, actually more common cause than TB for pediatric scrofula.
63
what is the reservoir for M scrofula?
water.
64
how do we treat scrofula infections?
surgically excise the infected nodes.
65
nonchromogens characteristics and organisms
no pigment. doesn't kill guinea pigs. M. avium/M. intracellularae hard to distinguish. they are highly drug resistant.
66
what do the nonchromogens causes?
they cause a pulmonary disease indistinguishable from TB in severely immunocompromised patients.
67
where do we find nonchromogens?
they are environmental found in soil and water.
68
how do we treat the nonchromogens
highly drug resistant so we need clarithromycin with ethambutol, rifabutin or cipro.
69
rapidly growing mycobacteria characteristics and organmis
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
where do we find M. fortuitum/M. chelonei
in soil and water
71
who gets infected with the M. fortuitum/M. chelonei?
prosthetic hips. indwelling catheters, immunocompromised, puncture wounds.
72
how do we treat M. fortuitum/M. chelonei
amikacin + doxy + surgical excision.
73
where do we find M. abscessus?
environment.
74
what does abscessus causes?
lung infections, skin, bone and joints. highly antibiotic resistant.
75
where we find M. smegmatis
normal flora under the foreskin of the penis
76
M. leprae characteristics
slowest growing human pathogen. 14 day doubling time
77
what temperature does M. leprae like?
30 C. thats why its found on the periphery
78
what are the reservoirs for M. leprae
humans and armadillos
79
how is M. leprae transmitted?
by prolonged contact with an infected patient. spread by nasal secretions and skin lesions.
80
where is M. leprae found?
worldwide. seen in the US: TX, LA, CA, HA.
81
what percentage exposed is actually infected?
only 10%. 90% + clear the infection.
82
what happens when infected?
the bacteria replicates within the skin histiocytes, endothelial cells, and schwann cells.
83
is there nerve damage in M. leprae infection?
yes, both by bacterial infection and by immunological response.
84
why do the symptoms range on a scale?
because the of CMI response.
85
tuberculoid leprosy characteristics
strong CMI response! CD4+ and Th1 cells. Th1 secretes gamma interferon, IL-2, 12. granulomas containing giant cells form.
86
how many bacteria are seen with tuberculoid leprosy?
few bacilli seen in this form
87
what is the lepromatin skin test in tuberculoid form?
the test will be positive due to strong response.
88
lepromatous leprosy characteristics
poor CMI response! there is useless Th2 response that forms non protective antibodies. anergic. foamy histiocytes form
89
what causes nerve damage in tuberculoid leprosy
the immunological response.
90
what causes the nerve damage in lepromatous leprosy
the bacterial infection in schwann cells.
91
how many bacteria are seen in the lepromatous form
there are a ton of bacilli present.
92
what is the lepromatin skin test show in lepromatous
it will be negative due to lack of immunity
93
what does the tuberculoid form look like?
hypopigmented macular or plaque-like skin lesions, thickened superficial nerves, anesthesia of the skin lesions
94
what does lepromatous form look like?
multiple nodular skin lesions, leonine facies,
95
labs for tuberculoid
they will be negative, diagnose on the exam
96
labs for the lepromatous
acid-fast stain of the skin lesions or nasal scrapings, lipid-laden macrophages full of acid-fast. VDRL and RPR + PCR also +
97
treatment for tuberculoid?
dapsone + rifampin for 2 years
98
treatment for lepromatous
dapsone + rifampin + clofazimine for 2 yrs or until the lesions clear.
99
what is a common complication of the treatment?
severe erythema nodosum.
100
how do we control the EN from therapy?
treat with thalidomide.
101
why do we bother distinguishing between the mycobacteria?
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.
© 2025 Bold Learning Solutions. Terms and Conditions