Brainscape's Knowledge GenomeTM

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


See full index

micro immuno 2 > Actinomyces and Nocardia (2/15/18) > Flashcards

Actinomyces and Nocardia (2/15/18) Flashcards

1
Q

morphology of actinomyces

A

gram-positive, filamentous
elongated rods that branch at acute angles
microaerophilic/strictle anaerobe

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

growth speed of actinomyces

A

slow growers (4-10days)

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

where are actinomyces found

A

commensal in the GI tract

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

actinomyces complexes in tissue/puss

A

sulfur granules

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

Actinomycosis causing disease species

A 
A israelli (most common)
A naeslundii (early colonizer during dental plaque formation)
A viscosus (dental caries formation)
A odontolyticus
A meteri
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

commonality of actinomycosis

A

rare

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

how does actinomycosis occure

A

Chronic inflammitory condition that originates in tissues near mucosal surfaces
resulting in local hardening of tissue

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

actinomycosis profession speed

A

slow

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

immune response to actinomyces

A

poor, Ab(TH2) can be detected

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

what type of infection occures via actinomyces

A

typically chronic that can only be resolved with antibiotics

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

most common site for actinomycosis

A

cervicofacial actinomycosis

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

cervicofacial actinomycosis is relateed to

A

poor dental hygeine
tooth extraction
trauma to mouth/jaw

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

thoracic and abdominal actinomycosis commonality

A

rare

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

why would one get thoracic abdominal actinomycosis

A

aspiration or trama

also intrauterine contraceptive devices can lead to chronic endometritis

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

ease of diagnosis of thoracic and abdominal actinomycosis

A

delayed because of vague symptoms -easy to mistake for a malignancy

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

how would one go about diagnosis of actinomycosis

A

patient history (type of lesion, slow progesssion, trama, immunocompromised)
presence in pus-grow on plates
sulfur granules
biochemical tests to distingush from propionibacteria (anaerobic for 10 days) may also be contaminated with gram negative- use selective media

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

how treat actinomycosis

A 
penicilin G(high dose, followed by 6-12 months oral due to slow growth)
also: ampicillin, doxycycline, erythromycin, clindamycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how are patients treated for actinomyces

A

empirically if actinomyces is suspected

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

morphology of nocardia

A

strickaerobic, gram-positive(poor staining though-beaded), filamentous bacilli
cell wall of mycolic acid(causes poor staining)
similar to actinomyces

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

where is nocardia is found

A

in soil

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

observing/growing nocardia

A

2-3 days in blood agar or BHI, smelling like mood

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

staining of nocardia

A

weak acid-fastness

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

where can nocardiosis be found in body

A

gingiva and respiratory tract of healthy (not commensal though

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

disease of nocardiosis

A

pulmonary (systemic)

cutaneous

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

how is nocardiosis spread

A

not by person-to person

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

pathogenisis of nocardiosis

A

poorly understood but good in immunocompromised

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

virulence factors of nocardiosis

A

unknown:

resists phagocytes and can survive within them

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

what causes pulmonary nocardiosis

A

N. asteroides

N. farcinica

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

Pulmonary nocardiosis leads to

A

acutre neutrophili inflammation
pus formation and destrucutre of parenchyme
abscesses form
dissemination to other sites, while traving in other cells

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

cause of cutaneous nocardiosis

A

direct inoculation of nocardia (N. brasiliensis)

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

Cutaneous nocardiosis leads to

A

superficial (pustule

longer inflection leads to similar to actinomycosis (draining sinuses, sulfur granules)

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

Immunity to nocardia

A

cell mediate immune response (Th1 response)

little effective humoral response (live inside the macrophage and antibodyes can’t get to ti)

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

diagnosis of nocardio

A

easier than actinomycosis (more at site and grow fast)
use morphology, gram stain, and acid fastness
plate with selective media(buffered charcoal yeast and Thayer-Martin agar)

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

treating Nocardia

A

systemic sulfonamides alone or combined with trimethoprim

also: new beta-lactams, minocyclin, doxycycline, erythromycin

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

reistance of nocardia

A

older penicilins

anti-TB and antifungals ineffective

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

anaerobes

A

can’t grow in less than 10% O2

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

the ability of an organism to survive the presence of )2 for breif time

A

oxygen tolerance

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

how do anaerobes get anergy

A

fermentase

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

how do anaerobes neutralize O2

A

produce catalase and superoxide dismutase

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

how to classify anaerobes

A

biochem and culture tests: difficult

cellular fatty acids and metabolic products

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

where do anaerobic bacteria live

A

sebaceous gland
gingival crevice
lymphoid tissue in throat
intestinal and urogenital lumens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

infections from anaerobes come from

A

commensal microbiotia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

relation of anaerobes and aerobes to one another

A

aerobes eat up all the o2 so anaerobes can live

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

genus of clostridia

A

Clostridium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

morphology of Clostridia

A

GRam-positive bacilli, large

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

can clostridia form spores

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

exotoxins of clostridia

A

Hemolysin-lyses cell
Neurotoxin- nerves
Enterotoxin- enterocytes in GI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

endo vs exotoxin

A

endo: from the cell wall
Exo: secreted out of the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

morphology of clostridium perfringes

A

gram+, non-motile

50
Q

what was clostridium perfringes produce on blood agar

A

hemolytic colonies

51
Q

what does clostridium perfringes produce when given fermentable carbs

A

large mounts of hydrogen and carbon dioxide gas, causing gas gangrene

52
Q

toxins made by clostridum perfringes

A

Alpha-toxin
theta-toxin
Enterotoxin

53
Q

Phospholipiase that hydrolyses lecithin and sphinomyelin destroying cell membrane (hemolysin)

A

alpha-toxin

54
Q

similar to streptolysin O(pore former) altering capillary permeability and toxic to heart

A

theta-toxin

55
Q

forms pores in enterocytes membrane, changing permeability, and causing fluid loss

A

enterotoxin

56
Q

Clostridial Myonecrosis

A

Gas gangrene

57
Q

where does Gas gangrene develop

A

in traumatic wounds when contaminated with C. perfringens and other histotoxic clostrida

58
Q

when may gas gangrene occure

A

trama when time between injury and intervention is delayed
compound fracture
bullet wounds
wartime trauma

59
Q

when does Gas gangrene begin

A

1-4 days after injury

60
Q

characteristics of GAs gangrene

A

severe pain, sense of heaviness and pressure

61
Q

how does gas gangrene appear in anaerobic condition

A

spores germinate and produce hemolytic toxin
increase in vascular permeability leads to systemic toxin absorption and shock
systemic alpha-toxin, not bacteremia can be fatal

62
Q

food poisoning is caused by

A

Clostridum perfringens

63
Q

where does food poisoning occure

A

meat disshes and buffets

64
Q

what does food poisoning strains produce

A

enterotoxin in the ileum

65
Q

incubation period of food poisonig

A

8-24 hours

66
Q

what does food poisoning by clostridum perfringens lead to

A

nausa, ab pain, diarrhea, no fever, aiwth no vomit

67
Q

recovery of clostridum perfringes food poisoning

A

spontaneous after 24 horus

68
Q

treating clostridium perfringes

A

clinicl observation, since culture is not sufficient for diagnosis

69
Q

how to treat gas gangrene

A

get rid of the tissue and lots of penicillin

70
Q

morphology of clostridium botulinum

A

large gram+ rod

71
Q

what does clostridium botulinum resist

A

heat resistance

72
Q

what does clostridium botulinum produce

A

botulinum toxin (lethal at less than 1 microgram

73
Q

what id botulinum toxin

A

neurotoxin
blocks acetylcholine release and flaccid paralysis
damages the synapse is permant

74
Q

symptoms appear of clostridium botulinum when

A

12-36 hours after leading to nausea, dry mouth, blurred vision and severe respiratory paralysis

75
Q

where are clostridium botulinum is found

A

in environment in alkaline conditions (vegies, mushrooms, fish, and honey) with no change in food taste, odor and color

76
Q

can you kill botulinum toxin

A

head-labile(kill by heat)

77
Q

outbreaks of clostridium botulinum

A

small and stuck in family

78
Q

foodborne botulism is consider to be what

A

intoxication, not infection

79
Q

treatment of botulism

A

respiratory care
supportive care
antitoxin (for free toxin)

80
Q

morphology of clostridum tetani

A

slim, gram+ rod

strict anaerobic condition

81
Q

where is clostridum tetani found

A

environmet, spores last a long time in spoil

82
Q

what does clostridium teani produce

A

neurotoxin (tetanospasmin)

83
Q

what does tetanus toxin do

A

an irreversable neurotoxin that causes spastic paralysis

84
Q

how does teanus toxin work

A

prevent release of glycine and GABA from presynaptic neuron

85
Q

what does GABA do

A

inhibitor neurotransmitter

86
Q

destroying tetanus toxin

A

heat-labile
antigenic
destoyed by proteases
neutralized by antitoxin

87
Q

how does tetanus occure

A

spores enter through deep, penetrating wound (nail non-sterile instruments)

88
Q

once C. tetani is in the body, what does it do

A

multiplies locally and does not invate tissue,

instead toxin travels to CNS via retrograde axonal transport

89
Q

incubation of tetanus

A

4 week- several weeks (shorter incubation leads to worse disease)

90
Q

muscles affected by tetanus

A

masseter 1st

respirator, swallowing, back afterward

91
Q

diagnosis of tetanus

A

clinical

92
Q

treat tetans

A

neutralize free toxin with human tetanus immune globulin (HTIG)
nonspecific supportive measures (dark envirnoment(decrease scares(, sedation, ensure adequate airways
benzodiaepines (GABA receptor to block spasm)
preventative vacine

93
Q

what does the prevetative vaccine of tetanus work for

A

tetanus toxoid (inactive toxin)

94
Q

morphology of clostridium defficile

A

gram+ rod

95
Q

where is clostridium difficile found

A

in the envrinoment and as a commensal

96
Q

why would clostridium difficile form spores

A

trigggered by taurocholate (Bile salt)

97
Q

toxins made by clostridium dificile

A

Toxin A and B

C. difficile binary toxin (CDT)

98
Q

action of Toxin A and B from clostridium difficile

A

disrupt cytoskeleton signal transduction (disrupts tight junction)

99
Q

action of CDT

A

inhibits actin polymeration

100
Q

what causes antibiotic-associated diarrhea (AA)

A

antibiotics destroying natural microflora

101
Q

where can you get clostridium difficile

A

is presnet in 2-15% of pop

also as a spore in a hospital-acquired infection

102
Q

how to prevent C. difficile

A

the colonic microbiota prevent C. diff from colonizing

103
Q

C. Diff can create what as a faulse membrane by secretaing toxins that destory cells and stick in the colon

A

Pseudomembranous colitis

104
Q

affect of Clostridium Difficile

A

mild, watery, bloody poop
abdominal cramping, leukocytosis, fever
lasts weeks
also pseudomembranous colitis (Can get so bad it creates toxic megacolon and explode)

105
Q

diagnosis of C. Diff

A

stool culture

106
Q

treat C. Diff

A

Vancomycin, metronidazole (Mild and moderate)
fidaxomicin
do a pulsed-treatment
probiotics, toxin-specific Ab, toxin neutralizer
fecel transplant
comepetive inhibitors of bile salts

107
Q

morphology of bacteroides fragilis

A

gram-, rod, capsulated, anaerobic commensal

108
Q

growing speed of bacteroidies fragilis

A

overnight growth on blood agar

109
Q

how may bacteroides fragilis resist o2 for 3 days

A

superoxide dismutages and catalase

110
Q

toxin part of bacteroides fragilis

A

LPS (less toxic though than most gram-

some produce enterotoxin

111
Q

roll of bacteroides fragilis polysaccharide capsule

A

resistant to phagocytosis
hinders macrophage migration
helps with bacterial adhesion
contribute to abscess formation

112
Q

what does enterotoxin do from bacteroides fragilis

A

water, self limiting diarrhea

113
Q

how does bacteroides fragilis enter

A

non-invasive

114
Q

what does bacteroides fragilis do

A

abscess formation, patient has abdominal pain, tenderness, mild fever
can spread infection to blood

115
Q

how to clear bacteroides fragilis

A

classical complement acitvation

cell-mediated immunity

116
Q

tretament of bacteroides fragilis

A

drain and debride

clindamycin and metronidazol

117
Q

why is antimicrobial therapy diffcult for bacteroides fragilis

A

most make Beta-lactamase

resist tetracyclins

118
Q

morphology of petrosrteptococcus

A

gram+, slow grow, anaerobic, coccus

119
Q

type of pathogen for peptostreptoccus

A

opportunistic

120
Q

the most common G= anaerobic coccus in oral cavity

A

P. anaerobius

P. micros

121
Q

what infections does Peptostreptococcus cause

A

gingivits and periodontisi
abscesses
soft tissue infections

micro immuno 2 (8 decks)

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