Actinomyces and Nocardia (2/15/18) Flashcards
(121 cards)
1
Q
morphology of actinomyces
A
gram-positive, filamentous
elongated rods that branch at acute angles
microaerophilic/strictle anaerobe
2
Q
growth speed of actinomyces
A
slow growers (4-10days)
3
Q
where are actinomyces found
A
commensal in the GI tract
4
Q
actinomyces complexes in tissue/puss
A
sulfur granules
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
6
Q
commonality of actinomycosis
A
rare
7
Q
how does actinomycosis occure
A
Chronic inflammitory condition that originates in tissues near mucosal surfaces
resulting in local hardening of tissue
8
Q
actinomycosis profession speed
A
slow
9
Q
immune response to actinomyces
A
poor, Ab(TH2) can be detected
10
Q
what type of infection occures via actinomyces
A
typically chronic that can only be resolved with antibiotics
11
Q
most common site for actinomycosis
A
cervicofacial actinomycosis
12
Q
cervicofacial actinomycosis is relateed to
A
poor dental hygeine
tooth extraction
trauma to mouth/jaw
13
Q
thoracic and abdominal actinomycosis commonality
A
rare
14
Q
why would one get thoracic abdominal actinomycosis
A
aspiration or trama
also intrauterine contraceptive devices can lead to chronic endometritis
15
Q
ease of diagnosis of thoracic and abdominal actinomycosis
A
delayed because of vague symptoms -easy to mistake for a malignancy
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
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
18
Q
how are patients treated for actinomyces
A
empirically if actinomyces is suspected
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
20
Q
where is nocardia is found
A
in soil
21
Q
observing/growing nocardia
A
2-3 days in blood agar or BHI, smelling like mood
22
Q
staining of nocardia
A
weak acid-fastness
23
Q
where can nocardiosis be found in body
A
gingiva and respiratory tract of healthy (not commensal though
24
Q
disease of nocardiosis
A
pulmonary (systemic)
cutaneous
25
how is nocardiosis spread
not by person-to person
26
pathogenisis of nocardiosis
poorly understood but good in immunocompromised
27
virulence factors of nocardiosis
unknown:
| resists phagocytes and can survive within them
28
what causes pulmonary nocardiosis
N. asteroides
| N. farcinica
29
Pulmonary nocardiosis leads to
acutre neutrophili inflammation
pus formation and destrucutre of parenchyme
abscesses form
dissemination to other sites, while traving in other cells
30
cause of cutaneous nocardiosis
direct inoculation of nocardia (N. brasiliensis)
31
Cutaneous nocardiosis leads to
superficial (pustule
| longer inflection leads to similar to actinomycosis (draining sinuses, sulfur granules)
32
Immunity to nocardia
cell mediate immune response (Th1 response)
| little effective humoral response (live inside the macrophage and antibodyes can't get to ti)
33
diagnosis of nocardio
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)
34
treating Nocardia
systemic sulfonamides alone or combined with trimethoprim
| also: new beta-lactams, minocyclin, doxycycline, erythromycin
35
reistance of nocardia
older penicilins
| anti-TB and antifungals ineffective
36
anaerobes
can't grow in less than 10% O2
37
the ability of an organism to survive the presence of )2 for breif time
oxygen tolerance
38
how do anaerobes get anergy
fermentase
39
how do anaerobes neutralize O2
produce catalase and superoxide dismutase
40
how to classify anaerobes
biochem and culture tests: difficult
| cellular fatty acids and metabolic products
41
where do anaerobic bacteria live
sebaceous gland
gingival crevice
lymphoid tissue in throat
intestinal and urogenital lumens
42
infections from anaerobes come from
commensal microbiotia
43
relation of anaerobes and aerobes to one another
aerobes eat up all the o2 so anaerobes can live
44
genus of clostridia
Clostridium
45
morphology of Clostridia
GRam-positive bacilli, large
46
can clostridia form spores
yes
47
exotoxins of clostridia
Hemolysin-lyses cell
Neurotoxin- nerves
Enterotoxin- enterocytes in GI
48
endo vs exotoxin
endo: from the cell wall
Exo: secreted out of the cell
49
morphology of clostridium perfringes
gram+, non-motile
50
what was clostridium perfringes produce on blood agar
hemolytic colonies
51
what does clostridium perfringes produce when given fermentable carbs
large mounts of hydrogen and carbon dioxide gas, causing gas gangrene
52
toxins made by clostridum perfringes
Alpha-toxin
theta-toxin
Enterotoxin
53
Phospholipiase that hydrolyses lecithin and sphinomyelin destroying cell membrane (hemolysin)
alpha-toxin
54
similar to streptolysin O(pore former) altering capillary permeability and toxic to heart
theta-toxin
55
forms pores in enterocytes membrane, changing permeability, and causing fluid loss
enterotoxin
56
Clostridial Myonecrosis
Gas gangrene
57
where does Gas gangrene develop
in traumatic wounds when contaminated with C. perfringens and other histotoxic clostrida
58
when may gas gangrene occure
trama when time between injury and intervention is delayed
compound fracture
bullet wounds
wartime trauma
59
when does Gas gangrene begin
1-4 days after injury
60
characteristics of GAs gangrene
severe pain, sense of heaviness and pressure
61
how does gas gangrene appear in anaerobic condition
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
food poisoning is caused by
Clostridum perfringens
63
where does food poisoning occure
meat disshes and buffets
64
what does food poisoning strains produce
enterotoxin in the ileum
65
incubation period of food poisonig
8-24 hours
66
what does food poisoning by clostridum perfringens lead to
nausa, ab pain, diarrhea, no fever, aiwth no vomit
67
recovery of clostridum perfringes food poisoning
spontaneous after 24 horus
68
treating clostridium perfringes
clinicl observation, since culture is not sufficient for diagnosis
69
how to treat gas gangrene
get rid of the tissue and lots of penicillin
70
morphology of clostridium botulinum
large gram+ rod
71
what does clostridium botulinum resist
heat resistance
72
what does clostridium botulinum produce
botulinum toxin (lethal at less than 1 microgram
73
what id botulinum toxin
neurotoxin
blocks acetylcholine release and flaccid paralysis
damages the synapse is permant
74
symptoms appear of clostridium botulinum when
12-36 hours after leading to nausea, dry mouth, blurred vision and severe respiratory paralysis
75
where are clostridium botulinum is found
in environment in alkaline conditions (vegies, mushrooms, fish, and honey) with no change in food taste, odor and color
76
can you kill botulinum toxin
head-labile(kill by heat)
77
outbreaks of clostridium botulinum
small and stuck in family
78
foodborne botulism is consider to be what
intoxication, not infection
79
treatment of botulism
respiratory care
supportive care
antitoxin (for free toxin)
80
morphology of clostridum tetani
slim, gram+ rod
| strict anaerobic condition
81
where is clostridum tetani found
environmet, spores last a long time in spoil
82
what does clostridium teani produce
neurotoxin (tetanospasmin)
83
what does tetanus toxin do
an irreversable neurotoxin that causes spastic paralysis
84
how does teanus toxin work
prevent release of glycine and GABA from presynaptic neuron
85
what does GABA do
inhibitor neurotransmitter
86
destroying tetanus toxin
heat-labile
antigenic
destoyed by proteases
neutralized by antitoxin
87
how does tetanus occure
spores enter through deep, penetrating wound (nail non-sterile instruments)
88
once C. tetani is in the body, what does it do
multiplies locally and does not invate tissue,
| instead toxin travels to CNS via retrograde axonal transport
89
incubation of tetanus
4 week- several weeks (shorter incubation leads to worse disease)
90
muscles affected by tetanus
masseter 1st
| respirator, swallowing, back afterward
91
diagnosis of tetanus
clinical
92
treat tetans
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
what does the prevetative vaccine of tetanus work for
tetanus toxoid (inactive toxin)
94
morphology of clostridium defficile
gram+ rod
95
where is clostridium difficile found
in the envrinoment and as a commensal
96
why would clostridium difficile form spores
trigggered by taurocholate (Bile salt)
97
toxins made by clostridium dificile
Toxin A and B
| C. difficile binary toxin (CDT)
98
action of Toxin A and B from clostridium difficile
disrupt cytoskeleton signal transduction (disrupts tight junction)
99
action of CDT
inhibits actin polymeration
100
what causes antibiotic-associated diarrhea (AA)
antibiotics destroying natural microflora
101
where can you get clostridium difficile
is presnet in 2-15% of pop
| also as a spore in a hospital-acquired infection
102
how to prevent C. difficile
the colonic microbiota prevent C. diff from colonizing
103
C. Diff can create what as a faulse membrane by secretaing toxins that destory cells and stick in the colon
Pseudomembranous colitis
104
affect of Clostridium Difficile
mild, watery, bloody poop
abdominal cramping, leukocytosis, fever
lasts weeks
also pseudomembranous colitis (Can get so bad it creates toxic megacolon and explode)
105
diagnosis of C. Diff
stool culture
106
treat C. Diff
Vancomycin, metronidazole (Mild and moderate)
fidaxomicin
do a pulsed-treatment
probiotics, toxin-specific Ab, toxin neutralizer
fecel transplant
comepetive inhibitors of bile salts
107
morphology of bacteroides fragilis
gram-, rod, capsulated, anaerobic commensal
108
growing speed of bacteroidies fragilis
overnight growth on blood agar
109
how may bacteroides fragilis resist o2 for 3 days
superoxide dismutages and catalase
110
toxin part of bacteroides fragilis
LPS (less toxic though than most gram-
| some produce enterotoxin
111
roll of bacteroides fragilis polysaccharide capsule
resistant to phagocytosis
hinders macrophage migration
helps with bacterial adhesion
contribute to abscess formation
112
what does enterotoxin do from bacteroides fragilis
water, self limiting diarrhea
113
how does bacteroides fragilis enter
non-invasive
114
what does bacteroides fragilis do
abscess formation, patient has abdominal pain, tenderness, mild fever
can spread infection to blood
115
how to clear bacteroides fragilis
classical complement acitvation
| cell-mediated immunity
116
tretament of bacteroides fragilis
drain and debride
clindamycin and metronidazol
117
why is antimicrobial therapy diffcult for bacteroides fragilis
most make Beta-lactamase
| resist tetracyclins
118
morphology of petrosrteptococcus
gram+, slow grow, anaerobic, coccus
119
type of pathogen for peptostreptoccus
opportunistic
120
the most common G= anaerobic coccus in oral cavity
P. anaerobius
| P. micros
121
what infections does Peptostreptococcus cause
gingivits and periodontisi
abscesses
soft tissue infections
