2/15: Actinomyces, Nocardia and anaerobes Flashcards
Actinomyces is gram pos or neg
is aerobic or anaerobic
gram pos
aerobic
Actinomyces are commensal bacteria often found in ___
GI tract
When actinomyces do infect, they form ___
sulfur granules
What are sulfur granules
formed by actinomyces infection
they are tissue and pus complexes
____ are hallmarks of actinomyces infection
sulfur granules
___ is the most common type of actinomyces
actinomyces israelii
What are the 2 types of actinomyosis
cervicofacial actinomyosis
thoracic/abdominal actinomyosis
What is actinomyosis
chronic inflammatory condition tha torigines in tissues near mucosal surfaces (50% of cases originate near mouth)
What is the immune response to actinomyosis
very poor – requires antibiotics
Which is more common: cervicofacial actinomyosis or thoracic/abdominal actinomyosis
cervicofacial
Cervicofacial actinomyosis is caused bY___
tooth extraction, poor hygiene or trauma to the mouth
this allows bacteria to get into breaks in the epithelium
Thoracic / abdominal actinomyosis is caused by __
Diagnosis ____
aspiration or trauma
hard to diagnose because often mistaken for a tumor
How do you diagnose actinomyosis?
presence of sulfut granule – requires a 10 day grown in ANAEROBIC CONDITIONS
Nocardia is gram pos/neg
aerobic/anaerobic
gram pos
aerobic
Is nocardia a commensal bacteria?
no
found in soil
Nocardia cell wall is composed of ___
mycolic acid
Nocardia bacteria cna infect ____
respiratory tract or cutaneosu areas
if exposed 0– can find in gingiva and gI
Pulmonary nocardiosis is caused by ____ and ____ (strains of nocardiosis)
nocardia asteroids
nocardia facinia
What are the symptoms of pulmonary nocardiosis?
acute neutrophilic inflammation and pus and destruction of parenchyma due to neutrophil recruitment
can form abscess and disseminate
Cutaneous nocardiosis is caused by ___
nocardia brasiliensis getting into an open cut
not as severe as pulmonary nocardiosis
The severity of cutaneous nocardiosis is dependent on ____
how soon it is treated
can be a pustule (non severe) to a sulfur granule)
Wha tis the immune response to nocardiosis?
Th1 – good because nocardiosis can survive in a phargocyte!! (we don’t know why)
Clostridium is found in the ___
intestine
What are the 3 strains of clostridium?
clostridium perfringens
clostridium botulinum
clostridium tetani
clostridium difficile
Clostridium perfringens is nonmotile/motile?
non-motile
If given carbsm, clostridium perfringes will ___
ferment them into H2 and CO2 gas
Clostridium perfringes leads to ___
gas gangrene
What are the 3 virulence factors of clostridium perfringes?
alpha toxin
theta toxin
enterotoxin
What is the alpha toxin in clostridium perfringes?
hemolysin - phospholipas that destroys cell membrane via lysis
What is the theta toxin in clostridium perfringes?
forms pores, increasing capillary permeability
What is the enterotoxin in clostridium perfringes?
forms pores in enterocyte membrane which leads to fluid loss (more common in strains that affect GI)
Clostridium perfringes leads to gas gangrene. What is thsi?
disease that occurs when there is a delay between trauma and intervention (compound fracture, bullet wound, wartime trauma)
begins 1-4 days after tauma, causes pressure and heaviness, the severe pain.
if conditions are anaerobic - ALPHA TOXIN is produced, can lead to increased vascular permeability – DEATH
Clostridium perfringes can also lead to food poisoning. Describe this.
strains that produce ENTEROTOXINS
incube 8-24 hours, causes nausea, stomach pain, diarrhea and spontaneous recovery in 24 hours.
Clostridium botulinum is found in _____
environment or in ALKALINE conditions of canned food
Clostridium botulinum has sproes that are heat ___
resistant
Clostridium botulinum produces ___
botulinum toxin
What is bolutlinum toxin?
produced by clostridium botulinum
neurotoxin that blocks Ach in the NMJ leading to FLACCID PARALYSIS
symptoms begin 12-36 hours after ingestion
cause nausea, dry m outh, blurred vision. respiratory paralysis can lead to death.
BOT TOXIN IS HEAT LABILE.
Bot toxin is heat ___
labile!!
Clostridium tetani is strictly anaerobic and associated with ___
deep penetrating wounds
CLostridium tetani produces ___ which causes __
tetanospasmin (causes spastic paralysis)
this prevents release of GABA from presynaptic neurons
tetanospasmin is heat ___
produced by clostridium tetani
this is heat LABILE
How do you destroy tetanospasmin
heat labile
antigenic
readily destroyed in the GI
Clostridium tetani causes ____ (disease)
tetanus
What is the pathology of clostridium tetani before getting tetanus disease?
clostridium tetanis PORES enter into deep pentrating wound
germinate, multiply locally, produce toxin that travels to CNS via RETROGRADE AXONAL TRANSPORT.
What is the first sign of tetanus disease?
masseter muscle is the first affected
then respiratory tract, then swallowing, and back
How is tetanus disease diagnosed?
clinically
What is the treatemnt for tetanus disease
from clostridium tetani
neutralize the free toxin with HTIG
make patient comfortable - antibiotics can antagonize toxin effects
YES THERE IS A VACCINE (duh)
Where can clostridium difficile be found?
environmentally or commensal
Spore germination of clostridium difficile is triggered by ____
bile salts
What are the 3 toxins that clostridium difficile produces/
- toxin a
- toxin b
- CDT (clostridicum difficle binary toxin)
What do toxin a and toxin b do in clostridium difficile?
disrupt TIGHT junctions
What does CDT (clostridium difficile binary toxin) do in more virulent strains of clostridium difficile?
inhibits epithelial actin polymeraization
Clostridium difficile is the most common cause of ____
antibiotic associated diarrhea and nosocomial infection
Clostridium difficule can lead to diarrhea (watery, mild or bloody with some cramping or fever).
This can last for weeks and lead to ____
PSUEDOMEMBRANOUS COLITIS
What is psuedomembranous colitis?
enterocytes are damaged by toxins produced from clostridium difficile
enterocytes die, immune cells come in.
psuedomembrane is formed from dead epithelial cells and immune cells prevent the fulid from being absorbed in gI tract.
This can lead to bolus getting STUCK in colon (toxic megacolon)
What is toxic megacolon?
What is it a result of?
toxic megacolon is when bolus is stuck in colon because immune cells are blocking teh reabsoprtion in GI tract.
This is because clostridium difficile has killed the enterocytes and a psuedomembranous layer is covering the GI tract
toxic megacolon is a possible result of psuedomembraneous colitis
What is the treatment for psuedomembraneous colitis and toxic megacolon?
diagnose with stoool sample
pulsed-treatment with antibiotics
probiotics
FECAL TRANSPLANT
Bacteriodes fragillis is found in the ___
intestine
Bacteriods fragillis : capsulated or non?
capsulated (helps evade phagocytosis)
Bacteroids fragillis leads to __ disease?
abscess
may cause abdominal pain, tenderness, mild fever, severity depends on integrity, size, where it is of abscess and could possbly spread to blood
What is the immune response to bacteroids fragillis abscess?
must activ ate classical COMPLEMENT PATHWAY
and TH2 immunity
What is the treatment for bacteroids fragillis?
drain, debride abscess, antiobiotcs are hard due to resistance
Peptostretococcus is gram pos/neg
anaerobic/aerobic
gram pos
anaerobic
Peptostretpcoccus is an opportunistic pathogen that commonly resides in the ___
oral cavity
What diseases is peptostreptococcus associated with?
gingivitis, periodontitis, abscesses
What is the treatment for the diseases caused by peptostretpcoccus?
(gingivitis, periodontitis, abscesses)
drain, debride, antibiotics
