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56 Cards in this Set

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has no cell wall and cant be identified by gram stain
this feature distinguishes M. penumoniae from e.g M. hominis, orale, and salivarium
the fact that M. pneumoniae ferments glucose
during early stages of mycoplasma pneumonia serum taken from patients might show what three things
1. cold hemagglutinins
2. positive C fixation test
3. DNA probes
how does M. pneumonia attach to epithelial surface
P1 protein complex at tip of bacterium
what is ciliotosis - caused by what organism.
elaboration of H2O2 and superoxide resulting in host cell membrane and DNA damage, as well as altered metabolism
(seen in M. pneumonia infections
How to Variable Lipoproteins (VLPs) play a role in pathogenesis of M. pneumonia
VLPs are on surface and variation in their structure is one mechanism to avoid prior immunity. they also surve as structural componenets to stabilize the bacterial membrane
2 organisms which might have come from unpasturized milk
Brucella and Campylobacter
What antibiotics do you use to treat M. pneumonia
erythromycin or tetracycine.
why would you not treat M. pneumonia with penicillin
it inhibits cell wall synthesis and this organism does not have a cell wall
resistant to erythromycin and sensitive to tetracycline
M. hominis
produces super antigen and may be responsible for some infectious arthritis
M. arthritidis
role in RA
m. arthritidis
motile gram negative fermenter, comma shape, polar flagellum
Vibrio cholerae
what do colonies of vibrio cholerae look like
yellow opaque colonies on special TCBS medium (EMB platesw may inhibit growth)
motility of vibrio cholerae abolished by
major colonization factor in vibrio cholerae
toxin coregulated pilus (TCP)
Vibrio cholerae form microcolonies where
intestinal crypts
what does the cholera toxin bind?
ginds GM1 gangliosides of Cell Membrane
Neuraminidase of V. cholerae converts
other gangliosides to GM1 and htereby increases amount of toxin binding sites
cholera toxin enters intestinal cells by
The cholera toxin stimulates adenylate cyclase and increases cAMP - resulting in massive intestinal fluid loss via what two mechanisms
1. villus cells: decreased NaCL absorption from gut
2. secretory cells: increased CL and increased HCO3 secretion into gut along with H20
what are the clinical features of cholera
1. painless, profuse watery diarrhea and isotonic volume loss (10-15 liters/day) and dihydration, low blood pressure "shock" and possible death
transmission of vibrio cholerae is through
water (food)
campylobacter species

Gm neg rod
comma shaped
how does one contract campylobacter
contaminated food or water. usually raw chicken or unpasteurized milk (it is a zoonotic disease)
campylobacter causes inflammation of
small and large bowel (rare bacteremia)
primary symptom of campylobacter
most common etiologic agent of diarrhea in world
one in a thousand people w/ campylobacter develop
immunity to their own nerves - leading to paralysis that lasts for several weeks
infectious dose of campylobacter
low - fewer than 500 organisms
diagnosis of campylobacter
in stool culture on selective media -
treatment for campylobacter
supportive therapy
sometimes anti-microbial therapy
C jejuni and C. coli are part of what species
most common causative agent of the campylobacter species

which is the most common cause of diarrhea
main metabolic characterisitics of Y. pestis
large rod gram neg
aerobic or faculatatively anaerobic
Y.pestis - ferment lactose?

it does ferment glucose though
it is oxidase negative and a facultative anaerobe
cause of plague
Yersinia pestis
F1 antigen
anti-phagocytic capsule required for virulence in Y. pestis
other anti-phagocytic properties present before visible capsule in Y. pestis
V and W
Anti-phagocytic properties of Y. pestis are present at what temp
mammalian temp 37
but not 28 degrees (flea)
F. tularensis cause skin lesion enter lymphatics and after producing local lymphadenopathy they
go into blood (bacteremia) and form granuloma in liver and spleen
F. tularensis survives intracellularly in
specific syndromes caused by this organism include skin ulcer and painful adenopathy (inguinal and axillary)
f. tularensis
a progression from untreated bubonic or pneumonic plague which results in abdominal pain, shock, bleeding into skin and other organs
septicemic plague
what happens then a the buuboes ulcerate in someone with bubonic plague
bacteria invade the blood stream
pneumonic plague is rapidly fatal - how many days and what is the cause of such fatality
2-4 days then fatal due to respiratory failure and shock
pathogeniesis of septicemic plague and why it might ahve been called black death throughout history
DIC - Disseminated intravascular coagulation
diagnosis of plague is based on
isolation of Y. pestis or four fold rise in specific AB to capsule
Handling infectious animal tissue or fluid. Tick bits. Ingestion of contaminated food, water, or soil. Or inhalation of infective aerosols from animals are all ways you might contract
tularemia pneumonia

usually not spread from person to person
how many organisms required for infection of tularemia
10-50 organisms (inhaled or intradermally)
most common clinical presentation of tularemia
ulcerogladular tularemia (skin ulcer and adenopathy)

if bacteremia results you might get granuloma
why do you not want to culture tularemia
dangerous (aerosol) and requires special media
how might you diagnose tularemia
fluorescent Ab staining of node
serologic (rise in Ab)
requires 10% CO2 to grow (and is still slow)
Three major pathogenic Brucella species fro human
1. brucella melitensis (goat and sheep)
2. brucella abortus (cattle)
3. brucella suis (pigs)
transmission of brucellosis
1. contaminated goat milk (b. melitensis)
2. direct tissue contact (B. abortus, B. suis)
3. urine contact (B. canis)
4. inhalation
note: more common in countries with unpasturized milk
two disease that result in granuloma formation in spleen and liver
F. tularensis and Brucella

they both replicate w/in macrophages
occasionally this organism causes osteomyelitis and endocarditis along with symptoms resembing colds

as well as FUO