Cholera, Mycoplasma, Campylobacter, Plague, Etc

Front 1

has no cell wall and cant be identified by gram stain

Back 1

mycoplasma

Front 2

this feature distinguishes M. penumoniae from e.g M. hominis, orale, and salivarium

Back 2

the fact that M. pneumoniae ferments glucose

Front 3

during early stages of mycoplasma pneumonia serum taken from patients might show what three things

Back 3

1. cold hemagglutinins
2. positive C fixation test
3. DNA probes

Front 4

how does M. pneumonia attach to epithelial surface

Back 4

P1 protein complex at tip of bacterium

Front 5

what is ciliotosis - caused by what organism.

Back 5

elaboration of H2O2 and superoxide resulting in host cell membrane and DNA damage, as well as altered metabolism
(seen in M. pneumonia infections

Front 6

How to Variable Lipoproteins (VLPs) play a role in pathogenesis of M. pneumonia

Back 6

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

Front 7

2 organisms which might have come from unpasturized milk

Back 7

Brucella and Campylobacter

Front 8

What antibiotics do you use to treat M. pneumonia

Back 8

erythromycin or tetracycine.

Front 9

why would you not treat M. pneumonia with penicillin

Back 9

it inhibits cell wall synthesis and this organism does not have a cell wall

Front 10

resistant to erythromycin and sensitive to tetracycline

Back 10

M. hominis

Front 11

produces super antigen and may be responsible for some infectious arthritis

Back 11

M. arthritidis

Front 12

role in RA

Back 12

m. arthritidis

Front 13

motile gram negative fermenter, comma shape, polar flagellum

Back 13

Vibrio cholerae

Front 14

what do colonies of vibrio cholerae look like

Back 14

yellow opaque colonies on special TCBS medium (EMB platesw may inhibit growth)

Front 15

motility of vibrio cholerae abolished by

Back 15

antisera

Front 16

major colonization factor in vibrio cholerae

Back 16

toxin coregulated pilus (TCP)

Front 17

Vibrio cholerae form microcolonies where

Back 17

intestinal crypts

Front 18

what does the cholera toxin bind?

Back 18

ginds GM1 gangliosides of Cell Membrane

Front 19

Neuraminidase of V. cholerae converts

Back 19

other gangliosides to GM1 and htereby increases amount of toxin binding sites

Front 20

cholera toxin enters intestinal cells by

Back 20

endocytosis

Front 21

The cholera toxin stimulates adenylate cyclase and increases cAMP - resulting in massive intestinal fluid loss via what two mechanisms

Back 21

1. villus cells: decreased NaCL absorption from gut
2. secretory cells: increased CL and increased HCO3 secretion into gut along with H20

Front 22

what are the clinical features of cholera

Back 22

1. painless, profuse watery diarrhea and isotonic volume loss (10-15 liters/day) and dihydration, low blood pressure "shock" and possible death

Front 23

transmission of vibrio cholerae is through

Back 23

water (food)

Front 24

campylobacter species

gm?
anaerobic?

Back 24

Gm neg rod
comma shaped
aerophilic

Front 25

how does one contract campylobacter

Back 25

contaminated food or water. usually raw chicken or unpasteurized milk (it is a zoonotic disease)

Front 26

campylobacter causes inflammation of

Back 26

small and large bowel (rare bacteremia)

Front 27

primary symptom of campylobacter

Back 27

most common etiologic agent of diarrhea in world

Front 28

one in a thousand people w/ campylobacter develop

Back 28

immunity to their own nerves - leading to paralysis that lasts for several weeks

Front 29

infectious dose of campylobacter

Back 29

low - fewer than 500 organisms

Front 30

diagnosis of campylobacter

Back 30

in stool culture on selective media -

Front 31

treatment for campylobacter

Back 31

supportive therapy
sometimes anti-microbial therapy

Front 32

C jejuni and C. coli are part of what species

Back 32

most common causative agent of the campylobacter species

which is the most common cause of diarrhea

Front 33

main metabolic characterisitics of Y. pestis
gm?

Back 33

large rod gram neg
aerobic or faculatatively anaerobic

Front 34

Y.pestis - ferment lactose?

Back 34

no

it does ferment glucose though
it is oxidase negative and a facultative anaerobe

Front 35

cause of plague

Back 35

Yersinia pestis

Front 36

F1 antigen

Back 36

anti-phagocytic capsule required for virulence in Y. pestis

Front 37

other anti-phagocytic properties present before visible capsule in Y. pestis

Back 37

V and W

Front 38

Anti-phagocytic properties of Y. pestis are present at what temp

Back 38

mammalian temp 37
but not 28 degrees (flea)

Front 39

F. tularensis cause skin lesion enter lymphatics and after producing local lymphadenopathy they

Back 39

go into blood (bacteremia) and form granuloma in liver and spleen

Front 40

F. tularensis survives intracellularly in

Back 40

monocytes

Front 41

specific syndromes caused by this organism include skin ulcer and painful adenopathy (inguinal and axillary)

Back 41

f. tularensis

Front 42

a progression from untreated bubonic or pneumonic plague which results in abdominal pain, shock, bleeding into skin and other organs

Back 42

septicemic plague

Front 43

what happens then a the buuboes ulcerate in someone with bubonic plague

Back 43

bacteria invade the blood stream

Front 44

pneumonic plague is rapidly fatal - how many days and what is the cause of such fatality

Back 44

2-4 days then fatal due to respiratory failure and shock

Front 45

pathogeniesis of septicemic plague and why it might ahve been called black death throughout history

Back 45

DIC - Disseminated intravascular coagulation

Front 46

diagnosis of plague is based on

Back 46

isolation of Y. pestis or four fold rise in specific AB to capsule

Front 47

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

Back 47

tularemia pneumonia

usually not spread from person to person

Front 48

how many organisms required for infection of tularemia

Back 48

10-50 organisms (inhaled or intradermally)

Front 49

most common clinical presentation of tularemia

Back 49

ulcerogladular tularemia (skin ulcer and adenopathy)

if bacteremia results you might get granuloma

Front 50

why do you not want to culture tularemia

Back 50

dangerous (aerosol) and requires special media

Front 51

how might you diagnose tularemia

Back 51

fluorescent Ab staining of node
serologic (rise in Ab)

Front 52

requires 10% CO2 to grow (and is still slow)

Back 52

Brucellosis

Front 53

Three major pathogenic Brucella species fro human

Back 53

1. brucella melitensis (goat and sheep)
2. brucella abortus (cattle)
3. brucella suis (pigs)

Front 54

transmission of brucellosis

Back 54

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

Front 55

two disease that result in granuloma formation in spleen and liver

Back 55

F. tularensis and Brucella

they both replicate w/in macrophages

Front 56

occasionally this organism causes osteomyelitis and endocarditis along with symptoms resembing colds

as well as FUO

Back 56

Brucella