Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
178 Cards in this Set
- Front
- Back
what is the gram stain and morphology of neisseria gonorrhea?
|
gram negative
diplococcus |
|
what can neisseria gonorrhea cause? (4)
|
urethritis
cervicitis proctitis pharyngitis |
|
how does urethritis manifest in gonorrhea? (3)
|
thick pus
scar tissue may obstruct the urethra may result in sterility |
|
what can cervicitis in gonorrhea result in?
|
scar tissue that may cause sterility or ectopic pregnancy
|
|
what offers resistance to penicillin and tetracycline in gonorrhea?
|
R plasmids
|
|
what STD has opa proteins?
|
neisseria gonorrhea
|
|
what allows for gonorrheal attachment to many different types of cells?
|
chromosomal rearrangement of pili genes
|
|
what does the chromosomal rearrangement of pili genes allow for with gonorrhea?
|
attachment to many different cell types
|
|
what do opa proteins do in neisseria gonorrhea? (3)
|
increase adherence between gonococci
increase adherence to eukaryotic cells attach to receptors on CD4 t cells and then prevent activation and prolferation of the lymphocytes |
|
why have attempts to make a gonorrhea vaccine been futile?
|
antigenic variaton makes the body incapable of forming antibodies
|
|
how do you treat neisseria gonorrhea?
|
penicillin
|
|
what does chlamydia cause? (3)
|
urethritis
cervicitis proctitis |
|
what is the infectious form of chlamydia?
|
elementary body
|
|
what is the causative agent in chlamydia?
|
chlamydia trachomatis
|
|
what is the replicating form of chlamydia?
|
reticulate body
|
|
what do cells infected with chlamydia release and what does this lead to? (2)
|
cytokines leading to an intense inflammatory reaction and cell mediated response
|
|
when chlamydia attaches to spern, what can it cause in females?
|
pelvic inflammatory disease leading to fallopian tube damage
|
|
what damage can occur asymptomatically in women with chlamydia and what can this lead to? (2)
|
tubal damage which can result in sterility or ectopic pregnancy
|
|
what problem can other variations of chlamydia cause?
|
blindness
|
|
how do you diagnose chlamydia and why?
|
immunoflourescence
although the cell wall structure is similar to gram negatives, gram stains so not work well with it |
|
what is the causative agent in syphilis?
|
treponema pallidum
|
|
how is primary syphilis manifested?
|
as a chancre
|
|
what is a chancre?
|
a painless, red ulcer with a hard rim at the site of entrance of the syphilis organism
|
|
how is syphilis transmitted?
|
the chancre coming into contact with partners body
|
|
how is secondary syphilis manifested? (5)
|
runny nose
watery eyes aches sore throat rash |
|
what is a characteristic lesion of secondary syphilis?
|
gumma on the roof of the mouth
|
|
what is secondary syphilis due to?
|
immune complexes
|
|
how is tertiary syphilis manifested? (3)
|
mental illness
blindness stroke |
|
what is tertiary syphilis due to?
|
hypersensitivity to treponema
|
|
what is the morphology of treponema? (2)
|
motile spirochiete
|
|
what does not work well for diagnosing syphilis?
|
gram stain
|
|
where can syphilis not be cultured?
|
in vitro
|
|
how is syphilis identified microscopically? (2)
|
dark field or flourescent
|
|
what syphilis patients do you use immunodiagnostics for?
|
those without chancres
|
|
what are 2 nontreponemal antibody tests for syphilis?
|
rapid plasma regain (RPR)
venereao disease research laboratory (VDRL) |
|
what type of test can detect antibodies to cardiolipin and other lipoidal indicators of tissue damage?
|
nontreponemal antibody test
|
|
what can nontreponemal antibody tests detect? (2)
|
antibodies to cardiolipin
other lipoidal indicators of tissue damage |
|
how can nontreponemal antibody tests become false positives? (3)
|
febrile infections
pregnancy AI disorders |
|
what are 2 confirmatory tests for syphilis?
|
flourescent teponemal antibody absorption (FTA-ABS)
microhemagglutination (MHA-TP) |
|
what is the gram staining and morphology of haemophilis ducreyi?
|
gram negative bacillus
|
|
what type of toxin does haemophilis ducreyi release?
|
cytolethal distending toxin
|
|
what does haemophilis ducreyi cause?
|
soft tissue chancroid
|
|
how is haemophilis ducreyi different from syphilis?
|
the chancre is tender but not indurated; in syphilis it s a hard chancre
|
|
what are 3 high risk groups for haemophilis ducreyi?
|
uncircumscribed males
heterosexual men female prostitiues |
|
what is a major co-factor in the transmission of HIV?
|
haemophilis ducreyi
|
|
how do you diagnose haemophilis ducreyi? (3)
|
1 or more painful genital lesions
no evidence of t pallidum test results for HSV are negative |
|
what is the causative agent in donovanosis?
|
calymmatobacterium granulomatis
|
|
what is the gram stain and morphology of donovanosis?
|
gram negative encapsulated
|
|
is calymmatobacterium granulomatis motile?
|
no
|
|
what bacteria has a capsule similar to klebsiella?
|
calymmatobacterium granulomatis
|
|
how do you diagnose calymmatobacterium granulomatis (2)?
|
intracellular donovan bodies
beefy-red ulcers |
|
what bacteria will have beefy red ulcers?
|
calymmatobacterium granulomatis
|
|
what pathogen has escape proteins gC, gE, and gI?
|
HSV
|
|
how does escape protein gC work?
|
binds to C3 complement protein thus removing it from the complement repertoire and inhibiting complement activation
|
|
how do escape proteins gE/I work?
|
bind to the Fc portion of the antibody thus camoflaguing the virus and virally-infected cells
|
|
what happens in reactivation of HSV?
|
viruses travel down bundle of neurons connected to the original site of infection
|
|
how can HSV be reactivated? (4)
|
stress
trauma fever sunlight |
|
what is the MOA of acyclovir and peniclovir against HSV?
|
activated by the viral enzyme thymidine kinase and become substrates for the viral DNA polymerase
thus become incorporated into and prevent elongation of viral DNA |
|
how are acyclovir and peniclovir activated?
|
viral enzyme thymidine kinase
|
|
how does HSV develop resistance to acyclovir and peniclovir?
|
mutations that inactivate thymidine kinase
|
|
how does the viral genome of HPV exist?
|
extrachromosomal DNA in the host cell
|
|
what can happen to neonate infected with HPV?
|
warts can obstruct the respiratory tract
|
|
how does HPV cause cervical cancer?
|
integrates its genome into the host cell DNA and codes for a protein that causes uncontrolled cell growth
|
|
what CD4 level will AIDS symptoms develop?
|
<450/uL
|
|
what pathogen is known to cause strawberry cervix?
|
trichonomas vaginalis
|
|
what organisms does trichonomas vagnialis infect?
|
humans only
|
|
what is the green, frothy discharge in trichinomas vagialis due to?
|
the production of hydrogen gas
|
|
what pathogen is known to cause green, frothy discharge?
|
trichinomas vaginalis
|
|
what predisposes an indivisual to vaginitis? (6)
|
broad spectrum antibiotics
douching overused, retained tampons intrauterine contraceptives multiple sex partners history of STDs |
|
what are the 3 typical microorganisms of vaginitis?
|
gardnerella vaginalis
gardnerella mobiuluncus mycoplasma hominum |
|
what are 2 findings with vaginitis?
|
strong, fishy odor
itching |
|
what are clue cells and what are they associated with?
|
sloughed off epithelial cells covered with bacteria
associated with vaginitis |
|
what organism has phenotype switching?
|
vulvovaginal candidiasis
|
|
what enables candidia to survive in many different places in the human body?
|
phenotypic switching
|
|
how is candidia predominately transmitted?
|
endogenous - predominant source of infection is the patient herself because we're colonized by candidia
|
|
how can candidia be transmitted exogenously? (4)
|
contaminated irrigation solutions
cardiac valves corneas person to person |
|
what type of prep will you use for candidia?
|
KOH prep
|
|
what type of stain will you use for candidia?
|
flourescent stain
|
|
how do you identify candidia microscopically?
|
budding, yeast-like forms and pseudohyphae seen in flourescent microscope
|
|
what is a selective media for candidia?
|
CHROMagar
|
|
what is so helpful about CHROMagar?
|
each species will work on the substrate in a slightly different way to produce a different color
|
|
how will candidia albicans appear on CHROMagar?
|
green
|
|
how will candidia krusei appear on CHROMagar?
|
rose
|
|
how will candidia tropicalis appear on CHROMagar?
|
steel blue
|
|
what candidia species will appear green on CHROMagar?
|
albicans
|
|
what candidia species will appear rose on CHROMagar?
|
krusei
|
|
what candidia species will appear steel blue on CHROMagar?
|
tropicalis
|
|
how do azoles work?
|
inhibit fungal CYP450 which disrupts membrane synthesis in fungal cells
|
|
how do echinocandins work?
|
inhibit the synthesis of beta-(1,3)-glucans which are key components of the fungal cell wall (mammals do not have this comonent)
|
|
how does flucytosine work?
|
interferes with the synthesis of fungal DNA, RNA, and proteins
|
|
how do allylamines work?
|
inhibits the fungal enzyme squalene epoxidase
|
|
when is teratogenicity worst with rubella?
|
first trimester
|
|
what virus is not cytolytic?
|
rubella
|
|
how does rubella damage the fetus? (3)
|
alters normal growth, mitosis, and chromosomal structure
|
|
what is the budding mechanism for rubella?
|
inside the host cell it lines viral proteins along the membrane
the nucleocaspid then becomes enclosed by the viral envelope which is composed of the host's plasma membrane and viral proteins |
|
how long can rubella persist in a neonate and where is it likely to persist?
|
3-4 years
the eye |
|
what may the presence of rubella create and thus prevent?
|
may create tolerance and prevent clearance
|
|
what are the most common manifestations of rubella? (3)
|
cataracts
mental retardation deafness |
|
what may prevent the spread of rubella to the fetus?
|
maternal immunity
|
|
what is opthalmia neonatorum?
|
a purulent ocular infection of gonorrhea acquired by neonates at birth
|
|
how do you treat opthalmia neonatorum? (3)
|
silver nitrate
tetracycline erythromycin |
|
what has an 80% mortality rate in neonates?
|
congenital syphilis
|
|
what is hutchinson's teeth caused by?
|
congenital syphilis
|
|
what is often fatal when the infant is infected during birth?
|
HSV
|
|
how will a baby infected with HSV present?
|
initially appears septic with a vesicular lesion
|
|
why does HSV disseminate so quickly in neonates?
|
the baby does not have cell mediated immune response
|
|
what is the causative agent in group B strep?
|
streo agalectiae
|
|
what is the gram staining and morphology of group B strep?
|
gram positive cocci
|
|
how does group B strep manifest in newborns? (3)
|
bacteremia
pneumonia meningitis |
|
what is the gram stainign and morphology for listeria monocytogenes?
|
small gram positive rods (very skinny)
|
|
why is listeria monocytogenes sometimes mistaken for and why is this important?
|
strep pneumonia or enterococcus
important because strep pneumonia also causes meningitis |
|
does listeria monocytogenes form spores?
|
no
|
|
how does listeria monocytogenes respirate?
|
facultative anaerobes
|
|
what is the characteristic motility of listeria monocytogenes/
|
end over end tumbling motion
|
|
what bacteria has characteristic end of end tumbling motion?
|
listeria monocytogenes
|
|
what is the key to the pathogenecity of listeria monocytogenes?
|
facultative intracellular pathogen
|
|
what cells does listeria monocytogenes grow in? (3)
|
macrophages
epithelial cells cultured fibroblasts |
|
what is listeria monocytogenes entry into cells mediated by?
|
internalisn - interact with glycoprotein receptors
|
|
what 3 hemolysins does listeria monocytogenes produce?
|
listeriolysin O
2 phospholipases |
|
how does listeria monocytogenes move from cell to cell
|
builds an actin tail using Act-A and then pushes into the next cell
|
|
how does listeria monocytogenes avoid humoral immunity?
|
it is pushed through the cell membrane into an adjacent cell so it never sees the outside world
|
|
what patients are even more susceptible to listeria monocytogenes?
|
patients will cellular immunity defects
|
|
what is typically associated with food-borne illnesses?
|
listeria monocytogenes
|
|
what allows listeria monocytogenes to survive in a wide variety of food?
|
its ability to survive in a wide range of pH and temperatures
|
|
what has the potential to be grossly contaminated with listeria monocytogenes?
|
refrigerated food
|
|
what is granulomatosis infantiseptica cause by?
|
listeria monocytogenes
|
|
what is characterized by the formation of disseminated abcesses and granumomas in multiple organs?
|
granulomatosis infantiseptica caused by listeria monocytogenes
|
|
how does late onset neonatal listeria monocytogenes manifest?
|
meningitis or meningoencephalitis
|
|
what presents similarly to group B strep disease?
|
late onset listeria monocytogenes
|
|
what is listeria monocytogenes naturally resistant to?
|
cephalosporins
|
|
how does listeria monocytogene gain antibiotic resistance?
|
plasmids on transposons (jumping genes)
|
|
what is the morphology of group A strep?
|
chains
|
|
what are 4 virulence factors of group A strep?
|
superantigen exotoxin
exotoxin B C5a peptidase lipoteichoic acid |
|
how does superantigen exotoxin work and what bacteria is it associated with?
|
exotioxin A
associated with GAS |
|
how does exotoxin B work and what bacteria is it associated with?
|
protease which destroys and breaks down tissue proteins
associated with GAS |
|
how does C5a peptidase work and what bacteria is it associated with?
|
neutralizes C5a chemotaxis
associated with GAS |
|
how does lipoteichoic acid work and what bacteria is it associated with?
|
allows for attachment on mucous membranes
associated with GAS |
|
what mediates the autoimmune reaction in GAS?
|
M protein
similar to myosin and can stimulate antibodies to bind to the human heart sarcolemma makes the organisms resistant to phagocytosis |
|
what 3 things does the M protein do?
|
makes the organism resistant to phagocytosis
inhibits activation of alternative complement pathways stimulates antibodies to bind to the human heart sarcolemma |
|
what is the morphology of staph aureus?
|
clusters
|
|
how does protein A work and what bacteria is it associated with?
|
binds to the Fc regions of the antibody, preventing phagocytes with Fc receptors from engulfing the microorganisms
associated with staph aureues |
|
how does luekocidin work and what bacteria is it associated with?
|
kills WBC
associated with staph aureues |
|
how does hyaluronidase work and what bacteria is it associated with?
|
degrades hyaluronic acid that holds tissues together
associated with staph aureues |
|
how does protease work and what bacteria is it associated with?
|
degrased various host proteins
associated with staph aureues |
|
how does alpha toxin work and what bacteria is it associated with?
|
punches holes in the host cell membrane
associated with staph aureues |
|
what bacteria is coagulase associated with?
|
associated with staph aureues
|
|
how do superantigens work and what bacteria are they associated with?
|
override the specificity of the t cell response and short circuit the normal mechanisms in antigen presenting
associated with staph aureues |
|
what is characterized by sudden onset of fever, chills, vomiting, diarrhea, muscle aches, and rash?
|
staph toxic shock
|
|
what can rapidly progress to severe hypotension and multisystem dysfunction?
|
staph toxic shock
|
|
what can result in desquamation on palms and soles 1-2 weeks later?
|
staph toxic shock
|
|
what type of toxin does menstrual toxic shock produce?
|
toxic shock syndrome toxin-1 (TSST-1)
|
|
what type of toxin does non-menstrual toxic shock produce? (3)
|
TSST-1 or enterotoxin B or C
|
|
what bacteria can toxic shock also be caused by?
|
strep pyogenes
|
|
how does clostridium respirate?
|
obligate anaerobe
|
|
is clostridium a spore former?
|
yes
|
|
where is clostridium found? (4)
|
saprophytic
soil GI tract female genital tract |
|
what cell types does clostridium's alpha toxin attack? (4)
|
erythrocytes
leukocytes platelets muscle cells |
|
how does beta toxin work and what bacteria is it associated with?
|
necrotizing
associated with clostridium |
|
how does epsilon toxin work and what bacteria is it associated with?
|
permease
associated with clostridium |
|
how does iota toxin work and what bacteria is it associated with?
|
necrotizing
associated with clostridium |
|
what type of toxin does menstrual toxic shock produce?
|
toxic shock syndrome toxin-1 (TSST-1)
|
|
what type of toxin does non-menstrual toxic shock produce? (3)
|
TSST-1 or enterotoxin B or C
|
|
what bacteria can toxic shock also be caused by?
|
strep pyogenes
|
|
how does clostridium respirate?
|
obligate anaerobe
|
|
is clostridium a spore former?
|
yes
|
|
where is clostridium found? (4)
|
saprophytic
soil GI tract female genital tract |
|
what cell types does clostridium's alpha toxin attack? (4)
|
erythrocytes
leukocytes platelets muscle cells |
|
how does beta toxin work and what bacteria is it associated with?
|
necrotizing
associated with clostridium |
|
how does epsilon toxin work and what bacteria is it associated with?
|
permease
associated with clostridium |
|
how does iota toxin work and what bacteria is it associated with?
|
necrotizing
associated with clostridium |
|
what is the gram stain and morphology of leptospirosis?
|
gram negative spirochite with hooked ends
|
|
how does leptospirosis respirate?
|
obligate anaerobe
|
|
what is the source of leptospirosis? (2)
|
recreational exposure to contaminated water
exposure to the urine of infected animals |
|
how does leptospirosis gain access to the body?
|
through cuts and abrasians
|
|
how does leptospirosis spread through the body?
|
blood
|
|
where can leptospirosis be found early in the disease? (2)
|
blood
CNS |
|
where can leptospirosis be found late in the disease?
|
urine
|
|
how does leptospirosis manifest? (4)
|
meningitis
hepatitis renal dysfunction hemorrhage |