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274 Cards in this Set

  • Front
  • Back
which gram(+) rods produce spores?
bacillus and clostridium
which gram(+) rods are anaerobic? aerobic?
bacillus are aerobic, clostridium are anaerobic
club shaped morphology
c.diphth
loeffler's medium selects for ______
selects for coryne. diphth
tellurite plate test for which bacteria, mechanism and positive test result?
tellurium salt is reduced to elemental tellurium by c.diphth. positive test = gray-black color
metachromatic granules (Babes-Ernst granules), bacteria and which stain
coryne. diphtheria, methylene blue
pseudomembranes?
coryne. diphtheria, c.diff
clinical pictures of diphtheria?
laryngitis, myocarditis, nerve weakness, cutaneous diphtheria (ulcerating skin lesions covered by a gray membrane, non-invasive)
clinical pictures of listeria?
meningitis in pregnant women, newborns, IC patients. GI from ingestion of raw milk, meat, veggies
pathogenic factors for listeria?
internalin binds to cadherin, listeriolysin allows escape from phagosome, actin rockets
shows narrow zone of beta-hemolysis
listeria
shows double zone of hemolysis (which toxins are in each zone?)
C.perf, alpha toxin outside and theta toxin inside
2 bacteria that produce toxins that ADP-ribosylate, and what mechanism?
B.cereus, diphtheria
expresses hemolysin, DNase, hyaluronidase, collagenase?
c.perf
why hyperbaric O2 for c.perf?
suppresses growth (c.perf is anaerobic) and encourages growth of new vessels in wound to improve phagocytic activity
C.diff toxins do what to what molecule?
toxin A and toxin B are both glucosyltransferases. they add glucose to G protein Rho GTPase. toxin B causes depolymerization of actin→loss of cell integrity and apoptosis
clinical pictures of C.perf?
gas gangrene (necrotizing fasciitis), alpha toxin produces gas in tissues, jaundice shock, death. food poisoning by enterotoxin action.
C.perf normal flora of what body parts
colon and vagina
Naegler (egg yolk) test for which bacteria
c.perfringens
three superantigen enterotoxin producing bacteria?
staph A, B.cereus, C.perf
tennis racket
C.tetani
opisthotonos
arching of back (from tetanus)
8 antigenic types of this toxin, which are medically relevant
botulinum (A, B, E most important)
3 clinical pictures of botulism?
canned food, wound botulism, infant botulism
tetanus toxin has how many antigenic types?
1
anthrax toxins? what mechanisms?
edema factor and lethal factor, both A-B. B unit is "protective antigen", forms pores in membrane allowing EF and LF to enter. EF A unit is an adenylate cyclase that ↑cAMP causing edema. LF is protease that cleaves phosphokinase activator of MAP kinase, inhibiting cell growth.
clinical findings of anthrax?
cutaneous anthrax: malignant pustule (painless ulcer with black eschar/scab) progressing to bacteremia. Pulmonary anthrax: RTI progressing to mediastinitis, pleural effusions, spetic shock. GI anthrax: vomiting, abd pain, bloody diarrhea
reheated fried rice
B.cereus
alpha toxin
C.perf. lecithinase activity.
bacteria producing exotoxin A and B causing depolymerization of actin and death of enterocytes
C.diff
meningitis in newborns?
listeria
nonmotile?
shigella
motile?
poly-d-glutamic acid capsule
anthracis
edema factor and lethal factor
anthracis
black eschar (painless scab with local edema)/malignant pustule, id and prognosis?
anthracis, progress to bacteremia and death
2 forms of food poisoning based on different toxins
b.cereus, diarrheal by heat-labile enterotoxin, emetic by heat-stable enterotoxin
gamma phage assay
b.anthracis
zoonotic viruses
brucella x 4, c. jejuni, e.coli, francisella, pasteurella, salmonella, yersinia pestis, yersinia enterocolitica, bartonella x 2, anthrax, erysipelothrix, listeria
V or L-shaped morphology
c.diphth, listeria
tumbling movement
listeria
blocks GABA/glycine release
tetanospasmin
blocks Ach release
botulinum toxin
protective antigen
bacillus anthracis B-subunit
protease that cleaves MAPK activator
LF
ADP-ribosylates EF2
diphtheria toxin
host cell receptor for diphtheria toxin
HB-EGF (abundant on heart and nerve cells)
elek test
3 strips (+ control, patient's, - control) with an antitoxin strip
lab dx of listeria?
gram+ rods forming small, gray colonies with narrow zone of beta-hemolysis. tumbling MOTILITY (as opposed to corynebacteria)
traveler's diarrhea and ROT
ETEC, fecal-oral
undercooked meat
EHEC
neonatal meningitis
e.coli (also GBS)
e.coli adhesin
pili
e.coli enterotoxins and mechanisms
heat-labile toxin (LT): stimulate adenylate cyclase→PK phos ion transporters→diarrhea. heat-stable toxin (ST) stim guanylate cyclase→reduced ability to reabsorb sodium ions
e.coli exotoxin mechanism
A-B protein. removes adenine from 28S rRNA, CPE could lead to HUS
UTI e.coli adhesin binding site
gal-gal dimer, aids in ascension through urinary tract
laboratory diagnosis of e.coli
pink on MacConkey's. green on EMB. produces indole from try, decarboxylates lysine, uses acetate as carbon source, and is motile. EHEC does not ferment sorbitol
does ETEC ferment sorbitol? does EHEC?
ETEC sorbitol+, EHEC sorbitol-
tx e.coli?
UTI: ampicillin or trimethoprim. sepsis: cephalosporin (cefotaxime) w/ aminoglycoside. neonat meningitis: amp + cefotaxime. diarrhea: imodium or trimethoprim.
contents of MacConkey's agar?
lactose, pH indicator, crystal violet (inhibit gram+), bile salts inhibit commensals.
lactose fermenters
enterobacter, e.coli, klebsiella
non-lactose fermenters
proteus, salmonella, shigella, yersinia
EMB agar
selects against gram+ and differentiates lactose fermenation (green sheen by e.coli)
TCBS agar selects for ______
selects within vibrio because of 8.6 pH. then differentiates based on sucrose: cholera (sucrose+ = yellow) from parahaemolyticus and vulnificus (sucrose- = green)
which vibrio grows in 1% and which in 8% NaCl
parahaemo grows in in 8%
CAMPY agar
selective for campylobacter→jejuni if also susceptible to nalidixic acid and resistant to cephalothin.
is EHEC invasive? PMNs in stools?
not invasive thus minimal PMNs
methylene blue stain of fecal sample for what reason? which bacteria are positive?
presence of neutrophils; bacteria is invasive: shigella, salmonella, campylobacter. non-invasive (rather, toxin-producing): v.cholera, e.coli, c.perf.
pathogenesis for shigella? factors?
must invade through M-cells first using outer membrane protein IPA (invasion plasmid antigens). once inside, escape vacuoles and use actin-based motility to navigate cytoplasm (like listeria). invasion of adjacent lamina propria, then basal surface of epithelials. inflammation→tight junction loosening→further pathogenesis. bloody diarrhea. also shiga toxin.
rose spots
salmonella typhi
causes sequela esp. with concurrent disease i.e. osteomyelitis, pneumonia, meningitis
salmonella septicemia
likes to infect vascular grafts and site of previously damaged tissue (sites of infarcts, aneurysms)
salmonella septicemia
virulence factor
salmonella typhi
TSI results for salmonella?
alkaline slant, acid butt, gas+, H2S+. salmonella typhi is exception with no gas and little H2S. alkaline b/c lactose- glucose+.
pathogenesis for salmonella?
fimbriae encoded on plasmids attach to microvilli. pathogen-directed endocytosis. ruffled membranes due to salmonella-induced alteration of cell signal transduction. effector molecules injected through Type III secretion encoded on pathogenicity island 1 (SPI-1). effect is to inh phagosome-lysosme fusion. multiplies in vacuole. translocates to basal side, exocytosis into lamina propria. survival/growth in macrophages. possible bacteremia. eventually inflammatory response is protective (responsible for the inflammatory diarrhea and mild fever). phase variation of h antigen.
typhoid fever
salmonella typhi. primary asymptomatic bacteremia. secondary lasts 4-8 weeks long with fever, chills, headache, muscle pain. carriage in gall bladder by biofilm formation on gallstones.
tx typhoid fever/septicemia/metastatic infection?
ceftriaxone or ciprofloxacin. amp on carriers
comma shaped
vibrio, campylobacter, helicobacter
sensitive to stomach acid
salmonella, vib cholera
salmonella that cause endocarditis?
s.cholerasuis, s.typhimurium
vaccines for salmonella?
Vi capsule, live attenuated, and conjugated Vi for childrren.
mucinase
vibrio cholera, clears glycoprotein covering of intestinal cells for adherence.
cholera enterotoxin
choleragen: A-B protein. B binds to GM1 ganglioside. A-unit ADP-riboslyates adenylate cyclase, phos of membrane transporters causes watery diarrhea with NO neutrophils/RBCs. gene on CTX bacteriophage.
cholera pili important for…
adherence to gut, receptor for CTX bacteriophage
rice water stool
vib cholera
lab dx of cholera
lactose-, oxidase+ (distinguishes from all enterobacteria), sucrose+ so acid/acid on TSI. O1 ab
Tcp A
toxin coregulated pili (adheres to gut). regulated by same system that governs toxin production.
MOT of vib parahaemolyticus?
ingestion of raw/undercooked seafood
distinguishing dx of vib parahaemolyticus?
8% NaCl
sx of vib parahaemolyticus?
mild to severe watery diarrhea, vomiting, abd cramps, fever, lasting about 3 days.
vib vulnificus clinical picture?
cellulitis, bullae esp. in shellfish handlers with skin wounds. septicemia in IC people eating raw shellfish.
liver damage predisposes to _______
vib vulnificus
causes guillain barre
campylobacter jejuni
microaerophilic (5%)
campylobacter
further classification of vibrio cholera?
all vib cholera has O1. among O1 are Classical and El Tor (responsible for epidemics and higher asymptomatic carrier rates)
reactive arthritis/reiter's syndrome
campylobacter. large joint arthritis (knee/back) w/ relative sparing of small joints. dysuria and eye involvement as well.
lab dx of camp. jejuni?
failure to grow at 25% O2, oxidase+, sensitivity to nalidixic acid.
peptic ulcers
helicobacter pylori. risk factor for MALT lymphomas
differences between helico and camp pylori?
h.pylori is urease+
MOT of c.pylori?
domestic animals, fecal-oral. young puppy with diarrhea
MALT lymphoma? mechanism?
h.pylori chronic inflammation leading to B-cell prolif and eventually lymphoma
pathogenesis of h.pylori?
attach to mucus-secreting cells of gastric mucosa. urease creates ammonia, damaging mucus layer. neutralization of stomach acid makes better growing environment but inflames stomach. no bacteremia.
urea breath test
radioactive urea ingested and cleaved by urease leading to radiolabeled CO2 breath
causes primary (asymptomatic) and secondary bacteremia
salmonella typhi (typhoid fever)
gal-gal dimers
e.coli pilin binding site (UTI strains)
red pigmented colonies
serratia marcescens
bacteria that has large polysacch capsule giving its colonies a mucoid appearance
klebsiella pneumoniae
swarming effect on agar
PPM group (particularly proteus)
struvite
caused by urea producing PPM, damages urinary epithelium, obstructs urine flow, serves as "nidus" for other bacteria
e.coli pathogenic factors
pili, capsule, endotoxin, three exotoxins (LT, ST, shiga toxin)
GM1 ganglioside
receptor for binding of ETEC LT and ctx toxin
starts off as foul-smelling, watery diarrhea into bloody diarrhea
c.jejuni
sensitive to nalidixic acid
c.jejuni
4 characteristics of all enterobacteriaceae
facultative anaerobes, glucose+, cytochrome oxidase-, reduce nitrates to nitrites (as part of energy production)
causes reiter's syndrome complications
salmonella, campylobacter, yersinia
toxins increase cAMP
EF, ctx, e.coli LT, pertussis toxin, adenlyate cyclase
location of mucin
small intestine
bacteriocin
inhibitory substances secreted by normal flora
O, H, and K antigens are what and help to classify what family
O=outer polysaccharide, H=pili, K=capsular. helps identify enterobacteriaceae
fluoresces yellow-green under UV light
pyoverdin produced by pseudomonas
biochem differences of pseudomonas from enterobacteriaceae
oxidase+, non-fermenter (strict aerobe)
clinical pictures of pseudomonas
sepsis, pneumonia, UTI in IC patients, chronic LRT in patients with CF, cellulitis in burn patients, otitis externa in diabetic patients
mucoid isolates from CF patients
pseudomonas, klebs??
pseudomonas is normal flora of _____
colon, skin (moist areas), URT in hospitalized patients
can grow in antiseptics and low nutrient environments (distilled, tap water)
pseudomonas
pseudomonas virulence factors
endotoxin, exotoxin A, elastase, proteases, pyocyanin, sec III system
exotoxin A action and mechanism
tissue necrosis by ADP-ribosylation of EF2 (same as diphtheria toxin)
damages cilia and mucosal cells in resp tract
pyocyanin
pseudomonas sec system and purpose
sec III, injects toxins (namely ExoS) directly into cell
Exo S
ADP-ribosylates a Ras protein, damaging cytoskeleton
ecthyma gangrenosum
bacteremic pseudomonas spreading to skin, causing black, necrotic lesions (sign of high mortality)
underchlorinated pools/hot tubs
pseudomonas
puncture wounds in shoe soles causing osteochondritis
pseudomonas
dirty contact lenses causing corneal infection
pseudomonas
biochem dx of pse. aeruginosa
lactose-, oxidase+, metallic sheen on TSI agar with blue-green pigment on ordinary agar (and fruity aroma)
tx for pseudomonas
high resistance, so antipseudomonal penicillin + aminoglycoside
common agent of acute epiglottitis
hib
polyribitol phosphate capsule
haemophilus influenza
IgA protease
hib
only toxin produced by haemophilus influenza
endotoxin
most common cause of meningitis in children 2 months to 5 years old until vaccine development
hib
epidemiological concern with hib vaccine success?
appearance of nonencapsulated strains including aegyptius, ducreyi, aphrophilus
hib conjugate vaccine target, mechanism?
capsular PRP antigen, activates TI-2
name 4 species of haemophilus, diseases caused, and growth factors
influenzae causing URT/sepsis in children and pneumonia in adults (X and V), aegyptius causing acute purulent conjunctivitis (X and V), ducreyi causing STD chancroid disease (X), aphrophilus causing subacute endocarditis with heart valve damage (neither X/V)
septic arthritis, cellulitis, sepsis
haemophilus influenza
lab dx of haemophilus?
chocolate agar with X and V or tests to detect capsule
tx for haemophilus
high resistance (beta-lactamase), ceftriaxone
morphology of bordetella
coccobacillary, encapsulated gram- rod
attacks ciliated epithelium leading to severe coughing episodes
bordetella p.
path. factors for bord. p?
filamentous hemagglutinin (adhesin), pertussis toxin (ADP-ribsolyte Gi protein), adenylate cyclase, tracheal cytotoxin (bacterial peptidoglycan fragment, induces NO production to kill ciliated cells)
produces lymphocytosis in pertussis. how?
pertussis toxin. inhibits transduction by chemokine receptors → lymphocytes cannot enter lymphoid tissue
whooping cough lasting 1-4 weeks in children, months in adults
bordetella pertussis
isolate from nasopharyngeal swabs during paroxysmal stage, grow on Bordet-Gengou medium
bordetella pertussis (Bordet-Gengou contains high % of blood to inactivate inhibitors)
highest period of risk for spread of bord.p?
catarrhal stage (prodromal symptoms)
toxin that inhibits neutrophil activation and chemokine signaling. also acts as T lymphocyte mitogen
pertussis toxin. ADP-ribosylation of Gi
toxin internalized by PMNs disrupting PMN oxidative funciton. needs which activator?
adenylate cyclase, requires calmodulin
BvgA, BvgS responsive to what factors? belongs to which bacteria?
environmental signals like Mg, sulfate ion conc., temperature. bord.p
name 5 2-component regulatory systems
sarA/agr, VanS/VanR, PilS/PilR, PhoP/PhoQ
components of aPertussis vaccine?
Fha, pertussis toxoid, fimbriae, pertactin
name the events in formation of legionella phagosome
pseudopod coiling, surround by smooth vesicles from vacuolar membrane, surround by mitoch., assc. of ribosomes, multiplication and then rupture
requires iron and cysteine to grow
legionella
hot tubs and other water sources
legionella
only virulence factor from legionella
endotoxin
do secondary cases of legionella occur?
no
mental confusion, nonbloody diarrhea, proteinuria, hematuria, hyponatremia
legionella
charcoal-yeast agar
medium supplemented with iron and cysteine (selects for legionella)
tx legionella
erythromycin
pseudomonas iron scavenger, competes with transferrin
siderophore
purpose of elastase, exotoxinA in pseudomonas
damages tissue, releasing iron
response to low phosphate in pseudomonas
phospholipaseC
causes pulmonary infection in CF patients, why?
pseudomonas, core polysaccharide adheres to chloride channel protein in CF patients
pseudomonas virulence factors
core polysachh of LPS, glycocalyx (alginate biofilm)
pseudomonas pigment, damages cilia/mucosal cells
pyocyanin
cellulitis in burn patients
pseudomonas
malignant otitis externa in diabetics
pseudomonas
able to grow in distilled water and disinfectants
pseudomonas
blue-green color in agar
pseudomonas
turns pus in a wound blue
pyocyanin produced by pseudomonas
fluoresces yellow-green under UV light
pyoverdin produced by pseudomonas
biochem differences of pseudomonas from enterobacteriaceae
oxidase+, non-fermenter (strict aerobe)
clinical pictures of pseudomonas
sepsis, pneumonia, UTI in IC patients, chronic LRT in patients with CF, cellulitis in burn patients, otitis externa in diabetic patients
mucoid isolates from CF patients
pseudomonas, klebs??
pseudomonas is normal flora of _____
colon, skin (moist areas), URT in hospitalized patients
can grow in antiseptics and low nutrient environments (distilled, tap water)
pseudomonas
pseudomonas virulence factors
endotoxin, exotoxin A, elastase, proteases, pyocyanin, sec III system
exotoxin A action and mechanism
tissue necrosis by ADP-ribosylation of EF2 (same as diphtheria toxin)
damages cilia and mucosal cells in resp tract
pyocyanin
pseudomonas sec system and purpose
sec III, injects toxins (namely ExoS) directly into cell
Exo S
ADP-ribosylates a Ras protein, damaging cytoskeleton
ecthyma gangrenosum
bacteremic pseudomonas spreading to skin, causing black, necrotic lesions (sign of high mortality)
underchlorinated pools/hot tubs
pseudomonas
puncture wounds in shoe soles causing osteochondritis
pseudomonas
dirty contact lenses causing corneal infection
pseudomonas
biochem dx of pse. aeruginosa
lactose-, oxidase+, metallic sheen on TSI agar with blue-green pigment on ordinary agar (and fruity aroma)
tx for pseudomonas
high resistance, so antipseudomonal penicillin + aminoglycoside
myelitis
spinal cord tissue
entryways into CNS
circulation, olfactory nerve, peripheral nerves, choroid plexus
bacterial meningitis in infants (<2 months)
GBS, E.coli (K1), listeria
causes of bacterial meningitis in childhood (CA)
meningococcus, pneumococcus, hib
bacterial meningitis in adults (CA)
meningococcus, pneumococcus, listeria
nosocomial bacterial meningitis
e.coli, pseudomonas, klebs, streps, staphA, staphE
what do GBS and K1 e.coli have in common?
sialic acid capsules
cat scratch disease
bartonella henselae
bacillary angiomatosis
bartonella henselae, bartonella quintana
trench fever
bartonella quintana
human body louse
bartonella quintana
cat reservoir
bartonella henselae
undulating fever? why?
brucella. localizes in small granulomas in lymphoid tissue, then periodically release into blood
name 4 brucellas and their reservoirs
melitensis (goats/sheep), abortus (cattle), suis (swine), canis (dogs)
adenopathy of nodes surrounding site of entry
francisella tularensis
infected rabbits, ticks/mites/lice
francisella tularensis
yersinia virulence factors
yad adhesin, yops, Fra1 protein capsule, pla protease (plasminogen activation), LPS, iron-acquisition systems, endotoxin, V and W antigens
Yersinia pla purpose?
degrades fibrin clots, and c3b/c5a
name two epidemiologic forms of yersinia p.
urban, sylvatic
bipolar staining
yersinia pestis, pasteurella
yops purpose?
inhibit phagocytosis and cytokine production. i.e. YopJ protease cleaves two proteins required for TNF synthesis
giemsa/wayson stain
plague
tx plague
streptomycin/tetracycline
cat and dog bites? sutures?
pasteurella
tx pasteurella
penG
erysipelothrix reservoir
meat/fish, causes eryseipelas
notable distinguishing characteristics of mycobacteria
obligate aerobes, non-motile, non-spore forming, non-toxin producing, acid fast, grows extremely slowly, resistent to chemicals (acids/bases) and dehydration, niacin+, catalase+
Lowenstein-Jensen medium
contains complex nutrients (egg yolk) and malachite green dye (inhibits normal flora in sputum)
components of mycobacteria cell wall
mycolic acid (long chain FA), wax D, phosphatides (play role in caseation necrosis)
correlated to high virulence in tuberculosis
production of cord factor and cell wall component called phthiocerol dimycocerosate
antibiotic genes on M. tuberculosis located where?
chromosome
mechanism of KatG mutation
mutates catalase-peroxidase that activates INH
definition of MDR?
resistant to at least INH and rifampin
acute inflammatory response in the lungs at site of initial infection, M. tuberculosis
exudative lesion
GI tuberculosis associated with ________
cow's milk
M. tuberculosis mechanism of survival in phagosomes
inhibition of: phagosome-lysosome fusion, oxidative burst, acidification of phagosome, inhibitory cytokine responses
protein inhibiting phagosome-lysosome fusion
exported reptitive protein
giant cells containing tubercle bacilli surrounded by epithelioid cells
granulomatous lesion
Langhan's giant cells
contain tubercle bacilli
tubercle
granuloma surrounded by fibrous tissue that has undergone central caseation necrosis. heals by fibrosis and calcification
Ghon complex
single parenchymal lesion and caseation resulting in calcified bronchial lymph nodes (visible on X-ray)
miliary tuberculosis
dissemination of tuberculosis, causing hepatosplenomegaly, organ dysfunction, adrenal insufficiency, meningitis, osteomyelitis. IC patients predisposed. millet seed x-ray of lungs
point mutations responsible for tuberculosis drug resistances
antibiotic receptors, drug activator molecules (KatG)
immunity involved in M. tuberculosis infection
cellular (macrophages and Th1 helper T cells)
NRAMP protein
located in membrane of phagosome in macrophages, mutations = high rate of tuberculosis
scrofula
mycobacterial cervical adenitis (swollen but nontender)
non-respiratory forms of tuberculosis
GI, renal, oropharyngeal
erythema nodosum
tender lymph nodes along leg representing active cell-mediated immunity response. tuberculosis and leprae.
auramine-rhodamine stain
makes mycobacteria fluoresce yellow-orange
common acid-fast stain for mycobacteria
Kinyoun's acid-fast stain with carbolfuchsin
niacin test
M. tuberculosis lacks niacin ribonucleotide enzyme so free niacin react with cyanogen bromide to form yellow compound.
BACTEC medium
medium with radioactive metabolites. more sensitive for mycobacteria.
luciferase assay
detects presence of ATP with flashes of light
IFN-gamma release assay or Quantiferon-TB
expose blood cells to tub. antigen and measure IFN-gamma release.
BCG vaccine significance
can result in false positive in PPD. contains attenuated M.bovis Calmette-Guerin. Suppresses tuberculosis disease but not infection.
optimal growing temperature for M.leprae and significance?
30degC, grows on skin and superficial nerves.
MOT for leprosy?
nasal secretions, skin lesions
site of replication for leprosy?
skin histiocytes, endothelial cells, Schwann cells
forms granulomas
brucella, francisella, mycobacteria tuberculosis, tuberculoid leprosy
tuberculoid leprosy characteristics
infection limited by CMI. few acid-fast bacilli seen. granulomas. lepromin skin test+
lepromatous leprosy characteristics
poor CMI response. large numbers of organisms in skin/mucous membranes. foamy histiocytes rather than granulomas. negative lepromin.
disfiguring appearance of leprosy is from what?
skin anesthesia, resorption of bone, thickening/folding of skin due to infiltration
foam cells
lipid-laden macrophages. tuberculoid leprosy
tx leprosy
dapsone
very small, walless bacteria with sterols in membrane
mycoplasma
fried egg colony
mycoplasma
SP4 blood agar
contains several lipids including sterols that allow mycoplasma growth
shape of mycoplasma? why?
pleomorphic, lack cell wall, very flexible membrane
rod-shaped with tapered tip containing proteins? what do the proteins do?
mycoplasma pneumoniae. proteins serve as attachment point to resp epithelium.
pathogenesis of m. pneumoniae?
inhibits ciliary motion, necrosis of epithelium
m. pneumonia produces what molecule?
hydrogen peroxide
cold agglutinins
autoantibodies produced during infection by m.pneumoniae against RBCs, brain, lung, liver cells. can be used in serologic testing; agglutinates cells at 4degC but not 37degC
most common type of atypical pneumonia
mycoplasma pneumoniae
extrapulmonary manifestations of m.pneumoniae
stevens-johnson syndrome, erythema multiforme, raynaud's, cardiac arrythmia, arthralgia, hemolytic anemia, GBS
main lab dx
serologic testing. cold agglutinin titer of 1:128 or higher but half patients will have false negatives. false positives during flu and adenovirus infections. ab titer in complement fixation test.
what can you NOT treat m.pneumoniae with? why?
penicillin, cephalosporins (no cell wall)
tx for m.pneumoniae and m.hominis?
tetracycline for both pneumoniae and hominis; erythromycin for m.pneumoniae
diseases caused by m.hominis and ureaplasma?
hominis: pelvic inflammatory disease. ureaplasma: urethritis. both cause inflammation of chorioamniotis and postpartum fever and are isolated from fetal CSF (transferred during pregnancy and/or childbirth)