Gram Positive Bacteria Flashcards

Terms Definitions
Micrococcus
Catalase-positive
Aerobic
Cocci
Gram-positive
Enterococcus
Catalase-negative
Aerobic
Cocci
Gram-positive
Mycobacterium
Acid-fast
Aerobic
Bacilli
Gram Positive
Nocardia
Aerobic
Bacilli
Gram Positive
Staph. epidermidis
Coagulase-negative
Catalase-positive
Aerobic
Cocci
Gram-positive
Other staphylococci
Coagulase-negative
Catalase-positive
Aerobic
Cocci
Gram-positive
Peptostreptococcus
Anaerobic
Cocci
Gram Positive
Bacillus anthracis
G+ rodaerobic/facultativespore-formingBacillus motile except B anthracisIn soil (anthracis), air, dust, water2 virulence factors required for activity - capsule, exotoxinExotoxin - PA + LF = lethal toxin, PA + EF = edema toxinDeath due to massive bacteremiaIntestinal, cutaneous, pulmonary formsNo hemolysis (anthracis), most Bacillus are hemolyticTreat w/ ciprofloxacin b4 culture, then penicillin/tetracyclines if not resistantPA used in vaccine, B. cereus seen in mastitis
identify staphylococcus saprophyticus
NOVOBIOCIN-RESISTANT
 
gram positive coccus
 
blood agar: white colonies
 
catalase positive
 
coagulase negative
 
mannitol-salt agar test negative (cannot ferment mannitol)
neonatal tetanus
tetanus neonatorum
clostridium tetani
common 1* infection site: umbilical stump (dirty tools to sever cord)
symptoms: excessive crying, trismus, tetanic spasms, opisthotonus
fatality: >90% (survivors have developmental defects)
Arcanobacterium (pyogenes)
AKA actinomyces/corynebacterium pyogenesG+ pleomorphic rods, swollen at endsLives in mm of nasopharynxEntrance via injury, has weak hemolysins that act as cytotoxins, get heavily encapsulated abscesses w/ anaerobic bacteria in themCattle/sheep/swine - suppurative pneumonia/mastitis, metrits, joint infSlow-growing (48-72hrs) coloniesBeta hemolysis, catalase negSusceptible to most antibiotics
staphylococcus saprophyticus diseases
cystitis (inflammed bladder)
pyelonephritis
*commonly present w/ dysuria and/or pyuria
 
bacterial UTI in sexually active women (7-20%)
*E. coli the most common cause
 
side note: commonly drug resistant
hordeolum/style
most common cause: S. aureus (invasive & cutaneous)
 
folliculitis of eyelid
 
erythematous or pustular appearance
localized tetanus
clostridium tetani
confined to musculature of 1* site of infection
generalized tetanus
C. tetani
most common
masseter muscles (trismus, lockjaw); risus sardonicans
early signs: drooling, irritability, back spasm (opisthotonus)
Corynebacterium pseudotuberculosis
Caseous lymphadenitis in sheep/goatsProduces phospholipase D (exotoxin) - lyses RBCs, decreases neutrophil activity/complement activationHas lipid in cell wall (good for survival/leukotoxicity)Enters via abrasionsBeta hemolysis, crumbly coloniesIs bacterin/toxoid (must use in advance)
Impetigo
Bacterial cause: (S. aureus: 80%; S. pyogenes OR mixed: 20%) invasive & cutaneous disease
 
limited to epidermis
 
acute & contagious
 
common in children (face & limb) AND during summer/tropical climates
 
progression:small macule (small discolored spot on skin) --> pustule on erythematous base --> pustule ruptures & is replaced by honey brown crusting
bacteremia
when s. aureus (invasive & non-cutaneous disease) is the cause
 
> 50% acquired after surgery OR from contaminated IV catheter
 
usually from innocuous-appearing skin infections
staphylococcus epidermidis identification
gram positive coccus
 
catalase positive
 
coagulase negative
 
blood agar: white non-hemolytic colonies
 
mannitol-salt/tellurite-glycine agar negative
staphylococcus aureus colonization (prevalence)
community: 20-50%
 
healthcare workers: 90%
 
higher in hemodialysis patients
What organism is this?
 
gram positive coccus
 
coagulase positive
 
catalase positive
 
grape-like clusters
 
tellurite-glycine/mannitol-salt agar positive
 
blood agar: golden-yellow colonies exhibiting hemolysis
staphylococcus aureus
Clostridium perfringes epidemiology
most predominant (spores/vegetative bacteria): serotype A in human fecal flora & in soil (most virulent)
growth time: very fast (3xs faster than E. coli)
infections endo/exogenous
 
single greatest biological warfare threat
bacillus anthracis
bacillus anthracis epidemiology
commonly infects grazing herbivores
more serious w/o animal vaccination
human-->human transmission: RARE
human infection (US): RARE
Staphylococcus intermedius
Coagulase +Causes otitis, pyoderma, urinary calculi in dogs.Infections in any wound
Streptococcus suis
Group r-S strepAlpha or non-hemolytic34 serotypesmeningitis, pneumonia, arthritis, myocarditis in swine
Streptococcus zooepidemicus
Group C strepBeta hemolyticMucoid colonyVariable M protein - so, about 15 serotypes (from diff't capsules)Dogs, horses - resp tract infections, abscessesHorses also metritis, eyes, wounds - VERY IMPORTANT for HorsesPigs - abscesses, arthritis, abortion
Streptococcus dysgalactiae
Group C strepAlpha or non-hemolyticBovine mastitis
toxic shock syndrome
cause: enterotoxin or enterotoxin-like TSST-1
*in menstruation-associated TSS cases: >90% caused by TSST-1
 
mechanism: TSST-1 strains multiply in hyper-absorbant tampons 
 
presentation: abrupt (fever, hT, whole-body-erythematous rash); multiple organs involved; entire skin desquamates (2-3 wks); markedly red tongue
 
fatality: previously high, currently 5%
staphylococcal pneumonia
prevalence: 2% of community pneumonia (*PV leukocidins important role here); 20% nosocomial-pneumonia (15-40% fatality <= those who develop are already ill)
 
cause: aspiration of oral secretions OR hematogenous spread
 
presentation: tissue destruction, massive hemoptysis, septic shock (all due to toxins)
 
remember: streptococcus pneumoniae is the most common cause of bacterial pneumonia
osteomyelitis
most common cause: s. aureus (invasive & non-cutaneous disease)
 
cause: hematogenous spread OR extension from subcutaneous infection
 
children: in metaphyseal areas of long bones (from low flow areas => time for bacteria to get out of the circulation)
 
adults: vertebra (rarely in long bones)
 
presentation: sudden onset of localized pain AND high fever
mastitis
s. aureus intro into ductal system through cracked nipples (invasive & cutaneous disease)
 
presentation: tenderness, fever, fatigue, possibly aggressive, may require drainage
anthrax hemorrhagic meningitis
fatality: 100%
symptoms: lots of edema, blood CSF (w/ gram+)
"Cardinal's cap" appearance (lots of hemorrhage of leptomeninges)
spreads: to CNS from any kind of anthrax infection
cephalic tetanus
Clostridium tetani
head is the 1* site of infection
poor prognosis
identify cutaneous anthrax specimens
vesicular stage: vesicular fluid
eschar stage: eschar material
most virulent species of Mycabacterium tuberculosis Complex
Mycobacterium tuberculosis
aerobic weakly acid-fast genera:
actinomycetes (nocardia)
50-60 C length of beta chain
leprosy (Hansen's disease)
cause: Mycobacterium leprae (7xs slower growth than M. tuberculosis)
affects: skin & peripheral nerves
Streptococcus agalactiae
Group B strepBeta hemolytic or non-hemolytic sometimesProduces arrow on CAMP test (CAMP +)Obligate pathogen found mammary glandMay cause mastitis
Streptococcus equi
Group C strepBeta hemolytic, mucoid coloniesCapsulatedImportant herd problem - strangles in horses (may have carriers with ongoing guttural pouch infections)Has antiphagocytic distinct M proteinAnimals may have resistance after 1 infection
s. aureus id
 
tss
check vaginal samples, bacteria will be there
 
bacteria will NOT be in blood :(
food poisoning
most common cause of food borne illness: staphylococcus aureus (50% strains produce 8 distinct enterotoxins)
*heat stable (produced by bact in food @ RT, stable in re-heating)
 
superantigen mechanism? (not well understood)
 
presentation: severe vomiting (w/in 3-4 hrs)
*toxin w/in vomitus (bacteria absent)
 
therapy: fluid replacement NOT antibiotic (be/c this in an intoxication NOT an infection)
tx of clostridial myonecrosis
surgical debridement & frequently amputation
virulence of C. difficile
spores survive gastric acidity (germinate in LGT)
2 toxins: enterotoxin A & cytotoxin B (disrupt epithel cell barrier)
*pseudomembranes seen on colon endoscopy
identify gastrointestinal anthrax in these specimen:
blood, stool, rectal swab
three important Actinomycetes w/ mycolic acid:
1. Corynebacterium
2. Nocardia
3. Mycobacterium
types of actinomycosis (4)
1. cervicofacial: soft tissue swelling/abscess/mass lesion; often mistaken for neoplasm; potential spread
2. thoracic: involves pulm parenchyma/pleural space, may cross fissures/pleura; spread to mediastinum, contiguous bone, or chest wall
3. abdomen/pelvis: diff to dx; present as abscess or mass lesion (long time to develop)
4. cerebral (single brain abscess)
disease caused by Acintomyces israelii
Actinomycosis (acute/chronic pyogenic infec, both suppurative AND granulomatous)
char: multiple abscesses & interconn sinus tracts
*infected tissues show sulfur granules (pathognomonic)
usually: polymicrobial
several types
Corynebacterium renaleCorynebacterium pilosumCorynebacterium cystitidis
Found genitally in cattleInfection by urine splashHas pilusCauses pyelonephritis (cattle), urinary infections (swine)No hemolysisFlat, off-white/tan colonies
predominant site(s) of staphylococcus aureus colonization
#1: anterior nares
 
others: skin, vagina, axilla, perineum, & oropharynx
common transmission of staphylococcus aureus
(epidemiology)
from hands of healthcare provider
 
patient to patient (hospital setting)
 
not seasonal (except warm seasons' prevalence for food poisoning)
 
community: major cause of soft tissue infection
s aureus id
 
food poisoning
:) bacteria in food/toxin in vomitus
 
:( bacteria NOT in feces/vomitus
C. tetani virulence factors
common entry to body: implanting spores in wounds
under anaerobic conditions: spores germinate --> produce toxins --> retrograde mvmt w/in CNS
char sympt: convulsive muscle contraction (lockjaw, back muscles)
cause of death: cardiac/respiratory complic
Bacillus cereus virulence factors (2 toxins)
heat-labile (diarrheal): stim adenylate cyclase (=> cAMP); SLOW onset
heat-stable (emetic): RAPID onset
ALL gram+ anaerobic spore formers
Clostridium
part of normal colonic flora
most abundant: C. ranosum, then C. perfringes
most pathogenic: C. perfringes
clinical forms of TB
1. pulmonary TB *most common
2. extrapulmonary TB
Mycobacterium tuberculosis produces many genes for...
lipid synthesis, these lipids are cross-linked to fatty acids & arabinogalactan (impor for host interaction & survival in macrophage) & peptidoglycan layer => AFB & low permeability of cell wall
-complex cell wall => very slow growth
Ig bound to protein A elicits...
cell-mediated response => pus formation AND necrosis
s. aureus id
 
bullous impetigo
:) looking in blister fluid (bacteria found here!)
Clostridium difficile epidemiology
spores high conc in hospitals & LTCF (high antibiotic use)
risk of infection correl. to length of stay
 
name the 2 clinical outcomes of Nocardia disease
1. bronchopulmonary nocardiosis 
2. cutaneous nocardiosis:
Primary (mycetoma, lymphocutaneous infection, cellulitis)
Secondary (spread of organism from pulmonary diseases)
types of Mycobacterium leprae diseases (2)
1. Tuberculoid TB (paucibacillary PB)
2. lepromatous TB (multibacillary MB)
how is Nocardia usually acquired? pathogenesis?
inhalation of fragmented bacterial mycelia and usually => abscess w/ extensive PMN infiltration & necrosis
-toxins observed, no clear role
-produces catalase & SOD
-cord factor inhib acidification of phagosome (PMNs can phagocytose but not efficiently kill => CMI needed to eliminate infection)
2 potent toxins of C. tetani
1. chromosomally encoded 02 labile hemolysin (tetanolysin): unclear role 
2. plasmid encoded 02 labile neurotoxin (tetanospasmin-tetanus toxin): stationary phase, blocks release of inhibitory neurotrans
leading cause of death due to a single infectious agent (worldwide) & contributing factors:
tuberculosis
 
HIV epidemic
poorly managed TB programs
incr mvmt of ppl & overcrowding
Scalded Skin Syndrome (Ritter's disease)
caused by: exfoliative toxins A & B (s. aureus-toxigenic disease) break desmoglein-1 (polypeptide) in desmosome (connect adjacent skin cells)
*stratum granulosum is susceptible be/c it lacks the Dsg-3 (polypeptide) that usually compensates for ETA/ETB hydrolysis of Dsg-1 in other strata
 
presentation/progression: abrupt onset of perioral erythema (covers entire body in 2 d) --> large bullae/cutaneous blisters (like burns) --> desquamation (in 5-7 d) --> blisters (2 wks) & positive nikolsky's sign
 
*blisters do NOT contain organism
 
 
name the 4 types of C. botulinum diseases (all paralytic diseases)
1. foodborne botulism 
2. infant botulism
3. wound botulism
4. inhalational botulism
how is AFB growth inhibited (as seen w/in granulomas)?
where does MTB grow best? why?
low 02 & pH
 
kidneys/vertebral bodies (areas w/ high 02)
how does the host respond to M. tuberculosis?
monocytes present AFB-antigens to T cells => start CMI/HMI
@ 2-4 wks: 1. macrophage activating CMI (activated macroph kill AFBs)
2. tissue damaging response (kill un-activated macrophages w/ AFBs)
Clostridium
Anaerobic
Bacilli
Gram positive
Corynebacterium
Aerobic
Bacilli
Gram Positive
Peptococcus
Anaerobic
Cocci
Gram Positive
Staphylococcus aureus
Coaglulase-positive
Catalase-positive
Aerobic
Cocci
Gram-positive
Proprionibacterium
Anaerobic
Bacilli
Gram Positive
Bacillus
Aerobic
Bacilli
Gram Positive
staphylococcus epidermidis 
 
"CNS" or "CONS"
Coagulase Negative Staphylococcus
foodborne botulism
C. botulinum
characteristic: symmetric descending paralysis
*flaccid paralysis
initially: blurred vision, constipation, abd px, no fever
Streptococcus equisimilis
Beta hemolyticNon-capsulatedVery widely distributed among number/species animals
furuncle
most common cause: S. aureus (invasive & cutaneous)
 
boil: several hair follicles & adjacent tissues are affected
 
reduced risk: w/ good skin hygiene
causes 80% suppurative infections
 
2nd leading cause of nosocomial infections
Staphylococcus Aureus
bullous impetigo
localized SSSS
 
infection, NOT toxigenic => bacteria will be present w/in blister fluid
 
presentation: erythema does not extend beyond blister borders
intestinal anthrax
cause: eating anthrax-infected meat
fatality: 25-60%
symptoms: severe GI difficulty, vomiting blood, diarrhea, acute inflamm
(Bacillus anthracis)
 
Streptococcus uberis
Serologically diverseAlpha or non-hemolyticbovine mastitisCAMP +
Staphylococcus epidermidisStaphylococcus simulansStaphylococcus xylosusStaphylococcus saprophyticusStaphylococcus schleiferi
Coagulase (-)Usually not pathogensFound in wounds, surgical infections, UTI/cystitis (cats), mastitisepidermidis - opportunisticschleiferi - on skinsaprophyticus - in urine
s. aureus ID
 
bacteremia 
good: culturing blood
 
bad: staining blood (so few organisms)
carbuncle
S. aureus disease: (invasive & cutaneous)
 
coalesced furuncles (more serious disease); extended to deeper subcutaneous tissue (multiple sinus tracts)
 
common locations: nape of neck, upper back, or buttocks
 
progression: tight/erythematic skin --> effaces & releases pus
 
associated symptoms: chills & fever
 
 
most staphylococcus aureus infections result from:
own strains
other staphylococci (2)
 
and their associated diseases
staphylococcus haemolyticus
 
staphylococcus capitis
 
endocarditis, UTIs, wound infections, opportunistic infections
bioterrorism concern
inhalational botulism caused by Clostridium botulinum <= toxin can be aerosolized 
general characteristics of Actinomyces israelii
gram+
filamentous branching
anaerobic
non-acid fast
disease more common: men & w/ poor oral hygiene
virulence: low, infection w/ mucosal disruption
(endogenous)
usually present in oral cavities, colon, & vagina
Corynebacterium (general)
G+ small rodsVariable appearance, catalase +Are "diptheroids"Commensals of skin, mucosaSusceptible to many antibiotics - abscesses make treatment difficult
Staphylococcus hyicus
Coagulase +/-Non-hemolytic on sheep BAGreasy pig - exfoliative dermatitisEnters through wounds in skin - hypersensitivity, skin thickens - eventually kidney damageAutogenous bacterins beneficial for immunization against hyicus
Listeria monocytogenesListeria ivanovil
G+ rodmotilecatalase +facultative anaerobeIngestion from soil/feces,disseminated in blood stream, spreads along trigeminal nerve,Internalin allows movement across cell membranes, hemolysin, LPS, listeriolysin allows breaking out of phagosome into cellMeningoencephalitis (looks like rabies), abortionBeta hemolysis (narrow)Treat with sulfa/trimethoprim, erythromycin, oxytetracycline (difficult b/c in brain)
Enterococcus faecalis
Enterococcus is formerly fecal streptococci or enterococciSo... G+See in canine ears, all animals in woundsTreat with ampicillin, secondarily sulfa/trimethoprim, Gentamicin (systemic inf)E. faecalis: Group D (strep)weak alpha or non-hemolytic Normal flora intestine
wound infections
most commonly colonized by gram negative organisms
 
most common gram positive organism: staphylococcus aureus (invasive & cutaneous disease)
 
occurs after surgery/trauma
 
presentation: edema, erythema, pain, accumulation of purulent material
staphylococcus saprophyticus virulence factor
not known
 
can colonize periurethral skin & mucosa
s. aureus ID
 
ssss
good: look at nasopharyngeal sample
 
bad: looking at blister fluid (usually not here!)
septic arthritis
most common cause in most individuals:
s. aureus (however, N. gonorrhoeae (gram-negative coccus) is most common among the sexually active)
 
presentation: pain w/ mvmt, erythematous/swollen joints, pus in aspirated fluid
 
common location(s): knee (50% of cases), wrists, ankles, & hips
Staphylococcus aureus virulence factor 
(toxins-4)
1. alpha/beta/delta/gamma & leukocidins
(toxic for: leukocytes, RBCs, platelets, macrophages, & fibroblasts)
 
2. ETA & ETB = serine proteases (digest anchors holding epidermis to dermis)
 
3. TSST-1 (superantigen; systemic effects)
 
4. enterotoxins (A-E) (superantigens; stim T cells/cytokine release/inflamm med by mast cells; incr intestinal peristalsis/fluid loss/vomiting)
staphylococcus aureus virulence factors (structural-4)
1. capsule (inhibit chemotaxis/phagocytosis; adheres to foreign bodies)
 
2. peptidoglycan (inhibit phagocytosis; endotoxin-like)
 
3. teichoic acid (major component of cell wall; mediates attachment to mucosal surface; regulate cationic conc @ cell mem; bind Fn)
 
4. protein A (bind IgG-Fc frag; inhibit opsonization/complement activation)
antibiotic associated enterocolitis
most common cause: Clostridium difficile 
2nd: staphylococcus aureus (produce ETA & leukotoxin E/D)
 
presentation: watery diarrhea, abdominal cramps, fever, inflammation of intestinal mucous membrane (bacteria present in stool)
 
increased risk: w/ use of broad spectrum antibiotics
 
 
suppurative myositis
suppuration in muscle planes w/o necrosis or systemic symptoms
secondary tuberculosis
AFB contained in granulomas of activated macroph (not eradicated) = latent infection
if released (liquefaction allows bact growth) can cause disease years later (bacillary antigens => tissue dmg: bronchi erosion, spreading along bronchial tree)
little tissue dmg
PPD rxn+
identifying features of Nocardia
aerial hyphae
clinical specimen: sputum or pus
weakly acid-fast
growth improves w/ C02
Staphylococcus aureus
Coagulase +Cows - mastitis (including peracute gangrenous mastitis)Horse- wounds, jointsChickens - bumble footDouble zone hemolysisOften resistant to penicillin, ampicillin, tetracyclineMay use pirlimycin IMM
Streptococcus (general)
G+ coccus, single/pairs, long chains in abscesses, mucoid when run togetherCatalase (-)Facultative anaerobe or microaerophilicNormal floraM-protein and hyaluronic acid antiphagocyticM protein inhibits complement activation and binds Fc of AbsToxins and enzymes damage membranes, lyse RBCsAlpha, gamma hemolytics normal, betas are pathogensTreat w/ penicillin for beta hemolytics and erythromycin/ampicillin for others
Erysipelothrix rhusiopathiae
G+ rod, alpha hemolysis, catalase negNon-motileFacultative anaerobeNo toxins, causes hypersensitivity immune complexes, has hyaluronidase, neuraminidase (penetrates cell)Infects joints, heart, vessels, petechial hemorrhages in liver, lungsSwine: septicemia - "diamond skin dz", can vaccinate forSheep - after docking, castrationTreat with penicillin
Streptococcus canis
Infections in neonatal dogs and cats
s aureus id
 
blood agar
hemolytic and golden yellow colonies
3 Staphylococcus aureus virulence factors
1. structural
 
2. enzymes
 
3. toxins
identify inhalational anthrax in these specimen:
blood & sputum
gas gangrene=clostridial myonecrosis
what does the "gas" come from?
organism replication (there will be crepitus present)
extensive hemolysis
bacteria present
inflammatory cells absent
symptoms: shock, renal failure, death w/in 2d
aerobic, true acid-fast genera:
all Mycobacterium species
70-90 C length of beta chain
primary tuberculosis
clinical illness during 1st year after 1* exposure: caseous center enlarges --> tissue destruction --> releases bacilli from un-activ macroph
not assoc w/ high transmissibility
10%
presentation: flu-like illness; fever, cough, night sweats, weight loss, "snow storm" on Chest rad
characteristic: Ghon focus (CMI control of MTB => calcified lung lesions)
Mycobacterium avium complex (MAC)
1. M. avium
2. M intracellulare
causes: disseminated infect in immunocompromised (esp HIV+)
most common: non-TB mycobacterial infection (AIDS pts - 50% will develop MAC infec)
presentation: fever, swollen lymph nodes, diarrhea, fatigue, & wt loss
Actinomyces viscosus
G+ filamentous rodIn oral cavity of dogs, enters blood via wound/periodontal disease, get abscesses, fistulous tracts, pyothoraxSee granules in aspirateColonies form in 3-7 daysTreat with penicillin/tetracycline
staphylococcus epidermidis diseases (2)
1. major cause of infections associated w/ intravascular devices (ie. prosthetic heart valves, shunts, etc.); also in prosthetic joints, large wounds, and catheter induced UTIs
 
2. high incidence in hospital setting (contaminates pt care equipment/environmental surf w/ biofilm)
steps to C. difficile colitis:
1. exposure to antibiotics
2. exposure to C. difficile capable of producing toxins
3. inadequate immune response (antibodies to toxin A-protective)
2 most likely causes of colitis:
1. Clostridium difficile
2. Staphylococcus aureus
other gastroenteritis caused by C. perfringes (other than food poisoning)
necrotizing enteritis (enteritis necroticans, pig-bel)
cause: strains prod beta toxin
occurs w/: high protein/trypsin inhibitor (sweet potato)
incr risk: decr intestinal proteases
symptoms: peritonitis, abdom px, vomiting, bloody diarrhea, shock
fatality: 50%
organisms most commonly causing primary & secondary cutaneous nocardiosis:
1* N. brasillensis
2* N. asteroides
Actinomyces bovis
G+ filamentous rodsLive in mm or oral cavityCauses chronic granulomatous suppurative lesions "lumpy jaw" in cattleSuppurative mastitis in swineTreat w/ penicillin/tetracycline
staph infections caused by MRSA (in the US):
1974
1995
2004
1974: 2%
1995: 22%
2004: 63%
s aureus id
 
tellurite-glycine agar
positive: s aureus changes color --> black
 
glycine inhibits growth of species OTHER than staph
 
differential due to tellurite reduction to tellurium
identifying features of Bacillus cereus
beta hemolytic on sheep blood agar
string of pearls test-
motile
glutamyl-polypeptide capsule-
identifying M. tuberculosis
this is one of the few mycobacteria that can reduce nitrate
transmission of Mycobacterium tuberculosis:
droplet nuclei from pts w/ pulmonary TB (coughing, sneezing, or speaking)
pathogenesis of C. perfringes
growth requirements: ~14 AAs & 6 other factors (most body fluids are deficient of these materials EXCEPT necrotic tissues)
*produces ~12 toxins  (alpha toxin=gas gangrene)
explain the quantiFERON-TB Gold Test (QFT-G)
M. tuberculosis
dx: latent & active TB (cannot differentiate bt/w the two)
process: blood samples mixed w/ 2 MTB-specific antigens
results: w/ MTB+ sample, WBCs release measurable IFN-gamma
Quorum sensing - Staphylococcus aureus virulence factor
bacteria makes genetic changes due to changes in growth density (different growth phases)
*S. Aureus is a classic example 
 
during initial part of infection, S. aureus growth density is low: bacteria doesn't need to produce toxins, it needs to produce cell surface proteins (ie. Protein A) to establish a colony
*agr locus of S. aureus regulates many of its cell surface proteins (RNA molecule rather than the usual protein gene-expression-regulator)
 
later on, once the infection is established and the organism needs more room, this feature of the bacteria allows it to produce the toxins against the host => degraded host cells serve as bacterial nutrients (tissue damage/disease)
entry/action of anthrax toxin: PA binds anthrax receptor --> processed by furin on cell surf
--> PA oligomerizes => EF/LF binding sites --> toxins endocytosed --> PA conform chg w/ pH chg --> toxins in cytosol
 
EF (adenylate cyclase): releases cAMP
LF (protease): degrades MAPKK
rate of leprosy contracted after exposure
3-5% ("due to CMI, not readily contagious"?)
early stages - most infectious
transmission: skin/mucus lining (nose & throat)
higher risk: children
progression: infection begins attack on dermis --> spreads up nerve sheath
2nd or 3rd most common cause of food poisoning in the US
Clostridium perfringes, usually type A
induces Ca++ dependent alteration in permeability
symptoms: epigastric pain, nausea, cramps, watery diarrhea
1. most common Nocardia in the US
2. Condition of patients most commonly infected by Nocardia
1. Nocardia asteroides
2. AIDS and other immuno-deficiencies 
/ 134
Term:
Definition:
Definition:

Leave a Comment ({[ getComments().length ]})

Comments ({[ getComments().length ]})

{[comment.username]}

{[ comment.comment ]}

View All {[ getComments().length ]} Comments
Ask a homework question - tutors are online