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110 Cards in this Set

  • Front
  • Back
spirillum
rigid cell bodies, elongated with flagellar tufts at both poles, gram negative aerobic
Spirochetes
smal flexible helical cells, two axial filaments wrap around, gram negative, aerobic.
Cocci
spherical
Bacilli
rods
Clusters of bacteria
Staphylo-
Chains of bacteria
Strepto-
Lophotrichous
several flagella at one pole
Peritricous
Multiple flagella everywhere
H antigens
Flagellar antigens
Endoflagella
specific to spirochetes, around cell, within outer sheath, rotation causes cell movement
Gram-stain procedure
1. Crystal Violet (purple -positive)
2. Iodine
3. Alcohol
4. Safranin (red - negative)
Gram positive cell walls
Thick peptidoglycan layer
Teichoic Acids
Polysaccarides provide antigens
Gram negative cell walls
Thin peptidoglycan layer and an outer membrane that contains LPS, phospholipids, and protein.
Layers of Gram negative cell wall - inside to outside
Plasma membrane, periplasm, peptidoglycan, outer membrane, polysaccharides
Toxins in gram negative and positive cells
Gram positive - exotoxins
Gram Negative - endotoxins
Lipopolysaccarides in gram positive and negative cells
Positive - none
Negative - lots
Mycobacteria cell wall
Similar to gram negative but has mycolic acid. Use acid fast stain instead of gram stain.
Staining mycobacterium
neither gram pos or neg. Acid fast - they retain pink stain.
Gram pos vs. neg: sporulation
Some strains of Gram positive only
Layers of endospores
core, inner membrane, spore wall, cortex, outer membrane, protein coat, exoporium
Phases of the growth curve
1. Lag
2. Log
3. Stationary
4. Death
Penicillin target
Cell wall, usually gram positive
Cephalosporins
still beta lactams, more resistant to lactamase.1st generation - gram pos. 4th generation - gram neg.
Bacitracin
Topical only, targets cell wall
Cycloserine -
against mycobacterium tuberculosis
macrolides
Targets protein synthesis - binds to 50s
clindamycin
Blocks peptide bond formation
Linezolid
blocks 23s rrna
Tetracycline
30s
aminoglycosides
streptomycin and kanamycin, bind 30s subunit
Sulfamethoxazole
Folate synthesis, competitive inhibition of PABA
Quinolones
like Cipro - inhibits DNA gyrase
Rifampin
Blocks transcription by binding to RNA polymerase
Prototroph
an organism with wild type complement of genes enabling it to grow with a simple requirement of nutrients
Auxotroph
a mutant unable to synthesize a small molecule, requires supplements
Fastidious organism
complicated growth requirements
Lytic
host cell is lysed by virus
lysogenic
phage genome is integrated into host chromosomal DNA
pathogenicity islands
chromosomal regions that contribute to virulence
generally higher GC
Horizontally acquired
Endotoxin
LPS - arent released unless the cell is lysed
SZipper mechanism
bacterium tricks endocytosis into bringing in the cell
Membrane splash
another way for bacteria to enter cell. membrane folds around bacterium
AB toxin
B - binding portion
A - active portion
Group A
Strep pyogenes
Group B strep
S agalactiae
Group D
enterococcus. E faecalis
Streptococcus pyogenes
pus forming, aerotolerant anaerobes. human is the only reservoir. 10-30% asymptomatic carriage rate
Superantigens
proteins that simulataneously bind Vbeta (TCR) and MHC-II
m protein
antiphagocytic factor
hyaluronic acid capsule
hinders opsonization recognition
lipotechoic acid
adhesin, binds fibronectin, last of the 3 group A virulence factors
Quellung reaction
determines pneumococcus capsular type. you can see capsule swelling
Only coagulase positive bacteria strain
staph aureus
Coagulase
Clotting factor
Staphylokinase
can target Fc cleavage, cleaves antimicrobial peptides, cleavage of C3b to C3i.
Protein A
binds to Fc region of Ig
Catalase
converts h2o2 to water and oxygen
Carotenoid
Aureus - gold color, antioxidant
CHIPS
chemotaxis inhibitory protein, throws neutrophils off the scent
TSST
Toxic Shock Syndrome Toxin from Strep
How enterotoxin B causes death
hypovolemic shock
Bullous impetigo
bacteria in the skin
SSSS
Staphylococcal scalded skin syndrome - no bacteria in blisters
Staph food poisoning
from toxins, not infection. No fever. 24 hrs.
Faruncles
Extension of folliculitis. Underlying collection of necrotis tissue. From staph infection.
Carbuncles
Coalesced furuncles that extend to deeper tissues. Can lead to bacteremia. Chills and fever indicate systemic spread.
Acute endocarditis
Staph in blood can adhere to heart tissue. Sudden onset of high fever. High mortality. Valvular destruction and embolisms to brain or lung.
Pneumonia
rarely caused by staph.
Staphylococcus epidermidis
Coagulase negative, normal flora of skin.
Staph saprophyticus
causes UTI's in young sexually active women
Staph treatment;
not penicilin. New semisynthetic penicillins should work
MRSA treatment
Vancomycin is 1st line of defense
Strep skin infections:
cellulitis, necrotizing fascilitis, impetigo, erysipelase, myonecrosia
+RNA viruses
can make protein directly
-RNA viruses
must make +RNA to make protein.
Capsid
protein coat on virus
Envelope
bilayer membrane that covers capsid
Parvovirus
single stranded DNA virus
Herpes virus
double stranded DNA, envelope. Herpes, chicken pox, kaposi's sarcoma, Epstein-Barr
Picornavirus
+RNA virus, single stranded, non enveloped, hepA
HIV-1
positive sense, SS RNA, enveloped, diploid genome
Enterobacteriaceae
facultative anaerobic gram -
ETEC
Enterotoxigenic E coli, traveler's diarrhea, infant diarrhea in 3rd world.
EPEC
enteropathogenic E coli, infant diarrhea
EIEC
enteroinvasive e coli, mild shigella like dysentery.
EAEC
enteroaggregative e coli - infant and child diarrhea in 3rd world or immunocompromised adults.
DAEC
diffusely adhering e coli, watery diarrhea in children
EHEC
enterohemorrhagic e coli. bloody diarrhea
ETEC toxins
Labile - increases cAMP in intestinal cells to secrete water and ions
Stable - stimulates cGMP with same effect
EPEC toxins
destroy surface microvilli in intestines
EIEC toxins
factors similar to those of shigella, causes dysentery
EAEC
fimbriae attach to intestinal cells
EHEC toxins
Stx-1 and -2 on lysogenic phage are hemolysins. Vero toxin - shiga like.
Shigella
Gram neg rods. Human are the only reservoir. Fecal oral transmission.
Shigellosis
Intense diarrhea 3 days. can end here or can develop into dysentery with intestinal inflammation, abdominal pain, relatively scant stool with blood and pus (WBCs)
S. dysenteria
Causes worse shigellosis, contains shiga like toxin which prevents protein synthesis. AB toxin.
Shigella pathogenic process
1. invade intestinal cells
2. escape from endocytotic vesicles and multiply
3. directly invade adjacent cells
4. host cells die and mucosal abscess forms.
Treating shigellosis
manage dehydration, antibiotics use is controversial
Typhoid fever
Most severe of salmonella diseases. requires antibiotics: cephalosporin, fluoroquinolone, treatment must be long lasting to eliminate carrier state
B pseudomallei diseases
limited to southeast asia and australia, melioidosis
Pseudomonas
Gram neg rod, non spore. Obligate aerobe. Found everywhere, motile.
P aeruginosa
ubiquitous. Common nosocomial pathogen along with staph aureus.
P aeruginosa diseases - lung
pulmonary infections, frequent cause of pneumonia, problem for CF patients.
S
P aeruginosa disease - skin
Skin infections - burn patients, tissue necrosis. folliculitis from hot tubs. Gangrene
P aeruginosa disease - other
UTI's in catheter patients, ear infections (swimmer's ear), eye infections in contact lens wearers.
Legionella
gram neg bacilli. L. pneumophila causes most disease, common aquatic bacteria. Transmission by aerosol inhalation
Legionella cont'd
intracellular, survives inside macrophages, uses type IV secretion to inject proteins that delay phagosome fusion with lysosome
Legionella treatment
Fluoroquinolones and macrolides
Bordetella
Major pathogen - bordetella pertussis. causes whooping cough. Gram negative coccobacilli.
Bordetella toxins
adenylate cyclase/hemolysin - increases cAMP in cells.
tracheal cytotoxin - causes ciliostasis