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Urinary tract infections, most
Meningitis in neonates(<1MO)
2ndmost common agent
Traveler’sdiarrhea, infant diarrhea in
3rd World. Watery diarrhea with
cramps, nausea, sometimes vomiting.
Usually ends on its own in 5 days.
Major cause of infant diarrhea in 3rd
Mild shigella-likedysentery. Rare in
US.Common in Third World.
Infant and child diarrhea in 3rdWorld
Persistentwatery diarrhea that
generallylast >14 days
Oftenthe cause of chronic diarrhea
inimmunocompromised patients more susceptible.
Persistent, watery diarrhea in 1-6yr.
After 3-4 days, watery, non-bloody
diarrhea.25% get a bloody
diarrheawith cramps and maybe
vomitingafter 2-3 days. 5-10%
develophemolytic uremic syndrome.
Often,O157:H7 serotype. 3,529 cases
inUS in 2005.
Pili-attachment;on pathogenicity island
Adhesion for bowel and urinary tract
Pili-attachment;on pathogenicity island
Adhesionfor bowel and urinary tract. ROle of k1 capsule is unclear
1 to 4 enterotoxins, plasmid-mediated- pedastol
Variety of proteins that lead to attachment and destruction of microvilli. Plasmid-mediated. produces tir protein that allows it to enter cells. Intimin of EPEC will bind tir. Then type 3 secretion will further assist entering.
Variety of factors very similar to those of shigella.Plasmid-mediated. you can see bloody diarrhea. not as bad as shigella
Fimbriae which attach to intestinal cells.
- resembles shigellosis
not well known
Stx-1 and Stx-2 toxins which are very similarto toxins of shigella. Toxin genes are on a lysogenic phage. Hemolysins.
Natural reservoir: common in soil and waters ofSoutheast Asia and Australia. Not partof the normal flora.
Transmission: by inhalation or direct contactwith the environment through skin or mucosal breaks
-melioidosis which has many forms
-infections in skin or respiratory tract
-multisystem abscess formation
-bacteremia with shock
-symptoms can appear days or years after exposure
-symptoms often mimic pulmonary TB
-limited to Southeast Asia and Australia
-Virulence factors not well defined but can survive inside phagocytes. Use type 3 secretion.
-Organism can be cultured and this is needed for a definitive diagnosis
-Drugs of choice not clear. ceftazidime would be a reasonable choice.
Type 3 secretion. Bacteria use a number of proteinsthat will form a needle which will penetrate the plasma membrane of the hostcell. There are other proteins, called effector proteins that will be secretedthrough the syringe. All these proteins involved will make the needle that canchange the plasma membrane. Notice needles on EM. This is how effector proteinsare secreted.
Type 3 secretion system. ExoS and ExoT. Pseudomonasaeoginosa Virulence factors secreted through type 3 secretions.
Many species but L.pneumophila causes
85% of diseases.
Hard to grow, require cysteine invitro
Common aquatic bacteria. Found inmany lakes and streams. Contaminate many human devices thathold water, such as humidifiers, air conditioning condensers or cooling tanks,whirlpools, etc. Can survive in treated waters or hottemps by growing inside amoebae in these waters.
Transmission is probably byinhalation of aerosols of contaminated water from environment.
No evidence for person to persontransmission
No known animal hosts
thecausative agent cannot be grown in routine bacteriological media in the lab orthe disease does not resemble pneumococcal pneumonia.
SA can crosslink TCR, variable beta chain of Tcell can crosslink to the alpha chain of the MHC2 molecule. Cross reacts the 2proteins. Activates T cell in a non antigen specific way. You get about 30-50%activation of all your T cells. This is what leads to the rash. HTN.
SpeB, Mac1/Mac2, SIC, ScpA, ScpC :cleaves immunoglobulins,antimicrobial peptides (cathelicidin), complement factors (C3b, C5a), cytokines (IL-8)
Streptodornase (Dnase). Breaksdown NETS (neutrophil extracellular traps)
Sourceof b-lactamaseand Vancomycinresistance (vangenes)
Hasbeen transmitted to Staphylococcus aureus
Treatmentof VRE: linezolid, daptomycin,tigecycline
LeukocidalToxins: target leukocytes (but unable to formpores in erythrocytes). Bi-component toxins made of F and S subunits. Three Fvariants and two S variants…combinations can make up to 6 diff. toxins
S.aureushas5 cytotoxins,2 exfoliative,eight enterotoxins,1 TSST
Exfoliative toxin A and B:
causesSSSS = Staphylococcal Scalded Skin Syndrome
Foundin 5-10% of S. aureus strains.
Serineprotease—splits intercellular bridges in stratum granulosumof epidermis
Notassociated with inflammation or cytolysis
Bacterianot found at site of shedding skin
Seenin young children – possibly because ETA and ETB target GM4-like glycolipids
Heatand protease resistant
Requireshigh oxygen and neutral pH (therefore not often found to act during other typesof staph infections where abscess forms)
Ableto cross mucosal barriers
Superantigenàrelease of cytokines, leakage of endothelia
(EnterotoxinB causes half of nonmenstruation-associated TS)
Deathoccurs from hypovolemic shock
In1980-81, 942 diagnosed cases of tampon-related TSS -- 40 died
Diseasecan result from toxin alone or direct invasion and tissue destruction
1. toxin-dependent:SSSS, food poisoning, TSS
2. invasion:cutaneous, endocarditis, pneumonia, empyema, osteomyelitis, septic arthritis
StaphylococcalScalded Skin Syndrome = Ritten’s Disease
1stsign: peri-oralerythema, expanding to entire body. Large bulleaform—no bacteria within bullae. Result of toxin. Low mortality
BullousImpetigo: localized SSSS; fluid-filled blisters; Staph cells within blisters;erythema does not extend beyond blister
4hour incubation, doesn’t last longer than 24 hours
Vomit,diarrhea, stomach cramping, No Fever
Staphmay cause enterocolitis…oftenfollowingbroad-spectrum antibiotic treatment
Impetigo:Superficial infection of epidermis
Pus-filledvesicles or erythemitous; following rupture of vessicle,crusts over
2°infection and spread likely occurs after rupture.
Mostcommon in children
infectionaround hair follicle; pus-filled lesions form around follicle
Ifoccurs at base of eye – stye
Furuncles(akaBoils): extension of folliculitis.Large, painful, underlying collection of necrotic tissue. Erythemitous,raised, swollen.
Carbuncles:coalesced furuncles; extend to deeper tissues; can lead to spread to othersites of body and bacteremia
Ofteninclude chills and fever àindicates systemic spread
Bacteremia:Staph is a common cause of bacteremia. Large number of cases have unknown primarysite of infection (likely skin infection)
Halfof cases follow surgical procedure or prolonged catheter use.
Hematogenous pneumonia:acquired during bacteremia or rarely from the community – strains typicallyexpress the PV leukocidin
Canlead to rapid destruction of parenchyma, or development of empyema (pus in thepleural space)
in children, occurs at metaphysealarea of long bones
in adults, typically occurs in vertebrae
both present severe pain and fever
(coagulase-negativestaph…normal flora of skin)
Endocarditisin artificial valves
Cathetersand shunts (50%)
originate from skin
UTIin young, sexually active women
MRSA30-50% of clinical isolates
mechanism: PBP2’ (cell wall enzyme changed, no longer binds b-lactams)
hospital acquired strains different fromcommunity acquired
many community acquired contain PVL toxin
Vancomycinis 1stline of defense against MRSA
targets cell wall one step earlier than b-lactams
VRSA: Vancomycinresistance emerging
vanAgene from VRE—confers high levels of resistanceVISA: VancomycinIntermediate resistance SA (low level resistance)
S.aureusstrains with thicker cell wall
Community-acquired,more susceptible to sulfa drugs, tetracycline, tigecycline.Hospital-acquired,require linezolid, rifampin, clindamycin
Ageneral term for drugs, chemicals, or other substances that either kill or slowthe growth of microbes.
Adrug used to treat infections caused by bacteria and other microorganisms. Includessynthetically produced drugs. (Old definition only included microbially-produceddrugs).
inhibitionof growth of targeted microbe without damage to the host. Antibiotictreatment is chemotherapy.
acompound that inhibits growth or reproduction of a microorganism, but does notdirectly kill the organism.
adrug that is administered in an inactive form. Activation occurs in vivo upon it being metabolized. (e.g.Isoniazid is activated by Mycobacterium’s catalase enzyme)
targetonly certain classes of bacteria (examples: Gram-negatives, anaerobes, Mycobacterium, etc.)
capableof targeting both Gram-negative and Gram-positive bacteria.
Kirby-BauerDisc Diffusion.This will spread out. If the antibiotic ispotent, you will get “ zones of clearing”. This is where the bacteria can’tgrow. Qualitative. You can measure the zone but it’s not the best way t measurethe miniminum inhibition. Qualitative measurement of Minimum InhibitoryConcentration (MIC)
Quantitativeanalysis for determining antimicrobial susceptibility. typically recorded in mg/ml (micrograms/milliliter).does notdetermine if bactericidal or bacteristatic.Commerciallyavailable strips. Serial dilution of antibiotic across strip. Placed on agarplate containing bacteria. View edge of clearing at lowest concentration ofantibiotic.
Inoculatefrom MIC cultures into fresh growth medium lacking antibiotics
MBCwill always be greater-than or equal-to MIC.
Vancomycin,penicillin and cephalosporins are the ones that are mainly used. They targetthe end steps. When cells are growing, they must reassemble cell wall. Rebuildafter you divide. Cell wall inhibitors are effective after growing bacteria.
Vancomycin willbind to the cell wall. Only place with fluourescen is where the cells aredividing. You wouldn’t see vancomycin stain if the cells weren’t growing.Bactericidal because bacteria have enzymes that tear apart the cell wall. Theseenzymes will tear apart the cell wall.
How do you recognize B lactam ring structures of bacteria?
Ceftriaxone (S. pneumo)
Verysmall b-lactam. Broadest antibacterial coverage. Often given with cilastin(inhibitor of liver enzyme that breaks down this drug). One of few remainingdrugs used to treat b-lactam-resistantbacteria.
Containgene NDM-1 (New Delhi metallo-beta-lactam-1). Effective against carbapenems.
Glycopeptide.Treatment of MRSA and Clostridiumdifficile(C.diff).Vancomycin-ResistantEnterococcus strains= VRE
mycolic acid biosynthesis inhibition
drugs: Thiolactomycin, Isoniazid,
80S(40S + 60S)
70S(50S + 30S)
chelatesCa2+;treats Chlamydia, tick-borne diseases, acne; phototoxic
Oxazolidones: Linezolid(zyvox):best against MRSA and VRE. Very expensive. Long-term use has high rates oftoxicity.
Tetracycline. selectivityis not at the level of ribosome, but is taken up by bacteria much moreefficiently.
bind30S or 50S subunits. Two modes of action: inhibits initiation complex andcauses misreads of mRNA.
Ex. Streptomycin and kanamycin
SynergisticTMP+SMX (called Bactrim)
Vancomycin-reistanceà change cell-wall component from
D-Alanine-D-Alanine à D-Alanine-D-Lactate
1.Enzymatic cleavage of b-lactams
2.Changing target of penicillins:PBPs penicillin-binding-proteins
3.Decreased permeability to drug (change pore sizes)4.Tolerance/Persistence: drug inhibits cell wall synthesis, but bacteria do notdie
(from D-Ala-D-Ala to D-ala-D-lactate)
1.modification of ribosome
a. acquiring mutation in ribosome
b. acquiring modifying enzyme (horizontal genetransfer)
2.decreased permeability to drug
2.molecular efflux pumps
2.modification of enzyme target
- Strict dependence on hostcells to multiple
- Infection of bacteria, plantsand animals
a. Provide the structural symmetry of the virus particle..
b. Facilitate transfer of thevirus nucleic acid from one cell to another.
c. Protect the viral genomeagainst inactivation by nucleases.
d. Determine the antigeniccharacteristics of thevirus
a. Regulators of viral gene expression
b. Enzymes for the viralreplicative cycle when virion enters a host cell.c. Down regulation of hostantiviral defenses
- Herpes simplex 1 (oral or ocular lesions)
- Herpes simplex 2 (genitallesions)
- Varicella-zoster virus(Shingles and chickenpox)
- Epstein-Bar virus (humancancers)
- Human herpevirus virus 8 (Kaposis’ sarcoma)
-Flaviviruses (hepatitis C virus)
-Orthomyxoviruses (influenza virus)
-Paramyxoviruses (measles virus)
Binding of viruses to receptor sites on the host cells. Different viruses use different receptors.
This occurs by endocytosis or fusion of viral envelope with cellmembrane.
This is the separation of the viral nucleic acid from its protein coat.
General principles of DNA replication (from DNA viruses to mammaliancells)
(1)They usually replicate completely in the cytoplasm.
(2) They replicate their genomes via mechanisms different from cellularmechanisms in that they transcribe RNA from RNA. Thus they must encode their own enzymes forthis purpose
Compared to DNA viruses, much higher mutation rates are found in RNAviruses because the RNA-dependent RNA polymerases do not have proof-readingfunction
In contrast, (+) strand viral particles lack a virion polymerase. Thus, deproteinized RNA genomes of these viruses are infectious
gag (group specific antigen): viral nucleocapsid and core proteins.
pol (polymerase): reverse transcriptase has 4 activities: RNA to ssDNA, ssDNA to dsDNA, RNase H, integrase.
env (envelope): envelope glycoproteins provide the ligand to bind hostcell receptors for the virus and areresponsible for viral entry.
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