Micro Bio Final ALL

Consists of a great deal of words and vocab esque questions term

Antibiotics that target
Bacterial cell membrane

Polymyxin, Tyrocidn and Gramicidin

Polymyxin (colistin, polymyxin B)

Target Outer-membrane of Gram - bacteria by binding to lipopolysaccharides LPS and phospholipids. Disrupts membrane integrity and causes leakage of cell contents. Impact on host Major Toxicities- Nephrotoxicity (liver damage) and Neurotoxcity Only used in severe resistant infections

Tyrocidin

Cyclic peptide antibiotic disrupts bacterial membrane causes loss of ion gradients and leakage and rapid bacterial death- For gram POSITIVE bacteria Impact on host is too toxic for systemic use as it damages mammalian membrane with higher exposure

Gramicidin

Linear peptide forms ion channels (pores) in bacterial membranes allows uncontrolled flow of monovalent ions collapses membrane potential mainly gram positive too toxic for systemic use— think A gram is one and monovalent ion

Antibiotics that affect DNA synthesis and Integrity

Metronidazole. Sulfonamides and Quinolones

Metronidazole

Is activated after being metabolized by microbial protein cofactors ferredoxin found in anaerobic and microaerophilic bacteria - aerobic microbes are resistant as they don’t have the ETC proteins that reduce metronidazole— Think METROOO sound dude and fear cuz he scary cuz it pops out of nowhere and ferredoxin is like fear

Sulfonamides

Inhibit nucleic acid synthesis by blocking folic acid which is needed for tetrhydrofolate (coenzyme) folic acid is made from PABA in bacteria. the drug competitively inhibits the enzyme Dihydropteroate synthase which uses PABA in folate synthesis they act as PABA anaolgs No folic acid production

this is bacteriostatic

SULFUR -FOLIC SURFOLIC

Quinolones

DNA gyrase bound to DNA and inactivated by a quinolone will block progression of a DNA replication fork

topoisomerase 2

Quinolone

quinolone wants to be together and not separates into a fork so it stops that

Antibiotics targeting RNA Synthesis

Rifampin

Rifampin

Selectively binds to bacterial RNA polymerase and prevents transcriptoin

also treats tuberculosis and menigococcal meningitis

Bacterial RNA polymerase B subunit

Antibiotics that inhibit Protein synthesis

All the translation ones targetting 30s and 50s

30s subunit translation antibiotic

Aminoglycosides tetracyclines and glycylcyclines

50 s ribosomal affecting antibiotics

chloramphenicol, macrolides, lincosamides, oxazolidinones, and streptogramins

Aminoglycosides

cause misreading of mRNA and inhibit peptidyl-tRNA translocation

Tetracyclines

Bind to the 30S subunit and prevent tRNA carrying amino acids from entering the A site

Glycylcyclines

bind to 30S subunit and inhibit entry of aminoacyl-tRNA into the A site; able to function in tetracyline resistant cells

chloramphenicol

Prevents peptide bond formation by inhibiting peptidyltransferase in the 50S subunit—think ora ora ora 50 punches

macrolides

bind to 50S subunit and inhibit translocation of tRNA from the A site to the P site—think macros think a to p think location is macro not micro and macro has 5 letters so 50

lincosamides

bind to peptidyltransferase and prevents peptide bond formation from the ribosome—— lin think lena think 5 foot tall for 50S and think Rib as she has ribs so ribosome

oxazolidinones

bind to 50S and prevent assembly of the 70S ribosome— idk think that z looks like a 7 or think that X in oxo is an X to building that ribosome

Streptogramins

Bind to 50S and block tRNA entry into A site while blocking exit of a growing protein from the ribosome— think about that one time i got strep throat and i was older than 5 so 50 and i was unable to eat and enter food into my mouth and i was not growing as there was no food

Anti Virals

Amantadine, Oseltamivir(tamiflu) and zanamivir (Relenza), and Zidovudine and Acyclovir, and Protease Inhibitors Nelfinavir and lopinavir , and then the entry inhibitors CCR5 inhibitor Maraviroc

Influenza contains what 2 things

Hemagglutinin-binds to the host membrane receptors for entry by phagocytosis and Neuraminidase-cleaves sialic acids to allow virus particles to escape from infected cells

Amantadine

Prevents virus from uncoating and exiting by changing the pH of the phagolysosome—think manta ray and they change pH with their stinger

Oseltamivir(Tamiflu) and zanamivir (Relenza)

neuraminidase inhibitors prevent the virus particles from leaving the cell- think zany is neuronic aliens and Oselta is frocking nothin bro just memorize it

Zidovudine

A nucleoside reverse transcriptase inhibitor that terminates viral DNA chain synthesis

Acyclovir

A guanosine analogue inhibits viral DNA polymerase causing chain termination

Protease inhibitors- target the HIV protease enzyme

Nelfinavir and lopinavir

Entry inhibitors Maraviroc

Block virus envelope protein gp120 from binding to host receptor CCR5 and stops viral membrane fusion with the host cell

Antifungal agents

Polyenes, Azoles, Allylamines, Echinocandins, Griseofulvin, Flucytosine

Polyenes

Disrupts membrane integrity

Azoles

Interferes with ergosterol synthesis

Allylamines

Interferes with ergosterol synthesis

Echinocandins

Blocks fungal cell wall synthesis

Griseofulvin

blocks cell division

Flucytosine

inhibits DNA synthesis

Anti Parasitic agents

Anti Protozoan- Metronidazole and Chloroquinine, Primauqine most are fairly toxic and then Anti-helminthic agents Niclosamide Praziquantel Mebendazole and albendazolee and ivermectin

Metronidazole

Causes DNA breakage. Used to treat giardiasis and Trichomonas infections

Chloroquinine, Primaquine(antimalarials)

Increased accumulation of iron radicals in red blood cells

Niclosamide

Blocks ETC and prevents ATP generation in Tapeworms

Praziquantel

increase uptake of calcium alters membrane permeability

Bebendazole and albendazole

Interferes with beta tubulin polymerization and blocks nutrient absorption

Ivermectin

Increase inflow of Cl ions reduces cell polarity in neuronal cells and leads to paralysis of helminths

Nosocomial disease

acquired in hospital setting

Subclinical disease

no noteacable signs or symtpoms inapparent infection

subacute disease

symptoms between acute and chronic in

Virulence factors

Toxins, Adhesion factors, capsules, Enzymes are examples

Stages of infectious disease

Incubation, Prodromal, Invasive phase , decline phase, Convalescence phase

zipper mechanism

Englufment

membrane fusion

GLycohydrolases

Degrades hyluronic acid that cements cells together to promote spreading through tissues

Nucleases

Degrades DNA released by dying cells (bacteria and host cells) that can trap the bacteria thus promoting spread

Phospholipases

degrades the phospholipid bilayer of host cells causing cellular lysis and degrade membrane of phagosomes to enable escape into cytoplasm

proteases

degrades collagen in connective tissue to promote spread

Focal infection

systemic infection that began as a local infeciton

Sepsis

toxic inflammtory condition arising from spread of microbes especially bacteria or their toxins from a focus of infection

septicemia

growth of bacteria in blood

Exotoxin

Gram positive, Protein composition, Effect- specific damage to cells , most are heat sensitiev, Low LD50

ENdotoxin

Gram negative , Compositive Lipid A component of lipopllysacchardie, general systemi symptoms of inflammation and fever, heat stable, high LD50

Super antigens

streptococcus and staphlycoccus -Stimulates excessive activation of immune cells and release of cytokines from immune system, life threatening fever inflammation and shock are result

Intraceullar targeting toxins

Cholera - Actiation of adenylate cyclase increased cAMP and scretion of fluids etc out of cell causing diarrhea, Tentanus toxin ihibits the release of inhibitory- botulin inhibits release of neurotransitter flaccid- Dipthereia inhibition of protein synth causing death

Membrane disrupting toxins

Streptococcus and staph A proteins that assembes into pores in cell membrane disrupting function and killin cell- and alphatoxin and beta toxin phopholipaes that degrade cell membrane phosophlipids disrupting membrane function and killing cell

dipthereia

blocks protein synthesis by inavtivatin elongation factor 2 leading to cell death

Methyl mismatch repair (wrong base insertion)

The parental DNA is methylated, which allows it to serve
as a template for the DNA repair machinery to identify and
correct errors in the newly synthesized DNA strand.

Base excision repair (damaged base)

Recognizes a specific damaged base (deamination) and
removes it from the DNA backbone

SOS save our ship repair

The SOS response is activated in bacteria when DNA is heavily
damaged. It induces error-prone repair enzymes to quickly fix DNA,
allowing survival but often introducing mutations.
• Coordinated cellular response to damage that can introduce
mutations in order to save the cell.
• DNA polymerase IV and V performs translesion synthesis

Sterilization

All dead

sanitation

to safe levels

disinfection

disease producing dead

antisepsis

removal on living tissue

Ethanol Iodine Chlorine

Highly reactive compounds that damage proteins lipids and DNA

Surfactants such as detergents

Help in the mechanical removal of microbes

Aldehydes

Combine with and inactive proteins and nucleic acids

Phenols

Denature proteins and disrupt membranes

Heavy metals

Bind to proteins and inhibit enymatic activity

Peroxygen

Strong oxidizers, produce free radicals that damage cellular macromolecules

Streptococcus infections

Gram pos Cocci, S pyogenes spread by respiratoory droplets contact with fomites, sometimes other transmission- many ezymes contribute to the disease and many of its exotoxins are phage encoded- Scarlet fever is known to cause strep throat Erysipelas skin infection, pyoderman and impetigo alone or in combination make skin infection that makes pus-ceullilitis deeper than erysipelas necrotizing fascilits - treatment is antibiotics prevention is vaccines long term complications

HIV Aids

Transmission-sex blood exposure, perinatal- SIV is primate equivalent - HIV evolved from it after humans evolved it is a pos SSRNA and has 2 idential SSrna reverse transcirptase, inegrase, and protease and envelope and the envelope spikes are gp120. HIV 2 is weak mutation not found outside africa, Incubation 9months -20years person to person sexually or needles to CD4 receptor on a bunch of cells- Early symptoms fever fatugue swollen lymph nodes, diarrhea weight loss, cough and shortness of breath. Late symptoms soaking night sweats fever higher than 100 cough and shortnesss of breath chronic diarrhea. —Persistant white sponts or unusal lesions on tongue or mouth headaches weight loss skin rashes or bumps- diagnoesed though elisa pcr western blots— no cure

Gonorrhea

std incubation is 2-30 days person to person humans only hosts transmitted for 5-15 years by carriers 1000 organisms enough to infect. IgA protease break down mucus to get it - Pili help bacteria adhere to mucosal membrane - lipooligosaccharide LOS: causes inflammation and tissue damage. site of infection ASS PENIS CERVIX. SYmptomes painful urination for men and pus discharge. Women few symptoms but complication such as PID. men 95% pus drip in 14days- Most women asymptomatic 50-80 men 10-20 asymptomatic Pelvic inflamatorry disease infertility and pain and men get epidydmitis testicular pain infetitloity

Beta LActamase enzyme

ARE KILLED BY CLAVICULAR acid doing suicide attacks