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What are the 3 cell wall blockers that are effective against gram-pos cocci & treponema pallidum
amoxicillin, ampicillin, carbenicillin
(antifungal) binds ergosterol of fungal PM; binding causes leakage of monovalent cations
amphotericin B
cell wall blocker; most broad spectrum; must be given parenterally
cephalosporin
(antimalarial); blocks P. falciparum’s ability to hydrolyze hemoglobin, parasite accumulates cytotoxic levels of heme group
chloroquine
cell wall blocker; penicillinase-resistant penicillin
cloxacillin
plasma membrane blocker; good versus gram-pos microbes & biofilms
daptomycin
blocks ribosomal elongation; broad spectrum; low toxicity
erythromycin
antifungal; blocks sterol anabolism
fluconazole
inhibition of virion entry; binds to GP41 and blocks GP41 function
fuzeon
narrow spectrum; blocks mycolic acid formation in mycobacteria
isoniazid
antihelminth; misregulation of glutamate-gated chloride channels
ivermectin
2 cell wall blockers that are penicillinase resistant
methicillin, nafcillin
cell wall blocker (delaney’s worst enemy)
penicillin
inhibits ribosomal protein synthesis by blocking 23s peptidyl transferase activity (impetigo)
pleuromutilin
antimalarial; blocks P. falciparum ability to hydrolyze hemoglobin
quinone
transcription/ mRNA synthesis blocks anti-beta subunit
rifampin
inhibition of viral assembly and of neurominidase (needed for virion release)
tamiflu
blocks charged tRNAs (protein synthesis)
tetracycline
sulfa drug, blocks prokaryotic PABA; folate anabolism (UTI)
trimethoprim
Tetracycline is considered the most _______ antibiotic
broad
Isoniazid is considered the most _______ antibiotic
narrow
________ interferes with linking enzymes; Cross-bridges and ____ subunits remain attached to their neighbors. The cell ______ from osmotic pressure because the integrity of peptidoglycan is not maintained.
penicillin, NAM, bursts
__________ will attack the NAG NAM
lysozyme
Secreted bacterial proteins, usually enzymatic, usually from gram-pos microbes
exotoxins
kill by lysis
membrane-disrupting exotoxins
A-B exotoxins : A= ______ _____ and B= _________
active site, binding
affects neuronal transmission
neurotoxin
affects intestinal cells
enterotoxin
can affect all cells
cytotoxin
nonspecific overstimulation of host immune system in multi-organ failure
superantigens
Membrane disrupting exotoxin = _______________ ____________
clostridium perfringens
C. perfringens: Produces __________ with phospholipase activity; _______________ lyses host cells; Results in _______ tissue
exotoxins, phospholipase, necrotic
2 examples of species that use translation-blocking A-B exotoxins are ____________________ diphtheriae and shigella ______________
corynebacterium, dysenteriae
C. diphtheriae: Exotoxin gene= ____; exotoxins= ADP-__________; Modifies eukaryotic __-_ proteins (needed for translation elongation); Results in ______ protein synthesis
Tox, ribosylases, EF-2, halted
S. dysenteriae: Exotoxin gene= _____; STX = A-B exotoxin with ___________ activity; Shiga toxin removes a specific “___” nitrogenous base from the 28S rRNA (cannot form peptide bonds); Results in ______ protein synthesis
Stx, depurinase, A, halted
2 examples of species that use A-B exotoxins that inhibit nerve impulses are clostridium ___________ and clostridium ________
botulinum, tetani
C. botulinum: A-B exotoxin= ________ (neurotoxin); Botulin operates at the ________________ junction; AcH is essential for muscle ____________; Botulin inhibits _______-mediated exocytosis of AC+ TVs; Results in ________ paralysis; Death by failure ________
botulin, neuromuscular, contraction, SNARE, flaccid, inhale
C. tetani: A-B exotoxin= _____________ (neurotoxin); Glycine & GABA neurotransmitters are essential for muscle ___________; Results in ________ paralysis; Death by failure to ________
tetanospasmin, relaxation, spasmic, exhale
2 examples of species that use A-B exotoxins as enterotoxins are vibrio __________ and staphylococcus _______
cholerae, aureus
Tetanospasmin inhibits _______________-mediated exocytosis of ______ and glycine
synaptobrevin, GABA
V. cholerae: A-B exotoxin= ____; CTX operates on _____________; CTX has ADP-ribosylase activity; CTX modifies eukaryotic adenylate _______; Results in massive ______ efflux; Omosis ensues, enterocytes ___________
CTX, enterocytes, cyclase, solute, plasmolyze
Exotoxin forms ______ in the membrane, causing the cytoplasmic contents to ______ and water to ________ causing host cell to lysis.
pore, efflux, influx
Numerous activated T helper cell will hyper-activate the immune system in a non-specific fashion, patient immune system may undergo anaphylaxis
superantigen
Endotoxin (lipid ___) —> ___________ fever response
A, pyrogenic
Endotoxin: __________ eats microbe —> microbe is digested releasing __________ —> endotoxins induce macrophage release of _________ —> cytokines enter _____________ —> cytokines travel to ________________ —> cytokines induce hypothalamus to produce _____________ which induce fever
macrophage, endotoxins, cytokines, bloodstream, hypothalamus, prostaglandins
Lipid A misregulates blood _____ leading to multiple organ _______
clots, failure
Lipid portions of the LPS found on the ______ membrane of gram-___________ microbes
outer, negative
2 ways that endotoxin might kill a human host
pyrogenic fever response, misregulated blood clots
Daptomycin and polymyxin attack plasma ___________ of bacteria
membrane
Clostridium perfringens that makes exotoxin ______, can obliterate ___________ heads from tails and ______ the plasma membrane.
lipase, phosphate, melts
Bacterial vaginosis is caused by __________ species
candida
____________ species keeps candida growth in check, __________ can wipe out all the lactobacillus causing candida overgrowth.
lactobacillus, antibiotics
____________ is produced by staphylococcus lugduninsiensis
lugdunin
S. luguninsiensis is a bacteriocin that inhibits ________
MRSA
Toxins produced by the bacteria that kill closely related species
bacteriocin
___________ is produced by eleftheriae tarrae
teixbactin
E. terrae produces an __________ rather than inhibiting another molecule.
antibiotic
___________ acid (CA) is a beta-lactamase inhibitor
clavulanic
Bacteria with a beta-lactamase will cause beta-lactam _____ on -cillin drugs to be hydrolyzed. Clavulanic acid (CA) _________ beta-lactamase and protects the -cillin drugs from being broken down and allows them to _____ bacteria they would not have been able to without it.
rings, inhibits, kill
Beta-lactamase is another name for _______________, since CA inhibits it will have no effect on penicillinase-resistant penicillins.
penicillinase
_____________, ____________, and cloxacillin all have beta-lactam rings but are unaffected by beta-lactamases because they are penicillinase __________.
methicillin, nafcillin, resistent
A non -cillin antibiotic with a beta-lactam ring is ________________ species
cephalosporium
What antibiotics would you use for pulmonary tubercles? (4)
isoniazid, tobramycin, polymyxin, streptomycin
Antibiotics NOT useful against ____________ are anything to treat gram-pos microbes or cell wall blockers
mycoplasmas
What antibiotic would you use for pulmonary invasive aspergillosis? (2)
antifungal drugs, amphotericin B
High eosinophils = ___________ infection
helminth
High serum IgE antibody indicates ________ infection
parasite
Blocking of viral entry = __________ —> influenza uses viral ____________ protein to adhere to host glycoproteins decorated with _____ acid residues. DAS181 is an enzyme that cleaves sialic acids, blocking _________.
DAS181, hemagglutinin, sialic, adhesion
Viral genome assembly= __________, saquinavir, and __________ are ____ protease inhibitors.
indinavir, ritonavir, HIV
__________ inhibits the influenza M2 ion channel protein necessary for viral ________.
amantadine, assembly
Virion release = _______ and relenza inhibit influenza _________________
tamiflu, neurominindase
Neurominindase (N) is needed for influenza virion release as N ________ H::sialic acid events as nascent virion buds from host plasma membrane
cleaves
____________ antibiotic resistance mechanism includes a beta-lactam ring
catalytic
Shape change = antibiotic can no longer _____ and ______________ will form
bind, tetrapeptide
___-_________ antibiotic resistance mechanism includes MDR effluxes which constantly pumps antibiotic but can only work if respiratory chain is going.
non-catalytic
Ribosome antibiotics which can acquire _____ mutations
gene
C. sporogenes makes _____ for humans and gets nutrients in return
IPA
E. coli makes ________ ___ for human and gets nutrients in return
vitamin k
2 organisms that are mutualistic in the large intestines of synapsids
c. sporogenes, e. coli
Ancestral tetrapod and all mammals became _________ and all birds and reptiles become ________
synapsids, diapids
E. coli is ________ and salmonella/shigella is _______
synapsid, diapsid
N. gonorrhea, E. coli, Shigella species, and P. aeruginosa use _________ to adhere to their targets
fimbriae
S. mutans and S. sobrinus use glycocalyx _______ layer
slime
S. pyogenes uses gycocalyx _________ and _____________ acid
capsule, lipoteichoic
HIV uses _______ spike
GP120
The deliberate inoculation of an uninfected person with smallpox material
variolation
Are altered forms of exotoxins secreted by bacteria whose toxicity is weakened
toxoids
Blood poisoning by toxins from a local bacterial infection
toxemia
Flaccid paralysis = muscles cannot ________
contract
Spasmis paralysis = muscles cannot _______
relax
Which stage of pathogenesis? No signs or symptoms
incubation period
Which stage of pathogenesis? Mild signs or symptoms
prodromal period
Which stage of pathogenesis? Most severe signs and symptoms
period of illness
Which stage of pathogenesis? Signs and symptoms are subsiding
period of decline
Which stage of pathogenesis? Body returns to prediseased state
convalescence
Recuperating patients without symptoms; they continue to shed viable microbes and convey the infection to others
convalescent carriers
Individuals who shelter the infectious agent for a long period after recovery because of the latency of the infectious agent (TB, Typhoid fever)
chronic carriers
Medical and dental personnel who must handle patient materials that are heavily contaminated with patient secretions and blood risk picking up pathogens mechanically and accidentally transferring them to other patients
passive carriers
Infections acquired during the process of receiving healthcare that was not present during the time of admission
nosocomial
Inanimate object that harbors and transmits pathogens
fomites