MIC102

bacteriostatic

inhibit growth

bacteriocidal

kill cells

penicillins

inhibit cell wall synthesis/transpeptidation during peptidoglycan synth

inhibitors of protein biosynth

chloramphenicol, aminoglycosides, tetracyclines

antifungals

target chitin, ergosterol

mechanisms of drug resistance

enzyme degrades antibiotic, use efflux pump to throw out antibiotic, modifications of the antibiotic target site, make dummy product

high prevalence of ABX in?

hospitals and livestock

nosocomial infection

an infection acquired in a hospital

innate immunity

when born; physical (skin, mucous membrane, microbiome, endothelial), mechanical (eyelashes), chemical (tears: lysozymes and lactoferrin, sebum, pH, O2 levels, AMPs)

adaptive immunity

built up

mast cells

allergy/histamine, defend against pathogens

neutrophil

phagocytic, throw genome and trap pathogens (programmed cell death), produce cytokines

macrophages

main phagocytic cell, alert adaptive immune cells

eosinophil

allergy, cytotoxicity

NK cells

kill, throw lysozomes, produce effector cells, recruit adaptive immune system

dendritic

phagocytic, recruit T cells/alert adaptive immune response, produce proinflamatory signals

pathogen degredation

bacterial recognition (PRRs on host recognize MAMPs/PAMPs on non-self cells), phagocytosis, oxygen intake increases ROS, pH drops, enzyme conformation, oxidative burst, fragment release and presentation

T cells

helper: present antigen, recruit other cells to support immune response

cytotoxic: produce chemicals/granules that kill and attack cells

B cells

independent: secretes antibody

dependent: activated by T helper cells, make memory and plasma cells

neutralization

bind the binders

osponization

mark for degradation → AB covers bacteria → macrophage kill

agglutination

stick together → stuck in filters

antibody-dependent cell-mediated cytotoxicity

cut into smaller pieces

inactivated vaccines

whole pathogens killed/inactivated by heat, chemicals, or radiation; needs higher doses and boosters; weaker immunity but no severe risk of active infection

subunit vaccines

key antigens of pathogen, lower risk of side effects but no protection against variation

toxoid vaccines

not a whole pathogen, inactivated bacterial toxins, botox; not prevent infection but neutralize toxin

live attenuated

weakened strain of whole pathogen, long lasting immunity but has risk of growing stronger

signs

measurable, ex: HR, BP, temp

symptoms

subjection, ex: yowl

disease

normal structure/fxn of body damaged or impaired

infections

caused by pathogen

communicable

spread between hosts

contagious

easily spread

periods of disease

incubation → prodromal → illness → decline → convalescence

contagious at all points, but most at prodromal

stages of pathogenesis

exposure → adhesion → invasion → infection

adhesion

proteins or saccharides: flagella, pili, glycocalyx, extrapolymeric substance; attach to host cells

invasion

effector proteins and enzymes, hijack machinery, reprogram defense, subvert immune systems

coagulase + kinase: hide out in blood clot, proliferate, and get back into bloodstream at [high]

protease: destroy antibody and limit communication

capsule: mucous layer hides antigen, larger = evade phagocytosis

G+: exotoxin (heat stable, specific damage, released), endospores

G-: LPS endotoxin (released when die+binary fission, general inflammation, membrane bound), secretion systems

antigentic drift

single nucleotide polymorphism, slight change

antigenic shift

rearrangement of genes, large change

toxoplasma gondii

reproduce in cats, eukaryotic protists, maternal-fetal transmission

pandemic

global spike

endemic

always present in a region

epidemic

spike in cases in a region

quorum sensing

[SM] mediates cell-cell communication, trxnal regulation, coordinates gene expression, ex: V. fisheri: AHL/N-acylhomoserine lactone

host-induced trxnal cascade

SM from the host induces a series of trxn in the symbionts, ex: rhizobia and legumes, flavenoids → produce nod factors → conformational change for friendly microbe response → infection thread → tumorous growth

cheating in legumes + rhizobia

fertilizer increases usable nitrogen for legumes → rhizobia do less N2 fixation and still receive C and housing → rhizobia is the cheater → host control mechanisms

host control mechanism

expulsion, immune system (antibiotics), sanctioning, cut off resources, modulate environment (pH, O2)

farming

mutualistic, amoeba get food source, bacteria get safe place to grow

antibiotics

antagonistic, kills bacteria, resource intensive for host, toxic to host at [high], cheater fitness (ABX resistant bacteria expend no energy and no competition)

immobilization

CO2→sugars

mineralization

sugars→CO2

methanogenesis

archaea

nitrogen fixation

N2→NH3, nitrogenase, bacteria and archaea, haber bosch

ammonification

organic N from waste/death → NH3, fungi and bacteria

nitrification

NH3→NO2- →NO3-, ammonia then nitrate oxidized, small redox potential → easily changed/outcompeted, ARCHAEA and bacteria

denitrification

NO3- →N2, nitrate TEA in anaerobia respiration, bacteria and archaea, anammox (anaerobic ammonia oxidization - nitrite TEA)

mycorrhizae

increase phosphorous intake in plants

greenhouse gasses

CO2, methane, NOx (nitrous oxide); processing, beef

nutrient pollution

nitrogen from fertilizer + excess nutrients→ eutrophication; manure and fertilizer; microbes grow quickly from nitrogen runoff → aerobic respiration → deplete H2O of O2 → other organisms can’t grow, different environment

nutrient displacement

urban vs rural cycle disruptions, agricultural nutrients, coastal runoff, nutrients rapidly moved between microbial communities, shipping products around the world → removed from the cycle

role of microbes

CO2: carbon sequestration

CH4: methanotrophy

Nox: anammox returns N2 to environment