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Carbon fixation

any process through which gaseous CO2 is converted into primarily through photosynthesis; making a Carbon-carbon bond

Unique intermediate of Calvin Cycle

Ribulose 1,5-Biphosphate

Inputs of Calvin Cycle




Unique enzymes of Calvin Cycle

PRK, RubisCO


an organism that uses methane as its primary electron donor and source of carbon for carbon fixation


are named for the unique way of getting energy: they convert hydrogen gas and carbon dioxide into methane gas anaerobically

pathway of nitrification

use of reduced nitrogen compounds (NH3) as electron donor in aerobic respiration

pathway of denitrification

se of nitrate as electon acceptor in anaerobic respiration

Nitrosomonas europa

ammonia oxidizing bacteria

Nitrobacter winogradskyi

nitrite oxidizing bacteria

Electron acceptor for aerobic sulfur oxidation


Electron acceptor for anaerobic sulfur oxidation


Sulfate reduction

Sulfate-reducing bacteria use sulfate as an electron acceptor (anaerobic respiration), converting the sulfate to hydrogen sulfide

reaction center

a complex of several proteins, pigments, and other cofactors assembled together to execute the primary energy conversion reactions of photosynthesis; give rise to electron transfer

Light harvesting complex

Used by plants and phototrophic bacteria to collect more of the incoming light than would be captured by the reaction center alone

Role of light in phototrophy

Converted to chemical energy; generates a good electron donor

Cyclic phototrophy

electron returns to Reaction center

Noncyclic phototrophy

electron does not return to RC, makes NADPH, requires external electron donor (H2S, H2)

Combined phototrophy

also requires electron donor, water and oxygen produced

3 main classes of soilborne pathogens

Endospore Forming Firmicutes
Metabolically diverse Proteobacteria
Soli fungi (often dimorphic)

Purple bacteria

proteobacteria that undergo cyclic phototrophy

Green Sulfur bacteria

obligate anaerobic non cyclic phototrophy

Merismopedia, Gioeocapsa, Myxosarcina, Pleurocapsa, Cyanobacteria

Oxygenic phototrophy

Bacillus anthracis

Endospore forming firmicute soilborne pathogen

Pseudomonas aeruginosa

Metabolically diverse Proteobacteria soilborne pathogen


gram positive, aerobic respiration, forms endospores

Spore structure for B. anthracis

Inner part; core that houses chromosome and is tightly complexed to protective proteins
Next layer; cortex with thick layer of membrane and peptidoglycan
Outside layer; coat, a protein shell
Final layer; exosporium, another protein shell

3 modes of entry for B. anthracis

1. Cutaneous anthrax
2. Pulmonary anthrax
3. Gastrointestinal anthrax


plasmid of B. anthracis that contains toxin genes


plasmid of B. anthracis that contains capsule genes

What is the composition and role of the capsule in B. anthracis?

Made of polyglutamic acid, inhibits phagocytosis

Lethal toxin

A protease that cleaves proteins called MAP kinase kinases involved in signal transduction

Edema toxin

an adenylyl cyclase that synthesizes cAMP, a common cellular messenger

How can Pseudomonas aeruginosa grow in so many different environments?

can use many different compounds as carbon/energy source via aerobic respiration
is an opportunistic pathogen

What are the main virulence factors for P. aeruginosa?

1. Type IV pilli mediate attachment to cell membranes
2. can secrete alginate and other EPS to form biofilm in host tissues
3. secretes toxins and degradative enzymes (protein synthesis inhibitor and proteases to degrade host tissues and antimicrobial proteins)
4. injects effectors via Type 3 secretion system
5. Produces siderophores for iron acquisition

What is the significance of biofilm formation on P. aeruginosa?

hinders access to phagocytes, limits diffusion of antibiotics and complement proteins to bacteria

Yersinia pestis

the plague, fleas and rodents

What are factors needed for Y. pestis growth in human host?

Must survive inside macrophages and effect immune cells (Yops), Yersiniabactin (siderophore), F1 protein capsule (antiphagocytic), Psa (antiphagocytic) and Pla protein (degrades C3b and C5a and degrades clots)


Yersinia Outer Proteins- interfere with phagocytosis and the immune response

Bubonic plague

Y. pestis infection that colonizes the lymph nodes, eventually moves to bloodstream

Septicemic plague

Y. pestis infection that grows in blood stream

Pneumonic plague

Y. pestis infection that invades the lungs and eventually moves to bloodstream; can develop from bubonic or septicemic plague in primary infection then directly in secondarily infected patients

Life cycle of plasmodium

Sporozoites injected during bite and travel through blood to liver. Sporozoites develop in liver cell and multiplies to form the schizont which is made up of thousands of merozoites which bursts into the cytoplasm of the liver cell and enters the bloodstream to invade RBC, form vacuoles and replicate

Describe the basic process of liver infection of Plasmodium

Sporozoites travel through liver, glide over blood vessel lining and interact with heparan sulfate proteoglycan (HSPGs). They cross the endothelial barrier and migrate through liver cells. When reach the final cell, forms parasitophorous vacuoles, develop, multiply inside vacuole, and form schizant (thousands of merozoites) vacuole bursts and merozoites enter bloodstream

What is the significance of apical complex in RBC infection by Plasmodium

apical complex allows merozoites to rapidly invade RBC

What are 2 unique features of RBC that impact the ability of Plasmodium to grow and replicate inside RBC?

1. have no nucleus or ability to synthesize new proteins or lipids, cannot endocytose/exocytose
2. Do not present MHCI for antigen

How do the symptoms of uncomplicated malaria result from pathogen infection of RBC?

Destruction of RBC causes chills, fever, and sweats

How do the symptoms of severe malaria result from features associated with P. falciparum and its effects on RBC properties

Infected RBCs adhere to each other and uninfected RBCs and adhere to the lining of small blood vessels. This damages blood supply, tissues and organs. Decreased oxygen supply can lead to acidosis, brain infection, and severe anemia

DefinitionS of fermentation

1. Method to preserve fresh food via microbial production of preservatives
2. metabolic pathway using substrate level phosphorylation for ATP generation
3. growing microbes in large amounts
4. Incubating product for awhile until it changes (non microbial)


Pyruvate > Acetaldehyde > Ethanol

Propionic acid

Pyruvate > lactic acid > propionic acid

Homolactic fermentation

Sugar converted to lactic acid (glucose > pyruvate > lactic acid) net energy= 2 ATP/glucose

Heterolactic fermentation

Sugar converted to lactate, CO2, and ethanol net energy= 1 ATP/glucose

Ethanol fermentation

fermentation to ethanol and CO2 without lactic acid (used by bacteria and yeast)


microbial production of lactic acid


uses lactic acid to make propionic acid and CO2, makes holes in cheese


acetic acid and water, acetic acid is fermented from ethanol, water is electron acceptor

Cocoa fermentation

yeast and lactic acid bacteria degrade the sugars and produce lactic acid and ethanol. the ethanol is used by acetic acid bacteria to make acetic acid. This product formation inhibits the growth of spoilage organisms.

Campylobacter jejuni

Main cause of bacterial foodborne infection

Basic biology of Campylobacter jejuni

thermophile (42degreesC) survives well at 4degreesC not salt tolerant, sensitive to drying, pH, high O2, microaerophile (prefer 5% O2) capnophile (need increased CO2)

Molecular mimicry

pathogens decorate their surface with molecules that mimic host cell surfaces, in Campylobacter involves recognition of LOS on the bacterium and similar sugars on human cells.

Basic biology of Listeria monocytogenes

Gram positive Firmicute (related to S. aureus), salt tolerant to 10% NaCl, acid tolerant to pH 4.5, Psychotroph (optimal growth 30-37degreesC, grows 1-45degreesC), Ubiquitous in the environment (found in water, soil, fresh and decaying plants, intestine of healthy animals)

Virulence factors of Listeria monocytogenes

PrfA, internalins, Listerolysin O, ActA


regulates gene expression in response to host temperature


promote entry into cell (intracellular pathogen)

Listerolysin O

promotes escape from vacuole


used by actin-based motility to spread to other cells

2 different meanings of enteric pathogen

1. Causes disease in GI system
2. belonging to the Enterobacteriaceae


reaction to serum or antibodies

O antigen

lipopolysaccharide LPS

K antigen


H antigen


Probiotic E. coli

produces antimicrobials, exceptionally good colonist, no virulence factors, modulates immune system


EnteroPathogenic E. coli; developing countires, major cause of infant death, person-person spread possible


EnteroHemorrhagic E. coli;developed countries, shinga-like toxin


EnteroToxigenic E. coli; developing countries; fecally contaminated food/water


EnteroAggregative E. coli; children in developing countries; diarrhea with dehydration; growth retardation; chronic

EPEC result

disruption of intestional barrier function, water absorption and ion balance, causes diarrhea

EPEC inital attachment mechanism

Bacterium binds to host cell, T3SS is induced and injects effectors into host (Tir)

Intimin and Tir

adhesions of EPEC; Tir injected into host cell by T3SS and binds to intimin (bacterium outer membrane protein), induces cytoskeletal changes, produces pedestals and destroys normal microvilli structure

T3SE proteins

EPEC proteins; effacement of microvilli, mitochondrial dysfunction, affects ion transporters, affects tight junctions

EHEC initial attachment mechanism



T3SS effectors (toxin)

Shinga toxin in EHEC

released from bacterium at cell death, can enter blood and cause hemolysis

AB toxin of Shinga toxin

B subunit= binds host glypolipds (kidney and intestine) A subunit= enters cell, cleaves RNA, kills cell

EAEC result

diarrhea and vomiting with dehydration and fever

Attachment mechanism of EAEC

adhesions= Aggregative adherence fimbriae (AAF), forms biofilms, several toxins

EAEC role of 2011 E. coli outbreak

had characteristics of EHEC and EAEC, new pathovar? EAHEC

What is different about Shigella?

Human only colonist, low infectious dose, spread person-person via fecal-oral, causes shigellosis: sever inflammation of colon with strong abdominal cramps, fever, and bloody/mucous stool


shigella that produces Stx

What is the effect of Shigella?

1. Taken up by M cells in colon: undergo phagocytosis, escape phagosome
2. Invade and kill macrophages: induce inflammation
3. Invade intestinal epithelial cells and replicate: induces inflammatory response, peptidoglycan released by shigella is recognized by PRRS, taken up by cells via T3SS, spreads cell-cell via actin-based motility
4. Neutrophils: arrive and eventually kill shigella, disrupt tight junctions, promote shigella access to underlying layer


Extraintestinal pathogenic E. coli

What is the normal site of colonization for the ExPEC strains?

Colonize intestinal tract but don't cause disease there, if translocated to another location in body, has ability to cause disease if has appropriate virulence factors
-Urinary tract, blood, CNS
Not the same as GI pathovars


removal of disease causing pathogens from a living surface


treatment of object to make it safe to handle


acts on many cellular targets at once


acts on one cellular target

Most resistant microbes

Prions and bacterial endospores

Moderately resistant microbes

protist cysts, some fungal spores, naked viruses, Mycobacterium, Staphylococcus, Pseudomonas

Least resistant microbes

most vegetative bacterial cells, some fungal spores, fungal and protist vegetative cells, and enveloped viruses

What are the main cellular targets for chemical control agents?

dissolve membranes, dentature proteins, modify (inactivate) proteins or DNA

chemical control agents

solubility in water or alcohol matters, must consider toxicity to non target organisms, presence of other organic material is important

selective toxicity in antimicrobial function

highly specific to one or very few targets in cell, target is present in microbe but NOT in host


Minimum inhibitory concentration

How is MIC measured?

1. inoculate plate with liquid culture of test organism
2. antibiotic discs placed on surface of agar plate
3. incubate 24-48 hours
4. test organism shows susceptibility to some antibiotics indicated by inhibition of bacteria growth around discs

Steps of peptidogylcan synthesis

1. NAM is linked to peptide
2. special amino acid synthesis
3. transfer of NAM-peptide to bactoprenol carrier
4. addition of NAG to make PG subunit
5. transfer across membrane
6 & 7. incorporation into existing PG via transpeptidases and transglycosylases
8. Recycling of bactoprenol

Steps of cell wall disrupting antimicrobials

1. cycloserine: inhibits special amino acid synthesis (step 2)
2. Vancomycin: binds to peptide and inhibits addition to existing PG (steps 6&7)
3. Beta-lactams: inhibits transpeptidases (steps 6&7)
4. Bacitracin: inhibits recycling of bactoprenol (step 8)

How do antimicrobials that inhibit DNA replication work?

Quinolones inhibit DNA gyrase in bacteria, target bacterial RNA polymerase, target many steps of protein synthesis


nalidixic acid, fluoroquinolones, ciprofloxacin and novobiocin

Ritamycin B

from Amycolatopis rif amycina that targets bacteria RNA polymerase

Actinomycin D

from Streptomyces sp. that intercalates into DNA

What are some non-target effects of antimicrobials?

toxicity to host, allergies, alteration of microbiota (microbiota shift diseases)

What are the mechanisms of specific resistance to antimicrobials?

Intrinsic resistance- lack target, impermeable
Acquired resistance by mutation or horizontal gene transfer

Acquired resistance by mutation or horizontal gene transfer

1. reduced permeability of cell to antibiotic
2. inactivation of antibiotic
3. alteration of target
4. development of alternative pathway
5. Efflux of antibiotic out of cell (efflux pumps)
6. growth of biofilms helps cells resist killing
7. antifungals

Resistance to Quinolones

1. change in target (gyrA or gyrB)
2. Decrease in OM permeability
3. Increase in efflux pump activity
4. drug modifying activity

What are the basic steps in cloning a piece of DNA?

1. prepare DNA purified DNA or PCR
2. select and prepare vector
3. digest DNA and vector with restriction enzymes
4. ligate DNA and vector
5. introduce to host and select clones

Describe the requirements for PolymeraseChainReaction

Relies on basic DNA biology
denaturation and rennaturation of DNA, complementary hybridization of DNA strands, microbial DNA polymerase
Uses a simple machine (thermal cycler)

PCR steps

1. create reaction mix (primers determine the DNA to be amplified)
2. Denaturation (raise temperature to denature with heat)
3. Primer annealing (cool to allow primer annealing)
4. Extension (polymerase extends primers and makes DNA)
5. repeat
6. repeat

What types of microbes produce polymerases useful for PCR?

Thermus aquaticus (Taq polymerase)
Hypothermophilic Archaea (produce vent polymerase)

Basic features of plasmids needed for good cloning vector

1. antibiotic resistance marker
2. restriction enzyme sites
3. origin of replication

What do restriction enzymes do?

Facilitate cloning

What are two important features of how restriction enzymes recognize their target DNA site and how they cut the DNA?

1. Digest DNA at specific sequences- recognition sequences are usually palindromes of 6 bases in length, cutting DNA to leave staggered ends of single stranded DNA
2 insert genes into plasmid- identify a palindromic recognition site, attach same recognition site to the cDNA gene, add restriction endonuclease, sticky ends rest, insert gene into plasmid

Shikimate pathway

make aromatic amino acids

Bt toxin

Bacillus thuringiensis produces the toxin, produced as cell undergoes sporulation

Processing and activation of Bt toxin by insect

1. ingestion 2. alkaline pH of insects digestive tract causes release of protoxins 3. host proteases process into active toxin 4. specific receptor in insect gut (determines insect specificity) 5. death of insect larva

What are possible modes of resistance to Bt toxin?

1. altered protease activity
2. altered receptor

Retroviruses in gene therapy

1. insert RNA versions of normal allele into retrovirus
2. retrovirus infect bone marrow cells removed from patient and cultured
3. viral DNA carrying normal alleles inserts into chormosome
4. inject new cells back into patient

Listeria monocytogenes as antigen delivery system

1. cytoplasmic location allows entry o f antigens into MHCI antigen processing pathway, leads to priming of specific CD8+ T cell responses
2. attenuated Listeria expressing antigens may direct cellular immune response to area


intermediates and products of metabolism

Secondary metabolites

Not directly involved in normal growth, development, or reproduction of an organism
antibiotics, anticancer agents, immunosuppressive drugs

Microbial biofuels

hydrogen, ethanol, butanol, methane, longer hydrocarbons


Bacteria and enzymes
Ethanol fermentation


photosynthetic bacteria
side product of nitrogen fixation


clostridium bacteria

Major roles of microbes in wastewater treatment

Primary= separate solids from liquids
Secondary= Microbes!! biological to remove organic material and pathogens
Tertiary= allows reentry of products into environment


biological oxygen demand, rough measure of available organic material used for aerobic respiration


groups of microbes surrounded by a matrix

why is proper floc formation important for wastewater treatment?

controlling biomass removal (microbes by EPS productions)


for cleanup of oil, toxic chemicals, or other pollutants from environment


Not responsive

Why is microbial degradation of toxins important?

microbes can degrade insecticides, herbicides, and other toxins, some recalcitrant


hydocarbon chain, used by microbes to store carbon as storage if energy shortage

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