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119 Cards in this Set
- Front
- Back
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Terms from Lecture 19 |
Pathogen - organism that produces disease Opportunistic pathogen - infects host with weakened immune system (compromised) Carrier -infected individual, potential source of infection Zoonoses -disease transmitted from animals to humans Vectors - organism that transmit diseases to humans (Ex: mosquitoes), ticks, pleas Pathogenicity - ability to produce disease Virulence -degree of pathogenicity Virulence factors or determinants -genetic, biochemical, structural features which contribute to virulence Latency - pathogen stops reproducing, Dormant, can become active again
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Pathogenicity Island (19) |
Large segments of chromosomal or plasmid DNA, encoding virulence determinants Absent in non-pathogenic strains G+C content different from bacterial genome (evidence of transduction) -mobile |
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How to measure virulence? 19 |
Infectious Dose 50 (ID50) - number of pathogens required to cause clinical disease in 50% of innoculated hosts Lethal Dose 50 (LD50) - number of pathogens required to kill 50% of hosts Example Strain A = ID 3000 , Strain B = ID 5000 Strain A is more virulent than strain B - doesn't require as much doses to infect 50% of population |
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Viral Replication cycle 19 |
1. attachment 2. entry 3. uncoating 4. genome replication 5. gene expression 6. assembly 7. release |
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Viral attachment 19 |
Capsids and envelope spike proteins can mediate attachment Examples: GP120 of HIV binds to CD4 receptor Hemagglutinin of influenza binds sialic acid |
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Viral spread 19 |
Viruses can spread by using blood, neuronal and lymphatic system
Syncytia - multinucleated giant cells
Tropism - cell, tissue, organ specificity which is determined by host cell receptors |
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Effects of viruses on immune responses 19 |
Innate -block or breakdown complement -block interferon production
Adaptive -block antigen processing, MHC export -evade antibody - Antigenic variation Ex: amino acid changes in virion spikes (common in RNA viruses) |
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Mechanisms of bacterial pathogenicity 19 |
-Adherence -invasion and spread -colonization - establishing a site of microbial reproduction on or in host -evading innate an adaptive immune responses |
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Bacterial Adherence Factors 19 |
-Pili (fimbriae) Ex: Type I pili of Uropathogenic Escherichia coli binds mannose residues on human cells -capsules Examples of bacteria -Streptococcus pneumoniae -Haemophilus influenzae -Neisseria menigitidis Vaccines made of capsular polysaccharide can attack the above -some strains of Pseudomonas aeruginosa - opportunistic pathogen |
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Bacteria Invasion and Spread 19 |
-active penetration of host's mucous membranes or epithelium -can be passive penetration (Ex: wounds, insect bites) -once below mucous membrane, bacteria can spread to deeper tissues |
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Coagulase 19 (bacterial virulence factor BVF) |
Staphylococcus aureus MOA: coagulates (clots) the fibrinogen in plasma. the clots protects the pathogen from phagocytosis and isolates it from other host defenses |
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Streptokinase - BVF 19 |
also called fibrinolysin, staphlyokinase Group A, C & G of streptococci, staphlyococci
MOA: protein that binds to plasminogen and activates the production of plasmin, thus digesting fibrin clots; this allows the pathogen to move from the clotted area |
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Collagenase - BVF 19 |
Clostridium species MOA: breaks down collagen that forms the framework of connective tissues, allows the pathogen to spread |
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Hemolysins - BVF 19 |
Staphylococci, Streptococci, Escherichia coli, Clostridium perfringens
MOA: lyse erythrocytes; make iron available for microbial growth |
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Immunoglobulin A protease (IgA) - BVF 19 |
Streptococcus pneumoniae
MOA: cleaves immunoglobulin A into Fab and Fc fragments |
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Leukocidins - BVF 19 |
Staphylococci, pneumococci and other streptococci
MOA: pore forming exotoxins that kill leukocytes, cause degranulation of lysosomes within leukocytes, which decreases host resistance |
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Deoxyribonuclease - BVF 19 |
Group A streptococci, staphylococci, Clostridium perfringens
MOA: lowers viscosity of exudates, giving the pathogen more mobility |
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NET - 19 |
Neutrophil Extracellular Trap -DNA + antibmicrobial peptides and enzymes kill pathogens and engulf microbe secrete anti-microbials |
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Bacterial Colonization |
-occurs when pathogen finds appropriate environment in host
- some bacteria invade specific cells
-some bacteria can be found in blood
Bacteremia -bacteria present in bloodstream |
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Bacteria evading innate immune response |
Evading complement system by capsules - inhibit opsonization by C3b of membrane attack complex formation
Proteases Lengthened O-side chains Evading cytokines - Type III systems - deliver proteins that block TLR (toll-like receptors) signaling, cytokine expression results
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Bacteria invading adaptive immune response |
Capsules
IgA proteases
Antigenic variation -change cell surface outer membrane or pili proteins |
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Bacteria evading phagocytosis |
Capsules Blocking of phaogyctic cell (Ex: Streptococcus pyrogens M protein) Leukocidins - destroys phagocytes Proteases inactivate complement system for opsonization |
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Phagocytosis |
1. Pseudopodia surrounds food 2. Phagosome 3. fuses with lysosome (phagolysosome) 4,5. nutrients diffuse into cytoplasm, waste released |
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Bacterial intracellular pathogens |
Mycobacterium tuberculosis -Legionella -Chlamydia
Listeria monocytogenes -gram +, food borne pathogens -psychrophile -can cross placenta -> motile |
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Examples of biofilm forming bacteria invading immune responses |
Pseudomonas in Cystic Fibrosis lung Staphlyococcus and Enterococcus on heart valves -endocarditis Streptococcus pneumoniae - otitis media (ear infection)
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Bacterial biofilm invading immune response cycle |
1. planktonic cells are sensitive to antibiotics and are detected by host phagocytes and antibodies 2. planktonic cells settles to form a biofilm and become biofilm cells 3. biofilm cells resist antibiotics and antibody detection. Host phagocytes detect and attempt to destroy biofilm cells 4. Unable to capture biofim cells, phagocytes release antimicrobial products that kill host cells but not biofilm cells |
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Bacterial toxins |
Substances that damage host -Exotoxins - made by microbes, secreted to environment -Endotoxins - not secreted component of microbial cells |
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Exotoxins |
Four types -Membrane disrupting -AB toxin (A &B components) - can be host site specific -Superantigens |
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Membrane disrupting exotoxins |
-pore forming exotoxins -leukocidins - hemolysis
1. form a pore/MAC (membrane attack complex) in host cell 2. water moves in 3. cell lysis and death
Ex: beta -hemolysis |
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Superantigens |
-binds MHC and T cells together while no antigen is presented, T cells become very stimulated and produce lots of cytokine
- causes T cells (30%) to overexpress, release cytokines -failure of multiple host organs Ex: Toxic shock syndrome caused by Staphylococcus aureus superantigen |
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AB Exotoxins |
Two subunits A-toxic effect B-binds target cell receptor Ex: Corynebacterium diphtheriae 1. B binds to epidermal growth factor receptor 2. enters by receptor mediated endocytosis 3. Acidification - lowering of pH breaks disulfide bond between A and B, releasing A 4. ADP-ribosyl transferase catalyze the attachment of ADP ribose (from NAD+) onto EF-2 (translation elongation factor 2) 5. Stop synthesis |
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Specific host site exotoxins |
Examples: Vibrio cholerae -enterotoxin (associated with intestine) -ADP-ribosyl transferase modifies host G protein -controls adenylate cyclase and increase cAMP -altered Na, Cl transport -H2O loss Diphtheria and Cholera toxin genes are encoded by lysogenic prophage |
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Botulinum Toxin |
Clostridium botulinum -gram +, spore forming bacterium -produces neurotoxins - blocks acetylcholine release at neuromuscular junctions (die of suffocation) -flaccid paralysis NO muscle contraction acetylcholine cause muscle contraction |
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Exotoxins that are antigenic |
-antitoxin (antibody) can neutralize toxicity -exotoxins are generally unstable, can lose toxicity but remain antigenic -toxoid - inactivated toxin but still can elicit immune response - part of a DTaP vaccine (D & T components are toxoids) |
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Endotoxins |
mostly gram (-) -Lipid A of LPS -effects are often direct via TLR4 (toll like receptor 4) -stimulates endogenous pyrogen from macrophages (cytokine interleukin) -stimulates TNF release (tumor necrosis factor) -uncontrolled amount leads to capillary leak, hypotension (low blood pressure) Ex: tissue necrosis due to Nisseria meningitidis -septic shock (gram - shock leads to multiple organ failure and tissue destruction) |
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Type III secretion system |
-Gram (-) pathogens -inject effors invasion, control host immune response, intracellular survival -have injectisome (genes on pathogenicity islands) - needle like structure w/ hollow tube, bacteria shoot the protein up the hollow tube into the eukaryotic membrane and block phagocytosis |
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Targets for Type III secretion effectors |
Host cell cytoskeleton -actin Host cell signaling -NF kappa B Ex: Enteropathogenic Escherichia coli induces pedestral formation on host cells |
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Enteropathogenic E.coli (EPEC) type III secretion system |
EPEC - major cause of infantile diarrhea Binds host cells using bundle forming pili then delivers effectors, including protein Tir Tir represented on host cell surface - binds bacterial intimin |
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Microbial Control Terms |
Cidal - kills static - inhibits growth sterilization - completely remove or kill all microbes disinfection - reduction of microbial population, destruction of pathogens sanitization - reduction of microbial contamination to levels safe by public health standards Antiseptic - chemical reagent applied to tissue to prevent infection by inhibition or killing |
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Microbial control Methods |
Mechanical removal - filtration Chemical agents - gases Physical agents - radiation, heat Radiation -UV can sterilize but poorly penetrates, mostly used to disinfect -Ionizing radiation (X, gamma ray) - penetrates and sterilizes Heat -moist heat more effective than dry -steam under pressure (autoclave -> sterilizes) -15 lbs/sq in, 121C, 15 mins (standard operating condition) Pasterurization (milk) -62.8C for 30 mins, rapid cool or 72C for 15 sec, rapid cool -doesnt sterilize but kills most pathogen including Listeria, Salmonella |
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Antimicrobial agents |
used to treat disease destroy pathogenic microbes or inhibit growth most are antibiotics -microbial products that kill or inhibit Ex: Streptomyces spp, Bacillus spp, Penicillium |
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Development of Antimicrobial Therapy History |
Paul Enrlich (1904) - selective toxicity -compound that would kill a germ but wouldn't kill you Alexander Fleming (1928) - accidentally rediscovered penicillin Florey, Chain, and Heatley (1940) -purified penicillin, when injected into mice infected with Staphylococcus, mice survived Selman Waksman (1944) -cultured over 10,000 strains of soil bacteria and identified streptomycin also identified many types of media |
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Spectrum of antibiotics |
Broad - attacks many different pathogens ex: Mycobacterium Narrow - attack only a few different pathogens Ex: Penicillin, Bacitracin |
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Considerations for developing antibiotics |
-money -allergic? toxic? -resistance? 20 years to develop antibiotics and 2 years to develop resistance -broad vs narrow -reach effective concentration -Not inactivated -doesn't eliminate microflora - Pseudomembranous colitis - Clostridium difficile - anaerobic, spore-forming, toxin-producing bacillus |
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Mechanism of Action of Antimicrobial Agents |
Targets: -cell wall -plasma membrane -nucleic acid synthesis -protein synthesis -metabolic enzymes |
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Cell Wall inhibitors |
Penicilins -broad or narrow, cidal -MOA: inhibit transpeptidation enzymes involved in cross-linking the polysaccharide chains of peptidoglycan by beta-lactam structure, also inhibit bacterial penicilin binding proteins (PBPs) used for transpeptidation -Structure: R group for stability and spectrum, Penicillinases can attack beta lactam ring Cephalosporins -broad and cidal -same MOA as penicilins Vancomycin -narrow and cidal -inhibits transpeptidation by binding to terminal D-alanine Bacitracin
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Plasma Membrane inhibitors for bacteria |
Polymyxins - disrupt lipid bilayer (cidal, narrow spectrum), effective against gram negatives Ex: colistin (disrupts LPS) |
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Plasma membrane inhibitors for fungi Antifungal agents |
Miconazole - blocks sterol synthesis -candida yeast infections and athletes foot (fungus Tinea pedis) Nystatin - binds sterol -candida yeast infections Some target cell wall - Nikkomycin -blocks synthesis of chitin |
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Nucleic Acid inhibitors |
Quinolones (Nalidixic acid, Ciprofloxacin) -cidal, broad spectrum -synthetic -inhibits DNA gyrase -blocks DNA replication Rifampin -cidal, broad spectrum -binds bacterial RNA polymerase |
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Protein synthesis inhibitors |
Aminoglycosides -cidal, narrow or broad -bind 30S, cause mRNA misreading -ex: streptomycin, kanamycin Tetracyclines -static, broad -bind 30S, distorts A site, inhibits amino acyl tRNA binding Macrolides -static, broad -bind 23S rRNA of 50S, blocks peptide elongation -Ex: Erythromycin, Azithromycin -> treating Chlamydia Chloramphenicol -static, broad -Same MOA as macrolides -toxic, limited to life-threatening situations |
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Metabolic Enzyme inhibitors |
Sulfonamides and Trimethoprim -static and broad -synthetic -Antimetabolites -> disrupt metabolic pathways -Similar to metabolic intermediates (analogs) -bind enzymes for folic acid synthesis -block bacterial purine, pyrimidine synthesis Triclosan -broad spectrum antibacterial -binds enoyl reductase -> enzyme for fatty acid synthesis
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Antiviral drugs |
few- because viruses enter host cells and make use of host cell enzymes and constituents Ex: -Acyclovir -inhibits DNA polymerase of herpes viruses (guanine analog) -Tamiflu - blocks neuraminidase which is a catalytic enzyme in influenza |
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Anti-HIV drugs |
HAART - highly active antibial retroactive therapy Azidothymidine (AZT) -RT inhibitors -targets reverse transcriptase -nucleoside analog, causes DNA chain termination Ritonavir (protease inhibitor) -HIV protease processes viral proteins for virion assembly |
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Antiprotozoan Drugs |
Malaria -Chloroquine, Malarone -chloroquine blocks polymerization of heme polymerase which neutralize toxic heme metabolites to non-toxic form -toxins accumulates Malarone -blocks e- transport and pyrimidine synthesis Metromidazole -Giarida, Trichomons -> both protozoan parasites of STDs -also anaerobic and microaerophilic bacteria (Clostridium and Helicobacter-> peptic ulcers) -enters parasite -> activated by reduction -> DNA nicking |
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Superbugs |
Microbes that are resistant to many antibiotics Examples: Vancomycin Resistant Enterococcus (VRE) -vanA gene -encodes enzyme that replace D-Ala with D-Lactate Methicillin Resistant Staphylococcus aureus (MRSA) -mecA gene -encodes PBP resistant to penicillin |
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Mechanism of drug resistance |
1. Altered antibiotic target - prevent access to the target of antibiotic 2. Degrading antibiotic enzyme 3. Enzymes that chemically modified the antibiotic so its function is blocked 4. Rapidly extruding the antibiotic - ABC efflux pumps drugs before it functions Also contains R plasmid containing one or more resistance gene that can be transferred by transformation and conjugation |
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Overcoming drug resistance |
Antibiotic don't mutate microbes, but rather create environments that select for antibiotic resistant mutants Use drugs only when necessary, take prescribed course Don't treat viral infections with antibacterials Give drug in high concentrations Give two or more drugs at same time -Penicillin + Clavulanic Acid |
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LISTEX(TM) P100 |
new antimicrobial a culture of safe microorganisms (bacteriophage preparation) in use as a processing-aid, characterized by the broad spectrum toward Listeria monocytogenes |
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Furanones |
new antimicrobial
Furanones -block bacterial biofilm formation -inhibit AHL (Acylhomoserine lactone - autoinducer in Gram-) mediated QS - Quorum sensing used to study P.aeruginosa |
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Viral - Airborne disease |
Chickenpox and Shingles Influenza Measles, Mumps, Rubella |
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Viral - Arthropod-Borne |
yellow and West Nile Fever Dengue Fever |
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Viral-Direct contact |
Common cold, Mono Warts, AIDS Ebola |
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Viral - food and water borne |
Gastroenteritis Polio |
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Viral - Zoonotic |
Rabies |
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Chickenpox |
Varicella-Zoster virus Family Herpesviridae -enveloped viruses -icosahedral shape -DNA genome Inhalation or conjunctiva of eye Virus spreads via blood, lymphatic and neuronal system ~10 days infection of skin leads to vesicular rash Treatment - drug - acyclovir Attenuated (live) vaccine |
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Vaccines |
Inactivated (killed) -chemicals or heat -induce humoral -> B cells -> antibodies -drawback: require booster Ex: Rabies, Flu (shot) Attenuated (live but avirulent) -inactive specific genes -can reproduce, but weakened -humoral and cell-mediated -drawback: may revert Ex: chickenpox, MMR, Flu (intranasal) |
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Herd immunity |
Protection of unvaccinated people in a population where most people are vaccinated due to lessened risk of disease transmission |
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Shingles (Zoster) |
individuals who recover from chickenpox are often resistant to disease however, viral DNA can reside in dormant state in nuclei of nerves, sensory neurons -latency immunocompromised state (age, organ, transplant, AIDS, stress) can reactivate virus -leading to shingles assembled to infectious new virions |
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Influenza (flu) |
(-)ssRNA, segmented genome must bring in its own RNA replicase to convert to (+) Entry -endocytosis Release - Budding |
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Changes in Antigenicity of Influenza viruses |
Antigenic drift - minor -mutations in viral genes in single strain -viral RNA replicase -error prone Antigenic shift -major -different strains (animal or human) infect cell, genomes re-assort -Animal influenza -> zoonotic -Epidermic - sudden increase in disease -Pandemic - increase in large geographically widespread population ex: spanish flu |
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Measles, Mumps, Rubella |
RNA viruses MMR attenuated (live) vaccine Measles - bumpy Rubella -smooth Mumps -on face |
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Yellow fever, West Nile Fever, Dengue fever |
Arthropod-borne diseases - transmitted via mosquito 400 million infected yearly - trophic (Puerto Rico) subtrophic All caused by Flaviruses (+) ssRNA, enveloped, icosahedral
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Common cold, Mononucleosis, AIDS and Ebola |
direct contact diseases Common cold -major cause -> Rhinovirus -(+) ssRNA, naked, icosahedral ->100 different serotypes wash your hand! |
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Mononucleosis (Mono) |
-Epstein-Barr virus (Herpesviridae) -DNA, enveloped, icosahedral -enters, replicates in epithelial cells of throat -then infects B cells (latant) <- use MHC II to interact with B cells -Cancer - Burkitt's (B cell) lymphoma - primarily Africa, in children with Malaria |
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Warts |
Human Papillomaviruses (HPV) -naked, icosahedral, DNA ->100 different strains -Genital HPV - most common sexually transmitted infection -some are oncogenic -cervical cancer
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How do viruses cause cancer? |
Most viruses act as cofactor and have dsDNA genomes -called oncoviruses -encodes protein that binds and inactivate tumor suppressor proteins (Ex: Rb and p53) Ex: HPV - viral protein E6 targets destruction of host p53 (E-early) |
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Acquired Immune Deficiency Syndrome (AIDS) |
Human immunodeficiency virus (HIV) -retrovirus -enveloped, RNA genome -partly icosahedral, cone-shaped core -originated in Africa from non-human primates (HIV-1-Chimpanzees) -binds host CD4 & CCR 5 co-receptor -have gp120 and gp41 receptors on surface -reverse transcriptase, integrase, ssRNA , protease Gene: LTR-gag-pol-env-LTR gag - capsid proteins pol- RT, integrase, protease env - spike proteins
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HIV life Cycle |
1. Docking and fusion - bind CD4, enters by endocytosis 2. Internalization and uncoating 3. RT reverts ssRNA to ssDNA 4. ssDNA replicates into dsDNA and circularized 5. Integrase integrate DNA into host genome 6. the protein necessary gets transcribed. 7. Protease helped assemble the necessary viral proteins |
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HIV Transmission and Pathogenesis |
When infected blood, semen, or vaginal secretions come in contact with uninfected person's broken skin or mucous membranes (sexual contact, transfusion, needle sharing)
Pathogenesis -T cell depletion -also macrophages, dendritic cells -virus mutates rapidly, evades immune system
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HIV cure? |
HIV infected individual with <200 CD4+T cells/ul of blood. T cell destruction -> immune system collapse -> opportunistic infections (ex: samonella) no cure for AIDS, treatments are mostly -reducing viral load (HAART) -treating opportunistic infections and malignancies (Kaposi's sarcoma -> reactivation of Herpes virus) -education key to prevention and control -Latency - a challenge |
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Ebola Hemorrhagic Fever |
-virus ssRNA, filamentous, enveloped -contains 7 genes, RNA replicase in virion, glycoproteins (spikes), Nucleoprotein (N) Family Filoviridae -Viral protein block interferon, clot blood -transmission: direct contact w/ blood or body fluids of infected symptomatic person -Airborne transmission hypothesized but not demonstrated at this time in human -evidence zoonotic - fruit bats, primates treatment - largely supportive
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Gastroenteritis |
food and water borne Rotavirus -Noro (Norwalk-like) virus -Rota and Norovirus are naked, RNA viruses -fecal-oral, also person -person |
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Polio (infantile paralysis) |
Poliovirus (enterovirus, +ssRNA) -stable food, water (ingestion) -multiplies, throat, intestinal cells -targets motor nerve cells in spinal cord - paralysis Vaccines: Salk (killed) and Sabin (live, oral) |
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Viral Zoonotic diseases |
multiplies in animal salivary glands Rabies virus (bullet shaped, enveloped virion RNA) In human, targets muscle cells spread via CNS to brain (Negri bodies) -paralysis |
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Zoonotic diseases |
spread between animals and humans rodents, amphibians, reptiles, insects, domestic and wild animals causes: viruses, bacteria, fungi, protozoa, even malaria ~75% of recently emerging infectious disease affecting humans are diseases of animal origin viral examples: yellow, west nile and dengue fever, ebola, rabies |
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Bacterial - Airborne |
-Diphtheria -Tuberculosis -Streptococcal Diseases -Pertussis -Meningitis |
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Bacterial - Arthropod-borne |
-Plague -lyme disease |
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Bacterial - direct contact |
-anthrax -Staphylococcal disseases |
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Bacterial - food, water -borne |
-Listeriosis -Cholera -Botulism -Escherichia coli -Samonella typhimurium infections can be controlled and prevented by sanitation measures, antitoxins, and antibiotic therapy |
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Tuberculosis (TB) |
Mycobacterium tuberculosis -inhaled - lung -phagocytosed, survive intracellulary -mycolic acids in cell wall protection -host response - tubercles -latency -tubercles can liquidfy - bacteria spread to blood, organs - death Tubercle - bacteria, macrophages, Tcells, proteins |
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TB skin test |
Mantoux tuberculin skin test -standard method of determining whether a person has had TB or been exposed to M.tuberculosis -performed by injecting purified protein into forearm -Reaction (in duration) measured in mm (48-72 hours) -delayed hypersensitivity - memory T cells -care must be taken in interpreting -False positives -Infection with nontuberculosis Mycobacterium -previous BCG vaccination -incorrect administration or interpretation Follow up: Chest X ray, bacterial culture, microscopy with acid-fast staining |
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TB - Vaccines |
BCG vaccine - Bacille Calmette-Guerin -live avirulent M.bovis Diagnosis -bloody sputum, chest X-ray, acid-fast staining, culture Antimicrobial therapy -Rifampin + Isoniazid (acid synthesis) -daily, 6-9 months -MDR and XDR strains emerging |
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Streptococcal Diseases |
-Streptococcus pyrogenes (group A beta hemolytic) or S. pneumoniae -Infections - impetigo (skin), throat and lung infections, pneumonia, otitis media Diagnosis- strep test, culture Treatment - penicillins, erythromycin Carbohydrate group streptococcus |
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Streptococcal Virulence determinants |
-capsule -streptokinase -hemolysins -leukocidins M protein -attachment -inhibit C3b -Ab to M may x-react with heart tissue (Rheumatic fever) -similar amino acid sequences in M and human cardiac myosin |
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Group A streptococci |
-can cause invasive infections some strains make tissue destroying protease Necrotizing fasciitis fresh eating bacteria - also associated with tooth decay Streptococcus mutans part of dental plaque (biofilm) Fermentation -> acid -> enamel (decay)
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Whooping cough (Pertussis) |
-Bordetella pertussis (Gram -) -Colonizes ciliated cells of respiratory tract Stage 1: cold-like symptoms Stage 2: prolonged paroxysmal cough Virulence factors: -type III secretion, pili, siderophores -used by microbe to acquire iron -PTx -> AB exotoxin, same MOA as cholera toxin Subunit vaccine - DTP1940s -2 toxoids - heat killed Bordetella pertussia D- Diphtheria, T- Tetanus, P-pertussis DTaP currently Tdap booster Antibiotics -tetracycline, erythromycin |
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Meningitis |
Inflammation of brain, spinal cord meninges (membranes) -bacteria, viruses, fungi Bacteria -Haemophilus influenzae -Streptococcus pneumoniae -Neisseria meningitidis |
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Neisseria meningitidis |
leading cause meningococcal disease in children and young adults person to person, respiratory or throat secretions can cross mucosal barrier into blood -> bacterimia Serogroups - groups of strains with common surface antigens (A,B,C, Y, W) Virulence factors: pili, capsules , endotoxin |
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Clinical of Neisseria meningitidis |
clinical-initial sore throat, vomitting, confusion, stiffness in neck, rash Prevention (vaccines) -MCV4 - capsular polysaccharides (CPS) protects against A,C, Y and W (not B) -MenB -group B outer membrane proteins (CPS of MenB is identical to human polysaccharide) Diagnosis, treatment -gram stain spinal fluid, culture -antibiotics (cell wall, protein synthesis) |
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The plague (black death) |
Yersinia pestis (Gram - rod) 2 forms: Bubonic -fleas Pneumonic - person to person -flu like (almost 100% fatal if not treated early) Category A Bioweapon Agent Type III secretion system - major virulence factor -injectisome delivers effector proteins called YOPs into host cells including macrophages YOP-Yersinia outer protein |
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Lyme Disease |
Most commonly reported ticke-borne disease in US caused by spirochete - Borrelia burgdorferi Vector = blacklegged (deer) tick - lxodes Clinical - varies with stage of disease |
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Stages of Lyme disease |
Localized (7-10 days) -bull eyes rash (erythema migrans) flu-like symptoms -most treatable -doxycycline (tetracycline) -penicillins Disseminated (weeks or months) -muscle pain, arthritis (autoimmunity) Late (years) -nervous system |
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Anthrax |
Bacillus anthracis Virulence factors -capsule -toxin - AB but 3 parts 1. Protective antigen (PA) 2. Edema factor (EF) 3. Lethal factor (LF) -toxin and capsule genes encoded on separate plasmids |
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Anthrax toxin |
AB exotoxin 1. PA attaches to receptor on macrophages (7 PA +receptor complex - like a syringe) 2. PA complex binds to EF/LF 3. Engulfment and into endosome 4. PA forms a pore and pierce endosome membrane 5. EF/LF released. Edema forms EF +LF = fluid release, NF kappa B blockage, cell death EF - adenylate cyclase, ATP -> cAMP LF - protease, degrades MAP kinases -> needed for transcription of NF kappa B |
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Forms of Anthrax |
Cutaneous -cut, abrasion Pulmonary - inhaled spores -fatal if bacteria reach bloodstream -bioterrorism (2001) Treatment - ciprofloxacin -> DNA gyrase inhibitor (replication) |
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Staphylococcal Diseases |
Members of the gram-positive genus Staphylococcus are among the most important bacteria that cause disease in humans Two major species S.aureus - invasive, virulent (coagulase +) S. epidermidis - less invasive, less virulent (coagulase-) Disease include: boils, carbuncles, toxic shock syndrome, food poisoning |
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Virulence factor of S. aureus |
Superantigens -Toxic shock syndrome toxin (TSST-1) Capsules IgA protease Coagulase DNase - target NET Biofilms Biofilms and toxins controlled by QS and 2 component system |
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Escherichia coli O157: H7 O-antigen H flagella antigen |
Enterohemorrhagic E.coli (EHEC) Infectious Dose <100 carriers - cattle, swine Shiga-like toxin - Ab toxin -binds glycolipid receptors on kidney and intestinal cells and enters Cleaves human rRNA hemolytic uremic syndrome (kidney failure) Toxin genes on prophage |
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Fermentation process |
Substrate level phosphorylation ADP-> ATP Reduction NAD+ -> NADH NAD+ oxidized NADH reduced Oxidation NADH -> NAD+ 2 pyruvate accept electrons Glucose -> 2 pyruvate -> Lactic acid ethanol Propionic acid |
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Yogurt production |
Lactic acid bacteria Lactobacillus + Streptococcus -starter culture Lactose (in milk) hydrolyzed to glucose, fermented to lactic acid |
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Cheese production |
Lactococcus lactis starter culture and renin (enzyme, hydrolyzes casein in milk causing coagulation) Ripening by adding more microbes Propionibacterium - propionic acid fermentation Swiss Penicilium roqueforti - fungus Bleu cheese |
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Plastic and Lactic acid fermentation |
Polylactide (natureworks) bio-based plastic Dextose from corn fermented to lactic acid, purified, polymerized Bioengineered E.coli, Lactobacillus |
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Probiotics |
microbes added to diet to improve health Lactobacillus Bifidobacterium Potential benefits -vitamin production -improved digestion -pathogen inhibition |
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Beer |
Malting and mashing Plant enzymes breakdown complex, starches, proteins hops added for flavor
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Wine |
Must -> wine yeast = Saccharomyces ethanol fermentation |
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Biofuels |
fuels from biological material corn to ethanol with bacteria, yeast fermentation Industrial microbiology - microbial growth occurs in bioreactors |
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Metabolic products made by microbes |
Primary metabolites -required for growth -made during active growth - exponential phase Ex: amino acids Secondary metabolites -not required for growth -made under nutrient limiting conditions - end of stationary phase before death phase -following active growth Ex: antibiotics |
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Triclosan |
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Fermentation |
