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Microbiology
Unit 1
| Question | Answer |
|---|---|
| Prokaryote | A unicellular organism having cells lacking membrane-bound nuclei. Bacteria, Archaea, blue-green algae. |
| Eukaryote | A single-celled or multicellular organism whose cells contain a distinct membrane-bound nucleus. Fungi, protozoa, algae, multicellular animal parasites (microscopic in some stages of life). |
| Mycology | Study of fungi |
| Parasitology | Study of protozoa and parasitic worms. |
| Serotype | A group of microorganisms, viruses, or cells classified together based on their cell surface antigens. |
| Antigen | A molecule that binds specifically to an antibody. |
| Microbes | Free-living organisms so small they are visible only under the microscope (less than about 100 micrometers). Exceptions: some bacteria/protozoa are 1 millimeter in length or longer. |
| Three domains of life | Bacteria, Archaea, Eucaryota |
| Bacteria | Prokaryote. Unicellular. Peptidoglycan cell walls. Reproduce by binary fission. Diverse: Energy from organic or inorganic chemicals or photosynthesis. |
| Archaea | Prokaryote. Unicellular. Lack peptidoglycan cell walls. Have eukaryotic-like ribosomes. Live in extreme environments. Include methanogens, extreme halophiles (salt loving), extreme thermophiles. |
| Fungi (yeasts, mold) | Eukaryotes. Absorb nutrients. Use organic chemicals for energy. Chitin cell walls. Molds & mushrooms are multicellular consisting of masses of mycelia-composed of branching filaments called hyphae. Yeasts are unicellular. |
| Algae | Eukaryotes. Photosynthetic. Cellulose cell walls. Produce molecular oxygen & organic compounds. Multi & unicellular. Always colorful-absorb light to get energy. Make complex carbs from CO2. |
| Protozoa | Eukaryotes. All microbes not algae or fungi. Unicellular, complex cells. Absorb or ingest organic chemicals. May be motile via pseudopods, cilia, or flagella. Nonphotosynthetic. Pellicle (interconnected protein molecules) interior to plasma membrane. |
| Protozoa Example: Cryptosporidium | Causes 30% of diarrheal illness in developing countries. Transmitted via water in U.S. Protozoa have complex life cycles. Hard to treat/kill. Oocysts develop-protozoa can hunker down and stay for a long time. |
| Viruses | Acellular. DNA or RNA core. Core surrounded by a protein coat. coat may be enclosed in a lipid envelope. replicated only when in a living host cell. |
| Multicellular Animal Parasites | Multicellular animals. Parasitic flatworms and roundworms are called helminths. Microscopic stages in life cycles. |
| Protists | Algae and Protozoa. |
| Scientific Names | Italicized. Genus capitalized, species (specific epithet) lowercase. After first mention, Genus can be abbreviated to 1 letter. |
| History: Ibn Khatima | 14th century. Hypothesized that infectious diseases are caused by "minute bodies" which enter the human body and cause disease. |
| Spontaneous Generation | The hypothesis that living organisms arise from nonliving matter; a "vital force" forms life. Argued in the 1400s. |
| Biogenesis | Hypothesis that living organisms arise from other living organisms. |
| Francesco Redi 1668 | Experiment: three bottles. 1 cork, 1 mesh, 1 open. Supported spontaneous generation-needs air. |
| John Needham 1745 | Experiment: boiled nutrient broth in covered flasks. Microbial growth due to contaminated flasks. Supported spontaneous generation. |
| Lazzara Spallanzani 1765 | Boiled nutrient solutions in flasks. Microbes grow when seal is broken. Supported spontaneous generation: life requires air. |
| Discovery of microbes | Light microscope in 1600s. Improved after. Mid 1600s: Robert Hooke (wealthy) observes small eukaryotes. Proposes cells. 1676: van Leeuwenhoek (a tailor) discovers bacteria. Animalcules. |
| Pasteur 1822-1895 | Bent neck of boiled flask so microbes would get stuck, but air could get in. No microbes grew. Supported Biogenesis. |
| Pasteurization | Application of high heat for a short time. Spoilage bacteria can be killed by heat that was not hot enough to evaporate the alcohol in wine. |
| Rudolf Virchow 1858 | Cells arise from preexisting cells. He watches cells divide. Biogenesis. |
| Cell theory | All living things are composed of cells and come from preexisting cells. |
| The Germ Theory of Disease | 1835: Agostino Bassi shows that a silkworm disease is caused by fungus. 1865: Pasteur believes that another silkworm disease is caused by a protozoan. 1840s: Ignaz Semmelweis advocates hand washing to prevent transmission of puerperal fever among OB pts. |
| The Germ Theory of Disease and Robert Koch | 1876: Robert Koch proved that a bacterium causes anthrax & provided the experimental steps to prove that a specific microbe causes a specific disease. |
| Koch's Postulates | 1. Microorganism found in diseased animals, not healthy. 2. Microorganism isolated from animals & grows in pure culture. 3. Cultured microorganism causes disease in healthy host. 4. New microorganism isolated is identical to original. |
| Vaccination | 1796: Edward Jenner inoculated a person w/ cowpox virus, who was then protected from smallpox. |
| Immunology | The study of immunity. Vaccines & interferons being investigated to prevent & cure viral diseases. Identify bacteria according to serotypes-Rebecca Lancefield. |
| Chemotherapy | 1910: Ehrleic synthesized an arsenic agent he used to treat syphillus. 1928: Alexander Fleming discovers the first antibiotic. Penicillium fungus killed S. aureus. Penicillin tested & mass produced in 1940s. |
| Pathogenesis | The development of disease |
| Infection | Colonization of the body by pathogens. No symptoms. |
| Disease | An abnormal state in which the body i9s not functioning normally. Symptoms. |
| Etiology | The study of the cause of a disease. |
| Transient Microbiota | May be present for days, weeks, or months. |
| Normal Microbiota | Permanently colonize the host. |
| Symbiosis | The relationship between normal microbiota and the host. |
| Normal Microbiota protect the host by: | Occupying niches that pathogens might occupy. Producing acids. Producing bacteriocins. Microbiota form a protective barrier, aid digestion, make vitamins for us, and prime the immune system. |
| The Human Microbiome Project (HMP) | A national institute of health initiative. Aims to characterize the microbial communities found at several dif sites on the body and to analyze the role of these microbes in human health and disease. >300 healthy people studied. |
| Microbial antagonism | Competition between microbes |
| Probiotics | Live microbes applied to or ingested into the body, intended to exert a beneficial effect. |
| Microbes affect our metabolism | Bacteria can digest things we cannot. Bacterial fermentation contributes to 10% of our daily caloric intake. |
| Symbiosis | The relationship between normal microbiota and the host. |
| Commensalism | One organism benefits and the other is unaffected. |
| Mutualism | Both organisms benefit. Ex. E.coli makes our vitamins and has a place to live. |
| Parasitism | One organism benefits at the expense of the other. |
| Opportunistic Pathogens | Some normal microbiota are this. Ex. E.coli is normal in the intestine, but causes infection in the urinary tract. |
| Problems with Koch's Postulates | People have differing immunities. Some microbes cannot grow outside a host. Some microbes only affect humans-ethics. Some pathogens can cause several disease conditions. |
| Symptom | A change in body function that is felt by a patient as a result of disease. |
| Sign | A change in a body that can be measured or observed as a result of disease. |
| Syndrome | A specific group of signs and symptoms that accompany a disease. |
| Morbidity | Incidence of a specific notifiable disease |
| Mortality | Deaths from a notifiable disease |
| Morbidity rate | Number of people affected in relation to the total population in a given time period. |
| Mortality rate | Number of deaths from a disease in relation to the population in a given time. |
| Incidence | Fraction of a population that contracts a disease during a specific time. |
| Prevalence | Fraction of a population having a specific disease at a given time. |
| Acute Disease | Symptoms develop rapidly |
| Chronic Disease | Disease develops slowly |
| Subacute disease | Symptoms between acute and chronic |
| Latent disease | Disease with a period when the causative agent is inactive. Ex. Chicken pox. |
| The Stages of a Disease | Incubation period-no signs or symptoms. Prodromal period-mild signs or symptoms. Period of Illness-most severe signs & symps. Period of decline-signs & symps. Period of convalescence. |
| Endemic disease | Disease constantly present in a population. Ex. A cold in the U.S. |
| Epidemic disease | Disease acquired by many hosts in a given area in a short time. Ex. Seasonal flu. |
| Pandemic disease | Worldwide epidemic. Ex. Tuberculosis. |
| Herd Immunity | Immunity in most of a population. |
| Communicable Disease | A disease that is spread from one host to another. |
| Contagious disease | A disease that is easily spread from one host to another. |
| Noncommunicable disease | A disease that is not transmitted from one host to another. |
| Reservoirs of Infection | Human: Carriers may have inapparent infections or latent diseases. Animals: zoonoses transmitted to humans. Nonliving: Ex. botulism, tetanus, from soil. |
| Transmission of Disease | Airborne: > 1 meter distance. Contact: Direct, Indirect (fomites), Droplet. |
| Vehicle | Transmission by an inanimate reservoir (food, water, air). |
| Vectors | Arthropods, especially fleas, ticks, and mosquitoes. |
| Mechanical Transmission | Arthropod carries pathogen on feet (flies). |
| Biological Transmission | Pathogen reproduces in vector (malaria lives in mosquitoes). Bitten/stung. |
| Nosocomial Infections | Acquired as a result of a hospital stay. Affect 5-15% of all hospital pts. |
| Contributing factors to emerging infectious diseases | Genetic recombination. Evolution of new strains. Inappropriate use of antibiotics and pesticides (antibiotic resistant strains). Changes in weather patterns. Ex. Hantavirus. |
| MRSA | Methycilin resistant Staph aureus. 30% of people carry it w/0 problems in nasal cavities. |
| Ignaz Philipp Semmelweis | 1846-1849. Decreased mortality rate from 10-35% to <1% due to chlorine washes & hand washing. OB pts in hospital dying of puperal sepsis. Semmelweis not believed till 20 years later. |
| More factors for emerging infectious diseases | Modern transportation (west nile virus). Ecological disaster, war, & expanding human settlement. Animal control measures (lyme disease). Public health failure (diphtheria). |
| Epidemiology | The study of where and when diseases occur. CDC collects & analyses epidemiological info in U.S. Morbidity & Mortality Weekly Report (MMWR) |
| Predisposing Factors | Make the body more susceptible to disease. Inherited traits, climate, fatigue, age, lifestyle, chemotherapy, sex. |
| John Snow | 1848-1849. Mapped the occurrence of cholera in London. One of the first epidemiologists. |
| Florence Nightingale | 1858. Showed that improved sanitation decreased the incidence of epidemic typhus. |
| Case reporting | Health care workers report specified disease to local, state, and national offices. |
| Nationally notifiable diseases | Physicians are required to report occurrence. |
| Cocci | Round bacteria |
| Impetigo | Crusting (nonbullous) sores, spread by autoinoculation. |
| Sepsis | illness in which the bloodstream is overwhelmed by bacteria |
| Perspiration | Contains Nutrients, Salts, & Lysozymes. Salt inhibits microbes. Lysozyme is a protein which hydrolyzes bacterial peptidoglycan. |
| Sebum | Contains nutrients, salts, & fatty acids which inhibit some pathogens, but act as nutrient for others. |
| Defensins | Small peptide Antimicrobial molecules the skin secretes. |
| Normal Microbiota of the skin | Gram positive bacterial cell walls are extra thick and protect them from salts and other compounds. Salt tolerant. exs. staphylococci, micrococci, diphtheroids. Grow on oils. Aerobes on surface. Anaerobes in hair follicles. Yeast. |
| Exanthem | Skin rash arising from another focus of the infection. |
| Enanthem | Mucous membrane rash arising from another focus of the infection. |
| Vesicle | Small, fluid filled lesion. <1cm. |
| Bulla | Large, fluid filled lesion. >1cm. |
| Macule | Flat lesions that are often reddish. Ex. Measles. |
| Papule (pustule) | Raised lesions. Called pustules when they contain pus. |
| Staphylococcal Skin Infections | Classified by coagulase, an enzyme that clots blood fibrin. |
| Staphylococcus epidermidis | 90% of normal skin microbiota. Gram-positive cooci, coagulase-negative. |
| Staphylococcus aureus | Found in 20-60% of population. Has more DNA in genome mostly devoted to virulence factors. Gram-positive cocci. Coagulase-positive. Has toxins. Pathogenic. |
| Staphylococcus aureus pathogenic mechanisms | Antibiotic resistant. Leukocidin-kills leucocytes. Evades immune system. Neutralizes skin defensins. Lysozyme resistant. Exfoliative toxin (scalded skin syndrome). Superantigen-may cause TSS1 by hyperactivating the immune sys. |
| Biofilm | Microbes cluster & excrete extracellular matrix to protect them. On ponds, our teeth, etc. Prevents chemicals from getting in. Allows them to concentrate nutrients. |
| Steps to creating a biofilm | 1. Attachment 2. Growth & Division 3. Exopolymer production & biofilm formation 4. Attachment of other organisms to biofilm |
| Staphylococcal Skin Infections | Folliculitis, Sty, Furuncle, Carbuncle, Impetigo, Scalded Skin Syndrome, Toxic Shock Syndrome |
| Foliculitis | Staph. Infections of the hair follicles (white pimples) |
| Sty | Staph. Folliculitis of an eyelash. |
| Furuncle | Staph. Abscess; pus surrounded by inflamed tissue. |
| Carbuncle | Staph. Inflammation of tissue under the skin. |
| Impetigo | Staph. Crusting (nonbullous) sores, spread by autoinoculation (came from another part of the body). |
| Scalded Skin Syndrome | Staph. Skin exfoliates. |
| Toxic Shock Syndrome (TSS) | Staph. Overreaction of immune system. |
| Topical treatment for Staphylococcal Skin Infections | Neomycin binds double stranded RNA-antibiotic. Mupirocin inhibits RNA & protein biosynthesis gram positive bacteria. |
| Streptococcal skin infections | Streptococcus pyogenes. Group A beta-hemolytic streptococci (GAS). NOT coagulase positive. Erysipelas. Necrotizing fascitis. |
| Group A beta-hemolytic streptococci (GAS) pathogenic mechanisms | Hemolysins & Streptolysins lyse red blood cells. Hyaluronidase dissolves connective tissue. M proteins. |
| M proteins in GAS | Help adhere to mucous membranes & evade immune system by inhibiting phagocytosis. |
| Staphylococcal skin infections look and grow how? | Round in bunches like grapes. |
| Streptococcal skin infections look and grow how? | Round and grow in chains. |
| Erysipelas | Strep. Serious infection of the dermal layer, may progress to bloodstream causing sepsis. |
| Necrotizing fascitis | Strep. Flesh eating bacteria. Destroys tissue rapidly. Exotoxin A-a super antigen (M-protein type); TSS: M proteins complex w/ fibrinogen, bind to neutrophils, activate. Release damaging enzymes. Shock and organ damage. |
| Pseudomonas aeruginosa | Wide-spread in soil and water. Gram-negative, aerobic rod. |
| Pseudomonas dermatitis | Opportunistic pathogen. Grows in biofilms. Antobiotic resistant. Treatment: neomycin, acidification. Rash, pimples, folliculitis. Otitis externa (swimmer's ear). Post-burn infections. |
| Comedonal (mild) Acne | Sebun channels blocked with shed cells. Treatment: retinoids, salicyclic creams. |
| Inflammatory (moderate) acne | Propionibacterium acnes (gram +). Treatment: isotretinion (prevents sebum), antibiotics, blue light. This bacteria usually produces low pH of skin & keeps other microbes out. |
| Nodular cystic (severe) acne | Treatment: isotretinion |
| Buruli Ulcer | Mycobacterium ulcerans after trauma. Deep, damaging ulcers due to lipid toxins, myclolactone, an immunosuppresent as well as necrotising agent that simulates cell apoptosis. > incidence than leprosy. Treatment: surgical excision, antibiotics. Treatable. |
| Viral diseases of the skin | Chicken pox, Warts, Rubeola, Rubella, Fifth disease. |
| Chickenpox | Varicella-zoster virus (human herpesvirus 3) Transmitted by respiratory route. Causes pus-filled vesicles. May remain latent in dorsal root ganglia. Prevention=vaccine. Breakthrough varicella in vaccinated people. |
| Shingles | Reactivation of latent HHV-3 releases viruses that move along peripheral nerves to skin. Postherpetic neuralgia. Prevention: vaccine. Acyclovir may lessen symptoms (inhibits viral DNA polymerase). |
| Measles (Rubeola) | Measles virus. Transmitted by respiratory route. Macular rash & Koplik's spots. Prevented by vaccine. Encephalitis in 1 in 1,000 cases. Subacute sclerosing panencephalitis in 1 in a million cases. |
| Encephalitis | Inflammation of the brain. |
| Rubella (German measles) | Rubella virus. Macular rash and fever. Congenital rubella syndrome causes severe fetal damage. Prevented by vaccine. |
| Herpes Simplex | Human herpesviurs 1 (HSV-1) & (HSV-2). Cold sores or fever blisters-vesicles on lips. Herpes gladiatorum-vesicles on skin. Herpetic whitlow-vesicles on fingers. Herpes encephalitis. HSV-1 can remain latent in trigmeninal nerve ganglia. |
| Skin warts | Papillomavirus: common skin and plantar warts. Treatment: removal-cryotherapy, electrodesiccation, salicylic acid. Imiquimod-stimulates interferon production. Bleomycin causes DNA strand breaks. |
| Latent HSV | HSV-1 in the Trigeminal Nerve Ganglion. HSV-2 in the sacral nerve ganglia. Encephalitis: 70% fatality. Treatment: Acyclovir. |
| Fifth Disease | Erythema infectiosum. Human parvovirus B19 produces mild flu-like symptoms & facial rash. |
| Fungal Diseases | Dermatomycoses. Exs. Ringworm, athlete's foot. Treatment: topical miconazole. Topical allylamine. |
| Candidiasis | Fungal disease. Candida albicans (yeast). Candidiasis may result from suppression of competing bacteria by antibiotics. Occurs in skin & mucous membranes of genitourinary tract & mouth. |
| Thrush | Fungal disease. Candida albicans (yeast). An infection of mucous membranes of mouth. Topical treatment w/ miconazole or nystatin. Common in kids. |
| Conjunctivitis | Bacterial eye disease. Inflammation of the conjunctiva. AKA pink/red eye. Commonly caused by Haemophilus influenzae bacteria (antibiotic treatment). Various other microbes can also be the cause. Associated w/ unsanitary contact lenses. |
| Chlamydia trachomatis | Bacterial eye diseases. Causes trachoma. Leading cause of blindness worldwide. Infection causes permanent scarring; scars abrade the cornea leading to blindness. |
| Eukaryotic cell organelles | Nucleus-chromosomes w/ histones. Mitochondrion. Chloroplast. Lysosome-digestive enzymes (WBC) ER/Golgi-protein modification/membrane component factory & transport. Peroxisome-oxidation of fatty acids, destroys H2O2. Vacuoles brings food, store & support. |
| Eukaryotic cell division | Mitotic spindle |
| The Plasma Membrane | Selective permeability. Simple diffusion. Facilitative diffusion. Osmosis. Active transport. Endocytosis: phagocytosis & pinocytosis. |
| Phagocytosis | Pseudopods extend and engulf particles. |
| Pinocytosis | Membrane folds inward, bringing in fluid and dissolved substances. |
| Lysozyme | Breaks down cell wall of bacteria |
| Cell Membranes | Made of a fluid lipid bilayer of phospholipids. Proteins embedded in membrane ~50% of area-anchor membranes to envelope. Sense the outside world. Transport materials into cell. |
| Eukaryotic cell wall | Protozoa (pellicle, protein). Algae (cellulose). Fungi (chitin). |
| Glycocalyx | Carbohydrates extending from animal plasma membrane. Bonded to proteins and lipids in membrane. Helps cells stick together, strengthens cell surface, cell to cell recognition. |
| Eukaryotic flagella | Made of microtubules, tubulin, 9 pairs + 2 array. |
| Prokaryotic Cells | Most microbes are prokaryotes. Much smaller than eukaryotic cells. Most bacteria are monomorphic (single shapeed). A few are pleomorphic. |
| 3 Basic Shapes of Prokaryotes | Bacillus-rod shaped. Coccus (spherical). Sprial-spirillum-normal, vibrio-1 bend, spirochete-tight spirals. Also unusual shapes. |
| Arrangements of Prokaryotes | Pairs: diplococci, diplobacilli. Clusters: staphylococci. Chains: Streptococci, streptobacilli. |
| Prokaryotic cell | DNA often circular chromosome. Not enclosed w/i membrane. DNA not associated w/ histones, but w/ other proteins. Lack membrane enclosed organelles. Almost always have peptidoglycan cell walls. Divide by binary fission. 70S Ribosomes. |
| Eukaryotic cell | DNA in nucleus. Associated w/ histone & nonhistone proteins. Membrane enclosed organelles. Chemically simple cell walls when present. Divide by mitosis. 80S ribosomes. |
| Eukaryotic DNA | Mostly linear. |
| Structure of a prokaryotic cell | Cytoplasm. Inclusion body. Nucleoid (usually a single, circular chromosome). Ribosomes. Pili. Flagella. Sometimes a capsule on outside. Small molecules. |
| Glycocalyx | Capsule. Outside cell wall. Usually sticky. Capsule: neatly organized. Slime layer: unorganized and loose. Extracellular polysaccharide allows cell to attach. Capsules prevent phagocytosis. |
| The Cell Wall | Almost all bacteria have it. Prevents osmotic lysis. Provides structure. Made of peptidoglycan (in bacteria). Polymer of disaccharide: NAG & NAM. One layer after capsule. |
| Halting the Synthesis of Peptidoglycan | Many antibiotics inhibit cell wall synthesis: Lysozyme digests disaccharide in peptidoglycan-kills it. It breaks the bond between G & M (NAG & NAM). Penicillin inhibits peptide bridges (transpeptidation)-can't grow & divide. |
| Gram Positive cell wall | Thick peptidoglycan. Teichoic acids. Single, inner membrane. Cell wall on outside. Ex: staph & strep: help bacteria survive on skin. Our immune sys. recognizes peptidoglycan & teichoic acids. More susceptible to penicillin. |
| Gram negative cell wall | Thin peptidoglycan between 2 membranes: outer & inner. Periplasmic space.Immune sys. detects LPS-polysaccharide (O polysaccharide, core polysaccharide, lipid A). |
| Gram Positive cell walls in depth | Teichoic acids: Lipoteichoic acid links to plasma membrane. The wall teichoic acid links to peptidoglycan. May regulate movement of cations. Polysaccharides provide antigenic variation (evade immune sys.) |
| Gram Negative cell walls in depth | Lipopolysaccharides, lipoproteins, phospholipids. Lipid A=endotoxin. Forms periplasm between outer membrane & plasma membrane. Protection from immune sys. that targets peptidoglycan. Porins form channels through membrane. LPS causes huge immune response. |
| Mycobacterium/Nocardia | Atypical cell wall. Acid fast cell walls-waxy lipid bound to peptidoglycan. Causes a lot of diseases. |
| Mycoplasmas | Atypical cell wall. Lack cell walls. Sterols in plasma membrane. Most dependent on living in a host. |
| Archaea | Atypical cell wall. Wall-less or walls of pseudomurein (lack NAM & D-amino acids). Murein=peptidoglycan. |
| The Eukaryotic Cell Wall & Glycocalyx | Cell wall: Protozoa: pellicle, protein. Algae: cellulose. Fungi: chitin. |
| Flagella | Outside cell wall. Made of chains of flagelin filament w/ a hollow core. Anchored to the wall & membrane by the basal body & hook. |
| Flagella motion | Clockwise=tumbling. Counterclockwise=straight. Bacteria have sensors for food/toxins. Move toward or away (taxis). Flagella proteins are H antigens. |
| Arrangements of Bacterial Flagella | Peritrichous: all over. Monotrichous & polar: one on one side. Lopotrichous & polar: lots out of one location. Amphitricous & polar: 2 at ends of bacteria. |
| Spirochete (tightly wound shape) | Burrow deep into the tissue of organs. Move like a corkscrew. Bacteria that cause syphilis do this. They have endoflagella: embedded in cell. |
| Fibriae & Pili | Fimbriae allow attachment (may be 100s/cell). Pili are involved in motility & DNA transfer (1-2/cell). A crawl called twitching. |
| Prokaryotic Inclusion bodies | A lot like organelles. Membrane bound. Primarily used for storage. Exs. Magnetosomes: iron oxide. destroys H2O2. Magnets. Sense magnetic pull of Earth & their location in soil. Lipid inclusions store energy. Carboxysomes-CO2 fixation. |
| Endospores | Resting cells that can survive for >100 years. Resistant to desiccation, heat, chemicals. Bacillus, Clostridium (gram + bacteria). Sporulation: endospore formation. Germination: return to vegetative state. Imp for pathogenicity. Dif morphology. |
| Formation of Endospores by Sporulation | Stress signals. Spore septum begins to isolate newly replicated DNA & some cytoplasm. Plasma membrane surrounds. Spore septum surrounds isolated portion forming forespore. Peptidoglycan layer then spore coat forms. Freed from cell. |
| Endosymbiotic theory | Plants have same photosynthetic machinery as cyanobacteria. Mitochondrial energy system looks like proteobacteria. Prokaryotic ribosomes. Circular DNA. Flagella look like spirochete bacteria. |
| Microbe-Associated Molecular Patterns: MAMPS or PAMPS (Pathogen-) | Microbial patterns recognized by components of our immune system. Exs. Peptidoglycan, Techoic acid, LPS, 70s ribosome, Flagella, Capsules, Fimbrae, Pili. |
| The Plasma Membrane | Phospholipid bilayer. Peripheral, Integral, and Transmembrane proteins. Damage to the membrane by alcohols, quaternary ammonium (detergents), & polymyxin antibiotics causes leakage of cell contents. |
| Movement of materials across membranes | Diffusion, facilitated diffusion, Ion-coupled transport, ATP-binding cassette transporters, Group translocation. |
| Simple diffusion | Movement of a solute from an area of high concentration to an area of low concentration. |
| Facilitated diffusion | Solute combines with a transporter protein in the membrane. Specific & nonspecific transporters. Pore. |
| Antiport | Cells couple favorable reactions with unfavorable transport (large molecules or against a gradient). Opposite directions. |
| Symport (Ion-coupled transport) | Same direction. Uses gradient that already exists. |
| Active Transport | Requires a transporter protein and ATP. |
| Group Translocation | Requires a transporter protein and PEP. |
| Osmosis | the movement of water across a selectively permeable membrane from high water to low water concentration. |
| Osmotic Pressure | The pressure needed to stop the movement of water across the membrane. |
| Aquaporins | Let water in or out of cell. |
| General Characteristics of Viruses | Obligatory intracellular parasites. DNA or RNA. Protein coat (capsid). Some enclosed by envelope. Some have spikes. Most infect only specific types of cells in 1 host. Host range determined by attachment sites & cellular factors. |
| Virion | Nucleic acid (either DNA or RNA). |
| Capsid | Protein shell. |
| Nucleocapsid | Virion + Capsid. |
| Capsomers | Structural subunits of the capsid that self-assemble. Polyhedral (triangular faces) or Helical (spiral hollow core; long). |
| Morphology of a Polyhedral virus | Capsomeres in triangle shape around nucleic acid. Forms capsid. |
| Morphology of a Helical virus | Capsomeres wind around making a hollow tube for nucleic acid to be in. Capsid. |
| Morphology of a complex virus | Capsid (head) & sheath. Polyhedral & Helical. Typical of bacteriophages. |
| Taxonomy of Viruses | Family names end in -viridae (Retroviridae). Genus names end in -virus (Lentivirus). |
| Viral Species | A group of viruses sharing the same genetic information & ecological niche (host). Common names are used for species (Human immunodeficiency virus HIV-1, HIV-2). Subspecies designated by a number. |
| Growing Viruses | Viruses must be grown in living cells. Bacteriophages form plaques on a lawn of bacteria. Animal viruses may be grown in living animals or in embryonated egges or in cells (cell lines). |
| Culturing viruses | 1) A tissue is treated w/ enzymes to separate the cells. 2) Cells are suspended in culture medium. 3) Normal cells or primary cells grow in a monolayer across the container. Transformed cells or continuous cell cultures do not grow in a monolayer. |
| Virus Identification | Cytopathic effects (what makes the cell sick). Serological tests-detect antibodies against viruses in a pt. Use antibodies to identify viruses in neutralization tests, viral hemagglutination, & western blot. Nucleic acids-RFLPs, PCR. |
| Viral life cycle | Attachment: Viruses attach to a cell. Entry into cell. Biosynthesis: production of nucleic acid & proteins. Maturation: Nucleic acid & capsid proteins assemble. Release. |
| Viral Entry | Collision, adsoption, lignand/receptor interaction, then decoating (enter by fusion or phagocytosis) OR Ejection of nucleic acid. |
| Release of virus | Cell lysis (nonenveloped virus). Viral budding process (enveloped virus) |
| Lytic Cycle of a T-Even Bacteriophage | 1. Attachment 2. Penetration 3. Biosynthesis 4. Maturation (viral components assembled into virons) 5. Release (Host cell lyses. New virons released). |
| The Lysogenic Cycle of Temperate Phage (Lytic cycle usually induced by cellular stress) | 1. Attachment 2. Phage DNA circularizes 3. DNA integrates w/i bacterial chromosome by recombination becoming a prophage 4. Bacteria reproduces 5. Occasionally, the prophage may excise from bacterial chromosome by another recombination event. Lytic cycle. |
| Generalized Transduction | 1. Phage infects bacterial cell 2. Phage DNA & proteins made. Bacterial chromosomes broken down into pieces 3. Occasionally pieces of bacterial DNA are packaged in a phage capsid. 4. New bacterial cell 5. Recombination: genetic variation. |
| Specialized Transduction | 1. Prophage exists in galactose using host 2. Phage genome excises carrying gal gene 3. Phage released 4. Infects a cell that can't use galactose 5. Integrates into new host DNA 6. Lysogenic cell can metabolize galactose. |
| Multiplication of Animal Viruses | Attachment. Penetration by endocytosis or fusion. Uncoating by viral or host enzymes. Biosynthesis. Maturation. Release by budding or rupture. |
| CSF | An adult has 130 mL of CSF circulating. This has low levels of complement (antimicrobial substances secreted by the body) or circulating antibodies. |
| Inflammation | Memingitis: meninges. Encephalitis: Brain. Meningoencephalitis: Both. Sepsis=high risk for CNS infection due to leakage. |
| Bacterial Meningitis | More dangerous than viral. Initial symptoms: fever, headache, & stiff neck. Then nausea & vomiting. Diagnosis by gram stain & latex agglutination of CSF. Cephalosporins & vancomycin inhibit cell wall biosynthesis. Bacteria have capsules to protect them. |
| Neisseria meningitis (meningococcal meningitis) | Caused by N. meningitidis. Gram -, aerobic cocci w/ capsule. 10% of people are nasopharyngeal carriers. Begins as throat infection, rash. Common in kids <2. Vaccine. Mortality rate 9-12%. Deafness common. |
| Streptococcus pneumoniae Meningitis (pneumonococcal meningitis) | Caused by S. pneumoniae. Gram+ diplococcus. 70% of people are healthy nasopharyngeal carriers. Common in kids 1 mo-4 yrs. Mortality: 30% in kids, 80% in elderly. Vaccine. |
| Haemophilus influenzae Meningitis | Mostly in kids 6 mo-4 yrs. Gram-, aerobic bacteria, normal throat microbiota. Capsule antigen type b. Hib vaccine. Mortality rate 6%. |
| Listeriosis | Caused by Listeria monocytogenes. Gram-, aerobic rod. Usually foodborne, can be transmitted to fetus. Reproduce in phagocytes. Mortality rate 50%. Esp. dangerous to pregnant women. Can live in refrigerator. |
| Leprosy (Hansen's disease) | Caused by Mycobacterium leprae. Acid-fast rod that grows best at 30 deg. C. Grows in peripheral nerves & skin cells. Transmission requires prolonged contact w/ infected person. Tuberculoid (neural) leprosy & Lepromatous (progressive) leprosy. |
| Poliomyelitis (Polio) | Poliovirus. Transmitted by ingestion. Sore throat/nausea. Viremia may occur; if perisitent, virus can enter the CNS. Destruction of motor cells & paralysis in <1% of cases. Vaccine. |
| Arboviral Encephalitis | Arboviruses. Arthropod-borne viruses that belong to several families. Prevention: controlling mosquitoes. Four types: California, West Nile, EEE, WEE. |
| African Trypanosomiasis (African Sleeping Sickness) | Endemic in sub Saharan Africa. 2 stages: 1. fever, headaches, joint pain, itching, swelling of lymph nodes 2. Neurological phase: it invades blood brain barrier causing confusion, disruption of sleep cycle. Transmitted by Tsetse fly. Acute or chronic. |
| Treatment of African Sleeping Sickness | Prevention: Elimination of the vector. Eflornithine blocks an enzyme nexcessary for the parasite. Parasite evades antibodies through antigenic variation. |
| How Trypanosomes Evade the Immune system | Change outer surface proteins. Have around 100 types. Trypanosomes have life cycle stages in fly & in human. |
| Naegleria fowleri | Protozoan infects nasal mucosa from warm water: ponds, lakes, hot springs (stagnant pools). 98% mortality rate. Amphotericin B recommended. Headache. Grows & divides in brain & destroys tissues. Rare. |
| Chronic Fatigue Syndrome (myalgic encephalomyelitis (ME) | Unexplained fatigue that lasts at least 6 mo + 4 other symptoms. Experimental treatment promotes antiviral interferons (possible causes are Epstein-Barr or human herpes virus-6 HHV-6). |
| - Strand RNA virus (antisense strand) | 1. Attachment, entry & uncoating 2. RNA replication by RNA polymerase 3. Translation & synthesis of viral proteins 4. maturation & release. Never enters nucleus! |
| Herpesvirdae | Double-stranded DNA, enveloped viruses. Simplexvirus. Varicellovirus. Lymphocrytovirus. Cytomegalovirus. Roseolovirus. HHV-7. Kaposi's sarcoma. Some can remain latent in host cells. |
| Multiplication of DNA Virus | In nucleus. 1. Attachment, entry, uncoating. 2. Portion of viral DNA transcribed producing mRNA that encodes early viral proteins. 3. Viral DNA is replicated & some proteins made. 4. Late translation; capsid proteins synthesized 5. Maturation & release. |
| Retroviridae | Single-stranded RNA, 2 RNA strands, produce DNA. Use reverse transriptase to produce DNA from viral genome. Lentivirus (HIV) Oncogenic viruses-includes all RNA tumor viruses. Enter nucleus. |
| Multiplication of a Retrovirus (more info on slide) | Enters by fusion. Uncoating releases 2 viral RNA genomes & enzymes reverse transcriptase, integrase, & protease. DS DNA produced. Into nucleus & integrated into host chromosome as a provirus by integrase. Proteins processed by protease. Leaves cell. |
| Cancer | Activated oncogenes turn normal cells cancerous. Transformed cells have increased growth, loss of contact inhibition, tumor-specific transplant antigens, & T-antigens. The genetic material of oncogenic viruses becomes integrated into the host cell's DNA. |
| Oncogenic DNA Viruses | Adenoviridae, Herpesviridae, Poxviridae, Papovaviridae, Hepadnaviridae. Integration causes cancer. DNA or RetroRNA can integrate. |
| Oncogenic RNA viruses | Retroviridae. Viral RNA transcribed to DNA, which can integrate into host DNA. HTLV-1, HTLV-2 |
| Flavivridae | Single-stranded RNA, + strand, enveloped. Arboviruses can replicate in arthropods; include yellow fever, dengue, SLE, & West Nile virus. Hepatitis C Virus. |
| + Strand (Sense Strand) RNA virus | Doesn't travel to nucleus. Attachment, entry & uncoating. RNA replication by RNA polymerase. mRNA transcribed from - strand. Translation & synthesis of proteins. Maturation & release. |
| Orthomyxoviridae | Single-stranded RNA, - strand, multiple RNA strands. Envelope spikes can agglutinate RBCs. Influenzavirus (influenz viruses A and B), Influenza C virus. |
| The Influenza Virus | Hemagglutinin (HA) spikes used for attachment to host cells. Neuraminidase (NA) spikes used to release virus from cell. Spikes are proteins which change for dif viruses. Antigenic variation. |
| Influenza Serotypes | Proteins determine immune response. Serotypes vary by yaer. |
| Influenza Virus Antigenic shift | Changes in HA and NA spikes. Probably due to genetic recombination between different strains infecting the same cell. |
| Influenza Virus Antigenic drift | Point mutations in genes encoding HA or NA spikes. May involve only 1 amino acid. Allows virus to avoid mucosal antibodies. |
| Viral One-step growth curve | Acute infection when virons released from host cell. |
| Latent Viral infection | Virus remains in asympomatic host cell for long periods. Ex. coldsores, shingles. |
| Persistent Viral infection | Disease processes occur over a long period; generally fatal. Ex. Subacute sclerosing panencephalitis (measles virus). |
| Viroids | Only RNA, does not contain or encode proteins. Infect plants because they have an RNA polymerase that makes RNA from RNA. |
| Prions (Proteinaceous Infectious Particles) | Spongiform encephalopathies: Sheep scrapie, Crewutzfeldt-Jakob disease, Gerstmann-Strussler-Scheinker syndrom, fatal familial insomnia, mad cow disease. Inherited & transmissible by ingestion, transplant, & surgical instruments. |
| Resolution of the Human Eye | ~150 uM. Micro: small, skopos: to look at. |
| 1 millimeter (mm) | 10^-3 meter |
| 1 micrometer (um) | 10^-6 meter |
| 1 nanometer (nm) | 10^-9 meter |
| 1 picometer (pm) | 10^-12 meter |
| Eye Resolution | Dependent upon the distance between photoreceptors. |
| Microscopes | Use lenses to magnify images. Need contrast between the object & its surroundings. Wavelength must be smaller than the object of interest. |
| Resolution | The ability of the lenses to distinguish two points. Shorter wavelengths of light provide greater resolution. Max resolution of a light microscope is ~1,000x. |
| Numerical Aperture | How well a lens collects light. Function of an angle. |
| Compound Light Microscopy | The REFRACTIVE INDEX is a measure of the light-bending ability of a medium. Light may bend in air so much that it misses the small lens. Immersion oil is used to keep light from bending. |
| Simple microscope | Only one lens. |
| Compound Microscope | The image from the objective lens (you control) is magnified again by the ocular lens (by eye). Total magnification=objective*ocular. Ocular magnification almost always=10. |
| Oil Immersion Microscopy | Bends light more into lens. |
| Light Microscopy | Use any kind of microscope that uses visible light to observe specimens. Types: compound, darkfield, phase-contrast (standard), fluorescence, confocal. |
| Brightfield Illumination | Dark objects are visible against a bright background. Light reflected off the specimen does not enter the objective lens. |
| The Dark Field Microscope | Excludes the light that is unscattered (excludes the light that is used to illuminate). Specimen stand out with a lot more detail. |
| Phase Contrast Microscopy | Accentuates diffraction of light that passes through a specimen. Small phase shifts in light passing through a transparent specimen are converted into amplitude or contrast changes in the image. Phase shifts induced by refractive index of sample. Color. |
| Fluorescence Microscopy | Uses UV light. Fluorescent substances absorb UV light & emit visible light. Cells may be stained w/ fluorescent dyes (fluorochromes). Most widely used. GFP=Green Fluorescent Protein. |
| Confocal Microscopy | Cells stained w/ fluorochrome dyes. Short wavelength (blue) light used to excite the dyes. This light illuminates each plane in a specimen to produce a 3D image. Up to 100um deep. Expensive: big computer & heavy duty software. |
| Electron Microscopy | Shorter wavelength electrons gives greater resolution. Ultrathin sections of specimens. Light passes through spec, then an electromagnetic lens, to a screen or film. Specimens may be stained w/ heavy metal salts. Magnets focus e-s onto sample in a vacuum. |
| Transmission Electron Microscopy (TEM) | 10,000-100,000x resolution 2.5nm. Great for observing internal features of cells. Cells must be fixed and artifacts can be a problem. |
| Scanning Electron Microscopy (SEM) | An e- gun produces a beam of e-s that scans the surface of a whole specimen. Secondary e-s emitted from the specimen produce the image. 1,000-10,000x; resolution 2 nm. |
| Scanning Tunneling Microscopy (STM) | Scanned-Probe Microscopy. Uses a metal probe to scan a specimen. Resolution 1/100 of an atom. Max resolution we can get. |
| Atomic Force Microscopy (AFM) | Scanned-Probe Microscopy. Uses a metal-and-diamond probe inserted into the specimen. Produces 3D images. Take pictures of molecular structures. |
| Preparation of Specimens for Light Microscopy | Staining; Smear |
| Staining | Coloring the microbe with a dye that emphasizes certain structures. Usually kills it. Simple: acidic (-charge), basic (+charge) dyes. Negative stain. Gram stain. Acid-fast stain. Capsule stain, endospore stain, flagella stain. |
| What stain do you use on most bacteria? | Base (+) stain. Most bacteria have a -charge. |
| Preparing Smears for Staining | Live or unstained cells have little contrast w/ surrounding medium though researchers do make discovers by observing live specimens. |
| Smear | A thin film of a solution of microbes on a slide. Usually fixed (by alcohols or heat) to attach the microbes to the slide and kill them. |
| "Fixing Bacteria"-in contrast to the wet mount | Spread on slide & air dry. Fix. Air dry. Stain. Wash off stain. Blott off excess water. View under microscope. |
| The Gram Stain | Differentiates Gram- & Gram+ bacteria. Iodine is a mordant-binds crystal violet & helps it "stick." The decolorization disturbs the gram- outer membrane, the stain leaks out. |
| Gram Stain Steps | 1. Apply crystal violet dye 2. Apply iodine 3. Alcohol wash (decolorization) 4. Apply safranin (counterstain) Gram+ is purple. Gram- is pink. |
| Differential Staining | Acid-fast stain (mycoplasma). Endospore stain (C. botulinum) India Ink/Negative Stain (Gloeocapsa). |
| Atypical Cell Walls | Acid-fast: Like gram+. Waxy lipid. Mycobacterium, Norardia. Mycoplasmas: Only bacteria that lack peptidoglycan cell wall. Sterols in plasma membrane. Archaea: Wall-less or Walls of psudomurein (lack NAM & D-amino acids). |
| Acid-fast Cell Walls | Plasma membrane, peptidoglycans, arabinogalactan, mannosecapped lipoarabinomannan, plasma membrane and cell envelope-associated proteins, mycolic acids & glycolipid surface molecules. |
| Acid-fast Stain | Primary Stain: Carbolfuchsin (red). Decolorizing agent: Acid-alcohol (non acid-fast turn colorless). Counterstain: Methylene (blue). Stained waxy cell wall not decolorized by acid alcohol. -charge due to atypical +charged bacteria. |
| Special Stains | Used to distinguish parts of cells. Capsule, endospore, or flagella stains. |
| Negative stain for capsules | Cells stained. Negative stain for capsules. (Everything but capsule is stained). |
| Endospore (Spore) Staining | Primary stain: Malachite green, usually with heat. Decolorize cells: Water. Counterstain: Safranin. Used a lot to look for contamination in food. |
| Flagella Staining | Mordant on flagella. Carbolfuchsin simple stain. |
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